Why Celiac Disease is a Blankety-Blank
What Is Gluten?
Gluten is a mixture of proteins that occur naturally in wheat, rye, barley and crossbreeds of these grains.
The gluten-free diet is a treatment for Celiac Disease. Some people who don’t have celiac disease also may have symptoms when they eat gluten, however. This is called non-celiac gluten sensitivity. A Gluten-Free Diet is primarily used to treat celiac disease. Gluten causes inflammation in the small intestines of people with celiac disease. Eating a gluten-free diet helps people with celiac disease control their Signs and Symptoms and prevent complications.
The Food and Drug Administration issued a final ruling that defined what characteristics a food has to have to bear a label that proclaims it “gluten-free.” The rule also holds foods labeled “without gluten,” “free of gluten,” and “no gluten” to the same standard. the American Celiac Disease Alliance, notes that there is no cure for celiac disease and the only way to manage the disease is dietary—not eating gluten. Without a standardized definition of “gluten-free,” these consumers could never really be sure if their body would tolerate a food with that label.
Humans first started to cultivate grains in the Neolithic period (beginning about 9500 BCE) in the Fertile Crescent in Western Asia, and it is likely that coeliac disease did not occur before this time. Aretaeus of Cappadocia, living in the second century in the same area, recorded a malabsorptive syndrome with chronic diarrhoea, causing a debilitation of the whole body. His “Cœliac Affection” (coeliac from Greek κοιλιακός koiliakos, “abdominal”) gained the attention of Western medicine when Francis Adams presented a translation of Aretaeus’s work at the Sydenham Society in 1856. The patient described in Aretaeus’ work had stomach pain and was atrophied, pale, feeble and incapable of work. The diarrhoea manifested as loose stools that were white, malodorous and flatulent, and the disease was intractable and liable to periodic return. The problem, Aretaeus believed, was a lack of heat in the stomach necessary to digest the food and a reduced ability to distribute the digestive products throughout the body, this incomplete digestion resulting in the diarrhoea. He regarded this as an affliction of the old and more commonly affecting women, explicitly excluding children. The cause, according to Aretaeus, was sometimes either another chronic disease or even consuming “a copious draught of cold water.”
The Paediatrician Samuel Gee gave the first modern-day description of the condition in children in a lecture at Hospital for Sick Children, Great Ormond Street, London, in 1887. Gee acknowledged earlier descriptions and terms for the disease and adopted the same term as Aretaeus (coeliac disease). He perceptively stated: “If the patient can be cured at all, it must be by means of diet.” Gee recognised that milk intolerance is a problem with coeliac children and that highly starched foods should be avoided. However, he forbade rice, sago, fruit and vegetables, which all would have been safe to eat, and he recommended raw meat as well as thin slices of toasted bread. Gee highlighted particular success with a child “who was fed upon a quart of the best Dutch mussels daily.” However, the child could not bear this diet for more than one season.
Christian Archibald Herter, an American physician, wrote a book in 1908 on children with coeliac disease, which he called “intestinal Infantilism.” He noted their growth was retarded and that fat was better tolerated than carbohydrate. The Eponym Gee-Herter disease was sometimes used to acknowledge both contributions. Sidney V. Haas, an American paediatrician, reported positive effects of A Diet Of Bananas in 1924. This diet remained in vogue until the actual cause of coeliac disease was determined.
While a role for carbohydrates had been suspected, the link with wheat was not made until the 1940s by the Dutch paediatrician Dr Willem Karel Dicke. It is likely that clinical improvement of his patients during the Dutch famine of 1944 (during which flour was scarce) may have contributed to his discovery. Dicke noticed that the shortage of bread led to a significant drop in the death rate among children affected by coeliac disease from greater than 35% to essentially zero. He also reported that once wheat was again available after the conflict, the mortality rate soared to previous levels. The link with the gluten component of wheat was made in 1952 by a team from Birmingham, England. Villous atrophy was described by British physician John W. Paulley in 1954 on samples taken at surgery. This paved the way for biopsy samples taken by endoscopy.
Throughout the 1960s, other features of coeliac disease were elucidated. Its hereditary character was recognised in 1965. In 1966, dermatitis herpetiformis was linked to gluten sensitivity.
∗ Citied From Wikipedia, the free encyclopedia