March 2016
Volume 57, Issue 3
Open Access
Letters to the Editor  |   March 2016
Author Response: Light Levels and the Development of Deprivation Myopia
Author Affiliations & Notes
  • Cindy Karouta
    Centre for Research in Therapeutic Solutions, Biomedical Sciences, Faculty of Education, Science, Technology and Mathematics, University of Canberra, Canberra, Australia.
Investigative Ophthalmology & Visual Science March 2016, Vol.57, 825. doi:
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      Cindy Karouta, Regan Ashby; Author Response: Light Levels and the Development of Deprivation Myopia. Invest. Ophthalmol. Vis. Sci. 2016;57(3):825. doi:

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      © ARVO (1962-2015); The Authors (2016-present)

  • Supplements
We thank Galvis et al.1 for their comments regarding the possible role of ultraviolet (UV) exposure in the regulation of ocular growth. As we noted in our report,2 although much still is unknown, results from animal studies suggest that UV light is not critical for the regulation of ocular growth during experimentally induced changes in scleral growth rates, and more specifically, does not underlie the ability of bright light to retard the development of experimental myopia. As discussed in our study,2 and as noted by the authors, the protection provided by bright light against the development of deprivation myopia has been obtained using UV-free lighting systems in all animal models tested (chicks,25 tree shrews,6 and rhesus monkeys7). Normal emmetropization also is modifiable in chicks by alterations in light intensity, again using UV-free systems.8,9 Therefore, UV exposure does not underlie the ability of bright light to retard the development of deprivation-myopia, or the ability of bright light to maintain normal untreated eyes in a hyperopic state. However, we have not tested whether broadening the spectral output of our lighting system to include UV output can induce an even greater protective effect against the development of myopia. This seems unlikely, as the development of deprivation myopia can be abolished in rhesus monkeys (20,000 lux)7 and chicks (40,000 lux)1 by bright light alone; therefore, UV exposure seems unnecessary. Instead, our data suggest that the ability of light to retard the development of deprivation myopia is driven by intensity-dependent increases in retinal dopamine release,4 although the role of spectral composition, in the visible range, is an area of interest (for review see the study of Rucker10). 
In terms of experiments directly testing the role of UV exposure, we noted the report of Hammond et al.11 In this study, the investigators observed no difference in compensation to −10 diopter (D) or −20 D lenses under white light or UV light of matching illuminance. This suggests that the presence or absence of UV light does not modify compensation to negative lens wear and, hence, the emmetropization process. However, we agree with the authors that it would be interesting to see if greater intensities of UV exposure could alter the rate of compensation to optical defocus. The mechanism by which UV exposure may inhibit ocular growth has been postulated to involve elevated levels of vitamin D. Again, animal studies do not support a role for vitamin D in the regulation of ocular growth. Specifically, vitamin D3 supplementation does not affect the development of FDM or LIM in the tree shrew (Siegwart JT, et al. IOVS 2011;52:ARVO E-Abstract 6298). 
Whether UV exposure, and with it vitamin D levels, has a role in the protective effects of time outdoors still is unclear. An association between vitamin D receptor polymorphisms and myopia has been observed.12 Epidemiologic analysis has shown that increasing time spent outdoors is paralleled with increasing vitamin D levels, both of which show a negative correlation to incident myopia.1316 However, survival analysis has indicated that the critical factor for incident myopia is time spent outdoors, rather than vitamin D levels.16 In summary, the combination of animal experiments and survival analysis from epidemiological studies show that increased time outdoors and increased light exposure can prevent the development of myopia, but there is limited evidence that UV exposure or vitamin D has a causal role. Caution must be taken when interpreting any correlation between UV exposure, vitamin D levels, and myopia, as it is difficult to distinguish between a causative role and a simple biomarker for time spent outdoors. 
Galvis V,, Tello A, Parra MM, . Light levels and the development of deprivation myopia. Invest Ophthalmol Vis Sci. 2016; 57: 824.
Karouta C, Ashby RS. Correlation between light levels and the development of deprivation myopia. Invest Ophthalmol Vis Sci. 2014; 56: 299–309.
Ashby R, Ohlendorf A, Schaeffel F. The effect of ambient illuminance on the development of deprivation myopia in chicks. Invest Ophthalmol Vis Sci. 2009; 50: 5348–5354.
Ashby RS, Schaeffel F. The effect of bright light on lens compensation in chicks. Invest Ophthalmol Vis Sci. 2010; 51: 5247–5253.
Lan W, Feldkaemper M, Schaeffel F. Intermittent episodes of bright light suppress myopia in the chicken more than continuous bright light. PLoS One. 2014; 9: e110906.
Norton TT, Siegwart JT,Jr. Light levels, refractive development, and myopia—a speculative review. Exp Eye Res. 2013; 114: 48–57.
Smith EL,III Hung LF, Huang J. Protective effects of high ambient lighting on the development of form-deprivation myopia in rhesus monkeys. Invest Ophthalmol Vis Sci. 2012; 53: 421–428.
Cohen Y, Belkin M, Yehezkel O, Solomon AS, Polat U. Dependency between light intensity and refractive development under light-dark cycles. Exp Eye Res. 2011; 92: 40–46.
Cohen Y, Peleg E, Belkin M, Polat U, Solomon AS. Ambient illuminance retinal dopamine release and refractive development in chicks. Exp Eye Res. 2012; 103: 33–40.
Rucker FJ. The role of luminance and chromatic cues in emmetropisation. Ophthal Physiol Optics. 2013; 33: 196–214.
Hammond DS, Wildsoet CF. Compensation to positive as well as negative lenses can occur in chicks reared in bright UV lighting. Vision Res. 2012; 67: 44–50.
Mutti DO, Cooper ME, Dragan E, et al. Vitamin D receptor (VDR) and group-specific component (GC, vitamin D-binding protein) polymorphisms in myopia. Invest Ophthalmol Vis Sci. 2011; 52: 3818–3824.
Choi JA, Han K, Park YM, La TY. Low serum 25-hydroxyvitamin D is associated with myopia in Korean adolescents. Invest Ophthalmol Vis Sci. 2014; 55: 2041–2047.
Yazar S, Hewitt AW, Black LJ, et al. Myopia is associated with lower vitamin d status in young adults. Invest Ophthalmol Vis Sci. 2014; 55: 4552–4559.
Mutti DO, Marks AR. Blood levels of vitamin D in teens and young adults with myopia. Optom Vis Sci. 2011; 88: 377–382.
Guggenheim JA, Williams C, Northstone K, et al. Does vitamin D mediate the protective effects of time outdoors on myopia? Findings from a prospective birth cohort. Invest Ophthalmol Vis Sci. 2014; 55: 8550–8558.

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