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An unexploded bomb
In this issue of the BJO (p 538), Saw and colleagues show that, after exclusion of syndrome associated and retinopathy of prematurity (ROP) related myopia, there was no identifiable link between birth weight and refractive error in later childhood. Low birth weight has been linked to adult risk of cardiovascular disease (CVD), hypertension, diabetes, and cancer. The effects of low birth weight are increased by slow infant growth and rapid weight gain in later childhood.1 The so called “Barker hypothesis” suggests that antenatal factors may “program” physiology in later life. The absence of a clear association with refractive error suggests the process coordinating ocular dimensions does not fall under the control of a similar mechanism. Put simply, they show that bigger children have bigger eyes, but not necessarily (after correction for other socioeconomic factors) higher levels of myopia. However, it has been shown that children who are born small have small eyes, and that this trait is retained in adulthood. Fledelius examined 70 subjects with low birth weight (less than 2000 g) and 67 full term controls. The low birth weight-ocular size deficit remained an adult feature, even in seemingly normal eyes. There was also a parallel, permanent lack of “catch up” in height, head circumference, and other anthropometric factors.2
What marks this paper as interesting is the analytical method used by the investigators. Previous epidemiological studies of refractive error have used refraction as the sole end point.3,4 However, there is a growing recognition that the risk factors for, and natural history of, myopia and hypermetropia cannot be fully understood without recourse to ocular biometry.5–7 The inclusion of biometric data in the analysis has strengthened the authors’ abilities to examine the determinants of refractive error in this study of 1413 schoolchildren in Singapore. With the recognition that that bigger people have bigger eyes, without necessarily higher rates of myopia, the importance of correcting for co-determinants of axial dimensions, such as height, can be readily appreciated.8 Similarly, in the study of adult refractive error, changes in lens opacity are often accompanied by changes in refractive index, further complicating the modelling of risk factors.9
The size of the problem may parallel the rapid industrialisation and economic growth in China
The aetiology of myopia still excites considerable debate. Comparison of prevalence data between Asia and the West suggests substantially higher rates of myopia in industrialised regions of east Asia. It is tempting to propose a genetic basis for this observation. However, Saw and colleagues have also shown that greater reading exposure is associated with myopia in Singapore.10 This, once again, raises the “chicken and egg” debate of cause and effect, although there is a broad consensus that near work is causally linked to myopia.11 None the less, it is becoming more plausible that myopia has a genetic predisposition with environmental triggers, the interaction of which results in phenotypic plasticity. Studies of myopia genetics have concentrated almost exclusively on high myopia, with inconclusive results to date. Lower levels of myopia are likely to be an even more challenging proposition. “Common” myopia probably has a complex genetic mechanism for which Mendelian models of disease will be inadequate. Myopia will probably become one of the most fruitful areas of ophthalmology and visual science for the study of the interaction of genetic and environmental mechanisms in causation of disease.
The prevalence of myopia in east Asia appears to be increasing at an alarming rate. It seems likely that with the size of the problem will parallel the rapid industrialisation and economic growth in China. If this issue is not tackled immediately, we risk ignoring a ticking bomb.
Note in Proof
An unexploded bomb
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