This file contains postings made by the following professionals: Stefano Guandalini, M.D--a professor of pediatrics at the University of Chicago; formerly with the University of Naples in Italy. Dr. Guandalini is involved in research on pathophysiology of intestinal transport, and has an interest in coeliac disease in children that is mainly clinical, leading to re-definition of diagnostic criteria in childhood. Karoly Horvath, M.D.--an associate professor of pediatrics at the University of Maryland at Baltimore. Dr. Horvath set up the Pediatric Gastrointestinal and Nutrition Laboratory, and is now director of this lab. Donald D. Kasarda, Ph.D.--a research chemist with the United States Department of Agriculture. Dr. Kasarda has worked on grain proteins in relation to grain quality for 30 years. He has colloborated with medical groups working on celiac disease for about 25 years and has often been used as an informal consultant by support groups. Joseph Murray, M.D.--a gastroenterologist at the University of Iowa, USA, where they have a mutidisciplinary service for the clinical care of people with celiac disease. They are also involved with clinical research and medical education related to celiac disease. Kalle Reichelt, M.D.--senior researcher at the Department of Pediatric Research, University of Oslo, Norway. Dr. Reichelt is looking into the impact of gluten intolerance on certain individuals with developmental delays. Phil Sheard, Ph.D.--researcher in the Developmental Biology Unit, Department of Physiology, University of Otago Medical School, in Dunedin, New Zealand. Other expert posting files are available. The naming convention is: Disclaimer: Verify this information before applying it to your situation. ========================================================================= Date: Wed, 3 Jul 1996 17:56:48 PDT From: "Donald D. Kasarda" (kasarda@PW.USDA.GOV) Subject: Re: oatrim With regards to: ) ...I think the findings are that "OATRIM" is used in meats, colas, and ) other formulated foods. The Beta Glucans are the specific derivative from ) "OATRIM" that has been placed in ice tea, fruit juice, sports drinks, and ) even wine. The process was developed at USDA's Midwest Area Northern ) Regional research center and is commercially supplied by ConAgra and Quaker ) Oats. ) ) It is supposed to be a benefit to normal humans. How it acts on the villa ) of those with Celiac Disease/Dermatitis Herpetiformis is not something I ) would deign to presume. AMS AMS is correct in her posting on oatrim to the best of my knowledge. I know the inventor of Oatrim and will try to find out how it is made and how likely it would be to have oat prolamins (or wheat prolamins) as a contamination (although oat prolamins may not be harmful to celiac patients). Don Kasarda ========================================================================= Date: Sat, 6 Jul 1996 18:28:04 -0400 From: Stefano Guandalini (Sguandal@AOL.COM) Subject: Re: return to normal villi Return of villi to normal after GF diet is a process that may take a variable amount of time. However, I believe 2 years has just never been reported! Actually, in the original ESPGAN protocol for diagnosis of CD, the lack of return to normal after 1 year of GFD was taken as a convincing proof that the cause of flat mucosa can not be CD. Possibilities are: 1) You are actually still eating gluten in some hidden form (Holy Communion? Other?) Normal blood work-up however (IF including anti-endomysium antibodies!) speaks against it. 2) Histology was not performed accurately. Sometimes it may happen that the specimen is improperly orientated or tangentially cut, leading to the false interpretation of a still flat mucosa. Believe me, it takes a very experienced pathologist to realize that the specimen may not be perfectly handled for interpretation. 3) You have another disease leading to flat mucosa. This is obviously a real possibility, although full clinical and laboratory remission (which I simply assume) after GFD are an indirect but sound evidence for CD. Other causes of flat mucosa include Crohn's, food allergy (but particularly in the first 2 years of life!), small bowel bacterial overgrowth, infection by Giardia Lamblia. Ask your doctor about these entities. As for Helicobacter pylori infection, this microrganism is known to be able to colonize only gastric mucosa, and is not a known cause for inflammation of duodenal-jejunal mucosa leading to shortening of villi. Hope to have been of some help! Stefano Guandalini ========================================================================= Date: Tue, 9 Jul 1996 10:25:56 EDT From: Bill Elkus (Bill_Elkus@JEFCO.COM) Subject: Re: DH diagnosis )From Karoly Horvath, MD at University of Maryland's celiac clinic: Date: 07/09/96 09:07:49 AM Subject: Re: DH diagnosis If the skin symptoms suggest DH, the diagnosis is based on two tests: 1. Skin biopsy: immunofluorescent staining - linear deposits of IgA. 2. Serology test: positive antiendomysium antibody test. As a compromise: the positive serology and the typical skin symptoms are enough for a clinical diagnosis. However, I think most of the dermatologist consider the biopsy as "gold standard" for the diagnosis. It seems that dermatologist needs some education regarding the DH diagnosis ("gluten-sensitive dermatopathy"; this is only my terminology) Karoly Horvath ========================================================================= Date: Wed, 10 Jul 1996 16:50:12 EDT From: Bill Elkus (Bill_Elkus@JEFCO.COM) Subject: Dr. Murray on Biopsies From: Murray @ intmed-po.int-med.uiowa.edu Date: 07/10/96 "Negative biopsies" may be reported in a celiac patient due one of several reasons. -- The patient may already have been on a GFD -- The disease may be somewhat patchy therefore many would advocate doing 3-4 samples from the small intestine. -- The pathologist may not recognise subtle changes that can be due to celiac disease. -- There may be some other process such as peptic ulcer disease that may occur simultaneously and mask the celiac disease changes. Not medical advice Joe Murray ========================================================================= Date: Wed, 10 Jul 1996 16:45:47 EDT From: Bill Elkus (Bill_Elkus@JEFCO.COM) Subject: Dr Murray on complaints of bones hurting A forward from Dr Joe Murray about a prior question by Nadia )email@example.com): N)i'm writing mainly on my mom's behalf. she has been complaining that her N)bones hurt for over two years now, and nobody seems to be able to give a N)reasonable explanation. From: Murray @ ntmed-po.int-med.uiowa.edu Date: 07/10/96 08:43:36 AM This may be due to osteoporosis due to loss of bone mineral. This can result in fractures or even sponteneous collapse of vertebra leading to compression of nerve roots and severe pain. Osteomalacia , also can occur though I think it is less common in US patients due to high intake of vitamin D and sunlight. This can result in pseudofractures in the hips, pelvis, spine and shouldres with significant pain and weakness especially climbing stairs or getting out of a low chair. Vitamin D deficiency can also result in a skin pain syndrome. It is possible that these changes could progress in diagnosed celiac due to poor vit D intake and low calcium intake especially if they are milk in tolerant. There are many other reasons one could have bone pain, from injuries, arthritis, lupus and malignancies. A careful phyical , biochemical and radiographic examination may be warranted. Not medical advice ========================================================================= Date: Thu, 11 Jul 1996 10:43:25 PDT From: "Donald D. Kasarda" (kasarda@PW.USDA.GOV) Subject: Oatrim Comments from Don Kasarda, Albany, CA I have talked with the inventor of Oatrim about what it is and how it is prepared. The main constituent of this fat replacement product is carbohydrate, specifically malto-dextrins from oats. These are prepared by fungal amylase digestion of the starch in oats. Although there is not likely to be much contamination from oat proteins in the final product, slight contamination cannot be ruled out. It would require some extensive research