Diabetic retinopathy (DR) is a leading cause of blindness but it is not known why retinopathy should be so early and so severe a complication of diabetes. The sensory loss caused by minute retinal lesions is part of the problem, but the diabetic changes in the brain are different and less serious than in the retina, often described as an outpost of the brain. This has led to the concept of a local factor being responsible for the microvasculopathy of DR. There are physiological factors unique to the retina, and it is suggested below how these, by causing hypoxia very early in diabetes, could activate cytokines that produce the microvascular changes. If retinal hypoxia is an important causal factor in the production of DR, prevention of hypoxia should ameliorate DR. This hypothesis predicts that retinitis pigmentosa (RP) should prevent DR. Both old and new work is described, which indicates that this is in fact the case, thus pointing to new, simple, and effective ways of delaying the progress of diabetic retinopathy.

Direct comparison of retinal and brain capillaries taken from diabetics show very considerable differences1 (Table 1), which indicate a “local factor” in the development of DR. It has been suggested2 that the local factor is related to what is unique to the retina, the photoreceptors. The 120 million rods have the highest metabolic rate of any cell in the body. In darkness, the outer limb membrane “leaks”, causing an inward “dark current”. This current is reduced by light, and at normal photopic levels is shut off completely. In full dark adaptation sodium ions and water enter the outer limb at a maximal rate, and are pumped out in the inner limb.3 The entire cytosol volume is pumped in about 15 seconds.4 This process requires a …