Another paper about EOMs and myopia

From Spain and 2018.

“Because of the incipient surgical techniques at the time, the question of EOM involvement in myopia was prematurely abandoned in the early 20th century. As a result, the participation of the extra and intraocular muscles in scleral distension has not been appropriately dealt with.

" The EOMs are able to contract with fiber shortening (isotonic contraction) or without fiber shortening (isometric contraction). By a combination of both types of contraction, the eye rotates around two areas known as space and body centrodes, situated 13.5 mm behind the cornea and nasally displaced from the geometrical center of the globe (9). To accomplish the formidable task of accessing virtually infinite positions, the EOMs are endowed with unusual physiological characteristics that derive from their expression of specific contractile proteins including, myosin heavy chain isoforms, myosin light chains, tropomyosin, and troponin, connected in parallel or in series, and other special features. The EOM myofiber continuum hypothesis combined with the non-linearity of eye muscle contractile properties would explain a total central nervous system (CNS) control of muscle tone and eye position and velocity. In EOM there seems to be a continuum of myofiber types. Each myosin heavy and light chain isoform results in a distinct shortening velocity, which would translate in an increased plasticity in the control of muscle force generation (10)."

"It can be argued that an anterior group of recti muscles acting jointly with isometrical contraction would fix the eye, while the ciliary muscle would pull anteriorly the choroid. At the same time, the joint action of both oblique muscles, acting isotonically, would pull apart the posterior pole, with the result of eye enlargement. The angle formed by the obliques and the ocular axis ranges in the low fifties [51° for inferior oblique (IO) and 54° for SO]. Convergence is the position of the globe in which the elevator and depressor action of the obliques is maximal. This is the near (reading) position with a synergy with accommodation (and miosis). In this position, the four recti can maintain the globe fixed with a tonic grip, while the maximal conjunct action of the obliques pulls the posterior pole apart, causing the elongation of the globe in its post-equatorial half ( Figure 1 ). Scleral pulling would secondarily cause choroidal stretching and rarefaction.

Figure 1 Eye and extraocular muscles relationship in myopia. (A) Position of the insertion of the IO in the posterior pole in relation to the fovea. Measurements in millimetres: (a) Wolf 1954; (b) Massri 1963; © Whitnall 1932. [Inspired by drawings in references (11,12)]; (B) isometric contraction of the anterior muscles (4 recti) maintains the anterior segment fixed, while the metric contraction of the inferior and superior obliques pulls apart the posterior pole, enlarging the globe at expenses of the retro-equatorial half. The ciliary muscle, mainly the longitudinal portion, acts contracting isotonically as a tensor of the choroid; © convergence of the globe is the position of maximal effect of the obliques. These are coincidentally the reading position and general near vision, with the synkinesis accommodation, convergence, and miosis.

A recent study relates severe IO overaction to thinning of the subfoveal choroid (wow!!), attributable to external mechanical effect (13). Myopia and near-work are statistically related in many studies, although also here are appearing divergent results (14,15)."


"Fortunately, this theory can be disproved (or confirmed) in an experimental setting in which the experimentally induced myopia can be totally neutralized, as regard to the muscular action, by the use of botulinum toxin (BT) injected into the EOMs. BT should be tested with and without cycloplegic drops, to paralyze accommodation. The effectivity of the induced muscle paralysis can be monitored, in the experimental animal, with electromyography.

Purified BT, produced by the anaerobic bacterium Clostridium botulinum, specifically targets the release of acetylcholine. Out of seven distinct antigenic BTs (A to G) produced by different strains of Clostridium botulinum, the human nervous system responds to five toxin serotypes but is unaffected by serotypes C and D. Each species has its own response. Currently, only the A and B toxins are available as drugs. BT irreversibly binds to the presynaptic terminal of the neuromuscular junction, where it cleaves membrane proteins responsible for acetylcholine excretion. In the design of the experiment, it is essential to take into account that the peak action of the BT does not occur immediately, and its maximum effect may take up to a couple of weeks. Additionally, BT’s action slowly decreases over time (16)."

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You ARE a determined young bulldog - I like that. :grinning:

This is because I am a determined old bulldog, or, as my sign is Taurus with the moon in Aries, just an old bull-goat. :ox: - :goat: They don’t have a full bull as an emoji, so you will have to do with a castrated one. :roll_eyes:

I don’t take this stuff seriously, and let’s not start a long sidetrack that will waste time better spent. :wink:

So in your opinion that is a BS paper?

I think Hannie has meant the Moon stuff.

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No, no, I was referring to Astrological signs. I will read the paper with great interest.

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I have now read the paper, and I really enjoyed the brief overview of the history of research on myopia and some current ongoing research. It reminds me that anyone who claims to know what causes myopia is over-confident.


