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Showing results for tags 'osteoporosis'.
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More Links Between Celiac Disease and Osteoporosis
Jefferson Adams posted an article in Winter 2024 Issue
Celiac.com 11/20/2023 - Celiac disease and osteoporosis are known to be linked due to several interrelated factors. We recently did an article on the role of celiac disease in the development of skeletal alterations in patients with osteoporosis. In addition to the connections mentioned in that article, here are some additional connections between these two conditions: Malabsorption of Nutrients: Celiac disease, particularly when untreated or undiagnosed, can lead to damage in the small intestine. This damage impairs the absorption of various essential nutrients, including calcium and vitamin D. These nutrients are crucial for maintaining healthy bones. The malabsorption of calcium and vitamin D can contribute to the development of osteoporosis. Chronic Inflammation: Celiac disease is characterized by chronic inflammation in the gut. Prolonged inflammation can have systemic effects on the body, including the promotion of bone loss and the development of osteoporosis. Secondary Hyperparathyroidism: In celiac disease, the malabsorption of calcium can lead to secondary hyperparathyroidism. This is a condition where the parathyroid glands become overactive in response to low calcium levels in the blood. Hyperparathyroidism can further contribute to bone loss. Low Body Weight: Celiac disease can lead to weight loss and a lower body mass index (BMI), which is associated with an increased risk of osteoporosis. Low body weight can result in decreased bone density, making the bones more susceptible to fractures. Gluten-Free Diet and Nutrient Restoration: Fortunately, osteoporosis associated with celiac disease can often be managed or even reversed by adopting a strict gluten-free diet. When individuals with celiac disease eliminate gluten from their diet and allow their small intestine to heal, nutrient absorption improves. This, in turn, can lead to a recovery of bone density. Supplementation: In some cases, healthcare professionals may recommend calcium and vitamin D supplementation to help restore bone health in individuals with celiac disease. These supplements can be especially beneficial during the early stages of adopting a gluten-free diet when the body is still healing. Bone Density Monitoring: Individuals with celiac disease, particularly those who are newly diagnosed or have experienced severe bone loss, may benefit from bone density testing (e.g., dual-energy X-ray absorptiometry or DXA scans). Regular monitoring can help assess bone health and guide treatment decisions. Lifestyle Factors: Besides diet, other lifestyle factors like engaging in weight-bearing exercises, quitting smoking, and moderating alcohol intake can contribute to better bone health and help mitigate the risk of osteoporosis. It's important for individuals with celiac disease and osteoporosis to work closely with healthcare professionals, such as gastroenterologists, registered dietitians, and endocrinologists, to manage their conditions effectively. By maintaining a strict gluten-free diet and addressing nutritional deficiencies, many individuals can improve their bone health and reduce the risk of osteoporosis associated with celiac disease.-
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Celiac.com 06/06/2023 - Celiac disease, osteopenia and osteoporosis are conditions that have been found to be connected. A research team recently described celiac disease-induced osteoporosis in an attempt to enlighten new and lesser-known aspects, including the influence of the intestinal microbiome and sex-related differences, on bone health. The team included Lisa Lungaro, Francesca Manza, Anna Costanzini, Marianna Barbalinardo, Denis Gentili, Fabio Caputo, Matteo Guarino, Giorgio Zoli, Umberto Volta, Roberto De Giorgio, and Giacomo Caio. They are variously affiliated with the Department of Translational Medicine, University of Ferrara in Ferrara, Italy; the National Research Council, Institute for the Study of Nanostructured Materials (CNR-ISMN) in Bologna, Italy; the Department of Medical and Surgical Sciences, University of Bologna, in Bologna, Italy; the Mucosal Immunology and Biology Research Center, Massachusetts General Hospital—Harvard Medical School in Boston, MA, USA. Their review describes the role of celiac disease in the development of skeletal alterations, in order to provide physicians with an updated overview on this debated topic, and to improve the management of osteoporosis in celiac disease. It is important to note that not all individuals with celiac disease will develop osteoporosis. The risk varies depending on factors such as the duration and severity of the disease, adherence to a gluten-free diet, and individual variations in bone health and genetics. However, individuals with celiac disease should be aware of the increased risk of osteoporosis and take steps to manage their bone health, including ensuring adequate calcium and vitamin D intake, monitoring bone density through regular screenings, and maintaining strict adherence to a gluten-free diet. Several important connections between the conditions highlighted by the researchers include: Malabsorption Celiac disease is characterized by damage to the small intestine, leading to impaired absorption of nutrients, including calcium and vitamin D, which are essential for maintaining healthy bones. Malabsorption of these nutrients can result in reduced bone mineral density and increased risk of osteoporosis. Inflammatory Response Celiac disease triggers an immune response in the presence of gluten. This immune response involves the production of