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Found 11 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. The following piece was written by Ronald Hoggan who is a teacher at Queen Elizabeth High School in Calgary, Alberta, Canada. Gall bladder disease or malfunction is often associated with celiac disease. It can cause pain in the upper right quadrant of the abdomen, just at the lowest rib on the right side. In one study of 1300 celiacs in Canada, 9% indicated that gall stones were the earliest presentation, sometimes followed by many years prior to correct diagnosis of their celiac disease. In another report, Dr. Kozlowska indicated that 13 of the 41 newly diagnosed celiacs she investigated were suffering from atresia, a condition which is a partial or complete blockage of the bile duct. CCK (cholecystokinin) is the hormone responsible for gall bladder contraction. The bulk of this hormone is produced in the duodenum. Active celiac disease would be likely, then, to cause a reduction or a cessation of duodenal production of CCK. A radiologist in Hungary is currently researching this problem. In private correspondence, one gastroenterologist reports having found (accidentally) a gallstone in a 12 year old girl who had active celiac disease. The 30% incidence of atresia among celiac children, as reported by Dr. Kozlowska, would suggest an even higher number among adults with active celiac disease. Given the low level of clinical suspicion for celiac disease in North America, it would not be at all surprising if a large portion of patients with gall bladder disease were suffering from occult celiac disease. Future research may reveal that gall stones and atresia are only symptoms of celiac disease. I did a Medline search on cck and celiac disease. I got 65 hits. Researchers repeatedly identified a connection between celiac disease and gall bladder malfunction with such comments as: Thus the already impaired fat absorption in celiac sprue is magnified by the lack of bile delivery.....; and We conclude that there is a reversible defect of gallbladder emptying and cholecystokinin release in celiac disease. and Cholecystokinin (cck) release and gall bladder emptying in response to a fatty meal are completely abolished in celiac disease. and the abnormally decreased gallbladder contraction in celiac patients is the result of endogenous cck secretion and not a lack of end-organ responsiveness to cck. There just isnt much ambiguity there. If youve got celiac disease, you have gall bladder malfunction, of the sort that may well develop into atresia and gallstones. Upon receiving a diagnosis of gall bladder disease, whether gall stones or atresia, one might be wise to request a blood test for celiac disease. The anti-endomysial antibody test is currently the most reliable and available test. Now, given the low level of clinical suspicion for celiac disease, I anticipate the suggestion that absent gall bladder emptying, atresia, and gall stones might occur in the absence of celiac disease. I did another Medline search, and I cant find a single study that has tested atresia patients or gallstone patients for celiac disease. My answer to the suggestion that gall bladder disease may occur in the absence of celiac disease is that there is no evidence to support such a contention. Considerable evidence exists, however, which points to celiac disease as a likely cause of gall bladder malfunction, atresia, or stones. As for childhood gallstones, there appears to be only one answer.... it is associated with celiac disease. A view that incorporates the association of gall bladder disease, and celiac disease, but does not preclude the above, has been expressed by Dr. Joseph Murray, of the University of Iowa, who is a gastroenterologist specializing in treating celiac disease. He believes there are several triggers that can activate Celiac disease in genetically susceptible people. One of them is: Surgery, particularly GI (gall bladder, etc.) In any case, the connection between celiac disease and gall bladder disease is well known.
  3. Don Wiss forwarded the following post to me: I know you have studied celiac disease for a long time. However, I need to disagree with the statement that fibromyalgia indicates celiac disease. It has been proven that persons with fibromyalgia have a decreased amount of serotonin and an increased amount of substance P in their spinal fluid. This indicates it is a result of not enough serotonin in the brain. Many of us who suffer from fibromyalgia do not have any problems with the digestive system at all. There are also PET scans that indicate that fibromyalgia patients have less dopamine activity in the brain indicating it truly is more a brain disease than celiac. The posters first point differentiating celiac disease from fibromyalgia on the basis of reduced serotonin in fibromyalgia may be unaware of the finding that celiac patients have fewer serotonin receptors on their platelets (1). Although I dont know about the spinal fluid, elevated levels of substance P have also been reported in the intestinal mucosa of celiac patients (2,3,4,5). A lack of digestive problems does not rule out celiac disease, as one of the foremost researchers in that area has reported that 50% to 60% of untreated celiacs are asymptomatic (6). Altered dopamine activity has also been reported in celiac disease (7). As regards the posters contention that it is really more a brain disease than celiac disease, the connections between celiac disease and altered brain perfusion (8), epilepsy without cerebral calcifications (9), epilepsy with cerebral calcifications (10, 11), a wide variety of neuropathic symptoms (12), and a number of psychiatric ailments (13), all counter the posters perspective. Finally, if (the poster) says that her fibromyalgia symptoms go away when gluten-free, and return when she eats gluten, I believe her. Sources: Chiaravalloti G, et al. Platelet serotonin transporter in celiac disease. Acta Paediatr. 1997 Jul;86(7):696-9. Sjolund K, et al. Enteropathy of celiac disease in adults: Increased number of enterochromaffin cells the duodenal mucosa. Gut. 1982 Jan;23(1):42-8. Sjolund K, et al. Duodenal endocrine cells in adult celiac disease. Gut. 1979 Jul;20(7):547-52. Bloom SR. Hormonal peptides of the gastrointestinal tract. Eur J Clin Invest. 1979 Apr;9(2 Pt 1):111-3. Domschke S, et al. Celiac sprue: abnormalities of the hormone profile of gastroduodenal mucosa. Scand J Gastroenterol Suppl. 1989;167:86-9. Marsh MN, et al. Morphology of the mucosal lesion in gluten sensitivity. Baillieres Clin Gastroenterol. 1995 Jun;9(2): 273-93. Review. Hallert C, et al. Psychic disturbances in adult celiac disease. III. Reduced central monoamine metabolism and signs of depression. Scand J Gastroenterol. 1982 Jan;17(1):25-8. De Santis A, et al. Schizophrenic symptoms and SPECT abnormalities in a celiac patient: regression after a gluten-free diet. J Intern Med. 1997 Nov;242(5):421-3. Cronin CC, et al. Celiac disease and epilepsy. QJM. 1998 Apr;91(4):303-8. Bernasconi A, et al. Celiac disease, bilateral occipital calcifications and intractable epilepsy: mechanisms of seizure origin. Epilepsia. 1998 Mar;39(3):300-6. Hernandez MA, et al. Epilepsy, cerebral calcifications and clinical or subclinical celiac disease. Course and follow up with gluten-free diet. Seizure. 1998 Feb;7(1):49-54. Hadjivassiliou M, et al. Clinical, radiological, neurophysiological, and neuropathological characteristics of gluten ataxia. Lancet. 1998 Nov 14;352(9140):1582-5 Hoggan, R. Absolutisms Hidden Message for Medical Scientism. Interchange. 1997; 28(2/3): 183-189.
