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Found 8 results

  1. Celiac.com 05/15/2017 - For all the talk of studies touting evidence for non-celiac gluten sensitivity, the actual data don't stack up very well, according to an recent assessment by two researchers, whose results appear in Clinical Gastroenterology and Hepatology. In an effort to determine the accuracy of using a double-blind, placebo-controlled study to confirm diagnosis of non-celiac gluten sensitivity in patients who respond to a gluten-free diet, researchers Javier Molina-Infante, and Antonio Carroccio recently set out to assess data on a series of such studies. Both researchers are affiliated with the Department of Gastroenterology, Hospital Universitario San Pedro de Alcantara in Caceres, Spain. For their study, the pair analyzed data from 10 separate double-blind, placebo-controlled, gluten-challenge trials on a total of 1312 adults. The available studies varied significantly in many ways. The duration of the gluten challenge, for example, varied from 1 day to 6 weeks. The daily doses for those gluten challenges varied from 2 grams to 52 grams, with 3 studies administering 8 grams or less each day. The composition of the gluten-free placebo also varied considerably between tests; including variation by gluten-free product type, and levels of xylose, whey protein, rice, or corn starch containing fermentable carbohydrates. Most of the studies did find gluten challenge to significantly increase symptom scores compared with placebo. However, out of 231 NCGS patients, only 38 patients (16%) showed gluten-specific symptoms. Moreover, nearly half (40%) of these patients showed similar or increased symptoms in response to placebo; something researchers term a 'nocebo' effect. That leaves just 6 or 7 patients out of 231 showing gluten-specific symptoms. The researchers also point to heterogeneity and to potential methodology flaws in gluten challenge studies. They also present powerful questions about gluten as the trigger for symptoms in most patients with presumptive NCGS. Lastly, they highlight the importance of the nocebo effect in these types of studies. These results certainly invite more careful, rigorous studies on the matter, and challenge researchers to provide solid data from well-crafted double-blind placebo controlled studies. Basically, what little evidence we thought we had to support the existence of non-celiac gluten sensitivity has been shown to be thin at best. Until solid evidence arrives, the status of non-celiac gluten sensitivity will remain open to question and doubt by both researchers and potential sufferers. Source: Clin Gastroenterol Hepatol. 2017;15(3):339-348.
  2. Celiac.com 01/31/2017 - In my practice, I have had the pleasure and honor of helping hundreds of people reverse their diabetes and put their autoimmune diseases into remission. One of the many things that we test for is gluten reactivity. The research, much of which has been cited in our book on gluten, Lose the Gluten, Lose your Gut. Ditch the Grain, Save your Brain, clearly demonstrates the connection between gluten reactivity and most autoimmune diseases, including but not limited to: Hashimoto's thyroiditis, rheumatoid arthritis and psoriasis. I intentionally didn't mention celiac disease, because, although it is very well established and accepted that gluten triggers celiac disease, what most don't realize is that those with celiac disease represent only a small percentage of people with autoimmunity that are impacted by gluten reactivity. What's alarming and disappointing to me is how many doctors 'pooh pooh' the concept of gluten reactivity, especially among their chronically ill patients. Because of this disconnect, patients continue to suffer needlessly with chronic diseases that, with the removal of gluten from the diet, would in many cases, clear up or go into remission. Hundreds of my patients tell me that when they told their health practitioner they had eliminated gluten from their diet, the health care worker didn't believe gluten would make a difference, or that since they didn't have celiac disease, eliminating gluten wouldn't help them. All this was said in the face of autoimmune diseases going into remission, or diabetes reversing right before their eyes, following the elimination of gluten from their diet. The issue is that many health care practitioners are just not keeping current