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Found 1,261 results

  1. Celiac.com 09/10/2018 - Anyone diagnosed with celiac disease needs to eat a gluten-free diet if they hope to see their condition improve, and not lead to worse outcomes. So, how much gluten exposure do celiacs get on a gluten-free diet? William F. Balistreri, MD, Director Emeritus, Pediatric Liver Care Center; Medical Director Emeritus, Liver Transplantation at Cincinnati Children's Hospital in Cincinnati, Ohio presented data at this year's Digestive Disease Week that focused on the challenges celiac patients face in trying to follow a gluten-free diet. Gluten-free standards and labels help improve awareness, but even so, eating gluten-free can be a challenge. Anyone with celiac disease can tell you that the chances of accidental gluten contamination are many, and that consent vigilance is required. Even ”gluten-free foods" are not always free from variable amounts of gluten, whether by imprecise food production, processing, packaging, or preparation. Accidental gluten exposure can also come via non-foods, such as lipstick, shampoo, toothpaste and the like. Regular, low-level gluten exposure can cause many celiac patients to have mucosal inflammation despite maintaining a gluten-free diet. Product by product, gluten levels are generally well-known, but not much is known about how much gluten exposure levels in people with celiac disease who are following a gluten-free diet. Such information could be quite helpful in designing disease management and patient follow-up strategies. Gluten immunogenic peptide (GIP) analysis provides direct and quantitative measurement of gluten exposure, has proven useful in diagnosis and clinical management of non-responsive or refractory celiac patients. To figure out the amounts of gluten ingested by highly motivated, educated celiac patients following a gluten-free diet, the research team measured levels of GIPs in food, urine, and stool. They noted the connections between gluten exposure and persistent villous atrophy or related conditions. The study also analyzed food samples from restaurant “doggie bags" saved by the study subjects. The team detected gluten in at least one food sample from nearly 90% of patients consuming a gluten-free diet. That indicates that nearly nine out of ten people with celiac disease, who are trying hard to follow a gluten-free diet, as being exposed to gluten when they eat out. Overall, approximately 33% of food samples tested positive for GIPs above 20 ppm, and the estimated GIPs ingested ranged from 0.23 mg to > 40 mg per exposure. This new information confirms what many people with celiac disease have long suspected. Namely, that avoiding gluten is really hard to do, even for who are highly aware of gluten-related celiac disease issues, and who work hard to avoid gluten. Read more at: Medscape.com
  2. Celiac.com 09/01/2018 - Celiac disease is a common disease triggered by gliadin exposure in genetically sensitive individuals. It has long been known that untreated celiac disease is associated with intestinal malabsorption, but it is also associated with ongoing inflammation. This inflammation may have adverse effects on the uptake of important nutrients. This is probably the underlying reason for the increased risk of osteoporosis demonstrated in patients with celiac disease. Malabsorption and ongoing inflammation in untreated celiac disease could also potentially have a negative effect on fetal development. Several reports have indicated an adverse effect of untreated celiac disease on pregnancy outcome. We set out to use the national registers of Sweden to: Evaluate the association of untreated celiac disease and birth weight, pregnancy duration and intrauterine growth. Evaluate the same association in treated celiac disease. Compare the risk of the above two groups with a reference group of 2.8 million births to mothers who never had a diagnosis of celiac disease. A fourth objective was to evaluate placental weight to see if lower placental weight was more frequent in women with celiac disease. We found that untreated celiac disease (women diagnosed after pregnancy, but most likely having untreated celiac disease at time of pregnancy) was associated with a two-fold risk of low birth weight, pre-term birth, intrauterine growth retardation and cesarean section. The low birth weight and intrauterine growth retardation may have been mediated through malabsorption, since placental weight was lowest in women with untreated celiac disease. This study was published in Gastroenterology Aug 2005. A link to this paper can be found here: gastrojournal.org After that we set out to evaluate the association between adverse pregnancy outcome in males with untreated and treated celiac disease. In a previous paper, we had found an increased risk of adverse pregnancy outcome when the father had celiac disease (Ludvigsson et al, Gut, 2001). Now, taking advantage of the large Swedish national registers (all births since 1973 and onwards are recorded), we found no increased risk of low birth weight, pre-term birth or cesarean section in infants to fathers with untreated or treated celiac disease. This study was published in the Scandinavian Journal of Gastroenterology in Feb 2006.
  3. Celiac.com 08/28/2018 - There have been a number of studies that tried to estimate risk levels for celiac disease in patients with osteoporosis, but the data has been highly variable and inconclusive. To address this, a team of researchers recently set out to investigate rates of celiac disease among individuals with osteoporosis. The research team included M. Laszkowska, S. Mahadev, J. Sundström, B. Lebwohl, P. H. R. Green, K. Michaelsson, and J. F. Ludvigsson. They are variously affiliated with the Department of Medicine, Celiac Disease Center, Columbia University College of Physicians and Surgeons, New York, NY, USA, the Department of Medical Sciences, Uppsala Clinical Research Center, Uppsala University in Uppsala, Sweden, the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet in Stockholm, Sweden, the Department of Paediatrics, Örebro University Hospital in Örebro, Sweden, and with the Division of Epidemiology and Public Health, School of Medicine, University of Nottingham in Nottingham, UK. The team conducted a systematic review of articles that appeared in PubMed, Medline or EMBASE through May 2017 to find studies on rates of celiac disease in patients with osteoporosis. Search terms included “coeliac disease” combined with “fractures”, “bone disease”, “bone density”, “densitometry”, “osteoporos*”, “osteomal*”, “osteodys” or “dexa” or “dxa” or “skelet”. Non‐English papers with English‐language abstracts were included. To confirm their data, the team used fixed‐effects inverse variance‐weighted models, and tested heterogeneity through both subgroup analysis and meta‐regression. They found a total of eight relevant studies, containing data from 3,188 people with osteoporosis. From this group, the team found 59 individuals, or just under 2%, with celiac disease. A weighted pooled analysis showed biopsy‐confirmed celiac disease in 1.6% of osteoporosis patients. The team found moderate heterogeneity (I2 = 40.1%), which was influenced by the underlying celiac disease rates in the general population. After adding four studies covering a total of 814 people with celiac disease, based on positive tissue transglutaminase or endomysial antibodies, the pooled rate was comparable (1.6%; 95% CI = 1.2%‐2.0%). About 1.6% of people with osteoporosis have biopsy‐verified celiac disease. That’s about the same rate as the general population. Based on this data, the team sees no need to routinely screen osteoporosis patients for celiac disease, contrary to current guidelines. They suggest additional studies to assess the benefits and desirability of such screening programs. So, it looks like there’s no reason for people with osteoporosis, or their doctors, to be concerned about celiac disease unless patients shows some physical symptoms or signs. Read more in: Alimentary Pharmacology & Therapeutics
  4. 08/21/2018 - Does celiac disease have any kind of adverse effect on ovarian reserve levels in women of reproductive age? To get an answer, a team of researchers recently conducted a study of ovarian reserve in patients of reproductive age with celiac disease using anti-Müllerian hormone (AMH) levels, antral follicle counts (AFCs), and ovarian volume. The research team included Erol Cakmak, Savas Karakus, Ozlem Demirpence, and Banu Demet Coskun. They are variously affiliated with the Department of Gastroenterology, the Department of Obstetrics and Gynecology, the Department of Biochemistry, Cumhuriyet University Faculty of Medicine, Sivas, Turkey, and with the Department of Gastroenterology, Kayseri Training and Research Hospital in Kayseri, Turkey. For this study, their team included 46 female celiac patients and 40 healthy female subjects of reproductive age, 18–45 years of age. The team drew blood samples from both groups on days 2–4 of the menstrual cycle, and measured follicle stimulating hormone (FSH), luteinizing hormone (LH), estradiol (E2), prolactin (PRL), and AMH levels. On the same day, the team measured AFCs and ovarian volume for each patient. They also recorded patient body mass index (BMI), gravidity/parity/abortions/alive counts, disease duration, and Marsh histological classification. The results showed no statistically significant differences between celiac disease patients and control groups in terms of mean age, BMI, or median gravidity/parity/abortions/alive counts. Also, there were no statistically significant differences between the groups in terms of average FSH, LH, E2, PRL levels, right and left ovarian volumes, and median right and left ovarian AFCs. The team found AMH levels to be markedly lower in the celiac group. The Spearman correlation test showed no significant connection between AMH levels and age, BMI, FSH, LH, E2, PRL levels, right and left ovarian volumes, right and left ovarian AFCs, or Marsh histological classification. However, the team did find that, compared to healthy controls, female celiac patients of reproductive age showed decreased AMH levels and ovarian reserves that reflected the length of celiac duration; the longer the celiac disease, the greater the decrease. It appears that, especially over time, celiac disease can reduce ovarian reserves, which could have an adverse affect on fertility. Read more at: Med Sci Monit. 2018; 24: 1152–1157.
  5. Celiac.com 08/27/2018 - Imagine the difficulty of diagnosing celiac disease without the associated blood antibodies, with seemingly normal blood tests. Seronegative celiac disease is one of the most common causes of seronegative villous atrophy, so a biopsy is crucial in such cases, but it can be hard for doctors to justify a biopsy in the face of seemingly normal blood tests. How can researchers learn more? Seronegative celiac disease seems like a simple enough condition. It's just the presence celiac disease without the celiac-associated blood antibodies typically found in people with the disorder. Isn't it? Well, not exactly. For one thing, seronegative celiac disease is rare, and the little data that exist are contradictory. Some data has even indicated that seronegative enteropathies have lead to higher rates of death than standard celiac disease. Yet, seronegative celiac disease remains poorly defined, partly from an absence of consensus on an exact definition, and partly due to an imprecise use of specific celiac serology. Due to these factors, accurate celiac diagnosis can be extra difficult in patients with seronegative celiac disease. Even when doctors spot seronegative villous atrophy, they still need to exclude other enteropathies as a potential cause. To try to shed some light on the nature of seronegative celiac disease, a team of researchers recently set out to provide a critical summary of the most recent work on this topic, along with a working definition of seronegative celiac disease. The research team included A Schiepatti, DS Sanders, and F Biagi. They are variously affiliated with the Coeliac Centre/First Department of Internal Medicine, University of Pavia, Pavia, Italy, and with the Academic Department of Gastroenterology, Royal Hallamshire Hospital & University of Sheffield, UK. Finding an accepted definition of seronegative celiac disease is crucial in order to ensure that patients receive a correct diagnosis, and thus avoid inappropriate treatment, and the perils associated with long-term untreated celiac disease. Since cases of seronegative celiac disease are commonly dealt with individually, it is important to establish strict criteria for the diagnosis of seronegative celiac disease to ensure prompt identification and treatment of these celiac patients. Doing so will require further study, along with input from the scientific community. Source: Curr Opin Gastroenterol. 2018 May;34(3):154-158.