  4. This article appeared in the Spring 2005 edition of Celiac.coms Scott-Free Newsletter. Celiac.com 04/10/2005 - Celiac disease is, by definition, a condition in which the intestinal wall is damaged as a result of eating gluten. It is a chronic illness in which the symptoms wax and wane1 for reasons that are not yet understood. Celiac disease is the result of genetic and environmental factors. We now know two HLA markers (DQ2 and DQ8) for the predisposition for celiac disease2. One environmental factor is, of course, the consumption of gluten, but there may be other environmental contributors. Recent research reveals that about 1% of the population suffers from this condition3 although most remain undiagnosed. On the other hand, gluten sensitivity is characterized by antigliadin antibodies. This condition afflicts at least 12% of the general population4 and is found in patients with a wide variety of autoimmune diseases. In some studies of neurological diseases of unknown origin, a majority of patients show signs of gluten sensitivity4. These patients are mounting an immune response to the most common food in the western diet, yet many practitioners consider gluten sensitivity to be a non-specific finding, frequently counseling patients to ignore these test results. This is particularly unfortunate since a strict gluten-free diet has repeatedly proven helpful to patients who are fortunate enough to consult a practitioner who is versed in gluten sensitivity and its connection with autoimmunity. Untreated celiac disease carries an added risk for a wide variety of additional autoimmune diseases. The most likely cause of this predisposition to additional autoimmune disease is a condition sometimes referred to as leaky gut syndrome. We know that gluten causes intestinal damage. We also know that this damage allows large undigested and partly digested proteins to leak into the bloodstream through the damaged intestinal wall. This leakage results in immune system production of antibodies to attack these foreign proteins as if they were invading microbes. The result is the production of a huge variety of selective antibodies, and each type recognizes a particular short chain of amino acids located somewhere in the proteins structure. Unfortunately, our own tissues can contain very similar or identical sequences of amino acids. Hence, by a process called molecular mimicry, we are producing antibodies that attack both the foreign food proteins that are leaked into our blood through the damaged intestinal wall, and similar amino acid sequences in our own tissues, often resulting in an autoimmune disease5. The supposedly non-specific antigliadin antibodies in gluten sensitivity provide two important pieces of information: 1) That the intestinal wall has been damaged and is permitting leakage of food proteins into the bloodstream, and; 2) That the dynamic contributing to increased autoimmunity in celiac disease may well be an important contributing factor in gluten sensitivity5. The currently common view that celiac disease is a serious illness, while disregarding gluten sensitivity, is dangerous to gluten sensitive patients. This bias is also a divisive element in the gluten-sensitive/celiac community. Whether a person has "biopsy proven" damage to the intestinal wall, if this person gets sick from eating gluten, or mounts an immune response to gluten, we are all in the same leaky boat (please pardon the pun). We need to work together to get a better understanding of gluten sensitivity in all its forms (including celiac disease). As a community, we need to discourage any kind of dismissal of illnesses that are partly or wholly mediated by gluten. If we can stand together in our quest for widespread recognition of the damaging impact of gluten consumption, we can all enjoy a healthier life. Our descendants will also inherit a more gluten-savvy world. Ron Hoggan is an author, teacher and diagnosed celiac who lives in Canada. His book "Dangerous Grains" can be ordered at Celiac.com. Rons Web page is: www.DangerousGrains.com Sources: Cooke W, Holmes G. Coeliac Disease. Churchill Livingstone, New York, N.Y. 1984. Fasano A. Celiac disease--how to handle a clinical chameleon. N Engl J Med. 2003 Jun 19;348(25):2568-70. Fasano A, Berti I, Gerarduzzi T, Not T, Colletti RB, Drago S, Elitsur Y, Green PH, Guandalini S, Hill ID, Pietzak M, Ventura A, Thorpe M, Kryszak D, Fornaroli F, Wasserman SS, Murray JA, Horvath K. Prevalence of celiac disease in at-risk and not-at-risk groups in the United States: a large multicenter study. Arch Intern Med. 2003 Feb 10;163(3):286-92. Hadjivassiliou M, Grunewald RA, Davies-Jones GA. Gluten sensitivity as a neurological illness. J Neurol Neurosurg Psychiatry. 2002 May;72(5):560-3. Braly J, Hoggan R.. Dangerous Grains, Penguin-Putnam-Avery, New York, N.Y., 2002.
