For nearly 400 years, near work has held a special place at the center of the universe of environmental factors related to myopia. As early as 1611, Kepler proclaimed in Dioptrics that “Those who do much close work in their youth become myopic.”1 The great mind of Kepler discerned the laws governing the orbit of planets around the sun. Was he correct when it comes to myopia? No doubt the monumental effort Kepler expended in sifting through Tycho Brahe's data on the movement of the planet Mars through the night sky led him to believe that near work was an important cause of his own myopia. More influential in the ophthalmic world, Donders enumerated, in 1864, what he believed were the deleterious consequences of near work: “1°, pressure of the muscles on the eyeball in strong convergence of the visual axes; 2°, increased pressure of the fluids…; 3°, congestive processes in the fundus oculi, which, under the increased pressure of the fluids of the eye, give rise to extension of the membranes.”2 Classic 19th century work reinforced this view. Often the connection between near work and myopia was assumed to operate through an increased amount of education. Ware noted in 1813 that only 12 out of 10,000 rural, less educated recruits for military service over the previous 20 years had to be discharged for myopia. Yet at Oxford University, 32 out of 127 students were myopic.3 Cohn wrote in 1866 that myopia was quite common in the more rigorous town schools but rare in the village schools. Out of 240 village schoolchildren between the ages of 6 to 13 years, only 1% were myopic. The prevalence of myopia in a Breslau city school of 361 students increased from 13% in the youngest class to 60% in the oldest class.4 Numerous subsequent human studies have reinforced the connection between time in study, level of education, and myopia. Results from animal experimentation have been consistent with the idea of near work as a myopigenic factor. Hyperopic defocus appears to be a potent stimulant of excess axial elongation in a number of animal species.5–10 In humans, the combination of hyperopic defocus from accommodative lag and prolonged near work has been the dominant environmental hypothesis, the potential explanation for increased risk of both myopia onset and faster progression after onset.
The potential, however, has not been borne out by the clinical reality. Hyperopic defocus from an infant's own refractive error could be a visual signal for emmetropization. Yet studies in infants demonstrate that they have the ability to accommodate and therefore to attenuate their exposure to defocus from their own hyperopia (Mutti et al, unpublished data, 2009).11 The logical consequence of this accommodative ability is that no correlation was found between measured defocus and refractive error change during emmetropization (Mutti et al, unpublished data, 2009). Alternate and more complex hypotheses are possible, but a simple model of emmetropization as a dose-dependent response to hyperopic defocus is not consistent with these data. Taking the hypothesis beyond infancy, myopes do have increased levels of accommodative lag,12,13 but contrary to expectation, defocus in childhood does not seem to be a robust risk factor for onset of myopia or for faster myopic progression. In our Collaborative Longitudinal Evaluation of Ethnicity and Refractive Error, higher levels of accommodative lag were not seen in children before the onset of their myopia compared to children who were always emmetropic.13 Increased accommodative lag has been reported in children before the onset of their myopia,14 but the robustness of this finding may be questioned as the increase was only significant 2 years before onset and not in the year just prior to onset. Another test of the robustness of the hyperopic defocus hypothesis would be an examination of whether higher levels of accommodative lag accelerate myopic progression. Our recent analysis of this hypothesis showed no association between the level of defocus and the rate of myopic progression.15
Beyond lag and defocus, clinical data from two longitudinal studies have not found that the time spent in near work is associated with an increased risk of the onset of myopia. In a longitudinal study of Singaporean schoolchildren, the Singapore Cohort Study of the Risk Factors for Myopia assessed refractive error, parental myopia, near work activities, outdoor activities, nighttime lighting, and nonverbal intelligence (Raven Standard Progressive Matrices) in 994 non-myopic Chinese children aged 7 to 9 years over a 3-year period.16 Myopic parents and a higher IQ increased the risk of the onset of myopia but increased near work did not. Near work was assessed in detail as books per week, hours per day of reading, computer use, playing video games, and watching television. Yet none of these variables, alone or in the aggregate, was a significant risk factor for myopia. Children with higher IQs read more, but IQ, not near work, was the variable related to the risk of myopia. Genetic effects from myopic parents might operate synergistically with near work, conferring an increased environmental susceptibility to myopia. This hypothesis was tested by asking whether an interaction between parental myopia and near work was present, i.e., whether near work mattered more if children had myopic parents. There was no evidence for this hypothesis; the interaction was not statistically significant.16
