Eye (2014) 28, 169–179

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Emmetropisation DI Flitcroft

CAMBRIDGE OPHTHALMOLOGICAL SYMPOSIUM

and the aetiology of
refractive errors

Abstract human refraction has a distribution that, in

statistical terms, is referred to as leptokurtotic
The distribution of human refractive errors
and negatively skewed.3 This is demonstrated
displays features that are not commonly seen
in Figure 1, which shows data from Sorsby’s
in other biological variables. Compared with
1953 study of young male army recruits.4
the more typical Gaussian distribution, adult
Compared with a Gaussian distribution of the
refraction within a population typically has a
same mean and standard deviation, the
negative skew and increased kurtosis (ie is
refractive data show a great excess of subjects
leptokurtotic). This distribution arises from
clustered close to the mean and also a greater
two apparently conflicting tendencies, first,
degree of variation at the extremes. In adult
the existence of a mechanism to control eye
human refraction data there is also an excess of
growth during infancy so as to bring
myopes, especially high myopes, which is the
refraction towards emmetropia/low hyperopia
source of the negative skew.
(ie emmetropisation) and second, the
What proved particularly intriguing to early
tendency of many human populations to
researchers in this field was that the ocular
develop myopia during later childhood and
parameters that contribute to final refraction
into adulthood. The distribution of refraction
such as corneal curvature, anterior chamber
therefore changes significantly with age.
depth, lens thickness, and axial length were
Analysis of the processes involved in shaping
distributed in a more typically Gaussian
refractive development allows for the creation
manner. Steiger calculated the expected
of a life course model of refractive
refractive distribution if the biometric
development. Monte Carlo simulations based
components of refraction were randomly
on such a model can recreate the variation of
associated and this is shown in Figure 1 as the
refractive distributions seen from birth to
solid line.5 The excess of emmetropes (or
adulthood and the impact of increasing
perhaps more accurately low hyperopes and
myopia prevalence on refractive error
emmetropes) in human populations led to the
distributions in Asia.
suggestion that a mechanism exists to regulate
Eye (2014) 28, 169–179; doi:10.1038/eye.2013.276;
eye growth so as to minimise refractive errors.6
published online 10 January 2014
For many years this process was largely
hypothetical, but in recent years a number of
Keywords: emmetropisation; refraction;
longitudinal studies have provided direct Children’s University
myopia; ametropia; hyperopia; model
evidence for such a mechanism in human Hospital, Dublin, Ireland
infants.7–9 Animal studies have provided clear
evidence of the mechanisms that might drive Correspondence:
Introduction DI Flitcroft, Ophthalmology,
this process. It has now been demonstrated, in a
Children’s University
The statistical study of the distribution of wide range of species, that the retina is able to Hospital, Temple Street,
human refractions has a long and distinguished detect and use hyperopic and myopic defocus to Dublin Dublin 7, Ireland
history. Interest in refractive distributions stems control eye growth.10–12 Tel: +353 1 662 9207;
in large part from the fact that human refraction As will be explored in this paper, the Fax: +353 1 662 9207.
appears to be very different to many other combination of a leptokurtotic and negatively E-mail: [email protected]
biological variables such as height or skewed distribution of adult refractions arises
Received: 20 October 2013
intelligence test results, which typically display from two apparently conflicting tendencies. Accepted: 31 October 2013
a normal (ie Gaussian) or log-normal First, the existence of a mechanism to control Published online: 10 January
distribution.1,2 It has been long known that eye growth during infancy so as to bring 2014
 Emmetropisation and the aetiology of refractive errors
DI Flitcroft
170

