----
Neuron. 2004 Aug 19;43(4):447-68.
Homeostasis of eye growth and the question of myopia.
Wallman J1, Winawer J.
PMID: 15312645 DOI: 10.1016/j.neuron.2004.08.008
Abstract
As with other organs, the eye's growth is regulated by homeostatic
control mechanisms. Unlike other organs, the eye relies on vision as a
principal input to guide growth. In this review, we consider several
implications of this visual guidance. First, we compare the regulation
of eye growth to that of other organs. Second, we ask how the visual
system derives signals that distinguish the blur of an eye too large
from one too small. Third, we ask what cascade of chemical signals
constitutes this growth control system. Finally, if the match between
the length and optics of the eye is under homeostatic control, why do
children so commonly develop myopia, and why does the myopia not limit
itself? Long-neglected studies may provide an answer to this last
question.
----
Curr Biol. 2006 Apr 4;16(7):687-91.
What image properties regulate eye growth?
Hess RF, Schmid KL, Dumoulin SO, Field DJ, Brinkworth DR.
PMID: 16581514 DOI: 10.1016/j.cub.2006.02.065
Abstract
The growth of the eye, unlike other parts of the body, is not
ballistic. It is guided by visual feedback with the eventual aim being
optimal focus of the retinal image or emmetropization . It has been
shown in animal models that interference with the quality of the
retinal image leads to a disruption to the normal growth pattern,
resulting in the development of refractive errors and defocused
retinal images . While it is clear that retinal images rich in pattern
information are needed to control eye growth, it is unclear what
particular aspect of image structure is relevant. Retinal images
comprise a range of spatial frequencies at different absolute and
relative contrasts and in different degrees of spatial alignment. Here
we show, by using synthetic images, that it is not the local edge
structure produced by relative spatial frequency alignments within an
image but rather the spatial frequency composition per se that is used
to regulate the growth of the eye. Furthermore, it is the absolute
energy at high spatial frequencies regardless of the spectral slope
that is most effective. Neither result would be expected from
currently accepted ideas of how human observers judge the degree of
image "blur" in a scene where both phase alignments and the relative
energy distribution across spatial frequency (i.e., spectral slope)
are important.
----
-----
Exp Eye Res. 2013 Sep;114:16-24. doi: 10.1016/j.exer.2013.02.008. Epub
2013 Feb 20.
Is myopia a failure of homeostasis?
Flitcroft DI
PMID: 23454097 DOI: 10.1016/j.exer.2013.02.008
This review examines the hypothesis that human myopia is primarily a
failure of homeostasis (i.e. regulated growth) and also considers the
implications this has for research into refractive errors. There is
ample evidence for homeostatic mechanisms in early life. During the
first few years of life the eye grows toward emmetropia, a process
called emmetropization. The key statistical features of this process
are a shift of the mean population refraction toward emmetropia and a
reduction in variability. Refractive errors result when either this
process fails (primary homeostatic failure) or when an eye that
becomes emmetropic fails to remain so during subsequent years
(secondary homeostatic failure). A failure of homeostasis should
increase variability as well as causing a possible shift in mean
refraction. Increased variability is indeed seen in both animal models
of myopia such as form deprivation and in human populations from the
age of 5 or 6 onwards. Considering ametropia as a homeostatic failure
also fits with the growing body of evidence that a wide range of
factors and events can influence eye growth and refraction from
gestation, through infancy, childhood and into adulthood. It is very
important to recognize that the refraction of an eye is not a simple
trait like eye colour but the consequence of the complex process of
eye growth throughout life. To understand how an eye ends up with a
specific refraction it is essential to understand all the factors that
may promote the attainment and maintenance of emmetropia. Equally
important are the factors that may either disrupt early
emmetropization or lead to a loss of emmetropia during later
development. Therefore, perhaps the most important single implication
of a homeostatic view of myopia is that this condition is likely to
have a very wide range of causes. This may allow us to identify
subgroups of myopia for which specific environmental influences, genes
or treatments can be found, effects that might be lost if all myopes
are considered to be equivalent.
----
BA: I'm pleased to see this line of research going forward. Some years ago
I discussed with Bill Powers the possibility that differential eye growth
might be a means by which the retina gets positioned relative to the lens so
as to put the image in good focus. The idea was that a chronically
out-of-focus image would lead to the release of some kind of
growth-stimulating agent so as to promote growth on the sides of the eye,
thus moving the retina back relative to the lens and improving the focus.
(This assumes that during normal eye development the eyeball begins with the
retina too close to the lens.) As focus improved, this differential growth
would diminish and finally cease when perfect focus was achieved. The
question was, why does growth continue beyond this point in those
individuals who develop myopia?
Given the stereotype of the glasses-wearing "bookworm" child, I wondered
whether having to focus "up close" for many hours a day might be interpreted
by the focus "reorganizing" system as a chronic out-of-focus condition and
thus trigger renewed lateral growth of the eye, leading to myopia.
-----
Exp Eye Res. 2013 Sep;114:16-24. doi: 10.1016/j.exer.2013.02.008. Epub
2013 Feb 20.
Is myopia a failure of homeostasis?
Flitcroft DI
PMID: 23454097 DOI: 10.1016/j.exer.2013.02.008
This review examines the hypothesis that human myopia is primarily a failure
of homeostasis (i.e. regulated growth) and also considers the implications
this has for research into refractive errors. There is ample evidence for
homeostatic mechanisms in early life. During the first few years of life the
eye grows toward emmetropia, a process called emmetropization. The key
statistical features of this process are a shift of the mean population
refraction toward emmetropia and a reduction in variability. Refractive
errors result when either this process fails (primary homeostatic failure)
or when an eye that becomes emmetropic fails to remain so during subsequent
years (secondary homeostatic failure). A failure of homeostasis should
increase variability as well as causing a possible shift in mean refraction.
Increased variability is indeed seen in both animal models of myopia such as
form deprivation and in human populations from the age of 5 or 6 onwards.
Considering ametropia as a homeostatic failure also fits with the growing
body of evidence that a wide range of factors and events can influence eye
growth and refraction from gestation, through infancy, childhood and into
adulthood. It is very important to recognize that the refraction of an eye
is not a simple trait like eye colour but the consequence of the complex
process of eye growth throughout life. To understand how an eye ends up with
a specific refraction it is essential to understand all the factors that may
promote the attainment and maintenance of emmetropia. Equally important are
the factors that may either disrupt early emmetropization or lead to a loss
of emmetropia during later development. Therefore, perhaps the most
important single implication of a homeostatic view of myopia is that this
condition is likely to have a very wide range of causes. This may allow us
to identify subgroups of myopia for which specific environmental influences,
genes or treatments can be found, effects that might be lost if all myopes
are considered to be equivalent.
----