pro-inflammatory molecules, which can contribute to bone loss and increased bone turnover, leading to osteoporosis. Calcium Imbalance The malabsorption of calcium in individuals with celiac disease can disrupt the balance of calcium in the body. When there is insufficient calcium intake or absorption, the body may draw calcium from the bones, weakening them and increasing the risk of osteoporosis. Calcium intake in the young age is an essential determinant of the bone mass peak. Calcium metabolism defects are common in untreated children with celiac disease, and they return to normal with a gluten-free diet. Vitamin D Deficiency Vitamin D plays a crucial role in calcium absorption and bone health. Celiac disease can lead to reduced vitamin D absorption due to intestinal damage. Vitamin D deficiency further exacerbates the risk of osteoporosis. Gluten-Induced Autoimmunity Celiac disease is an autoimmune disorder, and individuals with autoimmune diseases, including celiac disease, have a higher risk of developing additional autoimmune conditions such as autoimmune osteoporosis. Autoimmune mechanisms may contribute to bone loss and the development of osteoporosis in individuals with celiac disease. Hormonal Imbalance Celiac disease can disrupt the endocrine system, leading to hormonal imbalances. Hormones such as estrogen and testosterone play a crucial role in maintaining bone health. Imbalances in these hormones can accelerate bone loss and increase the risk of osteoporosis. Sex Differences Women with celiac disease are at a higher risk of osteoporosis due to both indirect and direct effects. The indirect effects include factors such as early menopause and amenorrhea (absence of menstruation), which can have a negative impact on bone health. Early menopause refers to the cessation of menstruation before the age of 45, which can occur in women with celiac disease due to various factors, including hormonal imbalances and inflammation. Early menopause is concerning for bone health because estrogen, a hormone that helps maintain bone density, decreases significantly during menopause. Lower estrogen levels can accelerate bone loss and increase the risk of osteoporosis. Therefore, women with celiac disease who experience early menopause should be particularly vigilant about managing their bone health. Physicians should be aware of bone conditions linked to celiac disease that might contribute to the worsening of BMD, and should treat them promptly. There is little evidence regarding osteopenia and pharmacological osteoporosis treatment, specifically in celiac disease. Probiotic supplementation might become a novel strategy in preventing bone alterations, although the role of gut microbiota is still uncertain and not well-established yet. In the full report, the researchers offer a comprehensive dive into each of the areas mentioned above. Read more in Nutrients. 2023 Mar; 15(5): 1089 doi: 10.3390/nu15051089
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Hello everyone, I need a kick in the butt. I have struggled with my relationship with food my entire life. I was diagnosed a coeliac at 10 years old and I followed a pretty strict diet till I was 17 because I was living with my mum. After that, I moved by myself and I started struggling with money and paying everything off. I started buying gluten products because they were cheaper but then it became a vicious circle where I would eat gluten, feel bad for eating gluten and eat more gluten. I have developed osteoporosis, vitamin D deficit and Hashimoto's thyroiditis. I am now 24 and I am genuinely scared because I want to be able to conceive soon and also I am terrified of going to the doctors to see the damage I have done to myself. I know I am killing myself but for some reason I cannot stop. It's almost like I live for that feeling of misery that comes after eating gluten. I don't know what to do. Please help.
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Celiac.com 10/23/2020 - As people age, their bones become less dense, and their risk of developing osteoporosis, leaving them susceptible to fractures. A recent study indicates that celiac disease may increase that risk, even in younger people. According to the Canadian study, people with celiac disease have a higher risk of serious osteoporotic fracture that is unrelated to their fracture risk assessment tool (FRAX) score. FRAX scores accurately predict fracture risk when celiac disease is added as a secondary osteoporosis risk factor, or when BMD is included in the FRAX assessment. A research team used data from the Manitoba Bone Mineral Density Registry to determine the 10-year risk of major osteoporotic fractures in nearly 700 people with celiac disease, over a period of about seven years. They also followed just over 68,000 people from the general population subjects for a similar period. The research team included D.R. Duerksen, L.M. Lix, H. Johansson, E.V. McCloskey, N.C. Harvey, J.A. Kanis & W.D. Leslie. The team found that about 8.5 percent of people in each group suffered one or more major osteoporotic fractures, even though the celiac disease group was younger, and contained more men. In the general population, there FRAX predictions and the observed 10-year major osteoporotic fracture probabilities matched up cleanly. In patients with celiac disease, however, predicted and observed fracture predictions only aligned when celiac disease was factored as secondary osteoporosis; otherwise, FRAX underestimated the celiac patients' 10-year major fracture risk by more than 4 percent. Celiac disease patients face an increased risk of major osteoporotic fractures. When celiac disease is considered as a secondary osteoporosis risk factor, or when BMD is included in FRAX assessment, FRAX can accurately predict future fracture risk. Do you have celiac disease and also suffer from osteoporosis? Have you broken bones? Share your thoughts below. Read more in Osteoporosis International (2020)