with the research. As such, they are inadvertently preventing their patients from truly getting healthy. The additional travesty with this is that so many people look to their health care practitioners as 'experts'. When these providers, who are not 'experts' in a particular subject, (in fact, many are completely ignorant of how dietary changes and supplement therapy can help people thrive) advise a patient against something that the research shows would likely help them, it becomes an issue of negligence and, quite frankly, laziness. One patient in particular comes to mind when I think of this disconnect. I had the pleasure of working with a retired nurse who, in her seventies, had come to me with several medical issues. For purposes of this article, I will refer to her as Mary. Mary suffered with hypothyroidism, which we quickly discovered through additional testing, was caused by an autoimmune disease called Hashimoto's thyroiditis. Interestingly, it is estimated that roughly 90% of the 26 million people in the U.S. that have hypothyroidism actually have Hashimoto's. This is an autoimmune disease in which your immune system attacks and destroys the thyroid gland. The research, and our clinical experience, has demonstrated that gluten will cause your immune system to flare-up and attack the thyroid. In addition to Hashimoto's, Mary also suffered with cardiac arrhythmia and she had a history of blood clots and strokes. She also had a long-standing issue with another autoimmune disease, called pleva, whereby her skin would rash up, itch and scab. Mary was very overweight, and exhausted all of the time. Mary had a full functional work-up in our office and she was confirmed, with testing, to be very gluten-reactive. After working with her for several months, with one very important instruction to go completely gluten-free, she easily lost over 40 lbs (with no additional exercise), her energy increased to the point where she stated she hadn't felt that good in decades, and her arrhythmia and pleva cleared up completely. Her cardiologist was ecstatic and her general practitioner told her to keep up whatever she was doing because she was so healthy now. I hadn't seen Mary for almost 6 months when she emailed me one day to update me on something that had happened with her. She went to a food class taught by a vegan. At the class the guests were told very directly that eating gluten-free was a 'billion dollar hoax' and that eating gluten-free could be dangerous and bad for your health. Mary, even after all of her success, in part from going gluten-free, was suddenly doubtful of her diet. She tested it, and for 3 days brought back gluten-containing foods. She told me she reacted very badly and felt horrible. For Mary, the point was driven home that gluten-reactivity was a very real issue regarding her health. The difference in how she felt was like night and day. Lucky for her, she observed this first hand and immediately went back on her gluten-free diet before her skin disease and arrhythmia flared-up. Whether one is a doctor, a nutritionist, or a regular Joe, making statements about any subject without having researched that subject in earnest, is unethical, and may even be harmful. We have done the research and have seen first-hand, with thousands of patients reversing everything from psoriasis to diabetes, that eating gluten-free, while very 'trendy' right now, is a trend that is solidly backed up by the evidence.
  3. Celiac.com 09/09/2016 - Celiac disease incidence has increased in recent decades. How much do sex, age at diagnosis, year of birth, month of birth and region of birth have to do with celiac disease risk? A team of researchers recently conducted a nationwide prospective cohort longitudinal study to examine the association between celiac disease diagnosis and season of birth, region of birth and year of birth. The research team included Fredinah Namatovu, Marie Lindkvist, Cecilia Olsson, Anneli Ivarsson, and Olof Sandström. They are variously affiliated with the Department of Food and Nutrition, the Department of Clinical Sciences, Pediatrics, and the Department of Public Health and Clinical Medicine, Epidemiology and Global Health at Umeå University in Umeå, Sweden. Their study included 1,912,204 children aged 0–14.9 years born in Sweden from 1991 to 2009. They found a total of 6,569 children diagnosed with biopsy-verified celiac disease from 47 pediatric