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      Frequently Asked Questions About Celiac Disease   04/07/2018

      This Celiac.com FAQ on celiac disease will guide you to all of the basic information you will need to know about the disease, its diagnosis, testing methods, a gluten-free diet, etc.   Subscribe to Celiac.com's FREE weekly eNewsletter   What are the major symptoms of celiac disease? Celiac Disease Symptoms What testing is available for celiac disease?  Celiac Disease Screening Interpretation of Celiac Disease Blood Test Results Can I be tested even though I am eating gluten free? How long must gluten be taken for the serological tests to be meaningful? The Gluten-Free Diet 101 - A Beginner's Guide to Going Gluten-Free Is celiac inherited? Should my children be tested? Ten Facts About Celiac Disease Genetic Testing Is there a link between celiac and other autoimmune diseases? Celiac Disease Research: Associated Diseases and Disorders Is there a list of gluten foods to avoid? Unsafe Gluten-Free Food List (Unsafe Ingredients) Is there a list of gluten free foods? Safe Gluten-Free Food List (Safe Ingredients) Gluten-Free Alcoholic Beverages Distilled Spirits (Grain Alcohols) and Vinegar: Are they Gluten-Free? Where does gluten hide? Additional Things to Beware of to Maintain a 100% Gluten-Free Diet What if my doctor won't listen to me? An Open Letter to Skeptical Health Care Practitioners Gluten-Free recipes: Gluten-Free Recipes
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    Jefferson Adams

    Celiac.com 03/04/2009 - Millions of people currently suffer from a potentially deadly condition that can have little or no symptoms, but is easily diagnosed and treated. The condition is called celiac disease, and it is caused by an adverse autoimmune reaction to gliadin (found in wheat gluten), secalin (found in rye gluten), or horedin (found in barley gluten). Because of the broad range of symptoms that celiac disease can present, and the fact that many people will have no symptoms at all, it can often be very difficult for those who do have it to get properly screened for the disease.

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    According to Dr. Alessio Fasano, medical director of the Center forCeliac Research, 2.5 million to 3 million people in the USA have celiac disease—it istwice as common as Crohn’s disease, ulceric colitis and cystic fibrosiscombined—yet, to date, no more than 150,000 of them have beendiagnosed. This means that a full 2.35 to 2.85 million people in the USA have not been diagnosed and treated.

    Gluten-Free GirlThe symptoms of the disease can range from no symptoms at all, to mild weakness, bone pain, aphthousstomatitis (canker sores), chronic diarrhea, abdominal bloating, and progressiveweight loss. If people with celiac disease continue to eat gluten, studies show that their risk of gastrointestinal cancer increases by a factor of 40 to 100 times over the general population. Further, gastrointestinal carcinoma or lymphoma develops in up to 15 percent of patients with untreated or refractory celiac disease. It is thus essential that the disease be quickly diagnosed and treated.

    The last decade has seen an explosion in the understanding and awareness of celiac disease and in higher standards and increased availability of gluten-free foods.

    To help us better appreciate the dramatic changes and developments that have taken place, Celiac.com has put together a list of historical landmarks in the understanding and treatment of celiac disease. A glance at the time line will show that it really has taken centuries just to recognize and diagnose celiac disease, with the greatest strides being made in the last fifty years, and especially in the last decade.

    A Celiac Disease / Gluten-Free Diet Historical Timeline:

