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Dr. Ron Hoggan, Ed.D. posted an article in Spring 2006 IssueCeliac.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.
Celiac.com 02/14/2017 - In 1999, Loren Cordain, the renowned professor of Exercise Physiology at Colorado State University who has since popularized the Paleodiet, published an extensive exploration of why our cultivation and consumption of cereal grains has been disastrous for the human race, resulting in many autoimmune, nutrient deficiency, and other modern diseases (1). Previously, in 1987, the famous physiologist, Jared Diamond characterized humanity's shift to agriculture as "The Worst Mistake in the History of the Human Race" (2). A year later, medical doctor and professor of Anthropology, S. Boyd Eaton and colleagues suggested a mismatch between the human genome and our current agricultural diet/lifestyle (3). And more than a decade prior to that, gastroenterologist, Walter L. Voegtlin, M.D., self published a book apparently asserting, based on his treatments and observations of patients, that dietary avoidance of cereal grains and sugars, offset by increased consumption of meats and animal fats, is an effective treatment regimen for a variety of intestinal ailments including Crohn's disease, colitis, irritable bowel syndrome, and indigestion (4). Each of these perspectives was informed by a different but solidly scientific approach to human health. The academic field of each of these authors varied from Exercise Physiology to Physiology, to Gastroenterology, to Anthropology. Yet each of these specialist researchers arrived at the very similar conclusion that cereal grains are not healthful foods for humans. Their strident declarations to that effect leave little room for doubt. Dr. Cordain acknowledges that the roots of some of his thinking lie with Dr. Eaton and his colleagues. Nonetheless, there is a convergence here, of ideas and insights drawn from separate bodies of data and investigative approaches. While there is some overlap between these scientific disciplines, they all lead to a clear indictment of cereal grains as little more than a starvation food for humans. These scientists point to myriad signs of illness that arise more commonly when populations make the transition to eating diets dominated by grains, especially when the grains are refined and when they are combined with sugar. One critic of this paradigm is the evolutionary biologist, Dr. Marlene Zuk of the University of California at Riverside. According to Alison George at New Scientist, Zuk asserts that the 10,000 years that humans have been cultivating and consuming cereal grains is an adequate time period for humans to evolve an adaptation to these foods (5). But surely this is a Eurocentric view. Simply because some Europeans have been cultivating and consuming cereal grains for ten or more thousands of years does not mean that the entire world's population, or even all Europeans, would or could have adapted to consuming these foods. Let's look back to see what we currently know about our human roots and how those early humans spread all over the world. A group thought to number about 200 humans left Africa sometime between 85,000 and 70,000 years ago, during a glacial maximum that lowered worldwide sea levels by about 300 feet below current levels. The enormous glaciers of the time so depleted the oceanic barriers we see today, that these bodies of water were made navigable even with very primitive flotation devices. The progeny of this relatively small group of early modern people multiplied and went on to parent almost all of today's non-African people of the world with some 1% to 4% of today's human, non-African genes having been derived from the Neanderthal branch of the hominid tree (6). This predominantly early modern human group's progeny would quickly find its way to Australia, the South Pacific, across Asia, to China, east to the Americas and west across India, finally arriving in Europe, where they would supplant the long-time Neanderthal residents who had survived some of Europe's harsh and inhospitable glaciations but apparently could not survive having our forebears as neighbors. While specific paths and dates for exiting Africa, and worldwide patterns and timing of human distribution remain controversial, most experts now accept that indigenous Australians had arrived there at least 60,000 years ago (6). A similarly recent finding places people in the Americas by at least 55,000 years ago, long prior to the date at which the Bering Land Bridge was thought to be available for human movement from Siberia into the Americas (8). This newer, admittedly controversial date raises the likely possibility that people arrived in the Americas, from Asia, by boats or rafts on which they followed the shoreline east to what is now Alaska, then south of the glaciated wastelands of much of what is now Canada. (Or perhaps they arrived by some other means that we have not yet imagined.) But only a small portion of these early Americans would eat wheat, rye, oats, or barley before the last 200 years or so, especially those living on the Great American Plains, or in the frigid north, the dense jungles or places that were otherwise isolated from the encroaching wave of "immigrants" from Europe and beyond. And none of those aboriginal peoples of the