The pathophysiology underlying diabetes-associated hearing loss is unclear, which allows for speculation. A leading candidate explanation is the effect of diabetes-related microvascular disease on the cochlea (8). Unlike the retina, the cochlea is virtually impossible to examine visually, and its microcirculation is embedded in the temporal bone, which cannot be effectively examined, even under surgical conditions. Previous postmortem studies have invoked microvascular disease affecting the stria vascularis, the organ responsible for generating endolymph, which serves as the driving force for mechanotransduction of hair cells. Temporal bone studies have demonstrated pathology in the stria vascularis and in hair cells of postmortem studies of the inner ear in diabetic adults (9–10). Despite these findings, the pathophysiology of impaired hearing in diabetes remains uncertain. First, pathologic change in the stria vascularis and the outer hair cells is a known concomitant of aging. Second, some investigators have looked for these changes in diabetic patients and failed to find them. Third, studies in diabetic animals have shown decreased hearing function but no abnormality in hair cells or the stria vascularis (11–12).