This file contains postings made by the following professionals: Dr. Alessio Fasano--a pediatric gastroenterologist at the University of Maryland School of Medicine in Baltimore. Dr. Fasano is the director of the Division of Pediatric Gastroenterology and Nutrition at the University of Maryland. With his colleagues at the University of Maryland he conducted pilot studies suggesting that CD is highly underdiagnosed in the USA. His major goal is to expand these preliminary studies and to establish an educational program for colleagues to gain more insights on CD. Dr. Ivor Hill--a pediatric gastroenterologist at the University of Maryland School of Medicine in Baltimore. Dr. Hill is attempting to establish a network of collaborators that will be involved in gathering preliminary data to support his belief that if we actively look for CD we will diagnose many more cases at an earlier age. Dr. Karoly Horvath--an associate professor of pediatrics ath the University of Maryland at Baltimore. Dr. Horvath set up the Pediatric Gastrointestinal and Nutrition Laboratory, and is now director of this lab. Donald Kasarda--a grain specialist working for the United States Department of Agriculture. Dr. Joseph Murray--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. Dr. Kalle Reichelt--involved in research in Norway. He is looking into the impact of gluten intolerance on certain individuals with developmental delays. Paul Shattock--Senior Lecturer in Pharmacy, Autism Research Unit, School of Health Sciences, University of Sunderland; Sunderland, England. He is doing research on the relationship between gluten/casein and autism. His work has application to other developmental and mental disorders. ========================================================================= Date: Mon, 3 Apr 1995 23:47:44 -0500 From: "J. Murray" (jomurray@BLUE.WEEG.UIOWA.EDU) Subject: Re: causes of diarrhea in people with CD If someone has confirmed celiac disease and gets a bout of diarrhea I think the most likely reason is gluten. Looking very closely at the diet in the days before the event may explain the diarrhea. If everyone in the family have had diarrhea then it is more likely to be infectious. If there are several episodes of diarrhea happening say every month that is too often for infections, somethings in the diet. Joe Murray Not medical advice to be used in individual situations. More like general information. Individual problems need discussion with a personal physician. ========================================================================= Date: Mon, 3 Apr 1995 23:58:34 -0500 From: "J. Murray" (jomurray@BLUE.WEEG.UIOWA.EDU) Subject: Re: CELIAC disease viral connection The enteropathy that occurs in AIDS is a complex process that may be the result of may abnormalities including infections, HIV viral infection itself, and autoimmune processes that occur due to the dysregulation of the immune system. There are some slight similarities between the two conditions. I have yet to hear of the 2 conditions co-existing in the one individual. The use of the term gluten free in advertisements for food supplements for AIDS probably refects the growing awareness among these companies of the things to leave out of food supplements like lactose, gluten and other things. Wheat itself may not be completely digested in normal individuals and hence the challenged digestion of the unfortunate victim of aids enteropathy may have more difficulty with wheat than with other foods. the observation that CD may become apparent after a viral infection is a common phenomenon in many autoimune diseases as well as GI inflammatory states. I have seen 2 cases of inflammatory bowel that occurred after an attack of CMV ( a common and usualy very benign disease in healthy people. This could be related to the non-specific stimulation of the immune system or a more specific incutement of a reaction to a host ( patient ) protein leading to disease. The example that has been suggested in CD is Adenovirus 12. see multiple references under KAgnoff M. Joe Murray ========================================================================= Date: Tue, 4 Apr 1995 00:04:45 -0500 From: "J. Murray" (jomurray@BLUE.WEEG.UIOWA.EDU) Subject: Re: Communion wafers Forgive my theological ignorance but are GFD wafers acceptable to catholic churches in Canada? how about Episcopal or Anglican? In some churches canon law says that the host is not bread any more, therefore , theologically speaking, it can not contain any gluten! I would appreciate any suggestions that I can pass onto my multidenominational clinc patients. Joe Murray ========================================================================= Date: Tue, 4 Apr 1995 00:18:46 -0500 From: "J. Murray" (jomurray@BLUE.WEEG.UIOWA.EDU) Subject: Re: CELIAC Disease and osteoporosis Osteoporosis is not only more common in CD but decreased bone density is almost universal in people diagnosed as adults esp in women. The good news is that it usually imptroves with a gluten free diet. Joe murray ========================================================================= Date: Tue, 4 Apr 1995 00:26:55 -0500 From: "J. Murray" (jomurray@BLUE.WEEG.UIOWA.EDU) Subject: Re: terminology The term celiac disease does indeed refer to a disease. what you call a healed celiac I dont know. ideas. we could return to the original term used by Samuel Gee in 1888, the Coeliac affliction. or gluten sensitivity, I did overhear a waitress at hotel in Florida at which a number of people with celiac disease were staying and having b'fast call out in a wonderful cockney accent " Who are the GLUTONS" any one with any suggestions? ========================================================================= Date: Tue, 4 Apr 1995 19:38:31 -0500 From: "J. Murray" (jomurray@BLUE.WEEG.UIOWA.EDU) Subject: Re: CELIAC disease viral connection I think that asymptomatic peolpe with CD are quite common. 1/2 of affected family members have no symptoms. However if you have fatigue then you are not asymptomatic, just atypical rather than classic preentation. Joe Murray. Are there any married couples out there who both have CD and at least one developed after they met. Joe Murray ========================================================================= Date: Tue, 11 Apr 1995 08:30:21 PDT From: "Donald D. Kasarda" (kasarda@PW.USDA.gov) Subject: Re: Wheat grass )I am wondering about wheat grass. Reply from Don Kasarda, Albany, CA The vegetative tissues of wheat or wheat grass should not contain any of the harmful gluten proteins (harmful to celiac patients, that is). However, if heads have formed and grain development initiated, the developing wheat grains or grass seeds could have harmful proteins. Thus, if you are sure that no head development has occurred, you are probably safe in eating wheat grass. I am familiar with the sale of juices from wheat grass, but I am not familiar with actually eating wheat grass. In the case of the bottled juices (squeezings, pressings), it would be difficult to know the state of grass development when the wheat grass was harvested for pressing. I hope this will be of some help. ========================================================================= Date: Sun, 16 Apr 1995 20:19:09 -0500 From: "J. Murray" (jomurray@BLUE.WEEG.UIOWA.EDU) Subject: Re: HLA Typing Jim Lyles writes about the gene typing test to determiine risk for celiac disease. Hla typing May hepl in populations where the genetic make up of the celiac population is known and that of the general population is known also. Unless I am incorrect I have not seen any stiudy address the issue of negative predictive value of HLA typing. In the melting pot of the USA i would be a little more circumspect about its value. Joe Murray. PS If you are a HLA matched siblibg of a celiac patient then you will have a higher chance of getting it. JM ========================================================================= Date: Sun, 16 Apr 1995 20:29:41 -0500 From: "J. Murray" (jomurray@BLUE.WEEG.UIOWA.EDU) Subject: Re: Costs of tests Costs of tests for making a diagnosis are dependent on the patient problems 1. Antibodies can run anywhere from 120 -240 dollars a panel should include endomysial antibody IgA, and gliadin testing IgG, and IGA 2. The process of getting a biopsy involves a doctors visit fee and endoscopy charges, a pathology charge for the interpretation. These often are considerable charges and vary by location and insurer. Real dollar costs can vary 1000-2000 dollars and maybe higher in some circumstances/places. Remember price doesnt always reflect value or reliablilty. Joe Murray ========================================================================= Date: Mon, 17 Apr 1995 10:24:35 -0500 From: "J. Murray" (jomurray@BLUE.WEEG.UIOWA.EDU) Subject: Re: asymptomatic family members of people with celiac disease people with Syymptoms of CD and/or positive blood tests ( antibodies) should probably have a biopsy too confirm that they have CD. Why? Osteoporosis subtle symptoms like chronic fatigue, depression etc Risk of malignancy, Certainty: usually needed to motivate diet compliance for life Risk of developing symptoms later in life when it may not respond as well to gluten withdrawal. Perhaps to allow searches of another branch of the family related to 2nd person. as yet blood tests are not precise enough to make the diagosis without a biopsy. joe Murray Disclaimer( not specific medical advice. Individuals should discuss matters with their own doctor) ========================================================================= Date: Mon, 17 Apr 1995 10:36:59 -0500 From: "J. Murray" (jomurray@BLUE.WEEG.UIOWA.EDU) Subject: Re: Where are the irish? We here in the USA. The lack of participation probably