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Vitamin D, Antibiotics and the Immune System
John B. Symes, D.V.M. posted an article in Summer 2010 Issue
Celiac.com 06/28/2019 (originally published 07/12/2010) - The report by R.H. Wasserman titled “Vitamin D and the Dual Processes of Intestinal Calcium Absorption“ is very important. I have some writing to do (and corrections to make) as a result of reading this. It helps to explain why dogs don’t suffer from clinical osteoporosis. It’s obvious that there are processes taking place in the ileum of humans that do not take place in the dog. This came up as I was counseling an Internet acquaintance concerning his osteoporosis. He was not improving with conventional therapy and was also suffering from chronic lymphocytic colitis. I knew that the ileum actively absorbs calcium but the numbers in the study above were news to me. I’ve been telling people for years that one of the biggest difference between a person doing well after gastric bypass vs. crashing and burning had to be the health of their ileum and now I understand a little more as to why this is the case, especially when it comes to bone density. So, I’ve turned my attention to the health and wellbeing of the ileum. I have assumed for years that one of the biggest factors in humans is dairy products. So much points to that. But…is it the casein and other dietary glycoproteins causing villous atrophy that does it OR is there something IN the milk that is doing it? We know that Mycobacterium paratuberculosis can be involved in Crohn’s and that it can come from milk, even when pasteurized. Are there other pleomorphs that are doing this? I like to point out that, of the “big 4” foods, only dairy is of animal origin and that it is “public enemy number one” for a reason: It not only contains damaging lectins, loads of estrogen, and casomorphins (BCM7) but is a veritable petri dish of microorganisms. In fact, they now know that the bovine leukemia virus can cause leukemia in primates. What about mycoplasma, mycobacteria, and the myriad of pleomorphic bacteria is contains, some of which could take up to a year to culture out (e.g. mycoplasma). I’m working on a paper that deals with the zoonoses associated with cow’s milk. So…I still contend that dairy is one of the biggest culprits in Crohn’s and other chronic diseases of the lower intestine but these are likely to be more examples of “syndromes”, in which resident viruses and bacteria (including those viruses in the DNA) react to chronic insults like gluten, dairy, etc. and other man-made components of food along with newly acquired viruses and bacteria, some of which are coming from vaccines. (Gotta wonder about those weaponized versions of mycoplasma floating around.) Also, there is no place like the gut for secondary infections. Here is the application I am wondering about: Could antibiotics help a person with osteoporosis, knowing that pleomorphic bacterial infections are showing up in other areas of “autoimmune” disease, such as rheumatoid arthritis, scleroderma, and sarcoidosis? The process appears to be the same in all cases: The residential viruses and bacteria are all involved in adaptive processes throughout the body. They are reason for inflammation, as they react to immune challenges being brought against the cell. Once this process escalates and the immune system crashes, the bacteria become a significant secondary problem requiring specific treatment (see www.bacteriality.com and the “miracles” that are occurring using long-term doxycycline, etc.). As long as the immune system remains competent, these individuals can still be rescued by employing nutritional therapy, holistic approaches and avoidance of the obvious insults (food lectins, preservatives, pollutants, cigarettes, etc.). Vitamin D3 therapy would be crucial here for both calcium absorption and immune competence. But the dog, once again, may give us a clue as to which aspect of D3 is the most important in the pathogenesis of osteoporosis. I believe that the average dog is woefully deficient in D3, with their dismally high incidence of cancer being a leading indicator. Why wouldn’t they be low? They convert sunlight to D3 much less efficiently than humans, are covered with fur, and spend most of their time indoors. If and when we start measuring their D3 levels, we will likely be stunned at their low levels. And yet…they don’t suffer from clinical osteoporosis. Is it because they don’t live long enough? Hey, they get everything else. So again, I am wondering more and more about the immune aspects of osteoporosis in humans. Once the patient crosses the line and their immune system becomes incompetent (which is when many present initially), bad things happen. They go from subclinical to clinical, from bad to much worse, or from “stage two” (“autoimmune” diseases) to “stage three” (cancer). We know now that pleomorphic bacteria are involved in cancer, which makes perfect sense. They were involved in the adaptive processes from the start (through their influence on the cell’s mitochondria) and play a vital role in determining when the cell (and the viruses it contains) finally decides to form a tumor to escape further insults. This process is taking place all over the body in every tissue we have. So…this must be happening in the ileum, where they now say 70-80% of the calcium is absorbed. Could antibiotics of the right type be of help when these immune incompetent individuals need rescuing, even in cases of refractory osteoporosis? Certainly, we should try to avoid their use for as long as possible but we have to be realistic sometimes in what the patient or the owner of a pet is willing to do. Those who are into holistic medicine can avoid this last ditch effort for the longest time, even indefinitely. But if the last ten years have done anything for me, they’ve made me a realist. Sadly, most people want a quick fix. Source: Wasserman RH, Vitamin D and the Dual Processes of Intestinal Calcium Absorption, J. Nutr. 134:3137-3139, November 2004 Article Corrected 07/01/2019 - The original article was corrected as it referenced a study linking the measles portion of the MMR vaccine with ileum damage in humans, however, this study was retracted.- 3 comments
