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  1. Celiac.com 05/17/2019 (Originally published 10/08/2010) - There are many ways in which the immune system is compromised in the context of celiac disease. A lack of fats (due to fat malabsorption) can limit production of eicosanoids and other fat-dependent immune system components. Malabsorption of minerals such as zinc, copper, iron, selenium, or magnesium can also impair immune function in several ways. Malabsorption of non-metalic elements such as iodine can also impair our immune function through impairing T cell production by the thymus. The leaky gut, a chronic feature of untreated celiac disease can induce autoimmunity and deplete the very resources that protect us from infection and toxic agents. The recent successes of Larazotide are highly suggestive that it is the leaky gut that is at the very root of celiac disease, since many celiacs can consume gluten with little harm when taking this drug. Malabsorption Our cells can make use of three separate sources of energy. They can burn glucose, from carbohydrates, amino acids, from proteins, or fats which can be saturated, monounsaturated, or polyunsaturated fats. Any or all of these can be used for fuel at the cellular level. Celiac disease has long been characterized as a condition of fat malabsorption, and some fats are essential to our survival and wellness. Stephen Cunnane makes an excellent case for these essential fats in his book about the evolution of the human brain titled “Survival of the Fattest”. He shows that the human brain cannot develop normally without adequate supplies of omega 3 fatty acids. We also need fats to make many elements of the immune system. We must consume and absorb omega 3 and omega 6 fatty acids because our bodies are unable to efficiently produce them. Similarly, as our understanding has expanded, we have come to recognize that absorption of other nutrients such as minerals can also be compromised in untreated celiac disease. (Some people with celiac disease continue to battle mineral malabsorption for many years after adopting the gluten-free diet.) Patients with iron deficiency that does not respond to supplementation should be investigated for celiac disease, as refractory iron deficiency is common in untreated celiac disease (1). Iron is an important constituent of immune function and Stephen J. Oppenheimer has identified seven separate dynamics through which iron deficiency can compromise immune function. These include: Reduced neutrophil function which can be reversed through iron supplementation; Reduced numbers of T-lymphocytes; Reduced T-lymphocyte responsiveness; Impaired natural killer cell activity; Impaired interleukin 2 production; Altered macrophage migration; Altered cutaneous hypersensitivity (2). Magnesium deficiency, in the context of celiac disease, has been identified as a factor in damage to the parathyroid gland and consequent bone demineralization. Rude et al have shown that magnesium supplementation alone will reverse this problem (3). Similarly, mineral malabsorption may impede our supplies of zinc, copper, and selenium, each of which may have a negative impact on the immune system. Even a mild zinc deficiency can impair T cells, interfere with hormonal regulation of the thymus, and activation of tumor necrosis factor and natural killer cells (4). I have previously reported that natural killer cells are the body’s first line of defense against malignancy (5). Natural killer cells also help to protect us from a variety of infectious agents. Malabsorption of non-metallic elements such as iodine can also impair immune function. Not only does the thyroid gland require iodine to function properly, the healthy thymus gland contains large reserves of iodine and a wide range of immune functions require iodine. The antibacterial uses of iodine have a long history and this element was discovered early in the nineteenth century. Although iodine is now added to most table salts in the industrialized world deficiency continues to plague the third world causing preventable mental retardation. Failure to absorb this important nutrient can cause disturbances to many facets of the immune system and impair heat regulation through compromised thyroid function. Added problems with the thyroid gland can also come to the untreated celiac through autoimmunity induced by a process called molecular mimicry (more on this later) which is one of the means by which the leaky gut can also create havoc with the immune system. Leaky Gut Jon Meddings has characterized the gastrointestinal tract as a long tube running through our bodies that contains materials from the outside environment (6). Unlike our skin, we have only one layer of cells in the intestine that protects us from the outside world. These cells must selectively absorb nutrients from this material, while providing a protective barrier against constituents of our food that might harm us. These nutrients are absorbed through the epithelial cells and are released on the other side of the cells into the bloodstream. The leaky gut, as induced by gluten, is a state where excessive zonulin is produced in the intestinal lumen. This protein attaches to the epithelial cells that line the intestine. The epithelial cells move further apart leaving gaps between the cells, thus allowing matter to enter the bloodstream on the other side of the epithelial barrier. Depending on the size of these gaps, various toxins, infectious agents from our food, undigested and partly digested food particles, and even the friendly bacteria that inhabit our intestines may reach the bloodstream and beyond. Whether in the form of partial or complete proteins from foods, microbes from the external environment, or friendly bacteria from our intestines, once in the bloodstream our immune systems recognize these proteins as foreign. We produce antibodies to attack and destroy them. If these same proteins arrive in the circulation repeatedly, we will have elevated serum antibodies specifically sensitized to these proteins. Protein structures can contain enormously variable sequences of amino acids. Perhaps for the sake of efficiency, these selective antibodies recognize only one segment of the foreign protein structure, in the form of a single sequence of amino acids. According to the theory of molecular mimicry, this or a very similar sequence of amino acids may be found in proteins that form some of our own tissues. If we have elevated levels of antibodies that are made to attack such a string of amino acids, they will also attack self tissues. This is process results in autoimmune disease. Because it is difficult to predict what sequence of amino acids the immune system will choose, we cannot predict the specific self tissues that will be attacked by our immune systems. Nonetheless, if the theory of molecular mimicry is correct, gluten may be at the root of many forms of autoimmunity because of its impact on zonulin production. Celiac Disease vs. Gluten Sensitivity The greater hazard appears to lie with celiac disease rather than non-celiac gluten sensitivity, as celiac patients not only have to contend with all the problems that come from a leaky gut, they also have all the problems associated with malabsorption. However, Anderson et al report that people with gluten sensitivity showed a greater rate of all cause mortality as well as significantly increased rates of non-Hodgkin’s lymphoma and cancers of the digestive tract than were found among patients with celiac disease (7). These unfortunate data may be the direct result of the many physicians and other health care practitioners who consistently urge their patients to continue to consume gluten despite the clear evidence, in the form of anti-gliadin antibodies, that these patients are mounting an immune reaction against the most common food in their diet. Peter Green, professor of Medicine at Columbia University, has called for more attention to be paid to “the lesser degrees of intestinal inflammation and gluten sensitivity” (8). Sources: Farhad Zamani, Mehdi Mohamadnejad, Ramin Shakeri, Afsaneh Amiri, Safa Najafi, Seyed Meysam Alimohamadi, Seyed Mohamad Tavangar, Ardeshir Ghavamzadeh, Reza MalekzadehGluten sensitive enteropathy in patients with iron deficiency anemia of unknown originWorld J Gastroenterol 2008 December 28; 14(48): 7381-7385 Oppenheimer Stephen J, Iron and Its Relation to Immunity and Infectious Disease. The American Society for Nutritional Sciences Supplement, Journal of Nutrition. 2001;131:616S-635S. Rude RK, Olerich M. Magnesium deficiency: possible role in osteoporosis associated with gluten-sensitive enteropathy. Osteoporos Int. 1996;6(6):453-61. Prasad AS. Zinc and immunity. Mol Cell Biochem. 1998 Nov;188(1-2):63-9. Hoggan R. Considering wheat, rye, and barley proteins as aids to carcinogens. Med Hypotheses. 1997 Sep;49(3):285-8. Meddings J. National Conference, Canadian Celiac Association, Calgary, Alberta, Canada, 1999 Anderson LA, McMillan SA, Watson RGP, Monaghan P, Gavin AT, Fox C, Murray LI Malignancy and mortality in a population-based cohort of patients with coeliac disease or ‘gluten sensitivity’. World J Gastroenterol 2007 January 7; 13(1): 146-151 Green P H R, Mortality in Celiac Disease, Intestinal Inflammation, andGluten Sensitivity. JAMA. 2009;302(11):1225-1226.
