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Celiac.com 01/20/2024 - The tissue transglutaminase IgA antibodies (tTG-IgA) test is a crucial diagnostic tool for celiac disease. In individuals with celiac disease, the ingestion of gluten triggers an immune response, leading to the production of antibodies, including tTG-IgA. These antibodies target the tissues of the small intestine, causing damage and inflammation. The tTG-IgA test measures the levels of these specific antibodies in the blood. Elevated tTG-IgA levels are indicative of an active immune response to gluten and suggest the presence of celiac disease. This blood test is an essential component of the diagnostic process, helping healthcare providers identify individuals who may require further evaluation, such as genetic testing and an endoscopic biopsy, to confirm the diagnosis of celiac disease. Elevated tissue transglutaminase IgA antibodies (tTG-IgA) are primarily associated with celiac disease, but they can also be elevated in some other conditions. It's important to note that the presence of elevated antibodies alone doesn't diagnose a specific condition, and further clinical evaluation is needed. Conditions and factors that may lead to elevated tTG-IgA antibodies may include the following: Non-Celiac Gluten Sensitivity (NCGS) Wheat Allergy Inflammatory Bowel Diseases (IBD) Type 1 Diabetes Autoimmune Liver Diseases Rheumatoid Arthritis Thyroid Disorders Genetic Conditions Casein/Cow's Milk Intolerance Non-Celiac Gluten Sensitivity (NCGS) Although it doesn't involve the autoimmune response seen in celiac disease, NCGS can lead to symptoms similar to those of celiac disease and may be associated with elevated tTG-IgA. NCGS is characterized by gluten-related symptoms without the autoimmune response and intestinal damage seen in celiac disease. The exact mechanisms leading to elevated tTG-IgA in NCGS are not fully understood, but it's believed that gluten sensitivity in NCGS may still induce an immune response, even though it differs from the autoimmune process seen in celiac disease. The presence of elevated tTG-IgA in NCGS underscores the complexity of gluten-related disorders and highlights the need for further research to elucidate the underlying immune responses and mechanisms associated with different gluten-related conditions. Wheat Allergy Individuals with a wheat allergy may produce antibodies, including tTG-IgA, as part of the allergic response. Individuals with a wheat allergy may also exhibit increased tTG-IgA levels. Wheat allergy is an immune-mediated response to proteins in wheat, distinct from the autoimmune nature of celiac disease. The presence of elevated tTG-IgA in individuals with a wheat allergy is somewhat perplexing, as tTG is an enzyme involved in the pathology of celiac disease, and its elevation is not commonly associated with allergies. One possible explanation is that the immune response triggered by a wheat allergy might lead to some cross-reactivity or shared epitopes with components involved in celiac disease, causing an increase in tTG-IgA. However, the exact mechanisms behind this phenomenon are not well-elucidated, and more research is needed to understand the connections between wheat allergy and the elevation of tTG-IgA. It emphasizes the intricate interplay between the immune system and various wheat-related disorders, requiring further exploration to unravel the complexities of immune responses in these conditions. Inflammatory Bowel Diseases (IBD) Conditions such as Crohn's disease and ulcerative colitis can cause gastrointestinal inflammation, and elevated tTG-IgA levels have been reported in some individuals with IBD. Elevated tissue transglutaminase IgA antibodies (tTG-IgA) can also be observed in individuals with Inflammatory Bowel Diseases (IBD). IBD, which includes conditions like Crohn's disease and ulcerative colitis, involves chronic inflammation of the gastrointestinal tract. The link between IBD and elevated tTG-IgA is not as straightforward as in celiac disease, and the reasons behind this elevation in some IBD patients remain a subject of research. One hypothesis suggests that the chronic inflammation and alterations in the intestinal mucosa associated with IBD may lead to increased permeability of the gut barrier. This heightened permeability might allow gluten proteins to interact with the immune system in a way that triggers the production of tTG-IgA. The intricate relationship between IBD and tTG-IgA elevation underscores the complex interplay between autoimmune responses and gastrointestinal disorders, requiring further investigation to uncover the underlying mechanisms and clinical implications. Type 1 Diabetes Some individuals with type 1 diabetes may have elevated tTG-IgA antibodies, and there is an increased risk of celiac disease in individuals with diabetes. Elevated tissue transglutaminase IgA antibodies (tTG-IgA) can be found in individuals with Type 1 Diabetes (T1D), establishing a connection between these two autoimmune conditions. Both celiac disease and Type 1 Diabetes involve an autoimmune response, where the body's immune system mistakenly targets its own tissues. In the case of celiac disease, the immune system reacts to gluten, while in Type 1 Diabetes, it attacks the insulin-producing cells in the pancreas. The shared genetic susceptibility to autoimmune disorders could explain the co-occurrence of celiac disease and Type 1 Diabetes. The presence of certain genetic markers might predispose individuals to develop multiple autoimmune conditions. Additionally, environmental factors and common triggers in the immune response pathways could contribute to the simultaneous development of these disorders. Clinicians often monitor individuals with Type 1 Diabetes for celiac disease-related antibodies, including tTG-IgA, to identify and manage celiac disease early, highlighting the importance of understanding these interconnected autoimmune processes for comprehensive patient care. Thyroid Disorders Conditions such as autoimmune thyroiditis (Hashimoto's thyroiditis) and Graves' disease may be associated with elevated tTG-IgA antibodies. Elevated tissue transglutaminase IgA antibodies (tTG-IgA) can be associated with thyroid disorders, particularly autoimmune thyroid conditions such as Hashimoto's thyroiditis. Hashimoto's thyroiditis is an autoimmune disease where the immune system attacks the thyroid gland, leading to inflammation and potential impairment of thyroid function. The link between celiac disease and autoimmune thyroid disorders has been observed, suggesting a shared genetic predisposition for autoimmune conditions. Individuals with celiac disease may have an increased risk of developing autoimmune thyroid disorders, and vice versa. The interconnected nature of autoimmune diseases suggests that the immune system's response to gluten in celiac disease might trigger or exacerbate autoimmune reactions in other organs, including the thyroid. Monitoring thyroid function and related antibodies, such as tTG-IgA, is crucial in individuals with celiac disease to identify and manage potential thyroid complications early. Understanding these complex interactions between autoimmune disorders is essential for comprehensive patient care and effective management of associated health conditions. Autoimmune Liver Diseases Certain autoimmune liver diseases, such as autoimmune hepatitis and primary biliary cirrhosis, may be associated with elevated tTG-IgA antibodies. Elevated tissue transglutaminase IgA antibodies (tTG-IgA) may be detected in individuals with autoimmune liver diseases, particularly autoimmune hepatitis (AIH). Autoimmune hepatitis is a chronic inflammatory condition where the body's immune system erroneously attacks liver cells, leading to liver inflammation and potential damage. The connection between celiac disease and autoimmune liver diseases, although not fully understood, suggests shared autoimmune mechanisms. In some cases, individuals with celiac disease may experience immune system dysregulation that extends beyond the small intestine, leading to autoimmune reactions in other organs such as the liver. The presence of elevated tTG-IgA in individuals with autoimmune liver diseases underscores the complex interplay between various autoimmune conditions. Monitoring liver function and related antibodies is essential for comprehensive healthcare in individuals with