Annual Changes in Refractive Errors and Ocular Components before and after the Onset of Myopia in Chinese Children.

Annual Changes in Refractive Errors and Ocular Components before and after the Onset of Myopia in Chinese Children. (2012)
Xiang F, He M, Morgan IG.State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China; ARC Centre of Excellence in Vision Science and Visual Sciences Group, Research School of Biology, College of Medicine, Biology and Environment, Australian National University, Canberra, Australia.Ophthalmology. 2012 May 9

In this study, participants had their eyes examined every year from 2006 to 2010 -- kids who developed myopia were followed.  The question is, why do children develop myopia, especially if there is a low or no genetic predisposition?  Animals generally seem to not develop myopia in their natural environments (but in the lab, they can become myopic under certain conditions); I read an article that   said that dogs can become myopic naturally...  In this study, it is suggested that myopic defocus possibly slows myopic development, though it does not stop it.  According to this theory, becoming myopic and experiencing defocus sends a signal to the eye to slow down axial growth.  In most  infants these visual input is enough to direct the eye towards emmetropic refraction: unaided good vision at near and far.  Why does this process fail in myopic children?
From the text:"Children who were not myopic at the first examination and myopic in at least 1 subsequent examination from 2006 to 2010 were included in the analysis. Annual change in SER increased slowly from 4 years before the first detection of myopia to 2 years before myopia onset (-0.25 to -0.4 diopter [D]). The rate of progression was the highest during the year of onset (-0.92 D). After the first detection of myopia, the rate of progression decreased to -0.71 D in the following year and kept decreasing. Annual change in axial length showed a similar, but inverse, shape to that of SER. Annual change in lens power did not change significantly around the onset of myopia.Before the onset of myopia, axial elongation and progression accelerate. After a myopic refraction is established, axial elongation and progression decrease. We suggest that the increases before myopia may be due to increased intensity of study and decreased time outdoors. In contrast, the rapid slowing after the onset of myopia may represent an inhibitory effect of myopic defocus on eye growth."
Link to abstract:
http://www.ncbi.nlm.nih.gov/pubmed/22578257

The effect of bright light on lens compensation in chicks.

The effect of bright light on lens compensation in chicks.
Ashby RS, Schaeffel F.
Institute for Ophthalmic Research, Section of Neurobiology of the Eye, University of Tübingen, Tübingen, Germany. regan.ashby@anu.edu.au
Invest Ophthalmol Vis Sci. 2010 Oct;51(10):5247-53.

This study looked at how bright light affected the development of refractive error (myopia or hyperopia) induced by optical defocus (caused by plus or minus lenses, +7 or -7).   The chicks with minus lenses that were exposed to 15, 000 lux (brighter than a SAD lamp, much brighter than typical indoor lux levels) for 5 hours per day developed myopia at a slower rate than those exposed to 500 lux (what one might be exposed to typically indoors).    The role of dopamine was found to be important: when the chicks were injected with a dopamine antagonist,  the protective effect of the light against myopia was negated.

From the abstract:
"It has been shown that sunlight or bright indoor light can inhibit the development of deprivation myopia in chicks. It remains unclear whether light merely acts on deprivation myopia or, more generally, modulates the rate of emmetropization and its set point. This study was conducted to test how bright light interacts with compensation for imposed optical defocus. Furthermore, a dopamine antagonist was applied to test whether the protective effect of light is mediated by dopamine.

Exposure to high illuminances (15,000 lux) for 5 hours per day significantly slowed compensation for negative lenses, compared with that seen under 500 lux, although full compensation was still achieved. 


High illuminance also reduced deprivation myopia by roughly 60%, compared with that seen under 500 lux. This protective effect was abolished, however, by the daily injection of spiperone, but was unaffected by the injection of a vehicle solution.

High illuminance levels reduce the rate of compensation for negative lenses and enhance the rate for positive lenses, but do not change the set point of emmetropization (target refraction). The retardation of myopia development by light is partially mediated by dopamine, as the injection of a dopamine antagonist abolishes the protective effect of light, at least in the case of deprivation myopia."