phase of eye growth there are changes in all the major

determinants of refractive power namely: corneal
curvature,19 axial length,20 and lens power.21 The
reduction in hyperopia is more than can be attributed to
simple scaling effects (or passive emmetropisation)22 and
appears to be attributable to modulation of axial growth.
Like the reduction in spherical refractive error, there is
also a marked reduction in astigmatism over the first few
years23 that appears to be independent of the change in
spherical refractive error.7
Figure 2 shows four distributions of refraction from
two different studies9,24 from 3 months of age to 3.5
years. During this time three separate processes can be
observed. First, there is a progressive shift in mean
refraction from þ 2 D to approximately þ 0.75 D. Second,
there is a significant reduction in the standard deviation
Figure 1 A representation of the refractive data from Sorsby or variability of refraction. Finally, although at this age
et al4 and a prediction for the distribution of human refraction
based on an uncorrelated combination of ocular components as
the population is still approximating a Gaussian
measured by Steiger.5 distribution, the subjects falling outside the best-fit
Gaussian are predominantly hyperopic (hatched in grey
in Figure 2), leading to a positively skewed distribution.
refraction towards emmetropia/low hyperopia (ie These higher hyperopes appear to have failed to
emmetropisation) and second, the tendency of many emmetropise or to be doing so very slowly. Effectively
human populations to develop myopia during later these hyperopes have been ‘left behind’ as the rest of the
childhood and into adulthood. The distribution of population has been regulated towards low hyperopia/
refraction therefore changes with age. Although the emmetropia.
process of emmetropisation does not appear to have Emmetropisation continues at a slower rate after this
changed in the past few decades, the prevalence of early rapid phase and by 6 years of age most populations
myopia has increased dramatically.13–16 This had led to display a definitely leptokurtotic distribution, although
significant changes in the distribution of adult refractions unlike adult populations this remains positively skewed
over time and geographically. Analysis of the processes (ie an excess of hyperopes, as shown in Table 1). At this
involved in shaping refractive development allows for age, the rate of myopia is low even in countries such as
the creation of a life-course model of refractive Japan that display much higher rates of myopia in older
development, as presented below. Monte Carlo children/adults than are seen in Australia or European
simulations based on this model can recreate the wide countries. The mean refraction is hyperopic in all three
variation in refractive distributions seen from birth to studies but it is lowest (closest to emmetropia) in Japan.
adulthood and the impact of increasing myopia If emmetropisation is considered to be the process
prevalence on refractive error distributions in Asia. whereby human refractive errors are minimised, then
this process would appear to be largely complete in most
populations by this age in terms of spherical refractive
The development of human refraction errors over time error, astigmatism, and anisometropia.23,25

To understand the relevance of emmetropisation to the

aetiology of human refractive errors it is necessary to first Refractive development after 6 years of age
define how refraction develops from birth all the way
After the age of 6, refraction starts to display divergent
into adulthood.
patterns of refractive development. In some populations,
such as Australia26 and the South Pacific island of
Vanuatu,27 emmetropisation appears to continue and the
Development of refraction up to age 6
population becomes even more leptokurtotic with a low
At birth neonates display a wide range of refractions, incidence of myopia and hyperopia. In most populations
which are distributed in the typical Gaussian pattern of that have been studied to date, an opposite pattern is
so many other biological variables.9,17,18 This distribution observed with an increasing level of myopia leading to
undergoes a shift in mean and a substantial reduction in increased variance, reduced leptokurtosis, and a negative
standard deviation within the first year.9 During this skew, as opposed to the positive skew observed in

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 Emmetropisation and the aetiology of refractive errors
DI Flitcroft
171