celiac disease, as the autoimmune cascade can impact multiple organs. Understanding these connections aids in early detection, proper management, and improved overall outcomes for individuals with autoimmune liver diseases and concurrent celiac disease. Genetic Conditions Some genetic conditions, such as Down syndrome, may be associated with an increased prevalence of celiac disease and elevated tTG-IgA. Elevated tissue transglutaminase IgA antibodies (tTG-IgA) in individuals with genetic conditions such as Down syndrome can be attributed to the increased prevalence of autoimmune disorders in this population. Down syndrome, characterized by the presence of an extra copy of chromosome 21, is associated with a higher susceptibility to autoimmune conditions, including celiac disease. The genetic link between Down syndrome and celiac disease suggests a shared vulnerability to immune dysregulation. Individuals with Down syndrome may exhibit an elevated risk of developing autoimmune disorders due to alterations in immune system function associated with the genetic anomaly. The complex relationship between genetics and autoimmune responses underscores the importance of monitoring individuals with Down syndrome for various health conditions, including celiac disease. Early detection and management of celiac disease in individuals with Down syndrome are crucial for optimizing their overall health and well-being, considering the potential impact of untreated celiac disease on nutrient absorption and long-term health outcomes. Rheumatoid Arthritis Elevated tTG-IgA levels have been reported in some individuals with rheumatoid arthritis. The presence of elevated tissue transglutaminase IgA antibodies (tTG-IgA) in individuals with rheumatoid arthritis (RA) can be linked to the complex interplay between autoimmune disorders. Rheumatoid arthritis is a chronic inflammatory condition primarily affecting the joints, but it is increasingly recognized that individuals with RA may have an elevated risk of coexisting autoimmune diseases, including celiac disease. The shared genetic predisposition and immune dysregulation mechanisms contribute to the observed association between RA and elevated tTG-IgA. In the context of rheumatoid arthritis, the immune system mistakenly attacks the joints, leading to inflammation and joint damage. This dysregulated immune response may extend beyond the joints and manifest as an increased susceptibility to other autoimmune conditions, such as celiac disease. The identification of elevated tTG-IgA in individuals with RA underscores the importance of comprehensive health assessments in autoimmune disorders, as coexisting conditions may impact the overall management and prognosis of these individuals. Regular monitoring and collaboration between healthcare providers specializing in different autoimmune diseases are crucial for a holistic approach to patient care. Casein/Cow's Milk Intolerance Recent studies have shown that elevated tTG-IgA levels have been reported in some individuals with casein/cow's milk intolerance. Conclusion While it's true that elevated tissue transglutaminase IgA antibodies (tTG-IgA) can be associated with various conditions beyond celiac disease, including autoimmune disorders and genetic conditions, the tTG-IgA test remains a valuable tool in the diagnosis of celiac disease. In individuals with celiac disease, there is a specific immune response triggered by the ingestion of gluten, a protein found in wheat, barley, and rye. People with celiac disease often have higher levels of tTG-IgA in their blood due to the immune system's reaction to gluten. When gluten is ingested, individuals with celiac disease produce antibodies, including tTG-IgA, which target and attack the tissues of the small intestine. The elevated tTG-IgA levels are indicative of this immune response and the damage occurring in the intestinal lining. However, it's important to note that the interpretation of tTG-IgA levels should be done in the context of the individual's overall health, medical history, and the possibility of other conditions. A definitive diagnosis of celiac disease typically involves a combination of blood tests, genetic testing (HLA-DQ2 and HLA-DQ8), and, in some cases, an endoscopic biopsy of the small intestine. In summary, while elevated tTG-IgA levels are a common feature in celiac disease, the diagnosis involves a comprehensive assessment, and healthcare providers consider various factors to ensure accurate identification of the condition. It's crucial to interpret antibody test results in the context of the individual's clinical symptoms, medical history, and additional diagnostic tests. If tTG-IgA antibodies are elevated, further evaluation by a healthcare professional, typically including endoscopic procedures and biopsies, is often necessary to confirm or rule out celiac disease.

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 04/05/2019 (Originally published on 10/19/2009) - Gluten intolerance caused by celiac disease, or non-celiac gluten sensitivity, may affect virtually any part of the body. A culprit in multiple health disorders, gluten intolerance is a major driver of health care delivery and associated costs. While this may seem to be an outrageous claim, a review of the many ways in which gluten intolerance can adversely affect the body will illustrate this point. So, let’s work our way down from head to toe. Celiac Disease Can Cause Hair Loss Normal, healthy hair is usually glossy and thick. An autoimmune disorder known as alopecia areata results in abnormal loss of hair, either in patches, or totally, and is one of many autoimmune disorders associated with celiac disease. Malabsorption severe enough to cause malnutrition can also result in thin, sparse, fragile hair. One of the outward signs of hypothyroidism is thinning hair and a loss of the outer third of the eyebrow; hypothyroidism is strongly associated with celiac disease. How Celiac Disease Affects the Brain Now let’s look at the brain. There are, unfortunately, a large number of neurological disorders associated with gluten intolerance and celiac disease, including narcolepsy, depression, ADD/ADHD, Autism Spectrum Disorders, and schizophrenia. There are also movement and balance disorders associated with gluten intolerance, including ataxia - the inability to coordinate movements and balance (gluten ataxia, celiac ataxia, some cases of sporadic idiopathic ataxia). In some cases, when symptoms are severe, this disorder mimics other disorders such as Parkinson’s, Normal Pressure Hydrocephalus, and even Alzheimer’s disease. Headaches Common in Celiac Disease Headaches are a very common symptom of wheat allergy, as well as gluten intolerance. Migraines are common in those with celiac disease and gluten intolerance, as are sinus headaches. These symptoms often decline dramatically after excluding gluten grains from the diet. Sinus problems are common in those with celiac disease, gluten intolerance, and sensitivity to dairy products as well, and are often reversible by making dietary changes. Some people with celiac disease seem to have an altered, highly acute sense of smell – for unknown reasons. Night Blindness from Vitamin A Deficiency Night blindness associated with vitamin A deficiency is reversible when malabsorption is resolved and with the addition of a vitamin A supplement. Xeropthalmia, or chronic, often severe, dry eyes, is also related to severe vitamin A deficiency. It is rare in developed countries, but can be found in some people with malnutrition due to celiac disease. Canker Sores Common in Celiac Disease Apthous stomatitis is the name for the mouth ulcers associated with food allergies and intolerances, and is strongly associated with celiac disease and gluten intolerance. Even people who do not have gluten sensitivity get these once in a while but in those with gluten intolerance they are more frequent and especially long-lasting. Dental Enamel Defects Can Indicate Celiac Disease While they are usually identified in childhood, they can continue to cause problems throughout life, because they often lead to more frequent dental cavities. Halitosis, or bad breath, is a reflection of our internal environment and gastrointestinal health, and is often present in those with untreated celiac disease, gluten sensitivity, or gut dysbiosis – an upset in the balance of our internal microorganisms caused