    • 100 A.D.—The first written account of celiac symptoms in western medicine occurs when the Greek Physician, Aretaeus the Cappadocean, known as Galen, describes the characteristic stool, noting that the disease was more common in women than men and that children can also be affected.
    • 1669—The Dutch physician Vincent Ketelaer publishes a book that contains an account of a diarrheal illness in which he notes feces so voluminous that, "several basins or pots scarcely hold these accumulations."
    • 1737—John Bricknell writes of patients who suffer from what he terms the "white flux.” Both Ketelaer and Bricknell were likely describing celiac disease, though that name would not be attached it for another century and a half.
    • 1887—Dr. Samuel Gee ushers in the modern era of celiac disease, when he drew attention to the disorder in a lecture delivered at the Hospital for Sick Children, Great Ormond Street, London.
    • 1888—Dr. Gee publishes his classic paper, "On the Coeliac Affection,” in which he describes aspects of the celiac disease with great accuracy and suggests that, "if the patient can be cured at all, it must be by means of diet.” He experimented with various diets and noted that children who were fed a quart of the best Dutch mussels daily, throve splendidly, but relapsed when the season for mussels ended.
    • 1889—R.A. Gibbons, MD., M.R.C.P. publishes The Celiac Affection in Children in the Edinburgh Medical. Journal.
    • 1908—British Physician Christian Herter becomes the first to discover that celiac disease can cause stunted growth, especially among children in their middle years.
    • 1921—British Physician John Howland devises the healthy, three-stage diet for celiac patients known as the milk/protein diet.
    • 1932—Danish physician Thorwald Thaysen provides the first clinical explanation of celiac disease in adults, though he lacks detailed knowledge on intestinal pathology for a full understanding of the disease.
    • 1936—Dutch pediatrician Willem Karel Dicke isolates cereal grains as the factor in aggravating the symptoms of celiac disease, especially in children, and begins treating children with the gluten-free diet. Afterwards his Ph.D. thesis was published and he was laughed out of the NYC gastroenterology meeting in 1950 and vowed not to return to the USA.
    • 1954—Experimenting with surgical biopsy material, Doctor J. W. Paulley makes the first discovery of the intestinal lesions caused by celiac disease in patients.
    • 1955—Margo Shiner invents the tiny biopsy tube that is still used today for confirming the presence of celiac disease in the small intestines. The important celiac disease discoveries of Paulley and Shiner meant that, from the mid 1950s onwards, doctors had a means by which to reliably diagnose the disease. Their discoveries gave rise to an explosion in the understanding of celiac disease that continues to this day.
    • 1965—Dermatologists recognize that people suffering from the itchy skin rash, dermatitis herpetiformis, have an abnormal jejunal biopsy just like those with celiac disease and that the rash usually subsides with the observance of a gluten-free diet.
    • 1970—In the early 1970s, researchers identify genetic markers for celiac disease. Even though the gene or genes that cause celiac disease have not been identified, researchers remain hopeful that they will succeed in doing so, and thereby give rise to a new generation of celiac treatments that do not require a gluten-free diet.
    • 1980s—Fiber optic technology enables doctors to take small bowel biopsies using fiber-optic endoscopes, while the development of reliable screening blood tests greatly increases the number of celiac diagnosis.
    • 1981—The Codex Alimentarius Commission establishes the earliest standards for gluten-free food. Under this original standard, foods labeled “gluten-free” must be made from naturally gluten-free grains, such as corn or rice or from gluten grains (wheat, barley, rye) that had been rendered gluten free through processing. At the time, there was no way to test for the presence of gluten, so tests gauged the levels of gluten by measuring nitrogen levels, an imprecise method.
    • ~1985—It is discovered that gliadin initiate damage to the absorptive epithelium of the small intestine toproduce symptoms of celiac disease in susceptible individuals.
    • 1990s—Early in the decade, doctors thought celiac disease to be rare and affect just 40,000 or so Americans. Over the last decade or so, the number of Americans diagnosed with celiac disease has nearly tripled, to 110,000, but that’s just the start. The National Institutes of Health now estimates that about 1% of the population, or about 3 million people suffer from celiac disease, and that only about 3% of existing cases have been diagnosed. A full 97% of celiac cases remain undiagnosed. That’s about 2.9 million people who remain undiagnosed and in danger. More and more of those who are diagnosed are reporting no symptoms.
    • 1995—In San Francisco, California, Scott Adams launches the Web site that evolves into Celiac.com, the first website on the Internet dedicated solely to celiac disease. The site quickly evolves into one of the most authoritative, informative, and comprehensive sources for celiac disease and gluten-free diet information. The celiac.com forum is one of the most popular places on the web for people with celiac disease to get answers and share information.
    • 1998—Codex Alimentarius revises its standards for foods labeled ‘gluten-free’ to be made from naturally gluten-free ingredients and contain 20 parts gluten per million, or less, while foods processed to be reduce gluten, such as wheat starch, can have no more than 200 parts per million gluten.
    • 1998—The Gluten-Free Mall (www.GlutenFreeMall.com) launches its "Special Diet Superstore!" to provide home delivery of top quality foods and other products that are free of wheat, rye and barley gluten, soy, dairy, eggs, corn, and other common allergens. The Gluten-Free Mall now sells thousands of gluten-free products including breads, cookies, cakes, pizzas, mixes, full meals, frozen foods, cosmetics, gluten-free guides, books, and more.
    • 1997 to 2007, the number of people under-18 diagnosed with food or digestive allergies rises nearly 20%, and nearly 3 million people young people now suffer from food allergies. About 12 million Americans suffer from a food allergy, according to the American Academy of Allergy, Asthma and Immunology, with nearly 90% of all food allergies arising from reactions to just eight foods: Cow’s milk, eggs, peanuts, tree nuts, shellfish, soy and wheat.
    • Since 2004, food retailers have added nearly 2500 new gluten free products to their shelves.
    • 2000—Scientists at the University of Maryland discover Zonulin, which is a protein that participates in tight junctions between cells of the wall of the digestive tract.
    • 2003—Alessio Fasano, MD, publishes his seminal study in the Archives ofInternal Medicine that indicates that 1 in 133 people in the USA haveceliac disease.
    • 2007—Studies show a high instance of arthritis and osteoporosis in people with celiac disease, and other studies show a high prevalence of celiac disease among people with type-1 diabetes.
    • 2008—A team of researchers works to develop a simple saliva test after concluding that it is possible to accurately measure salivary tTG-Abs; both at initial diagnosis for celiac disease, and also while patients are following a gluten-free diet.
    • 2008—Rates of celiac disease are shown to be 2.5 times higher among elderly people than among the general population.
    • 2009—Canada debuts the home celiac disease test kit as part of its national health care plan.
    • 2009—The company Nexpep is currently preparing for a clinical trial program for a peptide-based therapeutic vaccine, and intends to commence a Phase 1 in the first half of 2009. According to Nexpep, the peptide-based therapeutic vaccine is designed to treat the main problem T-cell epitopes of gluten, and has the potential to treat at about 80% of people with celiac disease and the appropriate genetic background.
    • 2009—Sometime this year the USFDA is expected to adopt long awaited regulations for the use of the term "gluten-free" on USA food labels. The new regulation would require foods with "gluten-free" on their labels to contain less than 20 parts per million of gliadin.
    • Several pharmaceutical companies are currently working on treatments for celiac disease, such as Alvine Pharmaceuticals (enzyme therapy), and Alba Therapeutics is developing a zonulin receptor antagonist called AT-1001, which is currently in phase 2 clinical trials.
    • 2012—All food made in the E.U. with ‘gluten-free’ on its label must contain less than 20 parts per million of gliadin, in accordance with the Codex Alimentarius standards.