  5. This article originally appeared in the Autumn 2002 edition of Celiac.coms Scott-Free newsletter. Copyright © 2002 Scott Adams. All rights reserved worldwide. Five years ago I became concerned about weakness in my bones after a couple of surprising fractures. At one point, I broke a rib while shingling a storage-shed roof. I leaned across the peak of the roofs ridge to pick up a shingle. I never expected such light pressure to cause a problem, however, I felt a sudden, sharp pain, and heard an odd sound. This, along with a couple of less dramatic, but similar injuries, caused me enough concern to begin looking into the question of celiac disease and bone strength. My explorations taught me that calcium absorption probably is not our main problem. People with celiac disease seem to be able to absorb adequate calcium1, but the primary problem appears to come from excreting too much of it, thus causing us to lose more calcium than we are absorbing. I also learned that research shows little or no benefit from calcium supplementation for celiac patients, while magnesium supplementation alone results in significant improvements2. The explanation for this may be that some of the antibodies caused by active celiac disease attack the parathyroid gland3. This organ is an important player in regulating calcium metabolism. Magnesium is necessary for the body to repair the parathyroid and to maintain its continued good function. Being convinced by this research, I began to take magnesium supplements without any calcium. I found that I had to be careful. Too much had me visiting the washroom frequently, and I was afraid that too little would fail to provide me the benefits I was seeking. At the same time, I also requested a bone density test. I wanted objective information that would allow me to evaluate the progress I hoped to make. The first test was conducted in March of 1997. The results (called "T scores") are reported based on comparison with the density of bones found in young adults. For instance, a score of 0 indicates that the bone density is about the same as would be found in an average young adult. A score in the minus range indicates a bone that has less mineral and more pores than is found in the same young adult. Thus, a score of –1.0 to –2.5 indicates mild mineral losses, while a score of –2.5 or lower indicates osteoporosis. My test results were not as bad as I had feared. The mineral density in my lower back was normal for my age, at –0.23. However, my upper leg, where it fits into my hip, was reported as –2.02, and my forearm was slightly stronger than that of a normal young adult at +0.19. As I saw it, there were only two causes for concern. First, at the tender age of 50, my hips were very close to osteoporotic, and certainly at a substantially increased risk of fracture. Such fractures can be very serious. Secondly, since only three skeletal areas had been tested for mineral density—and since there was such a wide range of density reported for each of these areas, it seemed impossible to estimate the density of the rest of the bones in my body. About three years after my first bone density test, some Calgary-based research made me suspect that the amount of vitamin D supplements I was taking might be too low4. I increased my intake to 1,000 IU daily. By the fall of 2001, I began to wonder if I was being foolish by avoiding calcium supplements based on the reports I had read. I therefore began to supplement 350 mg of calcium each day. In July of 2002, I underwent a second bone scan. They did not test my forearm, but the other two areas appear to have improved substantially. The T score for my lower back was now at + 0.06, and the T score for my hip had improved to –0.72. I realize that what I am reporting is just one persons experience. It is what the medical professionals call "anecdotal," and does not usually carry much weight. However, my experience does support the only published research of the impact of mineral supplements on bone density in celiac patients that I can find. Based on my own experience, and the relevant research, I am now convinced that magnesium is the most important supplement to consider in the context of celiac disease. I was thrilled to read my latest bone density report. Vitamin D may also be an important factor, but limitations of time and space force me to leave this topic for another day. References: Marsh MN. Bone disease and gluten sensitivity: time to act, to treat, and to prevent. Am J Gastroenterol. 1994 Dec;89(12):2105-7. Rude RK, Olerich M. Magnesium deficiency: possible role in osteoporosis associated with gluten-sensitive enteropathy. Osteoporos Int. 1996;6(6):453-61. Kumar V, Valeski JE, Wortsman J. Celiac disease and hypoparathyroidism: cross-reaction of endomysial antibodies with parathyroid tissue. Clin Diagn Lab Immunol. 1996 Mar;3(2):143-6. Embry AF, Snowdon LR, Vieth R. Vitamin D and seasonal fluctuations of gadolinium-enhancing magnetic resonance imaging lesions in multiple sclerosis. Ann Neurol. 2000 Aug;48(2):271-2. Ron Hoggan is an author, teacher and diagnosed celiac who lives in Canada. His new book "Dangerous Grains" is available at Celiac.com.
  6. Celiac.com 01/05/2012 - I was disappointed to read this opinion article in The Atlantic (titled: A Gluten-Free Diet Reality Check) when there are three U.S. studies demonstrating that about half of overweight and obese children and/or adults with newly diagnosed celiac disease lose weight following institution of a gluten free diet (GFD) (2,3,4). Some of these researchers make statements such as “The GFD has a beneficial effect upon the BMI [body mass index] of overweight children with celiac disease” after following 27 children who, at diagnosis, were overweight or obese (2). Similarly, Cheng et al reported that “A GFD had a beneficial impact on BMI, underweight patients gained weight and overweight/obese patients lost weight” (3). Murray et al report that only 30% of their obese patients with celiac lost weight after six months of following a gluten free diet (4). There isn’t much ambiguity in any of these three studies conducted by three separate groups of reputable medical scientists and published in the peer reviewed medical and scientific literature. Clearly, the gluten free diet is an effective weight loss tool for some of the individuals investigated. Yet Fontenot asserts that “there is no evidence that gluten-free foods promote weight loss….” (1). Exactly what evidence does she want? She goes on to say that “The only condition that necessitates a gluten free diet is celiac disease” (1). Yet she previously states, when discussing several other conditions that have been connected with gluten that “the research shows mixed results” (1). Surely the “mixed results” suggests that there is evidence that at least some cases benefit from a gluten free diet. Neither does the notion of ‘necessity’ apply to celiac disease. A person with celiac disase can consume gluten. They may place their health at risk by so doing, but that applies equally to those individuals with other conditions that have been shown to benefit from a gluten free diet. So the distinction she makes is, at best, one of degree. For decades many highly regarded investigators have published test results clearly showing that a gluten free diet is beneficial in the conditions listed by Ms. Fontenot, as well as many other ailments. These range from autism (5,6,7) to schizophrenia (8,9,10,11) to a variety of