by poor diet and other factors. And, one of the autoimmune disorders strongly associated with celiac disease, and one of the most prevalent is Sjogren’s syndrome, which impairs the normal production of body fluids like tears, saliva, and vaginal secretions. Strong Link Between Celiac Disease & Eosinophilic Esophagitis Following the path our food takes to the stomach, we can look for effects in the esophagus too. Eosinophilic esophagitis is a rarely encountered inflammation in the tissue of the esophagus which makes swallowing painful and difficult and can result in bleeding ulcerations. When doctors do see it, they sometimes test for celiac disease, since there is a strong correlation. Fortunately, in cases where this condition is caused by gluten intolerance, this painful chronic disorder clears up on a gluten free diet, too. GI Complaints Common in Celiac Patients Now we’re getting to the area most people associate with gluten intolerance – the gastro-intestinal system. In the past, celiac disease was usually described as causing gas, diarrhea, bloating, discomfort, cramping, and malabsorption. But as you’ve already seen above, there is a whole lot more to this disorder, and we’re only halfway to the toes. Celiac Can Be Misdiagnosed as IBS In addition to the above symptoms, the body’s reaction to gluten can cause inflammation anywhere, but a common location is in the illeo-cecal junction and the cecum. This can sometimes be confused with appendicitis, or ovarian pain or an ovarian cyst in women experiencing right-sided lower abdominal discomfort. Irritable bowel syndrome is suspected to affect at least 10-15% of adults (estimates vary). It is differentiated from IBD, or inflammatory bowel disorders (which include Crohn’s disease and ulcerative colitis). But, taken together, there are an awful lot of people out there with uncomfortable gut issues. One fact to consider is that many of those with celiac disease were previously, and wrongly, misdiagnosed with IBS before discovering they actually had celiac disease. Kidney & Urinary Problems Let’s take a look at the urological system. Even though gluten from the food we eat isn’t directly processed here, can it still be affected? The answer is yes. Kidney problems in association with celiac disease are well documented, including oxalate kidney stones. Bladder problems are increasingly shown to be responsive to a gluten-free diet. This is kind of my specialty and I would estimate that about a quarter of those with interstitial cystitis, and many people with recurrent urinary tract infections, have a sensitivity to gluten. Even prostate inflammation in some men can be triggered by eating gluten grains. Adrenal Fatigue in Celiac Disease Sitting just atop the kidneys are our adrenal glands. They have a difficult job, helping to direct our stress response system, our immune system, and our hormone output, and controlling inflammation in the body. Every time we experience a reaction to gluten, and our adrenals respond by sending out a surge of cortisol to help control inflammation, we are depleting our adrenal reserve. When this happens chronically, over time, our adrenal system cannot keep up and becomes fatigued. Symptoms of adrenal fatigue have far-reaching consequences throughout the body, including, of course, feeling fatigued and run down. But, adrenal fatigue can also affect our hormones, our blood sugar regulation, our mental acuity, our temperature regulation, and our ability to cope with food allergies, environmental allergies, and infections. Celiac Disease Common in Hepatitis Patients Can the liver, the body’s largest internal organ, be affected by gluten intolerance too? One example is autoimmune hepatitis, in which can be untreated celiac disease can be found in large numbers. Early screening testing for celiac disease is now strongly recommended for patients diagnosed with autoimmune hepatitis. Gluten Intolerance, Pancreas and Blood Sugar The pancreas, which is key in blood sugar regulation, is highly affected by gluten intolerance. Autoimmune disease triggers the development of Type I Diabetes, and is becoming more closely associated with celiac disease. Testing for celiac disease is now becoming a routine part of examination when a child develops Type I Diabetes, and now that physicians are looking for celiac disease in juvenile diabetes, they’re finding it with greater frequency. Blood sugar regulation problems are also associated with non-diabetic hypoglycemia in those with gluten intolerance, and appear to resolve with a low-glycemic gluten free diet. Celiac Disease Can Affects Limbs and Extremities So, we’ve covered most of the body’s major internal systems. Now, let’s look at the extremities, our upper and lower limbs, where gluten-associated problems are also found. Ehlers-Danlos Syndrome, a collagen disorder resulting in shoulder, elbow, and wrist joints that dislocate easily (and other characteristics) is a genetic disorder that may also be associated with celiac disease. I had mild symptoms of this disorder as a child, but never knew it had a name until I ran across it recently. With a child who has this disorder, a simple game of swinging a child by the arms, or swinging a child between two sets of their parent’s arms, can result in a trip to the emergency to put their joints back into proper alignment. This is not to say that a reaction to gluten causes this genetic disorder, but that if you have a personal or family history of Ehlers-Danlos Syndrome, and symptoms that may be related to celiac disease, you should consider being tested. Arthritis Associated with Celiac Disease Rheumatoid arthritis is another of the autoimmune disorders associated with celiac disease, and often affects the fingers with crippling joint deformation. Other joints in the body can also be affected. Scleroderma is another terribly disfiguring and sometimes fatal autoimmune disorder affecting every part of the body. It is often first identified in the extremities, particularly the fingers. In scleroderma, normal tissue loses it’s flexibility as the body’s autoimmune response produces inflammation and an overproduction of collagen. Collagen is the tough fibrous protein that helps form connective tissues including tendons, bones, and ligaments. Excess collagen is deposited in the skin and body organs, eventually causing loss of function. Scleroderma can be associated with celiac disease. Skin Conditions Common in Celiac Patients The arms and legs are also common spots for yet another autoimmune disorder, psoriasis, to develop. Some patients with psoriasis are responsive to a gluten-free diet, but unfortunately, not everyone. Another skin condition that often shows up on the arms is dermatitis herpetiformis (DH), although this itchy blistering skin rash can occur in other places as well. Common sites are the backs of the elbows and the backs of the knees, or on the lower legs. Peripheral Neuropathy Common in Celiac Disease Peripheral neuropathy is a disorder that results in numbness, tingling, and sometimes severe nerve pain in the extremities. Finger, hands, toes, feet, and lower legs may all be affected. Although usually associated with diabetes, peripheral neuropathy shows up fairly frequently in those with celiac disease, and is fortunately reversible on a gluten free diet supplemented by B-vitamins and some specific amino acids. Peripheral neuropathy is usually associated with older people, but some of the cases I’ve observed recently have been in very young children who had severe malabsorption issues. Fortunately they healed quickly and their neuropathy symptoms resolved completely. Malabsorption and Vitamin Deficiency There a few last symptoms related to malabsorption that tend to show up in those with celiac disease or gluten intolerance. Easy bruising and bleeding, either due to a deficiency of Vitamin K, or to an autoimmune platelet disorder, is one. Rickets, or osteomalacia – a softening of the bones in the legs related to vitamin D deficiency – is another. As we said before, inflammation goes along with celiac disease and gluten intolerance, and a common site for inflammation is the lower extremities. Sometimes this can be profound, and trigger doctors to think heart disease, but it’s often unresponsive to Lasix and other diuretics. This condition, too, may also clear up on a gluten-free diet. As for me, I’ll be happy to be gluten-free, from head to toe.

