Jump to content

Important Information

This site places cookies on your device (Cookie settings). Continued use is acceptance of our Terms of Use, and Privacy Policy.

  • Sign Up
  • Join our community!

    Do you have questions about celiac disease or the gluten-free diet?

  • Member Statistics

    84,923
    Total Members
    4,125
    Most Online
    Beckyok
    Newest Member
    Beckyok
    Joined
  • 0

    More Evidence Links Gut Bacteria to Celiac Disease


    Roy Jamron

    Celiac.com 11/06/2008 - Previously, the possible link between gut bacteria and celiac disease has been discussed in "Do Vitamin D Deficiency, Gut Bacteria, and Gluten Combine in Infancy to Cause Celiac Disease?"[1] A 5-year European study, DIABIMMUNE, is currently underway focusing on some 7000 children, from birth, investigating the development of intestinal bacterial flora and its influence on the development of the human immune system and autoimmune disease, including celiac disease.[2] Hopefully, this study will provide some much needed answers. Now a Spanish group of scientists has produced further evidence supporting a possible role for gut bacteria in the pathogenesis of celiac disease by investigating whether gut microflora present in the feces of celiac disease patients participates in the pro-inflammatory activity of celiac disease.[3]

    The makeup of fecal microflora in celiac disease patients differs significantly from that of healthy subjects. To determine whether gut microflora is a participant in the pro-inflammatory milieu of celiac disease, the Spanish research team incubated cultures of peripheral blood mononuclear cells from healthy adults with fecal microflora obtained from 26 active celiac disease children, 18 symptom-free celiac disease children on a gluten-free diet, and 20 healthy children. The scientists additionally investigated possible regulatory roles of Bifidobacterium longum ES1 and B. bifidum ES2 obtained from the feces of healthy individuals, co-incubating the Bifidobacterium with the test subject fecal microflora and the peripheral blood mononuclear cell culture.

    Fecal micrflora from both active and, notably, treated, symptom-free celiac children caused a significant increase in pro-inflammatory cytokine production and a decrease in anti-inflammatory IL-10 production in the peripheral blood mononuclear cell cultures compared to the fecal microflora from healthy children. However, cultures co-incubated with the Bifidobacterium strains exhibited a suppression of the pro-inflammatory cytokine production and an increase in IL-10 production. IL-10 is a cytokine which promotes immune tolerance.

    The scientists concluded that the makeup of the gut flora of celiacs may contribute to pro-inflammation in celiac disease, possibly in a synergy with gliadin, and that certain strains of Bifidobacterium appear to suppress and reverse pro-inflammatory effects and offering therapeutic opportunities for the treatment of celiac disease.

    It would have been interesting if the scientists had also investigated the effect of adding vitamin D to the fecal microflora and the peripheral blood mononuclear cell cultures. It is likely the addition of vitamin D might also have resulted in a suppression of pro-inflammatory cytokine production and an increase in IL-10 production. This is borne out by experiments with Mycobacterium tuberculosis and its culture filtrate antigen in peripheral blood mononuclear cell cultures where the addition of vitamin D resulted in a suppression of pro-inflammatory cytokine production and an increase in IL-10 production.[4] It is possible that celiac disease may be entirely prevented in infancy by routinely administrating prophylactic doses of vitamin D and probiotics containing specific strains of Bifidobacterium before gluten is introduced into the infant's diet. The vitamin D and Bifidobacterium strains may provide an IL-10 anti-inflammatory environment in which the immune system learns to respond tolerantly to gluten, forever preventing the onset of celiac disease.

    The fact that certain strains of fecal Bifidobacterium from healthy individuals appear to suppress celiac disease inflammation brings to mind the concept of "fecal bacteriotherapy" or "fecal transplant", a therapy developed and used in practice by the world reknown Australian gastroenterologist, Prof. Thomas J. Borody, M.D., known best for his development of a triple-antibiotic treatment for H. pylori and ulcerative colitis.[5] Fecal bacteriotherapy involves transplanting feces from a healthly, screened donor into an ailing patient with a persistant bacterial gastrointestinal disorder whose own gut flora has first been reduced or eliminated with antibiotics. The fecal microflora from the healthy donor reseeds the gut of the ailing patient with a healthy mix of intestinal microflora curing the gastrointestinal disorder. The Bifidobacterium research done by the Spanish researchers suggests that fecal bacteriotherapy might be an option to treat or cure celiac disease in adults, replacing gut flora causing intolerance to gluten with a healthy mix of gut flora that encourages tolerance to gluten.

