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    Is Wheat Breeding Really Driving Higher Rates of Celiac Disease?


    Jefferson Adams

    Celiac.com 03/27/2013 - Increased rates of celiac disease over the last fifty years are not linked to wheat breeding for higher gluten content, but are more likely a result of increased per capita consumption of wheat flour and vital glutens, says a scientist working with the US Department of Agriculture (USDA).


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    Photo: CC--D. H. WrightThe researcher, Donald D. Kasarda is affiliated with the Western Regional Research Center of the U.S. Department of Agriculture's Agricultural Research Service.

    Kasarda recently looked into one prominent theory that says that increased rates of celiac disease have been fueled by wheat breeding that has created higher gluten content in wheat varieties. His research article on the topic appears in the Journal of Agricultural and Food Chemistry.

    Kasarda says that, while increased consumption of wheat flour and vital wheat gluten may have contributed to the rise in celiac disease over the last decades, "wheat breeding for higher gluten content does not seem to be the basis."

    He notes that vital gluten is a wheat flour fraction used as an additive to improve characteristics like texture, and commonly featured in numerous and increasingly popular whole wheat products. However, he says that there is a lack of suitable data on the incidence of celiac disease by year to test this hypothesis.

    Part of his article features statistics on wheat flour consumption throughout the two centuries. He notes wheat flour consumption from all types of wheat hit an all-time high of 220 pounds per person (100kg) in 1900, declined steadily to a low of around 110 pounds per person (50kg) in 1970, then gradually rose to about 146 pounds per person (66kg) in 2000, and then decreased to about 134 pounds per person (61kg) in 2008.

    He goes on to point out that, even though consumption of wheat flour "seems to be decreasing slightly in recent years, there was an increase in the yearly consumption of wheat flour of about 35 lb (15.9kg) per person in the period from 1970 to 2000, which would correspond to an additional 2.9 lb (1.3kg) of gluten per person from that extra flour intake."

    Kasarda suggests that 'crude estimates' indicate that consumption of vital gluten has tripled since 1977. He finds this fact very interesting, because, he says, "it is in the time frame that fits with the predictions of an increase in celiac disease."

    However, he says that attributing an increase in the consumption of vital gluten directly to the rise of celiac disease remains challenging, partly because consumption of wheat flour increased far more significantly in the same time frame.

    Additionally, Kasarda says that there is no evidence that farmers have been breeding wheat to ensure higher protein and gluten content over the years. He points out that numerous studies have compared the protein contents of wheat varieties from the early part of the 20th century with those of recent varieties. These studies have all shown that, "when grown under comparable conditions, there was no difference in the protein contents," he said.

    One factor that remains unanswered is the relationship between higher rates of celiac disease and higher rates of diagnosis. That is, are more people developing celiac disease, or are more people simply with celiac disease getting diagnosed than in the past?

    It's likely that more and more people with celiac disease are being diagnosed, but it's unclear whether celiac disease rates are rising. There is just not enough evidence yet to provide a solid answer, although studies in the US and in Finland suggest that rates of celiac disease may be on the rise.

    Kasarda's article points out how much more research needs to be done. We need to determine if there is, in fact, a genuine rise in celiac disease rates and, if so, how such a rise might relate to gluten consumption.

    For now, though, there just isn't any solid evidence that wheat has any higher gluten levels than in the past, or that gluten consumption is driving an increase in celiac disease levels.

    What do you think? Have you heard this theory about modern wheat having higher gluten levels, or being substantially different than wheat in the past? Have you heard that such a difference may be driving higher rates of celiac disease? Please share your comments below.

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    Guest Share

    Posted

    I have to wonder if this person even understands what celiac disease is, and how it develops in a person. It isn't just that wheat is bred for "more gluten"... it is that with the cross-hybridization of wheat to create a hardier grain with a shorter stalk, we have started introducing NEW forms of protein molecules in the gluten that are foreign to our bodies. When our bodies detect a foreign substance that they are having trouble producing antibodies for, it goes into lockdown mode, and attempts to use all its immune defenses to protect itself. Studies have found incidents of at least 20 NEW types of bacterium amongst celiacs in the human intestine...bacteria that has never been seen before. More study must be done by the medical community as well as scientists before making such a bold statement.

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    Guest Giordano Checchi

    Posted

    I do not think the issue is the amount of gluten in new breeds of wheat. I agree with the previous comment. Something changed in wheat. Born in Italy I ate pasta, bread, and pizza all of my life and I never suffered from gluten intolerance until I was well into my middle age. Then "bang", it hit me like a cannon ball. Why? My only answer is: wheat must have changed. And I will continue to think so until proven wrong.

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    I admit that I have jumped on the band wagon and been quick to blame wheat tampering for the rise in celiac disease. But I read an article recently speculating that modern medicine could be to blame. It turns out that many drugs can cause a leaky gut. Maybe once the gut becomes leaky, gluten proteins pass through and those with celiac genes react and develop the disease. Just another thought.

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    Guest Penny

    Posted

    I agree with the above entry. This man has no common sense and just knowing he is affiliated with the Agriculture Dept raises tons of red flags. You don't have to be an expert to look at how wheat has been modified over the years to realize this will have an effect on the population. And his statistics are just like any, they can be molded into almost any "outcome" you desire.

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    Guest ACurtis

    Posted

    I have to wonder if this person even understands what celiac disease is, and how it develops in a person. It isn't just that wheat is bred for "more gluten"... it is that with the cross-hybridization of wheat to create a hardier grain with a shorter stalk, we have started introducing NEW forms of protein molecules in the gluten that are foreign to our bodies. When our bodies detect a foreign substance that they are having trouble producing antibodies for, it goes into lockdown mode, and attempts to use all its immune defenses to protect itself. Studies have found incidents of at least 20 NEW types of bacterium amongst celiacs in the human intestine...bacteria that has never been seen before. More study must be done by the medical community as well as scientists before making such a bold statement.

    I agree completely with you, Share. You've hit the nail on the head. It would be nice if there were actually scientists who did real scientific research--regardless of who or what industry that "research" might hurt. We need good, honest-to-goodness research done that doesn't rely on anyone's money to fund it. That way, no scientists are watching over their shoulders, wondering who they might tick off with the research results--the right, correct, unbiased research results.

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    Guest Denise

    Posted

    Interesting article! I believe a combination of new strains of wheat, higher consumption, and more accurate diagnosis are all factors in the current higher rate of celiac disease. Looking at any one factor alone does not give a clear answer for the higher incidence of this disease. Remember this is a complicated genetic disorder.

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    I totally agree with the above two entries, also wheat is added to so many 'convenience' foods nowadays, people eat more packaged food than in the past and so are eating a large amount of 'hidden' gluten. It wasn't until I became gluten intolerant last year that I realized just how much gluten there is in everyday foodstuffs apart from bakery products.

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    Guest CeliacMom

    Posted

    I think both this article by Mr. Adams and the research that he describes by Dr. Kasarda (USDA) are very good science and very good way of interpreting science; very useful information for us trying to make sense of a poorly understood disease. We must base our opinions in facts that can be corroborated by real data. "Common sense" is meaningless; some years back slavery was "common sense," but now we know it is not; pardon my extreme example. Yes it is POSSIBLE that new wheat varieties MAY have new forms of gluten that MAY lead to more celiac disease, it is a good hypothesis, but it must be proven correct or not with facts, not musings of our imagination. This is said in the spirit of waking people up to reality, not to offend.

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    I think it's worth getting this discussion going. My father was a plant geneticist in Montana. He bred wheat grasses here, though others worked on wheat itself, but for 2 years in the 60s he worked in Turkey on a higher yield wheat. I remember buying "hi-protein" wheat through a co-op. So yes, what I have seen is that geneticists have been developing wheat strains with higher protein yield.