has retained a greater proportion of hyperopes and

acquired more myopes, and thereby leading to a
negatively skewed population with less kurtosis than
was apparent at the age of 6 years. The Japanese
population, although slightly younger, shows the highest
proportion of myopia of these three groups. Figure 4
shows the changes in mean refraction and standard
deviation of refraction for boys and girls in the CLEERE
(Collaborative Longitudinal Evaluation of Ethnicity and
Refractive Error) study from 6 to 14 years of age.29
Despite a relatively small shift in the mean refraction
over this 8-year period, there is a very large increase in
the variability of refraction despite the low rate of
myopia development in this study compared to eastern
populations.
In the Far East where rates of myopia are rising fastest
there is evidence that the shift towards myopia starts as
early as 6 years of age.15,30 What aspect of refractive
development is driving the recent rises in myopia
prevalence? A study of school children conducted over
13 years (from 1984 to 1996) in Japan provides a clear
indication that the increasing levels of myopia observed
during this period were not a reflection of any disruption
of early emmetropisation.30 Among 17-year-olds the
prevalence of myopia increased during the study period
from 49.3 to 65.6%, but this divergence only appeared
after the age of 5 years, as shown in Figure 5. Certain
eastern urban populations now display markedly
skewed distributions with a high prevalence of myopia
(Figure 6), although the prevalence remains lower in
rural populations.31,32
The onset of myopia after the age of 6 has been
Figure 2 Four distributions of refraction from two different observed to be associated with a greatly increased rate of
studies ((a) Mutti et al9 and (b) Ingram and Barr24) from 3
myopic shift after several years of relatively stable
months of age to 3.5 years. (a) 3–9 months. (b) 1–3 years.
refraction or slowly declining refraction.33,34 The early
phase of progression follows an approximately linear
course,35 but slows after several years and usually
Table 1 Distribution parameters of human myopia in three
different countries at 6–7 years of age
asymptotes towards a stable myopic refraction. This
process has been found to be very well described by a
Study Age Mean Kurtosis Skew double-exponent model that fits a range of different
(years) (D) index index
myopia onset and progression profiles.33 Despite the vast
Watanabe et al (Japan) 6 0.96 11.50 1.73 literature on the epidemiology of myopia, the triggers for
Ojaimi et al (Australia) 6–7 1.26 14.4 1.27 the sudden initial acceleration around the time of myopia
French et al (Northern 6–7 1.41 7.2 2.2 onset and the mechanisms responsible for arresting this
Ireland subjects)
process remain unknown.
The phase of myopia development and progression
commences in childhood but persists well into
younger cohorts. This is most apparent in eastern adulthood.36 In studies of myopia progression it is
populations with a high prevalence of myopia. apparent that the primary growth response is
Figure 3 shows data for 12–13-year-olds from increasing axial length,37–39 even when the onset
Australia, northern Ireland26,28 and 11-year-olds from occurs in adults.40
Japan. Whereas the Australian population has a highly In later life, refractive changes appear to primarily
leptokurtotic distribution with a low incidence of both reflect changes in the optical power of the lens rather
hyperopes and myopes, the North Ireland population than axial length. The lens continues to grow during

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 Emmetropisation and the aetiology of refractive errors
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172

Figure 3 Histograms of the distribution of refraction in 11–13 years in Australia, Northern Ireland, and Japan.

Figure 5 Prevalence of myopia in Japanese school children

from ages 3–17 over a 13-year period (1984–1996 inclusive,
Matsumura and Hirai30).

If emmetropisation exists, how can we explain the

existence of refractive errors?

When considering the aetiology of refractive errors it is

important to appreciate that emmetropisation is only one
of many homeostatic or disruptive processes affecting
Figure 4 Mean and standard deviation of refraction from the
ages of 6–14 in the CLEERE (Collaborative Longitudinal Evalua-
eye growth from conception to adulthood.44 By the age of
tion of Ethnicity and Refractive Error) study (Zadnik et al29). 6 the two principal determinants of refraction are the
refraction at birth and the degree of emmetropisation that
has occurred in the intervening years. The presence of a
adult life and also undergoes changes in refractive index significant refractive error at age 6 requires one of the
with time. The balance of these opposing factors gives following scenarios to apply: an initial refractive error
rise to the lens paradox, whereby the overall refractive too great to be corrected by emmetropisation, an initial
power of the eye remains relatively stable.41,42 In later life refraction within the normal range but deficient
the development of cataracts can lead to refractive shifts, emmetropisation, or a combination of both of these.
typically in a myopic direction.43 Refractive errors that are present at age 6 can therefore be

