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Found 7 results

  1. Celiac.com 07/10/2006 - Increased consumption of gluten, according to Dr. Michael Marsh, raises the risk of celiac disease symptoms1. Although these symptoms may not indicate celiac disease, they reflect some biological realities. Grain-based foods simply do not offer the nutrients necessary to human health and they damage the human body. USDA and Canada Food Guides notwithstanding, if people eat grain-laden diets, they may develop symptoms of celiac disease (but in most cases, without the diagnostic intestinal lesion). The connection between eating disorders and celiac disease is well known and well documented2,3,4,5. Thus, the dynamics at work in celiac disease may offer insight into the broader realm of obesity, especially among those who are eating the recommended, daily quantities of grain-derived foods, while attempting to keep their weight down by eating low-fat foods. The primary, defining characteristic of celiac disease is gluten induced damage to the villi in the intestinal lining. Since malabsorption of vitamins and minerals are well known in the context of celiac disease, it should not be surprising that some celiac patients also demonstrate pica (Pica is an ailment characterized by eating dirt, paint, wood, and other non-food substances). Other celiac patients eat excessive quantities of food, coupled with a concurrent failure to gain weight. Yet another, perhaps larger, group of celiac patients refuse to eat (One may wonder if the latter find that eating makes them feel sick so they avoid it). Perhaps the most neglected group is that large portion of untreated celiac patients who are obese. Dr. Dickey found that obesity is more common than being underweight among those with untreated celiac disease6. When I ran a Medline search under the terms "obesity" and "celiac disease" 75 citations appeared. A repeated theme in the abstracts and titles was that celiac disease is usually overlooked among obese patients. While obesity in celiac disease may be common, diagnosis appears to be uncommon. Given the facts, I certainly believe that some of the North American epidemic of obesity can be explained by undiagnosed celiac disease. However, that is only a small part of the obesity puzzle, and I suspect that celiac disease may offer a pattern for understanding much of the obesity that is sweeping this continent. One example, a woman diagnosed by Dr. Joe Murray when he was at the University of Iowa, weighed 388 pounds at diagnosis7. Dr. Murray explained her situation as an over-compensation for her intestinal malabsorption. I want to suggest a two faceted, alternative explanation which may extend to a large and growing segment of the overweight and obese among the general population. As mentioned earlier, anyone consuming enough gluten will demonstrate some symptoms of celiac disease. If large scale gluten consumption damages the intestinal villi—but to a lesser degree than is usually required to diagnose celiac disease—fat absorption will be compromised. Deficiencies in essential fatty acids are a likely consequence. The natural response to such deficiencies is to crave food despite having absorbed sufficient calories. Even when caloric intake is huge, and excess calories must be stored as body fat, the need to eat continues to be driven by the bodys craving for essential fats. Due to gluten-induced interference with fat absorption, consumption of escalating quantities of food may be necessary for adequate essential fatty acid absorption. To further compound the problem, pancreatic glucagon production will be reduced, compromising the ability of the individual to burn these stored fats, while the cells continue to demand essential fats. Poor medical advice also contributes to the problem. The mantra of reduced fat continues to echo in the offices of health professionals despite a growing body of converse research findings. In February of this year, the results of a powerful, eight year study of almost 49,000 women showed little difference between the health of women consuming low fat diets when compared to those consuming normal diets8. Alarmingly, this low fat diet seems to have resulted in weight gain, a well recognized risk factor for a variety of diseases. For some of us, this result was predictable. The