Eyeglasses and retail optometry are scams

[Agatha]

Knock off the accusations of lying, and do not personalise your posts.

Replying to this modbox in thread will be off topic  Posted By: Agatha

 

[Tippit]

Yep, the paper is here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1979094/

I assume the idea is that the juvenile tree shrew is an animal model for human children. And yes, they were made to wear lenses.

That’s one of two papers Tippit posted as his scientific evidence to support his procedure and justify the exaggerated rhetoric of his thread title.

There are tens of thousands of links to studies on google scholar in reference to the topics of pseudomyopia (near induced transient myopia), lens induced myopia (axial elongation of the eyeball as the result of wearing glasses due to hyperopic defocus, and even axial shortening, as the result of myopic defocus which is what we’re primarily concerned with here. Pseudomyopia is essentially chronic ciliary muscle spasm as the result of staring at near-objects like computer screens for extended periods of time without rest. Chronic pseudomyopia causes people to begin wearing glasses, which then induces hyperopic defocus causing axial elongation and progressive myopia.

What is fascinating, is that this can be reversed (axial shortening) by the simple process of inducing myopic defocus, that is, using reduced lenses to cause light to be focused just in front of the retina as opposed to behind it.

There are thousands of studies about pseudomyopia and lens induced myopia. It is well known that eyeglasses cause progressive myopia. Just search google scholar for “lens induced myopia” and read.

There are far fewer studies that myopic defocus causes axial shortening, but the evidence is compelling, especially since it corroborates what I already know personally to be true from experience. Here is one that shows cross-species examples of this phenomenon:

https://iovs.arvojournals.org/article.aspx?articleid=2189093

Eyes in Various Species Can Shorten to Compensate for Myopic Defocus

Abstract
Purpose.: We demonstrated that eyes of young animals of various species (chick, tree shrew, marmoset, and rhesus macaque) can shorten in the axial dimension in response to myopic defocus.

Where progressive myopia is caused by wearing overprescribed eyeglasses and doing near work resulting in axial elongation, it can actually be reversed by wearing reduced lenses resulting in shortening.

Now, who is going to fund studies in the species that matters? EssilorLuxxotica? Lol.

In the meantime, I have my vision back almost to emmetropia, and that’s all that matters. Certainly not convincing ascientific pseudo-cynics on the internet. Enjoy your nerdgoggles.


Sent from my iPhone using Tapatalk

 

[Andy_Ross]

can you link to some that you think relevant?

 

[hecd2]

There are no studies that myopic defocus causes axial shortening, but the evidence is compelling, especially since it corroborates what I already know personally to be true from experience. Here is one that shows cross-species examples of this phenomenon:

https://iovs.arvojournals.org/articl...icleid=2189093

Eyes in Various Species Can Shorten to Compensate for Myopic Defocus

But all the animals of all species used in this trial were juvenile (as was the case with the tree shrew and human child studies). The explicitly stated mechanism is an effect on the growing eye of juveniles, that is there is a feedback mechanism in juvenile animals which adjusts the rate of axial growth to compensate for defocus and achieve emmetropy. You have presented zero published evidence that this process operates or can opeate in the fully grown adult eye.

While it is true that the evidence shows compensation of pseudomyopia in children can result in axial elongation, there isn't any published evidence that I can find that reversal of elongation has been observed in human adults. Since you haven't cited any, presumably you can't find any either.

But whether or not what you claim to have achieved is a result of the process you followed (it's impossible to say based on a sample size of one, and with you being so invested in your claims), you are making an error in concluding that there are no genetic factors in progressive myopia, nor any environmental factors other than overcorrected pseudomyopia in children and adolescents.

Now, who is going to fund studies in the species that matters? EssilorLuxxotica? Lol.

I have pointed out before that not all funding (not even most funding) in ophthalmology comes from frame and eyeglass lens manufacturers. Did they fund all these studies into animal models? It's not a good excuse for the complete lack of published support for your hypothesis.