  2. Celiac.com 05/04/2018 - It has been recognized for several decades that both children and adults with celiac disease have a significantly increased frequency of osteoporosis and increased risk of fractures as compared to the age-matched non-celiac healthy individuals. Based on published data the prevalence of osteoporosis among celiac patients varies from as low as 4% to as high as 70%. The data from our clinic indicate that prevalence of osteoporosis among adults with gluten intolerance and celiac disease is in the vicinity of 30-40%. Characteristics and causes of osteoporosis Osteoporosis is a bone disease characterized by the reduced bone mineral density and impaired bone architecture that leads to an increased risk of fracture. The three main mechanisms by which osteoporosis develop include an inadequate peak bone mass, excessive bone resorption and inadequate formation of new bone during remodeling. At a given age, bone mass results from the amount of bone acquired during growth (the peak bone mass) minus the acquired bone loss due to variety of reasons including age-related processes, malabsorption syndromes, chronic steroid use etc. The rate and magnitude of bone mass gain during the pubertal years may markedly differ from one individual to another. It has been demonstrated that pediatric onset of celiac disease and poor compliance with gluten-free diet during childhood do significantly reduce peak bone mass. One of the main causes of osteoporosis is an alteration in bone remodeling due to imbalance between bone formation and resorption, with a predominance of resorption resulting in a reduction in bone mass and increased risk of fractures. Formation of the new bone is facilitated by specialized cells, osteoblasts, which actively synthesize bone matrix. Bone resorption is mediated by other specialized cells, osteoclasts. One of the main regulators of bone remodeling is the RANK/RANKL/OPG system. During bone remodeling, bone marrow cells and osteoblasts produce RANKL(receptor activator for nuclear factor kB ligand), which bonds with a transmembrane receptor of the osteoclast precursor, RANK(receptor activator of nuclear factor kB), causing their differentiation and activation. Osteoprotegerin (OPG) binds to RANKL before it has an opportunity to bind to RANK, and hence suppresses its ability to increase bone resorption. Normal bone remodeling is based on the permanent renovation of the skeleton and consists of an initial phase of bone resorption followed by a phase of formation, both of which are regulated by general (endocrine) factors and local (paracrine) factors. The main endocrine factors include parathyroid hormone [PTH] and vitamin D as well as estrogens and, to a lesser extent, testosterone, thyroid hormones, growth hormone and leptin. Local factors include various cytokines (IL-1, IL-6 and TNF-a playing a role) key growth factors that regulate the process. There are several well-characterized risk factors which contribute to the development of osteoporosis in celiac patients. These include: 1. Malabsorption of vitamin D and secondary hyperparathyroidism Villous atrophy in celiac patients reduces the active absorption surface and induces steatorrhea (exces fat in feces), which has a chelating effect on calcium and vitamin D, making their absorption difficult. This reduces levels of the vitamin D transporting protein (calbindin and calciumbinding protein) and increases PTH synthesis which, in turn, lead to increased bone resorption causing osteoporosis. 2. Malabsorption of vitamin K Malabsorption of fat soluble vitamins including vitamin K is a common finding in celiac patients. Three vitamin-K dependent proteins have been isolated in the bone: osteocalcin, matrix Gla protein (MGP), and protein S. Osteocalcin is a protein synthesized by osteoblasts. The synthesis of osteocalcin by osteoblasts is regulated by the active form of vitamin D—1,25-dihydroxy-cholecalciferol. The mineral-binding capacity of osteocalcin requires vitamin K-dependent gamma-carboxylation of three glutamic acid residues. MGP has been found in bone, cartilage, and soft tissue, including blood vessels. The results of animal studies suggest MGP facilitates normal bone growth and development. The vitamin K-dependent anticoagulant protein S is also synthesized by osteoblasts, but its role in bone metabolism is unclear. Children with inherited protein S deficiency suffer complications related to increased blood clotting as well as decreased bone density. The data on the role of vitamin K in osteoporosis came from the clinical observations indicating that a chronic use of vitamin K antagonists such as warfarin increases risk of vertebral and rib fractures. Accordingly, vitamin K supplementation significantly lowers risk of vertebral and hip fractures. 3. Magnesium deficiency Magnesium deficiency may be an additional risk factor for celiac-associated osteoporosis. This may be due to the fact that magnesium deficiency alters calcium metabolism and the hormones that regulate calcium. Several human studies have suggested that magnesium supplementation may improve bone mineral density. Magnesium deficiency is easily detected with laboratory tests (eg, low serum magnesium, low serum calcium, resistance to vitamin D) or clinical symptoms (eg, muscle twitching, muscle cramps, high blood pressure, irregular heartbeat). Screening for magnesium deficiency should be routinely included in the screening of celiac patients with osteoporosis. 4. Chronic diarrhea and metabolic acidosis Chronic diarrhea in patients with celiac disease results in significant bicarbonate losses and development of metabolic acidosis. Bone is a major site for the extracellular buffering of the retained acid. Therefore, one of the main compensatory mechanisms maintaining a stable serum bicarbonate level in the face of an uncorrected metabolic acidosis is the dissolution of bone buffers and net efflux of calcium from bone. Bicarbonate supplementation in patients with metabolic acidosis decreases urinary calcium, phosphorus and hydroxyproline wasting supporting the concept of negative effects of acidosis on bone health. 5. Hypogonadism Decline of estrogen production and activity is one of the main events in the development of age-related osteoporosis. It is well known that estrogen deficiency is important in the pathogenesis of osteoporosis not only in women but also in men. Increase in bone mineral density in young men and declines in older men are related to circulating free estrogen, not testosterone. In general, patients with celiac disease are characterized by low levels of circulating estrogens which contributes to the development of premature osteoporosis. 