  6. Celiac.com 08/15/2018 - Grain-free food has been linked to heart disease in dogs. A canine cardiovascular disease that has historically been seen in just a few breeds is becoming more common in other breeds, and one possible culprit is grain-free dog food. The disease in question is called canine dilated cardiomyopathy (DCM), and often results in congestive heart failure. DCM is historically common in large dogs such as Great Danes, Newfoundlands, Irish Wolfhounds, Saint Bernards and Doberman Pinschers, though it is also affects some Cocker Spaniels. Numerous cases of DCM have been reported in smaller dogs, whose primary source of nutrition was food containing peas, lentils, other legume seeds or potatoes as main ingredients. These reported atypical DCM cases included Golden and Labrador Retrievers, a Whippet, a Shih Tzu, a Bulldog and Miniature Schnauzers, as well as mixed breeds. As a result, the U.S. Food and Drug Administration's Center for Veterinary Medicine, along with a group of veterinary diagnostic laboratories, is investigating the possible link between DCM and pet foods containing seeds or potatoes as main ingredients. The good news is that in cases where the dog suffers no genetic component, and the disease is caught early, simple veterinary treatment and dietary change may improve heart function. According to Nutritional Outlook, an industry publication for makers of dietary supplements and healthy foods and beverages, there is a growing market for “free from” foods for dogs, especially gluten-free and grain-free formulations. In 2017, about one in five dog foods launched was gluten-free. So, do dogs really need to eat grain-free or gluten-free food? Probably not, according to PetMD, which notes that many pet owners are simply projecting their own food biases when choosing dog food. Genetically, dogs are well adapted to easily digest grains and other carbohydrates. Also, beef and dairy remain the most common allergens for dogs, so even dogs with allergies are unlikely to need to need grain-free food. So, the take away here seems to be that most dogs don’t need grain-free or gluten-free food, and that it might actually be bad for the dog, not good, as the owner might imagine. Stay tuned for more on the FDA’s investigation and any findings they make. Read more at Bizjournals.com
  7. Celiac.com 08/16/2018 - What is the significance of vitamin D serum levels in adult celiac patients? A pair of researchers recently set out to assess the value and significance of 25(OH) and 1,25(OH) vitamin D serum levels in adult celiac patients through a comprehensive review of medical literature. Researchers included F Zingone and C Ciacci are affiliated with the Gastroenterology Unit, Department of Surgery, Oncology and Gastroenterology, University of Padua, Padua, Italy; and the Celiac Center, AOU San Giovanni di Dio e Ruggi di Aragona, University of Salerno, Department of Medicine and Surgery, Salerno, Italy. Within the wide spectrum of symptoms and alteration of systems that characterizes celiac disease, several studies indicate a low-level of vitamin D, therefore recent guidelines suggest its evaluation at the time of diagnosis. This review examines the data from existing studies in which vitamin D has been assessed in celiac patients. Our review indicates that most of the studies on vitamin D in adult celiac disease report a 25 (OH) vitamin D deficiency at diagnosis that disappears when the patient goes on a gluten-free diet, independently of any supplementation. Instead, the researchers found that levels of calcitriol, the active 1,25 (OH) form of vitamin D, fell within the normal range at the time of celiac diagnosis. Basically, their study strongly suggests that people with celiac disease can recover normal vitamin D levels through a gluten-free diet, without requiring any supplementation. Source: Dig Liver Dis. 2018 Aug;50(8):757-760. doi: 10.1016/j.dld.2018.04.005. Epub 2018 Apr 13.
  8. Celiac.com 08/13/2018 - It’s not uncommon for people to have psychiatric reactions to stressful life events, and these reactions may trigger some immune dysfunction. Researchers don’t yet know whether such reactions increase overall risk of autoimmune disease. Are psychiatric reactions induced by trauma or other life stressors associated with subsequent risk of autoimmune disease? Are stress-related disorders significantly associated with risk of subsequent autoimmune disease? A team of researchers recently set out to determine whether there is an association between stress-related disorders and subsequent autoimmune disease. The research team included Huan Song, MD, PhD; Fang Fang, MD, PhD; Gunnar Tomasson, MD, PhD; Filip K. Arnberg, PhD; David Mataix-Cols, PhD; Lorena Fernández de la Cruz, PhD; Catarina Almqvist, MD, PhD; Katja Fall, MD, PhD; Unnur A. Valdimarsdóttir, PhD. They are variously affiliated with the Center of Public Health Sciences, Faculty of Medicine, University of Iceland, Reykjavík, Iceland; the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; the Department of Epidemiology and Biostatistics, Faculty of Medicine, University of Iceland, Reykjavík, Iceland; the Department of Rheumatology, University Hospital, Reykjavík, Iceland; the Centre for Rheumatology Research, University Hospital, Reykjavík, Iceland; the National Centre for Disaster Psychiatry, Department of Neuroscience, Psychiatry, Uppsala University, Uppsala, Sweden; the Stress Research Institute, Stockholm University, Stockholm, Sweden; the Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; the Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden; the Astrid Lindgren Children’s Hospital, Karolinska University Hospital, Stockholm, Sweden; the Clinical Epidemiology and Biostatistics, School of Medical Sciences, Örebro University, Örebro, Sweden; the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; and the Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts. The team conducted a Swedish register-based retrospective cohort study that included 106, 464 patients with stress-related disorders, 1,064 ,640 matched unexposed individuals, and 126 ,652 full siblings to determine whether a clinical diagnosis of stress-related disorders was significantly associated with an increased risk of autoimmune disease. The team identified stress-related disorder and autoimmune diseases using the National Patient Register. They used Cox model to estimate hazard ratios (HRs) with 95% CIs of 41 autoimmune diseases beyond 1 year after the diagnosis of stress-related disorders, controlling for multiple risk factors. The data showed that being diagnosed with a stress-related disorder, such as post-traumatic stress disorder, acute stress reaction, adjustment disorder, and other stress reactions, was significantly associated with an increased risk of autoimmune disease, compared with matched unexposed individuals. The team is calling for further studies to better understand the associations and the underlying factors. Source: JAMA. 2018;319(23):2388-2400. doi:10.1001/jama.2018.7028
  9. I was diagnosed with Severe Celiacs last November plus 2 forms of glaucoma and recently degenerative arthritis. I'm only 22 and finding all this out is exhausting and stressful, well recently I decided to take a break from the gluten free diet and ordered a stuffed crust pizza from pizza hut, a few things from taco bell and a buffet at golden corral! And I have not gotten sick! Maybe I rash but the rash was there before hand, now I'm concerned my doctor was wrong and misdiagnosed me somehow? Before I started the gluten diet I was severely sick, throwing up and couldn't eat, I thought I had cancer, can someone help idk who else to go to, is this normal? Getting sick and then not getting sick? Oh and the rash has been there for weeks doctor has no idea what it is gonna see specialist, auto immune diseases are in family, I did have pelvic inflammatory disease could that of caused something?
  10. Celiac.com 11/15/2010 - Fermentation of wheat flour with sourdough lactobacilli and fungal proteases decreases the concentration of gluten in wheat. Depending on the level of hydrolyzation, gluten levels can be reduced as low as 8 parts per million. A team of researchers recently conducted a small study to assess whether people with celiac disease can eat baked goods made with wheat flour that is hydrolyzed via sourdough lactobacilli and fungal proteases during food processing. The team included L. Greco, M. Gobbetti, R. Auricchio, R. Di Mase, F. Landolfi, F. Paparo, R. Di Cagno, M. De Angelis, C. G. Rizzello, A. Cassone, G. Terrone, L. Timpone, M. D'Aniello, M. Maglio, R. Troncone, S. Auricchio. They are affiliated with the Department of Pediatrics and European Laboratory for the Study of Food Induced Diseases, University of Naples, Federico II in Naples Italy. The team evaluated the safety of daily administration of baked goods made from this hydrolyzed form of wheat flour for patients with celiac disease. Patients who volunteered for the study were assigned at random to consume 200 grams per day of baked goods from one of three groups. The did so every day for 60 days. The first group of six patients ate natural flour baked goods (NFBG), with a gluten content of 80,127 ppm gluten. The second group of 2 patients ate baked goods made from extensively hydrolyzed flour (S1BG), with a residual gluten content of 2,480 ppm. The third group of patients ate baked goods made from fully hydrolyzed flour (S2BG), with just 8 ppm residual gluten. In the first group, two of the six patients consuming baked goods made with natural flour (NFBG) discontinued the challenge because of adverse symptoms. All six patients in this group showed increased levels of anti-tissue transglutaminase (tTG) antibodies and small bowel deterioration. The two patients who ate baked goods made from extensively hydrolyzed flour (S1BG) had no clinical complaints, but biopsy showed intestinal damage in the form of subtotal villous atrophy. The five patients who ate baked goods made with made from fully hydrolyzed flour (S2BG), at just 8 ppm residual gluten had no clinical complaints. Also, they showed no increase in anti-tTG antibodies, and Marsh grades of their small intestinal mucosa showed no adverse change. Evidence with this small 60-day dietary study shows that people with celiac disease can safely consume baked goods made from fully hydrolyzed wheat flour, manufactured with sourdough lactobacilli and fungal proteases. This flour shows no toxicicity to patients with celiac disease. The team notes that a combined analysis of serologic, morphometric, and immunohistochemical parameters is the most accurate method to assess new therapies for this disorder. The results need to be borne out by further study, but, in the future, baked goods made with fully hydrolyzed wheat flour, manufactured with sourdough lactobacilli and fungal proteases may become another option for people with celiac disease. Source: Clin Gastroenterol Hepatol. 2010 Oct 15. doi:10.1016/j.cgh.2010.09.025
  11. J Allergy Clin Immunol 2004;113:1199-1203. Celiac.com 07/30/2004 - According to a study by Italian researchers published in the June edition of the Journal of Allergy and Clinical Immunology, the prevalence of atopic dermatitis is much more common in those with celiac disease. The researchers looked at 1,044 adults with untreated celiac disease at the point of their diagnoses, as well as 2,752 of their relatives, and 318 of their spouses. They also looked at the prevalence of allergies in celiacs after one year on a gluten-free diet. The subjects filled out a standardized questionnaire upon their diagnosis, and those who reported having an allergy were tested for it using a standard makeup of 20 antigens for serum specific IgE. The researchers found that one celiac in 173 (16.6%) had at least one additional allergy, compared with 523 of their relatives (19%), and 43 of their spouses (13.5%). Patients with celiac disease were also more likely (3.8%) to have atopic dermatitis than their relatives (2.3%) or their spouses (1.3%). The amount of time that the celiac patients went undiagnosed and therefore untreated did not seem to influence the presence of allergy or atopic dermatitis. It is possible that a longer period of time on a gluten-free diet could influence the prevalence of allergy in those with celiac disease, and more research needs to be done to determine if being gluten-free longer can decrease allergies in those with celiac disease.