likely result of a low-fat diet is an increased intake of carbohydrates while food cravings are fuelled by a deficiency of essential fatty acids. If my sense of the underlying problem (caloric excess combined with essential fatty acid deficiency due to fat malabsorption at the microvilli) is accurate, then a low fat diet is exactly the wrong prescription. Many obese persons are condemned, by such poor medical advice, to a life of ever deepening depression, autoimmune diseases, and increasing obesity. At the end of the day, when these folks drop dead from heart attacks, strokes, or some similar disaster, the self-righteous bystanders will just know that the problem was a lack of willpower. I watched my mom steadily gain weight for 35 years. I watched her exercise more will power beyond the capacity of most folks. Still, she could not resist her compulsive eating. I have seen her take something from the freezer and chew on it while agreeing that she had just eaten a very large meal and should feel full. In December of 1994 I was diagnosed with celiac disease. According to the published experts in this area, my mom should also have been invited for testing. Yet, when asked for testing, her doctor refused her. Through persistence, and a pervasive faith in her son, mom finally (after months of negotiation) swayed her doctor to do the anti-gliadin antibody blood test. Despite the fact that she had been on a reduced gluten diet for the past year, her antibody levels were elevated. She never sought a biopsy diagnosis, and the EMA and tTG were not available here in Canada at that time. However, she has been gluten-free for the past seven years or so. She dropped a considerable amount of weight. Her weakness was never will power. She was battling an instinct so basic that few of us could have resisted. That, I think, is the story behind much of North American obesity. The widespread, excessive consumption of gluten at every meal, in addition to the low-fat religion that has been promulgated throughout the land, is resulting in intestinal damage and a widespread deficiency in essential fats is among North Americans. Ron Hoggan is an author, teacher and diagnosed celiac who lives in Canada. His book "Dangerous Grains" can be ordered at www.celiac.com. Rons Web page is: www.DangerousGrains.com References: Marsh, Michael N. Personal communication. 2002. Ferrara, et. al. "Celiac disease and anorexia nervosa" New York State Journal of Medicine 1966; 66(8): 1000-1005. Gent & Creamer "Faecal fats, appetite, and weight loss in the celiac syndrome" Lancet 1968; 1(551): 1063-1064. Wright, et. al. "Organic diseases mimicking atypical eating disorders" Clinical Pediatrics 1990; 29(6): 325-328. Grenet, et. al. "Anorexic forms of celiac syndromes" Annales de Pediatrie 1972; 19(6): 491-497. Dickey W, Bodkin S. Prospective study of body mass index in patients with coeliac disease. BMJ. 1998 Nov 7;317(7168):1290. Murray, J. Canadian Celiac Association National Conference. 1999. Howard BV, Van Horn L, Hsia J, et. al. Low-fat dietary pattern and risk of cardiovascular disease: the Womens Health Initiative Randomized Controlled Dietary Modification Trial. JAMA. 2006 Feb 8;295(6):655-66.
  2. Celiac.com 01/19/2017 - When celiac disease was originally described, one of its hallmark presenting signs was extreme underweight. Along with diarrhea, digestive pain and bloating, the severe weight loss was understood to 'always' be present. Fast forward over 100 years and things have changed. Not only are many celiacs overweight, but those with gluten sensitivity are increasingly falling into that category as well. Sadly, too often doctors miss testing for these life-long conditions because of a patient's weight status. Stuck in the historical definition, these doctors have missed the current face of celiac and gluten sensitivity – a person can be any weight, and they frequently have weight to lose. We often speak of the leaky gut, formally known as a condition of increased intestinal permeability, found in the small intestine. This situation is seen most often in those with an intolerance to gluten due to their upregulation of a protein only made by humans, called zonulin. Zonulin was discovered by Dr. Alessio Fasano and his team. The zonulin molecule dictates the opening and closing of the 'gates' of the small