Celiac.com 11/05/2021 - This is going to be a bit different from most of your medical lectures, I think. I hope you are up for “different”. If nothing else, the hard copy in your conference notes will give you something to read on the plane home. “Hmmm—which metaphor do I use to best illustrate the fate of conventional medicine as we now know it? Which one will give the clearest vision of the dramatic paradigm shift that is now taking place, one that will change the way we practice the art of healing for the rest of man’s days? Which will they grasp, take to heart, and run with to share with their clients, patients, and loved ones, to give them the good news—the fabulous news—this ‘gospel’ of medicine: That we are in sooooooo much more control of our health destinies than we have ever believed, certainly more than we have ever been told? This is awesome news. But how do I take them from the deception that we are “genetically-flawed organisms at the mercy of man’s mechanical and pharmaceutical creations” to the truth that we reap what we sow? Yes, even in medicine, that timeless principle applies. But once again, this is GOOD news.” Melodrama??? Is this opening statement simply a gimmick to get the attention of the audience? I personally don’t think so—but I hope it worked. It is the truth. We are all witnessing, at this very moment, the most important shift in medicine of all time as far as I can see. We should be extremely excited to be alive to observe this phenomenal event firsthand, especially those who have been waiting for years to see this transition occur as many of you have. Certainly, there have been many who have known the folly of long-term symptomatic medication: taking aspirin for fevers caused by viruses, stopping intestinal symptoms at all costs, and “relieving” the airway obstructions of nasal congestion and bronchoconstriction that were designed to limit the offending agents that caused the symptoms in the first place. “Oh, now you’re sounding like one of those holistic nuts!” Yup. And their wisdom has been suppressed long enough. The approach that the body never makes mistakes and that all symptoms serve a purpose has been buried long enough—too long—and it is time for it to be resurrected. So, on to our first metaphor. Man, I love Tolkien. What a phenomenally wise guy, his epic tales overflowing with truth and wisdom about man’s struggle with himself and the forces-at-be. And the conflict for the possession of Middle Earth serves as a fantastic parallel to the one that we face everyday, with every bite and every breath—and every pill—in the battle for our health. There are many foes and there are huge towers that loom over the battlefield, housing those that create the enemy and direct them into our fields. One of these towers was constructed by men and the forces that drive them in what will be seen as a vain attempt to control man’s medical plight through the use of “magic”, potions as they were once called, to reverse symptoms that came upon the unfortunate victims of illness. “Do you have fever? Not any more. We have a pill for that. Do you have heartburn? Not anymore. We have a bunch of pills for that. Do you have fibromyalgia? Well, we have lots of pills for that one. And, they work ‘OK’, but you will still suffer a bit—as your bank account dwindles. Do you have cancer? Well, we have soooo much that we can do, but it is a bit of a crap-shoot. You may survive your particular form of this disease with therapy or you may die actually sooner if we treat you. On the other hand, you may conquer this one but die of a different cancer. We won’t really know ‘til we try.” Folks, we are in the year 2005 as I write this piece. We have now placed man-made landers on the moon, Mars, and Titan—one of the moons of Saturn, on the other side of the asteroid belt and Jupiter (Wow!)—but we still don’t know that it is total folly to artificially kill a fever that our body produces solely to control the virus that caused it. Yes, we are still in the Dark Ages of medicine, so the Lord of the Rings analogy is very appropriate. We might as well be wearing animal skins to work instead of lab coats. If we don’t know that it is totally insane to stop a vital fever then we certainly can’t see that acid blockers unleash Helicobacter pylori, (who has been cultured from atherosclerotic plaques of coronary and carotid arteries) or that some of the immunosuppressive elements of cancer “therapy” are counterproductive when it comes to fighting all of the viruses that caused the cancer to begin with. (Just thought I’d quickly throw in a little actual medicine at this point.) But—BUT—here’s the cool thing. We have just been through the battle at Helm’s Deep. For you Tolkien fans, you know that this was a huge turning point in J. R. R. Tolkien’s portrayal of the battle for Middle Earth. The forces that were bent on the destruction of mankind were coming against the remnants of man, who were hold-up in a fortress built into a mountain. It was a seemingly solid foundation from which to defend against the oncoming hordes, but the numbers and armaments of the enemy were potentially devastating. As the evil forces approached and the battle ensued, it appeared hopeless for man, battling side by side with elves (angels) and dwarfs. The leaders of those in the fortress decided to ride out to meet the enemy, a valiant move but one that seemed certain to seal their doom. But then, over the hill—in a flash of light—came Gandalf and a tremendous army on horseback, who divided the enemy, slaying many and sending the remainder running back to their towers to recover and regroup. Victory was man’s, for the moment. We dodged a bullet as they say today. But shortly, the real battle was to begin—the final battle for Middle Earth and the ultimate survival of mankind. Oh, how myth puts things in perspective, eh? As a wise author named John Eldridge just wrote in his book Waking the Dead, myths are not simply fictional stories made up to entertain us. They are poignant tales that illustrate timeless truths. They paint mental pictures of these truths that we can draw upon to visualize things that we know to be true in our hearts. They give us faith, hope, and strength to go against what often seem like insurmountable odds to accomplish vitally important tasks and reach our goals. In those myths, we win Helm’s Deep against all odds; Cinderella rises from the ashes to marry the Prince; the Lion King grows up, remembers who he is, and takes his rightful place in the Kingdom; Fiona finds out that she would rather be an ogre and live happily ever after with Shrek than take her “rightful” place in her previous world. They all illustrate how man’s undying spirit can help conquer those circumstances that would hold him back. In my mind, nothing illustrates our struggle to learn the truth about medicine (and other life lessons) better than Tolkien’s trilogy. All of the elements are there, including things “seen” and “unseen”. It is the classic struggle involving good and “evil”, with man and his knowledge, beliefs, and shortcomings all working together and in opposition to produce the battle of—and for—our lifetime. All of the players are there: the wise masters; those that were seduced by “the dark side”; elements of greed, ignorance, and lust for power; and the undercurrent in which man searching desperately for truth, wisdom, and justice and the reason that all of this is taking place. “So, enough of the stage-setting.” you might be saying. “How in the world did you get Helm’s Deep out of the current medical situation in which we find ourselves and why all of the ‘prophetic’ references?” Well then, let’s get to it. We’ll start with a news flash. A relatively small band of men have finally understood the vital importance of—this is so cool—FOOD in our health. Wow! What year is it again? How long have we been saying, “You are what you eat?” But, how many have understood this and grasped the full meaning of that statement and what has unfortunately become a worn out cliché’? Many think in limited terms, I’m afraid, supposing that this expression means things like “eat your broccoli” or “don’t eat too much saturated fat”. Little do they know that the actual staples of their diet are harming them with every bite and setting the stage for most of the plagues that will befall them. When we add in the man-made chemicals, preservatives, colorings, and flavor enhancers, the self-induced nature of our suffering should become readily apparent. A whopping 75% of the calories in the Standard American Diet (appropriately abbreviated the S.A.D.) come from the number one and number two human, dog, and cat food allergens: cow’s milk and wheat. Why they are the top allergens and why soy and corn join them to round out the top four will be the main topics of this discussion. But as if this is not bad enough, 90% of prepared human foods have hydrogenated oils in them and 60% have MSG (monosodium glutamate), which we will be talking about very shortly. Throw in things like aspartame (a known neurotoxin and MSG’s evil twin), tons of sugar and salt, preservatives, chemicals, estrogens, pesticide residues, and more and you have a pretty good start on how we arrived at Helm’s Deep. When we see that the vast majority of pet foods are made with their main allergens, then we can understand why these little angels (elves) and dwarves are fighting right along side of us. Oh, and we can’t forget the horses. They are vitally involved in this battle. But, the real question (and this is huge) is “Why are cow milk and wheat the number one and two human, dog, and cat food allergens?” The answer is so simple that it is literally stupefying. There are substances in these “foods” and the other primary food allergens (soy and corn) that do physical harm to the intestinal tract, thereby eliciting an immune response. Part of this response is intended to go off to distant locations (skin, ears, lungs, brain, etc) to warn us that the damage is taking place. Yes, the enemy is sneaky and their initial attack on the headquarters of our camp is cloaked in secrecy. But, those with their eyes open should see the smoke rising from that assault. In cow’s milk the culprit is casein, a very powerful