    As to the question of a rise in incidence or a rise in testing with celiac, my experience would indicate the latter. It took me 10 years to figure out what was going on with me, and the only reason I did was that my son had very extreme symptoms, which led to us testing all of us. I remember my mom having very similar symptoms to mine in her 40-50s, but she just suffered through - it was never diagnosed. To this day, even though she has gone on to have additional celiac symptoms, she does not believe she has the disease. It's what's "normal" in her mind.

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    Guest Christine

    Posted

    Wonder how much wheat farmers paid this person to question the relation between celiac disease and wheat consumption?! I'm getting sick of telling family members and other wheat farmers that I can't eat their grain, only to have them (at best) look at me like I have 5 heads or (at worst) make me feel like a total pariah because I have celiac disease. And it's really humiliating to have to go into a small town restaurant where the main customer base is wheat farmers, only to read that their menu doesn't include any gluten-free choices. What really upsets me is how the owners of these small-town restaurants fail to learn about celiac disease and train their staff how to appropriately accommodate our needs. They then have the gall to turn the blame back on us for having celiac disease when they fail to educate their help about how to properly handle our food and make excuses for their staff. Appalling.

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    Guest Chris

    Posted

    I doubt that a rise in wheat consumption has led to more recognized cases of celiac disease. For me, a single crumb of something containing wheat can trigger a full reaction. It isn't a question of how much, but a question of whether I ate something containing wheat gluten. What might be a factor is the hidden wheat flour in many packaged foods. Wheat flour is added to sunflower seeds, peanuts, shredded cheese and many many others to prevent clumping. This wheat does not appear on the label! It should, but it doesn't.

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    Guest Nicole

    Posted

    I have to wonder if this person even understands what celiac disease is, and how it develops in a person. It isn't just that wheat is bred for "more gluten"... it is that with the cross-hybridization of wheat to create a hardier grain with a shorter stalk, we have started introducing NEW forms of protein molecules in the gluten that are foreign to our bodies. When our bodies detect a foreign substance that they are having trouble producing antibodies for, it goes into lockdown mode, and attempts to use all its immune defenses to protect itself. Studies have found incidents of at least 20 NEW types of bacterium amongst celiacs in the human intestine...bacteria that has never been seen before. More study must be done by the medical community as well as scientists before making such a bold statement.

    The pathology of celiac disease occurs NOT because our body can not produce an antibody for gluten, but because our body does produce an antibody for gluten triggering a damaging immune response in some individuals.

     

    As for the "new" bacteria. The technology to identify the hundreds of bacterial species living in the gut (both in healthy and diseased individuals) is relatively new. There is still a huge amount of work that needs to be done to characterize these bacteria (and other microbes), let alone understand the relationship between the bacteria and host.

     

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    Guest Nicole

    Posted

    I do not think the issue is the amount of gluten in new breeds of wheat. I agree with the previous comment. Something changed in wheat. Born in Italy I ate pasta, bread, and pizza all of my life and I never suffered from gluten intolerance until I was well into my middle age. Then "bang", it hit me like a cannon ball. Why? My only answer is: wheat must have changed. And I will continue to think so until proven wrong.

    There is such a thing as silent or latent celiac disease. A life event that alters immune regulation can trigger celiac disease symptoms. It is quite common for celiac disease to present later in life, especially in women. The disease is quite complex because the immune system is quite complex.

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    Guest Celia

    Posted

    Just for the record, my 12 year old son has had what I firmly believe to be the celiac rash (and soon will find out) on and off for the last 5 years. At first I was told it was a highly contagious skin infection caused by him picking his nose and getting the germs into a small skin lesion. I was given cream and I think antibiotics (it's been awhile, may have just been cream.) It didn't seem to be working to well but maybe a little. When summer and salt water pool time came, it faded away. I assumes the salt water helped heal it and perhaps some sun too. I was highly relieved that none of the other 5 people in our house caught it (3 not genetically related to the other 3.) and no one else at school caught it and I could stop worrying about who was sitting on his bed, etc. (interestingly, I had something like psoriasis on my legs that I was told was vitamin/ sun related and given a cream for, I can't remember what doc called the rash though, or what the cream was, but before my son's rash had cleared, one time I accidentally started to put my cream on him, and I noticed the pigmentation in his skin lightening everywhere I put the cream. Fortunately I just did his knees and right under them before I stopped and realized I had the wrong cream. When I washed it off, his pigmentation remained lightened. It has been about 5 years and it is still like that.) The rash has come and gone quite a few times since then and usually departs in the summer. When it comes it STAYS for an eternity (well a few months at least.) He usually only gets 1-5 spots but the first time had more. He's had one on the side of his neck for a few months now. In the winter he had a bad lingering cough and got very itchy hives, or so I thought. I gave him allergy med I take and it cleared up. Took him to doctor who diagnosed him with walking pneumonia because he had had "hives" which are a symptom along with the rest. My daughter gets "hives" all over if she doesn't take allergy med. so she was already taking it. Although his hives cleared out quick, the spot on his neck didn't. He had been taking antibiotics for pneumonia so I figured they'd clear out the spot in a few days. Nope. He scratches it constantly and so I decided to try some extra strength Benadryl itch cream. It seemed to start working but every time it wore off he kept picking at it and would make it raw again. So I figured that was the reason it wouldn't heal because he kept picking it. So I became Super-cream mom and made sure to keep slathering it on (he won't remember due to other issues.) It finally started to fade back into its old scar (from the first time) just when 2 more popped up on the back of his neck. When I checked photos of the celiac rash recently they didn't look like his rash. So I figured it wasn't. However in reading yesterday more about the rash on various sites, it sounded like his in so many ways...locations, extreme itchy/burn, can't sleep, itchy back, length of rash, etc. because so many other things factored in as well besides the rash, for him, sister, and me, I decided to look at more pics. I looked at like 200. Only a very few looked like his. But I found them. I will take a pic when he gets home to document his type of rash (and I'll confirm if its celiac for sure as soon as I know.) I'm pretty sure for other reasons I'll share later as this post is long enough.

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    Guest Celia

    Posted

    It seems to me that it is more of an allergic reaction to the new proteins in wheat than it is how much of the wheat someone eats. Just like pollen, if a person is severely allergic they will have a bad reaction when the first hint of pollen comes out and a bad reaction when the rest of it comes out too. Sure it may be worse with more pollen, but if they had a bad reaction with just a little, they are still going to go seeking an allergist/ allergy medication. So since those with severe reactions to wheat are the ones who made the name celiac disease possible before there were any new proteins in wheat, we associate those severe cases with the disease, who continue having reactions to the new proteins as well. But now that there are more proteins in the wheat (if that proves to be the case) more people are having reactions to them because our bodies tend to associate those new things as allergens/ bad guys. People get hives as reactions to allergens and we usually automatically know what it is if we have allergies as allergies are pretty common. Those with severe/classic celiac skin reactions/ symptoms will most likely have been reacting with the same statistical outcome all through the recorded history of celiac disease/gluten allergy (assuming that the doctors know what it is- which many don't- so there goes that.) (But assuming they did (since many of them did) then the doctors would be seeing a certain percentage of those patients with say, the skin rash. So if you factored in more people becoming sensitive/ allergic to new proteins in wheat, who didn't react before, I would think there would be a large increase in the number of celiac rashes (the most obvious sign) observed by doctors. If this could be singled out somehow perhaps it could help make more sense somehow of all the other variables like doctors who have a clue what it is, people becoming informed over incredibly speedy Internet education/ gossip train, etc., etc., etc.