departments. The team used Cox regression to examine the association between celiac disease diagnosis and season of birth, region of birth and year of birth. They found that children born during spring, summer and autumn had higher celiac disease risk, as compared with children born during winter: adjusted HR for spring 1.08 (95% CI 1.01 to 1.16), summer 1.10 (95% CI 1.03 to 1.18) and autumn 1.10 (95% CI 1.02 to 1.18). Increased celiac disease risk was highest for children born in the south, followed by central Sweden, as compared with children born in northern Sweden. The birth cohort of 1991–1996 had increased celiac disease risk if born during spring, for the 1997–2002 birth cohort the risk increased for summer and autumn births, while for the birth cohort of 2003–2009 the risk was increased if born during autumn. Both independently and together, season of birth and region of birth are associated with increased risk of developing celiac disease during the first 15 years of life. These seasonal differences in risk levels are likely due to seasonal variation in infectious disease exposure. Source: Arch Dis Child. doi:10.1136/archdischild-2015-310122
  4. Celiac.com 08/15/2016 - On May 3rd, 2016, as part of an ongoing effort to learn more about celiac disease, the U.S. Preventive Services Task Force (USPSTF) released its first-ever draft recommendation statement, and draft evidence review. The statement basically says that there just isn't enough evidence to adequately weigh the benefits and harms of celiac disease screening in asymptomatic patients. This is an "I" recommendation that does not apply to patients with symptoms of celiac disease such as diarrhea, abdominal pain and unexplained weight loss. They basically call for "[m]ore evidence on screening for celiac disease…before the task force can recommend for or against screening people who don't have any signs or symptoms of the condition," said USPSTF member Alex Krist, M.D., M.P.H., in a news release. "In the face of unclear evidence, physicians should use their clinical judgment when deciding whom to screen," Krist added. The USPSTF pointed out that their future recommendations for screening patients would benefit from research into: The effectiveness of targeted screening in patients at increased risk for celiac disease The accuracy of serological markers in asymptomatic patients, particularly those with risk factors The effect of treatment of celiac disease in asymptomatic patients who have positive blood tests for celiac disease, and The clinical outcomes such as changes in health and quality of life in people who are screened versus people who are not screened Read more at: AAFP.ORG.
  5. Celiac.com 04/14/2014 - Exposure to stressful stimuli, such as inflammation, cause cells to up-regulate heat shock proteins (Hsp), which are highly conserved immunomodulatory molecules. Research points to Hsp involvement in numerous autoimmune diseases, including autoimmune bullous diseases and celiac disease. To better understand the role of Hsp in autoimmune bullous diseases, a research team conducted the first investigation of the humoral autoimmune response to Hsp40, Hsp60, Hsp70, and Hsp90 in patients with dermatitis herpetiformis (DH; n = 26), bullous pemphigoid (BP; n = 23), and pemphigus vulgaris (PV; n = 16), the first representing a cutaneous manifestation of celiac disease. The research team included Kasperkiewicz M1, Tukaj S, Gembicki AJ, Silló P, Görög A, Zillikens D, Kárpáti S. They are affiliated with the Department of Dermatology at the University of Lübeck in Lübeck, Germany. In patients with active BP and PV, serum levels of autoantibodies against these Hsp matched the healthy control subjects (n = 9-14), while circulating autoantibodies against Hsp60, Hsp70, and Hsp90 increased at the active disease stage of DH. Further analysis showed that in patients who adopt a gluten-free diet, these anti-Hsp autoantibodies decreased in relation to serum autoantibodies against epidermal and tissue transglutaminase during remission of skin lesions. Larger groups of patients must be studied to confirm these findings, but these results indicate that autoantibodies against Hsp60, Hsp70, and Hsp90 play a key role in the development and maintenance of DH, possibly also in the underlying celiac disease, and may be important in potentially undiscovered disease biomarkers. Source: Cell Stress Chaperones. 2014 Mar 19.