These results are not specific to Asia. Singapore Cohort Study of the Risk Factors for Myopia results are nearly parallel to those from the Orinda Longitudinal Study of Myopia, our study of risk factors for myopia in a sample of mostly White children in the San Francisco Bay Area.17 Children who became myopic by the eighth grade in this longitudinal study (111) were compared with children who remained non-myopic (403). Parental myopia was a significant risk factor for the development of myopia. Two myopic parents increased the odds of myopia by 5.07 times and one parent by 2.08 times compared to having no myopic parents. Reading was not a significant factor, again either as an aggregate of various activities or as any single activity (reading, watching television, studying, using the computer or playing video games). Adjustment for near work did not affect the magnitude of parental influence (i.e., there was no evidence of a myopigenic environment created by myopic parents encouraging intense near work). There was also no interaction between parental myopia and near work (i.e., no genetic susceptibility to near work was inherited).17
The inconvenient truth in the animal data is that the eye appears to be far more responsive to inhibition of ocular growth than to stimulation of ocular growth. The myopia community has engaged in several years of debate over why the epidemiologic data on near work are not more compelling and more obviously connected to myopia. The answer was presumed to lie in the temporal integration of signals controlling the growth of the eye. Total time spent in reading, the usual form survey questions take on the topic, may not be as important as whether the reading took place in many short periods or less frequent longer periods. Several important animal studies took up this issue and came up with a consistent finding. Brief periods of visual experience that inhibit growth, such as in-focus viewing in a tree shrew or monkey, or myopic defocus in a chick, far outweigh and easily cancel the effects of much longer periods of exposure to myopigenic stimuli.18–21 These data are the complete opposite of those needed to support a near work theory of myopia. Supportive data would have the effects of defocus being cumulative, somehow remembered by the eye and translating into faster growth and a myopic state. Instead it appears that the eye is quite happy to forget whatever was accelerating growth. Nearly constant near work would be needed to divert the eye from its normal course. Perhaps this is what orthodox rabbinical students experience in their 16 h/d of study,22 but this is hardly the norm for most of the world's myopic children.
New clinical data are in agreement with these recent animal data: environmental influences are important but are more effective at slowing ocular growth and lowering the risk of onset. The data suggest that outdoor activity could be just such an influence. It appears to be both measurable and potent. Several cross-sectional studies have reported this effect.23–25 The robustness of the finding is underscored by the range of questions used to assess it. The effect is detectable whether the question is simple [“Activity Before and at Age 7 (which was mostly done): Outdoor activity or Indoor activity?”]24 or a detailed multi-page questionnaire.26 The probability of becoming myopic by the eighth grade is about 60% if a child has two myopic parents and does less than 5 h/week of sports/outdoor activity. We have estimated that this probability is about 20% if a two-myopic parent child does 14 h or more per week of sports/outdoor activity.17 Interestingly, the effect may be due simply to spending time outdoors rather than exercising or engaging in sports outdoors.25,27 The effect also does not seem to be backhanded evidence for near work, i.e., outdoor activity is the absence of doing near work; the amount of time outdoors was not correlated, let alone negatively correlated, with the time spent in near work.17,25
Study results are important when they provide a definitive answer, but another value may be raising good provocative questions, and that is the case with outdoor activity. The story is not yet completely and neatly wrapped. Longitudinal results from the Orinda Longitudinal Study of Myopia show that children who report more hours of “outdoor/sports activity” are at lower risk of onset of myopia,17 but this effect was not seen in the longitudinal results from Singapore Cohort Study of the Risk Factors for Myopia.16 The precise activity that confers the protective effect still needs to be found. A plausible mechanism for the effect would also be comforting. Several candidates have been proposed in the literature. One is that the distance fixation that would occur more frequently outdoors exposes the eye to the clear, unrestricted vision that has been the most consistent stop signal for ocular growth in mammalian models.17,21 Other candidates include a smaller pupil size for decreased retinal blur and light-mediated release of retinal dopamine, an inhibitor of ocular growth.25 Another possibility is an increase in exposure to more peripheral myopia or less peripheral hyperopia during distance viewing.28 The periphery has garnered increased attention in recent years. It covers a greater proportion of the internal ocular surface than the fovea, which is ordinarily assumed to be in charge of organizing growth. Ablation and occlusion experiments show that the periphery is quite capable of controlling the central refractive state.29–31 If defocus is important and if the periphery is capable of translating this signal into modulated growth, far objects viewed in the outdoors could slow ocular growth. Clinical trials using interventions such as ortho-keratology could test this hypothesis.32
This discussion has not mentioned genetic effects on ocular growth and the risk of myopia (see refs. 33–35 for recent reviews). These are no doubt important; the risk of onset was found to be reduced with high levels of outdoor activity, but not to nothing.17 Having two myopic parents still confers more risk than having none, regardless of the amount of outdoor activity. A tremendous amount of energy is being devoted to finding genetic loci associated with myopia and to determining how these loci influence the refractive state of the eye. How these influences might interact with the effect of time outdoors is another potentially productive avenue for study.