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    Guest Celia

    Posted

    Something I forgot to mention, I have read about toxins, substances and environmental factors being able to mutate genes. So if that's true, then all this stuff like autism, celiac, etc. being genetic as opposed to externally influenced is nonsense.

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    Guest Harold

    Posted

    Wonder how much wheat farmers paid this person to question the relation between celiac disease and wheat consumption?! I'm getting sick of telling family members and other wheat farmers that I can't eat their grain, only to have them (at best) look at me like I have 5 heads or (at worst) make me feel like a total pariah because I have celiac disease. And it's really humiliating to have to go into a small town restaurant where the main customer base is wheat farmers, only to read that their menu doesn't include any gluten-free choices. What really upsets me is how the owners of these small-town restaurants fail to learn about celiac disease and train their staff how to appropriately accommodate our needs. They then have the gall to turn the blame back on us for having celiac disease when they fail to educate their help about how to properly handle our food and make excuses for their staff. Appalling.

    I doubt anyone has "paid " any farmers to "support" the new grain-they are always anxious to be the first to adopt and use the newest things and it causes these changes in the product available on the market.

     

    If it produces higher yields they fall over themselves to get with the NEW. This is probably the opposite of a generation or two back when change was opposed!

     

    Don't forget, most of them are eating "the new" themselves too!

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    Scott Adams
    By R.A. Gibbons, MD., M.R.C.P., Physician to The Grosvenor Hospital for Women and Children, Physician for the Diseases of Women and Children at the St. George's and St. James's Dispensary.

    Footnote: (1) This title is adopted by Dr. Gee, who was the first to direct my attention to the disease, at the Hospital for Sick Children, Great Ormond Street, and I have therefore thought it best to retain it.
    The subject of this paper is one which has not been described, to my knowledge, in any of the text-books, either on general medicine or on the diseases of children. As it is one of great importance, and one which is readily overlooked, even by excellent physicians, I have thought that it would be of interest to publish a few of the cases which have come under my own observation of this somewhat uncommon disease. These cases are very similar, and it is therefore unnecessary to burden my paper with more than four, which will serve as examples of all.
    The name "coeliac" is derived from the Greek Koilia, which means belly. The "coeliac flux" is a well-known and o1d expression signifying diarrhea, in which the undigested food is passed from the bowel. The name of the affection under consideration does not necessarily imply diarrhea, and is taken for want of a better one; it means merely that the disease pertains to the abdomen. It has, however, the merit of not conveying anything actually erroneous. The disease is not distinctly a diarrhea although undoubtedly children suffering from this affection are liable to attacks of diarrhea. In the latter affection, if the larger bowel is affected, we get dysenteric symptoms; if the smaller bowel is the seat of the trouble, it is generally considered that we have three different conditions affecting it, namely, increased movement, increased secretions, or a diseased condition of the mucous membrane. The coeliac affection corresponds with neither of these conditions, as will presently be shown.
    The following cases are epitomized from notes taken of some of the patients who have been under my care in private practice:
     
    Case I -- J.F., a boy, aged 2 years, was first seen on the 26th of April 1883 (1)
    He was lying in his nurse's lap, looking flushed, and complaining of pain over the abdomen. He had been languid and vomiting during the morning. I ascertained that the motions had been copious, frothy, and offensive. He had been latterly losing flesh. As to the previous history, I learned that the child had been brought up by hand, and there was nothing of importance to relate until last December, since which time he had been out of health, and seemed to be gradually getting worse. In that month they had sought advice, and he had caused his parents anxiety ever since, sometimes being a little better, at other times worse. On examination I found that the temperature was over 99, the pulse 108; but no definite disease could be made out. The examination of the chest yielded nothing. The abdomen was soft and doughy, but painful to the touch, and he cried out when any attempt was made to palpate. The spleen and liver were not enlarged, and I could detect no enlarged lymphatic glands. The flesh was soft and flabby. As he was having rather frequent actions of the bowels, a mixture of bismuth and compound tincture of camphor was ordered.
    His diet consisted of cream, with two or three times as much water or scalded whey. For a drink at breakfast, at 11 o'clock in the morning, and at bedtime, whey made wit essence of rennet; if mixed with cream, it was to be scalded. Pounded raw meat prepared in the ordinary way, and rubbed through a sieve; of this one, two, or three tablespoonfuls to be taken for dinner, with a little sifted sugar or fruit jelly. A tablespoonful of mashed floury potato. Rusks, plain biscuits, or toast with fresh butter; Savory & Moore's food made with whey, and a teaspoonful of cream added. Half a pint of asses' milk in the morning, and the same quantity- in the evening. One or two teaspoonfuls of raw meat in the after part of the day. The following day I carefully examined some motion microscopically, and could detect no pus and nothing extraordinary.
    Family History:-- The mother was a healthy woman. She had had no miscarriage.
    She had no history of any important disease. There was no trace of tubercle on her side. Her mother suffered occasionally from gout. The child's father appeared a healthy man; he occasionally passed free uric acid, and had symptoms rather like those of renal calculus. There was no history of syphilis obtainable, and no reason to suspect it. There were two other children, a boy and girl, older than this patient. The girl had suffered from suppuration of the submaxillary glands.
    The child improved considerably until 5th July, when he had an attack of watery- diarrhea, which prostrated him. The motions were extremely offensive. Dr. Gee saw him with me, and suggested, instead of the compound kino powder, which he was taking, that he should have minute doses of mercury and chalk every two hours; forty-eight hours later the diarrhea had stopped. Without going further into detail, it may be stated that this attack nearly proved fatal. He, however, gradually recovered, the first favorable sign being that the motion contained some solid material. There was no change in the diet, except that the meat was omitted and Brand's essence substituted.
    The following month left London for the seaside. He occasionally had attacks of diarrhea there. Six months afterwards I again saw him, when he seemed in excellent spirits, looked fat, and, although flabby, ran about and played with the other children with apparent enjoyment.
    This boy died of acute purpura haemorrhagica, the details of which illness I have already published in the Medical Times and Gazette for 1885.
     
    Case II -- S.H., aged 2 years and 8 months. First seen on 10th May 1885
    Her condition is as follows:-- She is very anaemic in appearance. She is not thin or wasted, but her flesh is flabby, and her legs and arms, though apparently well covered with flesh, are soft to the touch. Nothing is to be discovered on examination of the chest, the heart sounds being normal, and the lungs acting well. On palpation of the abdomen, it is found to be doughy, blown out with flatulence, and looking very large. The liver can be felt about one finger's breadth below the edge of the ribs, and the spleen is slightly enlarged. No enlarged lymphatic glands can be made out anywhere. She walks with difficulty, and has a great disinclination to go upstairs. A very little exertion makes her tired, and break out into a profuse perspiration, especially about the head. Her appetite is poor, and it is with great difficulty that she can be coaxed to eat. Her motions are light in color, frothy, and intensely offensive. Microscopically they contain nothing abnormal. Sometimes the actions vary from one to three in the twenty-four hours. The urine contains no albumen, sugar, or bile.
    Previous History:-- With the exception of an acute attack of laryngitis, there is nothing to report about her former health. She was nursed as a baby by her mother. She first began to complain in July last, but as the weather was very hot, it was thought that she was suffering merely from the effects of the heat. At that time her motions were clay colored, and she was very pale and languid, with occasional attacks of diarrhea; but in the beginning not much attention was paid to these symptoms. Soon after, becoming worse, advice was sought concerning her; and in a letter to me from her medical attendant, it was stated that the saw her for what he considered were symptoms of mesenteric disease, but that she greatly improved under treatment. She soon afterwards relapsed, and owing to the extreme
    debility and pallor, her case was considered hopeless.
    Family History:-- Her mother is perfectly healthy, with no history of any importance. Her father is at present healthy; he suffered some years ago from abscess of the hip joint. From this he perfectly recovered, and is in excellent health. The other children, three sisters, are all healthy.

