The autoimmune coeliac disease results from ingestion of gluten in genetically predisposed individuals. The inflammatory damage caused to the mucosal lining of the small intestine gives rise to malabsorption and associated nutrient deficiency, and has been linked to a wide range of other medical conditions.
A link between diet and coeliac disease (CD) had been assumed since the beginning of the 20th century, but it was an acute observation by a Dutch paediatrician, Willem Dicke, that marks the beginning of our current understanding. He noted an improvement in the condition of his young coeliac patients when bread was not available in war-torn Holland for a period in 1944–1945. Later, after allied planes began regular drops of bread supplies, the condition of his patients deteriorated again. In studies exploring this observation he demonstrated the all-important association between ingestion of wheat or rye and the development of coeliac symptoms. Two years later, gluten, the collective name for storage proteins in wheat, was identified as the toxic component. The gliadins have since been identified as the class of protein principally responsible for CD. Related storage proteins in rye (hordein) and barley (secalin) have also been implicated.
By 1960 the curative effect of a gluten-free diet (exclusion of all foods containing wheat, rye and barley) had been demonstrated both in terms of symptom elimination and normalisation of the intestinal mucosa. Over the intervening years, much has been learned about how gluten causes intestinal damage, and the necessary genetic (inherited) factor has been identified. Arguably the most significant recent finding is that CD is a very common condition and that most affected people remain undiagnosed and quite unaware of the insidious damage to health that their diet may cause.
Some experts now argue that, as the disease is so common and the treatment so effective, everyone should be offered a serological screening test for CD. The more conservative prevailing view is that such testing should be reserved for those who are symptomatic and those known to be at high risk. All agree that the improved rate of case recognition through more widespread serological testing is now an important public health objective.
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