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Myopia: was mother right about reading in the dark?
  1. Dartmouth Hitchcock Medical Center, Dartmouth Medical School, Hanover, New Hampshire, USA Douglas.R.Fredrick{at}

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    Perhaps one of the most universal experiences of childhood involves parental admonishments warning of dire outcomes as a result of unacceptable behaviour. Tree climbing leads to “broken skulls and necks,” television viewing leads to “mushy brains,” and sweet consumption to “rotten teeth.” Ocular admonishments are particularly prevalent with stick playing leading to “putting one's eye out,” voluntary eye crossing becoming “permanently stuck,” and reading in the dark “ruining your eyes.” The notion that how we use our eyes will determine eventual refractive outcome has long been held a popular truism but dismissed as a scientific fact by many eye care professionals. While most agree that refractive error is, for the most part, genetically determined, there is a growing body of evidence that how we use our eyes influences eventual refractive status.1

    In this era of high index spectacles, modern contact lens materials, and refractive surgery one may ask the question, “why study myopia?” The answer lies in the understanding that myopia and pathological myopia are common causes of vision loss and blindness in both developed and emerging countries.2 In Taiwan, the prevalence of myopia approaches 75% and in many east Asian countries, pathological myopia is one of the leading causes of blindness.3 Myopic macular degeneration and myopic retinal detachment are not prevented through refractive surgery, a fact often not understood by many high myopes undergoing this form of surgery. The prevention of the development of high myopia has become a priority in many Asian countries and accounts for a significant portion of the research funding in these countries. Myopia research asks the question, “Is refractive status determined by some genetically predetermined mechanism or does the visual environment influence this process?” This nature versus nurture question has been asked for decades but most myopia research is severely limited by problems of study design. Most studies on the incidence of myopia are actually prevalence studies. Longitudinal studies on the incidence of myopia are difficult to conduct, as children tend to be mobile, making long term follow up difficult. Until recently only some of the components of refractive state (axial length, corneal curvature, lens thickness, anterior and posterior segment depth) were recorded, making the distinction of axial versus corneal myopia difficult to distinguish. Interventional trials often are limited by poor randomisation, retrospective design, poor compliance, lack of adequate control group, and high dropout rate. Finally, studies conducted to look at the effect of visual environment during childhood often rely on patient recall concerning near work duration and intensity and rarely look at parental refractive state.4 In recent years, efforts have been made to devise standard study definitions and protocols to define and quantify the refractive state in large populations, and last year saw the first publications of results of these myopia prevalence studies from China, Nepal, and Chile.5-8 The extreme differences in prevalence of myopia between different ethnic groups underscores the importance of genetic determinants of refractive state.

    It is rare for an infant to be born emmetropic, with most children being hyperopic in the first few years of life becoming less so with the approach towards emmetropia. This process of emmetropisation is most assuredly affected by both genetic substrate of the individual and the visual environment of the developing eye. The genetic component of refractive state has been well documented by studies correlating the refractive state between parents and siblings, between siblings, and in twin studies.910 Zadnik and coworkers have shown that children of myopic parents tend to have longer eyes even before developing myopia.11 Several pedigrees of familial myopia have been described, and the gene for myopia has been characterised in these families.1213While “myopes tend to beget myopes” heredity is not destiny and other factors are at work in determining refractive state of the eye. For centuries, the correlation of near work and myopia has been characterised by vision researchers. Epidemiological surveys have shown that myopia is more prevalent in individuals who spend more time reading or performing close work than those who spend more time not using their eyes at near. Myopia has been correlated with the amount of school work and level of educational attainment.14-16 The process continues into the third decade of life with graduate students, microscopists, and military conscripts becoming more myopic with more near work.17 Studies of Aboriginal peoples and Inuits have shown increasing incidence of myopia correlating to the increased near work demands.18 Showing correlation of near work with myopia is simple but proving causation is more difficult owing to the limitations of studies described above. To better understand and study the effect of visual environment on the developing eye, animal models have been described.

    The two animal models commonly used to study myopia are the primate model and the avian model. The primate model was developed by Raviola and Weisel during their research of visual cortical development.19 Suturing closed the eyelid of a young monkey led to abnormalities of the visual cortical development but also led to axial myopia in the sutured eye. This was found to be a locally controlled process and subsequent primate studies have shown that ocular growth is influenced by both visual deprivation as well as optical defocus. The avian model using newborn chicks also clearly demonstrates that affecting the visual environment of the developing eye leads to biochemical and structural changes in the retina and sclera, which are both reversible and focal in occurrence.20 Visual deprivation and optical defocus leading to myopia can be blocked by biochemical interventions in the avian model.21 These primate and avian models will be invaluable in developing therapeutic interventions to prevent myopia in humans.

    These animal studies in myopia led to inquiries regarding early visual experience in children and eventual refractive status. It was well known that pathological conditions which altered visual experiences early in life, such as congenital cataract and periocular haemangioma, were associated with the development of myopia. In 1998, Quinn et al22 reported a high correlation between light exposure at night time (night light or room light) with myopia later in childhood. In this issue of theBJO (p 527), Saw and coworkers present a study which does not find the correlation and implied causation of night light exposure with myopia. This paper joins others that have examined the issue of night time light exposure and refractive status, with all authors emphasising the limitations inherent in conducting myopia research warning readers not to invoke causation from correlation which may be spurious, confounded, uncontrolled, or unproved.23-25

    Numerous interventions have been proposed and studied to prevent myopia progression. These include optical interventions with bifocals and contact lenses; pharmacological interventions with ocular hypotensives, atropine, or pirenzepine; surgical (scleral sling) and behavioural changes.2627 No intervention has been shown to prevent pathological myopia and efficacy of any intervention has been limited to a few dioptres at best. There are currently well controlled prospective trials examining the use of progressive bifocals, rigid gas permeable lenses, and antimuscarinic agents. Ophthalmologists should become involved in these clinical trials as well as in conducting basic research into the physiology and biochemistry of ocular development and refractive state. Most of us spentour formative years reading at bedtime with poor light, listening to our mothers tell us we were going to ruin our eyes. Let's find out if, as usual, mother was right.


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    • Scientific correspondence
      Seang-Mei Saw Hui-Min Wu Ching-Ye Hong Wei-Han Chua Kee-Seng Chia Donald Tan