Development of Ocular Refraction: Lessons from Animal Experiments

The size of the organs in the body is continuously regulated to match their functional capacity as required (review: Wallman and Winawer [79]). There is, however, probably no other organ so precisely controlled in size as the eye: to achieve full visual acuity, its length must be matched to the optical focal length of cornea and lens with a tolerance of about a tenth of a millimeter (equivalent to 0.25 D). A normalsighted (emmetropic) eye that increases in length by more than this amount will be slightly myopic and experience a detectable loss of visual acuity at far distances. Until about 1975, it was thought that this match was achieved by tight genetic control of growth, even though this appeared an improbable (or improbably impressive) achievement. About this time, it was discovered that, in monkeys whose lids were monocularly fused to study the development of binocular neurons in the visual cortex, the deprived eyes became longer and myopic [84]. This observation stimulated research into myopia in animal models. The idea was that eye growth, and therefore also refractive development, might be under visual control which is accessible to experimental studies in which the visual experience is intentionally altered. It also revived an older discussion as to whether myopia is environmental or genetic. Today, despite the results from animal models that demonstrate visually controlled eye growth, this discussion has not come to an end (e.g., [42]). Major studies in the United States concluded that “heritability was the most important factor” in myopia development and that only less than 20% can be modulated by visual experience (Orinda study [43]; twin studies, e.g., [18]). In contrast, a recent major review of the literature reaches the conclusion that the significant increase in the incidence of myopia in the last 40 years must be due to environmental factors [39]. Development of Ocular Refraction: Lessons from Animal Experiments