6. Chronic use of Proton Pump Inhibitors Proton pump inhibitors (PPIs) are one of the most widely used classes of drugs. The commonly used PPIs include such drugs as Omeprazole (brand name: Prilosec), Lansoprazole (brand name: Prevacid), Dexlansoprazole (brand names: Kapidex, Dexilant), Esomeprazole (brand name: Nexium), Pantoprazole (brand name: Protonix) and Rabeprazole (brand name: AcipHex). Chronic use of PPIs for gastroesophageal reflux disease and other related conditions has been associated with impaired calcium and magnesium absorption and increased risk of vertebral and nonvertebral fractures. 7. Chronic use of Selective Serotonin Reuptake Inhibitors Selective Serotonin Reuptake Inhibitors (SSRIs) are frequently used in celiac patients for treatment of depressive disorders. The commonly used SSRIs include such drugs as Citalopram (brand name: Celexa), Escitalopram (brand name: Lexapro), fluoxetine (brand name: Prozac), fluvoxamine (brand name: Luvox), Paroxetine (brand name: Paxil) and Sertraline (brand name: Zoloft). It has been demonstrated that SSRIs increase extracellular 5-HT (5-Hydroxytryptophan) levels that have deleterious skeletal effects. The skeletal serotonergic system consists of 5-HT receptors and the 5-HT transporter (5-HTT) in osteoblasts and osteocytes. 5-HTT is a transmembrane protein targeted by SSRIs. 5-HT restrains osteoblastic activity, thus leading to bone loss. 8. Autoimmune mechanisms Autoimmune mechanisms have been long suspected as risk factors contributing to development of osteoporosis in celiac patients. Near a decade ago, it was demonstrated that sera from celiac patients with osteoporosis contains significantly high titers of antibodies against bones as compared to non-celiac osteoporotic patients. The immunostaining was localized in areas where an active mineralization process occurred and was similar to the distribution of the native bone tissue transglutaminase. Recently, it has been described that a subset of patients with celiac disease has autoantibodies to osteoprotegerin, which block the inhibitory effect of osteoprotegerin on signaling by the receptor activator of nuclear factor (NF)-kappaB (RANK), and are associated with severe osteoporosis and high bone turnover. 9. Chronic inflammation Chronic inflammatory diseases, including celiac disease, are associated with overproduction of proinflammatory cytokines such as TNF-a, interleukin(IL)-1, IL-6, IL-11, IL-15 and IL-17 among others which activate osteoclasts and accelerate bone resorption leading to osteoporosis. In conclusion, osteoporosis associated with celiac disease is not a coincidental problem. It is a consequence of disease-specific (autoantibodies to osteoprotegerin), disease-nonspecific (malabsorption of vitamin D, K and magnesium, hypogonadism, chronic inflammation, chronic diarrhea and metabolic acidosis) and jatrogenic (overuse of PPIs and SSRIs) events accelerating resorptive processes in the skeleton. Correction of the aforementioned risk factors in celiac patients can reverse the development of osteoporosis and reduce the risk of osteoporosis-associated fractures. Bibliography: Bab I, Yirmiya R. Depression, selective serotonin reuptake inhibitors, and osteoporosis. Curr Osteoporos Rep. 2010 Dec;8(4):185-91. Bianchi ML. Inflammatory bowel diseases, celiac disease, and bone. Arch Biochem Biophys. 2010 Nov 1;503(1):54-65. Ito T, Jensen RT. Association of long-term proton pump inhibitor therapy with bone fractures and effects on absorption of calcium, vitamin B12, iron, and magnesium. Curr Gastroenterol Rep. 2010 Dec;12(6):448-57. Katz S, Weinerman S. Osteoporosis and gastrointestinal disease. Gastroenterol Hepatol (N Y). 2010 Aug;6(8):506-17. Riches PL, McRorie E, Fraser WD, Determann C, van't Hof R, Ralston SH. Osteoporosis associated with neutralizing autoantibodies against osteoprotegerin. N Engl J Med. 2009 Oct 8;361(15):1459-65. Stazi AV, Trecca A, Trinti B. Osteoporosis in celiac disease and in endocrine and reproductive disorders. World J Gastroenterol. 2008 Jan 28;14(4):498-505. Sugai E, Cherñavsky A, Pedreira S, Smecuol E, Vazquez H, Niveloni S, Mazure R, Mauriro E, Rabinovich GA, Bai JC. Bone-specific antibodies in sera from patients with celiac disease: characterization and implications in osteoporosis. J Clin Immunol. 2002 Nov;22(6):353-62. Turner J, Pellerin G, Mager D. Prevalence of metabolic bone disease in children with celiac disease is independent of symptoms at diagnosis. J Pediatr Gastroenterol Nutr. 2009 Nov;49(5):589-93. Vasquez H, Mazure R, Gonzalez D, Flores D, Pedreira S, Niveloni S, Smecuol E, Mauriño E, Bai JC. Risk of fractures in celiac disease patients: a cross-sectional, case-control study. Am J Gastroenterol. 2000 Jan;95(1):183-9.
  3. Hello, hope to find some help here, because my doctors are quite unsure. I had nerve pain in my ulnar nerve (elbow, pinky finger) for about 7 years with an escalation about 2 years ago (28 yo btw). Eating a lot of pizza and beer, combined with stress of a long period of time, my nerve pain got worse to the point I could not use my hands any longer. There were some ups and downs but quickly other symptoms appeared, like muscle aches, cold hands, joint pain, dry eye, finger pain on the other fingers and increased sensitivity in general. After seeings tons of doctors, one found in Nov, 2016 increased ttG-AK, AGA and thyroglobulin antibodies as well as slightly increased free t4 with TSH and T3 being normal. I have always been low on Vitamin D, Selen, Q10 and had bad cholesterol and increased CK from time to time - which all relate to eighter celiac disease or hashimoto. Iodine is also low, but was measured only recently. He told me to go gluten free and both conditions - the celiac disease and hashimoto - will improve quickly. The diagnosis was clear for him, even without a colonoscopy. Most pain improved quickly and overall I felt better, however I got new symptoms: iron deficiency, cold hands all day and bowel sounds with bowel pain. My bowel movements became much more voluminous (!) than ever before and I've lost 15 Kg within 2 months (85 Kg vs 70 Kg now). I started eating huge amounts, but my small intestines seems not to be able to handle it. I had never noticeable bowel problems (or weight loss/gains before) - only after eating special foods (like pizza), but I never recognized it a problematic. I did not lose or gain weight. But after going gluten free, my intestines seem to be on a war. It should be the opposite, shouldn't it? (I'm strictly gluten free, read a lot of articles and books and I always had a very healthy lifestyle concerning food - except a few phases like the one mentioned above - ... mostly organic, lots of fruits and vegetables) Thanks for your help!