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 Emmetropisation and the aetiology of refractive errors
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173

resolve spontaneously and almost as many arise.46 As the

variation in refraction increases up to age 12–15, so too
does the amount of anisometropia (5.77%).25
Anisometropia is also associated with the magnitude of
refractive error, increasing in frequency with increasing
myopia, hyperopia, and astigmatism.25,47 Loss of well-
regulated patterns of growth from age 5–6 years
therefore manifests as increased variability between
subjects and between the two eyes of a single subject.
A similar pattern is seen in monozygotic twins that
show increased discordance with increasing refractive
error.48,49 Table 2 shows the variation between refractive
error and intra-pair difference in monozygotic twins
from Sorsby et al.48 There is a significant association
between the refractive error and the degree of refractive
discordance with the discordance increasing with
absolute refractive error (Fisher’s exact test, two-tailed
Figure 6 Distribution of refraction in adult population in Japan
with a myopia prevalence showing a highly skewed distribution P ¼ 0.016).
that has lost the classical feature of leptokurtosis seen, for
example, in Figure 1.
Clinical examples of a failure of emmetropisation
considered as primary failures of emmetropisation.44 The Large congenital refractive errors do exist but are rare50
overall variation of refraction and the proportion of and often associated with genetic disorders.51,52
significant ametropes are lowest at this age; therefore, it Examples of clearly genetic congenital refractive errors
can be concluded that primary failure of include the congenital and non-progressive myopia
emmetropisation is not the dominant factor in the associated with Stickler’s syndrome53 and Leber’s
aetiology of refractive errors as a whole. It is however amaurosis.54 In such cases there appears to be a strong
clear that hyperopes and myopes have a different life genetic bias away from emmetropia and the large initial
course. The positive skew of the refractive distribution at refractive errors remain largely unmodified by any
age 6 indicates that most hyperopia arises from the emmetropisation mechanism.
persistence of infantile hyperopia due a failure of Keeping in view the visually guided nature of
emmetropisation. The low incidence of myopia at age 6 emmetropisation, conditions that prevent clear vision
compared to older ages indicates that the vast majority of from birth are associated with a lack of emmetropisation
myopia develops in eyes that have successfully and a broad range of refractions. As is observed in visual
emmetropised earlier in life. Myopia is therefore most deprivation studies in animals, the refraction in such
commonly due to a secondary failure of the children is shifted towards a myopic mean.55,56 In
emmetropisation mechanisms to maintain emmetropia/ contrast, visual deficits that are not congenital but
low hyperopia. develop in the first 3 years are associated with hyperopic
Another factor that might also contribute to the errors.57 Visual deficits such as those associated with
aetiology of refractive errors is stochastic influences on albinism and other causes of nystagmus are also
eye growth. Such influences are well described in associated with impaired emmetropisation and broad
biological systems and can be manifested at a phenotypic refractive distributions.58 Astigmatism is also greatly
or genetic level.45 The existence of such stochastic factors increased in albinism and one analysis suggests that the
can be inferred from the existence of anisometropia and, vertical refractive meridian, which is unaffected by the
to a lesser extent, discordant monozygotic twins. The two motion blur of horizontal nystagmus, may display some
eyes of an anisometrope share both the same degree of emmetropisation.59
environment and genome yet display different There is a poorly understood interaction between
refractions. Early onset anisometropes may have an amblyopia and emmetropisation. Induced amblyopia in
ocular development that is complicated by amblyopia monkeys leads to hyperopia in the amblyopic eye which
but anisometropia often develops later and is associated correlates with the density of the amblyopic deficit.60 The
with both hyperopia and myopia. Deng and Gwiazda development of amblyopia leads to a failure in
demonstrated that the prevalence of anisometropia compensatory growth to imposed lenses.61 In humans
declines to a small extent from 6 months (1.96%) of age to the situation is less clear cut but studies have suggested
5 years (1.27%). Between 1 and 5 years of age many cases that anisometropia may be a consequence of amblyopia

