Otis's and everybody else's.

Who?

Gee, Otis.  A theory.  How marvelous.

YOU, too, have a theory.  Unfortunately, it fails to hold up in HUMAN
clinical trials AND it induces DOUBLE VISION in people naive enough to
listen to you.

Let's go back ... once again ... to Scientific Method 101 for Dummies
like yourself:

    Recognize the problem

    Observe the problem

    Formulate a hypothesis (this is as far as you've ever gotten)

    Devise and conduct experiments to test the hypothesis (using the
results of this testing to inform and revise your hypothesis.              You
seem to detest this part)

    Come to a conclusion based on the testing.

Hurting unsuspecting people (or the children of desperate parents),
helping nobody (ask your myopic niece), mangling statistics, and
occasionally throwing out Greek letters doesn't make you a scientist.

Not even close.

Now that Otis has discovered this article by Hung and Ciuffreda, I am
eager to see where he goes with it.  I must say that quoting Alex
Eulenberg -- who himself has not read the article, is not a very
encouraging sign.

Otis and Alex have now taken hold of the proverbial rope.  Let's see
just how long it will take them to hang themselves with it.

DrG (who has read the entire article)

Dear Prevention minded friends,

Subject:  Professor Hung's theory -- simplified.

In order to understand this "de-focus" theory, you
should review the animation of it produced
by Dr. Wildsoet on:

http://vision.berkeley.edu/wildsoet/myopiaprimer.html

What the theory predicts is that if you place
a -3 diopter lens on the eye, it will change its
refractive STATE by -2 diopters in six months.

[See the refractive change on the blue-tinted
eye on this site.]

Here is Dr. Hung's verbal description of that proven
process the eye uses to control its refractive STATE.

Best,

Otis

=================

    A unifying theory of refractive error development.

    Hung GK, Ciuffreda KJ.

    Department of Biomedical Engineering, Rutgers University, 617
Bowser Road, Piscataway, NJ 08854-8014, USA.

    shoane@rci.rutgers.edu

    While retinal defocus is believed to be myopigenic in nature,
the underlying mechanism has remained elusive.

    We recently constructed a theory of refractive error
development to investigate its fundamental properties.    Our
Incremental Retinal-Defocus Theory is based on the principle that
the change in retinal-defocus magnitude during an increment of
genetically-programmed ocular growth provides the requisite sign
for the appropriate alteration in subsequent
environmentally-induced ocular growth.

    This theory was tested under five experimental conditions:
lenses, diffusers, occlusion, crystalline lens removal, and
prolonged nearwork.

    Predictions of the theory were consistent with previous
animal and human experimental findings.  In addition, simulations
using a MATLAB/SIMULINK model supported our theory by
demonstrating quantitatively the appropriate directional changes
in ocular growth rate.    Thus, our Incremental Retinal-Defocus
Theory provides a simple and logical unifying concept underlying
the mechanism for the development of refractive error.

    PMID:  11127515 [PubMed - indexed for MEDLINE]

    Ghung8.txt

    Incremental retinal-defocus theory of myopia
development-Schematic analysis and computer simulation.

    Hung GK, Ciuffreda KJ.

    Department of Biomedical Engineering, Rutgers University,
Piscataway, NJ 08854, USA.

    Previous theories of myopia development involved subtle and
complex processes such as the sensing and analyzing of chromatic
aberration, spherical aberration, spatial gradient of blur, or
spatial frequency content of the retinal image, but they have not
been able to explain satisfactorily the diverse experimental
results reported in the literature.

    On the other hand, our newly proposed incremental
retinal-defocus theory (IRDT) has been able to explain all of
these results.    This theory is based on a relatively simple and
direct mechanism for the regulation of ocular growth.

    It states that a time-averaged decrease in retinal-image
defocus area decreases the rate of release of retinal
neuromodulators, which decreases the rate of retinal proteoglycan
synthesis with an associated decrease in scleral structural
integrity.

    This increases the rate of scleral growth, and in turn the
eye's axial length, which leads to myopia.

    Our schematic analysis has provided a clear explanation for
the eye's ability to grow in the appropriate direction under a
wide range of experimental conditions.    In addition, the theory
has been able to explain how repeated cycles of nearwork-induced
transient myopia leads to repeated periods of decreased
retinal-image defocus, whose cumulative effect over an extended
period of time results in an increase in axial growth that leads
to permanent myopia.

    Thus, this unifying theory forms the basis for understanding
the underlying retinal and scleral mechanisms of myopia
development.

    PMID:  17150204 [PubMed - as supplied by publisher]

==========

This is a dynamite paper, by the way, and should appeal to any person
who calls himself an engineer.  Unfortunately for Otis, it won't
support most of his ideas, especially as it pertains to the use of
strong plus for the prevention of myopia.  In fact, it puts Otis into
an even tighter corner.

Remember how we have been discussing the concept of retinal defocus as
opposed to accommodation, and how Otis keeps dragging us back to the
junkheap of outdated ideas?  This paper makes that even more obvious.

DrG