glycoprotein, from which they make waterproof industrial adhesives. “What?” Yes, they make GLUE from casein. Who’s picture is on the bottle of a very popular brand of household glue, one that the kids could eat in elementary school if they had a craving for it (which we will also cover)? Yep, a well-known dairy company makes that glue and the cow is on the label. It is made from casein. And, it DOES stick to your (and your pet’s) gut, primarily that first stretch of the intestinal tract known as the duodenum, keeping this vital section of bowel from functioning optimally. Its adhesive properties are advertised in the form of a moustache in the ever-popular “Got glue?” ads. Stick out your tongue after drinking milk. Yuck! Is it really a stretch to think that it sticks to our intestinal tracts? The thinking person is saying, “But the stomach breaks it down, doesn’t it?” The bad news is that, even with the tons of acid it produces—and the heartburn and chronic gastritis that follows—the glue still survives to reach the duodenum. (Only the fermentation process that takes place in the fore stomachs of the ruminant destroys this glue.) Who knows this and how do we know? Most doctors both know and don’t understand this. (“Huh?”) It’s a conundrum to me, too. How can they know to tell you not to take certain medications with milk because it will block the absorption of that drug and not know that milk physically blocks other things at the same time? How can some pediatricians tell new moms not to give cow milk products until the baby is on an iron-rich diet and not see that this same milk blocks iron absorption in adults, contributing to the fact that iron-deficiency anemia is the number one nutritional deficiency in the world, including in these United States—the red-meat-consumption capital of the world. How can that be? Simply stated, we are not absorbing what we consume. And now we know EXACTLY why, don’t we? But, cow’s milk and casein are only the beginning. (Note: Why do I keep specifying cow’s milk? Here is the neat thing: goat milk is nearly devoid of casein, which is real reason why goat milk is considered the “universal foster milk”—and why the Greeks elevated the goat into the heavens—for the milk it gave. All mammals could be successfully raised on goat milk. BUT, feed those same infant mammals cow‘s milk and watch how many come apart at the seams. The casein is the culprit, NOT the lactose. Goat‘s milk has plenty of lactose. So much for that deception.) Here is the important thing. The other “foods’ that coat (and subsequently damage) the intestinal villi—and the ONLY ones that do this along with casein—are gluten, soy, and corn. These are the big four or the “four horsemen of the apocalypse” as I now like to call them. And it is man and animals against casein, gluten, soy, and corn as the title implies. The strongest evidence of their potential harm is found in the fact that all of these food elements are used to make adhesives—powerful adhesives. Casein, gluten and soy are the strongest, stickiest, and most powerfully antigenic glycoproteins while corn is a slightly less powerful but nonetheless very significant player (especially the corn that we have recently created). They put cars together with the super-glues manufactured from soy protein. They make waterproof industrial adhesives from casein and gluten that are used for numerous purposes ranging from the glue on stamps and envelopes to putting metal together. But, the “best” they can do with corn glues is to put cardboard boxes together. So, we see why the FDA and veterinary lists of food allergens are what they are: in order, the (primary) food allergens are cow’s milk, wheat, soy, and corn. (We will discuss “secondary” allergens in a moment.) Soy could become number one—if that were possible. Fortunately, there are too many soy opponents who will keep this from happening. Now, here is what should really grab attention of veterinarians and (hopefully) not let go. Talk about hindsight being 20:20. When I graduated from vet school 26 years ago, dog foods were corn-based. (Keep in mind that corn has been modified to “death” over the past 25 years. Ever hear the term “hybrid corn”? Do you remember the Starlink /CRY9C corn scare a while back and how Taco Bell took the fall for that one? You only heard the beginning of that story.) The bottom line is that corn was bad enough and was, in retrospect, causing so many of the problems that we saw back then, especially in the “trouble breeds”: the German shepherd, Poodle, Cocker, Shar Pei, some giant breeds, and the Irish setter. (Remember when there were Irish setters around? We’ll be getting to that soon.) But—BUT—when we started adding wheat to the diet of pets about ten years later, we effectively landed the single-most devastating blow to veterinary health that we had struck since adding a milk coating to the puppy and kitten chows. Don’t let that last part slip past you, either. The cow’s milk coating we had on the growth formulas was a HUGE problem that we are just now seeing the vital importance of. In a recent medical study, researchers in human medicine found that our children that ingested cow’s milk in the first five days of life had a staggering 40-50 times higher rate of asthma, type-1 diabetes, and juvenile-onset rheumatoid arthritis when compared to the general population. Oh, no! How could that be? You need to remember what is going on in the gut and immune system of the newborn during the first five days of life as well as understand the concept of “lectins”—antibody-sized glycoproteins derived from the big four—to really grasp the importance of this cataclysmic mistake. Much of this particular issue is outside of the time restraints of this presentation but I think you will find that this “fun fact” fits right into the grand scheme of things. We will discuss lectins a bit later, however. So, we added wheat to the pet foods about 16 years ago. Why? Did we not know better? Yes, we did. Veterinary texts in print at that time boldly listed cow milk and wheat as the leading food allergens. So, why did we do it? (Hmmm—Remember those powers and principalities I alluded to in the opening comments. Their two most formidable manifestations are greed and ignorance.) Actually, there was a geopolitical phenomenon that occurred at that time. We had a “wheat glut” develop in this country as a result of numerous factors, including the fact that China became the number one grower of wheat in the world and thereby stopped importing it from us (an amazing transition in their diet which has its own prophetic implications). We had more wheat in this country than we knew what to do with (and we are repeating history with SOY right now. There is no new thing under the sun. Ecclesiastes 1:9). Therefore, wheat became cheaper than corn and the pet food companies started making kibble from wheat instead of corn. So easy to see—in retrospect. The fact is that I remember that time now like it was yesterday. I was practicing in California and suddenly my colleagues and I were talking about how sick dogs and cats were rather than our golf games when we went to lunch. It is now a well-defined moment of time in my memory that still shocks me when I think about it. Man, talk again about 20:20 hindsight. Suddenly, every dog had allergies, immune-mediated diseases, and cancer, not just the usual suspects. When I went to school the subject of allergies (atopy) was just another lecture, not the lecture. In an instant, the mutts from the pound were just as riddled with allergies as the pure-breeds. The old adage of “Heinz 57” dogs being healthier than pure breeds was becoming less and less true. Breeds like the Golden retriever were turning into money pits and their owners were saying things like “I love this breed but I can’t afford to have another one.” You as veterinarians remember this all happening, don’t you? If not, you may be too young or just need your memory jogged—or your glasses adjusted—as did some of my educators. I was at an orthopedic seminar recently put on by the guys who taught me at Auburn University. They were concentrating on the topic of juvenile bone diseases and the same breeds kept popping up on the slides: the Rottweiler, the Lab, the German shepherd, the Rottie again, another Lab, another Lab, and yet another Lab. You get the picture. They also mentioned how they had learned through experience that the puppy chows were harming these dogs more than the adult foods. They weren’t sure exactly why that was so but they no longer recommended the “high-powered” puppy foods for rapidly growing breeds that were prone to these conditions. I was squirming in my chair like a four year old that needed to go to the restroom. After the lecture, I approached one of the instructors (one of my favorites of all time—still is) and asked him a question. “Where are all of the Irish setters these days? I noticed that you don’t have them up there in your slides anymore,” and I smiled a really big, leading smile. He said, “I don’t know. Now that you mention it, we don’t see that breed much anymore, do we? Why do you ask? Do you know why we don’t see them?” (Chuckle, chuckle.) I said “As a matter of fact, I do know why they’re not around much anymore. That’s what happens when you feed a celiac lots and lots of wheat.” (Blank stare). I asked, “Do you remember what celiac disease is?” He thought for a pretty long moment and said that he didn’t. It sounded familiar but he couldn’t recall. I reminded him that celiac disease was gluten intolerance, an immune-mediated reaction to gluten in wheat, and that the Irish setter was the only breed KNOWN to be afflicted with this condition in the veterinary literature. I went on to explain how we transitioned from corn to wheat after I graduated and that once we did, the Irish setter became nearly “extinct”—end of story. He was truly amazed at my insight. As people were starting to crowd around him, I told him that this was just the tip of the tip of the tip of the iceberg and that I would talk to him more about it later. I went on to compose a five-page letter on my laptop that day and give it to all of the lecturers at the end of the session, explaining how this had become my “mission” (and