The beauty of Kepler's insight into planetary motion was that he was able to imagine orbits that were other than circular. He also put the sun in the right place, at the center of the solar system. His move away from the dominant paradigm led him to the correct explanation for the retrograde motion of Mars. Perhaps it is time for us to take to heart the hard-won data from these large epidemiological studies and dare to imagine that reading is not a harmful activity. Perhaps there are more productive paths to take than any invoking new and elaborate explanations of how reading might still cause myopia. Hopefully near work's fall from the center of myopia's environmental risk factor universe is more beginning than end, more big bang than apocalypse.
Donald O. Mutti
1. Mark HH. Johannes Kepler on the eye and vision. Am J Ophthalmol 1971;72:869–78.
2. Donders FC. On the Anomalies of Accommodation and Refraction of the Eye: With a Preliminary Essay on Physiological Dioptrics. London: New Sydenham Society; 1864.
3. Ware J. Observations relative to the near and distant sight of different persons. Philos Trans R Soc Lond A 1813;103:31–50.
4. Cohn HL. The Hygiene of the Eye in Schools. London: Simpkin, Marshall; 1886.
5. Wildsoet C, Wallman J. Choroidal and scleral mechanisms of compensation for spectacle lenses in chicks. Vision Res 1995;35:1175–94.
6. Smith EL, III, Hung LF. The role of optical defocus in regulating refractive development in infant monkeys. Vision Res 1999;39:1415–35.
7. Graham B, Judge SJ. The effects of spectacle wear in infancy on eye growth and refractive error in the marmoset (Callithrix jacchus). Vision Res 1999;39:189–206.
8. Siegwart JT, Norton TT. Refractive and ocular changes in tree shrews raised with plus or minus lenses. Invest Ophthalmol Vis Sci 1993;34(suppl.):1208.
9. McFadden SA, Howlett MH, Mertz JR. Retinoic acid signals the direction of ocular elongation in the guinea pig eye. Vision Res 2004;44:643–53.
10. Irving EL, Sivak JG, Callender MG. Refractive plasticity of the developing chick eye. Ophthalmic Physiol Opt 1992;12:448–56.
11. Gabriel GM, Mutti DO. Evaluation of infant accommodation using retinoscopy and photoretinoscopy. Optom Vis Sci, 2008;86: in press.
12. Gwiazda J, Thorn F, Bauer J, Held R. Myopic children show insufficient accommodative response to blur. Invest Ophthalmol Vis Sci 1993;34:690–4.
13. Mutti DO, Mitchell GL, Hayes JR, Jones LA, Moeschberger ML, Cotter SA, Kleinstein RN, Manny RE, Twelker JD, Zadnik K. Accommodative lag before and after the onset of myopia. Invest Ophthalmol Vis Sci 2006;47:837–46.
14. Gwiazda J, Thorn F, Held R. Accommodation, accommodative convergence, and response AC/A ratios before and at the onset of myopia in children. Optom Vis Sci 2005;82:273–8.
15. Berntsen DA, Sinnott LT, Mutti DO, Zadnik K, the CLEERE Study Group. Accommodative lag is not related to myopia progression. Optom Vis Sci 2007;84: abstract nr 070049.