reflects the relative lack of access of the public to the internet in ireland. only Universities and some companies( usually computer companies have e-mail) I will personally try to recruit some of my countrymen and women to the list. Joe Murray ========================================================================= Date: Mon, 17 Apr 1995 10:45:39 -0500 From: "J. Murray" (jomurray@BLUE.WEEG.UIOWA.EDU) Subject: Re: Gliadin IgG postive only test I believe I have written before on this topic to the list. The IgG anti gliadin may be postive alone for many reasons including 1. The person doesnot have CD 2. The person has CD and IgA defiency 3. The person has latent gluten senstivity i.e. There is evidence for serum antibodies but a completely normal small intestine and no symptoms 4. The other antibody tests are wrong and the person does have CD 5. Occassional low level positives can be seen in normals , people with giardiasis, crohn's disease. Joe Murray disclaimer( not medical advice) ========================================================================= Date: Mon, 17 Apr 1995 11:05:27 -0500 From: "J. Murray" (jomurray@BLUE.WEEG.UIOWA.EDU) Subject: Re: CELIAC Disease and hives There may be an increased risk of hives in celiacs due to the leaky gut which allows macromolecules into the blood system where they dont belong. This makes the developement of allergic reactions to the allergens more likely. On the good side The permeability can iimprove with strict adherence to a GFD. Avoidance of the allergen if known is helpful if known Prescription mediacation may help to reduce the severity of the illness. The other consideration is whether this could an atypical form of dermatitis herpetiformis. Joe Murray Disclaimer( not mediacl advice) ========================================================================= Date: Mon, 17 Apr 1995 11:18:23 -0500 From: "J. Murray" (jomurray@BLUE.WEEG.UIOWA.EDU) Subject: Re: CELIAC Disease and dermnatitis herpetiformis I have put a post on this subject before to the list so search the archives. The GIG of seattle have a very nice synopsis on the topic that they give/send to health professionals and They may give to you too. I am not sure if everyone with a confirmed case of DH needs to have a biopsy of the intestine. Certainly a definite postive biopsy of the skin confirms gluten sensitivity of the individual. If The person adheres to a strict gluten free diet to manage their skin condition then It is not always necessary to biopsy the intestine. The biopsy can provide useful additional information, but if it to persaude anwilling patient/dermatologist that a diet if beneficial then a careful explanation of the scientiific information should suffice to persuade most. The eventual should be to control the skin condition with the GFD alone. There is no doubt that the drugs used dapsone and sulfa drugs are very useful to get the itch under control but they can have side effects and do not benefit the intestinal damage that often co-exists. Joe Murray disclaimer( not medical advice) ========================================================================= Date: Mon, 17 Apr 1995 16:48:06 PDT From: "Donald D. Kasarda" (kasarda@PW.USDA.gov) Subject: Re: mouth ulcers and white flecks on the nails Information that might be of interest provided by Don Kasarda, Albany, CA Cliona O'Farrelly writing in "Gastrointestinal Immunology and Gluten-Sensitive Disease" (Eds., C. Feighery and C. O'Farrelly, Oak Tree Press, Dublin, 1994, pp. 169-180) states: "However, there is evidence to suggest that gluten sensitive ROU (recurrent oral ulceration) also occurs in the absence of classic celiac disease. The oral lesion in patients with normal small intestinal architecture responds to treatment with vitamin B12 and folate suggesting that a malabsorptive process was active even in the absence of any detectable small intestinal lesion (7, 61). The small intestinal lesion in these patients may be too subtle to be seen by routine histology and yet be sufficient to activate a pathogenic process which manifests itself more visibly and actively in the buccal mucosa. It has been proposed that wheat protein plays a primary pathogenic role in some of these cases (52, 53)." )My 6 year old daughter was diagnosed as having celiac disease 2 years )ago. Since starting a gluten-free diet she has been very healthy, and )has a good appetite and lots of energy. However, she does have a problem )with mouth ulcers, which come and go quite frequently. In addition, she )has small white flecks in some of her finger nails, which I believe may )indicate some vitamin or mineral deficiency. If anyone can offer any )suggestions regarding these two complaints, I would be very grateful. ) )Robert Hewitt ========================================================================= Date: Wed, 19 Apr 1995 11:30:15 -0500 From: "J. Murray" (jomurray@BLUE.WEEG.UIOWA.EDU) Subject: Re: CELIAC Disease and atypical symptoms As physicians start to biopsy the small intestine more frequently there is an increased awareness of the atypical nature of the symptoms of celiac disease. The majority of the patients I see have not presented with the Classic symptoms but much more vague ( Not directly due to the small intestinal malabsorbtion) presentations. Certainly I have seen patients who have had reflux as their presentation which gradually tends to improve after several months of the diet. I dont know why this but I suspect it may be due motor incoordination between the stomach and inflammed small intestine. This might lead to retention of food in the stomach for a longer time and a greater risk of reeflux of the acidic stomach contents nto the esophagus. Acid reflux is a very common condition and it may be that it just co-exists with the celiac disease. The only way of knowing for sure is if all of the symptoms go away after a year of a totally gluten free diet. Not medical advice Joe Murray ========================================================================= Date: Thu, 20 Apr 1995 17:05:32 PDT From: "Donald D. Kasarda" (kasarda@PW.USDA.gov) Subject: Gluten in corn? There is much confusion in terminology when it comes to gluten. Here is the way I understand it. The term gluten in reference to the cohesive, elastic protein mass remaining after starch is washed from a dough goes back to Beccari in 1745. Strictly speaking, gluten is found only in wheat because it is difficult to wash a cohesive protein mass even from rye, the closest relative to wheat, let alone from barley or oats or anything else. Unfortunately, a misuse of the term by the corn industry has become common in recent years. It has become fairly common to call corn storage proteins "corn gluten." Personally, I think there is no justification for such usage. Corn may contain prolamins, as does wheat, but gluten--no way! When it comes to celiac disease, a similar corruption of the term has become very common. There are certain related proteins in wheat, rye, and barley that give rise to particular peptides during digestion that are capable of triggering the responses typical of celiac disease. Only in the case of wheat can these be strictly considered to be derived from the gluten proteins. But for lack of a suitable term, patients and their physicians began speaking of gluten-free or gluten-containing foods. People ask me, "How much gluten is there in quinoa?" I have to translate this into, "Are there any harmful peptide sequences in the proteins of quinoa?" There is nothing in quinoa that is like gluten prepared from a wheat flour dough, which has an unusual, perhaps unique, viscoelastic character. Anyway, as far as we know, corn does not seem to cause harm to celiac patients. Corn has not been studied in the extensive way that wheat has in relation to celiac disease, but for 40+ years patients and their physicians have seemed to agree that corn is OK. The sequences in the corn zein (prolamin) fraction are suspicious, but they do differ in an apparently crucial way from the protein sequences of the wheat gliadin (prolamin) fraction. So, I have to admit that there have been no modern biopsy based studies of the effects of purified corn proteins on the celiac intestine as there have been for wheat, but the mass of evidence still seems to point in the direction of corn being safe for celiac patients. Disclaimer: The above is my opinion, it should not be considered definitive in a legal sense nor should it be considered medical advice by anyone. Don Kasarda, Albany, CA ========================================================================= Date: Sun, 23 Apr 1995 15:05:11 PDT From: "Donald D. Kasarda" (kasarda@PW.USDA.gov) Subject: Re: Is diagnosis necessary? John Tisdale states (an excerpt from a longer communication): )A close friend and physician suggested that it was the gluten in the )wheat that was the problem. After removing wheat from my diet at age )23, all headaches subsided (bleached wheat did not cause headaches for )me). I would just like to point out that bleaching of flour has no effect on gluten proteins that I am aware of. The amino acid sequences found in gluten proteins that trigger the intestinal changes of celiac disease would still remain and be released to contact with the intestinal surface during digestion. I would also like to make an additional comment: I continue to be concerned that the myriad personal symptoms described on this list might make many other people with celiac disease think that these symptoms are necessarily part of having celiac disease. I think there is value in having this information on the list, but whether many of these symptoms and the remedies indicated have anything to do with celiac disease should be considered completely