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Table 2 Variation between refractive error and intra-pair where, R(t) is the refraction at time t; Ro is the refraction
difference in monozygotic twins from Sorsby et al48 at birth; Eg is the gain of emmetropisation controller; Rs is
Absolute refractive error (D) Absolute intra- Number of twin pairs the refractive set-point target; Et is the emmetropisation
pair differences time constant; Rc is the myopic offset; a, is the myopic
progression shape; to is the myopia onset time; Gn(t) is the
o0.5 D 40.5 D growth associated biological noise; Gb(t) is the genetic bias
o0.5 24 1 25 In essence, this model combines the four components
40.5 37 16 53 described above. First, the starting point of refraction at
birth is captured by the term Ro. Emmetropisation is
Additional breakdown of 40.5 D group captured in the simplest possible manner as an
0.75–2.0 30 9 39
2.25–4.0 6 2 8
exponential model (with parameters for the gain of
44.25 1 5 6 emmetropisation, the set-point towards which the eye
grows, and a time-constant reflecting the time-limited
There is a significant association between the refractive error and the
degree of refractive discordance with the discordance increasing with nature of the process). The modified Gompertz formula
absolute refractive error (Fisher’s exact test, two-tailed P ¼ 0.016). developed by Thorn et al33 is included to capture the
process of myopic progression as it describes this better
as much as a cause.62,63 Amblyopic eyes display different than any other model to date. The Rc and a parameters of
patterns of vitreous chamber growth to the fellow eye.64 the original model are maintained for ease of comparison
Prematurity, even in the absence of retinopathy of but the Rc parameter is omitted as the starting refraction
prematurity, has been demonstrated to impair is determined by the first two terms. The biological noise
emmetropisation in at least a subset of children.65,66 and bias terms (Gn(t) and Gb) are specified as generalised
A more dramatic failure of emmetropisation can be functions, although in general these factors only seem to
observed in Down’s syndrome despite the good visual be dominant in limited range of clinical scenarios.
acuity usually observed in this condition.67,68 It has been Equation 1 has been specified to allow calculation of
proposed that the apparent absence of emmetropisation refraction at a given age depending on the value of the
in Down’s syndrome would reveal the underlying various parameters and does not allow for interaction
pattern of genetically determined eye growth.69 The between the different components. This is clearly a
patterns of refractive development in Down’s syndrome simplification but the first three factors are largely
are instead highly variable and display the mathematical independent on the basis that the operative factors have
features of a random walk typical of a stochastic little or no temporal overlap. A more complete
process.67,68 mathematical description would specify all four
processes as part of a differential equation incorporating
stochastic components as this would provide for the
A comprehensive model of the mechanisms involved in interaction between each of the processes. Such a
refractive development treatment is beyond the scope of the current paper.
This paper has reviewed the major influences on This model allows the simulation of the distribution of
refractive development from birth to adulthood. These human refraction from birth into adulthood and each of
are the initial refraction at birth, the efficacy and duration the parameters can be estimated from existing clinical
of the emmetropisation process in the first few years of studies. To model a population, each of these parameters
life, the poorly understood mechanisms of myopia onset can be subjected to random variation using either a
and progression, stochastic influences on eye growth, Gaussian or Beta probability function, and once again
and, more rarely, sources of major genetic bias towards existing studies provide a basis for estimating such
myopia or hyperopia. This allows the creation of a model parameters. The following Monte Carlo simulations are
for the development of refractive errors from birth to based on 20 000 subjects with the parameters given in
adulthood. This model encapsulates each of these Table 3 and performed using custom Matlab (Mathworks
processes in a simple mathematical form. Equation (1) Inc., Natick, MA, USA) functions that are available from
provides a mathematical description of this model and the author on request. With the exception of the variation
Figure 7 provides an annotated explanation of each in the gain of emmetropisation (Eg), the distributions
component and parameter. chosen for the parameters listed in Table 3 were based on
published data for such parameters33 or estimated from
  human distribution data from a variety of sources. As the
 t
RðtÞ ¼ Ro þ Eg ðRo  Rs Þ 1  e Et stochastic and bias elements are dominant only in
  pathological situations, these elements have not been
t  to
þ Rc 0:07295a þ Gn ðtÞ þ Gb 1 included in the following simulations.