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    Guest candy collins


    I enjoy this information, I was just told I have celiac disease. The more information the better!

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    Guest Dr. Bailey


    The body's response to wheat and all grain products is a natural response, not a disease process. We do not need to find another pharmaceutical to mask the body's response to a foreign antigen. People need to stop looking for the quick fix and learn to respect and treat your body as the hunter/gatherer it was genetically determined to be. Eating grains began an increase in the inflammatory process in the body which has lead to a variety of afflictions today. A drug is a band-aid.

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    Guest Michal S.


    Well "Dr.", if I could take a pill to end or at least control this disease I might get back the 2+ hours a day I lose having to do things strictly related to combating the disease, i.e. constantly having to read every word of every label of everything I eat and then still have to call the companies to be absolutely positive they are gluten-free if it isn't on the label, much lost time having to hunt down gluten-free food (the markets here don't have a section for them) and constantly having to prepare meals when I could be happy with a quick sandwich. Just once I'd like to grab some fast food when I don't have the time to cook. Don't even get me started on the expense. I like pasta but I now have to pay 250-300% more for mine than the general public. I'd also like a soft piece of bread once a year. I like sandwiches but I haven't had one in years because I just can't bear eating the hard always toasted bread that I'm forced to eat now. I've found some tasty bagels but they cost $8 for 5. I don't make a lot of money but this disease has cost me in more ways than just dollars and cents. The bad skin, foul smelling feces and constant sore gut are just a few of the problems I have to deal with. Finding a place to eat out means traveling quite a distance. Just finding gluten-free food is time-consuming. So Yes, if I could take a pill and reduce some of this aggravation I'd do it in a heart-beat. So get off your high horse and realize that real people are really affected by this and maybe some of us would appreciative a 'band-aid' to stop the bleeding.

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    Guest Danika


    I would have to agree that celiac disease is, more than likely, America's most under diagnosed health problem....the question is WHY??

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    The body's response to wheat and all grain products is a natural response, not a disease process. We do not need to find another pharmaceutical to mask the body's response to a foreign antigen. People need to stop looking for the quick fix and learn to respect and treat your body as the hunter/gatherer it was genetically determined to be. Eating grains began an increase in the inflammatory process in the body which has lead to a variety of afflictions today. A drug is a band-aid.

    That's right...no need to mask the body's response.

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    Guest Has Celiac's_1


    The body's response to wheat and all grain products is a natural response, not a disease process. We do not need to find another pharmaceutical to mask the body's response to a foreign antigen. People need to stop looking for the quick fix and learn to respect and treat your body as the hunter/gatherer it was genetically determined to be. Eating grains began an increase in the inflammatory process in the body which has lead to a variety of afflictions today. A drug is a band-aid.