    Sources

    [1] Do Vitamin D Deficiency, Gut Bacteria, and Gluten Combine in Infancy to Cause Celiac Disease?
    Roy S. Jamron
    https://www.celiac.com/articles/21605/

    [2] European Study Will Focus On Relation Of Gut Bacteria to Autoimmune Disease in Children
    Roy S. Jamron
    https://www.celiac.com/articles/21607/

    [3] Journal of Inflammation 2008, 5:19.
    Bifidobacterium strains suppress in vitro the pro-inflammatory milieu triggered by the large intestinal microbiota of coeliac patients.
    Medina M, De Palma G, Ribes-Koninckx C, Calabuig M, Sanza Y.
    http://www.journal-inflammation.com/content/pdf/1476-9255-5-19.pdf

    [4] J Clin Immunol. 2008 Jul;28(4):306-13.
    Regulatory role of promoter and 3' UTR variants of vitamin D receptor gene on cytokine response in pulmonary tuberculosis.
    Selvaraj P, Vidyarani M, Alagarasu K, Prabhu Anand S, Narayanan PR.
    http://www.springerlink.com/content/d67236620021j84u/

    [5] Prof. Thomas J. Borody, M.D., Bio and Publication List http://www.cdd.com.au/html/hospital/clinicalstaff/borody.html http://www.cdd.com.au/html/expertise/publications.html


    0


    User Feedback

    Recommended Comments

    Dear Mr. Jamron, After 2 years of a gluten free diet

    my health remained very bad. That is when I learned about heavy metal toxicity. When the gut barrier isn't strong anymore,there is no good protection anymore and we get stuff in our system which is very bad for our health. I don't believe bacteria are THE CAUSE or THE CURE for celiac disease. The reason people with celiac disease have different bacteria in their gut is because the immune system is not working correctly anymore because of the toxins and heavy metals. When these toxins and heavy metals are removed, perfect health will be regained, BUT the celiac disease will remain.

    Share this comment


    Link to comment
    Share on other sites

    Thanks Roy for that. It makes me feel so much better about my banging on about gut dysbiosis and rogue bacteria being behind so many health issues. Celiac is just one condition among many and just the tip of the iceberg. I am sure a lot more will come out on this subject.

     

    It's encouraging when you get information that proves you are on the right track. Now I have a little more evidence to back up my belief.

    Share this comment


    Link to comment
    Share on other sites
    Guest Michelle Grace

    Posted

    Very informative and interesting. Makes absolute sense to me. I have long believed there are many factors contributing to the disorder/disease. Thanks for the article.

    Share this comment


    Link to comment
    Share on other sites
    Guest MaryClare

    Posted

    Healthy intestinal flora from birth on will provide a strong defense and immune system that will be much more likely to keep at bay many auto-immune disorders.

    Share this comment


    Link to comment
    Share on other sites

    Thanks for this article. I'm pretty firmly convinced that expression of the celiac genes is primarily facilitated by a gut that is out of balance -- too much bad bacteria, not enough good. Curses to all those dozens of antibiotics I took as a child!!

     

    I suspect it would do all celiacs good to follow the GAPS diet for some time, as a means to heal the gut. Alas, it's pretty challenging to do in the real world, without a very high level of motivation...

    Share this comment


    Link to comment
    Share on other sites


    Your content will need to be approved by a moderator

    Guest
    You are commenting as a guest. If you have an account, please sign in.
    Add a comment...

    ×   Pasted as rich text.   Paste as plain text instead

      Only 75 emoji are allowed.

    ×   Your link has been automatically embedded.   Display as a link instead

    ×   Your previous content has been restored.   Clear editor

    ×   You cannot paste images directly. Upload or insert images from URL.


  • About Me

    Roy S. Jamron holds a B.S. in Physics from the University of Michigan and an M.S. in Engineering Applied Science from the University of California at Davis, and independently investigates the latest research on celiac disease and related disorders.

