An interesting article at Scientific American. War-related food shortages can save lives, it turns out.
CD [celiac disease] acquired a name in the first century A.D., when Aretaeus of Cappadocia, a Greek physician, reported the first scientific description, calling it koiliakos, after the Greek word for “abdomen,” koelia. British physician Samuel Gee is credited as the modern father of CD. In a 1887 lecture he described it as “a kind of chronic indigestion which is met with in persons of all ages, yet is especially apt to affect children between one and five years old.” He even correctly surmised that “errors in diet may perhaps be a cause.” As clever as Gee obviously was, the true nature of the disease escaped even him, as was clear from his dietary prescription: he suggested feeding these children thinly sliced bread, toasted on both sides.
Identification of gluten as the trigger occurred after World War II, when Dutch pediatrician Willem-Karel Dicke noticed that a war-related shortage of bread in the Netherlands led to a significant drop in the death rate among children affected by CD—from greater than 35 percent to essentially zero. He also reported that once wheat was again available after the conflict, the mortality rate soared to previous levels. Following up on Dicke’s observation, other scientists looked at the different components of wheat, discovering that the major protein in that grain, gluten, was the culprit.
it is the only example where the addition or removal of a simple environmental component, gluten, can turn the disease process on and off. (Although environmental factors are suspected of playing a role in other autoimmune diseases, none has been positively identified.)
Many more interesting details in the article, including recent research on the mechanism of the autoimmune reaction and prospects for non-dietary treatments of the disease. Finally, something to think about if you've got celiac in the family and are still having babies: The author and colleges have
...begun a long-term clinical study to test whether having infants at high risk eat nothing containing gluten until after their first year can delay the onset of CD or, better yet, prevent it entirely. “High risk,” in this case, means infants possess susceptibility genes and their immediate family has a history of the disorder.
We suspect the approach could work because the immune system matures dramatically in the first 12 months of life and because research on susceptible infants has implied that avoiding gluten during the first year of life might essentially train that developing immune system to tolerate gluten thereafter, as healthy people do, rather than being overstimulated by it. So far we have enrolled more than 700 potentially genetically susceptible infants in this study, and preliminary findings suggest that delaying gluten exposure reduces by fourfold the likelihood that CD will develop. It will be decades, however, until we know for certain whether this strategy can stop the disease from ever occurring.