    Do you actually have celiac or are you just saying that because if you actually have celiac then you would understand?

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    The body's response to wheat and all grain products is a natural response, not a disease process. We do not need to find another pharmaceutical to mask the body's response to a foreign antigen. People need to stop looking for the quick fix and learn to respect and treat your body as the hunter/gatherer it was genetically determined to be. Eating grains began an increase in the inflammatory process in the body which has lead to a variety of afflictions today. A drug is a band-aid.

    This article was excellent. Dr. Hunter/Gatherer apparently doesn't understand what the "gatherer" part is. Not too sure when he/she believes this advent of eating grains occurred. Not sure he/she suggests one experiencing this disorder is to cope without moving to a local cave. My son has the disorder (a severe case) and very minimal cross-contamination means disaster for him. This doctor's hypothetical utopia isn't reality for the lifetime of my son. -- Respectfully!

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    Guest JenniferW


    As someone who began suffering with multiple autoimmune disorders, the hunter-gatherer (Paleo) diet has changed my health for the better. Is it easy? Absolutely not. It takes commitment and effort to reprogram the way you eat. I think the comments above don't understand that it is a grain-free diet (also free of dairy/sugar/processed foods) that is completely manageable -- no cave needed. We all know that organic meats, fruits, and vegetables are healthiest for us, but I guess some people want to act like they can't live without processed foods. We all have a choice!

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    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
    Celiac.com 09/09/2011 - A team of researchers recently set out to assess the effects of milk-feeding behavior and the HLA-DQ genotype on intestinal colonization of Bacteroides species in infants with a risk of developing celiac disease.
    The research team included E. Sánchez, G. De Palma, A. Capilla, E. Nova, T. Pozo, G. Castillejo, V. Varea, A. Marcos, J. A. Garrote, I. Polanco, A. López, C. Ribes-Koninckx, M. D. García-Novo, C. Calvo, L. Ortigosa, F. Palau, and Y. Sanz.
    They are affiliated with the Ecofisiología Microbiana y Nutrición, Instituto de Agroquímica y Tecnología de Alimentos (CSIC) in Valencia, Spain.
    The team studied 75 full-term newborns with at least one first-degree relative who suffered from celiac disease. They classified the newborns according to milk-feeding practice (breast-fed or formula fed) and HLA-DQ genotype, which indicates high or low genetic risk.
    The team used PCR and denaturing gradient gel electrophoresis (DGGE) to analyze stools at 7 days, 1 month, and 4 months. They found that formula-fed infants showed greater Bacteroides species diversity than did breast-fed infants.  Breast-fed infants showed a higher prevalence of Bacteroides uniformis at 1 and 4 months of age, while formula-fed infants had a higher prevalence of B. intestinalis at all sampling times, of B. caccae at 7 days and 4 months, and of B. plebeius at 4 months.
    Infants with low genetic risk showed greater colonization of B. ovatus, B. plebeius, and B. uniformis, while those with high genetic risk showed a greater colonization of B. vulgatus.
    Among breast-fed infants, those with low genetic risk had greater colonization of B. uniformis than those with high genetic risk, who showed higher rates of B. vulgatus.
    Among formula-fed infants, the prevalence of B. ovatus and B. plebeius was increased in those with low genetic risk, while the presence of B. vulgatus was greater in those with high genetic risk.
    The results indicate that both the type of milk feeding and the HLA-DQ genotype influence the types of Bacteroides that colonize in the intestinal tract, and possibly also influence risk for developing celiac disease.

    Appl Environ Microbiol. 2011 Aug;77(15):5316-23. Epub 2011 Jun 3.

    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.

    Jefferson Adams
    Celiac.com 05/12/2014 - Currently, researcher know almost nothing about the natural history and evolution of celiac disease in ancient populations.
    But, a set of recently unearthed bones from ancient Rome show signs of a struggle with celiac disease, and may help researchers to better understand the natural history and evolution of the condition.
    Researchers believe the bones are those of an 18 to 20-year old upper class Roman woman, who likely had celiac disease or gluten intolerance, as her skeleton reveals signs of malnutrition and osteoporosis and her attempts to manage it by changing her diet.
    DNA analysis has confirmed that the woman carried two copies of an immune system gene variant strongly associated with celiac disease. Although celiac disease can be influenced by numerous environmental factors, the gene variant is found in nearly all contemporary celiac populations.
    The combination of genetic risk factors and malnutrition in someone likely to have good access to nutritious food, make celiac disease a reasonable diagnosis, says Gabriele Scorrano, a biological anthropologist at the University of Rome Tor Vergata.
    An article about the study appears in Nature, and the study itself appears in the American Journal of Physical Anthropology.