  4. Hey guys. I'll try to keep it short. I recently had tests done in Denmark and found all my food sensitivities, with the hope of getting better. It's been 5 years adhering a super strict diet. Nothing seemed to work as it should. Let me rewind. A few years back I went on the SCD (simple carbohydrate diet). I was so thin and my weight rushed down every day. I couldn't keep any weight on me no matter how much I ate. Bmi of about 13-14, I was a constant skeleton outfit for halloween. Great for that one day of the year, not the rest ;P After a ton of reading I came across "Breaking The Vicious Cycle", by Elaine Gottschall B.A. She explains why many diseases have carbohydrate issues, and how to solve it. At the time it didn't work. Fast forward. I adher strictly to the food sensitivity chart I got back from DK with all foods I don't react to, but still having digestive issues. Foods seem to go unprocessed. Oddly enough mostly quinoa and such. So the pieces begun to fall to place. I re-read the book, and sure enough it seem that poly and disaccharides can't get absorbed through the lining, feeding the bad bacteria, the bacteria makes mucus which again cover the lining even more, making it impossible to absorb, and creating this endless loop of malabsorbtion. Not only for those foods, but for EVERYTHING i ate in the same meals. So how can we survive without carbos? Easy. Monosaccharides! Bananas, honey and the likes. They can pass through and get absorbed in the small intestines without being broken down. Their low sugar contents makes them ideal for celiacs, so we can eat a whole bunch without getting any issue. Before you go and chow down bananas as a substitute, make sure this is the root cause for you, and also try to do a fast for a day, then eat a ton of fiber with lots of water (add lemon and salt) to clear out your intestines. You don't want bacteria from old food rests gobbling on anything. So I've found some good charts. I prefer the one posted below. They will help aid in digestion. Will report back, but I am 99% certain this will be the nail in the coffin to get my health back as I have already gone up about 20 kg from where I was just two years ago, mostly muscle mass. Besides eating well I take, a lot of supplements that Nordic Labs recommended, yes they are a lab, not doctors. They know their stuff, so if you got the money I highly recommend it, as these tests are brand new and very very precise. If it's too expensive to travel, call them, and get it arranged to send blood samples. I'll answer any questions to the best of my ability. Let me know if anything was unclear.
  5. Celiac.com 09/15/2016 - Some doctors and clinicians have reported cases of severe sprue-like enteropathy associated with olmesartan, but, until now, no clear demonstration of an increased risk has been documented by epidemiological studies. Now, a French nationwide observational cohort study has shown a connection between severe intestinal malabsorption and the drug olmesartan, according to results presented by a team of researchers. Olmesartan is an angiotensin II receptor antagonist which has been used for the treatment of high blood pressure. Olmesartan is also sold commercially under the name Benicar. The research team included Mickael Basson, Myriam Mezzarobba, Alain Weill, Philippe Ricordeau, Hubert Allemand, Francois Alla, and Franck Carbonnel. They are variously affiliated with the French National Health Insurance Fund, Paris, France, and the Université Paris-Sud, Assistance Publique-Hôpitaux de Paris and Gastroenterology unit, Hôpitaux Universitaires Paris Sud, Le Kremlin Bicêtre, France. The team set out to assess, in a nationwide patient cohort, the risk of hospitalization for intestinal malabsorption associated with olmesartan compared with other angiotensin receptor blockers (ARB) and ACE inhibitors (ACEIs). From the French National Health Insurance claim database, they included all adult patients initiating ARB or ACEI between 1 January 2007 and 31 December 2012, with no prior hospitalization for intestinal malabsorption, no serology testing for celiac disease, and no prescription for a gluten-free diet product. Their main endpoint was incidence of hospitalization with a discharge diagnosis of intestinal malabsorption. The team included 4,546,680 patients, for a total of 9,010,303 person-years, and observed 218 events. Compared with ACEI, the adjusted rate ratio of hospitalization with a discharge diagnosis of intestinal malabsorption was 2.49 (95% CI 1.73 to 3.57, p Average length of hospital stay for intestinal malabsorption was longer in the olmesartan group than in the other groups (p=0.02). Compared with ACEI, the adjusted rate ratio of hospitalization for celiac disease was 4.39 (95% CI 2.77 to 6.96, p<0.0001). These results show that olmesartan is assoc qiated with higher rates of hospitalization for intestinal malabsorption and celiac disease. Source: Gut. doi:10.1136/gutjnl-2015-309690
  6. Hello Celiac Forum, I will try to keep this brief but my story is a bit lengthy...I have been sick with severe gastrointestinal "issues" for 2 years. After a battery of tests by a NJ gastro (who's initial thought was I had Celiac), including a celiac panel, colonoscopy, ultrasounds, SIBO test, and an abdominal CT scan, my doctor dismissed my condition as IBS-D and told me to deal with it. I then went to another doctor who also suspected Celiac and he ran another panel which also came up negative. He ran a few more tests and indicated I had "mild malabsorption syndrome" but could not tell me why. This was based on a positive fecal fat test. Probiotics and digestive enzymes have proven ineffective, and sometimes make me worse. He then dismissed me saying it's IBS-D and sent me on my way. The reason I continue to be slightly alarmed is my intestinal issues are drastically different than they have ever been in the past. I've always has problems with IBS....this is WAY worse. It's an everyday problem and NO over the counter medications work at all. The positive fecal fat makes me nervous as well. That usually indicates small bowel disease, but I have never had a small bowel scope. So, long story short, is it REALLY possible to have a negative celiac panel and still have Celiac? I read somewhere that it's possible, especially if you have Hashimoto's....yeap, got that too. Anyone had a negative test and positive biopsy? The two doctors I saw said no way. Articles indicate otherwise. Please help! Immuniglo. 259 (ref 91-414) IGA Glia 7 (ref 0-19) Igg Glia 2 (ref 0-19) IGA Ttg <2 (ref 0-3)
