Dear Prevention minded friends,

Here is an Ophthalmologist who recommends
that we begin dealing with the "cause",
and not spend so much time with the
consequences.

We have been using the same negative-lens method
and theory for the last 400 years.  It works
(i.e., consequence) but this is the 2005, and
perhaps consider preventive alternatives.

The Donders-Helmholtz concept is an
ex-post-facto theory -- built AROUND
the traditional method.  Maybe the
we should consider the "second opinion"
i.e, dealing with the cause, more
seriously, as optometrist Steve Leung
is doing it.

www.chinamyopia.org

Enjoy our thoughtful analytic discussions, including
the opinion of a highly qualified ophthalmologist.

Otis
Engineer

__________________________________________

       Br J Ophthalmol 1998;82:210-211 ( March )

             D I FLITCROFT

 Institute of Ophthalmology, University College Dublin, Dublin,
                Ireland

               Commentary

 Ophthalmologists should consider the causes of myopia and not
         simply treat its consequences

    Myopia has been undergoing a major re-evaluation in recent
years both by ophthalmologists and basic scientists, though for
different reasons.  For ophthalmologists the rise of refractive
surgery in the past decade has seen myopia changing from a
condition requiring optical correction to one that can be managed
surgically with the aid of the excimer laser and other techniques.
For basic scientists interested in the control of eye growth, the
past decade has been equally revolutionary with a huge increase in
the understanding of mechanisms by which eye growth is regulated
by the quality of the retinal image.

    This research offers insights into why myopia develops in
humans and offers clinicians a novel perspective from which to
approach the management of myopia.  Rather than attempting to
alter corneal curvature to "treat" myopia, it may be possible to
prevent or "cure" myopia by directly manipulating the growth
mechanisms of the eye.

    Epidemiological studies indicate that myopia represents a
growing public health problem, particularly in the Far East.
Singapore, for example, has seen an increase in the prevalence of
myopia in young adults from 26% to 43% over a decade, reaching 65%
in university graduates.  1

    This increase largely reflects the increasing levels of youth
onset myopia and adult onset myopia.  There is a wide variety of
epidemiological evidence that suggests that environmental effects
can influence the development of these forms of myopia.  Within
the Singaporean population, both the prevalence and degree of
myopia correlate with the time spent in full time education.  2

    In populations with little genetic heterogeneity, such as
Inuit populations, studies have revealed that within a generation,
the incidence of myopia has risen dramatically in line with the
onset of formal education and literacy.  3 4

    In addition to this evidence for an environmental
contribution to the aetiology of myopia, there is also abundant
evidence for a genetic influence.  These contrasting lines of
evidence have stimulated the long running "nature versus nurture"
debate, although it is now clear that myopia results from the
interaction of environmental and genetic factors. 5

    However, the observed increases in myopia over a generation
indicate that the modern myopic epidemic is being fuelled by
environmental changes.    Furthermore, environmental influences are
more easily altered than our genetic make up.  Understanding how
the visual environment can influence eye growth should therefore
be central to any attempts to alter the natural history of myopia.

    The link between the visual environment and myopia lies in
the quality of the retinal image.  Experimental evidence in a
range of species has revealed that in the absence of a clear
retinal image, eye growth is disturbed resulting in deprivation
myopia. 6-8

    Of much more relevance to human myopia are the recent
findings that the primate eye can alter its growth depending on
the direction and degree of defocus within the retinal image,
modifying its growth to neutralise the effects of lenses placed in
front of the eye during development. 9

    Such work demonstrates the role of the retinal image in the
process that has become known as emmetropisation.  This notion
initially arose from the observation that the frequency of
emmetropia in the population is far higher than expected from the
observed variation in ocular variables influencing the refractive
state such as corneal curvature and axial length.

    In most individuals these variables are balanced in order to
achieve emmetropia, implying some form of optical regulation of
eye growth.  Myopia clearly represents a failure of the normal
emmetropisation mechanisms.  For late onset myopia, the
association with educational attainment suggests that increased
near work either disrupts normal emmetropisation mechanisms or
results in regulation of ocular growth towards myopia as an
adaptation to prolonged near work.