  • Recent Articles

    Jefferson Adams
    Celiac.com 04/19/2018 - Previous genome and linkage studies indicate the existence of a new disease triggering mechanism that involves amino acid metabolism and nutrient sensing signaling pathways. In an effort to determine if amino acids might play a role in the development of celiac disease, a team of researchers recently set out to investigate if plasma amino acid levels differed among children with celiac disease compared with a control group.
    The research team included Åsa Torinsson Naluai, Ladan Saadat Vafa, Audur H. Gudjonsdottir, Henrik Arnell, Lars Browaldh, and Daniel Agardh. They are variously affiliated with the Institute of Biomedicine, Department of Microbiology & Immunology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; the Institute of Clinical Sciences, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden; the Department of Pediatric Gastroenterology, Hepatology and Nutrition, Karolinska University Hospital and Division of Pediatrics, CLINTEC, Karolinska Institute, Stockholm, Sweden; the Department of Clinical Science and Education, Karolinska Institute, Sodersjukhuset, Stockholm, Sweden; the Department of Mathematical Sciences, Chalmers University of Technology, Gothenburg, Sweden; the Diabetes & Celiac Disease Unit, Department of Clinical Sciences, Lund University, Malmö, Sweden; and with the Nathan S Kline Institute in the U.S.A.
    First, the team used liquid chromatography-tandem mass spectrometry (LC/MS) to analyze amino acid levels in fasting plasma samples from 141 children with celiac disease and 129 non-celiac disease controls. They then crafted a general linear model using age and experimental effects as covariates to compare amino acid levels between children with celiac disease and non-celiac control subjects.
    Compared with the control group, seven out of twenty-three children with celiac disease showed elevated levels of the the following amino acids: tryptophan; taurine; glutamic acid; proline; ornithine; alanine; and methionine.
    The significance of the individual amino acids do not survive multiple correction, however, multivariate analyses of the amino acid profile showed significantly altered amino acid levels in children with celiac disease overall and after correction for age, sex and experimental effects.
    This study shows that amino acids can influence inflammation and may play a role in the development of celiac disease.
    PLoS One. 2018; 13(3): e0193764. doi: & 10.1371/journal.pone.0193764

    Jefferson Adams
    Celiac.com 04/18/2018 - To the relief of many bewildered passengers and crew, no more comfort turkeys, geese, possums or other questionable pets will be flying on Delta or United without meeting the airlines' strict new requirements for service animals.
    If you’ve flown anywhere lately, you may have seen them. People flying with their designated “emotional support” animals. We’re not talking genuine service animals, like seeing eye dogs, or hearing ear dogs, or even the Belgian Malinois that alerts its owner when there is gluten in food that may trigger her celiac disease.
    Now, to be honest, some of those animals in question do perform a genuine service for those who need emotional support dogs, like veterans with PTSD.
    However, many of these animals are not service animals at all. Many of these animals perform no actual service to their owners, and are nothing more than thinly disguised pets. Many lack proper training, and some have caused serious problems for the airlines and for other passengers.
    Now the major airlines are taking note and introducing stringent requirements for service animals.
    Delta was the first to strike. As reported by the New York Times on January 19: “Effective March 1, Delta, the second largest US airline by passenger traffic, said it will require passengers seeking to fly with pets to present additional documents outlining the passenger’s need for the animal and proof of its training and vaccinations, 48 hours prior to the flight.… This comes in response to what the carrier said was a 150 percent increase in service and support animals — pets, often dogs, that accompany people with disabilities — carried onboard since 2015.… Delta said that it flies some 700 service animals a day. Among them, customers have attempted to fly with comfort turkeys, gliding possums, snakes, spiders, and other unusual pets.”
    Fresh from an unsavory incident with an “emotional support” peacock incident, United Airlines has followed Delta’s lead and set stricter rules for emotional support animals. United’s rules also took effect March 1, 2018.
    So, to the relief of many bewildered passengers and crew, no more comfort turkeys, geese, possums or other questionable pets will be flying on Delta or United without meeting the airlines' strict new requirements for service and emotional support animals.