Americas were eating these grains prior to 1492. The epidemics of autoimmunity and obesity that may be seen among indigenous Americans are clear reflections of their recent shift to the gastronomic wonders of foods derived from these European grains. Further, even among Europeans, grain cultivation and consumption had not uniformly spread across most of Europe until, at most, less than half of the 10,000 years that Zuk says would be sufficient for human adaptation. In Britain, for instance, grain farming was only getting under way about 4,000 years ago, and availability of grains varied according to local geographies and economies. Also, in parts of Scandanavia, wheat bread was a rare treat until after World War II. Some Europeans are thought to have been cultivating grains for even longer than the 10,000 years ago suggested by Cordain, but the evidence is contradictory and accompanied by a range of expert opinions. Further, the health consequences of this nutritional path are consistently seen in the skeletal remains of those early farmers, many of which can now be seen reflected among indigenous peoples of the Americas, as they assimilate our grain and sugar dominated diet. Adaptation to eating grains is not a gentle, joyful process. Early farmers may have produced many more children than their hunting and gathering neighbors, but their lives were shorter, their bodies were less robust, with substantial reductions in stature, and they experienced widespread infectious diseases and ailments driven by nutritional deficiencies. By the time grains became a cash crop for many European farmers, cereals were disproportionately consumed by affluent urbanites. Those who were large consumers of cereal grains did not include all Europeans, even where yields were prodigious. In more remote, northerly, or mountainous areas, cereal grains, or foods made from them, were likely a rare treat rather than a daily staple. Jared Diamond points out, that in addition to "..... malnutrition, starvation, and epidemic diseases, farming helped bring another curse upon humanity: deep class divisions." He goes on to argue that only with farming and the storage and accumulation of food can Kings "and other social parasites grow fat on food seized from others". He also presents evidence that farming led to inequality between men and women. Conversely, contemporary hunter-gatherers have repeatedly been shown to be quite egalitarian, both regarding gender and political leadership (9). Roger Lewin is another critic of the health impact of European grain cultivation on humans. He points out that even in the very heart of the Fertile Crescent, where agriculture got its start, there was not a uniform adoption of farming. One agricultural center at Abu Hureyra, experienced two cycles of abandonment, one at 8,100 B.C.E., lasting about 500 years, and another at 5,000 B.C.E. These periods when agriculture at this locale was abandoned are "thought to be related to climatic change that became less and less conducive to agriculture" (10). Lewin also harkens to Mark Nathan Cohen's collation of "physical anthropological data that appear to show increasingly poor nutritional status coincident with the beginnings of agriculture.... " (10) suggesting, again, that grains were a starvation food. Eaton et al also approach grain cultivation from an anthropological perspective, suggesting that increased dietary protein and fats from animal/meat sources likely gave rise to increased stature of earlier humans, along with providing the necessary fatty acids for building larger brains, and allowing smaller gut sizes over the past 2.5 million years. It seems reasonable to assume that if it took our pre-historic ancestors that long to adapt to eating meats and animal fats, the very irregular adaptation period of between less than one hundred years and about 10,000 years that various world populations have been cultivating and consuming wheat, rye, barley and oats would be insufficient to allow full adaptation to eating these immune sensitizing cereal grains. Dr. Zuk's perspective might be tempered a bit if she considers that Europeans and their descendants do not comprise the entirety of the world's populations. There are several Asian populations that are not insignificant when compared with European populations and their progeny, including the residents of China, India, Pakistan, and South-East Asia. Even among those of us who appear quite European, there may be a mixture of genes derived from peoples of any of the other five populated continents. The approximately 10,000 year maximum period since humans began to cultivate cereal grains would have little adaptive impact on populations that have only been exposed to these grains for a period of somewhere between four or five centuries and seven or eight decades, as is the case among the indigenous people of the Americas, Australia, New Zealand, and much of Asia (6). Even if all humans had been cultivating and consuming cereal grains for the 10,000 years since this practice was first begun in the Middle East, the high frequency of intestinal, autoimmune, and other diseases that can be mitigated by a gluten free diet, even among descendants of Europeans, leaves little room to doubt that Dr. Zuk's projected adaptation simply has not occurred. The current prevalence of celiac disease and non-celiac gluten