    Unravelling how near work interacts with normal
emmetropisation represents one potential avenue for blocking the
environmental contribution in late onset myopia.

    The degree of defocus of the retinal image is dependent on
the refraction of the eye, viewing distance, and the state of
ocular accommodation.

    Although accommodation has been invoked as a cause of myopia for
decades, early theories relied largely on unsubstantiated
mechanical effects of ciliary muscle activity on the sclera rather
than the impact on retinal image quality.  If prolonged near work
promotes the development of myopia as a result of retinal image
quality, then the interaction between viewing distance and
accommodation is likely to be of particular significance.  Myopic
children have been found to have poor accommodation for near
targets 10 resulting in hyperopic blur within the retinal image.

    Under such conditions myopia may represent a physiological
adaptation to prolonged near work with the mechanisms of
emmetropisation regulating eye growth to a state that minimises
retinal image blur for near.  This can only occur at the expense
of producing myopia and retinal blur for distance.  Such reasoning
has led to a renewed interest in possible optical solutions, such
as bifocal or varifocal lenses to prevent late onset myopia in
high risk populations.

    Bifocal spectacles apear to reduce myopic progression, 11
particularly when there is associated esophoria.

    If myopia is an adaptive physiological response to prolonged
near work, correction of myopia with lenses during childhood may
increase the final degree of myopia by requiring further adaptive
changes in axial length to neutralise the effects of the lenses.

    Certainly in animal studies minus lenses do result in ocular
growth towards myopia.    Whether this implies that myopic children
should be undercorrected remains controversial.  Ultimately,
resolving whether these findings are applicable in humans can only
be achieved by appropriate clinical studies.

    Another possible avenue that might allow manipulation or
prevention of myopia has arisen from developments in our
understanding of the pharmacological mechanisms by which retinal
image quality influences eye growth.  The possible impact of
accommodation on myopia has been investigated in the past by using
atropine to block accommodation. 12

    However, atropine also acts to block experimental myopia in
species where the ciliary muscle is unaffected by atropine such as
the chicken, 13 implying that it is acting by a non-accommodative
mechanism.

    It has been found that experimental myopia can be prevented
by application of the selective muscarinic antagonist pirenzepine
which acts on the M1 receptor subtype.    14

    This subtype of muscarinic receptors is found within the
retina rather than the ciliary muscle.    In addition to muscarinic
mechanisms, two other neurotransmitters have been implicated in
the optical regulation of ocular growth namely, dopamine 15 and
VIP (vasoactive intestinal peptide).  16

    Dopamine and VIP are found within specific subpopulations of
amacrine cells, suggesting a role for this poorly understood cell
type in the regulation of eye growth.  Amacrine cells represent a
diverse population of neurons that are likely to perform a number
of roles within the retina, but with their synaptic connections
within the inner plexiform layer they are well placed to respond
to retinal image quality.

    Pharmacological manipulation of these growth mechanisms
clearly offers a very direct means of altering the natural history
of myopia.  Selective muscarinic antagonists such as pirenzepine,
a drug already in human use as a treatment for peptic ulcers,
offer the prospect of influencing the signals that promote myopia
without the confounding effects on the retinal image that result
from the cycloplegia generated by atropine.

    The one common thread in the various lines of research into
the regulatory mechanisms of eye growth and experimental myopia is
that this work has remained largely within the realms of the basic
sciences.  Indeed, a major criticism of this field is that much of
the work has relied on animal models, such as the chicken, that
are of questionable application to humans.

    Nevertheless, there is growing evidence that the primate eye
displays similar regulatory growth mechanisms to the avian eye.
Although a great deal of further research will be required to
transfer this work to humans, there is a real prospect for
dramatic alterations in the clinical management of myopia.