unproven. Psychological/neurological effects experienced upon eating wheat seem to be real, but it is also quite possible that the mechanisms involved are different from those involved in celiac disease. There is little or no solid information available right now. Are there biopsy proven celiacs out there who do not recall having psychological disturbances (other than what might be expected by anyone who is sick, perhaps from the flu or a bad cold)? If there are, it would be helpful to have brief messages from them. Also, are there any celiac patients out there, again preferably biopsy-proven, who do not have any problems with white vinegar or vanilla extracts. It would be helpful to have brief message from them as well? Don Kasarda, Albany, CA ========================================================================= Date: Sun, 30 Apr 1995 17:05:34 PDT From: "Donald D. Kasarda" (kasarda@PW.USDA.gov) Subject: Re: Gluten and distillation I am in complete agreement with what Richard Abrams has written. Accordingly, I am puzzled as to why some celiac patients feel so strongly that they cannot use white vinegar, which I have been given to understand is prepared through fermentation of distilled alcohol. Perhaps, there is some component of the alcohol or the fermentation inoculate (other than gluten peptides) that causes some people to react, somewhat the way a few people react to sulfites in wine. I will try to obtain some more detailed information about the process by which white vinegar is made. Don Kasarda, Albany, CA )I have no experience with the manufacture of distilled beverages, but my )understanding of so basic a chemical procedure as distillation is that )distillation through a moderately efficient reflux tower is very )effective at separating volatile from non-volatile components. Even any )micro-droplets of pot-liquor carried up as spray should be trapped in the )upper parts of the distilling apparatus so that non-volatiles such as )gluten or peptides if they are formed do not get into the distillate. )What does get over are the volatile components of the fermentation )mixture, alcohol, esters, and aldehydes and other fusel oil components. )It is these non-alcoholic volatile organic components that vary depending )upon the grain that was used for fermentation, and they, especially the )esters are responsible for the taste of the beverage. I had hoped that )someone experienced in the manufacture of alcoholic liquors would have )answered your question, hence my delay in responding. ========================================================================= Date: Fri, 5 May 1995 16:57:19 -0400 From: Ivor Dennis Hill (ihill@UMABNET.AB.UMD.EDU) Subject: Re: Growing out of CD On Fri, 5 May 1995 MOTORADD@AOL.COM wrote: ) I understood from a gastrointerologist that one should periodically perform ) a "gluten challenge" presumably because it is possible to "grow out of it" ) being CD. Does anyone have more info on this? Celiac disease is a permanent (lifelong) condition which affects genetically predisposed individuals who are exposed to gluten and related products from rye, barley and oats. Once the diagnosis has been confirmed there is absolutely no indication for periodically undertaking a gluten challenge. It is well known that patients with celiac disease who start ingesting gluten again after having been on a gluten free diet may go for years without apparently having any symptoms. Despite this there will be ongoing histological damage to the intestines. It was this apparent prolonged symptom free state that led doctors in the past to believe that people could "grow out" out of the condition. This is no longer accepted as correct. Ivor D. Hill Professor of Pediatrics Clinical Director, Pediatric Gastroenterology University of Maryland School of Medicine ========================================================================= Date: Tue, 9 May 1995 01:05:11 -0400 From: Don Wiss (email@example.com) Subject: Re: HD symptoms Evelyn Loy (Evey129@AOL.com) asked: )I was just wondering if someone could please send some info on HD. I have )read some posts about it, but still don't know to much about it. Does it )always show up as lesions? or could it show up as single pimple-like rash? I )have been experiencing the rash and can't figure out where these little spots )are comming from. Are you referring to DH? If so, the following is from Peter Thompson's web page at http://www.demon.co.uk:80/webguides/nutrition/diets/glutenfree/ and was written by Joe Murray: Dermatitis Herpetiformis The following represents my views about this curious and very itchy condition. In general DH is a severely itchy skin condition that often starts abruptly, affecting the elbows knees buttocks and scalp and the back. It usually starts as little bumps that can become tiny blisters and then are usually scratched off. It can occur in one spot only but usually occurs in many differnt areas. The condition is related to the deposit under the skin of IgA deposits. These occur in response to the ingestion of gluten in the diet. However once deposited there, they are only slowly cleared by the body even when the individual is gluten free. While most individuals with DH do not have obvious GI symptoms almost all have some damage in their intestine. They the potential for all of the nutritional complications of celiac disease. The diagnosis is made by taking a skin biopsy and preforming immunoflorescence studies on it ( a specialised type of stain in major laboratories) The test is usually reliable but it takes a signifigant dedication to detect early cases where there is a short history of rash rather than years or months of rash. It is unusual to develope DH after the the start of a GFD for CD. About 5 % of CD patients will develope DH usually in the first 6-12 months. This probably reflects the long lasting nature of the deposits under the skin. treatment for DH is 2 fold. Remove the cause Gluten suppress the skin response with drugs Dapsone or some other sulphones The latter is the most common treatment used as it is rapidly relieves the the itch. However there are some side effects associated with these mediacations and they need to be taken under mediacal monitoring with blood tests to detect side effects. It is my practise that DH should be treated with a GFD for life and use of drugs to get immediate relief in the short term. It is usually possible to get pateint off the dapsone after several months of a strict GFD. The most common complication of DH is scarring which ususally fades with time. Occassionally there can be secondary infection from scratching. There is probably a slightly increased chance of malignancy in DH not on a gfd diet. Several physical triggers are known to set off an attack of DH. especially exposure to iodides and bromides which are contained in household cleaners. A very good reference for DH is available from the GIG in washington. Joe murray ========================================================================= Date: Tue, 9 May 1995 16:47:55 PDT From: "Donald D. Kasarda" (kasarda@PW.USDA.gov) Subject: toxicity of uncooked beans Comments from Don Kasarda, Albany, CA Almost all plants have some toxic components in them, some more than others. In general, wheat is a good food with low levels of toxic components (except for celiac patients, of course) and wheat protein is highly utilized in animal feeding studies, but most uncooked beans and peas have significant amounts of protease inhibitors in them, such as trypsin/chymotrypsin inhibitors. These inhibitors make it unwise to eat beans and peas raw. They stop the action of digestive enzymes (specifically, in this case, proteases), especially those of the pancreas, so the pancreas responds by making ever more of the enzymes. This, however, is not a desirable situation on a constant basis. So, eating a raw bean or two will probably not cause any harm--they are not going to cause systemic poisoning, but I think it is generally desirable to cook beans and peas of all sorts before they are eaten. This tends to inactivate the protease inhibitors. Sprouting certainly will produce changes in composition, but these can sometimes be harmful as well as helpful. Alfalfa sprouts will have saponins in them (I think more than in alfalfa seeds themselves, although I am not going to take the time to research this), for example. A sprinkling of sprouts on a sandwich on occasion is probably not harmful and the other good components of the sprouts may be more important than the presence of the bad components. Still, I think it probably would not be a good idea to make something like alfalfa sprouts a major part of the diet (piles of them for breakfast, lunch, and dinner). A varied and balanced diet is best. The body is generally capable of dealing with the small amounts of toxic components present in all plant foods, but defenses can be overwhelmed. The preceding is not medical advice. It is somewhat educated opinion. Let the reader beware. ========================================================================= Date: Tue, 9 May 1995 22:35:15 -0500 From: "J. Murray" (jomurray@BLUE.WEEG.UIOWA.EDU) Subject: Re: differential diagnosis of CD THe differential diagnosis for CD is very broad indeed. If one takes classic malabsorptive CD then the differential includes the follwing not exclusive list Giardiasis Common variable hypogammaglobulinemia IgA def Crohn's disease Whipple's disease Cow milk allergy( in kids) Pseudoobstruction Ischemic bowel Scleroderma of the small intestine intestinal diverticulosis rare cangenital defects in the mucosa Bacterial overgrowth syndromes Pancreatic failure Effects of some drugs HIV enteropathy protein losing enteropathy( lymphangiectasia) The list goes