Outdoor light and the prevention of myopia

Abstract

The management of myopia is facing an unprecedented challenge, as the prevalence of myopia has ascended rapidly in the last decades. Although there is still no clinically acceptable and satisfactory management available, growing evidence has suggested that outdoor exposure, mediated by outdoor light, is a simple and useful option to prevent the development of myopia. In my thesis, I have investigated the roles of spectral properties of indoor light and of high light intensity on experimental myopia, the dose-effect response and the temporal function of the exposure, and the possible molecular mechanism underlying the light-mediated protective effect against myopia.

I found that with the same spectral property (i.e. spectral composition and distribution), high-level light intensity prevented myopia development compared with low-level intensity. However, there was no significant difference in the protection effect between the sunlight-like and fluorescent lighting presented at the same level of intensity, indicating that high level of light intensity is the primary reason for the outdoor light to display a powerful inhibitor against myopia. Furthermore, the dose-effect response of bright light exposure was found to be not linear, but rather saturate at approximately 5 hours of treatment, suggesting that additional protection could not be obtained through simply increasing the exposure duration. By contrast, frequent and short episodes of exposure were found to enhance the protection effect than a single continuous exposure even though the light intensity and total dose of exposure was the same. With regard to the underlying mechanism, I found that wearing diffusers dramatically suppressed dopamine release from the retina and also the expression of ZENK protein in the retinal glucagonergic amacrine cells (GACs). Bright light, no matter presented continuously or intermittently, could significantly reduce the suppression of dopamine release. But no any difference in the rescue effect of dopamine release was detected between these two exposure patterns. Neither continuous nor intermittent bright light could rescue the suppression of ZENK induced by wearing diffusers.

As a whole, my doctoral thesis has extended our knowledge of the mechanism underlying outdoor light against myopia: high level of intensity is the major reason for the protective effect of sunlight, which depends not only on the total duration but also the temporal property of the exposure. Findings in the thesis provide further evidence for a role of dopamine in the signaling cascade of the bright-light-mediated protection, but a role of ZENK in glucagon amacrine cells, representing an important element in the retinal circuitry for the detection of the sign of defocus, is unlikely. The reason why intermittent bright light had a more prominent suppressive effect on myopia than continuous bright light exposure is still unclear and needs further investigation.