  6. Celiac.com 11/06/2008 - Previously, the possible link between gut bacteria and celiac disease has been discussed in "Do Vitamin D Deficiency, Gut Bacteria, and Gluten Combine in Infancy to Cause Celiac Disease?"[1] A 5-year European study, DIABIMMUNE, is currently underway focusing on some 7000 children, from birth, investigating the development of intestinal bacterial flora and its influence on the development of the human immune system and autoimmune disease, including celiac disease.[2] Hopefully, this study will provide some much needed answers. Now a Spanish group of scientists has produced further evidence supporting a possible role for gut bacteria in the pathogenesis of celiac disease by investigating whether gut microflora present in the feces of celiac disease patients participates in the pro-inflammatory activity of celiac disease.[3] The makeup of fecal microflora in celiac disease patients differs significantly from that of healthy subjects. To determine whether gut microflora is a participant in the pro-inflammatory milieu of celiac disease, the Spanish research team incubated cultures of peripheral blood mononuclear cells from healthy adults with fecal microflora obtained from 26 active celiac disease children, 18 symptom-free celiac disease children on a gluten-free diet, and 20 healthy children. The scientists additionally investigated possible regulatory roles of Bifidobacterium longum ES1 and B. bifidum ES2 obtained from the feces of healthy individuals, co-incubating the Bifidobacterium with the test subject fecal microflora and the peripheral blood mononuclear cell culture. Fecal micrflora from both active and, notably, treated, symptom-free celiac children caused a significant increase in pro-inflammatory cytokine production and a decrease in anti-inflammatory IL-10 production in the peripheral blood mononuclear cell cultures compared to the fecal microflora from healthy children. However, cultures co-incubated with the Bifidobacterium strains exhibited a suppression of the pro-inflammatory cytokine production and an increase in IL-10 production. IL-10 is a cytokine which promotes immune tolerance. The scientists concluded that the makeup of the gut flora of celiacs may contribute to pro-inflammation in celiac disease, possibly in a synergy with gliadin, and that certain strains of Bifidobacterium appear to suppress and reverse pro-inflammatory effects and offering therapeutic opportunities for the treatment of celiac disease. It would have been interesting if the scientists had also investigated the effect of adding vitamin D to the fecal microflora and the peripheral blood mononuclear cell cultures. It is likely the addition of vitamin D might also have resulted in a suppression of pro-inflammatory cytokine production and an increase in IL-10 production. This is borne out by experiments with Mycobacterium tuberculosis and its culture filtrate antigen in peripheral blood mononuclear cell cultures where the addition of vitamin D resulted in a suppression of pro-inflammatory cytokine production and an increase in IL-10 production.[4] It is possible that celiac disease may be entirely prevented in infancy by routinely administrating prophylactic doses of vitamin D and probiotics containing specific strains of Bifidobacterium before gluten is introduced into the infant's diet. The vitamin D and Bifidobacterium strains may provide an IL-10 anti-inflammatory environment in which the immune system learns to respond tolerantly to gluten, forever preventing the onset of celiac disease. The fact that certain strains of fecal Bifidobacterium from healthy individuals appear to suppress celiac disease inflammation brings to mind the concept of "fecal bacteriotherapy" or "fecal transplant", a therapy developed and used in practice by the world reknown Australian gastroenterologist, Prof. Thomas J. Borody, M.D., known best for his development of a triple-antibiotic treatment for H. pylori and ulcerative colitis.