 

[Tippit]

But all the animals of all species used in this trial were juvenile (as was the case with the tree shrew and human child studies). The explicitly stated mechanism is an effect on the growing eye of juveniles, that is there is a feedback mechanism in juvenile animals which adjusts the rate of axial growth to compensate for defocus and achieve emmetropy. You have presented zero published evidence that this process operates or can opeate in the fully grown adult eye.

This is a reasonable point, and I don't know why they only studied juveniles. But here is an excerpt from the paper which I presume you didn't actually read:

It usually is assumed that, when eyes compensate for myopic defocus imposed by positive lenses, their rate of ocular elongation is reduced, so the eye either elongates at a slower rate than normal or, at the most, stops its growth. Even though it seems more natural that an eye in a growing animal should elongate rather than actually shorten (reduced length from the front of the cornea to the back of the sclera), there seems no obvious reason why an eye experiencing myopic defocus cannot axially shorten or shrink through a mechanism, such as extracellular matrix remodeling of the sclera, thereby further facilitating compensation. Given that tissues are remodeled continuously under homeostatic control, we ask why should axial shortening or shrinkage be more implausible than elongation or enlargement.

Clearly there are plenty of examples in human adult biology of tissue remodeling under homeostatic control. Chronic low blood pH results in the cannibalization and reforming of bone tissue for extracting calcium. Cellular autophagy reforms and removes diseased tissues throughout the body on a regular basis. Skin callouses are formed and removed as the result of environmental wear and tear, all outside of the post-natal growth phase in humans.

And perhaps the most important and relevant evidence of all? Hyperopic defocus results in axial elongation in adults of any age. Read any of the thousands of studies available on the topic. If you're too lazy to look any of them up, let me know and I will google scholar it for you. So while there is no peer reviewed science that directly addresses the hypothesis of axial shortening by way of myopic defocus in human adults, how likely do you think it is that we have cross species evidence of axial shortening in both mammals and fowl, AND peer reviewed science that confirms axial elongation in human adults? Do you think it's reasonable to assume that the eye's emmetropizing mechanism works only one-way (elongation) in adult humans, but two-ways in juvenile rhesus macaques, tree shrews, and chickens? It's a ridiculous notion, but that's what you're contending, arrogantly. Clearly, the human body can and does reshape the eye beyond the post-natal development phase of human biology, and I am living proof. Reading further into the paper:

Our data provided evidence that avian and mammalian eyes can shorten axially to compensate for myopic defocus. That eye shortening was found in a variety of species, regardless of the structural differences in the sclera and eye sizes, suggests that the same mechanism modulating eye growth is conserved evolutionarily.

Note the bolding, conserved evolutionary.

While it is true that the evidence shows compensation of pseudomyopia in children can result in axial elongation, there isn't any published evidence that I can find that reversal of elongation has been observed in human adults. Since you haven't cited any, presumably you can't find any either.

I've found mountains of evidence, starting with the results of my own experiment beginning in Jan of 2018. It's just not peer-reviewed, and therefore, worthless in your ignorant estimation (or, you accuse me of lying outright, which is ultimately what you have been reduced to). Read the endmyopia.org forums, and the youtube accounts of people using it.

But whether or not what you claim to have achieved is a result of the process you followed (it's impossible to say based on a sample size of one, and with you being so invested in your claims), you are making an error in concluding that there are no genetic factors in progressive myopia, nor any environmental factors other than overcorrected pseudomyopia in children and adolescents.

The sample size is many more than one, you're just disinterested because of authoritarian pseudo-skepticism that dismisses all non-peer reviewed hypotheses automatically, and with prejudice. Again, overcorrected pseudomyopia causes axial elongation in adults, and this is well-known. Order yourself a pair of glasses from zenni.com that are overcorrected by -3 diopters in each eye, then wear them religiously in front of the computer for two months. You will be practically blind without them even in that short span of time. This is not an exaggeration. Thankfully, it's reversible!

I never claimed that there are no genetic factors with regard to either pseudomyopia, or progressive myopia, and I am quite sure that there are. I claimed that it is not a genetic illness, which means that it is primarily epigenetic. If one fails to adequately look both ways before one crosses the street and then gets hit by a bus because of a genetic deficiency in the brain, the cause of death is still overwhelmingly epigenetic.