that this was going to be the contribution that the Upjohn representative was “expecting” when he handed me the Upjohn Award for outstanding senior student in small animal medicine—twenty-some-odd years late). I never heard from any of those instructors again, despite follow-up Emails. Why didn’t they see the vital importance of what I was trying to share with them? Why didn’t they see the link between celiac disease, the demise of certain breeds, and the fact that puppy chows were worsening juvenile bone diseases? It was right in front of their faces. Are we all that blind? Have we all had the brains washed right out of us in medical schools? Do we really think we know everything when, in fact, we understand very little and are confounded by the knowledge that we do have? Here is the key!!! As lecturers (and preachers) are fond of saying, “If you get one thing from what I say today then please get this.” The duodenum is “Pandora’s Box”. There. Got it? You can go home now. LOL. What? You don’t understand? I’ll say it more slowly. “The duodenum—is—Pandora’s—Box.” Of course you don’t understand—yet! But you will and this little gimmick will help to keep it in your frontal lobe, I hope. Why do I call the duodenum “Pandora’s Box”? Because, once you “open” it (damage it), you unleash the plagues—and potentially all of the plagues—that can befall man and animals. “Now wait a minute”, you might say. “I have been following this up to now but you are waaaay over the top now.” Hold on. This is going to be good—really good. The sad and startling fact is that I have yet to meet a health professional (MD, DVM, or nurse) that has been able to tell me what the duodenum ABSORBS. In fact, I have had numerous casual conversations with members of all of these professions during which they looked me in the eye and boldly stated that the duodenum absorbs “nothing”. Then, once I remove the dagger from my heart (not throwing stones, of course, because before five years ago, I didn’t know either), I go on to explain that the duodenum does nothing less than absorb the vast majority of our calcium, iron, iodine, B complex, vitamin C, zinc, boron, lithium, chromium, magnesium, manganese, blah, blah, and blah. In fact, it absorbs just about everything but our calories, proteins, fats, and fat-soluble vitamins (which is a lot of course). The amazing fact is that 95% of our vitamin D activity takes place in the proximal one-third of our duodenum, where the initial and majority of damage caused by the “big four” glue-foods take place. Yes, the “glue foods” (as I like to refer to them) leave the stomach—glug, glug, glug—and coat the villi of the duodenum (and jejunum), especially the first one-third of the duodenum. Then, those glycoproteins from the gluten grains (wheat, barley, and rye), casein, soy, and corn induce an immune response in susceptible individuals. Certainly, not all people or pets have an immune response to these glues, but according to recent studies, the incidence is so much higher than once thought that anyone who understands this should have the same medical “revelation” that I have had—that we have found the “mother lode”. When I was diagnosed as a celiac 5 years ago, it was considered a “rare disorder occurring in less than 1:5,000 people”. No wonder doctors (and veterinarians) had forgotten about it. But, in the first week of study about my new-found condition—the one that explained everything that was currently plaguing me and all that had been wrong with me since I could remember—I found that they were diagnosing people on the other side of the Atlantic at the rate of over 1:100. “Say what??? How could it be rare over here, when most of us came from those people—Anglo-Saxons, Italians, Scandinavians, French and Germans?” Yes, there was something amiss. So, I jumped into the study of celiac disease with both feet, discovering that casein, soy, and corn all did the same thing as gluten. I also found out the truth about hydrogenated oils, MSG, aspartame, sugar, the lactose myth, air pollution, and much, much more. (It was so profound that I started a parallel study in religion and prophecy. But that’s a whole ‘nother sermon. Smile.) I began writing to one of my best friends from high school, an internist at one of our biggest local hospitals. He casually stated that he was glad to see that I was feeling well but that celiac disease was “rare” and that I was simply doing what many do that finally get properly diagnosed with a chronic condition—projecting my illness upon others. At the time, that upset me and I started writing to him like an angry prophet, advising him that if he wanted to get way ahead of the pack, he would start learning all that he could about celiac disease. I even asked him if he believed in God, “because this revelation was Biblical in proportion”. That settled it—I was “nuts”. But, he was the one who sent me the New England Journal of Medicine article about eight months later that boldly labeled celiac disease as the most under-diagnosed (and misdiagnosed) condition in the country and stated that it was occurring in at least 1:250 Americans without their knowledge. “Na, na, na, na, na,!” (LOL). Actually, I did not call him and rub it in. By then, I had experienced a few of what I call “Jonah experiences”, learning that you catch more flies with honey. Plus, I had received a pretty good glimpse of how and why something this important could be so unknown and misunderstood—and why things were sooooo upside down. The fact is that the Mayo Clinic and Johns Hopkins University published their incidence studies last year and found celiac disease to afflict 1:122 Americans. Yes, that is the new “official” number. However, the unofficial number published by celiac authorities is 1:33. Whoa! But here’s the “bad news”. (Actually, you will come to see that this, again, is good news.) We are only talking about celiac disease here. And wheat is the number two food allergen. What is number one again? Cow’s milk (with casein). I wonder what the true incidence of casein-intolerance is? Is it more frequent than gluten intolerance? I would have to believe so. While wheat-containing foods (the targets of Dr. Atkins’ partial truth) make up nearly 25% of the calories of the S.A.D., cow milk products make up a whopping 40% of our overall caloric intake. Errrh!!! What about soy—the “third plague” as I like to call it.. Errrh, again!!! How about corn, the fourth horseman? Here’s a scary thought: What about a mix and match of the four—some or all of the “big four”? Think that happens? Of course it does. These guys can ride separately or they can form a gang. We all know a gang is harder to control, don’t we? Now for the pathophysiology that you have been waiting for. The food allergies are just the indicators. During the time that the body is reacting to the “glue” from these foods, the IgE antibody—the allergy antibody—is formed to go out and warn us of the damage that is taking place in the duodenum. Otherwise, this is a stealth condition in most cases, with only one-fourth of celiacs and related food intolerants having gastrointestinal symptoms. Get that? That is very important. In fact, this is CRITICAL for all to understand, as it explains much and opens a door through which all truth-seekers must pass. (“There he goes, getting all melodramatic again.”) Individuals—whether they are humans, dogs, cats, or horses—can go years and years before the bottom drops out of this condition. And it takes the bottom dropping out for most of us to wake up to what’s going on, doesn’t it? We are the masters of denial as well as the patsies of deception. “I’ll do it ‘til I have problems. Then, I‘ll quit.” (e.g. cigarette smoking, drugs, alcohol, or over-eating). The bad news is that by the time you have obvious problems with your lungs, liver, kidneys, heart, brain, immune system or duodenum, then you are waaaay down the wrong road. It is a consistent pattern that we can live on about 25% of our organ function—one half of one kidney, a fourth of our liver, multiple coronary arteries occluded, numerous neurons destroyed, etc. before (BEFORE) we even start having symptoms. That’s a good news/bad news thing isn’t it? As vets, we know that most of our conditions in the pet are “acute-on-chronic”—acute manifestations of chronic problems. I used to think that this was due to unobservant owners or the laid-back lifestyle of the pet. But when I started seeing friends and loved ones dropping dead of heart attacks and strokes without warning and I found out that atherosclerosis starts as early as 5 years old, I knew that we were missing something. Yep, we are made to take a licking and keep on ticking as the old Timex ads used to say. The bad news is that we are beating our poor bodies (and those of our pets) to death and don’t know it or, at least we don’t fully understand the magnitude of what we are doing with every bite—and breath. Imagine now that over 1:30 humans have celiac disease or are afflicted with the other related food intolerances (casein, soy, and/or corn)—food induced villous atrophy of the duodenum. It can affect the jejunum as well. We know that this also occurs in the dog, with our old “extinct” friend the Irish setter being the glaring example. (I was absolutely ecstatic to hear that there was a pathologist in a major university in the northeast who has reopened the book on celiac disease.) Now, combine that fact with the consequences of the chronic malabsorption of calcium, iron, iodine, B complex, C, and numerous trace minerals, all of which are vital in the development and normal functioning of our bodies and immune systems. Do you have it in your mind yet? Let it sink in for a second. (Pause) Which symptoms or clinical signs are likely to show up first? If you said gastrointestinal signs, you would be wrong (unfortunately). If you said signs associated with chronic calcium malabsorption or allergies you would be right. In some it is the former while in others the latter. The “worst of the worst”—those that have the earliest immune reaction to the glue foods—will have the IgE and IgG related symptoms first. These are your infants, human or pets, with congestion, itching, rashes, irritability, chronically sore throats, and