  12. Celiac.com 04/29/2010 - May is designated as National Celiac Awareness Month. As such, I thought it would be a great opportunity to explore the history of celiac disease. Most people think of celiac disease as a modern day ailment, which predominantly affects those of European descent and in Westernized societies. However in my research, I found that the best place to start when referencing the history of celiac disease, is actually the beginning of humans. In the beginning of humans, known as the Neolithic Period, humans were hunters and gatherers and primarily survived on fruits, nuts, and meat when available. During the Neolithic Period, humans evolved and began cultivating plants which quickly led to the agricultural revolution. With the agricultural revolution came a myriad of food antigens, such as dairy, eggs and processed grains. It was during this time that celiac disease was born. Some 8,000 years after making its debut, celiac was identified and named by a Greek physician known as Aretaeus of Cappadocia. In the first century A.D., Aretaeus documented information about, “The Coeliac Affection.” He named celiac disease, “koiliakos” derived from the Greek word for “abdomen”. In his descriptions of celiac Aretaeus stated, “If the stomach be irretentive of food and if it pass through undigested and crude, and nothing ascends into the body, we call such persons coeliacs”. While a name had been given to the disease, people with celiac still had no idea how to heal from the condition, and were still vastly unaware of the cause for their ailments. It wasn't until the early 19th Century that Dr. Mathew Baillie published his observations on celiac disease which he sited as, 'chronic diarrheal disorder causing malnutrition and characterized by a gas-distended abdomen'. In his observations, Dr. Baillie documented that some of his patients appeared to benefit from eating only rice. However important Dr. Baillie's findings were, they still went largely unnoticed by the medical community until 75 years later when an English doctor known as Dr. Samuel Gee, came into the scene. In 1888 Dr. Gee was working for the Great Ormond Street Hospital for Children in the United Kingdom when he demonstrated a set of clinical trials performed on children and adults with celiac disease. Dr. Gee was quoted as saying, “To regulate the food is the main part of treatment. The allowance of farinaceous foods must be small, but if the patient can be cured at all, it must be by means of diet.” As an example he sited a very sick child that was fed the best Dutch mussels every day during mussel season. The child thrived during mussel season, but as soon as the season was over, the child regressed and died before the next mussel season. In the 1920's, Sidney Hass presented the “Banana diet”. Sydney successfully treated 8 out of 10 children suffering with celiac disease using the banana diet. He claimed to have cured the 8 children that were on the banana diet, but the other 2 children not on the banana diet, died. The banana diet included the elimination of all bread, crackers, potatoes and cereals and for several decades, the banana diet was the only cure for celiac disease. Another important marker in the history of celiac disease were the findings by Dutch pediatrician, Dr. Willem Karel Dicke. In 1953 Dr. Dicke wrote his doctoral thesis for the University of Utrecht based on his observations that the ingestion of wheat proteins specifically, and not carbohydrates in general, were the cause of celiac disease. He was able to exemplify his findings based on bread shortages in the Netherlands during World War II. During the bread shortages, he found that the health of children with celiac improved tremendously. However, when the allied planes began dropping bread to the Netherlands, the same children quickly deteriorated. In the 1960's, it became evident that the best method for testing for celiac disease was to perform a biopsy. However, doctors were urged not to diagnose people as having celiac disease until it was proven that gluten was the cause for the damage. To determine if a patient had celiac disease, a biopsy would be performed to evaluate the damage done to the intestines. The patient would then be put on a gluten-free diet. Another biopsy would then be preformed to determine improvement in the intestines. After improvement the patient would be put back on a gluten diet, and another (3rd) biopsy would be preformed to determine reoccurring damages to the intestine, and thus the presence of celiac disease. This method was used for over 20 years as the best method for testing for celiac disease. Then in the 1980's studies by Dr. Stefano Guandalini, showed that the presence of celiac could be found in 95% of celiac cases by performing a single biopsy. In 1990 these findings helped create the new guidelines for celiac testing which were approved by ESPGHAN (European Society for Pediatric Gastroenterology). Also during this time, professionals starting recognizing celiac as an autoimmune disease and also began recognizing the correlation between gluten sensitivity and other autoimmune diseases. Here we are now in the year 2010; thirty years after the medical profession has successfully established the causes, tests and treatments for celiac disease, and thousands of years since celiac first made it's debut. Yet, as far as early diagnosis is concerned, we are still living in the dark ages. In this day and age, knowing what we know about celiac disease, childhood screening for celiac should already be mandatory. It's almost as if, when doctors were told in the 1960's to hold off on celiac diagnosis until they knew undoubtably that gluten was the cause for damage to intestines, they were never told, 'okay, now it's safe to diagnose for celiac'. Unfortunately, many (if not most) doctors still don't know how to appropriately diagnose patients for celiac disease, and therefor they continue to 'hold off' making celiac diagnoses, or misdiagnose regularly. Enforcing mandatory celiac screening in school age children has potential to eliminate the unnecessary suffering of millions of children and adults worldwide. My dearest hope is that we all get to see mandatory celiac testing in this lifetime. If you would like more information on “Celiac Awareness Month,” please check out the links below. The following links are trusted sites that also provide suggestions on how you can get involved and contribute to celiac awareness in your community. Celiac Disease Foundation Celiac Sprue Association Celiac Disease Timeline: Agricultural Revolution - celiac disease is born 1st Century A.D.- Aretaeus named celiac, “ koiliakos” 1st Century A. D.- Aretaeus documented“The Coeliac Affection.” 19th Century- Dr. Mathew Baillie published his observations on celiac 1888- Dr. Gee established the correlation between celiac and diet 1920's - Sydney Hass successfully treated celiac patients with “the banana diet” 1953 - Dr. Willem Karel Dicke confirmed wheat protein to be the cause for celiac disease 1960's - Biopsy established as the most accurate test for celiac 1980's - Dr. Stefano Guandalini established a single biopsy test for celiac 1990 - ESPGHAN established new guidelines for celiac biopsy testing Sources: Impact America's Silent Epidemic
  13. Celiac.com 08/21/2015 - Here's every celiac disease treatment currently in development in a single list: ALV003, by Alvine Pharmaceuticals, is a combination of two enzymes that break down gluten before it can provoke an immune reaction. The drug is a powder to be dissolved in water and taken before meals. ALV003 most recently passed a phase 2 clinical trial, results of which appeared in the June 2014 issue of Gastroenterology. Post-trial biopsies showed that ALV003 prevented intestinal damage in 34 volunteers with celiac disease who ate 2 grams of gluten each day for six weeks and also took the drug. Phase 2b, a 12-week trial, is now underway. AN-PEP, by DSM Food Specialties, is another enzyme that degrades gluten. AN-PEP is believed to work best when taken while gluten is still in the stomach. Results from a small 2013 study showing AN-PEP to be safe, appeared in the World Journal of Gastroenterology. For the study, 16 people ate 7 grams of gluten every day for two weeks and half of them also ate AN-PEP, and half took a placebo. However, the placebo group did not get sick enough during the course of the study to show that the enzyme had any effect, so further study is under way. ActoBiotics by ActoGenX uses Lactococcus lactis as an expression system to locally secrete bio-therapeutics such as cytokines, antibodies, hormones, etc. Early pre-clinical work with a genetically altered L. lactis secreting a peptide derived from gliadin demonstrated an in vivo suppression of gluten sensitization. Specifically, Huigbregtse et al. engineered L. lactis to secrete a deamidated DQ8 gliadin epitope (LL-eDQ8d) and studied the induction of Ag-specific tolerance in NOD ABo DQ8 transgenic mice [34]. Although apparently not part of the ActoGenX development program, recent work by Galipeau et al. also deserves mention in this context. The group treated gluten-sensitive mice with elafin, a serine protease inhibitor, delivered by the L. lactis vector, and found normalization of inflammation, improved permeability, and maintained ZO-1 expression. There is speculation that this is due to reduced deamidation of gliadin peptide. AVX176 by Avaxia Biologics, is an investigational oral antibody drug patented to provide "Antibody Therapy for Treatment of Diseases Associated with Gluten Intolerance." The patent, which expires on May 27 2029, provides broad coverage for treating celiac disease using orally administered antibodies produced by Avaxia's proprietary platform technology. BL-7010, by BioLineRx, is a novel co-polymer for the treatment of celiac disease, which significantly reduces the immune response triggered by gluten. This drug has been shown in mice to reduce the immune system response that leads to intestinal damage and villous atrophy in celiac disease. BL-7010 actually binds to the gluten protein, reducing the protein's toxicity.The drug, with the gluten molecule attached, then passes harmlessly through the digestive system to be expelled as stool. BL-7010 has undergone safety testing in humans and was found to be well tolerated. According to BioLineRx, testing will begin in mid-2015 to see if the drug works as expected to diminish gluten's effects on the body. However, BL-7010 is designed to protect only against gluten cross-contamination; it won't allow people with celiac disease to eat large amounts of gluten. CCR9, by Chemocentryx, is a drug called vercirnon, which is also known as Traficet-EN, or CCX282B), and was originally intended for patients with moderate-to-severe Crohn's disease. CCR9 has completed one Phase 2 trial in 67 patients with celiac disease. However, despite the completion of the trial several years ago, no results relating to celiac disease have been made public or published. Egg Yolk Enzyme. Little is known about efforts to develop a celiac treatment that uses egg yolk to coat gluten and allow it to pass through the body undetected, thus preventing an adverse gluten reaction in sensitive individuals. Like most other drugs being developed, this treatment would work to prevent reactions to small amounts of gluten, rather than as a cure. Larazotide Acetate by Alba Therapeutics. How it works: Larazotide acetate blocks a protein that carries pieces of gluten across the gut, where immune cells can see them. Fasano and his colleagues found that this carrier protein, called zonulin, is overproduced by celiac patients after they eat gluten. Results of the most recent phase 2 trial of larazotide acetate, published in February 2015 in Gastroenterology. The volunteers who took the drug experienced fewer days with disease symptoms during the 12 week-long study. Nexvax2, by ImmusanT, works much like an allergy shot. Nexvax2 exposes the immune system to gluten in a controlled way so that immune cells that are usually activated get turned off or eliminated. So far, Nexvax2 has completed a phase 1 trial showing it to be safe. More research is being done to test whether it is effective. Designed to work as a vaccine, Nexvax2 combines three proprietary peptides that elicit an immune response in celiac disease patients who carry the immune recognition gene HLA-DQ2. Similar to allergy shots, the vaccine is designed to reprogram gluten-specific T cells triggered by the patient's immune response to the protein. ZED1227 by Dr. Falk Pharma and Zedira recently announced the start of phase I clinical trials for the drug candidate ZED1227, a direct acting inhibitor of tissue transglutaminase. The small molecule targets the dysregulated transglutaminase within the small intestine in order to dampen the immune response to gluten which drives the disease process. Stay tuned for updates and progress reports as these drugs work their way through their various trial phases. Finally, share your thoughts on all these celiac drugs in the development pipeline. Are you excited, wary, both? Let us know by commenting below. Source: Gastroenterology Report
  14. Celiac.com 05/29/2017 - Currently, a gluten-free diet is the only way to manage celiac disease. Can a celiac vaccine change that? One company thinks so. ImmusanT corporation has developed a therapeutic vaccine, Nexvax2, that is specifically designed to treat celiac disease. The vaccine is an adjuvant-free mix of three peptides that include immunodominant epitopes for gluten-specific CD4-positive T cells. The vaccine is designed to neutralize gluten-specific CD4-positive T cells to further antigenic stimulation. As part of their efforts to evaluate the vaccine, a team of researchers recently set out to investigate the efficacy of epitope-specific immunotherapy targeting CD4-positive T cells in celiac disease. Specifically, they assessed the safety and pharmacodynamics of the Nexvax2 vaccine in patients with celiac disease on a gluten-free diet. An article detailing the findings of their most recent effort, titled Epitope-specific immunotherapy targeting CD4-positive T cells in celiac disease: two randomized, double-blind, placebo-controlled phase 1 studies, appeared in the Lancet. The research team included Gautam Goel, PhD, Tim King, MBBChir, A James Daveson, MBBS, Jane M Andrews, MBBS, Janakan Krishnarajah, MBBS, Richard Krause, MD, Gregor J E Brown, MBBS, Ronald Fogel, MDCM, Charles F Barish, MD, Roger Epstein, MD, Timothy P Kinney, MD, Philip B Miner Jr, MD, Jason A Tye-Din, MBBS, Adam Girardin, BS, Juha Taavela, MD, Alina Popp, MD, John Sidney, BS, Prof Markku Mäki, MD, Kaela E Goldstein, BS, Patrick H Griffin, MD, Suyue Wang, PhD, John L Dzuris, PhD, Leslie J Williams, MBA, Prof Alessandro Sette, DrBiolSc, Prof Ramnik J Xavier, MD, Prof Ludvig M Sollid, MD, Prof Bana Jabri, MD, and Dr Robert P Anderson, MBChB. To assess the safety and pharmacodynamics of the vaccine in patients with celiac disease on a gluten-free diet, ImmusanT recently conducted two randomized, double-blind, placebo-controlled, phase 1 studies at 12 community sites in Australia, New Zealand, and the USA, in HLA-DQ2·5-positive patients aged 18–70 years who had celiac disease and were following a gluten-free diet. The goal of the study was to document the number and percentage of adverse events in the treatment period in an intention-to-treat analysis. The study enrolled a total of 108 participants from Nov 28, 2012, to Aug 14, 2014, in the three-dose study, and from Aug 3, 2012, to Sept 10, 2013, in the 16-dose study. Overall, 62 (57%) of 108 participants were randomly assigned after oral gluten challenge and 20 (71%) of 28 participants were randomly assigned after endoscopy. None of the study participants, investigators, or staff knew which patients received a given treatment; these details were known only by the study’s lead pharmacist. In the three-dose study, participants received either Nexvax2 60 μg, 90 μg, or 150 μg weekly, or placebo over 15 days; in a fourth biopsy cohort, patients received either Nexvax2 at the maximum tolerated dose (MTD) or a placebo. In the 16-dose study, participants received Nexvax2 150 μg or 300 μg or placebo twice weekly over 53 days; in a third biopsy cohort, patients also received either Nexvax2 at the MTD or a placebo. In both studies, about 5% of the participants reported were vomiting, nausea, and headache. Among participants given the MTD, four of eight subjects in the third cohort experienced adverse gastrointestinal treatment-emergent events; zero of three participants had adverse events