neurological (12,13,14) conditions to attention deficit disorder (15,16), to many other forms of autoimmunity (17,18,19), learning disabilities (20) and even to AIDS patients (21). Ms. Fontenot even asserts that “A person with celiac disease has increased levels of certain autoantibodies circulating in their blood due to their intake of gluten”(1). Again, she overlooks seronegative celiac disease which is frequently seen in the context of IgA deficiency (22, 23, 24) and may be present in many other contexts. Opinion pieces are probably easier to write when ignoring relevant facts. In this case, the overwhelming body of personal bias that drives Ms. Fontenot’s article is offered in the absence of a single supporting research finding and only one other professional opinion which is offered by one of Ms. Fontenot’s colleagues. She certainly hasn’t let the facts get in the way of her story, but it is deeply disturbing to discover that The Atlantic has chosen to republish this unsupported rant. Sources: http://www.theatlantic.com/health/print/2012/01/a-gluten-free-diet-reality-check/250750/ Reilly NR, Aguilar K, Hassid BG, Cheng J, Defelice AR, Kazlow P, Bhagat G, Green PH. Celiac disease in normal-weight and overweight children: clinical features and growth outcomes following a gluten-free diet. J Pediatr Gastroenterol Nutr. 2011 Nov;53(5):528-31. 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. Murray JA, Watson T, Clearman B, Mitros F. Effect of a gluten-free diet on gastrointestinal symptoms in celiac disease. Am J Clin Nutr. 2004 Apr;79(4):669-73. Whiteley P, Haracopos D, Knivsberg AM, Reichelt KL, Parlar S, Jacobsen J, Seim A, Pedersen L, Schondel M, Shattock P. The ScanBrit randomised, controlled, single-blind study of a gluten- and casein-free dietary intervention for children with autism spectrum disorders. Nutr Neurosci. 2010 Apr;13(2):87-100. Reichelt KL, Knivsberg AM. The possibility and probability of a gut-to-brain connection in autism. Ann Clin Psychiatry. 2009 Oct-Dec;21(4):205-11. Knivsberg AM, Reichelt KL, Høien T, Nødland M. A randomised, controlled study of dietary intervention in autistic syndromes. Nutr Neurosci. 2002 Sep;5(4):251-61. Cascella NG, Kryszak D, Bhatti B, Gregory P, Kelly DL, Mc Evoy JP, Fasano A, Eaton WW. Prevalence of celiac disease and gluten sensitivity in the United States clinical antipsychotic trials of intervention effectiveness study population. Schizophr Bull. 2011 Jan;37(1):94-100. De Santis A, Addolorato G, Romito A, Caputo S, Giordano A, Gambassi G, Taranto C, Manna R, Gasbarrini G. Schizophrenic symptoms and SPECT abnormalities in a coeliac patient: regression after a gluten-free diet. J Intern Med. 1997 Nov;242(5):421-3. Dohan FC, Grasberger JC, Lowell FM, Johnston HT Jr, Arbegast AW. Relapsed schizophrenics: more rapid improvement on a milk- and cereal-free diet. Br J Psychiatry. 1969 May;115(522):595-6.. Singh MM, Kay SR. Wheat gluten as a pathogenic factor in schizophrenia. Science. 1976 Jan 30;191(4225):401-2. Hadjivassiliou M, Kandler RH, Chattopadhyay AK, Davies-Jones AG, Jarratt JA, Sanders DS, Sharrack B, Grünewald RA. Dietary treatment of gluten neuropathy. Muscle Nerve. 2006 Dec;34(6):762-6. Hadjivassiliou M, Rao DG, Wharton SB, Sanders DS, Grünewald RA, Davies-Jones AG.Sensory ganglionopathy due to gluten sensitivity. Neurology. 2010 Sep 14;75(11):1003-8. Turner MR, Chohan G, Quaghebeur G, Greenhall RC, Hadjivassiliou M, Talbot K. A case of celiac disease mimicking amyotrophic lateral sclerosis. Nat Clin Pract Neurol. 2007 Oct;3(10):581-4. Niederhofer H, Pittschieler K. A preliminary investigation of ADHD symptoms in persons with celiac disease. J Atten Disord. 2006 Nov;10(2):200-4. Zelnik N, Pacht A, Obeid R, Lerner A. Range of neurologic disorders in patients with celiac disease. Pediatrics. 2004 Jun;113(6):1672-6. Rodrigo L, Hernández-Lahoz C, Fuentes D, Alvarez N, López-Vázquez A, González S. Prevalence of celiac disease in multiple sclerosis. BMC Neurol. 2011 Mar 7;11:31. Malalasekera V, Cameron F, Grixti E, Thomas MC. Potential reno-protective effects of a gluten-free diet in type 1 diabetes. Diabetologia. 2009 May;52(5):798-800. Epub 2009 Feb 14. Iuorio R, Mercuri V, Barbarulo F, D'Amico T, Mecca N, Bassotti G, Pietrobono D, Gargiulo P, Picarelli A. Prevalence of celiac disease in patients with autoimmune thyroiditis. Minerva Endocrinol. 2007 Dec;32(4):239-43. http://www.timesonline.co.uk/tol/news/uk/article444290.ece Quiñones-Galvan A, Lifshitz-Guinzberg A, Ruíz-Arguelles GJ. Gluten-free diet for AIDS-associated enteropathy. Ann Intern Med. 1990 Nov 15;113(10):806-7 Evans KE, Leeds JS, Sanders DS. Be vigilant for patients with coeliac disease. Practitioner. 2009 Oct;253(1722):19-22, 2. Mozo L, Gómez J, Escanlar E, Bousoño C, Gutiérrez C. Diagnostic Value of Anti-Deamidated Gliadin Peptide Igg Antibodies for Celiac Disease in Children and Iga Deficient Patients. J Pediatr Gastroenterol Nutr. 2011 Dec 23. Wang N, Shen N, Vyse TJ, Anand V, Gunnarson I, Sturfelt G, Rantapää-Dahlqvist S, Elvin K, Truedsson L, Andersson BA, Dahle C, Ortqvist E, Gregersen PK, Behrens TW, Hammarström L. Selective IgA deficiency in autoimmune diseases. Mol Med. 2011 Aug 4.
  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 originally appeared in the Winter 2003 edition of Celiac.coms Scott-Free Newsletter. Evolution is an interactive process. Those of us who learn quickly and well are more likely to survive, thrive, and reproduce. Learning capacities then, are factors in the survival of our genes. Research is now revealing that cereal grains, along with other allergenic and highly glycemic foods, pose a serious threat to our sustained ability to learn. These foods have been shown to interfere at almost any stage of the learning process, impeding our attempts to focus our attention, observe, ponder, remember, understand, and apply that understanding. Grains can alter learning capacities in four specific ways: as sequelae of untreated celiac disease; through an immune sensitivity to gluten; through dietary displacement of other nutrients and; through the impact of grain on blood sugar/insulin levels. There are many reports of learning problems in association with untreated celiac disease. A majority of children with celiac disease display the signs and symptoms of attention deficit disorder (ADD/ADHD)1, 2 a range of learning difficulties3 and developmental delays4-6. Many of the same problems are found more frequently among those with gluten sensitivity7 a condition signaled by immune reactions against this most common element of the modern diet. Grain consumption can also cause specific nutrient deficiencies that are known to play an important role in learning. Grains can also cause problems with blood sugar/insulin levels resulting in reduced capacities for learning. Further, foods derived from grain are an important element in the current epidemic of hypoglycemia, obesity, and Type 2 diabetes8-10. Our growing understanding of the biological impact of cereal grain consumption must move educators to challenge current dietary trends. Part of our improved understanding comes from new testing protocols which are revealing that celiac sprue afflicts close to 1% of the general population, making it the most common life-long ailment among humans, with frequencies ranging from 0.5% to more than 5% of some populations11, 12. It is widespread and appears to occur more frequently among populations that have experienced relatively shorter periods