    Treatment:-- She was placed upon a diet exactly similar to the other cases related, but in her case it seemed necessary, on account of exhaustion, to give as an addition brandy once or twice a day. Attacks of diarrhea were treated as they arose, but the medicine she principally took was iron in some form. Cod-liver oil could never be borne; it invariably caused looseness of the bowels. At one time she developed purpuric patches all over the lower part of the abdomen, which, however gradually disappeared; and she also had an attack of stomatitis, which lasted for about ten days. She was under observation for a considerable time during each year, and I constantly heard about her when she was not in London. The diet and general treatment were carefully attended to, and she was allowed to have chicken, eggs, tapioca, milk, and everything of a plain description. when I last heard, her condition was most satisfactory, and she had gained considerably in weight.
     
    Case III -- E.H.W., aged 2 years and 1 month. Her mother came to consult me about her on the 10th of May, 1887, complaining that the child's digestion was out of order, and the first thing she noticed was that the motions were offensive and copious.
    Previous History:-- The mother declared that she considered the child had not been thoroughly well ever since she was born. She was only suckled a fortnight, after which she had cows' milk and water, then donkeys' milk for a time, and then again cows' milk.
    Family History:-- The patient is an only child. The mother is a healthy woman; has never suffered from any miscarriage; there is no history of tubercle. There is no history of syphilis obtainable, and no reason to suspect it.

    The child has always been nervous and easily frightened. For several months past she has been dieted by the mother. Sometimes she would give her a little meat, and sometimes not. She often has attacks of sickness; the least thing causes her to vomit, and the food is very easily brought back in an undigested state. The motions are very large in quantity, pale in colour, and extremely offensive. On examination the child is found to be generally flabby, and does not look strong; she is pallid, but not thin, and there is no yellow tint of the skin. On examination of the chest, the right side is seen to be slightly flattened anteriorly, and the percussion note is of a higher pitch as compared with the left, probably from thickened pleura. The breath sounds are natural; the heart seems normal. The liver is one finger's breadth below the ribs. The spleen is not enlarged, and there are no enlarged lymphatic glands to be discovered. On examination of the blood, there is observed to be an excess of white cells. The red are less colored than is natural, and there are numerous lymphoid particles present. It is spanaemic, the number of cells being greatly diminished. The tongue is white and coated. She was ordered some perchloride of iron and cod-liver oil, with occasionally some decoction of aloes, and the diet was to consist of cream, whey, also asses' milk, raw meat, and potato.

    A week later, I saw her on account of pain in the abdomen. Her legs were drawn up and she complained of great pain all over the abdomen. Her medicines were stopped, and I substituted for them a mixture containing bismuth and compound tincture of camphor, under which she improved. On the 11th of June she had an attack of sickness. She vomited frequently, and had three copious loose motions, the last being watery. This attack was probably because there had been some mistake about the milk, the child having had cows' milk instead of asses' milk during the morning.
    When I last heard of her from the country, I was told that she seemed very much better and improved in every way. She had, however, to be extremely careful about food, and could not make any change with impugnity, -- in fact, the diet had had to be altered to an ordinary one with the greatest of care.
     
    Case IV -- D.G., aged 2 years and 8 months. First seen on 9th September 1886. Her mother brought her to me, complaining of her not passing water for many hours, sometimes as many as 10 or 12 elapsing without any inclination on the part of the child to relieve herself.
    Previous history:-- The child had been brought up by hand, and there is nothing of consequence to report concerning her, with the exception of a severe attack of laryngitis, from which she suffered a year previously. Family History.-- The mother is a delicate-looking woman, thin, and by no means strong. There is no distinct history of phthisis on either side, and there is no syphilitic history obtainable, and no reason to suspect it. There is one other child, older than the patient and perfectly healthy. She also had a severe attack of laryngitis when a baby, but nothing else of consequence.
    On examination, she was seen to be a rather delicate-looking child, but apparently well developed, although her flesh was soft and flabby. No signs of rickets could be detected. The abdomen seemed large and doughy. The heart and lungs appeared to be normal. The spleen and liver were not enlarged, and no enlarged lymphatic glands could be felt. The urine proved to be distinctly albuminous and to contain crystals of uric acid. The mother, who had come with her from the country, had not brought the nurse, and could tell me nothing about the motions, or whether the bowels were regular or not. She was given a mixture containing some sulphate of soda and citte of potash. I soon afterwards received a letter telling me that the motions were copious, frothy, whitish, and intensely offensive, and that the bowels acted once or twice daily. On the 26th October I again saw her, and then heard from the mother that the child had been very poorly a fortnight previously, owing to what was considered due to a chill. She told me that the child was seized with what she termed "spasms of the abdomen," that she drew her legs up, and seemed in great pain. This attack of pain apparently lasted of several hours, and the mother states that she was not feverish. At that time the motions were too light in colour; they were very large and extremely offensive. She passed a slight amount of blood with the motion, but the mother is not quite sure whether this was merely from straining at the first, or whether it was mixed with the motion; probably the former would account for it, for I never again heard of the presence of blood. The nurse said the motions were so large in quantity that they quite astonished her, considering the amount of food eaten; that they were intensely offensive, and that there were never more than two in the twenty-four hours, although usually there was but one.
    There being no doubt as to the diagnosis in this case, I ordered the same diet as in the previous cases, viz., cream and whey, pounded raw meat with sifted sugar and floury potato, and to have some compound decoction of aloes and cod-liver oil. On the 4th of November I saw her in what her mother described as her "stomach attacks," and I then found that she appeared to have considerable abdominal pain, with the legs drawn up. I therefore omitted the compound decoction of aloe sand the cod-liver oil, and gave a mixture containing some compound tincture of camphor. On a microscopical examination of the motions, it was found that they contained no pus. There were many long, rod-like virbios, and very numerous spores, like the penicilium glaucum.
    It may be briefly stated that she was kept upon this diet for many months; that the attacks of pain from which she originally suffered gradually diminished in intensity until they entirely ceased, and that her general condition was greatly improved. The albumen disappeared form the urine; she became more muscular and walked without fatigue, and the motions gradually assumed a natural colour. This improvement, however, did not take place rapidly, but occurred during a period of about two and a half years. When I last heard of her, her condition was satisfactory, and although she could not be considered to be a perfectly robust child, there seemed to be nothing amiss with her. She ran about and played like other children, and seemed well. Her motions have always been natural for months past, an she has gradually returned to ordinary every day diet; but the nurse has been extremely careful in giving her only what has been ordered for her, and she has at all times been cautious not to give her anything which she feared would din the least disagree with her. The child has, therefore, had every possible care regarding her treatment.
    The coeliac disease, amongst hospital patients, is popularly called "consumption of the bowels," meaning by this one the several affections to which they apply this term. This disease is characterized by the passage of large, loose, white or whitish, frothy, intensely foetid motions; by pallor of the skin; wasting; loss of muscular strength, and by the fact that it is most frequently met with in children between 1 and 5 years of age. The youngest child I have seen attacked by it was between 10 and 11 months old. I have seen it in children with perfectly healthy parents, and, indeed, with sisters and brothers in every way healthy. In only one family can I trace any history of struma on the side of the father. No history of tubercle can be traced in the family of any of the patients whose cases are related, except one, and in that, consumption occurred in a paternal uncle of the patient, and in all there is no history of syphilis obtainable, and no reason to suspect it. In most cases there is a history to be obtained of gout, either on the side of the father or mother, or in distant relations. The examination of the faeces themselves throws no light upon the matter. In those I have submitted to careful microscopical examination I have never been able to discover anything abnormal, and I have failed to detect any tubercle bacilli although carefully searched for.
    Pathology:-- Under this head there is really nothing to be detailed. Examination of the bowel after death has led to the discovery of nothing. There is no sign of wasting of the mucous membrane, of engorgement, or of ulceration, and this statement refers to the whole of the intestinal tract. I am not aware that any wasting of Lieberkuhn's follicles has been detected. The liver and the spleen are not remarkable for anything abnormal. The spleen, however, is occasionally enlarged. The blood usually has signs of anaemia and except for the excess of small lymphoid particles, might pass of ordinary anaemic blood. As, however, these small particles are not peculiar to this affection, they really need hardly to be noticed, for I have myself found them, on many occasions, especially in children suffering empyema. Therefore, taking all the facts into consideration, it is quite clear that up to the present moment nothing has occurred to throw any light upon the pathology of this extraordinary affection.