  7. I have been on the run for a diagnosis for the past three years and have reached nowhere as most doctors I have met so far have either said that I have psychosomatic symptoms arising from a depression I once had or irritable bowel syndrome ( I'm not depressed anymore, I will be again due to the lack of not knowing what's ruining my life). I have severe migraine headaches which increased progressively over the years and have chronic rhinitis since a small age ( I am currently 21 yrs old). Over the last three years, my health started deteriorating. In February 2013, I started suffering from depression ( bouts of uncontrollable crying, extremely low and worthless feeling, sensitive to small unreasonable things, lack of focus and generally like i was dropped into a pit and trapped). I have always been a very strong person who is not generally sensitive. But from that particular point things have just changed. Now I believe I'm not depressed anymore, though I have been diagnosed as having an anxiety problem. Since then I have had other symptoms recurring ( they come and go and there are days I feel slightly better) including joint pain (everywhere) , dull annoying aching pain on the entire right side of my body that gives me a numb, extremely weak feeling, muscle spams and tightness (mostly in the thighs), severe brain fog ( I am a very ambitious person and it kills that I cannot concentrate or remember anything that I am studying anymore), migraine headaches ( pain in the right eye during the attack), cycles where I have acid reflux like symptoms, constant vomiting after every meal, alternating constipation and diarrhea. I always have mild stomach ache after eating and then have to use the bathroom. During these cycles, I have gone to doctors who said it was IBS and put me on medication that never worked on me. I have gone up until three weeks where I could not eat anything but drink ORS. I also have cycles of excessive sleeping where I sleep almost 15 hrs a day ( increases or decreases from 15) and still wake up extremely tired. Throughout the sleep I am constantly dreaming and get very unrefreshed sleep. I also have shortness of breath,nausea, chronic fatigue and exhaustion and can not do anything mentally or physically stimulating. There have been points where my hands were weak enough that opening bottles became a challenge. Also have a history of incessant hair pulling since I was a child and vitamin D deficiency ( from a blood test done in December 2014). My thyroid tests came back all normal. This summer I started NAET treatment and according to the muscle testing response I have been shown to be "allergic" to almost all food items and also deficient in vitamins and minerals. The treatment so far hasn't helped me and I came across Celiac disease and asked for me to be tested during the period while I was undergoing NAET. I suspected celiac due to the fact that including all these symptoms, I also have tooth discoloration and brown stains on my teeth that I get cleaned every 3-4 months. Dentists do not really know what causes them so far and the last one i spoke to said it may be due to enamel hypoplasia which occurs in gluten intolerant cases. I did a ttg-IgA and total IgA test but came back negative/normal. I have done IgE test in the past and have results that are sky-rocketing high ( as i have chronic rhinitis). But this time my IgE too came back normal as well despite having allergies. Again, this blood was drawn for testing in the middle of my NAET treatment. Should I trust this result? I hope to find some answer or diagnosis to what is going on with me. I cannot function properly and I am extremely exhausted with no energy all day. Life is crumbling at a very important age. If it may be helpful, my family has a history severe joint pain, spondylosis, migraines and couple of symptoms similar to mine. They all just deal with it. My sister who is 14 have been showing weakness on one side, tooth problems and keeps fracturing herself along with very irregular menstrual cycles. I too have noticed that my menstrual period has reduced to less than 3 days from the normal 5 over the past two years, and they are light. Is anyone facing similar health problems or am I a hypochondriac who is not "thinking positively enough" to get better? Sorry for the extremely long post.
  8. Celiac.com 06/17/2015 - Refractory celiac disease type II (RCDII) and EATL (Enteropathy Associated T-cell Lymphoma) are pre-malignant complications of celiac disease. However, there is scant medical literature and data what role malnutrition and intestinal absorption may play in these conditions. With this in mind, a team of researchers set out to conduct a comprehensive assessment of nutritional status and intestinal absorption capacity of patients with RCDII and EATL, and to compare that with data of newly diagnosed celiac disease patients. The research team included N.J. Wierdsma, P. Nijeboer, M.A. de van der Schueren, M. Berkenpas, A.A. van Bodegraven, and C.J. Mulder. They are affiliated with the Department of Nutrition and Dietetics, the Department of Gastroenterology, the Celiac Centre Amsterdam, the Department of Nutrition and Dietetics at VU University Medical Centre in Amsterdam, The Netherlands; and with the Department of Internal Medicine, Gastroenterology and Geriatrics at ATRIUM-ORBIS Medical Centre, Sittard, The Netherlands. They conducted an observational study in tertiary care setting in for 24 RCDII patients, averaging 63.8 ± 8.2 years of age, 25 EATL patients averaging 62.3 ± 5.7 years of age, and 43 celiac disease patients averaging 45.6 ± 14.8 years of age. At diagnosis, the team evaluated anthropometry (BMI, unintentional weight loss, fat-free mass index (FFMI), handgrip strength (HGS), nutritional intake, fecal losses and Resting Energy Expenditure (REE)). They found low BMI (<18.5) more often in RCDII patients than in celiac disease or EATL patients (in 33%, 12% and 12%, respectively, p = 0.029). Also, 58% of EATL patients had unintentional weight loss greater than 10% of total weight, compared to 19% of celiac disease patients, and 39% for RCDII patients (p = 0.005/0.082). The team found energy malabsorption (below 85%) in 44% of RCDII patients, and in 33% of EATL patients, compared with 21.6% in celiac disease (NS). Fecal energy losses were higher in RCDII than in celiac disease patients (589 ± 451 vs 277 ± 137 kcal/d, p = 0.017). REE was lower than predicted, with reulst greater than 10% in 60% of RCDII, 89% of EATL, and 38% of celiac disease patients (p = 0.006). Between one third and two thirds of all patients showed Low FFMI and HGS. Patients with RCDII and EATL show far worse nutritional profiles than untreated naïve celiac disease patients at presentation. This malnutrition is at least partly due to malabsorption as well as hypermetabolism. This study shows the importance of proper diagnosis, and of nutrition in the treatment of these conditions. Source: Clin Nutr. 2015 Apr 30. pii: S0261-5614(15)00124-7. doi: 10.1016/j.clnu.2015.04.014.
