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 celiac disease did not occur before this time. It wasn’t until the 20th century that the cause of celiac disease was identified.
In 250 A.D., Aretaeus of Cappadocia recorded a “malabsorptive syndrome with chronic diarrhoea.” When describing his patients he referred to them as “koiliakos,” which meant “suffering in the bowels.” The patient described in Aretaeus’ work had stomach pain and was atrophied, pale, feeble and incapable of work. 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 diarrhea.
Francis Adams translated these observations from Greek to English for the Sydenham Society of England in 1856. Adams gave the name “celiacs” or “coeliacs” to those suffering from this illness based on his studies of Aretaeus’ writings.
In 1888, the pediatrician Samuel Gee presented clinical accounts of children and adults with celiac disease at the Great Ormond Street Hospital for Children in the United Kingdom. Gee stated, “to regulate the food is the main part of treatment. The allowance of farinaceous foods must be small, but if the patient can be cured at all, it must be by means of diet.” September 13th is designated National Celiac Disease Awareness Day in honor of Gee’s birthday.
Christian Archibald Herter, an American physician, wrote a book in 1908 on children with celiac 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 pediatrician, reported positive effects of a diet of bananas in 1924. This diet remained in vogue until the actual cause of celiac disease was determined.
Dutch pediatrician, Willem Karel Dicke, MD, was recognized in 1952 for linking the ingestion of wheat proteins as the cause of celiac disease. Dicke noticed that while there was a shortage of bread during the Dutch famine of 1944 there was a significant drop in the death rate among children affected by CD – from greater than 35% to essentially zero. He also reported that once wheat was again available after the famine, 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.
The cause of celiac disease was eventually discovered to be an autoimmune reaction to gliadin, a gluten protein found in wheat, plus Secalin in rye and Hordein in barley. The lining of the small bowel is flattened, which interferes with the absorption of nutrients.
This gliadin molecule, found in wheat, is one of the triggers for the immune system reaction that causes celiac disease.
Originally called non-tropical sprue, terminology changed as research confirmed the adult sprue was the same thing as celiac disease diagnosed in children. The term “celiac disease” is now most commonly used. Another term for the same condition includes “gluten sensitive enteropathy.” Dermatitis herpetiformis and gluten ataxia are generally considered specific manifestations of celiac disease.
I’m very grateful to all of those who worked so hard through the years to find this disease and determine the treatment!
Sources: Celiac Support Association, www.csaceliacs.info; Wikipedia – Coeliac Disease
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