[5] Fecal bacteriotherapy involves transplanting feces from a healthly, screened donor into an ailing patient with a persistant bacterial gastrointestinal disorder whose own gut flora has first been reduced or eliminated with antibiotics. The fecal microflora from the healthy donor reseeds the gut of the ailing patient with a healthy mix of intestinal microflora curing the gastrointestinal disorder. The Bifidobacterium research done by the Spanish researchers suggests that fecal bacteriotherapy might be an option to treat or cure celiac disease in adults, replacing gut flora causing intolerance to gluten with a healthy mix of gut flora that encourages tolerance to gluten. Sources [1] Do Vitamin D Deficiency, Gut Bacteria, and Gluten Combine in Infancy to Cause Celiac Disease? Roy S. Jamron https://www.celiac.com/articles/21605/ [2] European Study Will Focus On Relation Of Gut Bacteria to Autoimmune Disease in Children Roy S. Jamron https://www.celiac.com/articles/21607/ [3] Journal of Inflammation 2008, 5:19. Bifidobacterium strains suppress in vitro the pro-inflammatory milieu triggered by the large intestinal microbiota of coeliac patients. Medina M, De Palma G, Ribes-Koninckx C, Calabuig M, Sanza Y. http://www.journal-inflammation.com/content/pdf/1476-9255-5-19.pdf [4] J Clin Immunol. 2008 Jul;28(4):306-13. Regulatory role of promoter and 3' UTR variants of vitamin D receptor gene on cytokine response in pulmonary tuberculosis. Selvaraj P, Vidyarani M, Alagarasu K, Prabhu Anand S, Narayanan PR. http://www.springerlink.com/content/d67236620021j84u/ [5] Prof. Thomas J. Borody, M.D., Bio and Publication List http://www.cdd.com.au/html/hospital/clinicalstaff/borody.html http://www.cdd.com.au/html/expertise/publications.html
  7. Celiac.com 12/02/2011 - Some rumors have been circulating in the health foods community that gluten-free eating can encourage weight loss. Unfortunately, this theory is completely unfounded. Wendy Marcason, a registered dietician, published an article in the Journal of the American Dietetic Association in November that reviews some of the theories and controversy surrounding this issue. The article concludes that there is no scientific evidence to support a connection between eating gluten-free and losing weight. For those of us with celiac disease who start a gluten-free diet, weight gain is more often the case. The healing of the damaged intestines allows better absorption of food, and unless you rapidly change the amount of food you eat when you go gluten-free, most celiacs gain a substantial amount of weight after the switch. If you do not have celiac disease, however, eating gluten-free is unlikely to have any affect on weight independent from decreases in the overall calorie intake due to eating more carefully. The consequence of this conclusion by the American Dietetic Association may be that more non-celiacs recognize that gluten-free does not necessarily mean more healthy. Unfortunately, some of the increased availability of gluten-free food over the last decade is owed to these non-celiac gluten-free folks. If these non-celiacs stop eating gluten-free, the demand for gluten-free food will fall and te number of options may decrease. All of that said, the paper said that no evidence exists because there are no studies that look at weight loss on a gluten-free diet. While it's impossible to conclude that gluten-free diets cause weight loss, its also impossible to conclude that they don't cause weight-loss. Only a clinical study will be able to put the issue to rest. Reference: Marcason W. "Is There Evidence to Support the Claim that a Gluten-Free Diet Should Be Used for Weight Loss?" Journal of the American Dietetic Association. Nov 2011; 111(11): 1786. Weight Loss and the Gluten Free Diet by Ron Hoggan, Ed. D.First, I’d like to set Dr. O’Connell’s mind at rest. The claims for weight loss following adoption of a gluten-free diet aren’t merely rumors. They are credible claims based on peer reviewed and anecdotal reports, as well as published data from a qualified medical practitioner. For instance, Cheng and colleagues found that “54% of overweight and 47% of obese patients lost weight” (1). They investigated 81 subjects who were overweight and had celiac disease. Congruently, Venkatasubramani et al found that one half of their eight overweight pediatric patients also lost weight on a gluten free diet (2). These reports alone cast an ominous shadow over Dr. Marcason’s claims if Dr. O’Connell has represented them correctly. Marcason, we are told, asserts that no research has been done on this question. Yet there are three such reports in the peer reviewed literature (1, 2, 3). One reports a preponderance of weight gain among overweight and obese celiac patients after beginning a gluten free diet, while the other two groups report that about half of the overweight and obese celiac patients, children and adults, lose weight on a gluten free diet. Not only has this research been conducted and most of the findings not only contradict the claim that no