of exposure to these grains13. The importance of this newly recognized high frequency of celiac disease becomes obvious when we examine the impact it has on learning and behavior. Research has identified ADHD in 66-70% of children with untreated celiac disease, which resolves on a gluten-free diet, and returns with a gluten challenge1, 2. Several investigators have connected particular patterns of reduced blood flow to specific parts of the brain in ADHD13-15. Other reports have connected untreated celiac disease with similarly abnormal blood flow patterns in the brain16. One might be able to dismiss such reports if viewed in isolation, but the increased rates of learning disabilities among celiac patients3, and the increased rates of celiac disease among those with learning disabilities leave little to the imagination17. Further, there is one report of gluten-induced aphasia (a condition characterized by the loss of speech ability) that resolved after diagnosis and institution of a gluten-free diet18. Still other investigations suggest a causal link between the partial digests of gluten (opioid peptides) and a variety of problems with learning, attention, and development. Gluten sensitivity, afflicting close to 15% of the general population19, 20 is an immune reaction to one or more proteins in found in grains. When a persons immune system has developed antibodies against any of these proteins, undigested and partly digested food particles have been allowed entry into the bloodstream21. The leakage of food proteins through the intestinal wall signals a failure of the protective, mucosal lining of the gastrointestinal tract, as is consistently found in untreated celiac disease. Many of the same health and learning problems that are found in celiac disease are significantly overrepresented among those with gluten sensitivity for the very good reason that many of the same proteins are being leaked into the blood of those with gluten sensitivity. Our cultural obeisance to grains is at odds with the remains of ancient humans. Archaeologists have long recognized that grains are a starvation food—one for which we are not well suited. Grains result in consistent signs of disease and malnourishment in every locale and epoch associated with human adoption of grain cultivation. Grains are a poverty food. As we increase our grain consumption, we cause deficiencies in other nutrients by overwhelming the absorptive and transport mechanisms at work in our intestines. For instance, diets dominated by grains have been shown to induce iron deficiency22—a condition that is widely recognized as causing learning disabilities23-29. This should not be surprising since iron is the carrier used to distribute oxygen throughout our bodies, including various regions of our brains. There is little room to dispute the hazards to learning posed by reductions in oxygen supply to the brain. Iron deficiency reduces available oxygen in the brain, revealing yet another dimension of gluten grains as mediators of learning difficulties. There is more. The impact of grain consumption on our blood sugar levels is yet another facet of its contribution to learning problems. We evolved as hunter-gatherers, eating meats, and complex carbohydrates in the form of fruits, vegetables, and seeds. Refined sugars were a rare treat wrested from bees with some difficulty. At best, it was a rare treat for our pre-historic ancestors. Today, with unprecedented agricultural/industrial production of refined sugars along with cultivation and milling of grain flours, these products have become very cheap and available, particularly over the last fifty years. During that time, we have added enormous quantities of grain-derived starches to the overwhelming quantities of sugar we consume. The result of this escalating dietary trend may be observed in the current epidemic rates of Type 2 diabetes, hypoglycemia, obesity, and cardiovascular disease. In the classroom, we see these trends manifest in students mood swings, behavioral disorders (fluctuating between extreme lethargy and hyperactivity), chronic depression, forgetfulness, and muddled thinking—all of which reflects the inordinate, counter-evolutionary burden placed on many homeostatic systems of the body, particularly those related to blood sugar regulation. The pancreas has many functions. One important activity of the pancreas is to stabilize blood sugar levels. When blood sugar is not well regulated, learning is impaired30. The pancreas secretes carefully monitored quantities of glucagon and insulin. The pancreas responds to the presence of proteins, sugar, and starch in the digestive tract by producing insulin. It produces glucagon in response to fats. The balanced presence of both of these hormones in the bloodstream is critical to learning because they regulate the transport of nutrients into cells. Too little or too much insulin can cause blood sugar levels go out of control inducing a wide range of symptoms. Today, when the insulin/glucagon balance goes awry, it is frequently due to insulin overproduction due to a diet dominated by sugars and starches. This overproduction is caused by chronic consumption of highly glycemic foods. The resulting elevated levels of insulin cause rapid movement of nutrients into cells, either for storage as fat, or to be burned as energy, causing increased activity levels, "hot spells", sweating, increased heart rate, etc. This energized stage requires a constant supply of sugars and starches to be maintained. Otherwise, it is soon followed by bouts of lethargy, light-headedness, tremors, and weakness, which are all signs of hypoglycemia or very low blood sugar levels. Despite having stored much of the blood sugars as fats, there is insufficient glucagon to facilitate its use for energy. As this condition progresses, and as blood sugar levels plummet, periods of irrational anger and/or confusion often result. These moods often result from adrenaline secreted to avoid a loss of consciousness due to low blood sugar levels. The next step in the progression, in the absence of appropriate nutritional intervention, is lapsing into a coma. In the short term, the answer to these fluctuations is more frequent consumption of sugars/starches. However, the long term result of such an approach is either a state of insulin resistance, where more and more insulin is required to do the same task, or a state of pancreatic insufficiency, where the pancreas is simply unable to keep pace with the demand for insulin. In either case, once this stage is reached, the individual may be diagnosed with type 2 diabetes. This disease has so increased among North Americans, particularly among children, that an autoimmune form of diabetes, previously called juvenile onset, had to be renamed to "Type 1 diabetes". By now, it will not surprise the reader to learn that Type 1 diabetes has also been shown to be significantly associated with gluten. Research reveals that there is considerable overlap between celiac disease and Type 1 diabetes. About 8% of celiacs also have Type 1 diabetes31-33, and 5-11% of Type 1 diabetics have celiac disease34-38. Further, Scott Frazer et al. have repeatedly shown, in animal studies, a causal, dose-dependent relationship between type 1 diabetes and gluten39-42. The growing reaction against gluten and other allergenic foods should not be confused with the several dietary fads of the 20th Century. The vegetarian perspective ignores the vitamin deficiencies