    Diagnosis:-- About this there can be no difficulty whatever, for the signs and symptoms are so clear that they cannot be mistaken. It is, however, of the greatest importance to examine the motions for one's self, for I am certain that if this had been done in several of the cases which have come under my notice, I should not have been the first to discover the child was suffering from anything beyond a little general debility. About this point one cannot be too strong, for, as there are usually no signs of ordinary diarrhea, and possibly but one action a day, the nurse, if not alarmed by the foetor, is apt to think nothing of the bowel, but to be more struck with the pallor and the generally increasing weakness of the child. The signs are so clearly indicative of this one affection, that there is no other with which it could be confounded.

    Prognosis:-- Unfortunately this is usually grave, and the majority of children suffering from this disease die. I have, however, with the exception of one, in the cases that have come under my observation, had the good fortune to witness their improvement; and I think it was partly due to the careful nursing that they had in their own homes, and to the fact that they have been the children of people who have been well off, and who have been able to give them everything that has been ordered, regardless of expense. I feel certain that this has a great deal to do with the well-being of the children, for, in one case, the second on the list, I am sure that without the most constant care and watching on the part of the mother and nurse, she would have died. As to the time at which death will take place, it is impossible to say, for, however bad these little patients are, they frequently have extraordinary rallies, and seem better for a time; but, without any warning, relapses take place, and after apparently progressing most favorably, they suddenly become exhausted, and rapidly fade away, usually from attacks of watery diarrhea.

    Symptoms and Progress:-- The onset is usually gradual, and there is nothing definite to call attention to the disease. The nurse or the mother generally states that the child has been a little out of health for some weeks, or possibly months, and yet there has been nothing special to cause alarm, with the result that no treatment has been adopted. The child becomes pale and anaemic, the blood evidently being affected, and sometimes there is a puffiness about the face. Possibly amongst the first indications, the motions have been marked by the nurse, and this has generally been owing to the colour being different, but above all, on account of their intensely foetid odor. This mal-odor is sometimes overpowering, and those who have not encountered can hardly realize it. The motions themselves, as already pointed out, are very large, soft, whitish in colour, and frothy. They resemble very much ordinary oatmeal porridge. The actions may be two or three in a day, but usually there is only one large one, and that may take place at a time to which the child is accustomed. Now and then there are attacks of so called diarrhea, that is to say, the child may have frequent evacuations of the bowels, that they may be very loose, and that they may be occasionally watery if the attack is severe, but these attacks of diarrhea are not an essential part of the disease, except in the cases of some children who have these constant attacks of diarrhea throughout the whole of the illness. The appetite is poor, usually capricious, sometimes large. The tongue is frequently coated with a whitish fur, at other times perfectly clean. In some cases there are attacks of crampy abdominal pain, possibly due to ordinary colic. These attacks were well marked in case 4. The abdomen is generally soft and doughy, although occasionally distended and hard. The liver is generally unaffected: now and then the spleen is found to be enlarged: no enlarged lymphatic glands can be detected. As a rule, the urine has nothing remarkable about it; occasionally it contains a trace of albumen. The temper of the child seems variable, most frequently he is extremely irritable, fretful, capricious, or peevish. Nothing seems to please him, and altogether he is quite unlike himself. Sometimes he is heavy and languid, complaining of headache, and wishing to lie down a good deal. The special senses seem to be normal. In all the cases that I have examined the various tendon reflexes were unaffected.
    The most remarkable sign about these children is that of loss of muscular power, with apparently no great loss of flesh; that is to say, to look at, the children do not seem to have wasted much, but on feeling the legs or arms, it is at once evident how soft and flabby and out of condition they are. A curious point is that they have a great objection to going upstairs, and in one case, on of the first symptoms which struck the nurse as being extraordinary was that the child did not care to mount the staircase, and that she had invariably to be carried up. The progress of this affection is as a rule slow. The children seem to gradually become more feeble, to waste away, and to lose power. Occasionally an attack of watery diarrhea, in those children who have been accustomed to suffer from diarrhea, may carry off the patient. In the case of colicky attacks I have seen a child in imminent danger from collapse. In non-fatal cases recovery is extremely gradual. An important point to note in this connection, is the tendency to relapses, each relapse taking a considerable time to make up for lost ground. When improvement begins to take place, it is usually shown in the healthier condition of the evacuations. The colour becomes better, the motions are more formed, and above all, less copious and less offensive. The child gains in strength, but is a long time gaining in colour. The muscular strength is the last to return, and mounting the stairs, or jumping, are amongst the very last things that can be done. The appetite generally improves but slowly, and is always capricious, or nearly so. Another important point concerning these patients is that the least thing apparently upsets them, and the smallest error in diet will bring on copious actions of the bowels, cause vomiting, or make the child quite ill again.