sensitivity identifies, at a bare minimum, between 7% and 12% of the American population that has not adapted to cereal grain consumption. While a few research projects suggest that molecular mimicry and the opioids from cereal grains contribute to autoimmunity, obesity, type 2 diabetes and cardio-vascular disease, current research does not provide any clear sense of how many cases or to what degree these health conditions are driven by gluten consumption. We know that foods derived from cereal grains are often laced with refined sugar, but the insulin stimulating properties of gluten alone are such that their role in these conditions cannot, reasonably, be denied. I feel vindicated by these many experts who decry the folly in humanity's embrace of the European grains. I wonder how long it will take for this information to filter into, and be acknowledged by, those who claim that science has led them to advocate cereal grain consumption for everyone without celiac disease and, more recently, non celiac gluten sensitivity? Sources: Cordain, Loren. Simopoulos AP (ed): Evolutionary Aspects of Nutrition and Health. Diet, Exercise, Genetics and Chronic Disease. World Rev Nutr Diet. Basel, Karger, 1999, vol 84, pp 19–73 http://thepaleodiet.com/wp-content/uploads/2012/08/Cerealgrainhumanitydoublesword.pdf Jared Diamond, "The Worst Mistake in the History of the Human Race," Discover Magazine, May 1987, pp. 64-66. http://www.ditext.com/diamond/mistake.html Eaton SB, Konner M, Shostak M. Stone agers in the fast lane: chronic degenerative diseases in evolutionary perspective. Am J Med. 1988 Apr;84(4):739-49. Voegtlin, Walter L. (1975). The stone age diet: Based on in-depth studies of human ecology and the diet of man. Vantage Press. ISBN 0-533-01314-3 George, A. " The Paleo Diet Is a Paleo Fantasy" New Scientist. April 7, 2013. http://www.slate.com/articles/health_and_science/new_scientist/2013/04/marlene_zuk_s_paleofantasy_book_diets_and_exercise_based_on_ancient_humans.single.html Oppenheimer, Stephen. The Real Eve: Modern Man's Journey Out of Africa. Basic Books, NY, NY. 2004 Fagan, Brian. Cro-Magnon: How the Ice Age Gave Birth to the First Modern Humans. Bloomsbury Press, New York. 2011 http://www.utep.edu/leb/Pleistnm/sites/pendejocave.htm Brody, Hugh. The Other Side of Eden: Hunters, Farmers and the Shaping of the World. Douglas 7 McIntyre Ltd., Vancouver, B.C., Canada. 2000 Lewin, Roger. A Revolution of Ideas in Agricultural Origins. Science. vol 240, May 20, 1988
Jefferson Adams posted an article in Refractory Celiac Disease & Collagenous SprueCeliac.com 06/04/2012 - Non-responsive celiac disease is very much what it sounds like: celiac disease where symptoms seem to resist treatment and continue even in the face of a gluten-free diet. A team of researchers recently set out to look for the most likely causes of persistent symptoms in celiac disease patients on a gluten-free diet. The research team included David H. Dewar, Suzanne C. Donnelly, Simon D. McLaughlin, Matthew W. Johnson, H. Julia Ellis, and Paul J. Ciclitira. They are variously affiliated with King's College London, Division of Diabetes and Nutritional Sciences, Department of Gastroenterology, and The Rayne Institute at St. Thomas' Hospital in London. Their goal for the study was to investigate all patients referred to our center with non-responsive celiac disease (NRCD), to establish a cause for their continued symptoms. For their study, the research team assessed all non-responsive celiac disease who were referred to their gastroenterology center over an 18-mo period. They then established the etiology of ongoing symptoms for these patients. For all patients, the team established a thorough case history and conducted a complete examination with routine blood work including tissue transglutaminase antibody measurement. Additionally, each patient was examined by a specialist gastroenterology dietician to try to spot any gaps in their diets, or any hidden sources of gluten consumption. When possible, the team conducted a follow-up small intestinal biopsy, and compared the results against the biopsies from the referring hospital. Patients with persistent symptoms received colonoscopy, lactulose hydrogen breath testing, pancreolauryl testing and a computed tomography scan of the abdomen. The team monitored patient progress over a minimum of two year period. Overall, the team looked at 112 patients with non-responsive celiac disease. They determined that twelve of those did not actually have celiac disease. Of the remaining 100 patients, nearly half, 45%, were not adequately following a strict gluten-free diet. Of these, 24 (53%) were found to be accidentally consuming gluten, while 21 (47%) admitted to not faithfully following a gluten-free diet. Microscopic colitis was found in 12% and small bowel bacterial overgrowth in 9%. Refractory celiac disease was found in 9%. Three of these were diagnosed with intestinal lymphoma. After 2 years, 78 patients remained well, eight had continuing symptoms, and four had died. In most cases of non-responsive celiac disease, the team found a reversible cause can be found in 90%. In the vast number of those cases, continued consumption of gluten was the main cause. The team is proposing the use of an algorithm for further investigation of the matter. Source: World J Gastroenterol. 2012 Mar 28;18(12):1348-56.