Progressive myopia is caused by wearing eyeglasses.

I have pointed out before that not all funding (not even most funding) in ophthalmology comes from frame and eyeglass lens manufacturers. Did they fund all these studies into animal models? It's not a good excuse for the complete lack of published support for your hypothesis.

There is plenty of published support for my hypothesis, you are just interested in dismissing it because of the specific omission of adults from the axial shortening studies, which, in context, is nonsensical and unreasonable given the circumstantial and other evidence. I don't know the reasons for the lack of studies, but I understand how selection bias plays a massive role in the (de)selection of studies to be funded and peer-reviewed.

 

[Andy_Ross]

There is plenty of published support for my hypothesis,

Which you haven't shown us.

 

[Tippit]

Also from the above paper:

In summary, we have presented an analysis of data from various established animal models of refractive error development showing the capacity of eyes in young, rapidly growing animals to shorten axially to facilitate compensation for myopic defocus. It would be interesting to determine if this phenomenon also exists in children or adolescents, since older adult human eyes have been shown to shorten axially, possibly in response to the increased refractive power of the cornea and the lens. 34 These results suggest the possibility that combining distance correction with some myopic defocus in the correct amount and duration might cause the developing human eye to shorten axially or shrink. If this were the case, then strategies for preventing or reducing the axial elongation of the eye that results in high myopia in human, and the associated ocular pathologies, might be treated feasibly.

 

[hecd2]

This is a reasonable point, and I don't know why they only studied juveniles.

Because the mechanism being studied is variations in the growth of juvenile eyes as a consequence of imposed defocus.

But here is an excerpt from the paper:

It usually is assumed that, when eyes compensate for myopic defocus imposed by positive lenses, their rate of ocular elongation is reduced, so the eye either elongates at a slower rate than normal or, at the most, stops its growth. Even though it seems more natural that an eye in a growing animal should elongate rather than actually shorten (reduced length from the front of the cornea to the back of the sclera), there seems no obvious reason why an eye experiencing myopic defocus cannot axially shorten or shrink through a mechanism, such as extracellular matrix remodeling of the sclera, thereby further facilitating compensation. Given that tissues are remodeled continuously under homeostatic control, we ask why should axial shortening or shrinkage be more implausible than elongation or enlargement.

It is clear the paper is about axial shortening or elongation in the growing eye of the juvenile. This is not carte blanche to conclude that the authors are endorsing the concept of lengthening or shortening in the adult eye.

Clearly there are plenty of examples in human adult biology of tissue remodeling under homeostatic control. Chronic low blood pH results in the cannibalization and reforming of bone tissue for extracting calcium. Cellular autophagy reforms and removes diseased tissues throughout the body on a regular basis. Skin callouses are formed and removed as the result of environmental wear and tear, all outside of the post-natal growth phase in humans.

All of which is reasonable as a hypothetical means for a hypothetical process, but is not evidence that that process can or does actually take place.

And perhaps the most important and relevant evidence of all? Hyperopic defocus results in axial elongation in adults of any age.

I couldn't find references to studies where hyperopic defocus causes a permanent axial elongation in adults. Could you you refer me to one. It is well documented that both axial elongation and shortening occurs as a result of transient defocus, but the effect is itself transient.

So while there is no peer reviewed science that directly addresses the hypothesis of axial shortening by way of myopic defocus in human adults,

Ah - we've got there at last. This is the point I was making which you repeatedly tried to sweep under the carpet. There is no published science which confirms that the process you claim can or does occur in human adults.

Reading further into the paper.
Note the bolding, conserved evolutionary.

Our data provided evidence that avian and mammalian eyes can shorten axially to compensate for myopic defocus. That eye shortening was found in a variety of species, regardless of the structural differences in the sclera and eye sizes, suggests that the same mechanism modulating eye growth is conserved evolutionarily

And note my highlight - this is about the growth of juvenile eyes not about long-term axial changes in adults.

Progressive myopia is caused by wearing eyeglasses.

