Abstract
We tend to view type 1 diabetes mellitus as a chronic autoimmune disease with a preclinical phase that usually lasts for a number of years.1 The classic symptoms of type 1 diabetes — hyperglycemia and ketosis — are thought to occur late in its course, only after 80 to 90 percent of the beta cells of the pancreatic islets have been destroyed. Data that provide strong support for this view have been obtained in numerous prospective studies of first-degree relatives of patients with type 1 diabetes; the relatives were followed because they had islet-cell antibodies.2 The conventional view of autoimmune . . .