on forever. Most can be distinguished on biopsy and with other tests but this is a very complex part of the body and not very accessible to examination Some of these can coexist with CD If one considers all of the possible presentations of CD then there is even wider number of possibilities. Joe Murray **Not medical advice** ========================================================================= Date: Tue, 9 May 1995 23:01:40 -0500 From: "J. Murray" (jomurray@BLUE.WEEG.UIOWA.EDU) Subject: Re: CELIAC Disease and colon cancer and Ireland There was one study looking at family histories of CD patients and an increased prevalence of colon cancer cases was hinted at. Intestinal cancer in the setting of celiac disease may actually be lymphoma or adenocarcinoma of the small intestine both directly? related to CD. A causal relationship to colon cancer is speculative. Holmes group in Britain di not reveal an increased incif=dence of colon cancer in their patients. Their is no ready explanation for the incidence in Ireland. One could speculate that Ireland's subsistence on the potatoe for 200years might have allowed celiacs to flourish unencumbered by gluten and the reintroduction of gluten lead to the disease. Other possibilities migt include early infant feeding practices or a limited genetic stock. Their are equally high areas of incidence in other places, parts of Sweden, Italy, and Israel. Joe murray ========================================================================= Date: Fri, 12 May 1995 10:03:01 PDT From: "Donald D. Kasarda" (kasarda@PW.USDA.gov) Subject: Re: Chickpea flour In regard to toxic substances in raw beans and peas, Paul Shattock indicated in a recent posting that lectins and hemagglutinins are the harmful substances in red kidney beans and chick peas. I had indicated in my posting that trypsin/chymotrypsin inhibitors are the main problem in beans and peas. In checking with colleagues, I find thatlectins and hemagglutinins are the most harmful components, with trypsin/chymotrypsin inhibitors coming in second. There may also be other toxic substances that are small molecules (proteins are large) and can be washed out to some degree. These various toxic components can be found in most (probably all) beans and peas. Paul stated also that lectins are destroyed by wet heat, but will not be affected by dry heat and that beans should be soaked before cooking to make sure that they are thoroughly hydrated. This will deactivate the lectins and hemagglutinins, and largely deactivate the inhibitors. Eating raw beans or bean flour that has never been cooked seems not to be a good idea. Perhaps beans could be cooked, dried, and then ground into flour? Don Kasarda, Albany, CA )I have been reading the posts on this topic. I like to go back )country camping and am always looking for food ideas. I met a person )who told me he takes a large bag of chick pea flour with him and makes )hummus while he's in the back country. He mixes it with water and )whatever spices he's brought along. Considering the discussion on the )possible toxicity of raw chick peas, does anyone have a comment on )how safe this is? It sounds like a great idea, and an excellent )alternative for GFer's. Would one be better served by heat treating )the flour, say in a warm oven or microwave (as the objective is to )keep it dry for travel). ) )Jennifer ========================================================================= Date: Wed, 17 May 1995 16:21:36 -0400 From: Karoly Horvath (khorvath@UMABNET.AB.UMD.EDU) Subject: Serological tests in celiac disease John Dennis asked me to explain the implications of serological tests in celiac disease. These are immunological tests. They are reflecting whether there is an activation of the immune system in the patients. The trigger for this immune response is the gliadin. The difference between a celiac and non-celiac individual is that a non-celiac does not have immune response to gliadin. If a patient has active disease and he/she is on a non-restricted diet the serological tests are positive, which means that he/she has high concentration of antibodies in his/her serum. We are performing three different tests: -anti-gliadin IgG antibody test -anti-gliadin IgA antibody test -anti-endomysium antibody test The most sensitive and specific test is the anti-endomysium test, however it can give false negative results in small children (Less Than 2 years of age) and in patients with selective IgA deficiency. IgA deficiency occurs in one out of 500-600 people. In IgA defificent patients only the anti-gliadin IgG test will be positive, and additional absorptive studies are necessary before the intestinal biopsy. The combination of these three antibody measurements allows us to reach an approximately 96% specificity and sensitivity. It means that we can miss 4% of patients if we rely on only the serological tests. If somebody on a gluten-free diet these tests become negative by 6 month of the gliadin-free diet. The decline of the initially high antibody levels may suggest a good compliance. In the absence of the "gliadin trigger" the immune system does not produce new antibodies, and generally it takes 6 months to eliminate the "old antibodies". A positive test during a long-term diet indicates accidental gluten consumption. The serological tests are useful in the diagnosis of celiac disease, and helpful in the estimation of strictness of the diet. If a celiac patients has some unusual symptom during the diet these tests can help to estimate whether these symptoms are related to the gliadin or we should look for some other reason. In Europe most of the patients have serological test results at the time of diagnosis, on diet, and during a rechallenge with gluten, which makes their management much easier. If you have any question concerning diagnostic tests in celiac disease me and my colleagues will be happy to answer them. We established a Celiac Center here at the University of Maryland to help children and adults with celiac disease all over the U.S. Karoly Horvath, M.D., Ph.D. ========================================================================= Date: Thu, 18 May 1995 18:26:52 PDT From: "Donald D. Kasarda" (kasarda@PW.USDA.gov) Subject: Re: Are oats safe for celiacs? (fwd) Reply from Don Kasarda, Albany, CA As Richard Abrams has indicated, the Irish work has not been published as a full paper yet. A final publication is being worked on. It is touchy for me to comment on this because of my position as a government employee and this work is not cleared for publication yet. Probably best to wait for full publication and then all can evaluate the study fully. However, I will stick my neck out, after reiterating that I am not a physician and the reader should beware, by saying that this work looks very good to me. The Dublin researchers used all the latest information and methods in the study. Of course, 10 patients is still a small number. I will also mention that they had considerable difficulty buying supplies of oats that were not contaminated with wheat and used extensive laboratory testing to clear their supplies. So how are you going to be sure that your oats are not contaminated? Wheat can grow in fields of oats quite readily and contamination can occur at many steps thereafter in the pathway to market. I think this work is important and that people should be aware of these findings, but if they wish to pursue a trial, it should be under the guidance of a knowledgeable physician and they should be well-informed about pitfalls and risks. Also,I think it is possible for a person to be sensitive/intolerant to oats without having celiac disease. With regard to Gln-Gln-Gln-Pro being in oats (a very good point!), I have recently done an identity search of the sequence data bases, which indicates that this sequence shows up in many, many proteins, including at least one zein (corn) and and one rice protein, so I now think it may be part of a toxic sequence, but is insufficient in itself. I don't think we can rule out the possibility that oats are non-toxic on the basis of Gln-Gln-Gln-Pro being present in the sequences of avenins. Again, I disclaim responsibility for the above opinions. They are presented for information purposes and for discussion purposes only. )How toxic are oats for celiacs? There is anecdotal evidence pro and )con. ) -Rich Abrams, Pittsburgh, PA ========================================================================= Date: Tue, 23 May 1995 09:51:33 PDT From: "Donald D. Kasarda" (kasarda@PW.USDA.gov) Subject: quinoa, amaranth, buckwheat, tef, millet From: Don Kasarda, Albany, CA I am afraid I am largely to blame for my "grains letter" not appearing in the archives because I was concerned about USDA regulations concerning publication and possible legal responsibility. I have decided that I am probably being overly conservative and will just post the letter here publicly--with permission as far as I am concerned to put it in the archive. A copy of the letter, which was sent originally to Phyllis Brogden follows: (The only updates I would like to make are that oats may be non-toxic on the basis of some recent testing, but I would recommend waiting until results are published and then consulting an experienced physician before trying oats and there is considerable anecdotal evidence developing, as I expected for these wheats, that spelt and Kawmut are harmful. August 27, 1991 Ms. Phyllis Brogden, Co-chairperson Celiac Sprue Support Group Greater Philadelphia Area 6318 Farmar Lane Flourtown, PA 19031 Dear Phyllis, Since you, Elaine Hartsook, Mary Alice Warren, Annette Bentley, and Elaine Monarch have all asked me from time-to-time about the safety for celiac patients of some particular