We read with interest the article on illumination levels and form-deprivation myopia in chicks by Karouta and Ashby.
1 As the authors explained, several epidemiological studies and data from some clinical trials have suggested that there is a light-stimulated protective effect of outdoors activities for the development of myopia.
2–6 Animal studies have supported that hypothesis.
7,8 A previous work by Ashby et al.
7 showed that the development of experimental deprivation myopia could be partially inhibited when the diffusers were removed daily for 15 minutes with exposure during that period of time to sunlight (around 30,000 lux), bright indoor light (UV-free, 15,000 lux) or even laboratory standard conditions (500 lux). The protective effect was greater when the birds were exposed to direct sunlight than when they were exposed to either intense indoor lighting or normal laboratory light levels. A similar effect of bright light (15,000 lux) was observed also in chicks that wore their diffusers continuously and were exposed to the light for a period of 6 hours per day.
7 Smith et al.
8 found a comparable effect in Rhesus monkeys. High ambient lighting (around 25,000 lux) retarded the development of form-deprivation myopia.
Findings on the effect on compensation for imposed optical defocus with lenses have been less definitive with different kinds of light sources. Ashby and Schaeffel
9 found that exposure to high ambient luminance (15,000 lux , wavelength 300–1000 nm, peaking at 700 nm) initially decelerated compensation for negative lenses in chicks. However, endpoint refractions at day 6 were not changed. Additionally, Hammond and Wildsoet
10 reported that in chicks reared either under low intensity (200 lux) near UV illumination or low intensity (200 lux) white light, no protective effect against the compensation to defocus imposed by negative lenses was seen. In monkeys, Smith et al.
11 did not find that high light exposure (25,000 lux) influenced the degree of myopia induced by negative lens wearing.
In the new study by Karouta and Ashby,
1 the lighting system used was composed of a mix of two light sources, with a spectrum of 400 to 650 nm and 430 to 700 nm, and did not emit in either the infrared or ultraviolet (UV) range. Authors explained that since the lighting systems used to inhibit the development of experimental deprivation myopia in this animal model did not produce light in the UV spectrum, UV exposure could not explain this protective effect. Other studies mentioned by the authors also used UV-free light sources and obtained similar results.
7,8 Additionally, authors cited the already mentioned study by Hammond and Wildsoet
10 where they found no significant differences in the compensation response of chicks to optical defocus under either white light or bright UV light. They considered those results as an argument supporting that UV exposure did not modify the compensation response to form deprivation. However, although plausible, that conclusion cannot be drawn from those data. In order to rule out any effect of bright UV light on form-deprivation myopia, an experiment with animals exposed to high levels of UV-light illumination would be necessary (higher than those used by Hammond and Wildsoet
10).
The finding, on the one hand, of a direct relation between the level of protection from the development of form-deprivation myopia and intensity of light and, on the other hand, that bright light arrested any further progression in already myopic eyes, are noteworthy. However, we still have a long way to go to understand with certainty the mechanisms leading to myopia.