ear problems. Some of them do have colic and diarrhea but these should not be required signs to make one suspicious of food problems. The “best of the worst” (and I rarely use the term the “best of the best” anymore) have the signs of calcium malabsorption first if they have any signs at all. Remember: the proximal one-third of the duodenum is greatly responsible for calcium metabolism and absorption. In the best-case scenario, these glue foods form a coating on these villi and keep them from performing optimally. (Here you go. Think of a beautiful coral reef with gorgeous sea anemones and multi-colored sponges. Got it? The “villi” of the anemones are swaying back and forth in the crystal clear water, absorbing small particles of food floating in the water. So serene, so perfect. NOW, imagine that same reef after the oil spill from the Exxon Valdez. Got that? How well do those anemones do when they are coated with oil? Some will survive but many, many will die. I think you have the picture.) This is what the glycoproteins from gluten, casein, soy, and corn do. They coat the villi—at best—and “kill” the villi at worst, with the first and most severe damage taking place in the proximal third of the duodenum. No wonder I had flat feet, short legs, rib abnormalities and painful joint laxity—and bad teeth—as a child and later developed rotator cuff problems, bilateral inguinal hernias, and premature disc ruptures of my neck and back. I’m a classic celiac. But now YOU know why the most food allergic dogs have the worst orthopedic problems. How cool is that??? Think about them: the Labs, Rottweilers, German shepherds, the Labs, the Rotties, the Labs, the Labs. Hmmm—I’ve heard that before. (smile). Why is it that they can’t nail down the genetics of hip dysplasia? Hmmm—again. AND, now you know why two of the most food allergic small breeds—the Cocker and Shi Tzu—hold the age record for when they start blowing intervertebral discs. Yep, they do it as early as ONE YEAR OF AGE, don’t they? Why again? They have been malabsorbing the building blocks of their skeletal system (calcium and vitamin C) since they were first put on the grain-infested puppy chows. What makes up collagen, again? So, you also know why the Cavalier King Charles Spaniel (and I have yet to see one that wasn’t severely food allergic) dies of acute mitral valve prolapse at 5 years of age. What is that valve made of again? How did we create the chondrodysplastic breeds like the food allergy afflicted, Demodex-encrusted, cherry-eyed, respiratory challenged, squatty body English bulldog, anyway? Shall I continue? I could give countless examples that would keep us into the wee hours of the morning. I think you are seeing the pattern here, right? The allergies are there to warn us that the damage is taking place in the gut. Again, the allergies are things “seen” to help us understand the things “unseen”. Watch for this pattern. It will come up again and again. This is only the beginning, unfortunately and fortunately. (Please keep in the very front of your mind that the malabsorption syndrome leads to chronic deficiencies in so many vital nutrients. This is paramount in importance. Keep chanting, “Pandora’s Box, Pandora’s Box.”) We are still on the tip of the tip of the iceberg. And perhaps this is a good time to throw in the other analogy with which I was considering opening this dissertation. Try this one on for size: Conventional medicine is steaming headlong into an enormous obstacle that is titanic in importance and yet has only a small piece of its mass protruding from the surface right now. The medical establishment (including both human and veterinary) has built a mighty vessel that many would deem unsinkable. “We have made such great gains in extending life” comes the announcement from the captain. “And one day, we will find the cures for cancer and the diseases that plague us all.” And the passengers all say “Hooray!!! It will be clear sailing from there!” The applause dies down and the captain exclaims, “And we are working on better ways to make these necessary drugs more available, more well-known by the public, and more affordable to you. Very soon, many of these drugs will be available over-the-counter and you will no longer need to even consult with your physician about them. Simply choose what is right for you by watching your television and then going to your local drugstore, supermarket, or gas station food mart to pick them up. You will be wise enough to choose for yourself.” Again, the crowd roars with approval. But, there is something looming in the waters, just off the port bow. Some call it an iceberg. Others call it a “rock”. I call it the Truth. This treatise so far has mapped out the tip of the tip of this iceberg. With the binoculars you now have, you can see it. Do you see it??? If your eyes are good enough, you can see much of what is below the surface, too. The water is a lot clearer out in the ocean than you may think. And this “unsinkable” vessel that man has created is heading straight for it. Why? They are not looking for it. Many are happy, quite content with the cruise they are on. Others don’t really know any other way to behave on a cruise like this. Others are desperately trying to keep those who would worry about icebergs distracted so that they don’t spoil the cruise for the others. Ignorance and greed are at the controls—our two biggest nemeses—with contentment being a first mate. Suddenly—WHAM—the mighty craft hits “the rock”. It starts to take on water. People are dying from drugs they have taken for years: HRT, NSAIDS, nasal decongestants, and what will be the next group- the cholesterol statin drugs. The epilepsy drugs don’t work anymore and the pets on board are being put to sleep for “non-responsive epilepsy”. The vaccines that were meant to protect us “turn on us”, making us question their role in everything from producing the full clinical disease to hard-to-detect/prove sub-total entities of that disease, such as epilepsy, chronic liver disease, immune glomerulonephritis, cardiomyopathy, or worse. The captain is shouting, “Don’t panic. We will figure out what to do. Calmly man the lifeboats.” But some do panic as they had so much faith in this indestructible piece of man’s technology, the same technology that put landers on the moon, Mars, and Titan. But, it is this same technology that does not seem to understand that taking an NSAID for a fever caused by a viral infection is not a wise thing to do. It is the same captain’s mates that don’t see that Helicobacter pylori—the opportunistic bacteria that causes deep stomach ulcers—hates an acid stomach and that heartburn is designed partly to control his growth. If they don’t know that, then they certainly can’t see how this beast that they have been feeding with antacids and problem foods leaves the stomach when the individual’s immune system takes a nose dive (after a lifetime of malabsorbing nutrients vital to its health) and takes up residence in a cholesterol plaque (that is safe-guarding a weakened artery) and causes it to break off, inducing a stroke or a myocardial infarction. How can they see that? They have their eyes on the moon and the stars. (And yet, a study done by a group of cardiologists found that a shocking 85% of atherosclerotic plaques that were cultured for H. pylori were positive for this critter. Think about that for a second. Sinking in?). Go to Part 2: Food Intolerance—Man and Animals versus Gluten, Casein, Soy, and Corn or How We Won the Battle of "Helm's Deep" (Part 2 of 2)

Celiac.com 07/14/2021 - Prior efforts to determine rates of celiac disease in individuals with autoimmune hepatitis (AIH) have shown highly variable data. To get better data and develop a clearer picture of the issue, a team of researchers recently set out to assess rates of celiac disease in individuals with AIH. For their study, the team employed two professional librarians to search PubMed, EMBASE, Cochrane and Web of Science Core Collection for entries through February 7th, 2020. Their search turned up nearly 2,500 unique publications that included any of the terms “celiac disease”, “celiac”, “transglutaminases”, “gluten”, “gliadin”, “EMA”, “TTG” and “villous” combined with “autoimmune”, “hepatitis”, “ANA”, “SMA” or “LKM”. The team then conducted a systematic review based on the PRISMA guidelines. They found 31 articles eligible for full-text review, 15 of which were deemed relevant. They included eight publications in their main analysis, using a fixed-effect inverse variance-weighted model, and also determining heterogeneity. Their final analysis included 567 individuals with AIH from eight studies, where they found biopsy-verified celiac disease equivalent to Marsh III in 23 individuals, for a rate of about 4%. The pooled rate of celiac disease in AIH was 3.5%, more than triple the 1% celiac disease rates found in most general populations. When 15 other studies of 1,817 AIH patients were included, where celiac disease had been diagnosed through positive serology without biopsy, the pooled rate of celiac disease was still about 3%. This study shows that celiac disease rates are higher in individuals with AIH compared to the general population. The study team recommends that doctors consider celiac screening in patients with AIH. Read more in Liver International The research team included Linnea Haggård, Ida Glimberg, Benjamin Lebwohl, Rajani Sharma, Elizabeth C Verna, Peter HR Green, and Jonas F. Ludvigsson. They are variously affiliated with the Department Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; School of Medical Sciences, Örebro University, Örebro, Sweden; Celiac Disease Center, Department of Medicine, Columbia University Medical Center, New York, NY, USA; the Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA; the Center for Liver Disease and Transplantation, Division of Digestive and Liver Diseases, Columbia University Irving Medical Center, New York, New York, USA; the Division of Digestive and Liver Diseases, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, New York, USA; the Department of Pediatrics, Örebro University Hospital, Örebro University, Örebro, Sweden; and the Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, UK.