that result from a strict vegetarian diet. The low-fat craze is another fad that has mesmerized the industrialized world for the last 30-40 years. Fortunately, this perspective has recently come under scrutiny. Despite having served as the driving force behind most physicians dietary recommendations during the last several decades, the low fat dictum is overwhelmingly being discredited by research reported in peer reviewed publications. Recognition and avoidance of allergenic and highly glycemic foods is a whole new trend that is based on scientific research and evidence. It reflects an improved understanding of the function of the gastrointestinal tract, the endocrine system, particularly the pancreas, and the immune system. Past dietary fads are consistently deficient in important nutrients that are necessary to our good health and survival. Further, they frequently contain substances that are harmful to us, such as the phytates that are abundantly present in whole grain foods, and interfere with absorption of many minerals. It is increasingly clear that grains, especially those that contain gluten, are contraindicated for human learning. The evidence is overwhelming. The mandate of eating to learn is learning to eat as our ancestors did. Ron Hoggan is an author, teacher and diagnosed celiac who lives in Canada. His book "Dangerous Grains" can be ordered here. References: Kozlowska, Z: (1991). Results of investigation on children with coeliakia treated many years with glutethen free diet Psychiatria Polska. 25(2),130-134. Paul, K., Todt, J., Eysold, R. (1985) [EEG Research Findings in Children with Celiac Disease According to Dietary Variations]. Zeitschrift der Klinische Medizin. 40, 707-709. Grech, P.L., Richards, J., McLaren, S., Winkelman, J.H. (2000) Psychological sequelae and quality of life in celiac disease. Journal of Pediatric Gastroenterology and Nutrition 31(3): S4 Reichelt, K., Sagedal, E., Landmark, J., Sangvic, B., Eggen, O., Helge, S. (1990a). The Effect of Gluten-Free Diet on Urinary peptide Excretion and Clinical State in Schizophrenia. Journal of Orthomolecular Medicine. 5(4), 169-181. Reichelt, K., Ekrem, J., Scott, H. (1990b). Gluten, Milk Proteins and Autism: DIETARY INTERVENTION EFFECTS ON BEHAVIOR AND PEPTIDE SECRETION. Journal of Applied Nutrition. 42(1), 1-11. Reichelt, K., Knivsberg, A., Lind, G., Nodland, M. (1991). Probable etiology and Possible Treatment of Childhood Autism. Brain Dysfunction. 4, 308-319. Hoggan, R. (1997a). Absolutisms Hidden Message for Medical Scientism. Interchange. 28(2/3), 183-189. Caterson ID, Gill TP. Obesity: epidemiology and possible prevention. Best Pract Res Clin Endocrinol Metab. 2002 Dec;16(4):595-610. Hennessy AR, Walker JD.Silent hypoglycaemia at the diabetic clinic. Diabet Med. 2002 Mar;19(3):261. Kue Young T, Chateau D, Zhang M. Factor analysis of ethnic variation in the multiple metabolic (insulin resistance) syndrome in three Canadian populations.Am J Human Biol. 2002 Sep-Oct;14(5):649-58. Wahab PJ, Meijer JW, Dumitra D, Goerres MS, Mulder CJ. Coeliac disease: more than villous atrophy.Rom J Gastroenterol. 2002 Jun;11(2):121-7. Catassi C, Ratsch IM, Gandolfi L, Pratesi R, Fabiani E, El Asmar R, Frijia M, Bearzi I, Vizzoni L. Why is coeliac disease endemic in the people of the Sahara?Lancet. 1999 Aug 21;354(9179):647-8. Langleben DD, Acton PD, Austin G, Elman I, Krikorian G, Monterosso JR, Portnoy O, Ridlehuber HW, Strauss HW. Effects of Methylphenidate Discontinuation on Cerebral Blood Flow in Prepubescent Boys with Attention Deficit Hyperactivity Disorder.J Nucl Med. 2002 Dec;43(12):1624-1629. 2: Kim BN, Lee JS, Shin MS, Cho SC, Lee DS. Regional cerebral perfusion abnormalities in attention deficit/hyperactivity disorder Statistical parametric mapping analysis. Eur Arch Psychiatry Clin Neurosci. 2002 Oct;252(5):219-25. Lou, H., Henriksen, L., Bruhn, P. (1984). Focal cerebral hypoperfusion in children with dysphasia and/or attention deficit disorder. Archives of Neurology. 825-829. De Santis A, Addolorato G, Romito A, Caputo S, Giordano A, Gambassi G, Taranto C, Manna R, Gasbarrini G. Schizophrenic symptoms and SPECT abnormalities in a coeliac patient: regression after a gluten-free diet. J Intern Med. 1997 Nov;242(5):421-3. Knivsberg AM. Urine patterns, peptide levels and IgA/IgG antibodies to food proteins in children with dyslexia.Pediatr Rehabil. 1997 Jan-Mar;1(1):25-33. Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 43-1988. A 52-year-old man with persistent watery diarrhea and aphasia.N Engl J Med. 1988 Oct 27;319(17):1139-48. Hadjivassiliou M, Boscolo S, Davies-Jones GA, Grunewald RA, Not T, Sanders DS, Simpson JE, Tongiorgi E, Williamson CA, Woodroofe NM. The humoral response in the pathogenesis of gluten ataxia. Neurology. 2002 Apr 23;58(8):1221-6. Hadjivassiliou M, Grunewald RA, Davies-Jones GA. Gluten sensitivity as a neurological illness.J Neurol Neurosurg Psychiatry. 2002 May;72(5):560-3. Review. Husby, V., Jensenius, C., Svehag, S.(1985). Passage of Undegraded DietaryAntigen into the Blood of Healthy Adults. Scandinavian Journal of Immunology. 22, 83-92. Ma A, Chen X, Zheng M, Wang Y, Xu R, Li J. Iron status and dietary intake of Chinese pregnant women with anemia in the third trimester. Asia Pac J Clin Nutr. 2002;11(3):171-5. Kapil U, Bhavna A. Adverse effects of poor micronutrient status during childhood and adolescence. Nutr Rev. 2002 May;60(5 Pt 2):S84-90. Review. Youdim MB, Yehuda S. The neurochemical basis of cognitive deficits induced by brain iron deficiency: involvement of dopamine-opiate system. Cell Mol Biol (Noisy-le-grand). 2000 May;46(3):491-500. Otero GA, Aguirre DM, Porcayo R, Fernandez T. Psychological and electroencephalographic study in school children with iron deficiency. Int J Neurosci. 1999 Aug;99(1-4):113-21. Guesry P. The role of nutrition in brain development. Prev Med. 1998 Mar-Apr;27(2):189-94. Review. Bruner AB, Joffe A, Duggan AK, Casella JF, Brandt J. Randomised study of cognitive effects of iron supplementation in non-anaemic iron-deficient adolescent girls. Lancet. 1996 Oct 12;348(9033):992-6. Soewondo S. The effect of iron deficiency and mental stimulation on Indonesian childrens cognitive performance and development. Kobe J Med Sci. 1995 Apr;41(1-2):1-17. McCarthy AM, Lindgren S, Mengeling MA, Tsalikian E, Engvall JC. Effects of diabetes on learning in children. Pediatrics. 2002 Jan;109(1):E9. Bertini M, Sbarbati A, Valletta E, Pinelli L, Tato L. Incomplete gastric metaplasia in children with insulin-dependent diabetes mellitus and celiac disease. An ultrastructural study.BMC Clin Pathol. 2001;1(1):2. Schuppan D, Hahn EG. Celiac disease and its link to type 1 diabetes mellitus.J Pediatr Endocrinol Metab. 2001;14 Suppl 1:597-605. Holmes GK. Coeliac disease and Type 1 diabetes mellitus - the case for screening.Diabet Med. 2001 Mar;18(3):169-77. x Saukkonen T, Vaisanen S, Akerblom HK, Savilahti E. Coeliac disease in children and adolescents with type 1 diabetes: a study of growth, glycaemic control, and experiences of families.Acta Paediatr. 2002;91(3):297-302. Spiekerkoetter U, Seissler J, Wendel U. General Screening for Celiac Disease is Advisable in Children with Type 1 Diabetes.Horm Metab Res. 2002 Apr;34(4):192-5. Barera G, Bonfanti R, Viscardi M, Bazzigaluppi E, Calori G, Meschi F, Bianchi C, Chiumello G. Occurrence of celiac disease after onset of type 1 diabetes: a 6-year prospective longitudinal study.Pediatrics. 