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The Origins of Celiac Disease

In this category you will find articles that cover ideas about how celiac disease came about, including theories of evolution, speculation on the underlying cause of the disorder, and information on the original doctors who studied and discovered celiac disease.


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    Can early infections in infants lead to celiac disease? Photo: CC--CaptMikey

    In previous studies, a team of scientists led by Professor Anette-Gabriele Ziegler had already shown an association between infections in early childhood and the development of type 1 diabetes. In that study, the researchers saw the highest risk for type 1 diabetes in children who experienced repeated respiratory infections in the first six months of life.

    Recently, Zeigler and another team of colleagues from the Institute for Diabetes Research at Helmholtz Zentrum München, a partner in the German Center for Diabetes Research (DZD), set out to determine whether infections during infancy are associated with increased risk for celiac disease later on.



    Why were bananas once regarded as a cure for celiac disease? Image: CC--jster

    Once upon a time, bananas were thought by many doctors to possess tremendous healing properties. Bananas were used to help diabetics to use weight. Doctors told mothers to feed bananas to their infants starting at 4 weeks. And for a long time, the diet seemed to help people "recover" from celiac disease.

    Invented by Dr. Sidney Haas in 1924, the high-calorie, banana-based diet excluded starches, but included bananas, milk, cottage cheese, meat and vegetables.



    Photo: CC--Yuri Samoilov

    Is a reovirus infection a prime cause of celiac disease? Researchers have suspected that viral infections may play a major role in celiac disease by causing a pathological response that triggers T helper 1 (TH1) immunity against dietary gluten.

    A team of researchers recently set out to test this hypothesis and to gain insights into mechanisms underlying virus-induced loss of tolerance to dietary antigens. To do so, they developed a viral infection model that makes use of two reovirus strains that infect the intestine, but which differ in their immunopathological outcomes.



    A paleo diet was the norm for the vast majority of human history. Image: CC--snowpea&bokchoi

    In 1999, Loren Cordain, the renowned professor of Exercise Physiology at Colorado State University who has since popularized the Paleodiet, published an extensive exploration of why our cultivation and consumption of cereal grains has been disastrous for the human race, resulting in many autoimmune, nutrient deficiency, and other modern diseases. Previously, in 1987, the famous physiologist, Jared Diamond characterized humanity's shift to agriculture as "The Worst Mistake in the History of the Human Race".



    Certain stomach viruses sharply increase celiac disease risk. Photo: CC--Vincent Tcheng Chang

    A new study confirms a link between intestinal viral infections and celiac disease.



    Photo: CC--Sander Van der Wel

    A new study looks at the impacts of introducing gluten to infants and the development of celiac disease. A research team recently set out to assess the evidence regarding the effect of time of gluten introduction and breastfeeding on the risk of developing celiac disease.



    Photo: CC--Pete

    Studies on early life infections and risk of later celiac disease (celiac disease) are inconsistent but have mostly been limited to retrospective designs, inpatient data, or insufficient statistical power.



    Photo: Wiki Media Commons--Roman skeleton woman

    What can bones from ancient Rome tell us about the natural history and evolution of celiac disease?



    Photo: CC--MDGLillehammer

    Pushback mounts against a controversial new report alleging that genetically engineered foods may trigger gluten sensitivity and celiac disease.



    Photo: CC--IvanWalsh.com

    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.



    Photo: CC--Dave Pearson

    Researchers don't know much about the genetic history of celiac disease. They know especially little about the age of specific gene sequences that leave people at risk for developing celiac disease.



    Photo: CC--D. H. Wright

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



    It is becoming increasingly clear that celiac disease affects many more people in the world than estimates from the past few decades suggested. 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.



    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.


    New article in Nature supports stone age human consumption of flours.
    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.


    SH2B3 offers protection against bacterial infection.
    A clinical team conducted a functional analysis of celiac risk loci, and found that SH2B3 offers protection against bacterial infection. The research team scientists hypothesize that the high prevalence of celiac disease might suggest that the process of natural selection favors genes that trigger celiac disease, and thus, that the gene may convey some evolutionary advantage to those who inherit them.


    Willem-Karel Dicke treats a patient Circa 1955.
    This article originally appeared in the Spring 2009 edition of Journal of Gluten Sensitivity.

    Willem-Karel Dicke was a Dutch pediatrician, and the first clinician to develop the gluten-free diet, and to prove that certain types of flour cause relapses in celiac disease patients.

    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).

    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?" 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. 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.

    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. 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. Pathogenic bacteria caused increased expression of vitamin D receptors in epithelial cells. Friendly bacteria did not.

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