  9. I feel hopeless and overwhelmed I’m a 29-year-old mom and newlywed undergoing testing for Celiac/NCGS, and I’m fairly certain that my dear husband is tired of hearing about it all the time…. So here I am. We’ve been together for three years, and I have to tell my husband that I swear that there was a time in my life where I was “normal.” I’m always achy, have crazy GI issues (not great for our sex life), my skin does insane things, and I alternate between raging irritability, anxiety, and depression. Basically, I’m not much fun to be around. We can’t eat out with friends. I don’t do fun things with my daughter. My life revolves around food and my stupid body. I just want to crawl in a hole and stay there. I started my gluten trial 11 months ago after realizing that the host of symptoms that I was experiencing weren’t normal and could potentially be diet-related. I mentioned the idea of cutting out gluten to some nurse (who, in hindsight, didn’t know jack!) and she told me to go ahead, “cut it out for four weeks and then reintroduce it and see what happens.” Then I could “‘call back’ and they’d enter a gluten allergy into my file.” Yes, she seriously said that. And in my naiveté I followed her advice—little did I know that any attempt at an actual diagnosis would be thwarted from there on out. Anyways, I was diagnosed with Salmonella after eating a bag of recalled lettuce in 2010. But other than that, I’ve always had an iron stomach. Nothing fazed me. But over the past four years my health has gradually deteriorated--and this has been so gradual a process that I can’t even pinpoint any onset, and I never even realized that what was happening to me wasn’t normal. [in case you’re curious, here’s a list of some of my symptoms: Neurological—anxiety (dx); depression (dx); irritability; brain fog; and memory problems. General—chronic rhinitis (dx); chronic sinus infections (dx); headaches; joint pain; weak dental enamel; fatigue; chronic dehydration; UTIs; dysmenorrhea (abnormal periods); night sweats; and water retention. GI—nausea; insatiable appetite; chronic diarrhea (dx); hemorrhoids (dx); painful gas; abdominal pain; and bloating. Skin—keratosis pilaris (dx); geographic tongue (dx); dark circles; adult onset cystic acne (dx); dry skin; eczema; and strange petechiae like rashes that look like I’m bleeding under my skin on my legs.] I do yoga. I’m a runner. I eat organic. I don’t eat processed food. I haven’t had fast food in over a decade (literally). I’m 5’6”, and depending on my water retention, range from either 112-120lbs. I’ve always considered myself a healthy individual. But over the past few years that notion has been destroyed. It finally took my husband, my daughter, and my family calling me out on my “antisocialness” to realize that something was wrong. I would seriously rather lie on my bed or sofa in my sweatpants than go anywhere, do anything, or see anyone. My stomach pain interfered with my quality of life that much! It was like there was a war going on inside. And my previously clear skin looked like a 16-year-olds! It was humiliating. I tried everything for that—clarisonic, topical antibiotics, prescription retinoids, creams, washes, masks, birth control—all to no avail. Over time, I guess I just assumed that multiple loose bowel movements a day was normal; that the stomach gurgling, gas, pain, and bloating were just unfortunate; and that the acne was just hormonal [P.S. That went away as soon as I cut out dairy. Quel surprise!] At that point I was desperate. I did a bunch of research online, and I decided I’d try cutting out gluten like the nurse suggested. And it helped! And when I cut out dairy a few months later it was like heaven on earth! All of my symptoms either went away or started to go away. And when I reintroduced either of them, all of my symptoms came back; so I knew something was up. I’ve since learned that I can’t tolerate dairy or gluten (all grains except for rice, and especially not corn). And it’s been do-able. Not fun, but do-able. [i used to consider myself a “foodie,” but not so much anymore]. The problem is, my husband and I are pushing 30 and we want to try to have another kid soon. Since I’m nervous about having such a restrictive diet, potential allergies, or a serious disease, as well as the impact that my health could have on a child, I talked to my PCP about it and she suggested that I see an allergist and a Gastroenterologist. So I did one more reintroduction test (wheat only) just to make sure, and lo and behold, my body freaked out! Except this time I got a crazy rash that I’d never had before (which four doctors haven’t been able to visually identify). That was in February. In March I did a second reintroduction test (again wheat only). The dumb rash came back. So I went to an allergist. She did a full food allergy blood panel on me and they all came back negative. She also did a Celiac panel on me and that came back negative too (though it’s no surprise since I had only eaten one serving of gluten/day for four days, and had been gluten-free for nine months prior). My PCP told me the blood work means nothing because of that. Anyways, a little over a week ago I got sick again, only this time, it was on accident. And the dumb rash came back, except it's spread more this time. My stomach is freaking out, I’ve had diarrhea for ten days, blood in my stool for three, and am passing undigested food. Basically anything I eat goes right through me. I’m starving, dehydrated, and look and feel like death. I saw my PCP and she said I need to go in for a colonoscopy and probably an endoscopy. I’m scared, frustrated, tired, and feel sort of crazy. I’m so tired of feeling like this! I don’t know what I’ll do when the GI tells me that I’m going to have to start eating gluten again! If I could hide I would. So this is where I’m at now. I truly appreciate those of you who took the time to read this! I just know I need to stop relying on my husband as my sole support because it’s not very healthy, and my family just doesn’t understand. Any words of advice, insight, or comfort would be much appreciated! Shannon Gluten-free since May 2013 DF since Sept 2013 Grain free (excl. rice) since Sept 2013 Allergy testing (negative) Mar 2014
  10. Good morning everyone, My name is April and I was just diagnosed with celiac disease last Thursday! I was hoping to share my story and see if anyone else out there is like me and can offer me any "what to expect" advice. Thank you all in advance. In a nutshell these were the weird symptoms I was experiencing: 1. Unexplained weight gain despite diet and exercise 2. Bone pain that progressed (I was scared of cancer) 3. Inability to sleep through the night or feel rested 4. EXTREME fatigue, all the time, no matter how much rest I got or caffeine I consumed Surprisingly I have absolutely NO GI symptoms when I ingest gluten. It never affected my GI tract which is why it took so long to track down I guess. I have always been a very thin person until the past 2-3 years after my dad died suddenly (a lot of my family kicked the bucket in a matter of a year) and I started to gain weight presumably from stress. Of course I thought this was from depression so over the past year and a half I have spent my time feverishly working out (Insanity, P90X, Turbo Jam, personal trainer, kettle bells, you name it!) and actually gained weight and inches much to my chagrin. I went back and forth to my doctor whining about how I am getting fat (I gained 35 lbs in a year and a half despite proper diet and exercise) only to be told I am eating too much and told to cut my calories down to 1100 a day (yeah right)(I currently weigh 140 lbs am 5'0" and going to be 30 later this month yikes!!). So a friend referred me to a lovely holistic medicine doctor who did a plethora of tests on me (ironically that I had begged my normal practitioner to do which she refused) and found that I have celiac disease (homozygous for all 4 genes) and am SEVERELY malnourished. Functionally I am starving to death she said. There was barely a measurable trace of vitamin D in my blood (29 and low normal is 75), I only had slight traces of biotin and one other B vitamin that I can't remember, all the rest were MIA and the same went with my amino acids, out of 26 essential amino acids I only had traces of 3 in my body. Alas she told me this was due to malabsorption and the more I worked out the more my body stored fat as it thought I was starving and the increased calorie burn made my body freak out even more when I was working out 90 minutes a day. This made sense to me until I read that most celiacs actually can't gain weight which is the exact opposite of me. I am interested to hear other experiences to know what I may expect and if I am "normal" so to say. I am excited to have answers but am still scared as I am still gaining a ton of weight although I don't eat much and am very active. Thank you!!
  11. hey all, I am a Gluten free newbie and a member of the community suggested I should introduce myself and explain my situation in a new thread, so here goes: The things you need to know about me: I am in my early 30s. I have had hemiplegic migraines inherited from my dad since I was six or 7. Aura with the migraines usually runs the full gamut from visual distrurbances, to numbness, to disorientation to severe headaches. I have been overweight since puberty hit, and have had GI issues since middle school or high school, but I have dropped 16 pounds since moving from CA to OR in August and trying to start a healthier lifestyle and I am still having GI issues. Somehow the "out of body" feelings and visual disturbances that I used to associate with my migraine aura, became prolonged to the point where I am now feeling them every day. Doctors tried to treat for migraines rather than GI issues and since they couldn't understand what my "out of body feelings were", I lost a few jobs in a row as the result of not being able to be reliable. In doing my own research to find out why I was feeling inexplicably sick every day, my symptoms matched those of malabsorption. My picture could have been next to the description. Gluten and possibly lactose intolerance seemed to be the underlying causes for malabsorption and possible depersonalization (my out of body feelings) so I am now attempting to go 100% gluten free to see if it will fix my issues. I am finding it really difficult for two reasons: #1 I don't know how to cook. I'm used to eating out and grabbing snacks or frozen foods. #2 I am a cheese-a-holic (not so good for avoiding dairy) and #3 hubby and I can barely pay the rent, let alone by all the food we need (though the financial assistance question someone asked in here was very helpful). My doctor just ran a test today for B12 deficiency and I am waiting on the results. She has recommended that I should see a psychiatrist, a GI Specialist and a neurologist, none of which I can do because I have no money! So....I am basically in a constant state of zombie mode, fatigued, stressed, gassy, constipated, sleep deprived, starving, and feeling completely lost when anyone mentions cooking. I just really need some help and advice!