You have not begun to show that that is the only or even the primary cause of progressive myopia.

There is plenty of published support for my hypothesis, you are just interested in dismissing it because of the specific omission of adults from the axial shortening studies

There is, as I have been saying for some time, no published study which confirms your hypothesis. Since your hypothesis is about axial shortening in adults then their omission is material.

which, in context, is nonsensical and unreasonable given the circumstantial and other evidence. I don't know the reasons for the lack of studies, but I understand how selection bias plays a massive role in the (de)selection of studies to be funded and peer-reviewed.

I will agree that your hypothesis is not an unreasonable one. But the fact remains that there is no published study to show that it is a correct hypothesis, as you have at last admitted in this post, and the circumstantial evidence, such as it is, is inadequate to justify your strong conclusion and the breathless rhetoric in the title of the thread. Could it be that no paper reporting long term axial shortening in adults has been published, because such changes do not occur?

I doubt that you would have got the same negative response to an OP entitled something like "My experience suggests a neglected area of research" or "A plausible hypothesis for correcting progressive myopia n adults" or some such. What people are reacting to is your claim that your personal anecdote proves the hypothesis and that you are justified in abusing the industry (and abusing those in this thread advocating proper trials to validate claims in healthcare) on those tenuous grounds. Your experience cannot validate the hypothesis. No-one's personal anecdote can.

 

[hecd2]

Also from the above paper:

In summary, we have presented an analysis of data from various established animal models of refractive error development showing the capacity of eyes in young, rapidly growing animals to shorten axially to facilitate compensation for myopic defocus. It would be interesting to determine if this phenomenon also exists in children or adolescents, since older adult human eyes have been shown to shorten axially, possibly in response to the increased refractive power of the cornea and the lens. 34 These results suggest the possibility that combining distance correction with some myopic defocus in the correct amount and duration might cause the developing human eye to shorten axially or shrink. If this were the case, then strategies for preventing or reducing the axial elongation of the eye that results in high myopia in human, and the associated ocular pathologies, might be treated feasibly.

Fine - it sets out a hypothesis that something along the lines of your process might work. As I said, your hypothesis is not unreasonable. But nor has it been demonstrated to be correct. Reference 34, by the way, is to a study where defocus caused transient axial shortening.

 

[Chanakya]

I haven't actually read any of the research referenced here, but I've followed the thread discussion with interest. Thread's interesting, fascinating even, on three counts.

First, it seems that lens correction is really a thing, in case of juveniles. Not necessarily human juveniles, but still. I hadn't known that. Further, it seems there is the possibility, backed by anecdotal results, that this might, just perhaps, find some application with adults as well -- although that's no more than just a possibility, that further research might, just perhaps, say something more definite about.

Second, it brings into sharp focus something I've myself encountered more than once IRL, how well educated, otherwise intelligent people are somehow unable to quite grok the whole scientific method thing. That's interesting, because it isn't such a difficult thing to understand, and a child of ten could, if properly explained, understand this: but yet, somehow this is something that many adults, educated intelligent adults, often have a hard time understanding. That's ...curious.

And three, I keep picturing in my mind these young tree shrew things running to their nests atop trees, to display to their disapproving parents these new blingy lenses those humans have fitted them with. If I were a film-maker I'd make a film on this. If I were a writer I'd write a children's book, maybe even a series of books, on that theme. And, hell, everyone's a writer, at least a latent writer, a potential writer, so who knows. If in a year or three you find bookstores (assuming they still have bookstores then) all full of this hot new publishing phenomenon involving tree shrews with glasses, then regardless of whether you buy it, be sure to look at the dedication: you'll find this forum and this thread mentioned there.

 

[Tippit]

Fine - it sets out a hypothesis that something along the lines of your process might work. As I said, your hypothesis is not unreasonable. But nor has it been demonstrated to be correct. Reference 34, by the way, is to a study where defocus caused transient axial shortening.

It works. The reason I know that it works, is because I (and many others) have used it effectively. The probability that my progressive myopia simply reversed itself, is null. As an aspiring scientist, you should be well aware that a hypothesis has to account for ALL the evidence, including the black swans.