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The Osteoporosis—Gluten Intolerance Connection
Dr. Vikki Petersen D.C, C.C.N posted an article in Autumn 2009 Issue
Celiac.com 01/02/2020 - Osteoporosis is the 11th leading cause of death. 1 in 2 women and 1 in 4 men is affected. We sometimes think of our bones like the walls in a room - they hold things up but we consider them rather inert. On the contrary, our bones are very much alive, constantly remodeling themselves by getting rid of old bone cells and rebuilding with new bone cells. Further, healthy bones are needed for immune function since all our red and white blood cells are made in the marrow of our bones. There are some drugs available to “treat” osteoporosis but they are laden with side effects. Some are even cancerous. In Nutrition Reviews 2007, a study report titled “Osteoporosis and Inflammation” revealed that inflammation triggers the shift from healthy bones to osteoporosis. So let’s look at how osteoporosis is related to digestive function. A recent article in Cell 2008 entitled “When the Gut Talks to Bone” revealed that certain genes (Wnt genes) trigger signaling factors required for the development of bones and nerve structures within the body. What was most interesting was the revelation that these genes are activated by serotonin. Where is the vast majority of serotonin made? In the gut! We have previously seen correlations between the brain and the gut, such as in chronic IBS which is strongly correlated to stress. But gut serotonin actually “talks” to our bone, thereby creating a strong connection between gut health and bone Health. This is quite new in the research. It substantiates something I’ve seen in my patients for years. The more inflammation is present, the more the gut makes serotonin which in turn leads to bone breakdown – osteoporosis. What does all this mean? It means that lowering inflammation in the body is critical in the prevention of osteoporosis (not to mention heart disease and cancer but we’ll leave those connections for another article.) How do we lower inflammation? One of the biggest inflammation inducing culprits is gluten. It not only creates local inflammation in the gut but it creates systemic inflammation through its affects on the immune system in sensitive individuals. And remember, current research considers 40% of the population to be gluten sensitive. In the New England Journal of Medicine 2007 it stated that celiac disease inflamed the gut, thereby creating bone loss. The good news in all of this is that reducing inflammation is something we have control over. We can find out if we’re among the 40% of the population that is gluten intolerant. We can change our diets. We can use supplements such as omega-3 fatty acids to reduce inflammation and help heal the lining of our intestines. These tools are within our reach. Further, remember that gluten reduces absorption of certain key vitamins and minerals such as calcium and Vitamin D, which are critical to bone health. Have your Vitamin D level evaluated and supplement as needed. Osteoporosis is a very debilitating disease. Now we know it doesn’t have to be.- 3 comments
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Celiac.com 05/04/2018 - It has been recognized for several decades that both children and adults with celiac disease have a significantly increased frequency of osteoporosis and increased risk of fractures as compared to the age-matched non-celiac healthy individuals. Based on published data the prevalence of osteoporosis among celiac patients varies from as low as 4% to as high as 70%. The data from our clinic indicate that prevalence of osteoporosis among adults with gluten intolerance and celiac disease is in the vicinity of 30-40%. Characteristics and causes of osteoporosis Osteoporosis is a bone disease characterized by the reduced bone mineral density and impaired bone architecture that leads to an increased risk of fracture. The three main mechanisms by which osteoporosis develop include an inadequate peak bone mass, excessive bone resorption and inadequate formation of new bone during remodeling. At a given age, bone mass results from the amount of bone acquired during growth (the peak bone mass) minus the acquired bone loss due to variety of reasons including age-related processes, malabsorption syndromes, chronic steroid use etc. The rate and magnitude of bone mass gain during the pubertal years may markedly differ from one individual to another. It has been demonstrated that pediatric onset of celiac disease and poor compliance with gluten-free diet during childhood do significantly reduce peak bone mass. One of the main causes of osteoporosis is an alteration in bone remodeling due to imbalance between bone formation and resorption, with a predominance of resorption resulting in a reduction in bone mass and increased risk of fractures. Formation of the new bone is facilitated by specialized cells, osteoblasts, which actively synthesize bone matrix. Bone resorption is mediated by other specialized cells, osteoclasts. One of the main regulators of bone remodeling is the RANK/RANKL/OPG system. During bone remodeling, bone marrow cells and osteoblasts