foods, I thought I would just put together a general statement for you covering a number of the concerns. I am supplying copies to the other group chairpersons. These are my opinions based on quite a few years of research in the area of proteins as they relate to celiac disease, but, of course, do not necessarily represent those of the Agricultural Research Service,U. S. Department of Agriculture. You may use any of the information that seems of interest in your newsletters, but if you attribute it to me, it would be best to indicate that the opinions are mine as a researcher and are not intended to define USDA policy. The only plants demonstrated to have proteins that damage the small intestines of people with celiac disease are those from wheat, rye, barley, and oats (and the man-made wheat-rye cross called triticale). These species are members of the grass family and are quite closely related to one another according to various schemes of plant classification (taxonomy). However, not all members of the grass family damage the intestines of celiac patients. Rice and corn, for example, are apparently harmless. Many other grains have not been subjected to controlled testing or to the same scrutiny as wheat, rye, barley, oats, rice, and corn in relation to celiac disease. If we accept corn and rice as safe, then members of the grass family that are more closely related to these species (on the basis of taxonomy) than to wheat are likely to be safe. Such grasses include sorghum, millet, teff, ragi, and Job's tears, which appear to be reasonably closely related to corn. In some cases, there are protein studies in support of this conclusion, although the studies are not sufficiently complete to provide more than guidance. Scientifically controlled feeding studies with celiac patients would provide a better answer. However, such studies are not likely to be carried out in the next few years because of high costs and the difficulty of obtaining patient participation (such studies would likely involve intestinal biopsy). In lieu of feeding studies, further studies of protein (and DNA) would provide the next best way to evaluate my suggestion that millet, sorghum, teff, ragi, and Job's tears are not likely to be toxic in celiac disease. The scientific name for bread wheat is Triticum aestivum--the first part of the name defines the genus (Triticum) and the second part, the species (aestivum). Species falling in the genus Triticum are almost certain to be harmful to celiac patients. Grain proteins of these species include the various types characteristic of the gluten proteins found in bread wheats (including the alpha-gliadins) that cause damage to the small intestine in celiac disease. Some Triticum species of current concern include Triticum spelta (common names include spelt or spelta), Triticum polonicum (common names include Polish wheat, and, recently, Kawmut), and Triticum monococcum (common names include einkorn and small spelt). I recommend that celiac patients avoid grain from these species. Rye (Secale cereale) and barley (Hordeum vulgare) are toxic in celiac disease even though these two species are less closely related to bread wheat than spelta and Kawmut. They belong to different genera, Secale and Hordeum, respectively, and lack alpha-gliadins, which may be an especially toxic fraction. You have asked especially for my opinion regarding spelta and Kawmut. Evidently there have been anecdotal reports suggesting a lack of toxicity in celiac disease for spelta and Kawmut. Controlled tests would be necessary to draw a firm conclusion. I don't consider anecdotal reports as reliable for the following reasons. The diagnosis, sometimes self-diagnosis, of celiac disease is occasionally made without benefit of reasonably rigorous medical or clinical tests, especially intestinal biopsy. Individuals who are "diagnosed" in this way without rigorous testing may not actually have celiac disease. Claims that particular foods cause this latter group no problems in relation to their celiac disease could cause confusion. Furthermore, celiac patients who report no problems in the short run with spelta or Kawmut might experience relapse later. There is now adequate evidence that when celiac patients on a "gluten-free" diet (that is, a diet free of any proteins or peptides from wheat, rye, barley, and oats) have wheat reintroduced to their diets, times-to-relapse vary enormously among individuals, ranging from hours to months, or even years. And this is for wheat, presumably the most toxic of all cereal grains to celiac patients. Additionally, the relapse may not be accompanied by obvious symptoms, but be recognized only by physicians through observation of characteristic changes in the small intestinal tissues obtained by biopsy. The reasons for the enormous variability of response times are not known. It may be speculated that they have something to do with the degree of recovery of the lining of the small intestine on a gluten-free diet, the degree of stress that the patient had been experiencing (including infections), and individual genetic differences. As I have indicated, all known grain species that cause problems for celiac patients are members of the grass family. In plant taxonomy, the grass family belongs to the Plant Kingdom Subclass known as monocotyledonous plants (monocots). The only other grouping at the Subclass level is that of dicotyledonous plants (dicots). Some other species about which celiac patients have questions actually are dicots, which places them in very distant relationship to the grass family. Such species include buckwheat, amaranth, quinoa, and rape. The seed of the last plant listed, rape, is not eaten, but an oil is pressed from the seeds that is becoming commonly used in cooking. This oil is being marketed as canola oil. Because of their very distant relationship to the grass family and to wheat, it is highly unlikely that these dicots will contain the same type of protein sequence found in wheat proteins that causes problems for celiac patients. Of course, some quirk of evolution could have given rise in these dicots to proteins with the toxic amino acid sequence found in wheat proteins. But if such concerns were carried to a logical conclusion, celiac patients would have to exclude all plant foods from their diets. For example, buckwheat and rhubarb belong to the same plant family (Polygonaceae). If buckwheat were suspect for celiac patients, should not rhubarb, its close relation, be suspect as well? It may be in order to caution celiac patients that they may have undesirable reactions to any of these foods--reactions that are not related to celiac disease. Allergic reactions may occur to almost any protein, but there is a great deal of individual variation in allergic reactions. Also, buckwheat, for example, has been claimed to contain a photosensitizing agent that will cause some people who have just eaten it to develop a skin rash when they are exposed to sunlight. Such reactions should be looked for, but for most people, buckwheat eaten in moderation apparently does not cause a problem. (Buckwheat is sometimes found in mixture with wheat, which of course would cause a problem for celiac patients.) It seems no more necessary for all people with celiac disease to exclude buckwheat from their diets because some celiac patients react to it than it would be for all celiac patients to exclude milk from their diets because some celiac patients have a problem with milk. In conclusion, scientific knowledge of celiac disease, including knowledge of the proteins that cause the problem, and the grains that contain these proteins, is in a continuing state of development. There is much that remains to be done. Nevertheless, steady progress has been made over the years. As far as I know, the following statements are a valid description of the state of our knowledge: o Spelt or spelta and Kawmut are wheats. They have proteins toxic to celiac patients and should be avoided just as bread wheat, durum wheat, rye, barley, oats and triticale should be avoided. o Rice and corn (maize) are not toxic to celiac patients. o Certain cereal grains, such as various millets, sorghum, teff, ragi, and Job's tears are close enough in their genetic relationship to corn to make it likely that these grains are safe for celiac patients to eat. However, significant scientific studies have not been carried out for these latter grains. o There is no reason for celiac patients to avoid plant foods that are very distantly related to wheat. These include buckwheat, quinoa, amaranth, and rapeseed oil (canola). Some celiac patients might suffer allergies or other adverse reactions to these grains or foodstuffs made from them, but there is currently no scientific basis for saying that these allergies or adverse reactions have anything to do with celiac disease. A celiac patient may have an allergy to milk, but that does not mean that all celiac patients will have an adverse reaction to milk. I hope this information will be helpful. Please contact me if you need further details or clarifications. Sincerely, Donald D. Kasarda Research Chemist Crop Improvement and Utilization Research Unit cc: Elaine Hartsook, Gluten Intolerance Group, Seattle, WA Mary Alice Warren, Gluten Intolerance Group of Florida, Cocoa Beach, FL Annette Bentley, American Celiac Society, Dietary Support Coalition, West Orange, NJ Elaine Monarch, Celiac Disease Foundation, Studio City, CA Antoinette Betschart, Director, Western Regional Research Center, Albany, CA Wilda Martinez, Associate Deputy Administrator, Agriproducts & Human Nutrition Sciences, Agricultural Research Service, Beltsville, MD ========================================================================= Date: Fri, 26 May 1995 10:02:17 EDT From: Bill Elkus (Bill_Elkus@JEFCO.com) Subject: Reichelt on hyperactivity and diet. As promised, here is a guest post from Dr. Reichelt. This may be of value to parents of ADHD children who are doing their own reading in the area (or to their doctors).. From: K.L.Reichelt @ rh.uio.no Date: 05/26/95 05:36:59 PM Hi. Just a few references to diet and hyperactivity syndrome. 