That’s interesting:

  1. I indeed have exotropia instead of esotropia in almost all vertical gazes when I look at bright yet cloudy sun, suffer moderate eye or other pain or very want to sleep. Excyclotorsion is another symptom, so probably inferior oblique muscle has the highest resting tone in my eyes. However, if I just close eyes and quickly alternate opened eye, esotropia appears.
  2. If I use maximal amount of divergence in upgaze, part of visual field goes dark (comparable to as I suddenly take vertical body position after long sitting), then majority of peripheral flashes of light disappear. Thus probably IO overaction indeed the cause of my retina weakness in right eye (that eye might have even more overacting IO).

Kinda stupid in my opinion. If so, EOMs would deform eyeballs like they want, but that could be intraocular pressure that locks axial length and lets it to change only by tiny fractions.

Often, increase in AL and increase in IOP go in pair.

@Ursa @halmadavid hehe, I seek shortcuts and should work a decade of years instead. Well, the species with human-like eyes only need even a decade of days to adapt :slight_smile:

Nothing to stop you from trying, and if you find one you can start your own movement and possibly become rich out of it. Do let us know when you have done so. In the meantime, just go a little along the EM road.


Mmh, not much of a study. Just an article to say that the exclusion of EOM was never conclusively done. The author doesn’t address the problem of Sherrington’s law. While the author correctly describes the action of the EOMs, he doesn’t explain how those actions may cause axial elongation or thinning of the choroid in an even fashion.

This article proves nothing, doesn’t really suggest how the obliques can stretch the eyes evenly (maybe the author doesn’t think axial length grow along the optical axis?), but makes no claims as well.

Although we won’t know for sure until someone funds a study to conclusively demonstrate the involvement of lack of EOM muscles to myopia. But it will probably never be done because mainstream optometry has it figured out already, and there’s very little incentive for ophthalmologist to investigate such a fringe idea that makes no intuitive sense. Also no financial incentive for any industry to study this so… Do EndMyopia. Still your best bet.


You’ve mentioned this several times as a reason for why EOM’s can’t all pull back on the eye at the same time.

However, I can make my bicep bulge at will without rotating my lower arm around my elbow. How is that possible with “Sherrington’s law”? It seems that the more I bulge my bicep, the more my triceps act to counter that. Thus it seems that both sets of muscles are pulling and balancing each other, both pulling on my upper arm bone. Does not the upper arm bone have a bit of stress from both sets of muscles pulling on the same time?

Reading on this “law”, it does does seem to indicate that the inhibition prevents full strength muscle use, but in the case of bicep/triceps, it’s not a complete inhibition, but seems to be balanced to allow both muscles to engage in equal amounts of force. IT’s actually cool that I can increase/decrease my biceps pull and the body automatically counters it exactly with the triceps.

When I use AF hard, my eyes don’t rotate, but are hard to rotate (look in a different direction) until I disengage AF, turn the eye, then reengage it. That’s now automated for me as I’ve done it so much, but it was the clue that made me think that AF was related to EOM’s as it works just like flexing the bicep (when you flex the bicep/triceps, it’s much harder to rotate the lower arm around the elbow, just like I feel when looking around with heavy AF)

So why can’t eye muscles do that? E.g. why can’t I “flex” my EOM’s all together? How are they different from my arm muscles where I can make my bicep bulge, get hard, seem to actually “pull” and get “countered” by my triceps? Why can’t I “flex” the right EOM and have it countered by the left EOM in the same way my bicep/triceps work? And if they can, what do those stresses do to the eye?

Co-activation (co-contraction) of muscles can happen, but it’s not well understood. We know that it’s often involved in joint stability, postural control and certain fine motor movements, the guess is that it’s a double inhibition.

As such, co-activation seem to be limited in its full power, the agonist and antagonist muscles cannot contract with 100% force. Maybe one does 30% the other does 50% power for a total of 80% of the power agonist alone. 60% power + 60% power for 120% power doesn’t happen. The joint is still under less than full power from either 100% agonist / 100% antagonist alone.

The eye isn’t a joint and there isn’t much evidence it does co-activation in the same way as bicep/tricep co-activation. Even if it did, it’s not really exerting more force than a single agonist would. Even if it could, the action would pull your eyes into the eye socket. If you can voluntarily pull your eyes into the eye socket, I rest my case. :laughing:

Oblique muscles stretch the sclera, not the eyes. Innards of eye are being inflated by IOP.

EOMs can contract without fiber shortening, without co-contraction it’s really not useful I guess.

EOMs are one of the most powerful muscles in body, so in my opinion, relatively small and tiny eye isn’t a big deal for them even in 10% of power.

How do you stretch the sclera and maintain eye shape? Keep in mind the obliques aren’t stretching along the optical axis. Which means the axial elongation will be in between the insertions of the oblique muscles not the optical axis. As far as I know, that’s not what happens in axial elongation.

Until you can retract your eyeball into your eye socket voluntarily, none of these discussion really matter.

Sorry, the first argument is too biased and the second is logically incorrect.

How about Bates’ experiments on non-fish animals without lens in?

Eye produces more myopic refraction without lens in while electrically stimulating it. When oblique muscles paralyzed by atropine or cut off, rabbit’s eye can’t produce more myopic refraction. Also, the same for rectus muscles and hyperopia. The same is for dogs (and maybe cats) if I remember correctly.