  • Related Articles

    Roy Jamron
    This article appeared in the Summer 2008 edition of Celiac.com's Scott-Free Newsletter.
    Celiac.com 06/16/2008 - Do vitamin D deficiency, gut bacteria, and timing of gluten introduction during infancy all combine to initiate the onset of celiac disease? Two recent papers raise the potential that this indeed may be the case. One paper finds that when transgenic mice expressing the human DQ8 heterodimer (a mouse model of celiac disease) are mucosally immunized with gluten co-administered with Lactobacillus casei bacteria, the mice exhibit an enhanced and increased immune response to gluten compared to the administration of gluten alone.[1] A second paper finds that vitamin D receptors expressed by intestinal epithelial cells are involved in the suppression of bacteria-induced intestinal inflammation in a study which involved use of germ-free mice and knockout mice lacking vitamin D receptors exposed to both friendly and pathogenic strains of gut bacteria.[2] Pathogenic bacteria caused increased expression of vitamin D receptors in epithelial cells. Friendly bacteria did not.
    If one considers these two papers together, one notices: (1) Certain species of gut bacteria may work in conjunction with gluten to cause an increased immune response which initiates celiac disease; (2) The presence of an adequate level of vitamin D may suppress the immune response to those same gut bacteria in such a way as to reduce or eliminate the enhanced immune response to gluten caused by those gut bacteria, thus preventing the onset of celiac disease.
    Vitamin D has recently been demonstrated to play a role in preserving the intestinal mucosal barrier. A Swedish study found children born in the summer, likely introduced to gluten during winter months with minimal sunlight, have a higher incidence of celiac disease strongly suggesting a relationship to vitamin D deficiency.[3] Recent studies found vitamin D supplementation in infancy and living in world regions with high ultraviolet B irradiance both result in a lower incidence of type 1 diabetes, an autoimmune disease closely linked to celiac disease.[4][5]
    Gut bacteria have long been suspected as having some role in the pathogenesis of celiac disease. In 2004, a study found rod-shaped bacteria attached to the small intestinal epithelium of some untreated and treated children with celiac disease, but not to the epithelium of healthy controls.[6][7] Prior to that, a paper published on Celiac.com[8] first proposed that celiac disease might be initiated by a T cell immune response to "undigested" gluten peptides found inside of pathogenic gut bacteria which have "ingested" short chains of gluten peptides resistant to breakdown. The immune system would have no way of determining that the "ingested" gluten peptides were not a part of the pathogenic bacteria and, thus, gluten would be treated as though it were a pathogenic bacteria. The new paper cited above[1] certainly gives credence to this theory.
    Celiac disease begins in infancy. Studies consistently find the incidence of celiac disease in children is the same (approximately 1%) as in adults. The incidence does not increase throughout life, meaning, celiac disease starts early in life. Further, in identical twins, one twin may get celiac disease, and the other twin may never experience celiac disease during an entire lifetime. Something other than genetics differs early on in the childhood development of the twins which initiates celiac disease. Differences in vitamin D levels and the makeup of gut bacteria in the twins offers a reasonable explanation as to why one twin gets celiac disease and the other does not. Early childhood illnesses and antibiotics could also affect vitamin D level and gut bacteria makeup. Pregnant and nursing mothers also need to maintain high levels of vitamin D for healthy babies.
    Sources:
    [1] Immunol Lett. 2008 May 22.
    Adjuvant effect of Lactobacillus casei in a mouse model of gluten sensitivity.
    D'Arienzo R, Maurano F, Luongo D, Mazzarella G, Stefanile R, Troncone R, Auricchio S, Ricca E, David C, Rossi M.
    http://dx.doi.org/10.1016/j.imlet.2008.04.006
    [2] The FASEB Journal. 2008;22:320.10. Meeting Abstracts - April 2008.
    Bacterial Regulation of Vitamin D Receptor in Intestinal Epithelial Inflammation
    Jun Sun, Anne P. Liao, Rick Y. Xia, Juan Kong, Yan Chun Li and Balfour Sartor
    http://www.fasebj.org/cgi/content/meeting_abstract/22/1_MeetingAbstracts/320.10
    [3] Vitamin D Preserves the Intestinal Mucosal Barrier
    Roy S. Jamron
    https://www.celiac.com/articles/21476/
    [4] Arch Dis Child. 2008 Jun;93(6):512-7. Epub 2008 Mar 13.
    Vitamin D supplementation in early childhood and risk of type 1 diabetes: a systematic review and meta-analysis.
    Zipitis CS, Akobeng AK.
    http://adc.bmj.com/cgi/content/full/93/6/512
    [5] Diabetologia. 2008 Jun 12. [Epub ahead of print]
    The association between ultraviolet B irradiance, vitamin D status and incidence rates of type 1 diabetes in 51 regions worldwide.
    Mohr SB, Garland CF, Gorham ED, Garland FC.
    http://www.springerlink.com/content/32jx3635884xt112/
    [6] Am J Gastroenterol. 2004 May;99(5):905-6.
    A role for bacteria in celiac disease?
    Sollid LM, Gray GM.
    http://dx.doi.org/10.1111/j.1572-0241.2004.04158.x
    [7] Am J Gastroenterol. 2004 May;99(5):894-904.
    Presence of bacteria and innate immunity of intestinal epithelium in childhood celiac disease.
    Forsberg G, Fahlgren A, Hörstedt P, Hammarström S, Hernell O, Hammarström ML.
    http://dx.doi.org/10.1111/j.1572-0241.2004.04157.x
    [8] Are Commensal Bacteria with a Taste for Gluten the Missing Link in the Pathogenesis of Celiac Disease?
    Roy S. Jamron
    https://www.celiac.com/articles/779/