    In terms of both the optical and pharmacological manipulation
of myopia, there are questions that can only be addressed by
clinical studies.  In light of recent developments such studies
should be given high priority.    However, such studies are only
likely to take place if there is sufficient interest and
enthusiasm from ophthalmologists.  While it is certain that
refractive surgery will play a major role in the ophthalmological
management of myopia in the future, ophthalmologists should also
recognise and take up the challenge of preventing or curing myopia
by addressing its cause and not simply treating the consequences

               References

1.   Tay MT, Au Eong KG, Ng CY, Lim- MK.  Myopia and educational
    attainment in 421,116 young Singaporean males.  Ann Acad Med
    Singapore 1992;21:785-791[Medline].

2.   Au Eong KG, Tay TH, Lim MK.  Education and myopia in 110,236
    young Singaporean males.  Singapore Med J
    1993;34:489-492[Medline].

3.   Morgan RW, Speakman JS, Grimshaw SE.  Inuit myopia:  an
    environmentally induced "epidemic"?  Can Med Assoc J
    1975;112:575-577[Abstract].

4.   Johnson GJ, Matthews A, Perkins ES.  Survey of ophthalmic
    conditions in a Labrador community.  I Refractive errors.    Br
    J Ophthalmol 1979;63:440-448[Abstract].

5.   Mutti DO, Zadnik K, Adams AJ.  Myopia:  the nature versus
    nurture debate goes on.  Invest Ophthalmol Vis Sci
    1996;37:952-957[Medline].

6.   Wiesel TN, Raviola E.  Myopia and eye enlargement after
    neonatal lid fusion in monkeys.  Nature
    1977;266:66-68[Medline].

7.   Hoyt CS, Stone RD, Fromer C, Billdon FA.  Monocular axial
    myopia associated with neonatal eyelid closure in human
    infants.  Am J Ophthalmol 1981;91:197-200[Medline].

8.   Wallman J, Turkel J, Trachtman J.    Extreme myopia produced by
    modest changes in early visual experience.  Science
    1978;201:1249-1251[Medline].

9.   Hung LF, Crawford MLJ, Smith EL.  Spectacle lenses alter eye
    growth and the refractive status of young monkeys.  Nature
    Med 1995;1:761-765[Medline].

10.  Gwiazda J, Thorn F, Bauer J, Held R.  Myopic children show
    insufficient accommodative response to blur.  Invest
    Ophthalmol Vis Sci 1993;34:690-694[Abstract].

11.  Goss DA, Grosvenor T.  Rates of childhood myopia progression
    with bifocals as a function of nearpoint phoria:  consistency
    of three studies.    Optom Vis Sci 1990;67:637-640[Medline].

12.  Bedrossian RH.  The effect of atropine on myopia.
    Ophthalmology 1979;86:713-719[Abstract].

13.  Stone RA, Lin T, Laties AM.  Muscarinic antagonistic effects
    on experimental chick myopia.  Exp Eye Res
    1991;52:755-758[Medline].

14.  Cottriall CL, McBrien NA.    The M1 muscarinic anatagonist
    pirenzepine reduces myopia and eye enlargement in the tree
    shrew.  Invest Ophthalmol Vis Sci
    1996;37:1368-1379[Abstract].

15.  Schaeffel F, Bartmann M, Hagel G, Zrenner E.  Studies on the
    role of the retinal dopamine/melatonin system in experimental
    refractive errors in chickens.  Vision Res
    1995;35:1247-1264[Medline].

16.  Stone RA, Laties AM, Raviola E, Wiesel TN.  Increase in
    retinal vasoactive intestinal polypeptide after eyelid fusion
    in primates.  Proc Natl Acad Sci USA
    1988;85:257-260[Medline].

             __________________________________

Canadian Medical Association Journal, Vol 112, Issue 5 575-577,
          Copyright © 1975 by Canadian Medical Association

     Inuit myopia:  an environmentally induced "epidemic"?

     R.  W.  Morgan, J.  S.  Speakman and S.  E.  Grimshaw

    Among Inuit less than 30 years old the prevalence of myopia
is far in excess of that of their elders.  This is especially true
for females.  There seems to be little, if any, genetic
contribution to this "epidemic" of myopia in the young.  The age
and sex distribution indicates the likelihood of an environmental
factor, probably cultural, being responsible for the current
pattern.  Other data implicate school attendance as a possible
etiologic factor.