    Jefferson Adams
    This article originally appeared in the Spring 2009 edition of Journal of Gluten Sensitivity.
    Celiac.com 05/15/2010 - Willem-Karel Dicke was born in 1905, in Dordrecht, Holland, and died Utrecht in 1962.  Dicke was a Dutch pediatrician, the first clinician to develop the gluten-free diet, and to prove that certain types of flour cause relapses in celiac disease patients.
    From 1922 until 1929, Dicke studied medicine in Leiden.  He then specialized in pediatrics in Juliana Children’s Hospital in The Hague from 1929 until 1933.  In 1936, at just 31 years of age, he was named medical director of the hospital. 
    In the 1940s and 1950s he went on to formally establish the gluten-free diet, forever changing treatment methods and clinical outcomes of children suffering from celiac disease.  By 1952, Dicke recognized that the disease is caused by the ingestion of wheat proteins, not carbohydrates. 
    From the late 1880s into the 1920s and 30s, doctors like R. A. Gibbons, Sidney Haas and others pioneered the use of specialty diets to treat celiac disease.  Diets such as the banana diet, the fruit diet, the carbohydrate diet (fruit, puree of potatoes or tomatoes), the beefsteak diet, the milk diet had all been tried, with some success.
    In his now seminal 1950 thesis on celiac disease and wheat-free diet, Dicke lays out the results of the detailed dietary study he conducted over several years at the Juliana Children’s Hospital on a patient with celiac disease.
    The study likely had its earliest beginnings at the advent of Dicke’s promotion to medical director, if not slightly before.  From the testimony of Dicke’s wife in 1991, we know that Dicke was convinced of the beneficial effect of wheat free diet even before 1940.  She confirmed that between 1934 and 1936, Dicke began to conduct experiments with wheat free diets confirming Christopher Booth’s comments in The Lancet, Feb 25, 1989:
    “It was a young mother’s statement of her celiac child’s rash improving rapidly if she removed bread from the diet that alerted his interest,” when Dicke was a pediatrician in The Hague in 1936.
    Dicke published his first report on a wheat-free diet in Het Nederlands Tijdschrift voor Geneeskunde in 1941.  (W. K. Dicke: A simple diet for Gee-Herter’s Syndrome).  At the time, celiac was still called Gee-Herter’s syndrome.  It reads, in part:
    “In recent literature it is stated that the diet of Haas (Banana-diet) and Fanconi (fruit and vegetables) gives the best results in the treatment of patients suffering from coeliac disease.  At present (World War II) these items are not available.  Therefore, I give a simple diet, which is helping these children at this time of rationing.  The diet should not contain any bread or rusks.  A hot meal twice a day is also well tolerated.  The third meal can be sweet or sour porridge (without any wheat flour).”
    In the Netherlands, the last winter of World War II, the winter of 1944/45 became known as the ‘Winter of Hunger.’ 
    Delivery of regular food staples, such as bread, was largely disrupted, especially in the western part of the country.  This meant that people had to turn to uncommon foods, such as tulip bulbs, for sustenance.  It was during this time that Dicke became even more convinced that eating less grain, along with unusual foods, such as tulip bulbs, improved the clinical condition of his patients. 
    Dicke’s next major confirmation came when Allied planes started dropping bread in the Netherlands, and these same children began to deteriorate rapidly. 
    After World War II, Dicke conducted a series of experiments with standardized diets were performed on four children in the Wilhelmina Children’s Hospital in Utrecht and in one child in the Juliana Children’s Hospital in The Hague.  These experiments involved excluding or adding wheat or rye flour over long periods in the diets of these children with coeliac disease. 
    In Dicke’s post-war experiments, children were challenged with different cereals under a strict dietary protocol with measurement of total fecal output, fecal fat content, and the fat absorption coefficient was calculated.
    Dicke worked closely with biochemist J. H. van de Kamer of the Netherlands Central Institute for Nutritional Research TNO in Utrecht, who developed the first accurate and easily available method for measure fecal fat content in wet feces.  Dicke also worked closely with H. A. Weyers, a pediatrician from the Wilhelmina Children’s Hospital in Utrecht, who developed a method that used the coefficient of fat absorption to analyze fecal fat excretion in children with celiac disease.
    Based on these findings Dicke concluded in his 1950 thesis that wheat flour, but not well-purified wheat starch (amylum), and also rye flour, triggered the anorexia, the increased fecal output, and the streatorrhea common in celiac patients.  Dicke presented his doctoral thesis on the subject at the University of Utrecht in 1950.
    Dicke’s 1950 thesis refers to a celiac disease patient he treated in 1936.  The patient’s symptoms disappeared and he returned to normal weight and growth patterns after following a strict wheat free diet in the hospital.  However, each time the boy went home and was unable to maintain a wheat free diet, he suffered a decline in his growth curve. 
    Dicke charted these advances and reversals over four long-term admissions.  Each time the trend towards normal growth was restored.  In his thesis, Dicke presents several growth curves of children treated with a wheat free diet.  In long term studies over several years he shows that, with a wheat free diet, these children gain weight, reaching normal growth patterns when compared with age matched controls.  At the end of chapter 3 of his thesis he concludes that:
    “- if certain types of meal, such as wheat and rye are replaced in the daily diet, the patient improves;
    - acute attacks of diarrhea, do not occur, provided these types of meal are not given;
    - after a latent period which can vary in length, deterioration and acute attacks of diarrhea re-occur, if the objectionable types of meal are added to the diet too soon....”
    In 1953, together with van de Kamer and Weyers, he subsequently published Coeliac disease IV “An investigation into the injurious constituents of wheat in connection with their action on patients with coeliac disease.”
    They wrote that the alcohol soluble or the gliadin component of the water insoluble protein of wheat was responsible for the fat malabsorption in patients with celiac disease. 
    Although these findings were quickly confirmed by researchers in Britain, Scandinavia, and Germany, some researchers, especially in America, questioned the wisdom of a gluten free diet.
    After the establishment of the intestinal biopsy technique for the diagnosis of celiac disease, it became apparent that a wheat free diet should be maintained for long periods before an adequate response occurred, as Dicke had predicted. 
    In 1954, Dr. Dicke, Charlotte Anderson, and a number of their colleagues, confirmed these findings, and described the damage to the lining of the small intestine as being directly related to celiac disease.
    In 1957 he was appointed a professor of Utrecht University and became a medical director of Wilhelmina Children’s Hospital.
    To honor Willem Karel Dicke, Netherland’s Society of Gastroenterology established a gold medal in his name, to be presented to pioneering researchers in the field.  Willem Dicke himself was named as the recipient of the first gold Dicke Medal.
    Dr. Dicke died in 1962 of cerebrovascular disease.  He was just 57 years old.
    Jefferson Adams is a freelance writer living in San Francisco.  His poems, essays and photographs have appeared in Antioch Review, Blue Mesa Review, CALIBAN, Hayden’s Ferry Review, Huffington Post, the Mississippi Review, and Slate among others.
    Sources:

    Willem Dicke.  Brilliant Clinical Observer and Translational Investigator.  Discoverer of the Toxic Cause of Celiac Disease, by David Yan and Peter R.  Holt , M.D. DOI: 10.1111/j.1752-8062.2009.00167.x GUT 1993; 34:1473-1475 Mulder, C.  “Pioneer in Glutenfree diet: Willem Karel Dicke 1905-1962 Over 50 Years of Gluten Free Diet.”  appended to: English translation by C.  Mulder June 1, 1993 of  Dicke, W.K.  “Coeliac Disease  Investigation of Harmful Effects of Certain Types of Cereal on Patients Suffering from Coeliac Disease.” Ph.  D.  Thesis, State University of Utrecht, 1950

    Jefferson Adams
    Celiac.com 11/29/2010 - Recent archeological evidence in the form of starch from ground grains found at Stone Age sites suggests early modern humans also consumed various kinds of flour, not just meat alone.
    For decades, there has been ample evidence to support meat-eating by early humans. Evidence such as stone blades used for hunting and animal bones bearing cut-marks have been are common finds. This evidence has supported a view that early humans were nearly total carnivores. 
    In contrast, very little evidence has been found to show plant and grain consumption. This may be due, at least in part to the lower environmental impact of plant use; plants leave far fewer traces.
    The evidence was partially obscured by standard archaeological practice of washing the grinding tools used to process plants, removing any preserved plant matter.
    In the latest discovery, scientists found flour residues on 30,000-year-old grinding stones from Italy, Russia and the Czech Republic. This indicates widespread processing and consumption of plant grains, according to Laura Longo, an archaeologist at the University of Siena in Italy and an author on the paper published in Proceedings of the National Academy of Sciences.
    These new finds provide some of the first evidence that early humans ate ground flour 20,000 years before the dawn of agriculture.
    "It's another nail in the coffin of the idea that hunter–gatherers didn't use plants for food," says Ofer Bar-Yosef, a Harvard University archaeologist not involved in the study.
    Additional work in recent years has also revealed a handful of Stone Age sites in the Near East with evidence for plant-eating.
    Source:

    18 October 2010 | Nature | doi:10.1038

    Jefferson Adams
    Celiac.com 01/08/2014 - Push-back mounts against a controversial new report alleging that genetically engineered foods may trigger gluten sensitivity and celiac disease.
    In the first salvo, Celiac Disease Foundation CEO Marilyn Geller derided the report, published last week by the Institute for Responsible Technology (IRT), as merely "speculative."
    Then followed comments by leading plant geneticist, Dr. Wayne Parrott, professor of crop science at the University of Georgia, that the report relied on "a handful of deeply flawed"studies and ignored "more than 1,000 studies that have been published in refereed journals and which show that GM crops are as safe as their counterparts."
    According to Geller, no one has offered scientific evidence "for a GMO/celiac disease link that is supported by the CDF Medical Advisory Board.
    For their part, the authors of the IRT report admit that there is no data to prove that GMO consumption causes gluten sensitivity.
    However, they try to hedge slightly by claiming that more and more research shows that GMO consumption may worsen celiac symptoms or lead to gluten sensitivity. Here again, they offer no good data to support their claims.
    Source:
    FoodNavigator.com

  • Recent Articles

    Jefferson Adams
    Celiac.com 06/18/2018 - Celiac disease has been mainly associated with Caucasian populations in Northern Europe, and their descendants in other countries, but new scientific evidence is beginning to challenge that view. Still, the exact global prevalence of celiac disease remains unknown.  To get better data on that issue, a team of researchers recently conducted a comprehensive review and meta-analysis to get a reasonably accurate estimate the global prevalence of celiac disease. 
    The research team included P Singh, A Arora, TA Strand, DA Leffler, C Catassi, PH Green, CP Kelly, V Ahuja, and GK Makharia. They are variously affiliated with the Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Lady Hardinge Medical College, New Delhi, India; Innlandet Hospital Trust, Lillehammer, Norway; Centre for International Health, University of Bergen, Bergen, Norway; Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Gastroenterology Research and Development, Takeda Pharmaceuticals Inc, Cambridge, MA; Department of Pediatrics, Università Politecnica delle Marche, Ancona, Italy; Department of Medicine, Columbia University Medical Center, New York, New York; USA Celiac Disease Center, Columbia University Medical Center, New York, New York; and the Department of Gastroenterology and Human Nutrition, All India Institute of Medical Sciences, New Delhi, India.
    For their review, the team searched Medline, PubMed, and EMBASE for the keywords ‘celiac disease,’ ‘celiac,’ ‘tissue transglutaminase antibody,’ ‘anti-endomysium antibody,’ ‘endomysial antibody,’ and ‘prevalence’ for studies published from January 1991 through March 2016. 
    The team cross-referenced each article with the words ‘Asia,’ ‘Europe,’ ‘Africa,’ ‘South America,’ ‘North America,’ and ‘Australia.’ They defined celiac diagnosis based on European Society of Pediatric Gastroenterology, Hepatology, and Nutrition guidelines. The team used 96 articles of 3,843 articles in their final analysis.
    Overall global prevalence of celiac disease was 1.4% in 275,818 individuals, based on positive blood tests for anti-tissue transglutaminase and/or anti-endomysial antibodies. The pooled global prevalence of biopsy-confirmed celiac disease was 0.7% in 138,792 individuals. That means that numerous people with celiac disease potentially remain undiagnosed.
    Rates of celiac disease were 0.4% in South America, 0.5% in Africa and North America, 0.6% in Asia, and 0.8% in Europe and Oceania; the prevalence was 0.6% in female vs 0.4% males. Celiac disease was significantly more common in children than adults.
    This systematic review and meta-analysis showed celiac disease to be reported worldwide. Blood test data shows celiac disease rate of 1.4%, while biopsy data shows 0.7%. The prevalence of celiac disease varies with sex, age, and location. 
    This review demonstrates a need for more comprehensive population-based studies of celiac disease in numerous countries.  The 1.4% rate indicates that there are 91.2 million people worldwide with celiac disease, and 3.9 million are in the U.S.A.
    Source:
    Clin Gastroenterol Hepatol. 2018 Jun;16(6):823-836.e2. doi: 10.1016/j.cgh.2017.06.037.

    Jefferson Adams
    Celiac.com 06/16/2018 - Summer is the time for chips and salsa. This fresh salsa recipe relies on cabbage, yes, cabbage, as a secret ingredient. The cabbage brings a delicious flavor and helps the salsa hold together nicely for scooping with your favorite chips. The result is a fresh, tasty salsa that goes great with guacamole.
    Ingredients:
    3 cups ripe fresh tomatoes, diced 1 cup shredded green cabbage ½ cup diced yellow onion ¼ cup chopped fresh cilantro 1 jalapeno, seeded 1 Serrano pepper, seeded 2 tablespoons lemon juice 2 tablespoons red wine vinegar 2 garlic cloves, minced salt to taste black pepper, to taste Directions:
    Purée all ingredients together in a blender.
    Cover and refrigerate for at least 1 hour. 
    Adjust seasoning with salt and pepper, as desired. 
    Serve is a bowl with tortilla chips and guacamole.