    Jefferson Adams
    Willem-Karel Dicke: Pioneer in Gluten-free Diet in the Treatment of Celiac Disease
    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.
    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

    Gryphon Myers
    An Evolutionary Explanation for Gluten Intolerance
    Celiac.com 07/04/2012 - It is becoming increasingly clear that celiac disease (or some form of gluten sensitivity) affects many more people in the world than estimates from the past few decades suggested. In the 1950s, celiac disease was estimated as affecting 1 in 8000 individuals worldwide, while today that number has grown to 1 in 100. Seeking to explain why this sizable portion of our population cannot tolerate gluten, Professor David Sanders, who is a Consultant Gastroenterologist at the Royal Hallamshire Hospital and University of Sheffield, looks to evolution for answers.
    It is hard to think of a world without bread, as even Ancient Romans harvested grain. But wheat is actually a new food for us: it was only widely introduced into the human diet roughly ten thousand years ago, which is a very small percentage (0.4%) of the 2.5 million years our species has walked the planet.
    So what were we eating that other 99.6% of our life as a species? We ate things that are edible raw, without the need for processing or refinement (which wheat is not). Our ability to process grains to an edible form was a technological development that did not occur until a relatively recent chapter in our history.
    In a sense, then, our ingenuity is ahead of our biology. As Dr. Sanders says, “... it makes sense that our bodies are still adapting to this food, and more specifically, the gluten it contains.” After millions of years of what is essentially gluten-free dieting, our bodies might be ill-equipped to process gluten, as it is still a relatively foreign substance.
    Source:
    http://www.science20.com/news_articles/being_glutenfree_determined_evolution_says_gastroenterologist-91578

    Jefferson Adams
    Do Bones from Ancient Rome Hold Clues to Celiac Disease?
    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.

  • Popular Contributors

  • Forum Statistics

    • Total Topics
      111,067
    • Total Posts
      953,252
  • Topics

  • Who's Online (See full list)