16. Saw SM, Shankar A, Tan SB, Taylor H, Tan DT, Stone RA, Wong TY. A cohort study of incident myopia in Singaporean children. Invest Ophthalmol Vis Sci 2006;47:1839–44.
17. Jones LA, Sinnott LT, Mutti DO, Mitchell GL, Moeschberger ML, Zadnik K. Parental history of myopia, sports and outdoor activities, and future myopia. Invest Ophthalmol Vis Sci 2007;48:3524–32.
18. Napper GA, Brennan NA, Barrington M, Squires MA, Vessey GA, Vingrys AJ. The duration of normal visual exposure necessary to prevent form deprivation myopia in chicks. Vision Res 1995;35:1337–44.
19. Smith EL, III, Hung LF, Kee CS, Qiao Y. Effects of brief periods of unrestricted vision on the development of form-deprivation myopia in monkeys. Invest Ophthalmol Vis Sci 2002;43:291–9.
20. Zhu X, Winawer JA, Wallman J. Potency of myopic defocus in spectacle lens compensation. Invest Ophthalmol Vis Sci 2003;44:2818–27.
21. Norton TT, Siegwart JT Jr, Amedo AO. Effectiveness of hyperopic defocus, minimal defocus, or myopic defocus in competition with a myopiagenic stimulus in tree shrew eyes. Invest Ophthalmol Vis Sci 2006;47:4687–99.
22. Zylbermann R, Landau D, Berson D. The influence of study habits on myopia in Jewish teenagers. J Pediatr Ophthalmol Strabismus 1993;30:319–22.
23. Mutti DO, Mitchell GL, Moeschberger ML, Jones LA, Zadnik K. Parental myopia, near work, school achievement, and children's refractive error. Invest Ophthalmol Vis Sci 2002;43:3633–40.
24. Onal S, Toker E, Akingol Z, Arslan G, Ertan S, Turan C, Kaplan O. Refractive errors of medical students in Turkey: one year follow-up of refraction and biometry. Optom Vis Sci 2007;84:175–80.
25. Rose KA, Morgan IG, Ip J, Kifley A, Huynh S, Smith W, Mitchell P. Outdoor activity reduces the prevalence of myopia in children. Ophthalmology 2008;115:1279–85.
26. Ip JM, Huynh SC, Robaei D, Rose KA, Morgan IG, Smith W, Kifley A, Mitchell P. Ethnic differences in the impact of parental myopia: findings from a population-based study of 12-year-old Australian children. Invest Ophthalmol Vis Sci 2007;48:2520–8.
27. Saw SM, Tong L, Gazzard G, Zhang X, Chia A, Rose K. Outdoor leisure is protective for myopia in Singapore teenage children. Invest Ophthalmol Vis Sci 2008;49:e-abstract 1551.
28. Stone RA, Flitcroft DI. Ocular shape and myopia. Ann Acad Med Singap 2004;33:7–15.
29. Smith EL, III, Kee CS, Ramamirtham R, Qiao-Grider Y, Hung LF. Peripheral vision can influence eye growth and refractive development in infant monkeys. Invest Ophthalmol Vis Sci 2005;46:3965–72.
30. Schippert R, Schaeffel F. Peripheral defocus does not necessarily affect central refractive development. Vision Res 2006;46:3935–40.
31. Smith EL, III, Ramamirtham R, Qiao-Grider Y, Hung LF, Huang J, Kee CS, Coats D, Paysse E. Effects of foveal ablation on emmetropization and form-deprivation myopia. Invest Ophthalmol Vis Sci 2007;48:3914–22.
32. Cho P, Cheung SW, Edwards M. The longitudinal orthokeratology research in children (LORIC) in Hong Kong: a pilot study on refractive changes and myopic control. Curr Eye Res 2005;30:71–80.
33. Young TL, Metlapally R, Shay AE. Complex trait genetics of refractive error. Arch Ophthalmol 2007;125:38–48.
34. Tang WC, Yap MK, Yip SP. A review of current approaches to identifying human genes involved in myopia. Clin Exp Optom 2008;91:4–22.
35. Mutti DO, Zadnik K. Heredity of refractive errors. In: Jaeger EA, ed. Duane's Clinical Ophthalmology. Philadelphia: Lippincott, Williams, & Wilkins, in press.