in the biopsy cohort in the three-dose study, while five events occurred in five (63%) of eight participants in the first cohort, and three events in two (29%) of seven participants in the biopsy cohort of the 16-dose study. Those who received the vaccine at the MTD on either schedule showed no significant difference between average villous height to crypt depth ratio in distal duodenal biopsies, as compared with those who received placebo. In the 4-week post-treatment period, ascending dose cohorts underwent a further double-blind crossover, placebo-controlled oral gluten challenge, which had a fixed sequence. Meanwhile, biopsy cohorts received a gastroscopy with duodenal biopsies and quantitative histology within 2 weeks without oral gluten challenge. Of the participants who completed the post-treatment oral gluten challenge per protocol, interferon γ release assay to Nexvax2 peptides was negative in two (22%) of nine placebo-treated participants in the three-dose study. Compared with two (33%) of six who received Nexvax2 60 μg, five (63%) of eight who received Nexvax2 90 μg, and six (100%) of six who received Nexvax2 150 μg (p=0·007); in the 16-dose study, none (0%) of five placebo-treated participants had a negative assay versus six (75%) of eight who received Nexvax2 150 μg (p=0·021). The MTD of Nexvax2 was 150 μg for twice weekly intradermal administration over 8 weeks, which modified immune responsiveness to Nexvax2 peptides with no adverse impact on duodenal histology. Patients who received the intradermal administration of the vaccine reported gastrointestinal symptoms were not subtantially different to those seen with oral gluten challenge. While the commercial release of a viable vaccine is likely still some time away, early-phase trials have shown promise. Based on these results, ImmusanT will continue clinical development of this potentially therapeutic vaccine for celiac disease. Both trials were completed and closed before data analysis. Trials were registered with the Australian New Zealand Clinical Trials Registry, numbers ACTRN12612000355875 and ACTRN12613001331729. Source: The Lancet Affiliations: The researchers are variously affiliated with the Division of Gastroenterology and Center for Computational and Integrative Biology, Massachusetts General Hospital, Boston, MA, USA, the Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, MA, USA; the Department of Gastroenterology, Auckland City Hospital, Auckland, New Zealand; the School of Medicine, University of Queensland, Brisbane, QLD, Australia; the Department of Gastroenterology & Hepatology, Royal Adelaide Hospital, Adelaide, SA, Australia; the Linear Clinical Research, Nedlands, WA, Australia; the Department of Gastroenterology, Alfred Hospital, Prahran, VIC, Australia; the Clinical Research Institute of Michigan, Chesterfield, MI, USA; the University of North Carolina School of Medicine, Chapel Hill, NC, USA; Wake Gastroenterology and Wake Research Associates, Raleigh, NC, USA; Atlantic Digestive Specialists, Portsmouth, NH, USA; Ridgeview Medical Center, Waconia, MN, USA; Oklahoma Foundation for Digestive Research, Oklahoma City, OK, USA; ClinSearch, Chattanooga, TN, USA; the Immunology Division, Walter and Eliza Hall Institute of Medical Research, Department of Medical Biology, University of Melbourne, Parkville, VIC, Australia; the Murdoch Children's Research Institute and Department of Gastroenterology, Royal Melbourne Hospital, Parkville, VIC, Australia; the Immunology Division, Walter and Eliza Hall Institute of Medical Research, Department of Medical Biology, University of Melbourne, Parkville, VIC, Australia; the Tampere Center for Child Health Research and Department of Pediatrics, University of Tampere Faculty of Medicine and Life Sciences and Tampere University Hospital, Tampere, Finland; the Tampere Center for Child Health Research and Department of Pediatrics, University of Tampere Faculty of Medicine and Life Sciences and Tampere University Hospital, Tampere, Finland; the Alfred Rusescu Institute for Mother and Child Care and Carol Davila University of Medicine and Pharmacy, Bucharest, Romania; Division of Vaccine Discovery, La Jolla Institute for Allergy and Immunology, La Jolla, CA, USA; the Tampere Center for Child Health Research and Department of Pediatrics, University of Tampere Faculty of Medicine and Life Sciences and Tampere University Hospital, Tampere, Finland; the Centre for Immune Regulation, KG Jebsen celiac Disease Research Centre, and Department of Immunology, University of Oslo, Oslo, Norway; the Oslo University Hospital-Rikshospitalet, Oslo, Norway; Department of Pediatrics, Department of Medicine, University of Chicago, Chicago, IL, USA; and ImmusanT in Cambridge, MA, USA.
  15. Celiac.com 02/08/2017 - "What if the kid you bullied at school, grew up, and turned out to be the only surgeon who could save your life?" --Lynette Mather If you ask any high school senior what in their life has changed the most since kindergarten, statistics show that many would answer moving from one school to another. However, the more drastic of changes are seen such as illnesses diagnosed during these critical school ages. In 2009 I was diagnosed with celiac disease, and that diagnosis has impacted my life in both positive and negative ways for my past, present, and future time at Indiana Area High School and beyond. Personally I have had to deal with bullying because of my disabilities. Bullying by definition is the use of force or coercion to abuse or intimidate others. I along with 20% of my peers nationwide in grades 9-12 (The Youth Risk Behavior Surveillance System) experience bullying in many different forms. Bullying can be teasing, hitting, leaving someone out, whispering behind backs, online harassment, shoving, remarks about race, sexuality, and disabilities. Before my diagnosis I was considered "normal" but as a result of my illness and "strange" dietary needs therefore I have been bullied. However, looking back on my experience I am happy to have dealt with the resistance because it has made me a better, more confident individual. I, like three million fellow Americans nationwide (National Celiac Disease), must deal with the stress of having celiac disease. I was diagnosed in 2009 after having lost my eyesight to a migraine. Celiac Disease is an often under-diagnosed autoimmune disease wherein the person cannot eat wheat, rye, barley, or oats, otherwise known as gluten, because their antibodies will attack their own system leading to other serious health issues such as cancer. Celiac Disease is spread through genes; my entire family, including my father, mother, and sister, has this disease. However, even with the growing awareness of celiac disease, there is also a growing skepticism. "Critics" of my disease claim that the gluten free diet is a fad. Many celebrities have tried to lose weight and failed to stay on this difficult diet. Restaurant chains are coming out with new gluten free menus every day to raise prices and profits, though they refuse to educate their servers about what someone with a gluten "allergy" cannot eat. While some people are sympathetic and know the outstanding facts about celiac disease, most of the population stays in the dark about this ailment. This causes frustration for people with celiac disease, like me, to have to deal with the resulting brick wall of resistance. In my small community it is very rare for someone to have such a disease that the public knows little about. This can cause doubt and disbelief, especially at a high school where everyone is just trying to "fit in". When I was diagnosed in 2009, I had just started ninth grade and I had also started playing two high school sports, softball and tennis. For the softball team it was a well-known fact that after every away game the softball boosters would buy each girl a twelve inch sub from a local deli to eat on the way home. Whenever my parents and I contacted the booster president to explain the situation with my disability and that I simply would like to have a salad, we were met with backlash. I did not understand at the time why a parent would refuse to supply another child with food after a physical activity when everyone else was getting a meal. This quickly made me an outcast on the softball team as the "strange girl with the made up disease", causing me to feel stressed and awful about myself over something that I could not control. I would have loved to have been able to "fit in" and eat the subs like my teammates rather than being different, especially after growing up able to eat gluten! It was a hard transition to make. I went from being able to eat the subs, donuts, pizza, and any other fast-food product to a strict dietary regime. After my long process through the education system, I finally got the meal I had a right to have. Unfortunately, the boosters' actions, forced us to go through the school system to "prove" I had a legitimate excuse not to eat the subs. I was distanced from other members of the team and, in subsequent years, had to deal with backlash from my teammates. They do not understand that it is not a personal choice to avoid gluten. I have a disability. I simply cannot eat it. Instead, they go back to the first year when I was eating the same foods they ate, and I get blamed for wanting to be "special" and get the more expensive food. I know that I am not alone in my struggle and that people with celiac disease around the world deal with what I deal with everyday - just like others who are bullied for being different. The after effects from my being bullied have shown themselves even in everyday situations. I have learned a great deal about myself and respect for other individuals' differences. I believe that if I had not been bullied I would not have the self-confidence, integrity, sense of right and wrong, or leadership skills that I have now. It has allowed me to go above and beyond in tough situations, knowing that I can overcome them. I know that even though the times are tough with my disability, and that while others may never understand mine, I can certainly understand and respect theirs. I respect and do not judge others simply based on what they can or cannot eat. I also know that just because someone does not "look" ill on the outside does not mean they are not dealing with something awful on the inside. This allows me to make friends easily and to understand others more effectively. Being bullied has also allowed me to learn new leadership skills that I use in my volunteer work. I am confident in myself that I can go forward into the world of higher education and succeed because of the values I now hold dear. The most drastic change I have encountered in my high school career is the diagnosis of celiac disease in 2009. This diagnosis has impacted my life in both positive and negative ways, in the past, present, and future at Indiana Area High School and beyond. I have had to deal with bullying because of my disabilities. Bullying, by definition. is the use of force or coercion to abuse or intimidate others. I along with 20% of my peers nationwide in grades 9-12 (The Youth Risk Behavior Surveillance System) experience bullying in many different forms. After dealing with the effects of my being bullied, I know that it has made me a better person. I can travel the world and make lasting relationships based on acknowledging and respecting differences in every person I encounter.
  16. The following piece was written by Ronald Hoggan who is a teacher at Queen Elizabeth High School in Calgary, Alberta, Canada. The Polish one is: Kozlowska, Z.E. Results of Investigation on Children with Coeliakia Treated many Years with Gluten Free Diet Psychiatria Polska 1991; 25(2): 130-134. The German one is: Paul, et. al. EEG-befunde Zoeliaki-kranken Kindernin Abhaengigkeit von der Ernaehrung Zeitschrift der Klinische Medizin 1985; 40: 707-709. The first indicates that 71% of celiac children, when newly diagnosed, demonstrate EEG abnormalities. Now please note this caution: I HAVE NO TRAINING IN THE INTERPRETATION OF EEG READINGS. Nonetheless, when I compare the authors descriptions of the EEG abnormalities in celiac children, and the abnormalities in children who have been diagnosed with ADD or ADHD, there are some startling similarities. Paul, et. al. are paraphrased by Reichelt et. al. in THE EFFECT OF GLUTEN-FREE DIET ON GLYCOPROTEIN ATTACHED URINARY PEPTIDE EXCRETION Journal of Orthomolecular Medicine 1990; 5: 223-239. They say: In celiac children provocation with gluten after diet causes alarmingly high frequency of EEG changes that persist up to a year (Paul et al 1985). I would urge (those with ADD) to be very careful to avoid contamination in (their) diets, and I would ask you to consider some alternatives to stimulant therapy (Ritalin is a brand name of the most commonly used stimulant.). The concept of drugging a child to facilitate learning is upsetting to me, especially when there is cause to suspect that, on the Gluten-free diet, she may improve without intervention. I know that she is falling behind now, but if her experience is similar to mine, many of my ADD type symptoms did go away during the first year. I will also forward a part of report that was forwarded to me, that showed that vitamin B-6 supplementation was as beneficial to a group of children with attention deficits, as Ritalin was. Especially in celiac disease, where vitamin deficiencies are so common, that seems a viable alternative.
  17. Celiac.com 09/18/2015 - That old saw about death and taxes might need a bit of amending to include complaints about pharmaceutical companies working on celiac drug treatments. One interesting facet of our coverage of the development of various drugs to treat and/or cure celiac disease has been the regular presence of comments questioning the motives,and actions of the companies involved. It's funny, but no one complains that companies still make money selling aspirin, and that no one has cured a headache, and that there must be some conspiracy to profit off of those who suffer a headache. There's no doubt that there's money to be made producing drugs that treat disease. But, if a company can develop and produce a safe drug to protect celiacs against contamination, or to help reduce symptoms, what's wrong with that? Just like an aspirin, I can take it or not take it. In the old days, ten years ago or more, people with celiac disease generally suffered in silence, with scant gluten-free food choices, and little information. However, in just a decade, we've got a wealth of information, and multi-billion dollar gluten-free foods market and a number of companies developing drugs to treat or cure celiac disease. To me, that's a good thing. Still, there are naysayers. Here's a rundown of comments by readers who seem less than enthused about celiac drugs in development. Our recent article, An Update on Every Celiac Disease Drug Currently in Development included the comment: "Article's fine. Concept's disturbing. Eating a gluten-free diet is the free, already-proven cure for celiac and gluten-intolerance. They don't have to torture mice and likely other animals to find a 'cure' for something that there already is a cure for. I imagine there is $$ for the researchers here and $$ for the animal labs and $$ for the pharmaceuticals." Of our article entitled, How Close Are New Celiac Disease Treatments? one reader wrote: "I would be very cautious about taking any of these until it was proven absolutely to have no side effects. There always are some and history has shown some to be deadly." Commenting on our article ALV003 Reduces Gluten Damage in Celiac Disease Patients, one reader commented: "I only want to know: how long until random internal organs begin to fail or malfunction as a result of yet another new mystery drug? I'd rather starve to death than be a guinea pig for big pharma again." Our article on NexVaxx, entitled Is a Vaccine for Celiac Disease Just Around the Corner? included the following comments: "Totally agree with vhill seems like a ploy to poison people with GMO foods that come up with a supposed "'cure'. Eat healthy whole foods this is not a curse its a wake up call to be healthy if you didn't have celiac you'd probably be eating processed crap." Balm wrote: "Thanks but no thanks. I'll remain a celiac and continue to eat healthy. While trying to fix one problem, some will end up with far worse problems." Jonnys wrote: "Stupid idea! Just another way to make more money off of people." These are but a few of the largely positive comments we receive, and we hope you enjoyed them as much as we do.