  • Posts

    • Maureen and Cyclinglady, Of the foods you listed. . .. I would focus on the Chocolate. Chocolate has Tyramine in it and it could/can cause rashes that  might be confused for DH. Sometimes Tyramine get's confused for/in high sulfite foods as triggers. Here is a great overview article on this topic. http://www.chicagotribune.com/lifestyles/health/sc-red-wine-headache-health-0608-20160525-story.html you might also have trouble with headaches if it tyramine is causing you your trouble. People who have trouble Tyramine might also have trouble with consuming cheeses. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2738414/ As for the Milk causing/triggering your DH don't rule Adult onset dairy allergy. While rare it does occur in the literature/research when you search it out. I am including the research here in the hopes it might help you or someone else entitled "Adult onset of cow's milk protein allergy with small‐intestinal mucosal IgE mast cells" https://onlinelibrary.wiley.com/doi/10.1111/j.1398-9995.1996.tb04640.x It is generally thought most of grow out of a Milk Allergy at approx. 3 years old. But for some lucky one (I guess) we never do apparently.  (I speak for my friend on this board JMG).  He found out he was having trouble with dairy as an adult better never realized until about 6 months ago. With delayed onset allergies it is often hard to tell if it (allergen) is effecting us because we might not associate it with our dairy consumption because it might happen a day or two latter. See this WHFoods article about food allergens/sensitivies.  It is very long/exhaustive but it is very helpful if you have time to study it in more detail. http://www.whfoods.com/genpage.php?pfriendly=1&tname=faq&dbid=30 I will quote some key points for your information. Symptoms of Food Allergies "The most common symptoms for food allergies include vomiting, diarrhea, blood in stools, eczema, hives, skin rashes, wheezing and a runny nose. Symptoms can vary depending upon a number of variables including age, the type of allergen (antigen), and the amount of food consumed. It may be difficult to associate the symptoms of an allergic reaction to a particular food because the response time can be highly variable. For example, an allergic response to eating fish will usually occur within minutes after consumption in the form of a rash, hives or asthma or a combination of these symptoms. However, the symptoms of an allergic reaction to cow's milk may be delayed for 24 to 48 hours after consuming the milk; these symptoms may also be low-grade and last for several days. If this does not make diagnosis difficult enough, reactions to foods made from cow's milk may also vary depending on how it was produced and the portion of the milk to which you are allergic. Delayed allergic reactions to foods are difficult to identify without eliminating the food from your diet for at least several weeks and slowly reintroducing it while taking note of any physical, emotional or mental changes as it is being reintroduced." Here is their information on Tyramine's. Tyramine "Reactions to tyramine (an amino acid-like molecule) or phenylalanine (another amino acid-like molecule) can result from eating the following foods: Fermented cheeses Fermented Sausage Chocolate Sour Cream Red wine Avocado Beer Raspberries Yeast Picked Herring Symptoms of tyramine intolerance can include urticaria (hives), angioedema (localized swelling due to fluid retention), migraines, wheezing, and even asthma. In fact, some researchers suggest that as many as 20 percent of migraines are caused by food intolerance or allergy, and tyramine intolerance is one of the most common of these toxic food responses." Here is an old thread on tyramine and especially how it can trigger headaches. https://www.celiac.com/forums/topic/95457-headache-culprit-is-tyramine/ I would also suggest your research a low histamine food diet.  Rashes/hives etc. can be triggered my disregulaton of histamine in the body. The other thing in chocolate that might be causing your problems is Sulfites. Here is a website dedicated to a Sulftie allergy. http://www.allergy-details.com/sulfites/foods-contain-sulfites/ Chocolate bars are on their list of sulfite contaning foods but probably most noted in dried fruits and red wine. Knitty Kitty on this board knows alot about a sulfite allergy. I want to go back to the possible dairy allergy for a second as a possible trigger. . .because it has been established as connected to DH . . .it is just not well known. Here is current research (as I said earlier) most dairy allergies are studied in children but it does occur in approx. 10 pct of the GP unless your of Asian descent where it is much more common. https://www.ncbi.nlm.nih.gov/pubmed/29555204 quoting the new research from this year on children. "When CMP (Cow's Milk Protein) was re-introduced, anti-tTG increased, and returned to normal after the CMP was withdrawn again." and if adults can also (though rarely) it seem develop "Adult onset of cow's milk protein allergy with small‐intestinal mucosal IgE mast cells" (see research linked above) as the research shows  you should at least trial removing dairy from your diet if you haven't already and see if your DH doesn't come back when you re-introduce it. It just takes 15 or 20 years for medical doctor' to incorporate new research/thinking into clinical practice.  And note the research on this happening in adults is 20+ years old and as far I know doctor's . . . are not aware of this.  I know I wasn't until recently and I research things alot of to help myself and my friends. But I know you can't do what you don't know about.  So this is why I am trying to share what I learned so that other might be helped and this research might not  lay hidden another 20 years before doctor's and their Celiac/DH patients become aware of it. And if it helps you come back on the board and let us know so it can help others too! If it helps you it will/can help someone else! if they know it helped you then they will/can have hope it might help them too and why I share and research these things for others'. . . who don't know or don't have time to research this for themselves. I hope this is helpful but it is not medical advice. Good luck on your continued journey. I know this is a lot of information to digest at one time but I hope at least some of if it helpful and you at least have a better idea of what in your chocolate could be causing your DH (idiopathic) as the doctor's say (of an unknown cause mild) DH symptom's. Or at least it is not commonly known yet that Milk can also cause trigger (DH) in children and adults who have a Milk allergy undiagnosed. . .because we don't don't typically think  or associate it with adults like maybe we should if we are not of Asian descent. Maureen if this doesn't help you you might want to start a thread in the DH section of the forum. As always  2 Timothy 2: 7   “Consider what I say; and the Lord give thee understanding in all things” this included. Posterboy by the grace of God,
    • I hooe you can get some answers with your new GI doc.
    • Many of us deal with doctor issues and diagnosis, you got a really bad draw indeed. Most doctors dismiss Celiac as their is no money in the cure for them IE a gluten free diet and not medications.

      Keep up updated on your new doctor and testing, good to see you finally found one that listens and can help, I got through on doc #5 I think it was.
  • Upcoming Events

  • Most Popular Articles

  • Blog Entries

  • Topics

×