2002 May;109(5):833-8. Hansen D, Bennedbaek FN, Hansen LK, Hoier-Madsen M, Hegedu LS, Jacobsen BB, Husby S. High prevalence of coeliac disease in Danish children with type I diabetes mellitus.Acta Paediatr. 2001 Nov;90(11):1238-43. Aktay AN, Lee PC, Kumar V, Parton E, Wyatt DT, Werlin SL. The prevalence and clinical characteristics of celiac disease in juvenile diabetes in Wisconsin.J Pediatr Gastroenterol Nutr. 2001 Oct;33(4):462-5. MacFarlane AJ, Burghardt KM, Kelly J, Simell T, Simell O, Altosaar I, Scott FW. A type 1 diabetes-related protein from wheat (triticum aestivum): cDNA clone of a wheat storage globulin, Glb1, linked to islet damage.J Biol Chem. 2002 Oct 29. Scott FW, Rowsell P, Wang GS, Burghardt K, Kolb H, Flohe S. Oral exposure to diabetes-promoting food or immunomodulators in neonates alters gut cytokines and diabetes.Diabetes. 2002 Jan;51(1):73-8. Scott FW, Cloutier HE, Kleemann R, Woerz-Pagenstert U, Rowsell P, Modler HW, Kolb H. Potential mechanisms by which certain foods promote or inhibit the development of spontaneous diabetes in BB rats: dose, timing, early effect on islet area, and switch in infiltrate from Th1 to Th2 cells.Diabetes. 1997 Apr;46(4):589-98. Scott FW. Food-induced type 1 diabetes in the BB rat.Diabetes Metab Rev. 1996 Dec;12(4):341-59. Of Relevant interest: Gormanous M, Hunt A, Pope J, Gerald B. Lack of knowledge of diabetes among Arkansas public elementary teachers: implications for dietitians. J Am Diet Assoc. 2002 Aug;102(8):1136-8.
  9. Celiac.com 05/17/2010 - Scott Adams and Ron Hoggan went on live radio last Saturday on the Love By Intuition Show with host Deborah Beauvais (Dreamvisions 7 Radio Network) in support of Celiac Disease Awareness Month. The show is broadcast live from Boston, MA on 1510 AM Revolution Boston, a progressive 50,000-watt station reaching 5 states locally, and on Energy Talk Radio in San Francisco, and it reaches over 1,000,000 listeners. The show will be re-broadcast several times and will hopefully reach many more listeners. The podcast is attached and can be downloaded or listened to from our server. Dreamvisions 7 Radio Network is holistic healing radio network with an eclectic group of radio hosts all with the common goal to help humankind by offering different modalities or programs combined with tools to bring awareness, joy and love to their listeners. Their vision is to continue to syndicate the Network of shows by having additional affiliates both terrestrial and Internet.
  10. This article appeared in the Autumn 2005 edition of Celiac.coms Scott-Free Newsletter. Celiac.com 01/11/2006 - There is an abundance of stories about people who begin a gluten-free diet, find that they feel better then decide they want a firm diagnosis of celiac disease. They are facing several problems. First, they may be gluten sensitive without the intestinal lesion of celiac disease. This is very likely since about twelve percent of the population is gluten sensitive, but only a little more than one percent of the general population has celiac disease. Another problem faced by gluten-free individuals who want a diagnosis is that it can take more than five years after returning to a regular gluten-containing diet before the characteristic damage of celiac disease can be seen on a biopsy1. Simply put, after beginning a gluten-free diet, only a positive biopsy is meaningful. A negative biopsy does not rule out celiac disease. A variety of opinions have been offered regarding how much gluten, for how long, should result in a definitive biopsy. The reality is that no such recommendation is consistent with the medical literature1-4. Some people with celiac disease will experience a return of intestinal damage within a few weeks of consuming relatively small amounts of gluten. Such brief challenges are valuable for these individuals. However, many people with celiac disease or dermatitis herpetiformis will require much larger doses of gluten, over much longer periods, to induce characteristic lesions on the intestinal wall. Unfortunately for these latter individuals, a negative biopsy after a brief gluten challenge can, and often is, misinterpreted as having ruled out celiac disease. Blood tests can compound this problem. If, as seems likely, celiac patients who are slow to relapse are also the ones who develop milder intestinal lesions, they are the very celiac patients for whom blood tests are very unreliable5. Claims to have ruled out celiac disease based on brief challenges with small quantities of gluten is a mistake that could lead to serious, even deadly, consequences. We may forget that gluten consumption by a person with celiac disease can lead to deadly cancers and a variety of debilitating autoimmune diseases. Any recommendation of a gluten challenge should be accompanied by a clear warning that the process may overlook many cases of celiac disease. The absence of such warnings is inexcusable. And what about non-celiac gluten sensitivity? The absence of an intestinal lesion does not rule out gluten induced damage to other tissues, organs, and systems. Evidence and research-based information in this area is sadly lacking but we do know that undigested or partly digested gliadin can damage a wide range of human cells6. Thus, one need only be consuming gluten and experience increased intestinal permeability for gluten-induced damage to be a factor in an almost infinite number of ailments. There are several partial answers to this problem. One, which Ive raised before, is to employ Dr. Michael N. Marshs rectal challenge for the diagnosis of celiac disease, particularly when the individual has already begun a gluten-free diet. This test permits a definitive diagnosis of celiac disease for up to six months after beginning a gluten-free diet. That would catch a great number of celiac patients who have found relief through a gluten-free diet and now want a diagnosis. Another piece of this puzzle is to test for IgG anti-gliadin antibodies. Although these antibodies are considered "non-specific," they inarguably identify an immune response to one of the most common foods in a regular North American diet. Although these individuals may experience improved wellness on a gluten-free diet, we just dont know enough about non-celiac gluten sensitivity to do more than recommend that they continue on this diet since it makes them feel better. Ron Hoggan is an author, teacher and diagnosed celiac who lives in Canada. His book "Dangerous Grains" can be ordered at Celiac.com. Rons Web page is: www.DangerousGrains.com. References: Kuitunen P, Savilahti E, Verkasalo M. Late mucosalrelapse in a boy with coeliac disease and cows milk allergy.Acta Paediatr Scand.1986 Mar;75(2):340-2. Bardella MT, Fredella C, Trovato C, Ermacora E, Cavalli R, Saladino V, Prampolini L. Long-term remission in patients with dermatitis herpetiformis on a normal diet. Br. J. Dermatol. 2003 Nov;149(5):968-71. Shmerling DH, Franckx J. Childhood celiac disease: a long-term analysis of relapses in 91 patients.J Pediatr Gastroenterol Nutr. 1986 Jul-Aug;5(4):565-9. Chartrand LJ, Seidman EG. Celiac disease is a lifelong disorder. Clin Invest Med. 1996 Oct;19(5):357-61. Rostami K, Kerckhaert J, von Blomberg BM, Meijer JW, Wahab P, Mulder CJ. SAT and serology in adult coeliacs, seronegative coeliac disease seems a reality.Neth J Med. 1998 Jul;53(1):15-9. Hudson DA, Cornell HJ, Purdham DR, Rolles CJ. Non-specific cytotoxicity of wheat gliadin components towards cultured human cells.Lancet. 1976 Feb 14;1(7955):339-41.
