I see near-identical objectives and conclusions in the Diabetes Control and Complications Trial Research Group's article [1] and writings of J.M. Brush, but the former did not cite the latter. Were Brush's studies not conducted in a different era, he could have coauthored the current paper.

His studies were done at a time when there were two conflicting schools of thought about management of diabetes: one chemical, championed by the Joslin School, and one clinical, followed by Tolstoi and his group. Brush occupied center stage more than 50 years ago with his intensive therapy for residual insulin secretion in patients with newly diagnosed type 1 diabetes. Without C-peptides and by relying on the much-maligned urine glucose testing, he arrived at the same conclusion as did the DCCT group. Both demonstrated that intensive therapy for type 1 diabetes helps to sustain endogenous insulin secretion.

Brush's patients paralleled the intensive therapy group of the DCCT. Potential variables (exercise and diet) were kept constant, and regular insulin was administered with four daily injections. Within a week, hypoglycemia was seen; this was heralded as a return of endogenous insulin production and was the signal to reduce administrative insulin. At time of discharge, children were receiving a single daily injection of 2 to 8 U of regular insulin. Unfortunately, in both studies, the steady state achieved at discharge did not last; the "honeymoon" was over in a year or two.

The message "hyperglycemia is glucotoxic" was embraced by many and was applied to the larger group of patients with type 2 diabetes, a group with windows of retained ß-cell function that were open for a longer period. The physiologic studies from early in this century demonstrating that overwork inhibited recovery of stressed islet tissue were picked up by and clinically applied by Brush in the 1940s. In the 1990s, the DCCT confirmed Brush's work that demonstrated the importance of initiating early aggressive intervention and also demonstrated the effect of such control on chronic complications.

Hyperglycemia has to remain a target even when a handle is placed on the autoimmune causes of diabetes. The golden opportunity for bringing about maximum functional recovery presents itself only once. Yes, yesterday may have had the answer to today's questions.