The Role of Diabetic Control in Diabetic Retinopathy

Abstract

In spite of the continuing debate, it is possible to summarize the present state of our knowledge and to draw the following conclusions: 1. Microangiopathy of diabetes can be produced by pure insulin-deficiency in human subjects and experimental animals. 2. Evidence supports the concept that the pathology is due mainly to the deranged metabolism following insulin deprivation. 3. Repair of the insulin deficiency in animals has been shown to prevent the vascular damage associated with insulin deficiency. 4. Present methods of therapy have not been successful in preventing vascular complications in the noninsulin-dependent middle-aged diabetic patient; and, based on the findings of the University Group Diabetes Program, there is reason to believe that new methods of therapy must be realized to improve this outlook. 5. The efficacy of "compulsive control" for prevention of microangiopathy in insulin-dependent diabetic patients has not been adequately studied. Based on the results of animal experiments, the prudent physician should make every attempt to restore a normal physiological cellular environment in these patients with the expectation that this will offer the patient the best opportunity to minimize degenerative complications. Prospective observations are needed on the effects of hypoglycemic episodes which may be inevitable under these circumstances, but there is no evidence at present to suggest that mild hypoglycemia is of itself detrimental. 6. All individuals interested in the prevention of the complications of diabetes using available therapeutic methods should work to encourage a prospective clinical trial carefully designed from both an ethical and scientific point of view to obtain answers to the questions raised here.