work to devise a method for measuring oat proteins or peptides at very low levels in the final product--and there may be none there. Because Oatrim is likely to be incorporated as a minor component of a food product, at most in 1:4 ratio with other constituents, this further diminishes the amount of oat proteins or peptides that might turn up in the final product. However, anyone who is allergic to oats may wish to avoid Oatrim. If there is any wheat contamination of the oats used to make the product, then wheat proteins or peptides might also make it into the final product, but because the amount of such contamination is likely to be very small, the chances for wheat proteins or peptides being passed along is also very small, much smaller than the possibility for the presence of oat proteins or peptides. As for celiac patients, some may not wish to take a chance on products containing Oatrim. It seems likely to me that the risk is extremely small insofar as I think the data on oats (at least in pure form) being harmless to celiac patients look quite good. This is not to be considered medical advice. My comments are correct to the best of my knowledge, but I hope it is clear that absolute statements are not possible. ========================================================================= Date: Fri, 12 Jul 1996 12:24:42 -0400 From: Karoly Horvath (khorvath@UMABNET.AB.UMD.EDU) Subject: Re: Return to normal villi (fwd) Ronal Hoggan cited a paper published in 1988 showing an incomplete histological and functional recovery in adult patients with CD. I have no doubt that the conclusion of this paper was correct that time. However, it is important to emphasize that the authors did not have the opportunity to check the sctrictness of diet by measuring the antibody titers or the in vitro cell-mediated immune response to gluten in their patients. It is well known that the immunological alterations return to the normal within months. If they are still present it suggest gluten ingestion. If a found an incomplete recovery of intestinal structure and function in children, all these patients had positive in vitro immune response to gluten suggesting accidental gluten consumption. To clarify this question a new well designed study necessary, which proves that the examined patients group do not ingest gluten. I agree with Dr. Guandalini and I believe in a complete restoration of intestinal structure in patients on a really strict gluten-free diet. Karoly Horvath, M.D., Ph.D. Baltimore ========================================================================= Date: Tue, 16 Jul 1996 10:59:53 +0000 From: Phil Sheard (phil.sheard@STONEBOW.OTAGO.AC.NZ) Subject: Re: Let's hear it for sprue! Hi all, with many scientific definitions the real is often less interesting than the fanciful. "Sprue" is derived from the Dutch word "sprouw", meaning "a kind of tumour". Sorry to disappoint those who thought it may have a more interesting derivation. To be an even bigger wet blanket for those of you who have DH and thought "herpetiformis" might have something to do with lizards, in fact it means "resembling Herpes". cheers Phil Philip Sheard Developmental Biology Unit, Department of Physiology, University of Otago Medical School, Dunedin, New Zealand. Ph (64 3) 479-7344 Fax (64 3) 479-7323 ========================================================================= Date: Thu, 18 Jul 1996 21:05:19 PDT From: "Donald D. Kasarda" (kasarda@PW.USDA.GOV) Subject: Re: Lemon Grass Comments from Don Kasarda, Albany, California. Lemon grass, Cymbopogon citratus, is a member of the grass family. According to Hitchcock it is placed in the same tribe as sorghum and therefore I think it is not likely to contain any proteins harmful to celiac patients on the basis of plant classification. Lemon grass has not been specifically tested, however, and I make my judgement only on the basis of its position in the taxonomy. )Can anyone on the list tell me about GF status of lemon grass? Is it a member )of the grass family? ) )Mildred Oberkotter, New York City ========================================================================= Date: Wed, 24 Jul 1996 20:25:00 CST From: Murray@INTMED-PO.INT-MED.UIOWA.EDU Subject: RE diabetes and celiac disease, gastroparesis There is a definite incidence of celiac disease in type one diabetes in causcasians at least. Anywhere from of 3.3% to 10 % of people with type one diabetes willl have or develope celic disease. Any form of diabetes can lead to gastroparesis, usually after many years of diabetes. The symptoms can be similar in many ways, bloating after meals, abdominal pain. Diarrhea is not usually caused by the gastroparesis itself. ( diabetic diarrhea may occur as part of the the nerve damage caused by the lonGstanding diabetes). I have several patients who have diabetes, gastroparesis and celiac disease. Certainly identifying the celiac disease oftenn makes a big difference to the symptoms. Joe Murray Univ of Iowa Not medical advice ========================================================================= Date: Thu, 1 Aug 1996 04:58:32 EDT From: Bill Elkus (Bill_Elkus@JEFCO.COM) Subject: Dr. Horvath on Intussusception & CD Recently, there was a post asking about a possible relationship between Intussusception and Celiac. I asked Dr. Karoly Horvath, one of the directors of the Celiac clinic at University of Maryland, for his thoughts, which follow: Bill Elkus Los Angeles Dr. Horvath writes: Intussusception is a common cause of intestinal obstruction between 3 month and six years of age. Generally a segment of intestine goes into the other segment, the circulation is compromised, which may lead to necrosis. It occurs frequently after infection involving the distal small intestine and causing lymph node enlargement in this area. Up to 75 % of causes can be solved by barium enema studies, which is diagnostic and therapeutic. The remaining cases need surgery. Even after surgery the prognosis is good, there are no complications associated with the surgery. There are cases of recurrent intussusception, they may need a sugery. In my knowledge there is no association between celiac disease and intususception. ========================================================================= Date: Tue, 13 Aug 1996 09:58:41 PDT From: "Donald D. Kasarda" (kasarda@PW.USDA.GOV) Subject: Re: GF Fast Food I was very pleased to see this posting (appended) as I suspect that for the majority of all celiacs the concern about gluten contamination in products that are not likely to have any gluten (or minute amounts, as in drugs taken occasionally) is far too great. Don Kasarda )...as many on the list know many )fast food hamburgers are NOT "diluted with fillers which may be oats or )heaven knows what else" -- to say "almost all" is quite misleading. All )french fries are NOT coated with wheat nor cooked in "forbidden oils". ) Lastly, milk shakes are typically GF....As we have )seen from the many posts on this subject, all fast food is not bad, nor is )all fast food GF. Let's not make GF life more difficult than it already is! ========================================================================= Date: Fri, 16 Aug 1996 14:34:00 CST From: Murray@INTMED-PO.INT-MED.UIOWA.EDU Subject: Maximum tolerable gluten debate My opinion based on seeing a large number of patients with celiac disease both in Ireland and in the USA, is that there is a remendous variablity in sensitivity to gluten in patients. I am frequently asked what is the most gluten a patient can tolerate and get away with it. How often can they deliberately cheat on the diet and get away it? How do they know if they have overdone it? Therre are no absolutely good answers to these questions. This is a short and generalised summary of my answers If eating it makes you sick avoid it.