  18. Addisons Disease Alopecia Anxiety and Depression Ataxia Attention Deficit Disorder / ADHD Autism and Celiac Disease Autoimmune Hepatitis / Chronic Active Hepatitis Bird Fancieris 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) Farmeris 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
  19. Abdominal Distention (children) Abdominal Pain, Steatorrhea Anemia - Folate-Deficiency / Iron Deficiency / Pernicious Arthralgia or Arthropathy Arthritis - Rheumatoid Carcinoma of the Oropharynx, Esophagus, and Small Bowel Collagenous Sprue Dermatitis Herpetiformis Diabetes (Type 1) and Celiac Disease Diarrhea Down Syndrome Enteropathy-Associated T-cell Lymphoma Failure to Thrive (children) Hypertransaminasemia IBS - Irritable Bowel Syndrome IgA Deficiency IgA Nephropathy Kidney Disease Liver Disease Low Bone Mass and Celiac Disease Microscopic Colitis / Collagenous Colitis Nerve Disease and Celiac Disease Osteomalacia, Osteoporosis and Celiac Disease Recurrent Aphthous Stomatitis, Recurrent Refractory Sprue / Celiac Disease Sjogrens Syndrome Thyroid Disease (Autoimmune) Ulcerative Jejunoileitis
  20. Celiac.com 04/24/2008 - Genetic tests for celiac disease and gluten sensitivity are readily available. Testing can be performed on either blood and mouth swab samples. If the testing is performed by certain laboratories not only will you have quite an accurate prediction of your risk of Celiac disease but also you may have information about the statistical probability that your children will inherit the risk, your likelihood of more severe Celiac disease, whether one or both of your parents had the risk gene, and for some laboratories you may determine your risk of gluten sensitivity without Celiac disease. The absence of any portion of the high-risk genetic patterns DQ2 and DQ8 nearly excludes the possibility of celiac disease with an approximate accuracy of 99.9%. However, there is a big caveat about relying on "negative celiac genetic testing". To definitively declare you have negative celiac genetic tests requires that the laboratory test for and report the presence or absence of the entire HLA DQ genetic pattern, including both alpha and beta subunits. The DQ genetic patterns DQ2 and DQ8 have two subunits but some laboratories only test for the beta subunit. This DQ typing is complicated and difficult to understand even by physicians and scientists. I have written an updated detailed review that appears in the Spring 2008 issue of Scott-Free newsletter published by celiac.com. Data collected by Dr. Ken Fine of Enterolab has supported the well-known fact that the absence of DQ2 and DQ8 does not exclude the risk of being gluten intolerance or sensitive though it now generally believed that one or both of those genetic white blood cell patterns are required to develop the autoimmune disorder known as Celiac disease or Celiac Sprue. However, there is a new study that reports that being negative for DQ2 and DQ8 does not completely exclude the possibility of celiac disease, especially in men. Previous studies have well documented blood test negative Celiac Sprue, also more common in elderly men with long-standing severe disease. Since DQ2 or DQ8 is almost universally present with the specific blood tests tissue transglutaminase and anti-endomysial antibodies are present it is not surprising that individuals without DQ2 or DQ8 that are negative for these two blood tests are being reported that meet criteria for Celiac disease. These new studies are also providing further information that the genetics of Celiac is gender specific. If you are a man, your risk of celiac disease may be higher than a woman if you don't have the classic genetic patterns. Again, in this situation your blood tests may be negative. If you are a woman, the risk for Celiac disease is generally higher than a man, especially if you have received the at risk gene from your father instead of your mother. Celiac is arguably the most common autoimmune disease. It is very common. It is easily treated. It affects 1/100 people worldwide. However, most people with celiac disease (~90%) are unaware, undiagnosed or misdiagnosed. Most adults finally diagnosed with celiac disease have suffered at least 10-11 years and have seen more than 3 or more doctors. Genetic testing is not only available but can be extremely helpful in determining your risk of developing Celiac disease, how severe it may be and the risk of your family members. Don't be one of those whose diagnosis is missed or needlessly delayed for over a decade. Get tested! Learn about the genetic tests for Celiac disease and if necessary educate your doctor about this testing. Here are ten facts you should know and remember about Celiac genetic testing. Genetic testing can help determine your risk as well as your children's risk. Celiac genetic tests can be done on blood or a mouth swab sample but your doctor may be unaware of the tests, not know how to order them, or know how to interpret the results. Genetic testing is not affected by diet. You can be eating gluten or on a gluten free diet. Blood tests for celiac disease antibodies, however, need to be done while eating gluten. They can become negative within a few weeks of restricting gluten so if you are going to get the diagnostic antibody blood tests don't begin a gluten free or restricted diet before being tested. Some insurance companies do not for the Celiac genetic test and almost all who do require pre-authorization first. The following diagnostic codes are helpful when requesting insurance coverage: 579.0 (Celiac disease); V18.59 (family history of GI disease); and/or V84.89 (genetic susceptibility to disease). Some laboratories do not perform the all of the necessary components of the test to completely exclude the possible genetic risk of Celiac disease and most don't test for or report the other gluten sensitive DQ patterns. Before you accept that have a negative test you need to know if your test included both the alpha and beta subunits of HLA DQ or did they just perform the beta typing. In some rare individuals, especially some men, a negative genetic test may not exclude the possibility of celiac disease anymore than a negative blood test. Men more commonly have negative genetic tests and blood tests, especially older men with long-standing severe disease. Both the DQ type, and number of copies you have, matter when determining not only your risk but also the possible severity of celiac disease. Two copies of DQ2 carries more risk than one copy of DQ8 or only partial DQ2. Even a single copy of DQ2 alpha subunit ("half DQ2 positive") carries risk for celiac disease but most of the commonly used laboratories for Celiac genetics do not test for or report the presence of this component of the celiac genes. The absence of at risk genes DQ2 and/or DQ8 does not exclude the possibility of being gluten intolerant or sensitive. You may respond to a gluten free diet even if you don't have DQ2 or DQ8 or true autoimmune Celiac disease. You can get genetic testing without a doctor's order and the tests can be done without having blood drawn or insurance authorization if you are willing to pay between $150-400 (www.kimballgenetics.com and www.enterolab.com). Laboratories in the U.S. that are known to offer complete alpha and beta subunit genetic testing include Kimball Genetics, Prometheus, and LabCorp. Bonfils, Quest and Enterolab only test for the beta subunit portions and therefore their test can miss part of a minor alpha subunit that carries a risk of Celiac disease. A negative DQ2 and DQ8 report from these labs may not necessarily be truly negative for the risk of Celiac disease. References and Resources: HLA-DQ and Susceptibility to Celiac Disease: Evidence for Gender Differences and Parent-of-Origin Effects. Megiorni F et al. Am Journal Gastroenterol. 2008;103:997-1003. Celiac Genetics. Dr. Scot Lewey. Scott-Free, Spring 2008.
  21. Celiac.com 03/04/2016 - For anyone who hasn't seen it, the website Glutendude.com has an article titled "Why Doesn't the Military Accept Those With Celiac Disease?" The article highlights the story of a smart, capable, American who was motivated to serve in the military, but who was medically disqualified by military policy, and all had failed in all attempts to secure an admission waiver. The man was further frustrated by the fact that he had very minimal symptoms, and felt that he had the ability to serve effectively. The article also highlights the military's uneven treatment of personnel with celiac disease. Medical fitness for the military is governed mainly by the Department of Defense Medical Examination Review Board (DoDMERB), which schedules, evaluates, and certifies all applicants as "medically qualified," or as "medically does not meet the medical accession standards" for the US Service Academies, ROTC Scholarship Programs, Direct Commission Programs, and the Uniformed Services University of the Health Sciences. Basically, current military policy is to reject potential recruits with known celiac disease, provide some accommodation for some troops already in the service, and to provide medical discharges other troops, as needed. The military doesn't reject you if they don't know you have celiac disease, and wouldn't likely test you for celiac disease unless you pressed the issue. But if there's no official diagnosis, or no debilitating symptoms, and the recruit says nothing, then celiac disease is not a barrier to military service. And, once in the military, if the disease is kept under wraps, then it's likely it will never come up, and thus pose no problem. Going back to GlutenDude's article, here's part of a quote from the soldier who was rejected due to celiac disease: "Two years ago I was diagnosed with celiac disease, and the military does not accept people with this disease. I was medically disqualified by DODMERB, and all waiver attempts have been denied. Years of hard work, a 3.9 GPA, a 32 MCAT, and a desire to spend my entire career in the service have been for naught. The most frustrating aspect of this situation is that I have almost no physical symptoms, am not on medications, and the few symptoms I have are completely controlled by diet. Yet even though my disease would not affect my ability to serve, my dreams have come to a screeching halt." The man also points out that: "Militaries in other countries accept celiac patients like Israel. Even in our military there are celiac patients that are accommodated for, albeit ones that have already been accepted and are diagnosed after being in for some time. The fact that one percent of the population, nearly 3 million people, have no chance to give their service to their country is a disgrace." What do you think? Is the current military policy of rejecting people with celiac disease only if it becomes known a bit like Don't Ask Don't Tell? Are potentially good recruits being turned away unnecessarily? Are existing soldiers being asked to cover up a treatable medical condition for fear of being discharged? Should people with celiac disease or gluten-intolerance be able to serve in the military?