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 Emmetropisation and the aetiology of refractive errors
DI Flitcroft
175

Figure 7 An annotation of equation 1 describing the biological mechanisms associated with each component of the model (a) and an
annotation of equation (1) describing the biological relevance of each component parameter (b).

Table 3 Parameters and distribution models used for development in this model up to the age of 6 because of
Monte Carlo simulations of refractive developments shown in the observed age range of the to parameter (myopia onset
Figures 8 and 9
parameter), but represents a dominant shape factor at
Parameter Distribution Values Notes/modifiers older ages.
Ro Gaussian m ¼ 2.5 D s ¼ 2.2 D
Figure 8 shows the results of Monte Carlo simulations
Eg Bimodal beta a¼8 b ¼ 0.5 High-gain population from 3 months of age up to 6 years. The evolution of the
a¼3 b¼6 Low-gain population refractive distribution from a normally distributed
Rs Gaussian m ¼ 0.5 s ¼ 0.5
Et Beta a¼5 b¼2 2.0  Beta
population with wide variation to a positively skewed
Rc Beta a¼1 b¼4  10  Beta leptokurtotic population closely mirrors that seen in
a Beta a¼7 b¼6 population studies. Figure 9 extends these models from
to Beta a ¼ 1.75 b¼6 5 þ 20  Beta
age 6 years up to age 24 years. The left-hand graphs on
this figure have set 15% of the population to be
susceptible to myopic progression and the right hand
To create the behaviour observed in human popula-
graphs 55%. Both in terms of increasing myopia
tions it proved necessary to divide the population
prevalence (o  0.5 D) and the shape of the distribution
into a proportion with a high gain of emmetropisation
these graphs also mirror the statistics of refractive
(90–95% of the population) and a corresponding
distributions in low and high myopia prevalence
proportion with low gain. The variation between modern
populations.
day Australian distributions (eg Figure 3), historic UK
distributions (eg Figure 1), young Asian and older Asian
distributions (eg Figures 3 and 6) could be created by
Discussion
varying the proportion of those who undergo later
myopic progression (ie those who are both genetically This analysis of emmetropisation and the development
sensitive and exposed to myopic environmental triggers). of refractive errors are intended to provide a
This proportion has minimal impact on refractive framework for a more rational discussion and

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 Emmetropisation and the aetiology of refractive errors
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176

Figure 8 Results of Monte Carlo simulations of human refractive development from 3 months of age to 6 years.

Figure 9 Results of Monte Carlo simulations of human refractive development from 8 years of age to 24 years. The left-hand panels
model a population with a low tendency to develop myopia and the right-hand panels a population with a high tendency to develop
myopia.