( dont assume its gluten that makes you sick ; it could be lactose intolerance) If you know it has gluten ( like wheat bread, bagels etc) avoid it. Follow up with your doctor with some objective test such as a biopsy and or blood tests ( antibodies to gliadin or similar tests). If these show there is still a problem, you must ask yourself if you gluten free enough? There are people who are exquisitily sensitive to minute quantities of gluten but they make up the minority of people with CD. What is minute? for some it is vinegar, others malt flavoring, others think of minute as a small slice of bread( wheat that is) What I mean by minute is less than the codex alimentarius agreed amount. People are unique, in their make up, hence their reactions to things are different both in type and severity. Those with a professional interest in any topic have to make some general assumptions based on aggregate data, Individuals must make their own minds up as to what is best for them, obviously and hopefully gaining some benefit from the experiences of others that gone before and from observers like Don Kasorda and myself. Discussing celiac disease can evoke some emotive issues, and responses, that in the e-mail world are not qualified by tonal inflections in the voice or gestures or mannerisms of the face to face conversations. Netiquette is a whole new skill that is strange to most of us, and we are all learning. Get well Stay well and be happy This opinion is not medical advice Nor is it the opinion of the US Government, the State of Iowa, the University of Iowa, Joe Murray MD University of Iowa ========================================================================= Date: Mon, 19 Aug 1996 09:17:49 EDT From: Bill Elkus (Bill_Elkus@JEFCO.COM) Subject: Reichelt on Fanconi and Downs syndrome Forwarded with permission: To: Bill_Elkus@jefco.com From: K.L.Reichelt@rh.uio.no (Kalle Reichelt) Date: 08/19/96 04:39:59 PM EDT Subject: Downs syndrome Hi. I know nothing about the mechanisms causing the Fanconi syndrome.It is correct that there is s slight increasein the frequency of coeliac disease in Downs. More important though is the fact that without Downs syndrome more than 1/3 of the children have extremely high IgA antibodies against gliadin, gluten,lactoglobulin and casein as well as ovalbumin without endomycium antibodies being increased.(1,2) There is an inverse relationship size of the children and level of IgA to gliadin and gluten. C P Reading in Australia thinks that there is a causal relationship Downs because of the increase in antibodies found also by him (3). Ref: 1:Kanavin \ et al (1988) Immunological studies of patients with Down's syndrome. Acta med Scand. 224: 474-477. 2: Reichelt KL et al (1994) Increased levels of antibodies to food proteins in Down Syndrome. Acta Paed japon 36: 489-492. 3:Reading CM (1984) Down's syndrome:Is Gluten/Alpha-gliadin sensitivity/coeliac disease the cause? Int J Biosocial Res 6: 62-65. All the best Cheers TINY K. Reichelt Pediatric Research Institute N-0027 Oslo, Norway Tel: +47 22 86 90 45 Fax: +47 22 86 91 17 E-mail: K.L.Reichelt@rh.uio.no ========================================================================= Date: Tue, 20 Aug 1996 16:00:04 +0000 From: Phil Sheard (phil.sheard@STONEBOW.OTAGO.AC.NZ) Subject: Fanconi G'day from the southern hemisphere. I read with interest a recent posting by Tom Hennessy which described a possible link between Fanconi syndrome and other disorders of interest to this group. His description did not resemble my memory of the disease, so I looked it up in the American Medical Association Encyclopedia of Medicine (1989). This book describes the disease as a rare kidney disorder occurring mainly in childhood, in which various important nutrients and chemicals such as amino acids, phosphates, calcium and potassium are lost in the urine. This leads to failure to thrive. It describes a number of possible causes, including inheritance, drug side effects, and ingestion of heavy metals. I looked up the url which Tom listed in his posting,and this seems to back up the encyclopedia's description. I found no obvious direct links with other diseases, and no mention of the endocrine abnormalities, although another (unrelated) disease (Fanconi's anaemia) is a fatal anaemia which may have associated endocrine changes. Since the latter is fatal and usually results in early death, it would be reasonable for most of you to assume you don't have it. I offer this information to contribute to the discussion, and it is no way intended as a criticism of Tom Hennessy or his findings, I am not a medical practitioner and my findings are also open to dispute. Tom mentioned one other thing which I would like to expand upon, as a point of general interest. He said "..the *muscle proteins* one of which is myosin which controls the face and throat..". Most of you will be aware that meat is muscle. Those of you who eat meat do so because it is a good source of dietary protein. The major proteins in muscle are the contractile proteins actin and myosin, these are the molecules which use energy to produce work, and which allow you to move your limbs (among other things). So, myosin is in all muscle (in various forms, but myosin nonetheless), and is not specifically related to face or throat musculature. best wishes Phil Philip Sheard Developmental Biology Unit, Department of Physiology, University of Otago Medical School, Dunedin, New Zealand. Ph (64 3) 479-7344 Fax (64 3) 479-7323 ========================================================================= Date: Sat, 24 Aug 1996 17:37:04 PDT From: "Donald D. Kasarda" (kasarda@PW.USDA.GOV) Subject: Re: the real culprit )I was under the impression that because gluten is insoluble in water, it is )pretty difficult to digest for a significant number of persons. And our )digestive systems have not evolved as quickly as cereal domestication. )We started out as hunter/gatherers. Dr. Lutz' article provided by Don Wiss )suggests this explanation. I have not read the article referred to (Dr. Lutz), but as a scientist specializing in gluten proteins, I am fairly aware of nutritional research related to the gluten proteins. I am not aware myself of any scientific evidence that gluten proteins are difficult to digest--there is some evidence in the direction that they are easy to digest. Also, most gliadin proteins (at present considered the most active fraction of gluten) are only slightly soluble in water, but are fairly soluble in acidic solutions. There is a high concentration of hydrochloric acid in the stomach where initial breakdown of proteins by the protease enzyme pepsin (which has low specificity, breaking down many different amino acid linkages) begins. The ability to be digested by various proteases probably outweighs solubility considerations for gluten proteins. Proteins that start out insoluble rapidly become soluble as enzymes fragment them into smaller pieces. The gluten proteins appear to be adequately attacked by the array of proteases available in our gastrointestinal tracts. I think it is not likely that the basis of celiac disease lies in the digestibility of the gluten proteins, although I know of one scientist who disagrees with me on this. I think, however, that most scientists would agree with me. Man no doubt started out as a hunter and gatherer, but that doesn't necessarily mean that he lived off easily digested materials only. I would guess that a wide range of plant foods were gathered and consumed, varying according to type in the degree of ease with which they could be digested. It is certainly possible, even likely, that wild wheats were gathered for a long time before they began to be cultivated (about 10,000 years ago, although I doubt that any special evolution of the digestive tract was necessary to adapt to the eating of grains, at least once they were cooked. If I recall correctly the pertinent publications on the subject, it is thought by anthropologists that adherent glumes (characteristic of wild wheats and spelt) had to be removed from the grains by charring, then the wheat grain was stone ground in a mortar for preparation of something like a gruel or porridge by cooking in water. Don Kasarda, Albany, California ========================================================================= Date: Mon, 26 Aug 1996 09:02:44 -0400 From: khorvath@MEM.po.com Subject: Endomysial IgA Peter L. Warren's question: "Does anyone know the range for positive and negative test results for endomysial IgA ?" We are