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    Stone Age Europeans Made and Ate Flour


    Jefferson Adams
    Image Caption: New article in Nature supports stone age human consumption of flours.

    Celiac.com 11/29/2010 - Recent archeological evidence in the form of starch from ground grains found at Stone Age sites suggests early modern humans also consumed various kinds of flour, not just meat alone.


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    For decades, there has been ample evidence to support meat-eating by early humans. Evidence such as stone blades used for hunting and animal bones bearing cut-marks have been are common finds. This evidence has supported a view that early humans were nearly total carnivores. 

    In contrast, very little evidence has been found to show plant and grain consumption. This may be due, at least in part to the lower environmental impact of plant use; plants leave far fewer traces.

    The evidence was partially obscured by standard archaeological practice of washing the grinding tools used to process plants, removing any preserved plant matter.

    In the latest discovery, scientists found flour residues on 30,000-year-old grinding stones from Italy, Russia and the Czech Republic. This indicates widespread processing and consumption of plant grains, according to Laura Longo, an archaeologist at the University of Siena in Italy and an author on the paper published in Proceedings of the National Academy of Sciences.

    These new finds provide some of the first evidence that early humans ate ground flour 20,000 years before the dawn of agriculture.

    "It's another nail in the coffin of the idea that hunter–gatherers didn't use plants for food," says Ofer Bar-Yosef, a Harvard University archaeologist not involved in the study.

    Additional work in recent years has also revealed a handful of Stone Age sites in the Near East with evidence for plant-eating.

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    Guest Celiac1

    Posted

    Now hopefully all of those people who mistakenly believe that celiac is simply a "natural" result of humans not "evolving" to eat grain will finally put their argument to rest. The fact is, celiac is an autoimmune DISEASE that occurs when the body loses tolerance for gluten and develops an autoimmune response to it. Yes it has a genetic component, but as a rule you are not born with it. Identical twin studies only have 70-80% concordance, and studies have shown that many patients develop celiac after testing negative for many years. I had no symptoms or positive blood work until one day I was exposed to the unknown environmental trigger(s) for celiac. In my case it seemed to be a viral infection and a vaccine given at the same time. In a matter of weeks, I had lost 20 lbs, and could not eat "normally" without immediately becoming sick. My blood work was off the charts positively, along with my biopsy. Celiac is a disease, much like Type 1 diabetes or Multiple Sclerosis, not a normal disposition. This is important so we can find a cure for celiac, and for ALL autoimmune diseases. Something in our environment is causing our immune systems to respond in a negative manner to "normal" stimuli. Celiac is NOT a "normal" or healthy response to a food protein

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    Guest Harriet Rimell

    Posted

    Very happy to have that settled and explained in an intelligent manner. I plan to use part of this explanation to help friends and co-workers realize this disease (I had a doctor correct me and call it a "condition') can be very dangerous like diabetes and is not to be dismissed as a condition or disposition! It is important that friends, relatives and your primary care doctor be educated to it's seriousness and be supportive to the same degree they would be to the well known autoimmune diseases.

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    Now hopefully all of those people who mistakenly believe that celiac is simply a "natural" result of humans not "evolving" to eat grain will finally put their argument to rest. The fact is, celiac is an autoimmune DISEASE that occurs when the body loses tolerance for gluten and develops an autoimmune response to it. Yes it has a genetic component, but as a rule you are not born with it. Identical twin studies only have 70-80% concordance, and studies have shown that many patients develop celiac after testing negative for many years. I had no symptoms or positive blood work until one day I was exposed to the unknown environmental trigger(s) for celiac. In my case it seemed to be a viral infection and a vaccine given at the same time. In a matter of weeks, I had lost 20 lbs, and could not eat "normally" without immediately becoming sick. My blood work was off the charts positively, along with my biopsy. Celiac is a disease, much like Type 1 diabetes or Multiple Sclerosis, not a normal disposition. This is important so we can find a cure for celiac, and for ALL autoimmune diseases. Something in our environment is causing our immune systems to respond in a negative manner to "normal" stimuli. Celiac is NOT a "normal" or healthy response to a food protein

    I would love to know what medical basis you have for stating the above, because you're wrong. Yes it is an autoimmune. Some people have symptoms younger than others. I had symptoms 20 years before I diagnosed myself. I also have a wide array of other autoimmune symptoms as do most people with gluten intolerance. Yes viral infections are implicated in late onset gluten sensitivities as compared to childhood celiac diagnoses, but it is more so because the viral overload weakens the body to a point it can no longer mask the symptoms. Celiac or gluten intolerance is the ROOT of autoimmune diseases and you would know this if you have done enough research as I have over the past 10 years. Many of my patients with autoimmune diseases can reduce or completely clear up their autoimmune symptoms by going on a gluten free diet. the reason for the growth of gluten issues is because of the hybridization of wheat, you would also know this if you actually did a little reading.

     

    And honestly this article doesn't prove anything about people eating grains. Maybe they ground the grains up to make glue. as Dr Weston Price showed people on native hunter-gatherer diets had no diabetes, osteoporosis, type 1 diabetes or autoimmune diseases. only when grains were added to the diets did stature change and the above mentioned diseases creep in. One thing that is not mentioned in the article that would be very telling is where these stone age sites were. I bet they were in the grain belt of the middle east.