Celiac.com 04/12/2021 - Celiac disease is an autoimmune disorder of the small bowel, classically associated with diarrhea, abdominal pain, and nutritional deficiencies. Rapid diagnosis of celiac disease is important, since strict adherence to a gluten-free diet can resolve most resolution of clinical and histologic manifestations of the disease. Celiac disease is commonly misdiagnosed, most often as one of these conditions. Numerous diseases and conditions can present with clinical and/or histologic features of celiac disease. In a recent review article, a pair of researchers highlight key clinical and histologic mimickers of celiac disease. Many conditions that mimic celiac disease offer clues to the underlying diagnosis, and many have a targeted therapy. It is important to provide patients with a correct diagnosis, and to avoid an unnecessary gluten-free diet for non-celiac patients. Two researchers recently set out to better understand the conditions that mimic celiac disease. Researchers Amrit K Kamboj, MD and Amy S Oxentenko, MD, are affiliated with the Department of Internal Medicine, Division of Gastroenterology and Hepatology, and the Department of Internal Medicine, Division of Gastroenterology and Hepatology, Mayo Clinic, Minnesota, USA. The diagnosis of celiac disease is made when there are compatible clinical features, supportive serologic markers, representative histology from the small bowel, and response to a gluten-free diet. Histologic findings associated with celiac disease include intraepithelial lymphocytosis, crypt hyperplasia, villous atrophy, and a chronic inflammatory cell infiltrate in the lamina propria. The evaluation of a patient with serologically negative enteropathy necessitates a carefully elicited history and detailed review by a pathologist. Medications can mimic celiac disease and should be considered in all patients with a serologically negative enteropathy. Clinical conditions that mimic celiac disease include: Autoimmune and/or inflammatory Conditions Can Mimic Celiac Disease Autoimmune and/or inflammatory conditions such as inflammatory bowel disease (IBD), microscopic colitis, thyroid dysregulation, and adrenal insufficiency may all cause clinical features that mimic celiac disease, or be concurrently present in patient known to have celiac disease. Infectious Diseases Can Mimic Celiac Disease Infectious mimickers include giardiasis and both viral and bacterial gastroenteritis, although most viral and bacterial infections are self-limited and do not cause the chronic symptoms that can be seen with Giardia infection, unless post-infectious IBS ensues. Other chronic parasitic infections may also cause symptoms that mimic celiac disease. Other less common clinical mimickers include tropical sprue, autoimmune enteropathy, drug-induced enteropathy, Whipple’s disease, and others. Irritable bowel syndrome (IBS) Can Mimic Celiac Disease Irritable bowel syndrome (IBS) is the most commonly diagnosed gastrointestinal disorder, and has features that mimic celiac disease.10 Symptoms include abdominal pain along with altered bowel form and/or frequency. IBS is often associated with other disorders including somatic comorbidities. Small Intestinal Bacterial Overgrowth (SIBO) Can Mimic Celiac Disease Small intestinal bacterial overgrowth (SIBO) is known to cause diarrhea, bloating, and weight loss, which may mirror symptoms of classic celiac disease; SIBO may also be a cause of recurrent or refractory symptoms in a patient with known celiac disease. The researchers divide the histological mimickers of celiac disease into early and late. The key difference being that early histologic mimickers are characterized by increased intraepithelial lymphocytes with no villous atrophy, and crypts that are either normal or have minimal hyperplasia. Late histologic mimickers are characterized by increased intraepithelial lymphocytes, partial or total villous atrophy, crypt hyperplasia, and chronic inflammation in the lamina propria. Early histologic mimickers include: Non-steroidal anti-inflammatory drugs Inflammatory bowel disease Small intestine bacterial overgrowth Helicobacter pylori Self-limited gastroenteritis Autoimmune conditions Unexplained Late histologic mimickers include: Medications (olmesartan, ipilimumab, colchicine, mycophenolate mofetil, methotrexate, and azathioprine) Common variable immunodeficiency Giardia Crohn’s disease Autoimmune enteropathy Collagenous sprue Tropical sprue Whipple’s disease Enteropathy-associated T-cell lymphoma CD4+ T-cell lymphoma Unclassified sprue Read the full report in Clin Transl Gastroenterol. 2017 Aug; 8(8): e114.

Celiac.com 04/15/2021 - Cases of celiac disease are on the rise. Celiac disease is associated with both gastrointestinal (GI) and extra-intestinal manifestations, with psychiatric disorders being among the most common extra-intestinal manifestations. The connection between celiac disease and associated psychiatric disorders has not been well documented or studied. A team of researchers recently set out to provide a greater understanding of the existing evidence and theories surrounding psychiatric manifestations of celiac disease. The research team included Emma Clappison, Marios Hadjivassiliou, and Panagiotis Zis. They are variously affiliated with the Medical School, University of Sheffield, Sheffield S10 2YN, UK; and the Academic Department of Neurosciences, Sheffield Teaching Hospitals NHS Foundation Trust and University of Sheffield, Sheffield UK For their study, the team conducted an online literature search using PubMed to locate eligible articles containing data on the rates of both celiac disease and psychiatric disorders. They also conducted meta analyses on odds ratios. In all, the team located 37 eligible articles. They detected a significant increased risk for patients with autistic spectrum disorder, attention deficit hyperactivity disorder, depression, anxiety, and eating disorders amongst the celiac disease population compared to healthy controls. They found no significant differences for bipolar disorder or schizophrenia. The data connects celiac disease to an increased risk of depression, anxiety, eating disorders, as well as ASD and ADHD. They point to the need for more research to investigate specific biological explanations as well as the potentially beneficial effects of a gluten-free diet. Data can be helpful in showing connections, and certainly the connection between celiac disease and psychiatric conditions is worthy of study, but further studies are crucial to understanding the connection in any meaningful way. Read more at MDPI.comNutrients 2020, 12(1), 142;