intestine. With a surface area of over 3,000 square feet, that involves a lot of gates! While only humans make zonulin, not all humans produce it. Twenty percent do not, 50 percent has a single copy of the gene and 30 percent of the population has both copies of the gene. Those with both copies are in the unenviable position of being two times more likely to die from all causes, and the diseases they do get tend to be more severe. When a lab test was done on rats highly predisposed to develop type 1 diabetes, two thirds of them never developed the disease when they were given a drug that inhibited zonulin. I know you're going to ask, so here's the answer: A drug does not yet exist for humans that performs this function. However, it is being developed, along with a test for zonulin, by Dr Fasano. A study published last Fall in Nutrition Research titled "Potential mechanisms for the emerging link between obesity and increased intestinal permeability” and lead by TF Teixeira, found a link that could well explain the obesity issue so commonly seen. Those with an intolerance to gluten not only tend to have a leaky gut due to the above mentioned zonulin connection, but they also have weakened immune systems due to the constant assault by gluten. The weakened immune system, predominantly housed in the small intestine, is thus less able to defend the body against the normal barrage of bacteria, amoeba, parasites and the like. Why do I call the presence of these organisms 'normal'? Because it is. Now, with that said, it is NOT normal for such organisms to gain a foothold in the intestine and procreate there, but their presence is a normal byproduct of eating food, putting one's fingers in one's mouth, etc. (These are microscopic organisms so don't get too grossed out.) The point is, that a healthy immune system easily kills them; an unhealthy immune system is unable to do its job. The result is a gut full of endotoxins (toxins released from inside bacteria when they disintegrate) or other inhospitable organisms. These bad organisms thereby fight against the good ones. The good bacteria in the gut (called the microbiome) literally have a population that exceeds the number of cells in the human body by 10 times. The genes associated with this population exceeds that of the human body by 100 times. We are talking about a part of the human body, long under-appreciated, that is now being considered influential enough to be considered an 'organ' in its own right. Emerging research reveals that when this organ is overwhelmed by toxins in the gut, its composition changes as far as the balance of certain organisms (probiotics), as does its ability to absorb nutrients and expend energy (burn calories). The result is not only weight gain but increased cholesterol, triglycerides, and insulin resistance – the latter leads to diabetes, heart disease and obesity. Intestinal permeability is also thought to be influenced by a high fat and high fructose diet, plus certain nutritional deficiencies such as zinc. Another study from the Journal of Parenteral and Enteral Nutrition titled "Gut Microbiota, Intestinal Permeability, Obesity-Induced Inflammation and Liver Injury” found much the same data. They found that eating a poor diet (high fat, high fructose) could affect the microbiome in as little as one to two days – the result being heart disease and obesity. So, how do we keep our microbiome happy? Discover if you have a gluten or dairy intolerance. If so, avoid those foods. Avoid excess, bad fats including fast food, trans fats, preprocessed, prepackaged foods, etc. Avoid ALL fructose. I'm not talking about the natural fructose in fruit, of course, but all added fructose, especially high fructose corn sweeteners. If you can, get your gut tested for the presence of any inhospitable organisms that have gotten a foothold in your system. This same test will evaluate the health of your microbiome. Another test that's good, as a verifier that you're on the right track, is one for a leaky gut. We tend to recommend this one once you've been on a reparative program for a while, to confirm that we are accomplishing our goal. Do ingest 9 servings of organic vegetables and fruits each day. These are naturally healing and prebiotic, meaning that they give strength and nourishment to your probiotic population. Ensure that you