  22. Celiac.com 07/09/2009 - Rates of celiac disease are four times higher today than they were just fifty years ago, according to the results of a new study by scientists at the Mayo clinic. In addition, the study showed that people with undiagnosed celiac disease died at rates four times higher than non-celiacs over the 45 year follow-up period. Celiac disease is an immune system reaction to gluten in the diet which, left untreated, celiac disease causes damage to the lining of the digestive tract and leaves sufferers at risk for various cancers and other associated conditions. When people with celiac disease eat wheat, barley or rye, a protein called gluten triggers an immune system attack, which damages the villi in the small intestine.Villi are finger-like folds in the intestine that increase surface area for nutrient absorption. Celiac disease symptoms may include diarrhea, abdominal discomfort, weight loss, anemia, unexplained infertility, loss of teeth or even premature or severe osteoporosis, among others. Joseph Murray, M.D., the Mayo Clinic gastroenterologist who led the study says celiac disease "now affects about one in a hundred people. We also have shown that undiagnosed or 'silent' celiac disease may have a significant impact on survival. The increasing prevalence, combined with the mortality impact, suggests celiac disease could be a significant public health issue." So, celiac disease is striking a higher than ever portion of the population, yet doctors don't yet fully understand the reasons for this reality. A team of Mayo Clinic scientists team performed celiac disease antibody tests on blood samples gathered at Wyoming's Warren Air Force Base (AFB) between 1948 and 1954. They then compared those blood test results with results from two recently collected groups from Olmsted County, Minn. Tests for the first group were matched by age to those from the Warren AFB group at the time of the blood draw, while the second group was matched by birth years. Researchers found that young people today are 4.5 times more likely to have celiac disease than young people were in the 1950s, while those whose birth years matched the Warren AFB participants were four times more likely to have celiac disease. Celiac disease was once thought to be rare, and many physicians still regard it as so, but, according to Dr. Murray, that is no longer the case. "Celiac disease is unusual, but it's no longer rare," he says. Dr. Murray adds: "Something has changed in our environment to make it much more common. Until recently, the standard approach to finding celiac disease has been to wait for people to complain of symptoms and to come to the doctor for investigation. This study suggests that we may need to consider looking for celiac disease in the general population, more like we do in testing for cholesterol or blood pressure." For Dr. Murray, the findings underscore the importance of raising awareness of celiac disease, both among physicians and patients. He adds that some studies "have suggested that for every person who has been diagnosed with celiac disease, there are likely 30 who have it, but are not diagnosed. And given the nearly quadrupled mortality risk for silent celiac disease we have shown in our study, getting more patients and health professionals to consider the possibility of celiac disease is important." One interesting point not touched on in the study is the increase in the gluten content of commercial varieties of wheat now being grown compared to gluten levels of 50 years ago. Additionally, people are eating more wheat and gluten than ever before. (http://www.mayoclinic.org/bio/13032852.html) Gastroenterology, July 2009;137(1)pp 373-374
  23. Celiac.com 09/24/2012 - With all the problems that go along with celiac disease, it can be hard to see any benefits to having the disease. However, it would seem that such benefits do exist: a recent study in Sweden shows that women suffering from celiac disease are actually at a decreased risk of developing breast, endometrial and ovarian cancer. Data was collected from 28 Swedish pathology departments, identifying 17,852 biopsy-diagnosed women diagnosed with celiac disease between the years of 1969 and 2007. Women in the celiac group were age-matched and compared with a control group of 88,400 women. Risk of breast, endometrial and ovarian cancer were all estimated using the Cox regression model in both groups. Results showed an inverse relationship between celiac disease and all three forms of cancer. With breast cancer rates, women with celiac disease had a hazard ratio of 0.89 (meaning for every 100 women in the control group, only 89 in the celiac disease group developed breast cancer). Women with celiac disease also had a hazard ratio of 0.89 for ovarian cancer. For endometrial cancer, the decreased risk was even more pronounced with a hazard ratio of 0.6. All calculations carried a confidence interval of 95%. These numbers became even more pronounced after omitting the first year of followup after diagnosis (presumably the gluten-free diet 'adjustment period'). Breast cancer's hazard ratio fell to 0.82, ovarian cancer's hazard ratio fell to .72 and endometrial cancer's hazard ratio fell to 0.58. The study suggests that this negative correlation could be a result of shared risk factors or early menopause associated with celiac disease. Looking at the numbers though, particularly the 'adjustment period' drop off, one has to wonder if the gluten-free diet has some part to play in this as well. Source: http://www.ncbi.nlm.nih.gov/pubmed/21953605
  24. Celiac.com 06/15/2015 - It's well-documented that people with active celiac disease are more likely to have osteoporosis and increased risk of fractures. High-resolution peripheral quantitative computed tomography (HR-pQCT) allows for three-dimensional exploration of bone micro-architecture, including measurement of cortical and trabecular compartments, and providing detailed information on bone disease pathophysiology and fracture. Using HR-pQCT, research team recently set out to assess the volumetric and micro-architectural characteristics of peripheral bones. that is the distal radius and tibia, in adult pre-menopausal women with active freshly diagnosed celiac disease. The research team included María Belén Zanchetta, Florencia Costa, Vanesa Longobardi, Gabriela Longarini, Roberto Martín Mazure, María Laura Moreno, Horacio Vázquez, Fernando Silveira, Sonia Niveloni, Edgardo Smecuol, María de la Paz Temprano, Hui Jer Hwang, Andrea González, Eduardo César Mauriño, Cesar Bogado, Jose R. Zanchetta, an dJulio César Bai. They are variously affiliated with the IDIM, Instituto de Diagnóstico e Investigaciones Metabólicas, and with the Cátedra de Osteología y Metabolismo Mineral, Universidad del Salvador, Buenos Aires, Argentina. For the study, their team prospectively enrolled 31 consecutive premenopausal women with newly diagnosed celiac disease (median age 29 years, range: 18–49) and 22 healthy women of similar age (median age 30 years, range 21–41) and body mass index. Using HR-pQCT, the team was able to successfully identify significant deterioration in the micro-architecture of trabecular and cortical compartments of peripheral bones. HR-pQCT revealed that most bone micro-architecture parameters were substantially reduced in celiac disease patients compared to a control group. Twenty-two patients showed symptomatic celiac disease. These patients had a greater bone micro-architectural deficit than those with sub-clinical celiac disease. Impaired bone micro-architecture could be one cause of diminished bone strength and higher risk of fractures seen in many celiac patients. The researchers are looking to conduct a follow-up of this group of patients. They want to know whether bone micro-architecture recovers with a gluten-free diet, and, if so, how quickly and to what extent. Source: BONE July 2015, Volume 76, Pages 149–157. DOI: http://dx.doi.org/10.1016/j.bone.2015.03.005
  25. Celiac.com 07/17/2015 - This article originally appeared in the Spring 2015 edition of Journal of Gluten Sensitivity. Why is a researcher whose field for twenty years has been autism now writing an article about celiac disease and its possible relationship to oxalate? This takes a little explaining. My training in graduate school was all about looking into old literature to find pieces of research that had been lost, or were never incorporated into current models. I learned that new science could provide a different context for old findings. The importance of this process came home when more than a decade ago I was sitting at an enormous oval table at the National Institutes of Health where an important meeting was addressing how the heads of various National Institutes of Health and the CDC would handle a theory about a possible environmental trigger related to autism. One scientist rose to the floor, and began to explain his reason for discounting the new theory's importance. He proposed that this theory did not fit into previous models of autism, and began to say that the scientific process worked like the construction of a brick wall. Everything added to that wall should fit into the foundation and bricks that had already been laid. How often does this view of science as being a construction of human beings, rather than a discovery of nature, keep us from accepting new lines of research? Has scientific consensus ever ended up wrong after the appearance of new findings? Yes, many times. In this meeting at the NIH, at that moment, a senior scientist, Dr, Bernard Rimland, rose to the floor. Those who knew this man realized he had singularly changed the view about the science of autism twice, accomplishing these major shifts of thinking during different decades. I don't have a transcript from that meeting, but Dr. Rimland rose to say something like this: "My experience is very different. I find that science is more like a crossword puzzle, in that you may have been working at the puzzle from one end and filled in places that looked correct until you began working from another side and discovered that something you filled in before must have been wrong. That's when you erase the part that you thought had been right, and you find another answer that will make the parts fit from both directions." That speech has been a guiding light to my own research since then, helping me have the motivation to recover all the pieces that were lost or misunderstood or left out from the past whose absence left a model that only approximately provided a place for all the known pieces, but left many other pieces "loose" and unable find a proper fit. In 2005 after spending ten years studying the biological roles of sulfate in the body, I began to investigate another negatively charged ion that travels on the same transporters. I reviewed the published literature on oxalate in any condition, looking at basic science and clinical research over the last two centuries. I was looking for gaps and opportunities for improving the identification of oxalate-related diseases outside the kidney. My work for twenty years had focused most intensely on autism, and I had found that oxalate was high in autism, but this finding needed to be put in context and studied formally. It was mystifying to me why work from basic science about oxalate was only being applied to patients with kidney disease. How could we identify others with oxalate-related disorders? In the fall of 2005, along with several associates, we started our Oxalate Project. Using the same methodologies I had developed in the previous decade using the internet to interact with a broad range of patients, we began seeking those with any condition that was already related to oxalate in the literature, and patients with other conditions where the science took us. Included in this effort was setting up a project at the Autism Research Institute that we named the Autism Oxalate Project. In October of 2006, I attended the International Celiac Disease Symposium in New York City. I was hoping that the findings in oxalate research on malabsorption and intestinal disease, and specific findings on oxalate in celiac disease published since the 1970's were being discussed at this conference. I heard not a word about oxalate there. These scientists probably did not realize that when oxalate levels in the blood become high, it can get stored all over the body where it can produce effects in any potential organ…not just the kidney. I had learned that systemic effects from oxalate could change the course of a condition in patients over years of time. For patients with celiac disease, this storage might have occurred primarily during the years before diagnosis when problems with fat digestion would have increased the percent of oxalate absorption from the diet. In autism, I had learned that, as in celiac disease, some investigators had noticed oxalate's elevation in urine in isolated individuals, but they had been taught by articles in peer-reviewed literature to dismiss this finding as irrelevant when those individuals didn't have kidney stones. Basically, the literature kept saying that kidney stones would always be the first presentation of an oxalate problem—but was that true? Why would that be true? As I began to attend numerous world conferences on oxalate, I was very surprised to find that the only people there besides botanists, were those involved in kidney research. My previous studies in the literature had identified many articles describing oxalate producing effects all over the body and in multiple systems. New work on oxalate transport was finding regulation of oxalate's movement all over the body. Why wasn't this research being applied to patient care outside the kidney and why were certain laboratories insisting on a kidney diagnosis before they would even measure oxalate? Since my own work at that point included running a support group for people reducing oxalate and our doors were open for people with any condition, we had seen patients with more than twenty different conditions report an easing of their symptoms or even complete cures when they brought their oxalate levels down. Would the scientists be able to catch up with this wealth of experience that today has involved more than 17,000 families? Here is an example: I worked with a team of oxalate and autism researchers in Poland to establish the prevalence of oxalate's elevation in autism. The study that this work produced became available online in 2011, but officially went to print in September of 2012 in the European Journal of Paediatric Neurology. It was the first study to examine whether the levels of oxalate in blood plasma would correlate to the levels in 24 hour collections of urine in those who were not in kidney failure. We discovered that the levels in these two compartments did not correlate at all, especially in the controls. This meant that the oxalate field's dependence on urine tests as sufficient to identify those with oxalate problems was probably misplaced. It made sense that the two compartments would not "agree" because oxalate's movement between tissues, we now know, is regulated and its regulation would be different in different organ systems. How many other conditions were experiencing effects from elevated oxalate in blood that were not accurately reflected by only using urine tests? What did we know about variability from day to day, or even rhythms within the day, for oxalate secretion in other conditions? What did we know about how any variability should affect the interpretation of lab results, or our interpretation about the timing and presentation of symptoms in other conditions? A striking finding in our paper seemed to have been also referenced in a paper from Mayo Clinic, showing that urine oxalate in normal controls seemed to stay below the reference level of 0.46 mmol/1.73 m2 (24 hr.) Perhaps the point of the kidneys regulating that level so tightly was to protect the kidneys from risks of kidney stones or nephrocalcinosis, but that particular control of urinary secretion seemed lacking in autism. Scientists were beginning to discover secretion to other compartments, such as the intestines, the lungs, and the skin for example. Why would someone doing research even think to measure oxalate secretion and regulation in these other sites in clinical settings? In the past, everyone had assumed that measuring urine was sufficient. The graph of plasma versus urine looked completely different in those with autism compared to controls. What would a similar graph look like in celiac disease? Would the graph show different patterns at different ages, or before and after treatment with a gluten-free diet? Data from a study from