1: Egger J et al (1985) Controlled oligoantigenic treatment of the hyperkinetic syndrome. The Lancet .march 9th :540-544. 2:Kaplan SJ et al (1989) Dietary replacement in preschool-aged hyperactive boys. Pediatrics 83:7-17. 3: Egger J et al (1992) Controlled trial of hyposensitisation with food-induced hyperkinetic syndrome .The Lancet 339:1150-1153. 4:Carter CM et al (1993) Effects of a few food diet in attention deficit disorder. Arch Dis Child 69:564-568. 5: Marshall (1989) Attention deficit disorder and allergy :A neurochemical model of the relationship between illnesses. Psychol Bulletin 106: 434-446. Furthermore high intake of low roughage ( purified ) carbohydrates cause rapid increases in blood sugar followed by rapid insulin increase and subsequent steep fall.This is prevented by high fiber additions concomitant with carbohydrate intake. It is possible to have an overshoot with postprandial hypoglycemia. This is more common in habitually violent offenders in Finland. Virkkunen M (1982)) Reactive hypogycemia tendency among habitually vioent offenders. Neuropsychopharmacol 8: 35-40. Finally we have found peptide increases (possibly phosphorylated/glycosylated?) in Hyperkinesia. ( Hole K et al ( 1988) Attention defciti disorders: A study of peptide-containing urinary complexes. j develop behav Pediatrics. 9: 205-212.). It should also be noted that concentrated glucose can increase the paracellular uptake in the gut .That is also more protein and peptides can be taken up. Ref : Pappenheimer JR and Madara JL (1993) Role of active transport in regulation of junctional permeability and paracellualr absorption of nutrients by intestinal epithelia .in Istonic transport in leaky Epithelia (Alfred benzen Symposium)Munksgaard ,Copehagen : pp 221-232. Hope this may be of some use to at least some parents. 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: Fri, 26 May 1995 09:53:39 EDT From: Bill Elkus (Bill_Elkus@JEFCO.com) Subject: Kasarda on cross contamination On May18th, Don Kasarda commented on the recent pilot study suggesting that oats may be safe for Celiacs (generally, he advised caution, the study was small, full study not published, etc.)... He also said in that May 18th post: DK I will also mention that they had considerable difficulty buying DK supplies of oats that were not contaminated with wheat and DK used extensive laboratory testing to clear their supplies. DK So how are you going to be sure that your oats are not DK contaminated? In a private email, I asked Don if there was something about oats in particular which makes them more likely to be contaminated with wheat than other grains, such as rice, corn, or the exotic grains. His reply follows (with his permission): DK With regard to your question about oats--I think oats may be more DK frequently contaminated with wheat (or rye or barley) than other DK grains because it may be grown in rotation with wheat or in DK adjacent fields so that volunteer wheat might well be present in DK the fields and be harvested with the oats. I am not sure, but I DK would make a guess that most farmers growing oats probably also DK grow wheat so that contamination from truck beds, machinery, and DK storage facilities is possible. Grains like corn are often grown DK separately from wheat, to some extent even in different parts of DK the country, and the way they are grown makes contamination less DK likely. This may be true of amaranth, quinoa, etc., as well. DK DK Beyond that, contamination during transportation and processing DK would probably not be much different than for other grains. I would add (from the little that I know about agriculture) that rice tends to be grown in a completely different climate from wheat, and should also be less likely to be contaminated in the fields. Bill Elkus ========================================================================= Date: Sun, 28 May 1995 16:09:26 PDT From: "Donald D. Kasarda" (kasarda@PW.USDA.gov) Subject: lemon grass harmful? Dain Smith requested information about lemon grass (Cymbopogon citratus). Reply from Don Kasarda, Albany, CA As far as we know, the proteins harmful in celiac disease are expressed only in the grain of certain grasses, wheat being the primary one, so stalks and leaves in themselves are not likely to be harmful unless contaminated with seeds or grain or exudates from seeds or grain (as in pressing). According to the Manual of Grasses of the Grasses of the United States (Hitchock, 2nd ed., U. S. Government Printing Office, 1950), lemon grass falls in Tribe 13, Andropoganeae. For comparison, in this particular taxonomy, wheat, barley, and rye fall in Tribe 3, oats in Tribe 4, rice in Tribe 9, and maize (corn) in Tribe 14. I interpret this as indicating that lemon grass is much more closely related to corn than to wheat and even the seeds (grain) are not likely to be harmful. This is not medical advice and I know of no scientific testing of lemon grass in regard to its potential toxicity in celiac disease. ========================================================================= Date: Tue, 30 May 1995 10:08:43 PDT From: "Donald D. Kasarda" (kasarda@PW.USDA.gov) Subject: vinegar )celiacs, in my view, should err on the side of safety! CSA/USA must have )some good reasons for prohibiting distilled vinegar. I certainly agree that full information should be available and then each person can make a decision based on that information. In this regard, I hope that someone from CSA/USA (or any other celiac group that prohibits grain alcohol based vinegar) will provide the basis for their prohibition. It would be helpful. If I knew what this belief was based on, perhaps I could do some checking. Don Kasarda Albany, CA ========================================================================= Date: Fri, 9 Jun 1995 10:43:33 PDT From: "Donald D. Kasarda" (kasarda@PW.USDA.gov) Subject: Patient Support Group Addition from Don Kasarda to list of support groups provided by Don Wiss. I think that Phyllis J. Brogden, Chairman of the Greater Philadelphia Celiac-Sprue Support Group, is doing an outstanding job with her group and felt that the Greater Philadelphia group should certainly be included in the listing of patient support groups. I am not sure what the membership fee is, but Phyllis can be contacted for information. I understand that an extensive information packet is supplied to each new member. Phyllis J. Brogden, Chairman Greater Philadelphia Celiac-Sprue Support Group 6318 Farmar Lane Flourtown, PA 19031 Telephone: 215/836-7518 ========================================================================= Date: Tue, 13 Jun 1995 09:46:55 -0400 From: Alessio Fasano (afasano@UMABNET.AB.UMD.EDU) Subject: CD and growth problems Dear Kathy, your question about CD and poor growth is one of the most frequent questions that I deal with in my practice and I am more then happy to try to give you more insight on this issue. Children with typical symptoms of the disease (i.e. chronic diarrhea, irritability, distended abdomen, etc.) present poor weight gain or weight loss, while the high is usually not affected, at least in the first stage of the disease. Consequently, they appear dystrophic (weight/high Lt 5 centile). These patients do not offer any problems in terms of diagnosis. More difficult to identify are the cases presenting atypical symptoms. Sometimes the short stature is the only symptom present. In other cases the weight and/or the high may fall off from the growth chart (i.e. weight gain unappropriate for their age, high growth LT 6.5 cm/year), but no gastrointestinal symptoms are present. As concern your child, the "drop" in centile at 15 month of age is not unusual and may be due to changes in diet, eruption of teeth, etc. On the other hand, he had a proportional growth since age two, remaining on the same centiles. Based on the previous considerations, it is unlikely that he is affected by CD. Different story would be if he is a first degree relative of a proved CD patients. Since the prevalence of CD among first relatives of celiacs is higher then in the general population, it is now general recommendation to screen them for the presence of antigliadin and antiendomysium antibodies in the blood, despite the presence of symptoms resembling CD. Alessio Fasano, M.D., Director Division of Pediatric Gastroenterology and Nutrition University of Maryland, School of Medicine 22 S. Greene St., PO Box 140 Baltimore, MD 21201 ========================================================================= Date: Tue, 13 Jun 1995 18:33:03 -0500 From: J. Murray (jomurray@BLUE.WEEG.UIOWA.EDU) Subject: Re: re skin rash that got better on GFD and RAST The improvement of an itching rash with the introduction of a GFD should suggest the possibility of dermatitis herpetiformis. This can be diagnosed by special biopsies done by a dermatologist that suspects the condition. See earlier postings on the subject. RAST testing is a very controversial topic with little hard scientific basis for its use in diagnosing food allergies( this is apersonal opinion) Serology testing for celiac disease is much more precise. I would regard a careful history , exclusion and rechallenge( perferable blinded as a better test of allergies. However these are not always possible or practical. The whole area of food allergies