using different dilutions of patient serum and incubate them with tissue slides. Generally, a fluorescence at the dilution of 1:4 or 1:5 is considered as borderline positive. Any fluorescence in the tissue above this dilution indicates a real positive result. Most of our patients with CD or DH have a value higher than 1:32. Karoly Horvath, M.D., Ph.D. Associate Professor of Pediatrics Director, pediatric GI and Nutrition Laboratory University of Maryland at Baltimore Tel: 410-328-0812 Fax: 410-328-1072 ========================================================================= Date: Wed, 28 Aug 1996 09:30:28 PDT From: "Donald D. Kasarda" (kasarda@PW.USDA.GOV) Subject: Re: the real culprit (If active celiacs )DON'T have achlorhydria, how is it that the peptides reach the gut intact )enough to be antigenic?). This comes about because in all people digestion of proteins in the stomach is incomplete so that peptides and some intact proteins pass into the small intestine where digestion continues by pancreatic enzymes and enzymes associated with the brush border of the intestinal epithelium. Don Kasarda, Albany, CA ========================================================================= Date: Thu, 5 Sep 1996 23:08:58 -0400 From: Bill Elkus (Bill_Elkus@JEFCO.COM) Subject: The Coeliac Symposium - Day 1 The following is a report from the international Coeliac Symposium currently being held at Tampere, Finland. This event occurs once every 4 years, and is the most important gathering of researchers in our field. We are very fortunate to have two volunteers as our reporters: Dr. Joseph Murray from the Celiac clinic at the University of Iowa, who is attending the conference and calling in his reports, and Ann Whelan, who is transcribing, summarizing and editing them. Many of you know Ann Whelan as the editor of the GLUTEN-FREE LIVING newsletter. This is an excellent printed newsletter which covers important topics at a level of detail which is difficult to do on a listserv just as ours. It is also an excellent product to give to medical professionals to assist them in keeping up with this field. It is well researched, and includes quotes and/or articles by many well-respected clinicans and researchers in the Celiac field. One year of 6 issues is $29, two years is $49. International orders are $5 extra. A sample issue is $5.95. Four issues have been published so far, the fifth is about to appear). Order from Gluten-Free Living, P.O. Box 105, Hastings-on-Hudson, NY 10706. Ann plans on covering a few selected topics from the Tampere symposium in greater detail (and with additional sources) in future issues. Bill Elkus for the Listowners ---------Ann Whelan / Joe Murray report #1 follows------------- THE DAILY REPORT Hi, everybody. Although I am not currently on the Internet, I am pleased to be involved in this effort to get the word out as quickly as possible. After listening to Joe Murray talk about the conference, I can tell you that I'd love to be there -- as I'm sure most of us would prefer. Joe says he didn't take a head count in the hall, but it's packed and just about everyone who is anyone in the celiac community -- with very few exceptions -- is in attendance. Today's rundown is pretty descriptive. Time permitting tomorrow I will try to get a bit more depth. But I think in the following information, you'll find plenty of interesting developments. So, here we go... The first speaker, Dr. Jarmo Visakorpi, from Finland, gave an overview of CD and how it started out being thought of as a rare gi disease of children and not a common disease that occurs at all ages and may not be limited to the gi tract. Joe remembered one quote that he felt would be well worth repeating -- and you'll see why. Dr. Visakorpi said: "Many people call parts of the celiac iceberg by different names, but that's not important. It's more important to know the size of the iceberg and how it floats...In Sweden, the whole iceberg is floating. In other European countries, the tips of the iceberg are showing. But in the United States, the whole iceberg is submerged." Wow! I'd call that a great image... Dr. Luigi Greco, from Italy, spoke next. He talked about origins of cultivation and how wheat was the first cultivated plant, at least in the middle east. The cultivation of wheat allowed people to change from being nomads to being settled. The next big occurrence relative to cultivation was that people discovered they could ferment wheat and make beer! Dr. Greco went on to comment that in the western part of Europe, exposure to gluten has only occurred very recently in genetic terms, with little time having elapsed for the population to adapt genetically! Dr. Greco also commented on the perceived differences in incidence rates that we see quoted and suggested that these differences may be actually due to the different ages of onset in different populations and there really is little difference statistically between different measures --1 250 and 1 in 500, for example. Dr. Henry Asher from Sweden spoke next. He discussed the Swedish experience, which has shown an increased incidence among children that is different from other countries. Dr. Asher made several observations about the gluten content of commercial foods, which has gone up dramatically since cow's milk protein has been eliminated from formulas and replaced with gluten-containing material. He says the amount of gluten given to young children is correlated with the onset of symptomatic disease. He looked at gluten consumption in children: It's highest in Italy, next highest in Sweden, next is Finland and the next is Denmark and these levels of gluten consumption parallel the rise in symptomatic cd in children. Dr. Asher went on to observe that the diagnosis of cd is related to a shorter duration of breastfeeding, the earlier introduction of solid foods and a higher amount of gluten in the diet. He showed news clippings from Sweden, including one that said the Justice Minister in Sweden has a daughter who has cd and the minister has called for an outright ban on gluten-containing baby food! Not surprisingly, Joe says there was a lot of comment on this question. Some suggested the need to look for other factors for the change in childhood incidence. Also, if the amount of gluten given to children is reduced, they may develop not symptomatic CD but silent or delayed CD. Joe says it's too soon to decide what can be done with childhood dietary content, but that it seems reasonable to prolong breastfeeding and to reduce the amount of gluten in the child's diet. Dr. Carlo Catassi, from Italy, spoke about screening. He used a quote (not his own) that said screening should only be undertaken if there's a risk of complications and we can alter the natural history of the disease in a significant proportion of those screened. Dr. Catassi claims in Italy, CD is one of the commonest lifelong disorders. He suggested that for every one diagnosed CD individual in Italy, there may be 7 others who have asymptomatic disease. In Italy, they screened 17,501 students and came up with a high incidence. Dr. Martin Stern spoke about the standardization of screening tests. Joe said his talk was very technical about standardization (not screening) in Europe. One important point that he made of interest to laypeople is that these tests can either be set as screening tests or as diagnostic tests but not both at the same time. What makes a good screening test does not make a good diagnostic test. Dr. Stern said the normal cutoff point needs to be adjusted for whichever aim you have. Dr. Pekka Collin, from Finland, spoke about diagnostic strategy and how to find CD. He did it on the basis of several things: actively screening high risk groups, including first-degree relatives, and those with insulin dependent diabetes mellitus, rheumatologic problems, especially sjogrens syndrome, problems of infertility, thyroid disease, and neurologic disease. The second thing he does is have a service where he gives open access endoscopy to primary care doctors who refer patients for endoscopy. Third, is to biopsy the duodenum of all patients who are endoscoped. Dr. Collin