Saccomani et al. may suggest that a limit to urinary secretion may be preserved in children with celiac disease, but would limiting secretion in the kidney sometimes lead to a greater accumulation of oxalate in tissues? Our autism study revealed that there are problems with assuming that a single urine test could be used to screen patients when oxalate could be elevated in blood and causing problems in the rest of the body. More than fifteen years ago (not published but presented at a think tank) I noticed problems in lab tests in autism with what looked like it could be caused by a variability in creatinine secretion. This would create a problem in interpretation for any urine test ratioed to creatinine, but the reason we would see this variability in autism made sense when a rat study recently found that oxalate in the kidney changes the movement of creatinine out of blood and into urine when oxalate was made to be high experimentally. This type of study urgently needs to be replicated in humans before anyone can have confidence that this affect on creatinine isn't compromising our data from spot urine tests. Suddenly it seems very sensible that in the oxalate field, it has become common practice to use 24 hour tests. Readers need to realize that this issue would affect anything measured in urine and ratioed to creatinine, not just oxalate! From data I've reviewed and analyzed statistically from more than a thousand organic acid tests, and from other literature, I also doubt that this single mechanism is solitary in contributing to problems in interpreting urine tests that use this ratio. Can we still legitimately think that physicians should not worry about oxalate levels unless their patients have developed kidney stones? Celiac disease is one of many conditions where high oxalate levels have frequently been found in patients. Some of the other conditions include bariatric surgery, cystic fibrosis, inflammatory bowel disease, short bowel syndrome, autism and more. Are doctors and nutritionists understanding that patients with these disorders will experience risks from oxalate to the rest of their body? Are they noticing when these patients develop issues outside the kidney that their symptoms might be related to oxalate? I've learned that the answers to these questions is most often, no. In our project's work with such patients we have reduced body oxalate levels through strategies of dietary modification, and by the use of specific vitamins, minerals and probiotics that have been shown to reduce oxalate. We've seen these changes alter the expression of their presenting disease in unforeseen but positive ways. It will take decades before all our findings from ten years of work in dozens of conditions can be confirmed by scientific studies. That does not mean these patients have to wait for academic studies to be published to see for themselves if reducing their exposure to this clearly recognized toxin will help improve their own health. Do physicians know that research on kidney stone patients have identified issues in their kidneys that lead to their increased risks of forming kidney stones from oxalate levels that would not produce stones in others? Could oxalate that was elevated in blood and tissues (and currently not being secreted at high levels in urine) cause problems to other parts of the body, contributing in unknown ways to comorbidities like those found in celiac disease? At the celiac symposium I attended, there were so many issues that were being discussed as being unresolved by the use of a gluten-free diet. That surprised me. Could those issues have been triggered by oxalate that was absorbed into the body before a gluten-free diet had resolved steatorrhea? Steatorrhea is the condition where excess fat stays in the feces, possibly causing the stool to float or have an oily appearance. Studies had shown that untreated celiac disease often was associated with steatorrhea. This condition elevates fat in the gut and that fat travels undigested all the way to the colon. Oxalate scientists had found that the fat left in the intestines during the journey to the colon would tie up calcium that ordinarily binds oxalate from the diet. About 80% of the calcium that travels through the gut stays in the gut. The purpose may involve the formation of a calcium oxalate salt in the feces that limits oxalate's absorption in the colon. Otherwise that oxalate could be transferred to blood if it is not first metabolized by the microbes in the gut. This is a bigger problem than the higher amount of oxalate in the diet. This might become a more serious problem when people with celiac disease use new grains that are gluten-free but which we know now are extremely high in oxalate. During the mid-nineteen thirties, prominent groups began recommending adding vitamin D to milk to prevent rickets, knowing that vitamin D enhances the absorption of calcium from the gut. Back then, oxalate research had not yet found a protective role for most of the calcium to remain in the gut to protect us from oxalate. Physicians had advised kidney stone patients to avoid calcium, but later determined that calcium in the diet was protecting patients from absorbing oxalate. Later studies showed that oxalate that remains in the intestines as a free anion (unbound to calcium) can and will be absorbed into the body once it reaches the colon. When this unbound oxalate is taken into the blood, there it was found to be able now to tie up free calcium that was needed to protect our bones and work in our metabolism. Free oxalate could a lso be taken into cells via oxalate transporters where it could disrupt calcium signaling inside cells and wreak havoc in the mitochondria and endoplasmic reticulum. Free oxalate can disrupt activity also in the nucleus where nature has supplied a specific oxalate binding protein. Is this protein sometimes overwhelmed when oxalate gets too high? Before I attended this celiac symposium, I had not heard that some of the autoimmune and cancer risks associated with celiac disease may still be there even with a gluten-free diet. Who was asking what else besides gluten could be contributing to these risks and were they being studied? Was oxalate one of those risks? People on our listserves that help people reduce dietary oxalate were telling us they experienced improvements in autoimmune conditions on a low oxalate diet. No one has had time to examine these reported changes formally yet, but could oxalate have a potential connection to the risks of autoimmunity or even transformed cells in celiac disease patients? I learned to ask these types of questions in graduate school and in the years that followed as I continued to find science that had been learned "out of order", and rejected as an important piece of the science because at the time there were missing pieces that were only discovered later. My intense study of medical literature's missing links brought to my attention so many valuable scientific discoveries that at the time they were published had been cast off as irrelevant. As I started to look intensively for more and more of these lost pieces, I made another astonishing discovery. I learned that we do not fund researchers to go digging through past scientific work to find links that may never be rediscovered after scientists with other priorities and agendas direct research efforts into other directions. Does science proceed linearly? Why should it? Are you personally one of the types of people that when doing a jigsaw puzzle, you first find all the outside pieces, and then start grouping colors and actually have a plan for which piece you will try to find next? My plan is to keep looking for pieces that didn't fit into models in the past to see if today's new findings will finally reveal how they now fit in well with today's insights. I don't think laboratory scientists or clinicians are the best equipped to do this sort of work, but organizations funding science expect that to be where this sort of integrative work will originate. I have found instead that most investigators who are up to their ears in current scientific projects or who are developing protocols for others to follow will not take very much time to dig deeply for lost pieces. There are rare exceptions to this observation. I have actually met a lot of this special breed of scientist, who loves to think outside the box and has respect for what might have been lost and loves to dig through old findings. Nevertheless, sociologists who study such things tell us that most scientific studies are never read outside of a small group of narrow interest and will only have influence for a few years. With this being the general expectations, who is left to do the work of recovering lost work from the past? Who also brings in work from other disciplines previously thought unrelated to a condition? In the oxalate field, molecular biologists have now discovered that oxalate shares transport with sulfate and bicarbonate, which means oxalate also gets into the regulation of pH. While these transporters regulate these ions, they also move a lot of water across cell membranes. In some places, oxalate shares transport with iodine, and of course, that makes us think of things related to the thyroid and all the histories of later onset thyroid disorders and autoimmune conditions. Pathologists found that the older you are, the more your thyroid gland will fill with oxalate, and this can be associated with a loss of thyroid activity. That makes sense now that we understand that these substrates are linked in the way the body handles them. But what about anemia that can develop in celiac disease? Scientists found that transferrin's carbonate ion can be replaced by oxalate if oxalate can gain access to this site at sufficient concentrations. When that happens, unlike the carbonate ion, the oxalate anion won't let go of the iron, so it sequesters iron irreversibly. This mechanism has never been thought to be related to the anemia in celiac disease. What about the tendency towards osteoporosis or osteopenia in celiac disease? Some remarkable studies conducted in the late 1930's (actually after Popeye made his appearance) fed groups of rats a basal diet deficient in a good calcium source, but they made up the rat "RDA" for calcium by using either turnip greens or spinach. Turnip greens are high medium in oxalate content, but spinach is extremely high. The rats fed the spinach, during their lifetime (and many died prematurely), had impaired growth (also seen with celiac disease). They had bones and teeth that wouldn't mineralize. The rats on spinach were unable to reproduce except for one litter of two pups that were quickly devoured by their mother at birth. In contrast, the rats fed turnip greens, which are roughly otherwise equivalently nutritious, completed the study in great health with shiny coats and all the perks of being a healthy rat. Did Popeye deceive us about the benefits of what has become a much more popular food, often called "the healthiest food there is?" By the way, one of these studies was conducted by Campbell Soup Company! Our oxalate project, which makes its home at www.lowoxalate.info with its associated support groups on Yahoo and Facebook, has now served more than 17,000 families in helping them discover for themselves how oxalate has been contributing to health issues…with problems that resolved as they brought down their body burden of oxalate. We've seen this one change fundamentally alter the course of more than twenty disorders, and these disorders are not very much alike. Some are genetic and some are probably not genetic, but are you wondering why they aren't alike if they are all associated somehow with oxalate? With new genetic tools and new basic science to help us, it is now a lot easier to figure that out. Members of the SLC26 family of oxalate transporters that move a special set of nutrients across cell membranes are expressed at different levels and in different combinations in different organs and cell types. Scientists are just now starting to ask the questions about how they may be regulated, or "turned on" or "turned off". When is the immune system involved in this regulation? When may we find genetic differences in the use or expression of these transporters? We already know a few observations related to their expression in the lungs and in the inner ear and in the mucosa, but at this stage in the game, there is much more science about their regulation that we don't know compared to what we already have discovered. We do know now that it was a mistake to think oxalate was only secreted in urine. How many studies in the past based their conclusions on urine being the only place to look? Oxalate is now known to be secreted in the lungs where scientists in Russia have been making much progress in understanding its roles in asthma and COPD, but I would just about guarantee that your immunologist or your pulmonologist doesn't know about that research yet, but it has been going on for years and years. Oxalate is also secreted to the skin and can cause terrible rashes. Is it related to dermatitis herpetiformis? Who has measured for oxalate in those lesions associated with gluten sensitivity? In primary hyperoxaluria, secretion of oxalate to the skin has led to serious lesions that can even turn into gangrene. People on our listserves have reported the swelling of blood vessels in the skin termed livedo reticularis, and others have described and pictured all sorts of skin lesions, including an odd appearance of glitter in the skin that appears imbedded, but glistens beautifully in the sun. No, these people were not vampires! Our bodies not only get oxalate from dietary sources. The body is also producing oxalate internally as a by-product of certain metabolic processes that normally keep oxalate levels low. In the genetic condition, Primary Hyperoxaluria Type I, still believed to be found in only one in a million individuals, these individuals lack a B6-dependent enzyme that ordinarily converts a normal byproduct of metabolism to a very safe amino acid. When this enzyme activity is lacking from this genetic defect or from B6 problems, oxalate builds up inside the cells where it is made and where it might produce local damage. The amount of oxalate produced with the genetic defect is so high that it spills out into the body, primarily from the liver, and produces a condition called oxalosis where oxalate damages tissues all over the body, and in the bones, and the heart, and often leads to death by kidney failure. Through the work of Marguerite Hatch and other scientists, we have learned that signals now being studied will instruct intestinal cells to take oxalate out of blood and secrete it into the stool. Even though a vast literature has associated inflammatory bowel diseases with producing an increased absorption of dietary oxalate through a leaky gut, that is apparently not the whole story. The body has mechanisms to rid itself of normal levels of excess oxalate, but in primary hyperoxaluria Type I, these efforts seem never enough to protect the body. In Mayo's database it was reported that 59% of those with this genetic disease experience abdominal pain. Oxalate is a known inflammatory molecule. Does oxalate secretion to the gut produce inflammation and pain? This certainly needs to be studied by gastroenterologists but does that discipline even know about this oxalate research? Who is showing them this science? Have you ever wondered if there is anyone who ensures that discoveries from basic science are applied by the physician to patient care when the finding isn't related to drug development? We humans do not have genes to degrade oxalate. That is why oxalate, once absorbed into blood can collect in our tissues and cause damage. Nature has provided a way for increased oxalate in our blood to join the contents of our intestines so that it can find and bind calcium in the gut and then can leave in the feces. That is not the only reason oxalate from blood is sent there. The gut is home to microbes that are capable of degrading oxalate. This purposeful removal of a substance toxic to humans happens only if the oxalate-loving microbes are there and healthy enough to perform this service for us. This wonderful system fails, however, in conditions like cystic fibrosis, where continuous use of antibiotics may have killed the microbes that perform this service for us. Unfortunately, even in those without cystic fibrosis, many commonly used antibiotics, like the Z-Pack, can kill our oxalate degrading microbial friends. Another problem is that widely used antibiotics can also kill back the biotin producing microbes in the gut. Why is