Both the name and that notion emerged in the mid-1970s, when it became clear that this form of diabetes has an autoimmune basis. Studies in identical twins showed that two of three initially unaffected cotwins would remain nondiabetic, an experiment of nature implying that type 1 diabetes was a disease involving a dose of happenstance, not solely of genetic predestination. Knowledge that the immune system was involved raised therapeutic possibilities because immunity had been successfully manipulated to our own advantage (eg, vaccines). Proof of principle for disease prevention emerged from rodent models of type 1 diabetes, and trials of immunosuppression with cyclosporin at disease onset showed that this could prolongβ-cell function in humans, if only transiently. Join this to the discovery that islet autoantibodies appeared in the circulation many years before clinical onset and could be used to predict disease development and one has a condition for which screening and intervention are justified, if such an intervention could be identified (1, 2).

The emerging therapeutic possibility has been matched to a growing need. The incidence of childhood diabetes continues to rise steadily, and the ever-increasing push toward more intensive management is limited by rising costs and the unremitting demand this form of therapy places on its recipients. It has been clearly demonstrated that improved clinical manage-