  11. The following piece was written by Ronald Hoggan who is a teacher at Queen Elizabeth High School in Calgary, Alberta, Canada. There is much evidence linking untreated celiac disease with malignancy. I have recently been notified of publication of a report I have written on that connection, which is promised for the September, 1997 issue of Medical Hypotheses (1). In that report, I combine a review of the literature with an outline of a possible biochemical pathway whereby psychoactive peptides derived from the pepsin digests of wheat, rye and barley may down-regulate the activation of natural killer cells, the bodys first line of defense against malignancy. This is not a postulation that glutinous grains are carcinogenic. Humankind has been exposed to carcinogens throughout its ~ two million year evolution. But it is only in recent centuries that malignancy has increased exponentially, and has struck so many children and adolescents. This is clearly a counter-evolutionary trend when youngsters are afflicted, because the incidence should be decreasing over time, as these youngsters genes are being pruned from the gene pool. There is some evidence that has come to light since my aforementioned report, which will be of interest to celiacs and members of their families. M. Stanislas Tanchou, a truly visionary physician, and campaigned with Napoleon Bonaparte, presented a paper to the Paris Science Society in 1843, which was a complex statistical examination of malignancy, offering evidence of increased malignancy with increased civilization (2). One of the prime indicators of a civilizing trend was a diet that included cereal grains. The greater the consumption of these foods, the greater the incidence of malignancy (3). Dr. Chris Reading, an orthomolecular psychiatrist, in Australia, has documented the treatment of five cancer patients for depression (4). His testing for food allergies, and subsequent treatment of depression with dietary exclusion of cereal grains resulted in total remission of the cancers (which were also given conventional treatments) in all five patients he reports treating. One of these patients did die, but that was from the cancer treatment. There are also two reports in the Journal of Clinical Gastroenterology (5) Lancet (6) that I cite in my Medical Hypotheses article. These reveal a total remission of malignancy in each patient. One report then recants the original diagnosis, and identifies the correct diagnosis as lymphadenopathy. In the other report, which spurs a heated debate, the original diagnosis is supported by a resected section of malignant bowel, and there can be no doubt as to the correct diagnosis. Further, in a 1977 report, in Nutrition and Cancer (8), from Stanford University, all the children suffering from radiation and chemotherapy damage to the small bowel recovered fully from their chronic enteritis, and suffered no relapse of either the bowel obstruction or the disease. The treatment they were given was a gluten-free, dairy-free, low fat, low residue diet. In an obscure Czech journal, a report has recently indicated that one or more of the gliadins, a sub-set of proteins in gluten, may also interfere with natural killer cell activation in peripheral blood (9). They tested the levels of natural killer cell activation in normal, and in treated celiacs, and found no significant difference. BUT, after 30 minutes exposure of the celiacs blood to gliadin, there was a reduced activation of natural killer cells. For the last hundred years, billions of dollars have been spent identifying carcinogens. Most of what we encounter in our environment appears to have some measure of carcinogenic potential. Unfortunately, we have failed to reconcile that Humanity has been exposed to most of these carcinogens throughout its evolution. Conventional wisdom has pointed to the increasing levels of chemical pollution and environmental damage. And I do not doubt that these factors are contributing to the current epidemic of malignancy. What I do doubt is that segment of the population, variously reported at 20% to 30%, which has the HLA factors which predispose to celiac disease and many other autoimmune diseases, can mount an adequate immune response, with natural killer cells, against malignancy. References: Hoggan R, Considering Wheat, Rye, and Barley Proteins as Aids to Carcinogens in press Medical Hypotheses, 1997. Tanchou S, Statistics of Cancer London Lancet 1843; Aug 5, 593. Audette R, personal communication. Reading C, Meillon R, Your Family Tree Connection, Keats; New Canaan, Conn.: 1988. Wink A, et. al. Disappearance of Mesenteric Lymphadenopathy with Gluten-Free Deit in Celiac Sprue, J. Clin. Gastroenterol, 1993; 16(4): 317-319. Wright DH, et. al. Celiac disease and Lymphoma, Lancet 1991; 337:1373. Wright DH, et. al. letter Lancet 1991; 338: 318-319. Donaldson SS, Effect of Nutrition as Related to Radiation and Chemotherapy, Nutrition and Cancer, Winick ed. 1977; Wiley & Sons, NewYork, 137153. Castany M, Nguyen H, Pospisil M, Fric P, Tlaskalova-Hogenova H, Natural Killer Cell Activity in Celiac Disease: Effect of in Vitro Treatment on Effector Lymphocytes and/or Target Lymphoblastoid, Myeloid and Epithelial Cell Lines with Gliadin, Folia Microbial, 1995 (Praha) 40; 6: 615-620.
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