Myopia—Yesterday, Today, and Tomorrow

Abstract

Ideas about the etiology of myopia used to be trapped in a debate of either/or. Early descriptions placed the blame on the environment, particularly long periods of close work.1 In the mid-20th century, Sorsby and Benjamin2 swung the pendulum strongly toward genetics when they stated flatly that “studies on twins have shown that all refractions of the eye—emmetropia, hypermetropia, and myopia—are determined genetically.” Nothing ruins a good dogma like data. The more recent view, informed by an explosion of information from research in the last 20 years, has moved toward a melding of these two extremes into a richly detailed combination of both nature and nurture. The idea that refractive error was hardwired into genes was shattered in 1977 when Wiesel and Raviola3 showed that eyelid suture produced myopia in monkeys and, then again, in 1978 when Wallman and coworkers4 showed that simple frosted occluders resulted in large amounts of myopia in chicks. The myopia research community truly lost one of its pioneers when Josh Wallman passed away in 2012. These deprivation experiments were followed by lens experiments by Schaeffel and coworkers5 whose powerful paradigm has shown that the eyes of young animals of an amazing variety of species respond to the sign and the magnitude of imposed defocus by modulating their rates of axial growth to compensate for the defocus and become effectively emmetropic. The fovea was originally assumed to be the seat of this local growth regulation because of its superior acuity, but later work showed that the retinal periphery also plays a role and can actually override the fovea during compensation for blur.6 This insight has stimulated interest in specialty refractive corrections such as multifocal contact lenses and orthokeratology, interventions that provide myopic defocus to the periphery in an attempt to rein in the growth of the myopic eye.