Sometimes, scientific hypotheses represent the beginning of the acquisition of scientific knowledge. Other times, they tear down pre-existing false hypotheses, and affirm what is already known by many. This is a case of the latter. Retail optometry is junk science, and it’s being demolished by people bold enough to wear an uncertified custom piece of plastic over their eyes.

Axial shortening (or lengthening) isn’t transient at all. It’s part of the built-in emmetropizing mechanism of the human eye which adapts to refractive stimuli. If the shortening changes to lengthening, its not “transience” but the application of hyperopic defocus.

We know that progressive myopia (axial elongation) gets worse in post-natal humans (adults), and so is semi-intransient. Do you, as a layman, have a hypothesis to explain why the human eye can grow longer in myopes, but presumably can’t grow shorter?


Sent from my iPhone using Tapatalk

 

[Tippit]

I doubt that you would have got the same negative response to an OP entitled something like "My experience suggests a neglected area of research" or "A plausible hypothesis for correcting progressive myopia n adults" or some such. What people are reacting to is your claim that your personal anecdote proves the hypothesis and that you are justified in abusing the industry (and abusing those in this thread advocating proper trials to validate claims in healthcare) on those tenuous grounds. Your experience cannot validate the hypothesis. No-one's personal anecdote can.

Since my personal anecdote reflects my actual reality, and since it relates an observation which represents an evidential “black swan”, as it were, it validates the hypothesis, for me.

I understand that you don’t find me credible. I could get my results certified, and then provide prior evidence from optometrist visits, and you probably still wouldn’t. Your implicit calculus is that billions of eyeglass-wearing people, with all the advice they’ve been given, are less likely to be wrong than I am. Perfectly reasonable, and yet, here I am, right.

I am well aware that the claim is extraordinary. Yet, I can read a Snellen chart to about 20/30, when before I was corrected for a refractive error of more than 20/300. You can’t explain that without accusing me of lying.

I titled the OP Because I am angry at the fact that I wasted the best years of my life being unnecessarily dependent on a medical crutch. The best case is that a few people here will try the method, and gain success.


Sent from my iPhone using Tapatalk

 

[Tippit]

Second, it brings into sharp focus something I've myself encountered more than once IRL, how well educated, otherwise intelligent people are somehow unable to quite grok the whole scientific method thing. That's interesting, because it isn't such a difficult thing to understand, and a child of ten could, if properly explained, understand this: but yet, somehow this is something that many adults, educated intelligent adults, often have a hard time understanding. That's ...curious.

I assume that since I am the antagonist here making what is, admittedly an extraordinary claim, that you’re accusing me of not understanding the scientific method.

The scientific method is about observation, hypothetical induction, experimentation, and deduction that may result in falsification of the hypothesis, or refinement of the hypothesis. Confusion arises from the fact that lots of bad science is done by bad scientists who arrive at bad deductions, sometimes with monumentally bad results (for instance, billions of people wearing lenses in front of their eyes to treat what begins as a muscle spasm). Is this a failure of science? The scientific method? No, it’s a failure of people. This is the limitation of the scientific method. People.


Sent from my iPhone using Tapatalk

 

[Chanakya]

I assume that since I am the antagonist here making what is, admittedly an extraordinary claim, that you’re accusing me of not understanding the scientific method.

The scientific method is about observation, hypothetical induction, experimentation, and deduction that may result in falsification of the hypothesis, or refinement of the hypothesis. Confusion arises from the fact that lots of bad science is done by bad scientists who arrive at bad deductions, sometimes with monumentally bad results (for instance, billions of people wearing lenses in front of their eyes to treat what begins as a muscle spasm). Is this a failure of science? The scientific method? No, it’s a failure of people. This is the limitation of the scientific method. People.


Sent from my iPhone using Tapatalk

No antagonism, Tippit. Just expressing my views on what I'm seeing here, kind of what we're here for, right? No offense intended.

And you're right, none on this thread have played the role of scientist. While you have, kind of.