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 Emmetropisation and the aetiology of refractive errors
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177

approach to refractive errors. Since refractive error is the eye growth lead to refractive errors, in particular
end result of a long, complex growth process over several myopia? An intriguing suggestion is that, as shown in
decades, it is no longer valid to consider refraction in the tree shrews, the older eye loses the ability to respond to
same manner as a simple trait. Adult hyperopes and myopic defocus that might slow or halt eye growth but
myopes errors have quite different life courses in terms continues to be sensitive to hyperopic defocus that
of ocular development and would appear to be the result promotes axial elongation.69
of fundamentally different processes. Furthermore, any It seems reasonable to assume that human infant
given refractive error can be the result of a wide variety emmetropisation reflects the optically guided growth
of influences. These influences include the following: mechanisms that have been identified in lens-rearing
where in the refractive distribution range of an eye starts studies in animals. Both are most active early in life74 and
at birth; the effectiveness (ie gain) and set-point of human infants display other features that are predicted
emmetropisation; the impact of stochastic factors when by an optically guided process.75,76 Partial hyperopic
emmetropisation is deficient; the susceptibility to later correction in infants does not seem to impair the end
myopiogenic factors; the exposure to such factors; and result of emmetropisation though it does appear to slow
the regulation of the adolescent phase of ocular growth in the process.77 In keeping with the predictions of an
axial length and lens power. Therefore, rather than optically guided control model, the rate of
accepting a single figure for the heritability of refraction emmetropisation has been reported to be correlated with
we should be asking what aspects of this process are the magnitude of the initial refractive error.78 We
genetically determined, what aspects are essentially therefore have a good animal model for emmetropisation
random (stochastic) and what aspects are influenced by but we do not have an animal that helps us understand
visual experience or other environmental factors. how, in later childhood, eyes undergo a rapid refractive
The model presented in this paper is based on well- acceleration in the direction of myopia. Until we can
defined, if not fully understood, phenomena within define and understand the triggers and growth
refractive development. That a single model can provide mechanisms mediating this initial acceleration and
a mechanistic explanation of both the evolution of subsequent stabilisation, we cannot claim to explain the
refractive distributions since birth through childhood aetiology of the vast majority of myopia.
into adulthood and the variations in refractive
distribution shape seen in different adult populations is a
Conclusion
testament to validity of the underlying concepts. The
parameters also have clinical relevance and are, in the The bulk of emmetropisation occurs in early childhood
most part, measurable. The question of examining and is largely complete by age 6. Therefore, refractive
genetic and environmental contributions to refractive errors that exist at this age can be considered failures of
error may become more tangible if the different aspects emmetropisation. The commonest refractive error at age
of the refractive life-course encapsulated within this 6 is hyperopia with both anisometropia and myopia
model and its parameters are considered in isolation. being far less common at this age. Since the prevalence of
Although the term emmetropisation is often used to myopia shows a marked increase in later years, only a
describe the process where older hyperopes ‘grow out of very small proportion of myopic refractive errors can be
their glasses’,70 it is clear from this review that true attributed to a primary failure of emmetropisation.
emmetropisation occurs early in life. The process of Therefore, an understanding of how and why
growing out of their glasses, that is observed in some but emmetropisation fails will be of particular importance in
by no means all childhood hyperopes, occurs at the same understanding hyperopia rather than myopia.
age that myopia is starting to emerge. Is this late Anisometropia remains the least understood refractive
hyperopic ‘emmetropisation’ merely another abnormality and a fuller understanding may require
manifestation of the processes driving myopia onset/ the addition of chance (ie stochastic factors) to the
progression or is it an entirely different process. This is traditional pair of nature and nurture. When considering
an interesting and unanswered question. If it were true the aetiology of refractive errors it is no longer tenable to
and the factors driving myopia onset and progression consider refraction as a trait without considering the
could be determined, then such factors could be used to developmental processes involved. It is hoped that the
develop novel management strategies for the hyperopia model presented in this paper may be of assistance in
and accommodative esotropia. bringing together different aspects of eye growth.
There is clear evidence from myopia intervention While myopia has public health implications in the
studies that the growth of the older human eye is adult population,79 within paediatric ophthalmology
sensitive to optical defocus.71–73 If the human eye it is hyperopia and anisometropia that create the
remains sensitive to defocus why does the later phase of greatest morbidity. Far less attention has been devoted

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178

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The author declares no conflict of interest.
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