is also affected by food intolerances which include lactose intolerance, chemical effects of foods, chocolate, coffee would be two examples. I regard CD as simple as compared to food allergies. Joe Murray (not medical advice) ========================================================================= Date: Thu, 15 Jun 1995 16:20:51 PDT From: Donald D. Kasarda (kasarda@PW.USDA.gov) Subject: rice bran )From Don Kasarda, Albany, California (firstname.lastname@example.org) There have been some questions on the list recently about bran as a fiber source. Unless wheat bran is very specially washed for the celiac market, I would expect it to have some endosperm contamination (endosperm being the part of the grain that has gluten proteins and is the source of white flour) and would not recommend it. I think rice bran is a good alternative for celiac patients. Rice is a major crop in California. There has been a problem with rice bran developing rancidity because of lipase enzymes and this laboratory has developed a process for rice bran stabilization that involves extrusion cooking, which inactivates the lipase. If anyone wishes to try to find some retail sources of the stabilized rice bran, he or she might might contact one of the companies using the extrusion cooking process developed here. The following address is for one of them: Food Extrusion, Inc. Daniel L. McPeak, CEO 1241 Hawk's Flight Court El Dorado Hills, CA 95630 Tel. 916/933-3000. Alternatively, if a full-fat fresh rice bran could be obtained right after milling (from the California or East Texas/Louisiana mills), storing the bran in a freezer should prevent development of rancidity. ========================================================================= Date: Mon, 19 Jun 1995 22:34:25 -0500 From: "J. Murray" (jomurray@BLUE.WEEG.UIOWA.EDU) Subject: Re: CELIAC Disease as a contagious entity? As far as we know CD is not an infectious disease. I have had only one husband/wife pair with celiac disease and have never seen unrelated adopted children both get it. If anyone has experience of that finding please e-mail me post it. There is certainly conflicting evidence on whether a infection triggers the presentation( not necessarily the start of the disease) in a genetically predisposed person. Not all of the cause is genetic in that 3 out 4 identiacl twins will have the diseae but not all pairs. Joe Murray ========================================================================= Date: Tue, 20 Jun 1995 00:12:28 -0500 From: "J. Murray" (jomurray@BLUE.WEEG.UIOWA.EDU) Subject: Re: latex allergy and biopsy The presence of latex allergy is becoming more common and can be serious. However more centers are becoming aware of this problem and can now carry out many mediacl and surgocal roceedures without exposure to latex. Endoscopically directe d biopsy can be done latex free so long a careful exclsion of latex is made. Most endoscopes dont not have latex components on the insertion tube. they can have elsewhere. medications need to be specially prepared also. it can also be reasonable to study the patient in a less precise way by antibodies and absorbtion tests. Joe Murray not medical advice ========================================================================= Date: Thu, 22 Jun 1995 14:40:44 EDT From: Bill Elkus (Bill_Elkus@JEFCO.com) Subject: Reichelt: Schizophrenia and diet A guest post from Kalle Reichelt, MD, PhD (in reply to the recent posts on this topic) Hi. I would like to draw your attention to a wee paper from us (1) on diet and schizophrenia ,where we followed completely blind 10 semichronic (not the best starting point) male schizophrenics for 1 year. We could conlcude : a) That both urinary peptide excretion and rating scales (Comprehensive Pyschopathological rating scale and Whitaker Index of schizophrenic thinking) as well as clinical state improved slowly on diet, with regression in those off. This was a crossover study. b) It is not unreasonable that changes will be slow because the kidneys are efficient peptide, aminoacid and protein preserving organs. c) The trophic changes in brain in schizophrenia established macroscopically and microscopically in a great many publications the last 10 years, would take time to correct if at all possible. Probably not completely being maturational defects to some extent ( 2).There is also the problem of an optimal timing for maturation of nerve cells as demonstrated in the visual cortex. This means that experiments on chronic cases is a poor way to test the hypothesis. Fairly fresh cases would be ideal. We have recently been able to demonstrate the presence of at least 5 (five) peptides with opioid activity in urines and dialysis fluid from schizophrenics that react to antibodies against bovine casomorphin 1-8.One of these cochromatogrpahs and has the same amino acid composition as bovine casomorphin 1-8.(Reichelt submitted ; as in autists (3)).The very fulminant psychosis seen in post-partum psychosis seems to be mediated by human casomoprhin (4) and demonstrates that such peptides do have access to the Central nervous system (CNS). Furthermore IgA antibodies against gliadin .beta-lactoglobulin and casein are increased in male schizophrenics (5)indicating a connection.NB: The biopsies were normal so that this is not coeliac disease, but a state with increased transmucosal protein/peptide transport. After all uptake in small amounts of intact protein and peptides is well documented (see earlier communications) WE think therefore that it is important to be gluten/gliadin free and milkprotein free if diet is to be used.The more so because gliadinomorphin and casomorphin are very similar and gliadinomorphin is part of the coeliac disease peptide B3142(6) Gliadinomorphin : Y-P-Q-P-Q-P-F Casomorphin(b) Y-P-F-P-G-P-I etc. There are a series og gluten derived opioids too. This is one of the reasons why we remove both protein sources in autistic syndromes too (2,7,8)with again long term but clearly measureable effects and regression in all who quit diet. The paper that was read to Dohan has been changed to : Can schizophrenia be reasonably explained by Dohan s hypothesis on genetic interaction with a dietary peptide overload? . It is hard ot get this published because it goes against the present trends. However, I think it extremely important so I keep trying ( I am of course rather partial to the hypothesis which makes it difficult). I find it remarkable that given the complete lack of aetiology directed treatment that a proper clinical trial should be so difficult to establish.After all also an American has published data along these lines (9) using our old urine screening assay.Our new technique based on Shattocks groups work in the UK but changed a little( Reichelt in prep) is of course available to anyone who is interested.It is fast and with fewer false positives.They are also wellcome here to learn by doing. Finally it should be stressed that opiods do have maturation inhibitory effects in rat brain (10),which would fit Crows(2) data quite nicely . References 1: Reichelt KL et al (1990) The effect of a gluten free diet on glycoprotein associated urinary peptide excretion in schizophrenia J Ort Mrd 5: 223-239. 2:Crow T(1994) Aetiology of schizophrenia .Current Opin.Psychiat7: 39-42 3:Reichelt Kl et al (1991) The probable etiology and possible treatment of childhood autism . Brain Dysfunct. 4:308-319. 4:Lindstr|m LH et al (1984) CSF and plasma beta-casomorphin-like opioid peptides in post-partum psychosis. Amer.j psychiat. 141:1059-1066. 5: Reichelt Kl and Landmark J (1995) Specific IgA antibody increases in schizophrenia. J Biol Psychiat37:410-413. 6. Wieser H et al (1984) Amino-acid sequence of the coleiac active peptide B 3142. Z Lebensmittel Untersuch Forsch 79:3371-3376. 7:Knivsberg A-M et al (1990) Dietary intervention in autistic syndromes. Brain Dysfun.3:315-327. 8: Knivbserg A-M et al (1995) Autistic syndromes and diet .A four year follow-up study of 15 subjects. Scand J Educat. Res : In press (accepted) 9: Cade R et al (1990)The effects of dialysis and diet in schizophrenia Psychiatry: A World prespective 3:494-500. 10:Zagon IS and Mclaughlin PJ (1987) Endogenous opioid systems regulate cell proliferation in the developing rat brain .Brain Res 412:68-72 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: Fri, 23 Jun 1995 09:44:33 -0400 From: Alessio Fasano (afasano@UMABNET.AB.UMD.EDU) Subject: Couple convicted in son's death - Reply Dear Mr and Mrs. Kennedy, I red your e-mail concerning the frustration about the resistance of doctors to "try a gluten free diet". It is out of discussion that there are many phisicians (including gastroenterologists) that are poorly knowdlegible about celiac disease and their advises may sometimes generate confusion. But it is also out of discussion that there are outstanding experts on the disease that spent a great deal of time and effort to come out with reccomendations and guidelines for the correct diagnosis of the disease. When you state: "..it IS possible to just try the diet rather then put kids.. thru the biopsy", you contribute to generate this confusion. As you well know, Celiac disease is a life-long condition (in other words, when you got, you got it!). You cannot commit yourself for the rest of your life to a challenging diet without being 100% sure of the diagnosis. Currently, there are no short cuts: testing for the antigliadin and antiendomysium antibodies, followed by the intestinal biopsy (if the antibodies are positive) is the ONLY way to make the diagnosis. Trying a diet, without being sure of the diagnosis, is like treating yourself as a "guinea pig". If we really want to avoid that other patients will experience the same frustrations that