We should consider "cause", begin dealing with it.

Discussion in 'Optometry Archives' started by otisbrown, Mar 8, 2005.

  1. otisbrown

    otisbrown Guest

    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

    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.


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



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


    Institute of Ophthalmology, University College Dublin, Dublin,


    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

    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


    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

    3. Morgan RW, Speakman JS, Grimshaw SE. Inuit myopia: an
    environmentally induced "epidemic"? Can Med Assoc J

    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

    6. Wiesel TN, Raviola E. Myopia and eye enlargement after
    neonatal lid fusion in monkeys. Nature

    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

    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

    14. Cottriall CL, McBrien NA. The M1 muscarinic anatagonist
    pirenzepine reduces myopia and eye enlargement in the tree
    shrew. Invest Ophthalmol Vis Sci

    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

    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


    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.
    otisbrown, Mar 8, 2005
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  2. otisbrown

    Neil Brooks Guest


    A couple of quick things:

    1) I suppose the bar for "proof" should be lower for you than for
    the rest of the scientific community because you want it to be? Seems
    a little narcissistic and self-serving, don't you think?

    2) In the wake of recent events (Aleve, Vioxx, Celebrex, Tysabri,
    etc.) I'm reminded that scientific hypotheses should be held to the
    highest of scrutiny before being labeled as "safe," "accurate,"
    "state-of-the-art," or "conventional wisdom." Reach for it, Mister.
    It's up there for you to surmount.

    Time and time again, you eagerly and blithely foist your theories on
    unsuspecting folks who stop by S.M.V. looking for help. The general
    public must rely on the kindly doctors to alert them to your lack of
    credentials, potential for harm, and untested hypotheses.

    Look, Otis, I'll allow for the possibility that all of the eye doctors
    on this NG are avaricious, self-serving monsters who have a lock on a
    huge chunk of change that comes from doing things "their" way. They
    may be a member of the vast ocular conspiracy that defends its wealth
    by maintaining the status quo. All of this may be true (though I
    don't think it is).

    But you still come across as a petulant, Napoleonic idiot and a
    dottering, old fool.

    The bar for proving your theories is the same as it is for all others.
    Go prove your theories (yes, the old fashioned way: proper testing,
    accurate data, peer-review) and -- if there's a kernel of truth in
    what you spout -- converts will be lining up to describe and prescribe
    your methods, you'll be rich, and you'll be right up there with
    Bagolini, Helmholz, Donders, Schirmer, Robert A. Strabismus, and all
    the other paragons whose names are memorialized in the annals of
    vision care.

    Until then, you're an intellectually inadequate troll . . . who
    creates risk for unsuspecting, often desperate, people seeking help.
    "Engineer" in your signature expiates some of your guilt. It does
    nothing to ameliorate the risk. Perhaps if your signature said, "I am
    not a doctor. My theories are my own, have not been proved, and are
    not shared by most in the medical community. Further, I am
    pathologically unwilling to make any efforts to see my hypotheses
    legitimately tested. Consult your doctor."

    Neil Brooks, Mar 8, 2005
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  3. otisbrown

    Dr. Leukoma Guest

    Indeed, Otis, this is 2005. Science marches on. You have not. You
    blithely choose to ignore the evidence that neither 1000 years of using
    plus lenses, nor 250 years of the bifocal lens have resulted in
    prevention of myopia. Now quit wasting our time and precious bandwith
    with your odd ruminations.

    Dr. Leukoma, Mar 8, 2005
  4. otisbrown

    g.gatti Guest

    You butcher: bring one patient you were able to cure from imperfect
    sight, if you are able.

    You are not.

    Your theories are all wrong, and the results are clear.
    g.gatti, Mar 8, 2005
  5. otisbrown

    RM Guest

    Otis Engineer is a zealot who advocates his "plus lens" prevention theory
    without good reason. There is no scientific data to prove what he proposes.
    He would ask that all myopes (=nearsighted persons) go around wearing plus
    reading glasses in hopes that it will eventually reverse their
    nearsightedness. Nevermind that the blurry distance vision that myopes
    complain about is made worse by plus lenses! Nevermind that there is no
    proof for what he claims.

    If you are interested in Otis' approach, I have some other links that you
    might also be interested in:






    Dear Prevention minded friends,
    RM, Mar 8, 2005
  6. otisbrown

    RM Guest


    I have snipped a few sections from this paper (which is just an overview
    paper and has no original research presented in it) that are germain to your
    "plus lens theory" of myopia prevention.