produce RANKL(receptor activator for nuclear factor kB ligand), which bonds with a transmembrane receptor of the osteoclast precursor, RANK(receptor activator of nuclear factor kB), causing their differentiation and activation. Osteoprotegerin (OPG) binds to RANKL before it has an opportunity to bind to RANK, and hence suppresses its ability to increase bone resorption. Normal bone remodeling is based on the permanent renovation of the skeleton and consists of an initial phase of bone resorption followed by a phase of formation, both of which are regulated by general (endocrine) factors and local (paracrine) factors. The main endocrine factors include parathyroid hormone [PTH] and vitamin D as well as estrogens and, to a lesser extent, testosterone, thyroid hormones, growth hormone and leptin. Local factors include various cytokines (IL-1, IL-6 and TNF-a playing a role) key growth factors that regulate the process. There are several well-characterized risk factors which contribute to the development of osteoporosis in celiac patients. These include: 1. Malabsorption of vitamin D and secondary hyperparathyroidism Villous atrophy in celiac patients reduces the active absorption surface and induces steatorrhea (exces fat in feces), which has a chelating effect on calcium and vitamin D, making their absorption difficult. This reduces levels of the vitamin D transporting protein (calbindin and calciumbinding protein) and increases PTH synthesis which, in turn, lead to increased bone resorption causing osteoporosis. 2. Malabsorption of vitamin K Malabsorption of fat soluble vitamins including vitamin K is a common finding in celiac patients. Three vitamin-K dependent proteins have been isolated in the bone: osteocalcin, matrix Gla protein (MGP), and protein S. Osteocalcin is a protein synthesized by osteoblasts. The synthesis of osteocalcin by osteoblasts is regulated by the active form of vitamin D—1,25-dihydroxy-cholecalciferol. The mineral-binding capacity of osteocalcin requires vitamin K-dependent gamma-carboxylation of three glutamic acid residues. MGP has been found in bone, cartilage, and soft tissue, including blood vessels. The results of animal studies suggest MGP facilitates normal bone growth and development. The vitamin K-dependent anticoagulant protein S is also synthesized by osteoblasts, but its role in bone metabolism is unclear. Children with inherited protein S deficiency suffer complications related to increased blood clotting as well as decreased bone density. The data on the role of vitamin K in osteoporosis came from the clinical observations indicating that a chronic use of vitamin K antagonists such as warfarin increases risk of vertebral and rib fractures. Accordingly, vitamin K supplementation significantly lowers risk of vertebral and hip fractures. 3. Magnesium deficiency Magnesium deficiency may be an additional risk factor for celiac-associated osteoporosis. This may be due to the fact that magnesium deficiency alters calcium metabolism and the hormones that regulate calcium. Several human studies have suggested that magnesium supplementation may improve bone mineral density. Magnesium deficiency is easily detected with laboratory tests (eg, low serum magnesium, low serum calcium, resistance to vitamin D) or clinical symptoms (eg, muscle twitching, muscle cramps, high blood pressure, irregular heartbeat). Screening for magnesium deficiency should be routinely included in the screening of celiac patients with osteoporosis. 4. Chronic diarrhea and metabolic acidosis Chronic diarrhea in patients with celiac disease results in significant bicarbonate losses and development of metabolic acidosis. Bone is a major site for the extracellular buffering of the retained acid. Therefore, one of the main compensatory mechanisms maintaining a stable serum bicarbonate level in the face of an uncorrected metabolic acidosis is the dissolution of bone buffers and net efflux of calcium from bone. Bicarbonate supplementation in patients with metabolic acidosis decreases urinary calcium, phosphorus and hydroxyproline wasting supporting the concept of negative effects of acidosis on bone health. 5. Hypogonadism Decline of estrogen production and activity is one of the main events in the development of age-related osteoporosis. It is well known that estrogen deficiency is important in the pathogenesis of osteoporosis not only in women but also in men. Increase in bone mineral density in young men and declines in older men are related to circulating free estrogen, not testosterone. In general, patients with celiac disease are characterized by low levels of circulating estrogens which contributes to the development of premature osteoporosis. 6. Chronic use of Proton Pump Inhibitors Proton pump inhibitors (PPIs) are one of the most widely used classes of drugs. The commonly used PPIs include such drugs as Omeprazole (brand name: Prilosec), Lansoprazole (brand name: Prevacid), Dexlansoprazole (brand names: Kapidex, Dexilant), Esomeprazole (brand name: Nexium), Pantoprazole (brand name: Protonix) and Rabeprazole (brand name: AcipHex). Chronic use of PPIs for gastroesophageal reflux disease and other related conditions has been associated with impaired calcium and magnesium absorption and increased risk of vertebral and nonvertebral fractures. 7. Chronic use of Selective Serotonin Reuptake Inhibitors Selective Serotonin Reuptake Inhibitors (SSRIs) are frequently used in celiac patients for treatment of depressive disorders. The commonly used SSRIs include such drugs as Citalopram (brand name: Celexa), Escitalopram (brand name: Lexapro), fluoxetine (brand name: Prozac), fluvoxamine (brand name: Luvox), Paroxetine (brand name: Paxil) and Sertraline (brand name: Zoloft). It has been demonstrated that SSRIs increase extracellular 5-HT (5-Hydroxytryptophan) levels that have deleterious skeletal effects. The skeletal serotonergic system consists of 5-HT receptors and the 5-HT transporter (5-HTT) in osteoblasts and osteocytes. 