such research has been done, but two of the three reports indicate that the gluten free diet helps with weight loss in some individuals. I think it is important to notice that the study showing that a large majority of overweight/obese celiacs was conducted where wheat starch is accepted as appropriate for celiac patients, while the two studies that showed weight loss were conducted in the USA. We still don’t know enough about the interaction between various constituents of gluten and people who lose weight on a gluten free diet. However, given the contradictions in findings, between research conducted in the USA and some parts of Europe, it is not unreasonable to suggest that these differences may result from wheat starch. Each of the three studies mentioned above have one large, consistent weakness. They are dealing with small numbers of patients. However, Dr. William Davis, a cardiologist has recently authored a book titled WHEAT BELLY, in which he reports that he has seen weight loss and other health improvements in more than 2,000 of his patients following adoption of a gluten free diet. And, of course, there are all the other anecdotal reports of similar benefits. Dr. O’Connell’s opposition to the use of a gluten free diet ignores the dynamics of appetite enhancement and satiation that are largely driven by hormones resulting from variations in nutrient density in various parts of the body. From insulin to glucagon to leptin to ghrelin, these and several other fat mobilizing hormones enhance and suppress our hunger based on the nutrients in our bloodstreams, gastrointestinal tract, and adipose tissues. Dr. O’Connell also ascribes Marcason’s views to the American Dietetic Association which is the body that publishes the journal in which Dr. Marcason’s opinion article appears. While it may be true that the American Dietetics Association takes this position, it would be unusual for a journal, and the association that operates that journal, to underwrite the claims of one of its authors so I am skeptical that it has done so. I am especially skeptical of endorsement by the association, if Marcason has, indeed, stated that no studies have been conducted to investigate changes in body mass resulting from the gluten free diet among people who are overweight or obese at diagnosis. Clearly, this is an inaccurate claim whether it emanates from O’Connell or Marcason or even the American Dietetics Association. I am also left wondering if there are any studies that show that “gluten-free does not necessarily mean more healthy” [sic]. I haven’t seen any and I would be very surprised if any exist. Dr. O’Connell didn’t cite any such studies, yet she asserts that a gluten free diet is not a healthy choice for those who do not have celiac disease. This is especially troubling in view of the growing recognition of non-celiac gluten sensitivity as a legitimate disease entity (5, 6, 7, 8, 9, 10). I frequently write opinion articles so I would not want to inhibit such writing. Nonetheless, I believe that taking a rigid stance on either side of this issue is premature. Clearly we all have a lot to learn about weight loss and the gluten-free diet. The scanty evidence that is currently available is entirely too limited to say, with confidence, that the gluten-free diet is an effective weight loss tool, even for overweight patients with celiac disease. It appears to work for some, but other, unseen factors may be at work here. Sources: Cheng J, Brar PS, Lee AR, Green PH. Body mass index in celiac disease: beneficial effect of a gluten-free diet. J Clin Gastroenterol. 2010 Apr;44(4):267-71. Venkatasubramani N, Telega G, Werlin SL. Obesity in pediatric celiac disease. J Pediatr Gastroenterol Nutr. 2010 Sep;51(3):295-7. Dickey W, Kearney N. Overweight in celiac disease: prevalence, clinical characteristics, and effect of a gluten-free diet. Am J Gastroenterol. 2006 Oct;101(10):2356-9. Davis W. Wheat Belly.Rodale, NY, NY 2011. Bizzaro N, Tozzoli R, Villalta D, Fabris M, Tonutti E. Cutting-Edge Issues in Celiac Disease and in Gluten Intolerance. Clin Rev Allergy Immunol. 2010 Dec 23. Ford RP. The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29. Sbarbati A, Valletta E, Bertini M, Cipolli M, Morroni M, Pinelli L, Tatò L. Gluten sensitivity and 'normal' histology: is the intestinal mucosa really normal? Dig Liver Dis. 2003 Nov;35(11):768-73. PubMed PMID: 14674666. Di Cagno R, De Angelis M, De Pasquale I, Ndagijimana M, Vernocchi P, Ricciuti P, Gagliardi F, Laghi L, Crecchio C, Guerzoni ME, Gobbetti M, Francavilla R. Duodenal and faecal microbiota of celiac children: molecular, phenotype and metabolome characterization. BMC Microbiol. 