    So myopia has both genetic and environmental influences huh. How do you
    think this relates to your "one size fits all" approach of putting plus
    lenses on all adolescent eyes. Do you think this approach works for all
    people. Could it possibly be effective for only some genetic types and not
    others? (BTW-- engineer pilots enrolled in a 4-year college and who are
    intelligent DOES NOT represent a homogeneous genetic group within the

    Once again Otis. Someone else besides the 2 billion people who have already
    told you in this forum is stating that objective studies must be performed
    before any of the bullshit animal (chickens, shrews, moneys, etc) studies
    that you derive your theory from can be applied to humans. Get it yet?

    Uh Oh Otis! What is myopia prevention has nothing to do with regulating the
    accommodative system in humans. What if it has to do with regulation of a
    transmitter that, in parallel, also affects the accommodative system. What
    if ciliary muscle contraction really is not cause-and-effect for myopia

    Do you even know what I'm talking about? Probably not since by your own
    admission you don't understand the anatomy/physiology/biochemistry of the
    human eye. And you don't even think it's relevant. That's why modern
    research of myopia prevention goes right over your head. You can only
    understand the yesteryear studies advocated by yesteryear "heros" of myopia
    like Young, etc. Otis-- they eye is more complicated that you understand!

    Once again Otis, another person is saying that more studies must be
    performed. Why don't you perform some instead of shoving your silly
    simple-minded theory on unsuspecting newbies who read this forum.

    I know why. You are incapable of understanding the current scientific
    status of myopia research because of your intellectual limitations.
    Ready-fire-aim is Otis approach. What a good engineer you must have been
    RM, Mar 8, 2005
  7. otisbrown

    otisbrown Guest

    Dear Rishi,
    Subject: Bashing Ophthalmologists who suggest the need for "Change".

    These ODs have this habit of "bashing" ANYTHING I post.
    If I said "the sky is blue" they would post a "bash" againt that!

    These people are not "thinking" at all -- just defending that
    traditional "quick-fix" of the last 400 years.

    And I think they react so strongly -- because in their
    hearts they know I am right about the dynamic behavior
    of the natural eye -- confirmed by direct, scientific testing.

    But that is why I seperate engineering-science, from

    As long as "Google" makes this site SCIENCE and "medicine",
    then keep an open mind.

    And Rishi, also remember that Bates considered his work
    to be Scientific. So if you wish to "Bash" something,
    then be clear -- Bash these "Medical" opinions if you


    otisbrown, Mar 8, 2005
  8. otisbrown

    RM Guest

    These ODs have this habit of "bashing" ANYTHING I post.
    You are right. We will bash just about anything YOU say. It's not about
    the subject that you post-- it's because you are an unlearned crotchity old
    fool who will not let an expert explain something to you that you do not
    understand. You do not utilize the knowledge of others to better understand
    the problems you are interested in.

    Your mind will therefore stay "static" instead of dynamic. Your mind is
    closed-off like a "box-camera"-- open up and learn something Otis!

    This is a 4000 year old problem. Stagnant minds get left behind and

    It reminds me of a poignant old story, "The Printer's Daughter"... blah blah

    We know all about the dynamic behavior of the eye. As a matter of fact we
    can tell you which parts of the eye are dynamic. We can also tell you some
    of the neural/physiological/biochemical signaling mechanisms that regulation
    the dynamic changes. Can you? Oh-- of course the answer is no because you
    admittedly don't know anything about the structure of the eye. I guess it
    has something to do with engineering science versus every other kind of

    But you do know the names of some old optometrists though don't you. That's
    worth something, right?

    Go invent a better vacuum cleaner.
    RM, Mar 8, 2005
  9. otisbrown

    Dr Judy Guest

    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

    (major snip of text of Flitcroft commentary)

    Thanks for the bravery in posting this Otis, since Flitcroft does not
    anywhere in this article say anything that supports your ideas. I was
    surprised that you posted this, since he spends a lot of time discussing
    emmetropization, which, in a previous post you said did not exist. And he
    calls for clinical studies on humans, (exactly the same thing ODs on this
    group have called for) which you pooh pooh as "medical" not "engineering"
    and therefore not worthy of consideration.

    Although Flitcroft does suggest researchers spend time on "causes", nowhere
    does he suggest spending less time on current treatments. These comments
    were published 7 years ago, since then, a number of the studies that he
    suggests have been done. The studies that used less minus to correct myopes
    or plus at near had disappointing results --- little to no effect in
    reducing myopia progression and, in one study, myopia was actually

    Here are some significant quotes from Flitcroft's commentary, anyone reading
    Otis's future posts should keep these in mind:

    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.

    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.

    Dr Judy
    Dr Judy, Mar 8, 2005
  10. otisbrown

    retinula Guest

    Real smart dude. You posted an 8-year old review article that doesn't
    support anything you believe! Did you understand any of the points the
    guy was saying?

    At least you are trying to read some real medical references on the
    subject. Maybe there's hope for you yet.
    retinula, Mar 8, 2005
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