5-HTT is a transmembrane protein targeted by SSRIs. 5-HT restrains osteoblastic activity, thus leading to bone loss. 8. Autoimmune mechanisms Autoimmune mechanisms have been long suspected as risk factors contributing to development of osteoporosis in celiac patients. Near a decade ago, it was demonstrated that sera from celiac patients with osteoporosis contains significantly high titers of antibodies against bones as compared to non-celiac osteoporotic patients. The immunostaining was localized in areas where an active mineralization process occurred and was similar to the distribution of the native bone tissue transglutaminase. Recently, it has been described that a subset of patients with celiac disease has autoantibodies to osteoprotegerin, which block the inhibitory effect of osteoprotegerin on signaling by the receptor activator of nuclear factor (NF)-kappaB (RANK), and are associated with severe osteoporosis and high bone turnover. 9. Chronic inflammation Chronic inflammatory diseases, including celiac disease, are associated with overproduction of proinflammatory cytokines such as TNF-a, interleukin(IL)-1, IL-6, IL-11, IL-15 and IL-17 among others which activate osteoclasts and accelerate bone resorption leading to osteoporosis. In conclusion, osteoporosis associated with celiac disease is not a coincidental problem. It is a consequence of disease-specific (autoantibodies to osteoprotegerin), disease-nonspecific (malabsorption of vitamin D, K and magnesium, hypogonadism, chronic inflammation, chronic diarrhea and metabolic acidosis) and jatrogenic (overuse of PPIs and SSRIs) events accelerating resorptive processes in the skeleton. Correction of the aforementioned risk factors in celiac patients can reverse the development of osteoporosis and reduce the risk of osteoporosis-associated fractures. Bibliography: Bab I, Yirmiya R. Depression, selective serotonin reuptake inhibitors, and osteoporosis. Curr Osteoporos Rep. 2010 Dec;8(4):185-91. Bianchi ML. Inflammatory bowel diseases, celiac disease, and bone. Arch Biochem Biophys. 2010 Nov 1;503(1):54-65. Ito T, Jensen RT. Association of long-term proton pump inhibitor therapy with bone fractures and effects on absorption of calcium, vitamin B12, iron, and magnesium. Curr Gastroenterol Rep. 2010 Dec;12(6):448-57. Katz S, Weinerman S. Osteoporosis and gastrointestinal disease. Gastroenterol Hepatol (N Y). 2010 Aug;6(8):506-17. Riches PL, McRorie E, Fraser WD, Determann C, van't Hof R, Ralston SH. Osteoporosis associated with neutralizing autoantibodies against osteoprotegerin. N Engl J Med. 2009 Oct 8;361(15):1459-65. Stazi AV, Trecca A, Trinti B. Osteoporosis in celiac disease and in endocrine and reproductive disorders. World J Gastroenterol. 2008 Jan 28;14(4):498-505. Sugai E, Cherñavsky A, Pedreira S, Smecuol E, Vazquez H, Niveloni S, Mazure R, Mauriro E, Rabinovich GA, Bai JC. Bone-specific antibodies in sera from patients with celiac disease: characterization and implications in osteoporosis. J Clin Immunol. 2002 Nov;22(6):353-62. Turner J, Pellerin G, Mager D. Prevalence of metabolic bone disease in children with celiac disease is independent of symptoms at diagnosis. J Pediatr Gastroenterol Nutr. 2009 Nov;49(5):589-93. Vasquez H, Mazure R, Gonzalez D, Flores D, Pedreira S, Niveloni S, Smecuol E, Mauriño E, Bai JC. Risk of fractures in celiac disease patients: a cross-sectional, case-control study. Am J Gastroenterol. 2000 Jan;95(1):183-9.
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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
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Celiac.com 05/01/2018 - Celiac disease is marked by a variety of intestinal and extra-intestinal symptoms. One of the most common and best described expressions of celiac disease outside the gut is the presence of osteopenia and osteoporosis, which make for a higher fracture risk. A team of researchers recently set out to see if a gluten-free diet (GFD) improves bone mineralization. The research team included MB Zanchetta, AF Costa, V Longobardi, R Mazure, F Silveira, MP Temprano, H Vázquez, C Bogado, SI Niveloni, E Smecuol, ML Moreno, A González, E Mauriño, JR Zanchetta, and JC Bai. They are variously associated with the Instituto de Diagnóstico e Investigaciones Metabólicas, Buenos Aires, Argentina; Research Institute, Universidad del Salvador, Buenos Aires, Argentina; the Department of Medicine, Dr C. Bonorino Udaondo Gastroenterología Hospital, Buenos Aires, Argentina; and with Consejo de Investigaciones en Salud, Health Ministry, Buenos Aires City Government, Buenos Aires, Argentina. These researchers previously identified a significant deterioration of bone microarchitecture in premenopausal women with newly diagnosed celiac disease using high‐resolution peripheral quantitative computed tomography (HRpQCT). In that study, the team also compared 1‐year results with those of a control group of healthy premenopausal women of similar age and BMI in order to assess whether the micro-architectural parameters of treated celiac patients had reached the values expected for their age. While that study showed that a year on a gluten-free diet had improved most of the women’s bone parameters, it also showed that those parameters continued to be significantly lower than those of healthy control subjects. In a recent paper, the team describes the results of their study that offers data to show improvements bone mineralization microarchitecture in celiac patients after three years on a gluten-free diet. Source: Clin Gastroenterol Hepatol. 2017 Oct 6. pii: S1542-3565(17)31200-4. doi: 10.1016/j.cgh.2017.09.054.