  12. Celiac.com 04/27/2011 - People with microscopic enteritis have microscopic and sub-microscopic changes that are associated with symptoms of gluten sensitive enteropathy, and which lead to micronutrient deficiencies. A team of researchers recently set out to examine microscopic enteritis and the pathomechanism of malabsorption. The research team included Kamran Rostami, David Al Dulaimi, Mohammad Rostami Nejad, Vincenzo Villanacci, and Mihai Danciu. They are affiliated variously with the School of Medicine, University of Birmingham, UK, the Department of Gastroenterology, Alexander Hospital in Redditch, UK, the Nejad Research Center of Gastroenterology and Liver disease, Shaheed Beheshti University, M.C., in Tehran, Iran, the 2nd Department of Pathology, Spedali Civili, University of Brescia Italy, and the “Gr. T. Popa” University of Medicine and Pharmacy in Iasi, Romania. Signs of microscopic enteritis include subtle mucosal abnormalities with no pronounced inflammation, villous effacement, erosions or ulcerations when observed with conventional light microscopy. In cases of microscopic enteritis intraepithelial lymphocytes usually fall within the normal range <25/100 enterocytes (microenteropathy), or increased (lymphocytic enteritis). Microscopic enteritis is the driving force behind atypical forms of celiac disease, previously known as 'potential' and 'latent' celiac disease. Even when there are no major mucosal changes, systemic, microscopic inflammation is a key player in pathophysiology of micro-nutrient deficiency. Microscopic enteritis or celiac disease with milder, Marsh 0–II, enteropathy is the most common feature of atypical gluten sensitivity, while celiac disease with macroscopic enteritis, and Marsh IIa–c is less common. Importantly, and in contrast to much prevailing belief, symptom severity in celiac disease seems to be unrelated to the degrees or length of affected bowel. The microenteropathy may eventually develop into pronounced villous atrophy, but one interesting finding was that severe mucosal damage does not necessarily mean worse symptoms. People with mild symptoms can have more severe damage, while those with little or no visible damage can have more severe symptoms. The finding that nutritional deficiency can be seen in patients presenting with even submicroscopic enteropathy casts doubt on the notion that severe mucosal changes, such as villous atrophy, are the sole driver of malabsorption. In fact, more and more, systemic inflammation seems to be the main driver of nutritional deficiency in such cases. Pro-inflammatory cytokines, such as TNF, appear to act at the enterocyte level, inhibiting the uptake of micronutrients like iron and phosphate. From this, it appears that malabsorption in celiac disease is secondary to inflammation and cytokine stimulation. This might explain why some patients experience milder, 'atypical' enteropathy that acts just like full-blown celiac disease. In fact, inflammation triggered by gluten-sensitized lymphocytes and cytokine stimulation seems to drive the micronutrient deficiencies in celiac disease patients, with or without villous atrophy. This finding is supported by several studies that show malabsorption syndrome to be no worse in patients with villous atrophy than in those with microenteropathy (Marsh 0–II). This theory is further bolstered by the fact that many people suffer from non-symptomatic, silent celiac disease with villous atrophy, and mucosal lesions that persist after years of successful gluten-free treatment. Over the last few years, the only type of gluten sensitivity doctors have identified is atypical presentation with microenteropathy resulting in micronutrient deficiencies. However, the team points to recent studies by Kurppa et al., and Ludvigsson et al., that suggest simple changes can improve life quality for celiac disease patients with milder enteropathy. The researchers feel strongly that patients with milder enteropathy and positive serology may benefit from a gluten-free diet, and that autoantibodies might have a more reliable positive predictive value than histology, especially in early enteropathy. Diagnosing celiac disease in its early stages, especially with little or no mucosal damage, can be very challenging. However, new studies are paving the way toward a better understanding of gluten sensitivity with microenteropathy. As a result, more patients with microenteropathy, symptoms of micronutrient deficiency and positive serology are being presented with the possible benefits of a gluten-free diet. Source: Autoimmun Highlights (2010) 1:37–38. DOI 10.1007/s13317-010-0006-4
  13. Celiac.com 05/12/2010 - Diarrhea, weight loss and malabsorption represent the major clinical presentation of celiac disease, but the exact mechanisms of these symptoms are not fully understood. A team of researchers recently set out to determine whether celiac disease impairs the function of solute transporters and aquaporins. The research team included U. Laforenza, E. Miceli, G. Gastaldi, M. F. Scaffino, U. Ventura, J. M. Fontana, M. N. Orsenigo, and G. R. Corazza. The team looked for possible alteration in the expression and localization of water channels, known as aquaporins, and certain solute transporters in duodenal mucosa of celiac disease patients. To do this, the team evaluated duodenal biopsies from untreated celiacs, treated celiacs, healthy controls and disease controls. The team used semi-quantitative RT-PCR and real time RT-PCR to determine the expression of some aquaporins and transporters mRNA in the duodenal biopsies. They relied on immunohistochemistry to evaluate the localization of aquaporin 3, 7 and 10, and of Na+/glucose cotransporter, H+/oligopeptide transporter and Na+/H+ exchanger. They found that the duodenal biopsies of healthy controls, treated celiac patients and disease controls expressed aquaporin 3, 7, 10, 11, Na+/glucose cotransporter, H+/oligopeptide transporter and Na+/H+ exchanger, cystic fibrosis transmembrane conductance regulator and Na-K-2Cl cotransporter mRNAs. Transcript expression was largely absent in the duodenal biopsies of untreated celiac disease patients, except for cystic fibrosis transmembrane conductance regulator and Na-K-2Cl cotransporter. Immunohistochemistry of healthy control subjects showed a labeling in the apical membrane of surface epithelial cells of duodenum. Immunolabeling was heavily reduced or absent in untreated celiac patients, but normal patients who had followed a gluten free diet for at least 1 year. The results of the study show that people with celiac disease have defects in their primary pathways for water and solute absorption that may play a role in the onset of malabsorption symptoms. Source: Biol Cell. 2010 Apr 26.