are not deficient in any major vitamins and minerals such as B's, D, zinc, magnesium, calcium, etc. While it seems like a 'no brainer' to take probiotics, here's a couple of things to keep in mind. a. Use a human strain b. Get a combination of organisms such as acidophilus, bifidus, etc. c. Due to dairy products being such a commonly sensitive food, get probiotics that are free of all dairy. d. Sometimes, if you have an infection in the gut, you may feel worse on probiotics. If this occurs, stop them, of course, but realize that you should look into step 4 above. I'm happy to help you! Don't cheat. I'm sorry, but being 'good' Monday through Friday and going crazy on the weekends just isn't going to cut it if you want to be healthy. And if your health is already compromised somewhat, cheating just isn't worth the dangerous repercussions. That microbiome can change in a day or two when you've been eating a poor diet. Remember that. I hope you found this helpful. It is interesting how much we are discovering about how the health of the gut dictates so much about our general health or tendency towards disease. And it's also quite revealing how much of a culprit gluten can be when trying to optimize the function of the small intestine and its immune system. Please send me your questions or comments. I am here to help! My clinic, HealthNOW Medical Center, is a destination clinic. You don't need to live locally to receive help with your health. You are welcome to call us anytime for a free health analysis – 408-733-0400. References: Nutrition Research. 2012 Sep;32(9):637-47. Potential mechanisms for the emerging link between obesity and increased intestinal permeability.Teixeira TF, Collado MC, Ferreira CL, Bressan J, Peluzio Mdo C. Journal of Parenteral and ENteral Nutrition 2011. Gut Microbiota, Intestinal Permeability, Obesity-Induced Inflammation and Liver Injury. Thomas H. Frazier, MD1; John K. DiBaise, MD, and Craig J. McClain, MD. Volume XX Number X
  3. Celiac.com 11/28/2014 - According to a new study, obesity plays a major part in triggering and prolonging autoimmune diseases, such as celiac disease, Crohn's disease and multiple sclerosis. The study appeared recently in Autoimmunity Reviews by Prof. Yehuda Shoenfeld, the Laura Schwarz-Kipp Chair for Research of Autoimmune Diseases at Tel Aviv University's Sackler Faculty of Medicine and Head of Zabludowicz Center for Autoimmune Diseases at Chaim Sheba Medical Center, Tel Hashomer. According to the research, obesity erodes the body's ability to protect itself, triggering a pro-inflammatory environment that promotes the development of autoimmune diseases, hastens their progression, and impairs their treatment. For some time now, says Professor Shoenfeld, researchers have been aware of the “negative impact of contributing disease factors, such as infections, smoking, pesticide exposure, lack of vitamins, and the like. But in last five years, a new factor has emerged that cannot be ignored: obesity.” According to the World Health Organization, about one-third of the global population is overweight or obese, nearly a dozen autoimmune diseases are now associated with excess weight, which now impact nearly 5-20% of the global population. That is why, according to Shownfeld, it is “critical to investigate obesity's involvement in the pathology of such diseases." The main culprit is not fat itself, but adipokines, compounds secreted by fat tissue, which impact numerous physiological functions, including the immune response. In tandem with their own study, Shoenfeld and his colleagues reviewed 329 studies from across the globe that focused on the connections between obesity, adipokines, and immune-related conditions like rheumatoid arthritis, multiple sclerosis, type-1 diabetes, psoriasis, inflammatory bowel disease, psoriatic arthritis, and Hashimoto thyroiditis. "According to our study and the clinical and experimental data reviewed, the involvement of adipokines in the pathogenesis of these autoimmune diseases is clear," says Shoenfeld. "We were able to detail the metabolic and immunological activities of the main adipokines featured in the development and prognosis of several immune-related conditions." One of the team’s more interesting findings was that obesity also promotes vitamin D deficiency, which, “once corrected, alleviated paralysis and kidney deterioration associated with the disorder… [and] improved the prognosis and survival of the mice.” Source: Science Daily, November 10, 2014