     

    Did you realize the reason why most people are addicted to wheat products is that it turns into opiates in the blood? It makes people feel good, therefore those deprived of their favorite yummy treat will go to all sorts of lengths to insist that there must be a cure so they can have that rush again. sigh.

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  • About Me

    Jefferson Adams is a freelance writer living in San Francisco. He has covered Health News for Examiner.com, and provided health and medical content for Sharecare.com. His work has appeared in Antioch Review, Blue Mesa Review, CALIBAN, Hayden's Ferry Review, Huffington Post, the Mississippi Review, and Slate, among others.

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  • 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/


    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

    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.
    Source:

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

    Jefferson Adams
    Celiac.com 11/06/2013 - Some researchers have questioned whether celiac disease may have arisen as a side effect of recent genetic adaptations since the domestication of wheat about 10,000 years ago.
    In his keynote address at the 2013 International Celiac Disease Symposium in Chicago, John Hawks spoke about the history of celiac disease and how he is using that history to explore the responses of complex gene networks to environmental changes during recent human evolution.
    Specifically, Hawks is "looking at how human genes evolved in the recent past to get an idea of how those genes work, especially in complex phenotypes."
    The risk of developing celiac disease has strong genetic factors, many are a function of immune system molecules called human leukocyte antigens, or HLAs.
    HLAs are one of the most variable gene systems in the human genome, with more genetic variants in the modern human population than any other type of gene.
    These molecules dot cell surfaces and help the immune system distinguish friendly particles from potentially dangerous pathogens.
    According to Hawks, as populations grew more dense after the rise of agriculture, infectious diseases likely became a more serious issue, which led to a situation where the positive effects of a strong immune system outweigh any negative effects such as autoimmune reactions.
    Hawks and former graduate student Aaron Sams recently published evidence of changes in other, non-HLA genes related to celiac disease risk.
    However, recent data suggest that the genetics of celiac disease may not be the result of recent evolutionary pressures and changes, but more likely, Hawks says is "characteristic of much more ancient humans."
    Hawks and others continue to explore how functional networks of different genes respond to environmental changes.
    Hawks hopes to look bring this approach to other autoimmune disorders, such as type 1 diabetes.
    Source:
    http://www.news.wisc.edu/22157

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    Jefferson Adams
    Celiac.com 06/21/2018 - Would you buy a house advertised as ‘gluten-free’? Yes, there really is such a house for sale. 
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    Advertising Banner-Ads
    Bakery On Main started in the small bakery of a natural foods market on Main Street in Glastonbury, Connecticut. Founder Michael Smulders listened when his customers with Celiac Disease would mention the lack of good tasting, gluten-free options available to them. Upon learning this, he believed that nobody should have to suffer due to any kind of food allergy or dietary need. From then on, his mission became creating delicious and fearlessly unique gluten-free products that were clean and great tasting, while still being safe for his Celiac customers!
    Premium ingredients, bakeshop delicious recipes, and happy customers were our inspiration from the beginning— and are still the cornerstones of Bakery On Main today. We are a fiercely ethical company that believes in integrity and feels that happiness and wholesome, great tasting food should be harmonious. We strive for that in everything we bake in our dedicated gluten-free facility that is GFCO Certified and SQF Level 3 Certified. We use only natural, NON-GMO Project Verified ingredients and all of our products are certified Kosher Parve, dairy and casein free, and we have recently introduced certified Organic items as well! 
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    Jefferson Adams
    Celiac.com 06/20/2018 - Currently, the only way to manage celiac disease is to eliminate gluten from the diet. That could be set to change as clinical trials begin in Australia for a new vaccine that aims to switch off the immune response to gluten. 
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    Read more at the website for Australia’s University of the Sunshine Coast Clinical Trials Centre.

    Source:
    FoodProcessing.com.au

    Jefferson Adams
    Celiac.com 06/19/2018 - Could baking soda help reduce the inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease? Scientists at the Medical College of Georgia at Augusta University say that a daily dose of baking soda may in fact help reduce inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease.
    Those scientists recently gathered some of the first evidence to show that cheap, over-the-counter antacids can prompt the spleen to promote an anti-inflammatory environment that could be helpful in combating inflammatory disease.
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    That message, which is transmitted with help from a chemical messenger called acetylcholine, seems to encourage the gut to shift against inflammation, say the scientists.
    In patients who drank water with baking soda for two weeks, immune cells called macrophages, shifted from primarily those that promote inflammation, called M1, to those that reduce it, called M2. "The shift from inflammatory to an anti-inflammatory profile is happening everywhere," O'Connor says. "We saw it in the kidneys, we saw it in the spleen, now we see it in the peripheral blood."
    O'Connor hopes drinking baking soda can one day produce similar results for people with autoimmune disease. "You are not really turning anything off or on, you are just pushing it toward one side by giving an anti-inflammatory stimulus," he says, in this case, away from harmful inflammation. "It's potentially a really safe way to treat inflammatory disease."
    The research was funded by the National Institutes of Health.
    Read more at: Sciencedaily.com

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