Except: First, to really play scientist, you've got to play it all the way through. You've only yet taken the first step there, in formulating a hypothesis that seems to explain your particular experience. There's a long way to go from that point. Although it's a start, sure.

And second, you don't really need to be a scientist in order to take advantage of the scientific method. Skepticism, to my understanding, is using the scientific method at the micro level, at one's individual personal level, to make sense of the world in a reasonable, rational manner. That necessarily involves standing on others' shoulders, and therefore knowing what that entails. Which isn't all that difficult or complicated, really.

Your past antagonistic exchanges notwithstanding, hecd2's recent summing up seemed apt: That there's a case for what you say as far as juvenile mammals, and therefore perhaps juvenile humans; that there is no such case for adults, thus far, no actual research as far as we know; but absolutely, this does seem to be a potential area for further research. That seems entirely reasonable to my layman's--as in, non-scientist's--ears. I wonder what reason you might have to object to that last position.


eta:
Your methods seem to have given you good results, and good for you. I wouldn't presume to dictate to you how you do things, but in your place, and having observed what you've observed about yourself, what I'd have done is done exactly what you're doing, but in consultation with and following the advice of a good optometrist/ophthalmologist, someone who's into (or at least aware of) actual research, so that I don't go blundering and end up somehow doing damage that might have been avoidable. And nor would I take my individual anecdotal experience as "proof" that all of this is a scam, but sure, I'd take that as grounds for some skepticism, as a tentative hypothesis that might merit initiating further research if I'm equipped to do that, or else at least keeping an eye out for new research in this area, why not. In fact I'm prepared to do that last even basis your experience.

 

[Dr. Keith]

I had a prospective client once who lost all of her hair. For reasons she could write about for pages, but never really made much sense, she added bleach to her shampoo. Shortly thereafter her hair began to grow back, but with some major differences from her hair before going bald. She really believed that this proved that bleach cured baldness across the board.

There were many other facts that came to light as I talked with her that better explained her miraculous return to a full head of hair, but she was sure it was down to the bleach. Luckily for me I was able to find prior art of treating baldness with bleach in a quick search, so I was able to convince her that patenting that broad concept would not be possible until she had something more specific. I suggested talking to a dermatologist or someone doing skin care research. She stopped responding to my communications rather abruptly.

I wonder sometimes if she found another patent attorney who was willing to take her money to file a worthless patent that would never go anywhere. It is an easy way to make money, but I found it interfered with my ability to sleep.

 

[Tippit]

On the topic of hyperopic defocus as the primary cause of progressive myopia, lets examine a paper that puts forth the theory of "Incremental retinal-defocus".

https://www.sciencedirect.com/science/article/abs/pii/S0010482506001922

From the abstract, bolding is mine:

Abstract
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.

First of all, I disagree with their deduction that axial growth is "permanent". It's not permanent, it is long-lasting, and will endure absent the proper stimulus, which is different than permanent.

They are putting forth the theory that simply engaging in near work for extended periods of time, let alone wearing lenses, leads to conditions that promote growth in the sclera, which cause the elongation. This may or may not be true, but the increased amount of defocus obtained by wearing eyeglasses, coupled with near work, definitely increases elongation.

But we have evidence here that defocus causes axial elongation, and that tissue remodeling within the eye is occurring.

 

[Tippit]

Here is another paper @ NIH:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3075061/

A role for hyperopic defocus is strongly supported by the finding that the eyes of young animals respond to minus lens wear with faster axial elongation.15–19 On the other hand, brief periods of clear vision completely negate the “grow” signal produced by otherwise constant hyperopic retinal blur across animal models.20–22 Because children would have to do constant near work to prevent exposure to the potent “stop” signal provided by brief periods of clear vision when viewing an object at distance, these results in animals question the importance of transient hyperopic retinal defocus due to accommodative lag during near work. There are also controversies over whether accommodative lag in children is elevated prior to the onset of myopia23, 24 and whether accommodative lag is associated with myopic progression.25–27

This study admits that elongation by defocus is strongly supported, but then attempts to undermine that theory by suggesting that mere brief periods of not staring at screens while wearing glasses are enough to negate the effects of previous hours.