    Celiac disease is an autoimmune condition that affects around 1% of the population. People with celiac disease suffer an autoimmune reaction when they consume wheat, rye or barley. The immune reaction is triggered by certain proteins in the wheat, rye, or barley, and, left untreated, causes damage to the small, finger-like structures, called villi, that line the gut. The damage occurs as shortening and villous flattening in the lamina propria and crypt regions of the intestines. The damage to these villi then leads to numerous other issues that commonly plague people with untreated celiac disease, including poor nutritional uptake, fatigue, and myriad other problems.
    Celiac disease mostly affects people of Northern European descent, but recent studies show that it also affects large numbers of people in Italy, China, Iran, India, and numerous other places thought to have few or no cases.
    Celiac disease is most often uncovered because people experience symptoms that lead them to get tests for antibodies to gluten. If these tests are positive, then the people usually get biopsy confirmation of their celiac disease. Once they adopt a gluten-free diet, they usually see gut healing, and major improvements in their symptoms. 
    Symptoms of celiac disease can range from the classic features, such as diarrhea, upset stomach, bloating, gas, weight loss, and malnutrition, among others.
    Celiac disease can often less obvious symptoms, such fatigue, vitamin and nutrient deficiencies, anemia, to name a few. Often, these symptoms are regarded as less obvious because they are not gastrointestinal in nature. You got that right, it is not uncommon for people with celiac disease to have few or no gastrointestinal symptoms. That makes spotting and connecting these seemingly unrelated and unclear celiac symptoms so important.
    Currently, most people diagnosed with celiac disease do not show symptoms, but are diagnosed on the basis of referral for elevated risk factors. 

    Gluten intolerance is a generic term for people who have some sort of sensitivity to gluten. These people may or may not have celiac disease. Researchers generally agree that there is a condition called non-celiac gluten sensitivity. That term has largely replaced the term gluten-intolerance. What’s the difference between celiac disease and non-celiac gluten-sensitivity? 
    Gluten triggers symptoms and immune reactions in people with celiac disease. Gluten can also trigger symptoms in some people with NCGS, but the similarities largely end there.

    There are four main differences between celiac disease and non-celiac gluten sensitivity:
    No Hereditary Link in NCGS
    Researchers know for certain that genetic heredity plays a major role in celiac disease. If a first-degree relative has celiac disease, then you have a statistically higher risk of carrying genetic markers DQ2 and/or DQ8, and of developing celiac disease yourself. NCGS is not known to be hereditary. Some research has shown certain genetic associations, such as some NCGS patients, but there is no proof that NCGS is hereditary. No Connection with Celiac-related Disorders
    Unlike celiac disease, NCGS is so far not associated with malabsorption, nutritional deficiencies, or a higher risk of autoimmune disorders or intestinal malignancies. No Immunological or Serological Markers
    People with celiac disease nearly always test positive for antibodies to gluten proteins. Researchers have, as yet, identified no such antobodies or serologic markers for NCGS. That means that, unlike with celiac disease, there are no telltale screening tests that can point to NCGS. Absence of Celiac Disease or Wheat Allergy
    Doctors diagnose NCGS only by excluding both celiac disease, an IgE-mediated allergy to wheat, and by the noting ongoing adverse symptoms associated with gluten consumption. WHAT ABOUT IRRITABLE BOWEL SYNDROME (IBS) AND IRRITABLE BOWEL DISEASE (IBD)?
    IBS and IBD are usually diagnosed in part by ruling out celiac disease. Many patients with irritable bowel syndrome are sensitive to gluten. Many experience celiac disease-like symptoms in reaction to wheat. However, patients with IBS generally show no gut damage, and do not test positive for antibodies to gliadin and other proteins as do people with celiac disease. Some IBS patients also suffer from NCGS.

    To add more confusion, many cases of IBS are, in fact, celiac disease in disguise.

    That said, people with IBS generally react to more than just wheat. People with NCGS generally react to wheat and not to other things, but that’s not always the case. Doctors generally try to rule out celiac disease before making a diagnosis of IBS or NCGS. 
    Crohn’s Disease and celiac disease share many common symptoms, though causes are different.  In Crohn’s disease, the immune system can cause disruption anywhere along the gastrointestinal tract, and a diagnosis of Crohn’s disease typically requires more diagnostic testing than does a celiac diagnosis.  
    Crohn’s treatment consists of changes to diet and possible surgery.  Up to 10% of Crohn's patients can have both of conditions, which suggests a genetic connection, and researchers continue to examine that connection.
    Is There a Connection Between Celiac Disease, Non-Celiac Gluten Sensitivity and Irritable Bowel Syndrome? Large Number of Irritable Bowel Syndrome Patients Sensitive To Gluten Some IBD Patients also Suffer from Non-Celiac Gluten Sensitivity Many Cases of IBS and Fibromyalgia Actually Celiac Disease in Disguise CELIAC DISEASE DIAGNOSIS
    Diagnosis of celiac disease can be difficult. 