    Dr. Ron Hoggan, Ed.D.
    Celiac.com 06/15/2018 - There seems to be widespread agreement in the published medical research reports that stuttering is driven by abnormalities in the brain. Sometimes these are the result of brain injuries resulting from a stroke. Other types of brain injuries can also result in stuttering. Patients with Parkinson’s disease who were treated with stimulation of the subthalamic nucleus, an area of the brain that regulates some motor functions, experienced a return or worsening of stuttering that improved when the stimulation was turned off (1). Similarly, stroke has also been reported in association with acquired stuttering (2). While there are some reports of psychological mechanisms underlying stuttering, a majority of reports seem to favor altered brain morphology and/or function as the root of stuttering (3). Reports of structural differences between the brain hemispheres that are absent in those who do not stutter are also common (4). About 5% of children stutter, beginning sometime around age 3, during the phase of speech acquisition. However, about 75% of these cases resolve without intervention, before reaching their teens (5). Some cases of aphasia, a loss of speech production or understanding, have been reported in association with damage or changes to one or more of the language centers of the brain (6). Stuttering may sometimes arise from changes or damage to these same language centers (7). Thus, many stutterers have abnormalities in the same regions of the brain similar to those seen in aphasia.
    So how, you may ask, is all this related to gluten? As a starting point, one report from the medical literature identifies a patient who developed aphasia after admission for severe diarrhea. By the time celiac disease was diagnosed, he had completely lost his faculty of speech. However, his speech and normal bowel function gradually returned after beginning a gluten free diet (8). This finding was so controversial at the time of publication (1988) that the authors chose to remain anonymous. Nonetheless, it is a valuable clue that suggests gluten as a factor in compromised speech production. At about the same time (late 1980’s) reports of connections between untreated celiac disease and seizures/epilepsy were emerging in the medical literature (9).
    With the advent of the Internet a whole new field of anecdotal information was emerging, connecting a variety of neurological symptoms to celiac disease. While many medical practitioners and researchers were casting aspersions on these assertions, a select few chose to explore such claims using scientific research designs and methods. While connections between stuttering and gluten consumption seem to have been overlooked by the medical research community, there is a rich literature on the Internet that cries out for more structured investigation of this connection. Conversely, perhaps a publication bias of the peer review process excludes work that explores this connection.
    Whatever the reason that stuttering has not been reported in the medical literature in association with gluten ingestion, a number of personal disclosures and comments suggesting a connection between gluten and stuttering can be found on the Internet. Abid Hussain, in an article about food allergy and stuttering said: “The most common food allergy prevalent in stutterers is that of gluten which has been found to aggravate the stutter” (10). Similarly, Craig Forsythe posted an article that includes five cases of self-reporting individuals who believe that their stuttering is or was connected to gluten, one of whom also experiences stuttering from foods containing yeast (11). The same site contains one report of a stutterer who has had no relief despite following a gluten free diet for 20 years (11). Another stutterer, Jay88, reports the complete disappearance of her/his stammer on a gluten free diet (12). Doubtless there are many more such anecdotes to be found on the Internet* but we have to question them, exercising more skepticism than we might when reading similar claims in a peer reviewed scientific or medical journal.
    There are many reports in such journals connecting brain and neurological ailments with gluten, so it is not much of a stretch, on that basis alone, to suspect that stuttering may be a symptom of the gluten syndrome. Rodney Ford has even characterized celiac disease as an ailment that may begin through gluten-induced neurological damage (13) and Marios Hadjivassiliou and his group of neurologists and neurological investigators have devoted considerable time and effort to research that reveals gluten as an important factor in a majority of neurological diseases of unknown origin (14) which, as I have pointed out previously, includes most neurological ailments.
    My own experience with stuttering is limited. I stuttered as a child when I became nervous, upset, or self-conscious. Although I have been gluten free for many years, I haven’t noticed any impact on my inclination to stutter when upset. I don’t know if they are related, but I have also had challenges with speaking when distressed and I have noticed a substantial improvement in this area since removing gluten from my diet. Nonetheless, I have long wondered if there is a connection between gluten consumption and stuttering. Having done the research for this article, I would now encourage stutterers to try a gluten free diet for six months to see if it will reduce or eliminate their stutter. Meanwhile, I hope that some investigator out there will research this matter, publish her findings, and start the ball rolling toward getting some definitive answers to this question.
    Sources:
    1. Toft M, Dietrichs E. Aggravated stuttering following subthalamic deep brain stimulation in Parkinson’s disease--two cases. BMC Neurol. 2011 Apr 8;11:44.
    2. Tani T, Sakai Y. Stuttering after right cerebellar infarction: a case study. J Fluency Disord. 2010 Jun;35(2):141-5. Epub 2010 Mar 15.
    3. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    4. Jäncke L, Hänggi J, Steinmetz H. Morphological brain differences between adult stutterers and non-stutterers. BMC Neurol. 2004 Dec 10;4(1):23.
    5. Kell CA, Neumann K, von Kriegstein K, Posenenske C, von Gudenberg AW, Euler H, Giraud AL. How the brain repairs stuttering. Brain. 2009 Oct;132(Pt 10):2747-60. Epub 2009 Aug 26.
    6. Galantucci S, Tartaglia MC, Wilson SM, Henry ML, Filippi M, Agosta F, Dronkers NF, Henry RG, Ogar JM, Miller BL, Gorno-Tempini ML. White matter damage in primary progressive aphasias: a diffusion tensor tractography study. Brain. 2011 Jun 11.
    7. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    8. [No authors listed] Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 43-1988. A 52-year-old man with persistent watery diarrhea and aphasia. N Engl J Med. 1988 Oct 27;319(17):1139-48
    9. Molteni N, Bardella MT, Baldassarri AR, Bianchi PA. Celiac disease associated with epilepsy and intracranial calcifications: report of two patients. Am J Gastroenterol. 1988 Sep;83(9):992-4.
    10. http://ezinearticles.com/?Food-Allergy-and-Stuttering-Link&id=1235725 
    11. http://www.craig.copperleife.com/health/stuttering_allergies.htm 
    12. https://www.celiac.com/forums/topic/73362-any-help-is-appreciated/
    13. Ford RP. The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29.
    14. Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A. Does cryptic gluten sensitivity play a part in neurological illness? Lancet. 1996 Feb 10;347(8998):369-71.

    Jefferson Adams
    Celiac.com 06/14/2018 - Refractory celiac disease type II (RCDII) is a rare complication of celiac disease that has high death rates. To diagnose RCDII, doctors identify a clonal population of phenotypically aberrant intraepithelial lymphocytes (IELs). 
    However, researchers really don’t have much data regarding the frequency and significance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. Such data could provide useful comparison information for patients with RCDII, among other things.
    To that end, a research team recently set out to try to get some information about the frequency and importance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. The research team included Shafinaz Hussein, Tatyana Gindin, Stephen M Lagana, Carolina Arguelles-Grande, Suneeta Krishnareddy, Bachir Alobeid, Suzanne K Lewis, Mahesh M Mansukhani, Peter H R Green, and Govind Bhagat.
    They are variously affiliated with the Department of Pathology and Cell Biology, and the Department of Medicine at the Celiac Disease Center, New York Presbyterian Hospital/Columbia University Medical Center, New York, USA. Their team analyzed results of TCR-GR analyses performed on SB biopsies at our institution over a 3-year period, which were obtained from eight active celiac disease, 172 celiac disease on gluten-free diet, 33 RCDI, and three RCDII patients and 14 patients without celiac disease. 
    Clonal TCR-GRs are not infrequent in cases lacking features of RCDII, while PCPs are frequent in all disease phases. TCR-GR results should be assessed in conjunction with immunophenotypic, histological and clinical findings for appropriate diagnosis and classification of RCD.
    The team divided the TCR-GR patterns into clonal, polyclonal and prominent clonal peaks (PCPs), and correlated these patterns with clinical and pathological features. In all, they detected clonal TCR-GR products in biopsies from 67% of patients with RCDII, 17% of patients with RCDI and 6% of patients with gluten-free diet. They found PCPs in all disease phases, but saw no significant difference in the TCR-GR patterns between the non-RCDII disease categories (p=0.39). 
    They also noted a higher frequency of surface CD3(−) IELs in cases with clonal TCR-GR, but the PCP pattern showed no associations with any clinical or pathological feature. 
    Repeat biopsy showed that the clonal or PCP pattern persisted for up to 2 years with no evidence of RCDII. The study indicates that better understanding of clonal T cell receptor gene rearrangements may help researchers improve refractory celiac diagnosis. 
    Source:
    Journal of Clinical Pathologyhttp://dx.doi.org/10.1136/jclinpath-2018-205023

    Jefferson Adams
    Celiac.com 06/13/2018 - There have been numerous reports that olmesartan, aka Benicar, seems to trigger sprue‐like enteropathy in many patients, but so far, studies have produced mixed results, and there really hasn’t been a rigorous study of the issue. A team of researchers recently set out to assess whether olmesartan is associated with a higher rate of enteropathy compared with other angiotensin II receptor blockers (ARBs).
    The research team included Y.‐H. Dong; Y. Jin; TN Tsacogianis; M He; PH Hsieh; and JJ Gagne. They are variously affiliated with the Division of Pharmacoepidemiology and Pharmacoeconomics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School in Boston, MA, USA; the Faculty of Pharmacy, School of Pharmaceutical Science at National Yang‐Ming University in Taipei, Taiwan; and the Department of Hepato‐Gastroenterology, Chi Mei Medical Center in Tainan, Taiwan.
    To get solid data on the issue, the team conducted a cohort study among ARB initiators in 5 US claims databases covering numerous health insurers. They used Cox regression models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for enteropathy‐related outcomes, including celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy. In all, they found nearly two million eligible patients. 
    They then assessed those patients and compared the results for olmesartan initiators to initiators of other ARBs after propensity score (PS) matching. They found unadjusted incidence rates of 0.82, 1.41, 1.66 and 29.20 per 1,000 person‐years for celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy respectively. 
    After PS matching comparing olmesartan to other ARBs, hazard ratios were 1.21 (95% CI, 1.05‐1.40), 1.00 (95% CI, 0.88‐1.13), 1.22 (95% CI, 1.10‐1.36) and 1.04 (95% CI, 1.01‐1.07) for each outcome. Patients aged 65 years and older showed greater hazard ratios for celiac disease, as did patients receiving treatment for more than 1 year, and patients receiving higher cumulative olmesartan doses.
    This is the first comprehensive multi‐database study to document a higher rate of enteropathy in olmesartan initiators as compared to initiators of other ARBs, though absolute rates were low for both groups.
    Source:
    Alimentary Pharmacology & Therapeutics