PURPOSE: To determine whether high light levels, which have a protective effect against form-deprivation myopia, also retard the development of lens-induced myopia in primates. METHODS: Hyperopic defocus was imposed on 27 monkeys by securing -3 diopter (D) lenses in front of one eye. The lens-rearing procedures were initiated at 24 days of age and continued for periods ranging from 50 to 123 days. Fifteen of the treated monkeys were exposed to normal laboratory light levels (∼350 lux). For the other 12 lens-reared monkeys, auxiliary lighting increased the illuminance to 25,000 lux for 6 hours during the middle of the daily 12 hour light cycle. Refractive development, corneal power, and axial dimensions were assessed by retinoscopy, keratometry, and ultrasonography, respectively. Data were also obtained from 37 control monkeys, four of which were exposed to high ambient lighting. RESULTS: in normal- and high-light-reared monkeys, hyperopic defocus accelerated vitreous chamber elongation and produced myopic shifts in refractive error. the high light regimen did not alter the degree of myopia (high light: -1.69 ± 0.84 D versus normal light: -2.08 ± 1.12 D; P = 0.40) or the rate at which the treated eyes compensated for the imposed defocus. Following lens removal, the high light monkeys recovered from the induced myopia. The recovery process was not affected by the high lighting regimen. CONCLUSIONS: In contrast to the protective effects that high ambient lighting has against form-deprivation myopia, high artificial lighting did not alter the course of compensation to imposed defocus. These results indicate that the mechanisms responsible for form-deprivation myopia and lens-induced myopia are not identical.
PURPOSE: To determine whether high light levels, which have a protective effect against form-deprivation myopia, also retard the development of lens-induced myopia in primates. METHODS: Hyperopic defocus was imposed on 27 monkeys by securing -3 diopter (D) lenses in front of one eye. The lens-rearing procedures were initiated at 24 days of age and continued for periods ranging from 50 to 123 days. Fifteen of the treated monkeys were exposed to normal laboratory light levels (∼350 lux). For the other 12 lens-reared monkeys, auxiliary lighting increased the illuminance to 25,000 lux for 6 hours during the middle of the daily 12 hour light cycle. Refractive development, corneal power, and axial dimensions were assessed by retinoscopy, keratometry, and ultrasonography, respectively. Data were also obtained from 37 control monkeys, four of which were exposed to high ambient lighting. RESULTS: in normal- and high-light-reared monkeys, hyperopic defocus accelerated vitreous chamber elongation and produced myopic shifts in refractive error. the high light regimen did not alter the degree of myopia (high light: -1.69 ± 0.84 D versus normal light: -2.08 ± 1.12 D; P = 0.40) or the rate at which the treated eyes compensated for the imposed defocus. Following lens removal, the high light monkeys recovered from the induced myopia. The recovery process was not affected by the high lighting regimen. CONCLUSIONS: In contrast to the protective effects that high ambient lighting has against form-deprivation myopia, high artificial lighting did not alter the course of compensation to imposed defocus. These results indicate that the mechanisms responsible for form-deprivation myopia and lens-induced myopia are not identical.