    Perhaps because celiac disease presents clinically in such a variety of ways, proper diagnosis often takes years. A positive serological test for antibodies against tissue transglutaminase is considered a very strong diagnostic indicator, and a duodenal biopsy revealing villous atrophy is still considered by many to be the diagnostic gold standard. 
    But this idea is being questioned; some think the biopsy is unnecessary in the face of clear serological tests and obvious symptoms. Also, researchers are developing accurate and reliable ways to test for celiac disease even when patients are already avoiding wheat. In the past, patients needed to be consuming wheat to get an accurate test result. 
    Celiac disease can have numerous vague, or confusing symptoms that can make diagnosis difficult.  Celiac disease is commonly misdiagnosed by doctors. Read a Personal Story About Celiac Disease Diagnosis from the Founder of Celiac.com Currently, testing and biopsy still form the cornerstone of celiac diagnosis.
    There are several serologic (blood) tests available that screen for celiac disease antibodies, but the most commonly used is called a tTG-IgA test. If blood test results suggest celiac disease, your physician will recommend a biopsy of your small intestine to confirm the diagnosis.
    Testing is fairly simple and involves screening the patients blood for antigliadin (AGA) and endomysium antibodies (EmA), and/or doing a biopsy on the areas of the intestines mentioned above, which is still the standard for a formal diagnosis. Also, it is now possible to test people for celiac disease without making them concume wheat products.

    Until recently, biopsy confirmation of a positive gluten antibody test was the gold standard for celiac diagnosis. It still is, but things are changing fairly quickly. Children can now be accurately diagnosed for celiac disease without biopsy. Diagnosis based on level of TGA-IgA 10-fold or more the ULN, a positive result from the EMA tests in a second blood sample, and the presence of at least 1 symptom could avoid risks and costs of endoscopy for more than half the children with celiac disease worldwide.

    Currently the only effective, medically approved treatment for celiac disease is a strict gluten-free diet. Following a gluten-free diet relieves symptoms, promotes gut healing, and prevents nearly all celiac-related complications. 
    A gluten-free diet means avoiding all products that contain wheat, rye and barley, or any of their derivatives. This is a difficult task as there are many hidden sources of gluten found in the ingredients of many processed foods. Still, with effort, most people with celiac disease manage to make the transition. The vast majority of celiac disease patients who follow a gluten-free diet see symptom relief and experience gut healing within two years.
    For these reasons, a gluten-free diet remains the only effective, medically proven treatment for celiac disease.
    There is currently no enzyme or vaccine that can replace a gluten-free diet for people with celiac disease.
    There are enzyme supplements currently available, such as AN-PEP, Latiglutetenase, GluteGuard, and KumaMax, which may help to mitigate accidental gluten ingestion by celiacs. KumaMax, has been shown to survive the stomach, and to break down gluten in the small intestine. Latiglutenase, formerly known as ALV003, is an enzyme therapy designed to be taken with meals. GluteGuard has been shown to significantly protect celiac patients from the serious symptoms they would normally experience after gluten ingestion. There are other enzymes, including those based on papaya enzymes.

    Additionally, there are many celiac disease drugs, enzymes, and therapies in various stages of development by pharmaceutical companies, including at least one vaccine that has received financial backing. At some point in the not too distant future there will likely be new treatments available for those who seek an alternative to a lifelong gluten-free diet. 

    For now though, there are no products on the market that can take the place of a gluten-free diet. Any enzyme or other treatment for celiac disease is intended to be used in conjunction with a gluten-free diet, not as a replacement.

    The most common disorders associated with celiac disease are thyroid disease and Type 1 Diabetes, however, celiac disease is associated with many other conditions, including but not limited to the following autoimmune conditions:
    Type 1 Diabetes Mellitus: 2.4-16.4% Multiple Sclerosis (MS): 11% Hashimoto’s thyroiditis: 4-6% Autoimmune hepatitis: 6-15% Addison disease: 6% Arthritis: 1.5-7.5% Sjögren’s syndrome: 2-15% Idiopathic dilated cardiomyopathy: 5.7% IgA Nephropathy (Berger’s Disease): 3.6% Other celiac co-morditities include:
    Crohn’s Disease; Inflammatory Bowel Disease Chronic Pancreatitis Down Syndrome Irritable Bowel Syndrome (IBS) Lupus Multiple Sclerosis Primary Biliary Cirrhosis Primary Sclerosing Cholangitis Psoriasis Rheumatoid Arthritis Scleroderma Turner Syndrome Ulcerative Colitis; Inflammatory Bowel Disease Williams Syndrome Cancers:
    Non-Hodgkin lymphoma (intestinal and extra-intestinal, T- and B-cell types) Small intestinal adenocarcinoma Esophageal carcinoma Papillary thyroid cancer Melanoma CELIAC DISEASE REFERENCES:
    Celiac Disease Center, Columbia University
    Gluten Intolerance Group
    National Institutes of Health
    U.S. National Library of Medicine
    Mayo Clinic
    University of Chicago Celiac Disease Center