went on to remark that the incidence of DH, which is an obvious condition, has been stable and unchanging over the years but the diagnosis of CD is increasing dramatically. Next were several short oral presentations not listed in the program. First, Dr. Ivarsson and colleagues from Sweden talked about different factors leading to cd in children. They mentioned the quantity of gluten, a shorter duration of breastfeeding and, interestingly Joe says, the socioeconomic status of those diagnosed. The lower the socioeconomic status, the greater the risk. Additionally, he found that those born in the summertime! have a greater risk and, of course, those genetically predisposed. Second, Dr. Hovdenak and his colleagues from Norway talked about blood donor screening. Joe said he thinks it's very interesting that he found a high incidence, 1 in 200, but did not find any difference in sex. Joe says that's different from symptomatic CD, which is predominately female. Third, Dr. Kaukinen from Finland looked at CD in patients who had positive antibody tests and normal architecture in the intestine. They show that many of these patients have some subtle changes in the intestine, but he's not sure yet what it means. (NOTE: The previous seems contradictory to me. I'll try to clarify tomorrow. Fourth, Dr. Bahedi from France talked about his findings that showed that only 43 percent of adult patients adhere to the GF diet. This was detected by biopsy and endomysial antibodies. He emphasized that when the antibodies are positive, patients are told they are not compliant, but if the antibodies are negative, it's not necessarily saying everything is okay. (NOTE: I'll see what else I can find out here tomorrow.) The next scheduled speaker, Dr. Anne Ferguson from the U.K., said that some people just eat a naturally low-gluten diet and that aspect needs to be considered when assessing for CD. She also talked about the latent forms of CD. Dr. Auricchio from Italy talked about patients who have symptoms due to gluten, but with normal biopsies. These people seem to have many differences from celiac patients. Dr. Auricchio suggested there may be different genes that determine sensitivity to gluten on one hand and the development of small bowel problems on the other. Dr. Lionel Fry from the U.K. talked about DH. He stated that all patients with DH have some degree of enteropathy, even though less than 1 in 10 patients with DH have GI symptoms. Dr. Fry also said 40 percent of DH relatives have gluten-sensitive enteropathy. He went on to say that the GF diet can take 6 months to two years to get healing of DH, and a relapse of the DH rash may take 2 to 12 weeks to occur after someone eats gluten. Total disappearance of IGA skin deposits may take up to 7 years after a GF diet is started. Dr. Reunala from Finland talked about associated diseases. He quoted others who said 5 to 14 percent of DH patients have thyroid disease and went on to say that DH patients have an increased incidence of lymphoma but a gf diet seems to protect against lymphoma. Dr. Holmes from the U.K. talked about malignancy in CD. He quoted that the is risk is between 0 and 7 percent, while in general it's 3 to 11 percent and this is reduced by being on a GF diet. Dr. Carazza from Italy talked about other conditions like refractory disease, hyposplenism, and something else, but there are no notes. Then there was a forum. Dr. Hallert talked about psychiatric illness in adult CD patients. He studied 180 CD patients and found that 22 percent had been to the psychiatric department prior to diagnosis of cd and the average time from going to the psychiatric department to the eventual diagnosis of CD was 14 years! (NOTE: I think I've got that right but think I should verify the figure tomorrow.) Dr. Hallert also said celiacs were four times as likely to be seen in the psychiatric department as the general population! He also went on to say that depression may occur after the CD diagnosis. Dr. Ventura from Italy talked about autoimmune disorders. He suggested it's more common in patients diagnosed later in life than those diagnosed in early childhood. Next, Dr. Murray himself presented information about seven patients who have duodenal strictures as a previously undescribed presentation/complication of CD. I'll see if I can get more information tomorrow, or perhaps it can wait until he returns. Dr. Bai, (sorry, don't know from where) described effects of the GF diet on bone density. Patients showed marked improvement in bone density with the GF diet, although it did not return to normal. The improvement was better in the spine than in the hip and better in the hip than elsewhere. Dr. Bai went on to say that premenopausal women did better than postmenopausal women. And that's it for today. I'll try to ask Dr. Murray more questions tomorrow, when he says the presentation might be much more technical. We were on the phone for a very long time just relaying the previous notes, which certainly provide a great deal of gluten-free food for thought! Talk to you tomorrow! ======================================================================== Date: Fri, 6 Sep 1996 23:53:00 EST From: James Lyles (firstname.lastname@example.org) Subject: The Coeliac Symposium - Day 2 )From an oral report by Dr. Murray; transcribed for the list by Ann Whelan, editor of the bi-monthly newsletter "Gluten-Free Living". To subscribe, write to P.O. Box 105, Hastings-on-Hudson, NY 10706. THE DAILY REPORT The big story today from Finland is oats. There were two talks and several posters presented about the topic. In the first talk, Dr. Risto Julkunen spoke about the Finnish five-year follow-up study in which oats were given to a population of well-controlled celiacs. They ingested an average of 34 grams, which is slightly over one ounce, daily for up to five years. The oats used in the study were specially grown and tested to be free of wheat, barley and rye. The researchers claim there was no difference in those allowed the oats and those who were not. There was a second study presented from Dublin, and reported by Dr. Conleth Feighery. This 12-week study looked at a small group of patients with healed CD to start with, who were given 50 grams of oats a day. Again, the oats were carefully screened and tested to make sure there was no contamination. After 12 weeks, no effect was seen on biopsy or through antibody tests. The researchers also took 2 of the 12 participants and did what they called a "micro challenge" of 500 milligrams of gluten a day. Both patients got reactions, so the researchers felt that at least two of the participants were sensitive celiacs -- and they still did not respond to the oats. A poster from Italy showed biopsies taken from celiacs that had been studied in the culture plate in the presence of oats, which did show some effect on the biopsies. In other words, tissue from biopsies from patients with treated CD were put in a plate and grown in the presence of oat protein, and the oat protein had an effect on the biopsies. This sounded odd, so I made sure I'd really understood what Joe reported and paraphrased: In other words, they're seeing no reaction from oats within the body in some studies but this one showed a reaction outside the body? "Yes," Joe said, "this of course is puzzling." Continuing on the oats issue, a series of short studies from several places also showed what the Finns had shown in the body, i.e., no problem in the short term. This is Joe's summary on Oats: Over the short term, in well-controlled, healed celiacs who are compliant in every other way, it may be safe for them to take oats that have been tested to be free of contamination of other grains. He also mentioned that there were a few studies showing that contamination of commercial oats may be common in several European countries. (NOTE: I went to Digestive Disease Week in May, where I met several Irish doctors who have studied oats. I would describe their strong beliefs about oats as very "adamant." They are adamant in believing that uncontaminated oats are safe for people with Celiac Disease. If all of this oats talk pans out as being acceptably correct to gluten-sensitive individuals in this country, that would seem to be pretty good news. Then, the next big challenge would be to figure out how gluten-sensitive people are going to get access to contamination-free oats. I, for one, will be all ears.) Moving on to other things: Dr. Paul Ciclitira spoke about in vivo gluten challenge and showed that one gram of gluten produces damage after only two hours. 