 

[Tippit]

An even more compelling study:

https://iovs.arvojournals.org/article.aspx?articleid=2189555

Abstract
Purpose.: To determine whether high light levels, which have a protective effect against form-deprivation myopia, also retard the development of lens-induced myopia in primates.

Methods.: Hyperopic defocus was imposed on 27 monkeys by securing −3 diopter (D) lenses in front of one eye. The lens-rearing procedures were initiated at 24 days of age and continued for periods ranging from 50 to 123 days. Fifteen of the treated monkeys were exposed to normal laboratory light levels (∼350 lux). For the other 12 lens-reared monkeys, auxiliary lighting increased the illuminance to 25,000 lux for 6 hours during the middle of the daily 12 hour light cycle. Refractive development, corneal power, and axial dimensions were assessed by retinoscopy, keratometry, and ultrasonography, respectively. Data were also obtained from 37 control monkeys, four of which were exposed to high ambient lighting.

Results.: In normal- and high-light-reared monkeys, hyperopic defocus accelerated vitreous chamber elongation and produced myopic shifts in refractive error. The high light regimen did not alter the degree of myopia (high light: −1.69 ± 0.84 D versus normal light: −2.08 ± 1.12 D; P = 0.40) or the rate at which the treated eyes compensated for the imposed defocus. Following lens removal, the high light monkeys recovered from the induced myopia. The recovery process was not affected by the high lighting regimen.

Conclusions.: In contrast to the protective effects that high ambient lighting has against form-deprivation myopia, high artificial lighting did not alter the course of compensation to imposed defocus. These results indicate that the mechanisms responsible for form-deprivation myopia and lens-induced myopia are not identical.

This study, in an attempt to ascertain the effect of high ambient lighting on form-deprivation vs. lens-induced, deduced that light had no effect, and that FDM and LIM have different causes.

Oh, and by the way, we can impose vitreous chamber elongation by putting distance lenses on monkeys for several months, and then it simply goes away after we remove the lenses!

Which means, if monkeys simply stop wearing glasses for near work, their eyes will adapt towards emmetropia! Amazing.

I guess it was unclear whether the monkeys could still drive, or operate their smartphones in the interim period. Maybe if they had been exposing themselves to hyperopic defocus for years instead of months, like humans do, they would conclude after removing their glasses "Wow, I'm ******* blind, give me back my glasses because I don't understand the basic science behind optical biology!"

 

[hecd2]

You made three posts presenting selected quotes from three separate papers.

They are all three about the development of myopia by axial elongation of the juvenile eye as a result of hyperopic defocus. There is no controversy there - there is, as you said, a wealth of published studies which confirms that hyperopic defocus over time induces myopia in the juveniles of a wide range of vertebrate species.

Post 1: Puts forward a hypothesis that near work induced myopia over time results in permanent myopia. Note that in this paper the primary mechanism for creating the myopic condition is near work and there is no mention of a role for eyeglass wear in the juvenile. You object to the conclusion that the myopia becomes permanent, but you omit any reason or grounds for your objection.

Post 2: Is a paper describing the recruitment of children for a study on the role of progressive addition lenses to correct or retard progressive myopia. Your quote is from the background section in the paper: it is actually a good review of the various hypotheses for the progression of myopia in children. The claim that "brief periods of clear vision completely negate the “grow” signal produced by otherwise constant hyperopic retinal blur across animal models" is not initiated in this paper but by the authors of references 20 - 22.

Post 3: Simply shows that in infant rhesus monkeys high ambient lighting has no influence on hyperopic defocus induced myopia and that removal of the hyperopic defocus stimulus resulted in recovery of the eye. The experiment was conducted in infant monkeys with an equivalent age of 2 to 15 months in humans so has nothing to say about the reversal of myopia in the adult eye.

In short, these papers do not change the conclusion that we reached earlier that there is no published evidence that myopia can be corrected by a process which results in axial shortening in adult humans. By posting them, you seem to be pummelling our fists with your nose.

 

[Andy_Ross]

Those cherries must taste good.