2011 Oct 4;11:219. Biesiekierski JR, Newnham ED, Irving PM, Barrett JS, Haines M, Doecke JD, Shepherd SJ, Muir JG, Gibson PR. Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double-blind randomized placebo-controlled trial. Am J Gastroenterol. 2011 Mar;106(3):508-14 Bizzaro N, Tozzoli R, Villalta D, Fabris M, Tonutti E. Cutting-Edge Issues in Celiac Disease and in Gluten Intolerance. Clin Rev Allergy Immunol. 2010 Dec 23. Amy O'Connell, MD, PhD's Reply to Dr. Ron Hoggan:This is Dr. O'Connell replying. My piece was merely a summary of an article in the Journal of the ADA. The short summary I wrote was not intended to be an end-all conclusive statement about the matter. That said, the Cheng article that is cited by Ron Hoggard. M.Ed. was not designed to look at the outcome of weight loss in overweight celiacs and is underpowered to make the conclusions that he cites. Another quote from the same article said, "Overall, 54% [of patients who started a gluten-free diet] gained weight and 38% lost weight." The same problem with a lack of statistical power exists for the Venkatasubramani paper. Four obese patients lost weight on a gluten-free diet but 2 gained weight and 1 was lost to follow up. I'd like to apologize if my brief summary seemed too closed-ended, but I will stand by my article conclusion, "While it's impossible to conclude that gluten-free diets cause weight loss, its also impossible to conclude that they don't cause weight-loss. Only a clinical study will be able to put the issue to rest."
  8. This article was posted to the Celiac Listserv by Ashton Embry at: embrya@cadvision.com in January, 1998: I became interested in the concept of a Paleolithic Diet in a circuitous way which began with the diagnosis of my oldest son with multiple sclerosis two and a half years ago. I hit the med library soon after I was told that there was no known cause and no effective treatment for MS. My goal was to determine the most likely cause and to then devise a therapy which countered this cause. After reading hundreds of papers and countless more abstracts I reached the conclusion that the main cause of MS is dietary and that dairy, gluten and saturated fat were the three main offending foods. I have summarized this analysis in an essay which is at The evidence I used to reach my interpretation was a combination of epidemiology, theory (molecular mimicry) and anecdotal data. After the essay was on the web I was contacted by Loren Cordain who pointed out that the foods implicated in MS were recently introduced to the human diet from a genetic point of view and he gave me the references to Boyd Eatons classic papers on Paleolithic Nutrition. From my geological background this concept seemed eminently reasonable so now I had an excellent unifying concept to go along with all the other data. One shortcoming of the evidence was that it was all circumstantial. There was no smoking gun evidence, that is, empirical evidence which demonstrates beyond a reasonable doubt that food proteins really do cause cell-mediated, organ-specific autoimmunity. As a dutiful civil servant, I made one of my required pilgrimages to Ottawa last week to participate in various mind-numbing meetings. I had a free afternoon so I went out to the Nutrition Research Division of Health Canada where I had the good fortune to meet with Dr Fraser Scott. Dr. Scott has been studying the effect of diet on the development of Type 1 Diabetes in BBdp rats for 20 years. He and co-workers have demonstrated conclusively that Type 1 diabetes can be generated by proteins derived from wheat, soy and milk. So now I had found the smoking gun. Food proteins can indeed induce cell-mediated autoimmunity and not surprisingly the foods which supply the pathogenic proteins are those added to the human diet during the Neolithic. I believe Dr. Scotts work is of great significance for understanding the cause of autoimmune disease and strongly supports Eatons suggestion the diet of our ancestors is the best defense against the diseases of civilization. References: The best reference for Scotts work is: Scott, FW, 1996, Food-induced Type 1 Diabetes in the BB Rat. Diabetes/Metabolism Reviews, v.12, p. 341-359. This paper summarizes all his results up to 1996 and contains references to all his earlier work.
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