(1, 2). At that time, severe VI (best corrected visual acuity of 20/200 or worse in the better eye) was 25 times as common in subjects with diabetes compared with those without diabetes. VI in subjects with diabetes resulted mainly from vitreous hemorrhage, tractional detachment of the macula due to proliferative diabetic retinopathy (PDR), and from macular edema involving the foveal area due to leakage from the breakdown of the blood-retinal barrier. Cataract and glaucoma also contributed to VI in individuals with diabetes. Poor glycemic control was common in subjects with diabetes at that time (3, 4). This was due, in part, to the fact that intensive appropriate insulin treatment was difficult to achieve. This was related to the technology that was available for monitoring glucose levels (self-monitoring of glycemic control was done by testing of spot urines; no glycosylated hemoglobin A1c was available) and to the way insulin was administered (no pump, treatment with one injection per day of a long-acting insulin). There was no definitive evidence that achieving good glycemic control would actually result in less DR; thus, there was a lack of consensus on optimal glucose levels among physicians caring for individuals with diabetes. Some clinicians believed that high blood glucose was less likely to result in the development of severe DR in subjects with type 2 diabetes than in those with type 1 diabetes (5). Blood pressure was also poorly controlled in individuals with diabetes at that time (3, 4).

In 1972, the efficacy of photocoagulation had not yet been demonstrated to prevent visual loss due to PDR or macular edema. Vitrectomy, a surgical intervention to restore vision in eyes with vitreous hemorrhage or tractional detachments of the macula, was in its developmental stages.