100 milligrams, that's 1/10th gram, produced some damage or slow damage and 10 milligrams produced no damage. The limitations of studies such as this are that they are highly invasive and there may be some risk. Joe said, "You must leave a biopsy capsule down for 24 hours, so it's not a small deal." Dr. Luigi Maiuri from Italy described an in vitro testing of intestine biopsies that showed a response could be produced. Joe said this wasn't new but what was interesting was that the little pieces of tissue could produce endomysial antibodies when exposed to gluten. Dr. Riccardo Trancone from Italy talked about rectal mucosal response to gluten challenge. He said he could get a measurable response in treated celiac disease patients to gluten, which Joe said was new. Dr. Trancone also talked about the idea that there may be two separate genetic factors involved in CD. One causes the individual to be sensitized to gluten and the second one is involved at the stage of severe gut damage. His work was based on examination of CD family members who don't have CD. Dr. Michael Marsh described the effects of specific peptide sequences from gluten. He had done studies in only two patients. Dr. Marsh said it was very expensive to do tests of this kind because it's very expensive to make the peptide artificially. He estimated a figure of about $5,000 (dollars) to do one test in one patient. Don Kasarda's talk was very hypothetical, Joe said. Don suggested that Celiac Disease may be the result of a collision of two separately evolving processes, the first being the storage proteins in the grasses and the second being control proteins in animals. Both of these have similarities in their proline and glutamine content and could lead to molecular mimicry. An explanation of what he meant is apparently quite complex, and after trying to explain, we gave up. It all has something to do with getting your lines crossed -- and this is hypothetical. Don also talked about the possible peptide fragments responsible for Celiac Disease. In his second presentation, Dr. Paul Ciclitira talked about the potential for identifying small amounts of gluten in foods. Based on what he said in his earlier talk about in vivo challenge, he took 10 milligrams per 100 grams of protein content in food as being the cutoff or threshold. He said that most commercial oats products are contaminated with gluten. Cooking does not alter the toxicity. Dr. Ciclitira also commented about toaster contamination and said he sees about one patient a year who gets contamination from using the same toaster as the rest of the family. Dr. Ciclitira also commented on the Skerrit test, which tests for gluten in food (it's the Australian test). He has "strong reservation" about the test and thinks it's because the test identifies omega gliadins, which are a minor component of gluten so the test can give variable results. Apparently this test is available in Canada. Dr. Ciclitira also mentioned other types of tests that really may not be specific and may pick up other non-toxic grains but may not pick up rye or barley. This brought on a lot of discussion, Joe said. The proposed CODEX Alimentarius threshold for something to be called gluten free is 200 parts per million. That's equivalent to 20 milligrams of gluten in 100 grams of protein. (I'm afraid I can't provide any more information about this.) There was a lot of heated discussion, and a women who may be the President of the European Celiac Societies objected to the allowance of wheat starch. Dr. Ciclitira and others said wheat starch is allowed only because the patients demanded it! Someone else also estimated that the market for GF foods in Europe was 500 million dollars! Joe said that really surprised him. Someone else, perhaps Dr. Ciclitira, said the Vatican now allows wheat starch communion hosts. Sorry, no more information available at this time. Dr. Thomas MacDonald from the U.K., gave a very technical talk on a model system for gut damage. Dr. Erkki Savilahti from Finland spoke about the role of lymphocytes in latent forms of CD. Dr. Markku Maki talked about the possible role of the antibodies in causing changes in the intestine. Dr. Per Brandtzaeg from Norway, whose talk was on "Development of intestinal immunity and its relation to coeliac Disease," made some interesting comments about the mismatch of our genetic makeup and the environmental pressure in the modern world. Again, sorry, no more information at this time. Dr. Brandtzaeg did mention several reasons why breast milk is particularly good for infants and the development of the immune system in that it provides antibodies the baby cannot make that helps protect the intestinal and respiratory tracts. He also talked about other things that are important to the gut like bacteria, age, and possible allergies. Dr. Kagnoff's presentation on "MHC and Coeliac Disease was very technical. He reviewed part of the genetic background on tissue types and CD. Dr. Kagnoff said virtually all celiacs have a specific tissue type but many people with the type do not have CD. Dr. Ludvig Sollid from Norway gave a very technical talk about lymphocytes and, finally, Dr. Joseph Michalski from the United States described how he has identified a new gene site, a small area on chromosome 6 that may be where the other gene for CD is located. Joe said it was interesting and mentioned a "race to find that gene." Dr. Michalski does his work at the University of South Alabama and uses patient material from County Galway, Ireland. (NOTE: I've spoken to Dr. Michalski a few times recently about genetics and HLA typing for a small article that will be in the September/October issue of Gluten-Free Living. He is very interesting and said he might consider writing an article for the newsletter about genes and the search for same. I'll keep you posted, because I'm really anxious to see an article that even the brain challenged among us on things scientific can understand about the genetic mysteries of Celiac Disease.) That's it for today. The last report will be tomorrow. I suspect we will all be talking about the Finland conference for quite a long time. I'm sure I'm just like you in being real anxious to know more about some of this tantalizing information. ========================================================================= Date: Sat, 7 Sep 1996 18:58:33 -0400 From: Jim Lyles (lyles@TIR.COM) Subject: The Coeliac Symposium - Day 3 )From an oral report by Dr. Murray; transcribed for the list by Ann Whelan, editor of the bi-monthly newsletter "Gluten-Free Living". To subscribe, write to P.O. Box 105, Hastings-on-Hudson, NY 10706. DAILY REPORT The thir d, and final, session at the conference in Finland was shorter and less packed than the previous two, but it was also much more technical in some instances. The first morning session was devoted to diagnostic criteria and was divided into two parts: child and adult diagnosis. Dr. Walker-Smith from the U.K. discussed historical issues of how diagnostic criteria were first generated. It started with the three biopsies: an initial biopsy, a second showing healing and a third done after a gluten challenge. This was in 1969. More recent criteria put together in 1989 suggested that in many children, one biopsy could be enough if there were some evidence of clinical improvement, demonstrated by antibody improvement or in some clinical situation like symptoms or anemia. There were some exceptions to this: o in patients where the initial biopsy was not entirely flat. o where the first biopsy was done under the age of two. o in communities where there were other diseases that could cause a flat biopsy (such as parasite infection). o if there was any doubt about the original diagnosis. o in