  4. Celiac.com 03/04/2013 - Morbid obesity is a common medical condition. In many cases, bariatric surgery is necessary. Although for decades celiac disease has been associated with chronic diarrhea and weight loss, and other classic symptoms, recent data shows that the clinical spectrum of celiac disease is extremely wide. A group of researchers recently reported on the benefits of diagnosing celiac disease during pre-operative work-up for bariatric surgery. The researchers included Federico Cuenca-Abente, Fabio Nachman, and Julio C. Bai of the Department of Surgery and Department of Medicine at Dr C. Bonorino Udaondo Gastroenterology Hospital in Buenos Aires, Argentina. They reported on the cases of five morbidly obese patients diagnosed with celiac disease during preoperative work-up for bariatric surgery. Celiac disease was suspected upon routine upper endoscopy, and confirmed by histology and positive celiac disease-specific blood tests. Interestingly, four of the five patients had no obvious symptoms. One complained of chronic diarrhea and anemia. All patients began a gluten-free diet. Due to their celiac disease diagnosis, doctors offered all five patients a purely restrictive bariatric procedure. At the time of the report, three of the patients had received a sleeve gastrectomy, while the other two were still undergoing pre-operative evaluation. The team's findings help to enlarge the clinical spectrum of untreated celiac disease. Even though rates of celiac disease in obese patients seems to be similar to that in the general population, the team recommends that patients with morbid obesity be tested for celiac disease in order to determine the best surgical strategy and outcome. Source: Acta Gastroenterol Latinoam 2012;42:321-324
  5. Celiac.com 08/04/2014 - Can excluding gluten, the protein complex present in many cereals, help to prevent diseases other than celiac disease? Seeking to gain insight into the effects of gluten-free diets on obesity, and its mechanisms of action, a research team set out to assess whether gluten exclusion can prevent the development and expansion of adipose tissue. Specifically, they wanted to determine if a gluten-free diet reduces adiposity, inflammation and insulin resistance associated with the induction of PPAR-alpha and PPAR-gamma expression. The researchers included F.L. Soares, R. de Oliveira Matoso, L.G. Teixeira, Z. Menezes, S.S. Pereira, A.C. Alves, N.V. Batista, A.M. de Faria, D.C. Cara, A.V. Ferreira, and J.I. Alvarez-Leite. The are affiliated with the Departamento de Alimentos, Faculdade de Farmácia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais in Belo Horizonte, Brazil. For their study, they fed a high-fat diet containing 4.5% gluten to a control group of C57BL/6 mice, and a gluten-free diet to another group of C57BL/6 mice. The team measured body weight and adiposity gains, leukocyte rolling and adhesion, macrophage infiltration and cytokine production in adipose tissue. They also measured blood lipid profiles, glycaemia, insulin resistance and adipokines, and determined expression of the PPAR-α and γ, lipoprotein lipase (LPL), hormone sensitive lipase (HSL), carnitine palmitoyl acyltransferase-1 (CPT-1), insulin receptor, GLUT-4 and adipokines in epidydimal fat. The gluten-free mice had less body weight gain and adiposity, with no changes in food intake or lipid excretion. These results are associated with up-regulation of PPAR-α, LPL, HSL and CPT-1, which are related to lipolysis and fatty acid oxidation. Gluten-free mice also showed improved glucose homeostasis and pro-inflammatory profile-related over-expression of PPAR-γ. Moreover, intravital microscopy showed a lower number of adhered cells in the adipose tissue microvasculature. The overexpression of PPAR-γ is related to the increase of adiponectin and GLUT-4. The study data support the beneficial effects of gluten-free diets in reducing adiposity gain, inflammation and insulin resistance. The data suggests that a gluten-free diet should be tested as a new dietary approach to preventing obesity and metabolic disorders. Source: J Nutr Biochem. 2013 Jun;24(6):1105-11. doi: 10.1016/j.jnutbio.2012.08.009.