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Celiac.com 06/08/2007 - In the first study, doctors Ibrahim S. Alghafeer, and Leonard H. Sigal conducted a routine gastroenterology follow-up of 200 adult celiac patients. Arthritis was present in 52 of 200 patients, or 26%. The arthritis was peripheral in 19 patients, Axial in 15 patients, and an overlap of the two in 18 patients. The doctors found that joint disease was much less common in those patients who were following a gluten-free diet (1). A related study by Usai, et al found that 63% of patients with celiac disease show axial joint inflammation (2). In that study, doctors conducted bone scintigraphy using 99m Tc methylene diphosphonate. 14 of these patients (65%) signs compatible with sacroiliitis. 11 of the 14 suffered from low back pain. In five of the 11 patients with low back pain, scintigraphy was negative. Sacroiliac radiographs were conducted on 4 of those 5 patients, and all of them were shown to have bilateral sacroiliitis. One patient had rheumatoid arthritis, but all patients in the studied showed negative HLA-B27 results. Rheumatoid Symptoms Less Common in Celiacs on Gluten-free Diet In patients with gluten enteropathy, symptoms of arthritis and other rheumatic complaints are common, and the associated clinical abnormalities routinely show improvement on a gluten-free diet. (3,4,5) In 9 of 74 patients with spondyloarthropathies, results show increased level of antigliadin antibodies, with 1 patient showing elevated antiendomysium antibodies and biopsy proven celiac disease (6). These results show that antiendomysial antibody testing is recommended as a screening tool in patients with suspected gluten enteropathy. Another study found that 3.3% of sprue patients had Sjogrens syndrome (7). 55 celiac patients who were tested for serial bone density showed osteoporosis in 50% of men and 47% of women. These findings confirm that celiac disease was an independent risk factor for osteoporosis (8). Bulletin on the Rheumatic Diseases, Volume 51, Number 2. Usai P. Adult celiac disease is frequently associated with sacroiliitis. Dig Dis Sci 1995;40:1906-8 Lubrano E, Ciacci C, Ames PR, et al. The arthritis of celiac disease: prevalence and pattern in 200 adult patients. Br J Rheumatol 1996;35:1314-8. Usai P. Adult celiac disease is frequently associated with sacroiliitis. Dig Dis Sci 1995;40:1906-8. Bagnato gluten-free, Quattrocchi E, Gulli S, et al. Unusual polyarthritis as a unique clinical manifestation of celiac disease. Rheumatol Int 2000;20:29-30. Borg AA, Dawes PT, Swan CH, Hothersall TE. Persistent monoarthritis and occult celiac disease. Postgrad Med J 1994;70:51-3. Collin P, Korpela M, Hallstrom O, et al. Rheumatic complaints as a presenting symptom in patients with celiac disease. Scan J Rheumatol 1992;21:20-3. Kallilorm R, Uibo O, Uibo R. Clin Rheumatol 2000;19:118-22. health writer who lives in San Francisco and is a frequent author of articles for Celiac.com.
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Celiac.com 07/01/2011 - People with celiac disease, who otherwise have no risk for osteoporosis, face a risk of developing progressive bone loss that is more than four times higher than the general population. This according to a study by the researchers from the Lancaster University School of Health and Medicine in the UK. In the latest study, the team took bone mass density readings of participants' skeletal health using dual-energy x-ray absorptiometry scans. They did this for more than 1,000 adults with celiac disease. The results showed that the lumbar vertebrae of individuals with celiac disease showed significantly lower bone density than those of healthy individuals. The team announced their findings at the European League Against Rheumatism's 2011 Annual Congress. No subject in the study had other risk factors for bone loss, and the team concluded that celiac disease increased the prospect of osteoporosis by a factor of four and a half, even among otherwise healthy adults. Because lumbar vertebrae sit at the base the spinal column, they take the most pressure, and thus, a more likely place for osteoporosis-related fractures. In the U.S., vertebral pressure fractures are the most common skeletal injury caused by progressive bone loss. Over a half a million vertebral pressure fractures occur each year, according to the National Osteoporosis Foundation. The UK study just the latest to show a connection between celiac disease and poor bone health. A 2010 report from Canada's University of Alberta that the average child with gluten allergies got less than half the amount of required vitamin K, as well as too little vitamin D. The research team suggests that dietary supplements may improve nutrition in children with celiac disease, and thus reduce the likelihood that they will develop osteoporosis. Source: endocrineweb.com
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Celiac.com 12/03/2009 - Clinicians recently described a case of severe osteoporosis with high bone turnover, in which they found neutralizing autoantibodies against osteoprotegerin to be present. They also report finding autoantibodies against osteoprotegerin in three additional patients with celiac disease. The clinical team reporting the findings was made up of Philip L. Riches, M.R.C.P., Euan McRorie, F.R.C.P., William D. Fraser, Ph.D., F.R.C.Path., Catherine Determann, B.Med.Sci., Rob van’t Hof, Ph.D., and Stuart H. Ralston, M.D. They are associated with the Rheumatic Diseases Unit, Institute of Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Edinburgh (P.L.R., E.M., C.D., R.H., S.H.R.); and the Unit of Clinical Chemistry, School of Clinical Sciences, University of Liverpool, Liverpool (W.D.F.) — both in the United Kingdom. The adult patient presented severe, high-turnover osteoporosis associated with subclinical celiac disease and autoimmune hypothyroidism. The clinicians found circulating autoantibodies against osteoprotegerin. Autoantibodies against osteoprotegerin block the inhibitory effect of osteoprotegerin on signaling by the receptor activator of nuclear factor (NF)-κB (RANK). The patient's osteoporosis did not respond to celiac disease treatment of a gluten-free diet, but completely reversed with bisphosphonate therapy. Immunoglobulins purified from specimens of the patient’s serum abolished the inhibitory effect of osteoprotegerin on RANKL-induced NF-κB signaling in vitro, while those from the control serum did not, which indicates the presence of neutralizing autoantibodies against osteoprotegerin. The clinicians used immunoprecipitation assay for osteoprotegerin on non-fasting patient serum samples at several points during the course of his illness, as well as from 10 age-matched healthy male controls, 15 patients with celiac disease, and 14 patients with autoimmune hypothyroidism. They used bicinchoninic acid assay to measure protein content. Serum samples from the 10 healthy controls and the 14 patients with autoimmune hypothyroidism showed no evidence of circulating autoantibodies against osteoprotegerin, while the serum samples from 3 of the 15 patients (20%) with celiac disease did show antibodies. Autoantibodies against osteoprotegerin may be connected to the development of high-turnover osteoporosis, but whether autoantibodies against osteoprotegerin contribute to the pathogenesis of osteoporosis in celiac disease patients remains unknown. Source: N Engl J Med 2009;361:1459-65.