that relevant to oxalate? An important class of enzymes called biotin-dependent carboxylases, were found to be invaded by oxalate when higher levels of oxalate travel to where these enzymes function. Since these enzymes function in critical roles in the mitochondrion (with only one enzyme of this type serving us in the cytosol) scientists learned that oxalate may seriously impair their enzyme activity, putting our mitochondria in great distress. Scientists also found this interference is fairly easily addressed by high doses of biotin. Many years ago, I realized that doses of biotin being recommended by physicians and others were in all likelihood too low to provide effective restoration of the function of biotin-dependent carboxylases whenever oxalate had become elevated in mitochondria . I read about doctors treating dystonia caused by a thiamine transport defect with high dose biotin at 5-10 mgs/kg/day. Children with this thiamine transport disorder were kept on this dose of biotin for years with no problems, but when the dose was lowered, the dystonia came back. Why are some physicians worrying about giving 5 to 20 mgs a day to grown adults? I can only guess that they were unaware of the literature on biotin's safety and were never able to witness how their patient's lives might change on higher doses. Competition at enzyme active sites will matter much more than blood or urine levels. Unfortunately, we have no way of measuring tissue or organelle levels of oxalate in routine patient care. Clearly, more work needs to be done in this area to see where and when higher doses are needed. Unfortunately, many doctors are in unfamiliar territory with higher doses of biotin, and may be unaware of biotin's track record of great safety even at very high doses. We must ask, if someone is dangerously high in oxalate, which choice will cause more harm to them, taking high dose biotin, or failing to take higher doses of biotin when that could lead to a loss of function of those important enzymes? Do scientists and doctors realize that anything which damages mitochondrial function might also lead to villous atrophy? Did elevations of oxalate happen before the changes that lead to a diagnosis of celiac disease? There are actually many other mitochondrial enzymes known to be inhibited by oxalate. If oxalate seriously affects mitochondrial function, what might that have to do with what else we know about celiac disease? Right now, the first two articles that come up in pubmed when searching on celiac disease and oxalate are articles that should get us thinking. The first is an article entitled, "Subclinical celiac disease and crystal­ induced kidney disease following kidney transplant". Its abstract says, "Subclinical celiac disease is commonly overlooked and hyperoxaluria is not usually investigated in kidney patients." This article described a patient with hyperoxaluria, but this patient was lacking overt diarrhea, fat malabsorption, or nephrocalcinosis. The article that comes up next on this search speaks of measuring children with celiac disease, and concludes, "In contrast to adults, increased urinary excretion of oxalate was not detectable in children with celiac disease." Was that happening because oxalate that was getting into the blood was being secreted at this age more appropriately to the gut, or the lungs, or the skin, instead? Or had their oxalate been collecting in tissues like the gut, where it might be starting to impair mitochondrial function, possibly leading in time to villous atrophy? It would be hard not to notice that currently in the US, it is becoming popular to try gluten-free eating even if someone does not have celiac disease. That situation also describes several members of my own family who do not have celiac disease, but found out about twenty years ago that being gluten-free turned around our health so significantly that we never were tempted to go back to eating gluten. I had actually gotten the idea to try life without gluten from autism research which had been looking at a different reason to be sensitive to gluten, termed "the opiate excess theory". When I was at the medical library doing research when I was in graduate school, I found this theory discussed in a decades old book talking about schizophrenia. Soon I was privileged to know two of the major scientists working in this area, Paul Shattock and Kalle Reichelt. They found a protein in wheat (gliadin) and in milk (casein) that as they were digested formed peptides that had opioid activity. These peptides were capable of producing signals at opiate receptors meaning they might produce reactions or side effects seen when taking opiate medications. Later work also discovered opioid peptides in soy. The reason that this research might be important to celiac disease is that part of the benefit seen by removing gluten may come from eliminating these opioid signals, but these signals may continue to be a problem if you are still consuming large amounts of milk or soy. Recently, some further implications have appeared in this research area. Another of my autism colleagues, Richard Deth, found at his laboratory that the peptides that form opiates also block the absorption of cysteine across cell membranes. This unexpected finding probably has its biggest implications in the gut (preventing sulfur absorption) and in the brain, where sulfur is regulated a little differently. I recommend his recent paper to tell you more details, but it simply means that some of the benefits people with celiac enjoyed on a gluten-free diet may have been related to this other characteristic of opioid peptides. These same individuals may find that their health will improve even more if they controlled milk and soy. In the second year of our project on oxalate, I spoke at a conference in Germany and was invited for lunch in the home of a family with a child with autism on a gluten-free diet, but I noticed that this child and the children with autism I met in Germany were not doing as well as I was used to seeing in the USA. As I sat at their table, I found out that most of their gluten-free bread was made with buckwheat as a major ingredient. Buckwheat is, a very high oxalate grain. Was this keeping their son from getting better? Because I knew so many children with autism who had done much better than before after they eliminated gluten and casein, this to me seemed a sufficient reason not to reintroduce these foods to children already off these foods as we looked into the role of oxalate in autism. That's why, as we began our research on oxalate, I purposefully set out to test the raw ingredients being used commercially and in households for individuals on gluten and dairy-free diets. Our project discovered that there was a problem with buckwheat, amaranth, quinoa, and two late arrivals, chia seeds and hemp. We already knew oxalate was high in seeds like sesame seeds and poppy seeds, and also high in nuts like almonds which were now being made into milks for those on dairy-free diets. Soy is also high in oxalate, meaning soy has two problems—its opioid peptides and its oxalate level. In grains, most of the oxalate is in the bran, so the more "whole grain" a product is, the higher it will be in oxalate. Our listserve was literally flooded with individuals who found they got "sick" soon after they adopted what they thought was a "healthy diet". Another issue was the high levels of oxalate in chocolate and carob, which are used extensively in gluten-free "comfort foods". Last year, I attended a gluten-free expo in my city and picked up a cookbook full of new exciting recipes that were put together for this expo, and I saw that most of the recipes contained grains, or nuts or seasonings that were extremely high in oxalate. I couldn't help but wonder: Is this going to backfire for people, and will they recognize what is happening if by using these recipes and foods that they will find their health does not improve and may even get worse? In helping so many thousands of people reduce oxalate, our oxalate project has learned one thing clearly, and that is that giving someone a one page list of foods to avoid rarely successfully reduces oxalate in anyone. We have been told this most often by kidney stone patients who were given these lists by their doctors. Patients have told us hundreds of times that health improvements were not realized until they made this diet more like calorie counting. This is what we do in our support groups where people also monitor the contribution to their total oxalate level that comes from medium oxalate foods. This is why I would ask those reading this article to please seek our help if you wish to reduce oxalate, and do not strike out into the unknown on your own or confine yourself to the use of lists you might find on the Internet or at your doctor's office. Hundreds of Listmates have told us these lists had serious inadequacies and misinformation and little overlap with what they actually had been eating. We have also learned something else that is critically important. People who have been on an extremely high oxalate diet and then have reduced their diet's oxalate content too quickly, have gotten themselves in trouble. Some have ended up in emergency rooms in metabolic crisis with the doctors there unable to help them, because the doctors had never had training about why someone in this situation would get so sick. Even before our project started, we knew from studying the literature on those with primary hyperoxaluria, that when oxalate supply is reduced quickly by removing the liver that was putting out so much oxalate into their bodies, after replacing it with a normal liver, the amount of oxalate that suddenly began to leave the tissues of their body could potentially damage the replacement organ. Doctors have reported a very high death rate with these patients, which is reported to be much higher than death rates from other reasons for liver transplants. But what about what happens when reducing dietary oxalate? The food industry's recommendation of multiple fruits and vegetables has happened at the same as they began promoting many foods as super-foods and nutrient rich. Unfortunately, many of these same foods are so high in oxalate that they can keep someone from being able to retain and utilize minerals that are coming from other foods in the same meal. This can promote hyperabsorption of oxalate and increase risks of mineral imbalances. Our support groups have been deluged with individuals coming to us now with diets containing thousands of milligrams of oxalate putting their urine oxalate levels in ranges formerly seen only in the genetic hyperoxalurias. A low oxalate diet tries to keep the total oxalate load to between 40-60 mgs per day in adults As we said before, people who have been eating extremely high levels of oxalate need to reduce oxalate very slowly while the body adapts to the change. We have amassed a lot of experience with helping such individuals. The need for caution and more gradual change should not surprise us, because scientists are now telling us how quickly dietary changes can alter the function and composition of our microbial community and can also quickly alter cellular regulation of whatever enters and exits cells. These are compelling reasons to change the oxalate level slowly. Our website is www.lowoxalate.info. Our Yahoo group and our Facebook group are both called Trying_Low_Oxalates. We are partnering with non-profits and scientists from many fields around the world to fill in the missing science for a long list of disorders. Our work has gone far beyond autism, and we have been monitoring labwork on many conditions. We want to help make this dietary alteration as easy and safe as possible. We hope some of you readers will begin to get educated in this area. If you begin to reduce your oxalate, please let us know what reducing oxalate accomplishes for you. Since my early years in autism research, I have been convinced of one main principle. People with a condition will know their own bodies well. They are more likely to make important observations of change compared to a professional who comes in with too many preconceived expectations and has only a limited acquaintance with their subject's previous life. The first step in the scientific process really happens before scientific steps are put into use. The first "pre-step" is observation of something that does not fit old models. Frankly, after twenty years in research on autism, I don't believe the first step is best done by scientists and/or physicians. Why? Often someone new seeing a problem for the first time will notice aspects of that problem that people relying on old models will think is irrelevant and leave alone. That is why, to me, careful observations of hundreds and thousands of patients interacting can become the opportunity for forming new hypotheses that a scientist can later be recruited to test. This coordination of this volume of patient input was impossible before the internet allowed patients to find each other. But now, I think this is the most fertile field there is for making new scientific discoveries. Please, let's not confuse those two processes. First, we need to observe changes without layering expectations on what we see that comes from experience with only one type of patient. By looking at a broader diversity of patients, and discovering the overlap of their observations, we have a much better chance at noticing unexpected patterns that are significant. When people with no expectations of what ought to be ignored end up making the same observation time and again when they don't know each other, THEN you have something to legitimately research. At that point, the scientist can get involved with the second step, which is verifying the observations and seeing how widely they apply in one disorder or even more broadly. Using both steps, and both sets of eyes, and the marvelous ability to combine observations from thousands of individuals using the internet, we are now likely to begin to understand the complex role of oxalate in celiac disease and in many other disorders. From the author: If you have ever been diagnosed with an autoimmune disease and have been trying to lower oxalate, will you participate in the development of this science by filling out a survey? We would also like to find out whether reducing oxalate has affected your autoimmune condition. The link to our survey is here: https://www.surveymonkey.com/r/CMN5KK7 References: Baker PW, Bais, R, Rofe, AM Formation of the L-cysteine-glyoxylate adduct is the mechanism by which L-cysteine decreases oxalate production from glycollate in rat hepatocytes. Biochem. J. (1994) 302, 753-757 Capolongo G, Abul -Ezz S, Moe OW, Sakhaee K . Subclinical celiac disease and crystal-induced kidney disease following kidney transplant . Arn J Kidney Dis . 2012 Oct ;60(4) :662-7 . Halbrooks PJ, Mason AB , Adams TE, Briggs SK, Everse SJ . The oxalate effect on release of iron from human serum transferrin explained . J Mol Biol. 2004 May 21;339 (1):217-26. Kohman, E.F. Oxalic acid in foods and its behavior and fate in the diet. The Journal of Nutrition, 1940 18(3): 233-246. Konstantynowicz J, Porowski T, Zoch-Zwierz W, Wasilewska J, Kadziela -Olech H, Kulak W, Owens SC, Piotrowska-Jastrzebska J, Kaczmarski M. A potential pathogenic role of oxalate in autism . Eur J Paediatr Neurol . 2012 Sep;l6(5) :485-91 Monico, CG, Persson, M, Ford CG, Rumsby, G, Milliner, DS. Potential mechanisms of marked hyperoxaluria not due to primary hyperoxaluria I or II. Kidney International, 2002 Aug;62(2):392-400. PubMed PMID: 12110000 Nishijima S, Sugaya K, Hokama S, Oshiro Y, Uchida A, Morozumi M, Ogawa Y. Effect of vitamin B6 deficiency on glyoxylate metabolismin rats with and without glyoxylate overload. Biomedical Research, 2006 Jun; 27(3):P93-P98. Novartis Foundation Symposium 273, Epithelial anion transport in health and disease: The role of the SLC26 transporters family. John Wiley and Sons, Ltd. 2006. Rare Kidney Stone Consortium Mayo Clinic. http://www.rarekidneystones.org/hyperoxaluria/physicians.html Saccomani MD , Pizzini C, Piacentini GL, Boner AL , Peroni DG . Analysis of urinary parameters as risk factors for nephrol ithiasis in children with celiacdisease . J Urol. 2012 Aug ;188(2):566-70 . Speirs, M. The utilization of the calcium in various greens, The Journal of Nutrition, 1939 17(6), 557-564. Trivedi MS , Shah JS, Al-Mughairy S, Hodgson NW , Simms B, Trooskens GA, Van Criekinge W , Deth RC . Food-derived opioid peptides inhibit cysteine uptake with redox and epigenetic consequences . J Nutr Biochem . 2014 Oct ;25(10) :1011- 8 .
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