  14. Eur J Gastroenterol Hepatol 2000;12:541-547. (Celiac.com 07/09/2000) Researchers in Sweden released a report that shows a high number of patients with chronic diarrhea also have bile acid malabsorption. Further, steatorrhea is also common, but appears to be independent of bile acid malabsorption. Their study evaluated 94 patients with chronic diarrhea for loss of bile acids using both 75-SeHCAT and a fecal fat excretion tests. The patients also completed a symptom questionnaire before during a 7 day period before taking the 75-SeHCAT test. Dr. Kjell-Arne Ung and his colleagues from Sahlgrenska University Hospital, in Goteborg reported their finding in the the May issue of the European Journal of Gastroenterology and Hepatology. They found that mild steatorrhea was present in 50% of patients with non-organic bile acid malabsorption, and in 38% of patients with functional diarrhea. Further, low 75-SeHCAT levels alone is not an indicator or risk for steatorrhea, although some patients with severe organic disease had a concomitant malabsorption of fat and of bile acids. Dr. Ungs study also shows that severe steatorrhea was common in patients with celiac disease, even in patients with high 75-SeHCAT values. When compared with patients who had functional diarrhea, those with bile acid malabsorption had significantly more frequent and looser stools, however, abdominal pain, distension and flatulence was equal between those with bile acid malabsorption and normal bile acid absorption. In conclusion Dr. Ung and colleagues state: The high prevalence of bile acid malabsorption and the absence of specific symptoms, with the exception of frequent and liquid stools, indicates that the 75-SeHCAT test should be performed early in the investigation of patients with chronic diarrhea.
  15. George Von Hilsheimer, 1977 (Celiac.com 06/12/2000) A way the hypothalamic choreographer might be deranged is by malabsorption syndrome. If this suggestion is valid it directly leads to some simple therapeutic guidelines and implications for inexpensive and productive research - I suggest that malabsorption syndrome is a whole complex of metabolic disorders which interact with psychosocial stress, infection, allergies and endocrine disorders. Malabsorption is a stressor in itself... ...Malabsorption is associated with high levels of circulating adrenocortocotrophic hormone (ACTH) and with high levels of acetylcholine (ACh). ACTH and ACh are in turn associated with modes of learning which are characterized by poor habituation (the animals do not learn or unlearn well), by high levels of avoidance, by efficient escape conditioning, by neophobia and by poor instrumental conditioning. The experimental evidence suggests that children with malabsorption will often be similar in their electrophysiological and conditioning patterns to animals with lesions to the hypothalamus and to the hippocampus. (Di SantAgnese & Jones, 1962.)... ...Many authors have remarked on the similarity of the symptoms of sprue and celiac disease to schizophrenia (Dohan, 1969). Abnormal levels of hydrochloric acid in the stomach are associated with hysteria and neurosis (Hepler, 1970). The classic celiac syndrome is said to occur in about one case in every two thousand patients seen by pediatricians, and there is a similar frequency of nontropical sprue in adults. However, one authority (Hodgkin, 1973) reported seeing only one case of celiac disease and no sprue in ten years on a British National Health Service with 2500 patients. My own experience is that many physicians are reluctant to diagnose celiac disease and that the variability of its frequency as a diagnosis may be even greater than that among expert clinicians diagnosing diabetes from laboratory results (viz. from 2 to 76%. Jarrett & Keen (1976)... ...Consequences of Malabsorption: The ecology of the gut would be poor; Imbalances in blood chemistries and developmental anomalies would indicate neonatal and fetal nutritional inadequacy; The adrenal glands would be depleted; The immune system would be over reactive... ...Evidence for Malnutrition in Middle Class Delinquents Summarizing the preliminary reports reviewed above and looking at my delinquents in their light suggest that compared to other children: Delinquents are more often products of unfortunate pregnancies; They suffer more pregnancy and birth complications; They are seldom breast fed; They have more colic and other early indications of GI distress and food intolerance; They are often victims of celiac syndrome and other inborn errors of metabolism; They are early addicted to diets high in sugar and refined carbohydrates; They have poor absorption of food deficient intestinal flora, and slow transit times for food products moving through their guts; They have thiamin, pyridoxine and pantothenic acid deficiencies as neonates. These facts suggest that delinquents are at high risk for unusual CNS development, CNS damage, poor continuing synthesis of CNS amino acids and neural transmitters, and are extremely vulnerable to derangements of the immune and allergy systems... ...Criminal, felon (schizophrenics), and chronic patients had the greatest evidence of malabsorption syndrome of all the subjects, who generally evidenced malabsorption. Felon (schizophrenic) had lower hair Cu than (schizophrenic) patients who were not actively delinquent...
  16. The following was sent to me from Rio de Janeiro by Dr. José Cesar da Fonseca Junqueira. If you have any questions you can e-mail him at: cjunqueira@ax.apc.org.br Rio de Janeiro - 05/27/96 - Celiac Disease. A Comparative study of two periods. Junqueira JC, Calçado AC, Percope S. 1996 Federal University of Rio de Janeiro Martagão Gesteira - Institute of Pediatrics. The aim of this study was to compare cases of celiac disease diagnosed in outpatients with malabsortion cases. The study was conducted at the Pediatric Gastroenterology Service of the Pediatric Institute Martagão Gesteira at the Federal University of Rio de Janeiro Brazil. It was done in two phases: from 1975 -1984 and from 1985 - 1994 (group 1, N=31 and group 2, N=21). Patients were selected based on the results of jejunal biopsy (group IV) and the favorable reaction to a gluten free diet. Data from the first interview (age, sex, nutritional status and prevalent symptoms) were analyzed. The number of biopsies and the level of compliance with the diet were also observed. The data collected was processed in a computer using EPI INFO 6.03 (January 1996)as software. The frequency of celiac disease over the studied years was compared with international data. There were no significant differences between the two groups in our study. However, the cases free of gastroenterological symptoms (atypical celiac disease) were not observed. The average age difference between the groups (group um X=24,39 months; group 2 X=32,03) was not statistically significant. A bigger study must be carried out to prove this theory. The analysis of nutritional status of the groups reveals the existence of severely undernourished patients. The number of biopsies and the level of compliance with diet were similar in the two groups. The decrease in the number of cases as well the increase in the age of patients were observed in group 2. These phenomena were probably due to a delayed exposure to gluten and to the expansion of the period of breast feeding. Other causes should be analyzed in a bigger research program. The conclusion of this study shows that there has been no change in the clinical features of the disease and points to the need for serological screening so that the entire spectrum of the disease can be established. Both groups had malabsorption and were very under-nourished (over 45%). One patient was diagnosed as having Diabetes Mellitus several years after and an other one is under investigation for poliarthrites. Serological investigation is not available in our country. The final conclusion is that we must have such serological screening to know the real spectrum of the disease. Adult celiac disease is not diagnosed in our country, mainly because the adult doctors do not know the full spectrum of celiac disease. Ill be presenting this work as a thesis at the University on May 29, 1996.
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