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Arch Intern Med. 2005;165:370-372, 393-399 Celiac.com 03/09/2005 - According to a new study by researchers at Washington University School of Medicine in St. Louis, Missouri, everyone with osteoporosis should also be screened for celiac disease. The study looked at 840 people—266 with osteoporosis and 574 without—who were screened for celiac disease using serum anti-tissue transglutaminase (tTG) and anti-endomysial (EMA) antibodies—those who tested positive for either were given a follow-up biopsy. The serological screening results indicated that 12 (4.5%) of the 266 osteoporotic patients were positive for celiac disease, while only six (1.0%) of the 574 non-osteoporotic patients tested positive. Out of the osteoporotic patients who were positive, 3.4% were confirmed by a biopsy, while only 0.2% of the non-osteoporotic patients were confirmed via biopsy (2 of the serological positive group refused a follow-up biopsy). In the group with both celiac disease and osteoporosis, the researchers found a direct correlation between the severity of both diseases, and the treatment of these patients via a gluten-free diet dramatically improved the symptoms of both diseases. According to the researchers: The prevalence of celiac disease among osteoporotic patients was much higher than among the non-osteoporotic population and high enough to justify a recommendation that all individuals with osteoporosis undergo serologic screening for celiac disease.
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Celiac.com 06/25/2003 - The following is an abstract of a recent study published in the June edition of the Journal of Association of Physicians of India by Dr. Y.A. Gokhale and colleagues from the Lokmanya Tilak Medical College and General Hospital, Mumbai (Bombay). The researchers conclude that symptomatic osteoporotic patients, especially those with associated anemia, who are younger than 55 years of age should be screened for celiac disease. Here is the abstract: Celiac Disease in Osteoporotic Indians YA Gokhale, PD Sawant, CM Chodankar, ND Desai, MV Patil, S Maroli, MN Patil, NK Hase J Assoc Physicians India June 2003;51:579-584 Abstract: Objective: The aim of the study was to identify the atypical celiac disease (celiac disease) in a cohort of symptomatic osteoporotic patients, younger than 55 years of age and 2) To study associated clinical and laboratory features and outcome with gluten-free diet. Material and Methods: We studied 33 patients (F:M =28:5),mean age 29 years (range 15-52 years) with osteoporosis (WHO diagnostic criteria, T-score less than -2.5 on DEXA scan) from January 2000-June 2002. Serological screening for celiac disease was done by detecting circulating IgA antibodies to tissue transglutaminase by ELISA. Patients with presence of antibodies to transglutaminase were subjected to biopsy from the 2nd part of the duodenum by upper GI endoscopy. The biopsies were reported independently by two pathologists who were blinded for the serology report. Measurement of mucosal thickness, crypts and villi were done with an ocular micrometer. Other parameters like complete hemogram, serum iron, total iron binding capacity (TIBC),calcium profile,25-OH-D, parathyroid hormone (PTH) were evaluated. Assessment of clinical and laboratory parameters was performed within 4-12 weeks of starting gluten-free diet (GFD). Results: Thirteen patients had circulating IgA antibodies to transglutaminase. Intestinal biopsies were performed on 11 patients and were consistent with the diagnosis of celiac disease (total villous atrophy -two, subtotal villous atrophy with crypt hyperplasia -nine). Patients with celiac disease had significant anemia when compared with non-celiac disease osteoporotic patients. Other important observations in these 11 patients were low serum calcium and phosphorus, low 25-OH-D, high PTH. Significant improvement in clinical and laboratory parameters was noted in all patients within 6-12 weeks of starting GFD. Conclusion: Symptomatic osteoporotic patients (younger than 55 years of age) especially with associated anemia should be investigated for celiac disease. Simple measures like omission of wheat from diet (GFD) lead to significant improvement in symptoms within weeks.
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The following was taken from a lecture given by Dr. Joseph Murray in October, 1996. It was published by the Sprue-Nik Press (Published by the Tri-County Celiac Sprue Support Group, a chapter of CSA/USA, Inc. serving southeastern Michigan) Volume 5, Number 9, December 1996. Dr. Joseph Murray, one of the leading USA physicians in the diagnosis of celiac disease (celiac disease) and dermatitis herpetiformis (DH). Dr. Murray (murray.joseph@mayo.edu) of the Mayo Clinic Rochester, MN, is a gastroenterologist who specializes in treating Celiac disease: Q: Can you touch on bone pain? A: The most common cause of severe bone pain with untreated celiac disease is osteomalacia, which is malformation of the bones due to lack of Vitamin D and calcium. It affects mostly the hips, and sometimes the shoulders and back. It usually gets better with specific treatment, which includes the gluten-free diet for celiacs and sometimes includes Vitamin D supplementation and other interventions. Another cause of bone pain is osteoporosis. It can often cause pain in the back, due to vertebrae which have become shortened and have begun squeezing the nerves. This condition is very painful and is not going to get better; once the vertebrae have shortened they are not going to stretch back up to their original size. Muscle pain can also occur, due to Vitamin D deficiency. I have seen some leg pains as the initial presentation of celiac disease which cleared up with the gluten-free diet.
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