teenage patients who were going to go off the diet anyway. (Apparently the feeling was that teens wouldn't follow the diet, and if they were going to be non-compliant, they should be encouraged to do it in a controlled fashion with a biopsy done before they would go off on their own.) Another point was made (not by Dr. Walker-Smith) about a finding in eight non-compliant teens in whom there was a flat biopsy but the endomysial antibodies were negative! (Sorry, no more information on that.) Then there was a discussion about serologic tests, and the feeling was that the tests are not yet good enough and can't completely replace the need for a biopsy. In adult biopsies, another doctor felt that in many cases, two biopsies are necessary, one before the gluten-free diet and one after starting the diet. It was also noted that how reliable this would be would depend on whether there were other diseases occurring in the community that could mimic the first biopsy. The next discussion concerned a Finnish study that suggested it didn't matter where in the duodenum the biopsies were taken as long as they were taken. Dr. Ferguson (I think there may be two Dr. Fergusons and don't know which one) commented that doctors should be aware of the personal and financial cost of the biopsy and the hope that there could be some way to replace this procedure. Then a general discussion pretty much held that a certain number of biopsies are essential and there is not yet a zero biopsy option. They could not overemphasize the importance of doing a biopsy before beginning the gluten-free diet, and that there are still some patients in whom more than one biopsy is necessary. Joe said the rest of the morning presentations were pretty scientific. In the afternoon, Dr. Lloyd Mayer from New York talked about how the cells lining the intestine can or cannot take up different proteins. Joe described Dr. Mayer as "not a celiac person." (NOTE: Since Dr. Mayer is here in New York, where I am, I'm going to see what I can find out about how his research work relates to Celiac Disease.) Dr. Cerf-Bensussan from France talked about T cells and said there were some very unusual T cells present in the intestines of celiacs. She also commented about a group of French children who seemed to be doing okay clinically on a gluten-containing diet although they did have a prior diagnosis of CD, but the children did have an increased number of these unusual T cells, which are called gamma delta cells, in their intestines. Next, Dr. Hayday from Connecticut talked about gamma delta cells seen in the lining of the intestines of celiacs that seem to be important for regulating immune responses. Next, Dr. Cerf-Bensussan presented and talked about some unusual populations of lymphocytes in patients with refractory sprue. These cells may represent a premalignant condition. She showed that five patients with refractory sprue had these identical types of cells. Dr. Auricchio from Italy was the last individual presenter. He outlined the six topics that are the most important for future research: 1. Understanding the entire clinical spectrum of gluten sensitivity. 2. Identifying the damaging peptides. 3. What is the mechanism of the damage that occurs (I hope I have this one right; my notes were a bit obtuse). 4. The other (non HLA) genes that contribute to CD. 5. Developing an animal model. 6. Developing strategies of immune therapy. Following his talk, there was a broad-ranging discussion on different possibilities for research. Then, a panel discussion suggested that there are several stages in what ends up with CD, the first being the initiation of gluten sensitivity, about which very little is known. Second, was non- immune reactions to gluten, meaning that the T cells are important in the damage, but they are probably not the only process in the initiation phase. At this point, a comment was made that Joe says was worth repeating. Here it is, to the best of our abilities, although it's obviously not a direct quote: "Some of the response seen in the challenge studies happen too fast to be purely due to immune cells or T cells. It was suggested that there are further stages and what we see in CD is a stage that is further beyond initiation." Another comment was made that it's important to replicate studies that have been done in only one center and in only two or three patients. Joe then summarized what he thought were the most exciting aspects of the conference: 1. The searches for the other non HLA genes. 2. The description of very early or possibly non-immune response to gluten. 3. The suggestion of non-gastrointestinal involvement (apparently some posters described early changes in the gut within one to two hours of a challenge (I'm not sure I have that absolutely correct). 4. That it seems as if major progress has been made in understanding the mechanism that causes the damage in the intestine. I asked about incidence, our perennial U.S. question, and Joe said there were several posters showing that in almost every place that was studied, the prevalence varies from between 1 in 100 to 1 in 500. In this regard, Dr. Fasano's Baltimore blood donor study was one of those presented. Here's the situation regarding publication of the material from Finland: There will be a book that will include all the presentations of all the invited speakers, which means they will not be on the internet. (Some of the studies already have been published elsewhere, so they are available in print.) Apparently there was some discussion of this, but Joe emphasized that studies will not be accepted by the scientific community unless they are subjected to the usual peer review process. And that's it ... the Finnish conference has ended. I'm sure there will be plenty to talk about over the next four years and plenty of leads to be investigated. I, personally, look forward to finding out more about many of the items discussed over the last three days. It was a pleasure to be able to reach so many people with this information and, especially, to work with Joe Murray. I should add that he was positively heroic in his efforts to transmit this information in such a timely fashion, and I think, as always with Joe, we all owe him an enormous debt of gratitude. -- Ann Whelan ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ )From the listowners: The listowners would like to express our appreciation to Dr. Murray for his efforts to keep the list informed. These reports were thorough, enlightening, and represented significant effort on his part in taking notes and transcribing them over the phone to Ann Whelan. We also want to thank Ann Whelan for her excellent job of capturing the information Joe relayed to her and turning it into three well-worded reports. Finally, we also appreciate the efforts of Sue Goldstein, who took Ann's reports and placed them on-line for our benefit. This truly was a team effort, from which we all benefitted. For the Listowners, Jim Lyles ........ (email@example.com) ........ Holly, Michigan, US) ========================================================================= Date: Wed, 18 Sep 1996 22:43:30 -0400 From: Karoly Horvath (khorvath@UMABNET.AB.UMD.EDU) Subject: Gliadin in pharmaceutical products I would like to make a correction. The cited paper was published in July 1994 from the Duke University. (Miletic et al. Identification of gliadin presence in pharmaceutical products. Journal of Pediatric Gastroenterology and Nutrition 1994; 19:27-33) They analyzed 59 prescription and non-prescription medications and summarized their results in a table. Their list included cold medications, pain-killer medications and medications used for gastrointestinal problems etc It is important to know that Lactase enzyme supplement (Dairy Ease) had gluten in both their tablet and drop form. Furthermore, Gas-X (simethicone), Pepcid (Famotidine), Tagamet (Cimetidine) also contained gliadin. Karoly Horvath, M.D., Ph.D. Associate Professor of Pediatrics University of Maryland at Baltimore Tel: 410-328-0812 Fax: 410-328-1072 ========================================================================= Date: Thu, 19 Sep 1996 08:59:05 PDT From: "Donald D. Kasarda" (kasarda@PW.USDA.GOV) Subject: Glutamine Glutamine is an amino acid. It is the major amino acid in wheat gluten proteins, making up 30-55% of the amino acids in these proteins. In itself and not as part of a protein or peptide, it is apparently harmless to celiac patients on the basis of one early paper. If the product in question includes only the purified amino acid and no proteins or peptides derived from wheat, it would not be harmful to celiac patients. The acid hydrolysis product of glutamine is glutamic acid, essentially the same as MSG. I do not know how large amounts of glutamine taken as the pure amino acid would affect humans, but I am fairly sure it would not trigger celiac disease in the strict sense. Don Kasarda, Albany, CA )...Can someone please explain the significance of glutamine. ========================================================================= Date: Tue, 24 Sep 1996 09:34:37 +0000 From: Phil Sheard (firstname.lastname@example.org) Subject: marmite Hi all, New Zealand dietitians maintain a register of commercial foods and their ingredients (using information supplied by the manufacturers), and this is called the NZ therapeutic database. From that database they supply the NZ coeliac society with a list of all commercial gluten free food products currently available in NZ, and the society sends the list to its members. The May 1996 list does not include Marmite, so NZ coeliacs would generally assume it not to be GF (although I have not called Sanitarium, the manufacturer, to check). However, a similar product, Vegemite (manufactured by Kraft) is included in the list, and is regularly consumed by my coeliac daughter with no ill-effects. Another beef/yeast extract (Bovril) is also included in the GF list. Some of you may also be interested in the following, which is included in the introduction to the GF foods booklet: "For the purposes of the GF list the criteria used for GF is that defined in the current New Zealand Food Regulations: When food products contain ingredients derived from wheat, triticale, rye, barley, and oats the nitrogen content of those ingredients shall not exceed 0.05 percent calculated as nitrogen on a dry weight basis; Starches prepared from gluten containing cereals are not considered to contain gluten if there is less than 0.3 percent protein in the dry matter." cheers Phil Philip Sheard Developmental Biology Unit, Department of Physiology, University of Otago Medical School, Dunedin, New Zealand. Ph (64 3) 479-7344 Fax (64 3) 479-7323 ========================================================================= Date: Tue, 24 Sep 1996 10:17:49 PDT From: "Donald D. Kasarda" (kasarda@PW.USDA.GOV) Subject: Re: Spelt Flour Spelt is wheat and nothing all thqt unusual about it beyond the adherent glumes, which represents a gene or two difference from normal bread wheat. There are slight variations in analysis of any given sample in comparison with an arbitrary sample or samples of bread wheat, but these differences don't impress me. It may have a slightly different flavor from normal bread wheat, as does durum wheat. I don't know about this as I have never eaten spelt although I have worked with it in the laboratory. On the basis of my experience in blind testing of someone with allergy who felt they could eat spelt, I would say that spelt is not suitable for use by people allergic to wheat and certainly is not suitable for anyone with celiac disease. Don Kasarda, Albany, CA )There was an article by Paul Heiney in the Times (UK Newspaper) on )Saturday 21st September on this very old variety of wheat which goes )back in the UK to Roman times. The flour is very high in protein )vitamins and minerals and the finished bread does contain gluten which )the growers say can be eaten by people normally intollerant to gluten. )Does anybody have experience of this flour? Are there any medical or )scientific opions on this variety of wheat? Is this similar to the Oats )debate? )-- )Deryk Ford ========================================================================= Date: Wed, 25 Sep 1996 09:33:00 CST From: Murray@intmed-po.int-med.uiowa.edu Subject: Inflammed duodenum in celiac disease The duodenum is the first part of the small intestine after you leave the stomach. It is exposed to acid and stomach digestive enzymes. It has a built-in defense against these corrosive materials. In many diseases the duodenum becomes inflammed. In duodenal ulcer disease, a bacterium, Helicobacter pylori damages alters the amount of acid the stomach produces and reduces the defense against the acid resulting in damage of the duodenum and ulcers. This is way and far the most common inflammation of the duodenum. However there are other things that inflame the duodenum and one of those is celiac disease. Celiac disease affects the first part of the small intestine ( duodenum more than any other part) the damage may get less furhter douwn the intestine. The extent of small intestine involved by the celiac damage may determine which symptoms the patient gets. If a lot of the small intestine is involved then diarrhea and malabsorption is more likely. However if only a short portion of the intestine is involved then there may be no diarrhea. The major consequence may be the result of the inflammation of the duodenum with pain bloating nausea and vomiting, that may be the same symptoms as those of the much more common peptic ulcer disease. Indeed some patients may even have ulcers that look like the peptic ulcers further confusing the picture and misleading the physician. Many patients biopsies taken by the endoscopists may have been called "non specific duodenitis " in the past where the pathologist may have assumed that the inflammation was caused by aicd damage and peptic ulcer disease. There some things that can be done to clarify this. 1. Have a high index of suspicion for CD, especially if the patient does not have helicobacter, or is not on large doses of anti-arthritis drugs. 2. Take biopsies in the duodenum past the area that have ulcers or obvious inflammation (the findings of celiac disease inflammation is more widespread than the damage with peptic ulcer disease which is usually located tio the spots whre the ulcers is. 3. The pathologist needs to look for intraepithelial lymphocytosis and the chronic inflammatory cells in the lamina propria( deeper layer) And draw the attention of the clinician to the alternate possibility. 4. Antibody tests may be helpful in differentiating the 2 conditions. The above represents a new approach to this problem and would not have been common or usual practise even 3-4 years ago. This is not medical advice and should not be used as such. It is intended to be general information and is part of the educational mission of the Univ of Iowa. Joe Murray MD Univ of Iowa ========================================================================= Date: Fri, 27 Sep 1996 21:33:17 -0400 From: "Donald D. Kasarda" (kasarda@PW.USDA.GOV) Subject: Re: dieticians and sugar )sugar cane is a grass and thus related to the wheat plant. Therefore )people who cannot tolerate wheat should not eat sugar. In regard to the query about sugar cane containing gluten. Sugar cane is a member of the grass family as are wheat, rye, and barley, the species that contain proteins harmful to celiac patients. However, not all grasses are harmful to celiac patients--for example, rice and corn. The scientific name of sugar cane is Saccharum officinarum and it belongs to the tribe Andropogoneae, which also includes sorghum. On the basis of closer relationship to corn or maize than to wheat, I would say that sugar cane is not likely to be harmful to celiac patients. Furthermore, as far as we know gluten proteins, or their equivalents in rye and barley, are found only in the endosperm of the grain of the plant and not in vegetative tissues, such as leaves. To the best of my knowledge, sugar is obtained from the stalks of the plant and, hence, even if the seeds of the plant contained harmful proteins (not likely), highly refined sugar would be safe to eat. Don Kasarda
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