  6. Celiac.com 05/25/2012 - A team of researchers recently set out to examine body mass and obesity risk in a large population of people with celiac disease who are following a gluten-free diet. The research team included T. A. Kabbani, A. Goldberg, C. P. Kelly, K. Pallav, S. Tariq, A. Peer, J. Hansen, M. Dennis & D. A. Leffler. They are affiliated with the Department of Medicine and Division of Gastroenterology at Beth Israel Deaconess Medical Center in Boston, Massachusetts. Diagnosis for celiac disease is on the rise, and many people who are diagnosed experience weight changes once they adopt a gluten-free diet. There's a pretty good amount of study data on weight change on a gluten-free diet, but a very limited amount of data regarding changes in body mass. The researchers wanted to look at a large population of people with celiac disease, who followed a gluten-free diet to better understand changes in body mass index (BMI) following celiac diagnosis. To do this, they looked at a total of 1018 patients with biopsy confirmed celiac disease. The patients had all previously visited the Beth Israel gastroenterology clinic in Boston. The team recorded data for initial and follow-up BMIs, and used an expert dietitian to assess patient compliance with a gluten-free diet. They found a total of 679 patients with at least two recorded BMIs and GFD adherence data, and used data from those patients in their study. The average amount of time from first BMI measurement to follow-up measurement was 39.5 months. When they compared the results against data for the general population, they found that celiac disease patients on a gluten-free diet were significantly less likely to be overweight or obese (32% vs. 59%, P < 0.0001). They also found that average body mass increased significantly after patients adopted a gluten-free diet (24.0 to 24.6; P < 0.001). Overall, 21.8% of patients with normal or high BMI at study entry increased their BMI by more than two points. The results of this study show that celiac disease patients on a gluten-free diet have lower BMI than the regional population at diagnosis, but that BMI increases with a gluten-free diet, especially in those who follow the diet closely. Still, even though overall risk of obesity is lower than the regular population, once celiac patients adopt a gluten-free diet, 15.8% of patients move from a normal or low BMI class into an overweight BMI class, and 22% of patients overweight at diagnosis gain weight. As a result, the study team feels that weight maintenance counseling should be an integral part of celiac dietary education. Source: Alimentary Pharmacology & Therapeutics. 2012;35(6):
  7. Celiac.com 03/08/2010 - Celiac, a genetic autoimmune disease, has long been associated with a medical picture of patients that lookunderweight, and malnourished. However, recent studies are findingthat obesity and a high BMI (Body Mass Index) may also be prominentin celiac patients. New studies were conducted to determine BMIchanges after initiation of a gluten-free diet, and they offer cluesto the importance of eating gluten free after being diagnosed withceliac disease. Doctors at the Celiac Disease Center ofColumbia University studied the BMI of 369 patients proven throughbiopsy to have celiac disease, spanning from 1981 to 2007. Men andwomen were evaluated separately for the sake of this study and thetest patients were classified as “classical” meaning diarrheaprominent, or “atypical” meaning they had no diarrhea at the timeof celiac diagnosis. Atypical patients were further divided intogroups of 'anemia present' and 'no anemia present' at time ofdiagnosis. Body Mass Index was then categorized into four groupsbased on the criteria of the World Health Organization. The BMI of all test celiac patientswere compared to the general United States population. Using theregression model, the study found that there are obvious predictorsfor low BMI; patients classified as “classical” celiac,female, and with severe villous atrophy, were all revealed aspredictors for low BMI. These findings further exemplify that themost dramatic changes in BMI rates were in underweight females withceliac disease. Celiac females had a considerably lower mean BMIthan the general population, thereby indicating an importantassociation between females with celiac disease and low BMI. In fact,celiac females that tested with a normal or low BMI were also foundto have higher rates of critical villous atrophy than those with ahigher BMI. However, more males with celiac were found to beoverweight compared to the general population. After initiating a gluten free diet,most BMI changes were shown to be directly associated with an initialbaseline appearance of “classical” symptoms. While on a glutenfree diet, over 50% of the overweight and obese patients lostweight, and of the group who initially had a low BMI, 42.4% attaineda normal weight. Thereby concluding that treatment of a gluten freediet after celiac diagnosis provides advantageouschanges in BMI results. Further evidence of the importance in earlydiagnosis and prompt treatment of celiac disease. Of course it is critical to note that,all the patients utilized for this study were monitored closely by a care center dedicated to celiac disease, and continually followed byan experienced dietician with expert knowledge of celiac disease. And, while you may not be able to afford the kind of dietician thesepatients were provided with, it is always very important to be underthe care of a doctor or clinic dedicated to treating celiac disease,as well as to be receiving experienced dietary counseling whentransitioning to a gluten free diet. Source: http://www.ncbi.nlm.nih.gov/pubmed/19779362
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