    Jefferson Adams
    Celiac.com 04/17/2018 - Could the holy grail of gluten-free food lie in special strains of wheat that lack “bad glutens” that trigger the celiac disease, but include the “good glutens” that make bread and other products chewy, spongey and delicious? Such products would include all of the good things about wheat, but none of the bad things that might trigger celiac disease.
    A team of researchers in Spain is creating strains of wheat that lack the “bad glutens” that trigger the autoimmune disorder celiac disease. The team, based at the Institute for Sustainable Agriculture in Cordoba, Spain, is making use of the new and highly effective CRISPR gene editing to eliminate the majority of the gliadins in wheat.
    Gliadins are the gluten proteins that trigger the majority of symptoms for people with celiac disease.
    As part of their efforts, the team has conducted a small study on 20 people with “gluten sensitivity.” That study showed that test subjects can tolerate bread made with this special wheat, says team member Francisco Barro. However, the team has yet to publish the results.
    Clearly, more comprehensive testing would be needed to determine if such a product is safely tolerated by people with celiac disease. Still, with these efforts, along with efforts to develop vaccines, enzymes, and other treatments making steady progress, we are living in exciting times for people with celiac disease.
    It is entirely conceivable that in the not-so-distant future we will see safe, viable treatments for celiac disease that do not require a strict gluten-free diet.
    Read more at Digitaltrends.com , and at Newscientist.com

    Jefferson Adams
    Celiac.com 04/16/2018 - A team of researchers recently set out to investigate whether alterations in the developing intestinal microbiota and immune markers precede celiac disease onset in infants with family risk for the disease.
    The research team included Marta Olivares, Alan W. Walker, Amalia Capilla, Alfonso Benítez-Páez, Francesc Palau, Julian Parkhill, Gemma Castillejo, and Yolanda Sanz. They are variously affiliated with the Microbial Ecology, Nutrition and Health Research Unit, Institute of Agrochemistry and Food Technology, National Research Council (IATA-CSIC), C/Catedrático Agustín Escardin, Paterna, Valencia, Spain; the Gut Health Group, The Rowett Institute, University of Aberdeen, Aberdeen, UK; the Genetics and Molecular Medicine Unit, Institute of Biomedicine of Valencia, National Research Council (IBV-CSIC), Valencia, Spain; the Wellcome Trust Sanger Institute, Hinxton, Cambridgeshire UK; the Hospital Universitari de Sant Joan de Reus, IISPV, URV, Tarragona, Spain; the Center for regenerative medicine, Boston university school of medicine, Boston, USA; and the Institut de Recerca Sant Joan de Déu and CIBERER, Hospital Sant Joan de Déu, Barcelona, Spain
    The team conducted a nested case-control study out as part of a larger prospective cohort study, which included healthy full-term newborns (> 200) with at least one first relative with biopsy-verified celiac disease. The present study includes 10 cases of celiac disease, along with 10 best-matched controls who did not develop the disease after 5-year follow-up.
    The team profiled fecal microbiota, as assessed by high-throughput 16S rRNA gene amplicon sequencing, along with immune parameters, at 4 and 6 months of age and related to celiac disease onset. The microbiota of infants who remained healthy showed an increase in bacterial diversity over time, especially by increases in microbiota from the Firmicutes families, those who with no increase in bacterial diversity developed celiac disease.
    Infants who subsequently developed celiac disease showed a significant reduction in sIgA levels over time, while those who remained healthy showed increases in TNF-α correlated to Bifidobacterium spp.
    Healthy children in the control group showed a greater relative abundance of Bifidobacterium longum, while children who developed celiac disease showed increased levels of Bifidobacterium breve and Enterococcus spp.
    The data from this study suggest that early changes in gut microbiota in infants with celiac disease risk could influence immune development, and thus increase risk levels for celiac disease. The team is calling for larger studies to confirm their hypothesis.
    Microbiome. 2018; 6: 36. Published online 2018 Feb 20. doi: 10.1186/s40168-018-0415-6