From the full text:
"A possible interaction that should be considered is the change of pupil size in bright light. Schaeffel et al.²⁷ found that the pupil size in chicks is reduced by roughly 50% of its maximum diameter under an illuminance of only 1000 lux. It is clear that a smaller pupil size increases the depth of focus and may therefore diminish the error signal driving emmetropization. However, changes in depth of focus cannot explain why bright light accelerated compensation for positive lenses. Furthermore, the development of deprivation myopia was also significantly suppressed under bright light, even though depth of focus does not play a role under the diffusers. In summary, changes in depth of focus cannot explain the effects of high illuminance on compensation for imposed defocus. Pupil constriction apparently also has no effect on refractive development in the uncovered fellow eyes.

Exposure to high illuminance levels reduces the rate of ocular growth normally seen in response to the fitting of negative lenses or translucent diffusers, and enhances the growth suppression of plus lenses, but does not alter normal ocular development. Further, the protective effect of light against the development of myopia appears to be mediated by dopamine, as the injection of a dopamine D2-specific antagonist abolishes the protective effect of light, at least in the case of deprivation myopia."
Link to the text

http://www.iovs.org/content/51/10/5247.full

Review of existing literature on myopia (2012)

Myopia
Prof Ian G Morgan PhD , Prof Kyoko Ohno-Matsui MD , Prof Seang-Mei Saw PhD 

The Lancet, Volume 379, Issue 9827, Pages 1739 - 1748, 5 May 2012

The authors of this article searched the Medline and Online Mendelian Inheritance in Man (OMIM) databases for research on myopia.  They note that there's is not enough epidemiological support for the idea that intense near work is related to myopia development; that environmental conditions (such as increased study indoors) might play a stronger role than genetics in many cases of school myopia ;  that peripheral defocus might be be a consequence rather than a cause of myopia,  and that orthokeratology might not work long term.   Here are some passages that seemed particularly interesting or informative to me:

From the text:
On myopia development:
"Most children are born hyperopic, with a normal
distribution of refractive errors.7 During the fi rst year or
two after birth, the distribution narrows,8 with a mean in
the hyperopic range of +1–2 dioptres (D). This change
indicates that there is an active process shaping the
distribution of refraction, known as emmetropisation.
After that period, the cornea stabilises,9 but refraction
can become more myopic as axial length can continue to
increase for another two decades. By contrast, lens power
decreases substantially up to the age of about 12 years,10
with slower decreases for most of adult life.9 Myopia
generally develops during the early to middle childhood
years, but significant myopia can also develop in the late
teenage years or early adulthood.11 Axial length is the
most variable factor during development, with the
strongest correlation with refractive status, with longer
eyes more likely to be myopic than shorter eyes.12 Control
of the axial elongation of the eye during development is
thus crucial for achieving normal vision, and therefore is
a primary site for prevention."


"Increased accommodation due to intensive near
work, such as reading and writing, could mediate the
association of myopia with schooling, but epidemiological
support for this idea is not strong. Although Saw and
colleagues31 showed that Singaporean children who read
more than two books per week were more likely to have
higher myopia than those who read less, the Sydney
Myopia Study showed that near work per se was a weak
factor, but that children who read continuously or at a close
distance were more likely to be myopic.32 Results from the
US Orinda Longitudinal Study of Myopia33 showed weak
albeit signifi cant eff ects of increased hours of near work,
and the authors of this study argued that the evidence did
not support a signifi cant effect of near work.27"



"A consistent finding is that children with myopic
parents have a higher prevalence of myopia,33,52,53 but the
relative risk varies substantially, and is lower in locations in which the prevalence of myopia is high, such as in east
Asia. No consistent relation with number of myopic
parents exists. At this stage, the impact of parental
myopia might be evidence of genetic effects. Differences
in family behaviour associated with myopic parents seem
less likely, but cannot be excluded at this time."



"The development of peripheral hyperopia now seems
to be a consequence, rather than a cause of myopia,
because it seems to appear in parallel with the
development of myopia, rather than before.90 Peripheral
hyperopia nevertheless could contribute to myopic
progression, and this perspective does not preclude the
use of localised manipulation of defocus to control
myopia, whatever the developmental mechanisms."



"Preliminary reports have also suggested overnight
orthokeratology contact lenses, which correct refractive
errors by physically flattening the cornea, might also
protect against myopic progression,96 and it has been
proposed that this might due to peripheral myopic
defocus imposed by the distorted cornea. However, the
eff ects might not be permanent and there might be
a rebound of progression rates of the cessation of
orthokeratology treatment."

Link to abstract:
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(12)60272-4/abstract