you and other people had suffered, we should work togheter to educate the american scientific community and the next generation of physicians to learn about the disease. We are working very hard on this task as well as to prove that celiac disease is not a negligible condition in USA. Alessio Fasano, M.D., Director Division of Pediatric Gastroenterology and Nutrition University of Maryland, School of Medicine Baltimore,MD email@example.com ========================================================================= Date: Fri, 23 Jun 1995 09:28:59 PDT From: "Donald D. Kasarda" (kasarda@PW.USDA.gov) Subject: schizophrenia, arthritis, ms Mike Johnson stated that: Schizophrenia, arthritis, and multiple sclerosis seem to be associated with gluten and that there seem to be practical and statistical indications to the contrary. Comment from Don Kasarda, Albany, CA I would be very much interested in the literature references that provide significant statistical indications of an association of the above mentioned conditions with gluten ingestion. I am mainly aware of studies in the area of schizophrenia where those that claim a significant correlation are canceled by others that haven't found such a correlation. This may well be a problem of experimental design rather than indicating a lack of any connection, but I haven't been convinced of a significant correlation by what I have seen so far. I understand the frustration that results when needed research isn't being done, but research costs money, often big money, and the funding frequently isn't available to researchers no matter how interested they might be in the problem. Also, when dealing with human subjects, there are major problems finding willing, suitable participants for studies and, in the case of schizophrenia, for example, with informed consent by subjects. ========================================================================= Date: Mon, 26 Jun 1995 08:28:33 -0400 From: Karoly Horvath (khorvath@UMABNET.AB.UMD.EDU) Subject: Biopsy or self-diagnosis? I have read the comments about the necessity of biopsy in celiac disease and a patient's letter who was diagnosed by biopsy and his/her symtoms did not improve. Let me write down my opinion shortly. -The biopsy is absolutely necessary in the diagnosis in CD,especially in adult. I do not want to list all the reasons. One of them, that there is a condition so called hypoplastic villus atrophy (CD is a hyperplastic diseas with increased mitosis number), which is not CD, but should be followed carefully, because of the possibility of malignancy. -A second reason: when we are performing a biopsy we analyze the activity of lot of digestive enzyme. Tipically the enzymes localized in the luminal part of intestinal cells can have low activities. It means that at the beginning we should start not only a gluten-free diet, but should consider the malabsorption of lactose, sucrose etc. If somebody does not improve in gluten-free diet immediately one reason can be a so-called secondary dissacharidase deficiency. The recovery time of the damaged intestine mucosa is generally much slower in adult than in children. -Third: I have written down in the Celiac BBS that the biopsy is nor a dangerous procedure and necessary for the diagnosis. -I understand the frustation of lot of people in this country having celiac disease. However, I feel a bit "upset" that this negative feeling are directed to gastroenterologist, who really have expertise in the diagnosis of this disease (e.g. I have 18 years experience with children), by questioning the necessity of intestinal biopsy and a proper diagnosis. Karoly Horvath, M.D. University of Maryland ========================================================================= Date: Tue, 27 Jun 1995 09:20:19 PDT From: "Donald D. Kasarda" (kasarda@PW.USDA.gov) Subject: reactions leanne Wenzel wrote: )In Canada French's mustard is considered to be safe. Tumeric is a spice and )does not contain any gluten. Cocoa processed with alkali definitely does not )contain gluten. If you have reactions to these substances it has nothing to )do with a gluten intolerance. Comment from Don Kasarda, Albany, CA My guess is that about 90% of the claims of "hidden gluten" made on this list have nothing to do with gluten intolerance. People react to all kinds of things and not always consistently. It seems to me unreasonable to attribute every twist and turn of the intestinal tract to "hidden gluten." ========================================================================= Date: Thu, 29 Jun 1995 15:08:23 PDT From: "Donald D. Kasarda" (kasarda@PW.USDA.gov) Subject: time req. for challenge Comment from Don Kasarda, Albany, CA. Laura Johnson-Kelly complained that no medical professional had replied to her question about guidelines on what is necessary for a challenge. I suspect the reason for a lack of response from the medical professionals has to do with the complexity of the issue. It would take many hours of literature review and writing to put together even a minimally adequate response. In the absence of comment from the medical professionals, however, I will offer some comments from a non-medical professional (me). Back in the mid 1970's, I thought it might be interesting to test celiac patients with bread from a wheat in which geneticists had removed a large block of alpha-gliadin genes (the protein product of which is known as A-gliadin) in the hopes that it might be a non-toxic wheat. At that time, we only knew for sure that gliadins as a whole were toxic and that the A-gliadin fraction was toxic (the only fraction that had been adequately tested). With the collaboration of a highly experienced and expert group at the National Institutes of Health (NCI), which had patients available for participation, we tested the nulli-6A bread (as I named it) by feeding it, and bread from a normal wheat as a control, to 6 well-characterized adult celiac patients. Characterization included biopsy. We fed either 1 loaf per week or 2 loaves per week (corresponding approximately to 4 grams and 8 grams of gluten, respectively, per day). Later we fed them the normal bread. This was almost entirely done with the patients hospitalized, so they were under complete control. The least responsive patient had only very minor symptoms after two weeks on the nulli-6A bread (4 loaves total), but showed mild to moderate villous atrophy when biopsied (biopsy had been normal at start). None of the patients showed severe symptoms on the nulli-6A bread, but all 4 who were biopsied showed at least some deterioration of the mucosa on biopsy. As a control, the normal bread was then fed to 4 of the same patients for 1 week (1 loaf) and all experienced diarrhea by the end of the week. Only 1 patient was biopsied at this point and showed mucosal damage. At that time, standard antibody screening had not been developed, so studies of antibody development upon challenge were not done. I should indicate that, unfortunately, when a paper on this work was submitted to the journal Gastroenterology, the referees and editor rejected the paper and so it has never been published. Personally, even after all these years, I don't think there was any adequate reason for rejection of the paper, which contained some very valuable information about gluten challenge with controlled amounts of bread only, as opposed to just putting the patient on a normal diet. Any defects in the presentation of the work in the manuscript could easily have been remedied, but rejection is not unusual in the world of scientific publishing. Some highly arbitrary decisions are made by very few people. Some junk gets published and some good work does not. We concluded that the nulli-6A bread was likely to be of lower toxicity than normal bread, but still definitely toxic. With our knowledge now that all gliadins are toxic, this would be expected. In another study that I know of, 0.5 gram of gluten per day (a relatively small amount) was fed to 4 adult patients for about 6 weeks. Two patients showed villous atrophy at the end of the period and the other two showed signs of infiltration by intraepithelial lymphocytes, which is considered to the be the very first sign of mucosal change in gluten challenge. In a paper published in 1988 by Ansaldi et al., they reported that of 13 children placed on a normal gluten-containing diet (Italy), 9 had symptoms at the end of one month and 12 showed a flat mucosal biopsy at that time. Finally, however, there are some reasonably well documented cases where properly diagnosed patients (usually children) have gone back to a normal diet for years before relapsing, as indicated by regular biopsies. Being aware of much of the literature involving challenges, I think it is extremely difficult to specify the amount of gluten and the time required for proper challenge because of the enormous variability among patients. Perhaps, however, the information I have given will be of some help to patients contemplating a gluten challenge. I am surprised by the number of people who write to the list about instant reactions to gluten. My long-time impression of many studies involving challenge has been that most celiac patients do not respond with immediate distress within hours of first eating wheat. Perhaps this is incorrect. Perhaps there has been a strong self-selection factor involved in that people who have severe reactions are not likely to volunteer for or agree to gluten challenge studies. There may also be a self selection factor for BBS communications in that the people who have the greatest problems and odd symptoms may tend to communicate to the list to a greater extent than those who have few problems.
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