Well, @SilentNote.

Conclusions are already drawn and even without my health problems I am not obliged to explain you everything :slight_smile:

We can find a gallon of arguments for and against each theory of axial elongation.

So, while scientists research things further, we can improve our eyesight instead of staring at screen doing goalless discussions.

We can’t know for now how it works, as you already subscribed in one of your previous posts. As well, we can’t know how fast it works or can work for me and you, as @NottNott said, some eyes might shorten more quickly as well as more slowly.

Jake got pretty balanced view. He doesn’t want to dive whether EOMs can or cannot elongate the eyeball, but drawn a usual improvement schedule. It all varies from person to person, both in the negative and positive deviations.

In short, that’s not crucial, but vision improvement is. We will go there (and there) very probably at some point. But arguments you provided can’t strongly knock out this theory, as well as pure chemical theory may also have some evidence for me.

Substantiate your claim.

Citations or it’s your bias.

That’s how fools think. Drawing conclusions when evidence is lacking.

I’m not trying to “knock out” a theory. I’m pointing out inconsistencies and problems in the “theory” that needs to be worked out before they are even worth doing experiments on. If a theory can’t even withstand simple criticisms then it’s got no grounds to be anywhere.

Hoping to use Jake to add credibility to your opinions? Jake and EndMyopia do not believe in eye exercises. Guess what muscles eye exercises work on? EOMs. LOL. Why doesn’t EndMyopia do EOM excercises. Obviously, it has little to no use for improving near work (lens induced) myopia, that’s why it’s ignored.

Anyway, I’ve got a couple diopters of reduction and you’ve got 0. So keep believing. Instead of studying what you’re doing wrong with EndMyopia, keep throwing out unsubstantiated theories to confuse people, like that will help anybody.

You also hadn’t substantiate your claim (except visual thought) so I can reply to your claim with basically everything.

About retraction, paper clearly states that rectus muscles hold eye forwards and obliques push eye backwards, that’s why it’s logically incorrect. Second logical incorrectness is that EOMs may be capable to involuntary contraction, as you have your permanent refractive state without voluntary control. That is the last explanation I give you.

It’s close to ad hominem, as well as your footnote.
Anyway, conclusions in that either chemical or mechanical theory lack evidence for now.

True, but that is not my obligation.

There are much more blur in chemical theories because they can’t explain how it works while mechanical theories find more arguments.

Myopia differ in cases. And claims you write are very low quality, as well as inappropriate emotional bias.

I already said you, maybe EOMs can contract involuntarily. As well as exercises only exercises isotonic contraction without isometric. Plus there’s an evidence EOMs play a role in accommodation due to increase in cyclotorsion with monocular accommodation.

I mute you and flag your last post because it has:

Sorry, but unlike you, I don’t have a claim regarding EOMs and Myopia. While you claim that EOMs are important for EndMyopia or that EOMs are related to Myopia somehow, I don’t pretend like I know if they are related or not. I’m only offering criticism on a theory that doesn’t seem to explain axial length sufficiently, which is actually important if you want to link EOMs to myopia.

Ah but the paper doesn’t, you have this backwards mate. I went back to check the paper and the authors didn’t get it wrong. Which means you can’t even read the paper correctly yet you’re calling me biased and illogical. * Slow clap *

Not sure what the voluntary control or involuntary control of the EOM has anything to do with my argument. Which is that if you you don’t see people’s eyes retracting in to the socket voluntarily or involuntarily, it’s a good enough clue that EOMs do not contract simultaneously (which is in contravention of Sherrington’s Law).

Missed this argument earlier so I’ll add it here: The eye isn’t a joint, so it’s unlikely that EOMs can do co-activations the way biceps and triceps can for joint stability. Even if they could, the eyes would retract into the socket in a simultaneous contraction of all the rectus muscles, and the simultaneous contraction of the obliques would rotate the eyes to the nose (cross eyed). This is self evident if you understood the anatomy of the eyes and actions of the EOM, which I have actually studied.

What? Who’s talking about your obligations? Do you think I expect you to come up with solutions to the problems of the theory? I’m just pointing out huge holes in the EOM theory so maybe, you will approach the whole EOM theory with some caution.

Look, do all the EOM exercises you need. It might actually be good for your strabismus, but blaming EndMyopia not working because it doesn’t address EOMs… It’s just sour grapes.

Provide the evidence or the link to the relevant papers. None of the articles you linked so far actually demonstrates this.

Hey mute all you want. I know I’m an expert at exposing people’s nonsense, and it totally overwhelms them when they know their game is up.

You’re just a 17 year old teen that has a multitude of health conditions (don’t know your medical history but I’d look into ruling out connective tissue diseases if I were you). Good on you that you’re looking for ways to improve your vision, but I also know you’ve failed to find AF in over 6 months, which frustrates you for sure. However, to claim that the method is deficient (for not considering EOMs) just because you have personally failed to achieve progress is just immature sour grapes behavior. Many people have succeeded in reducing myopia WITHOUT the need to pay attention to EOMs (a.k.a eye exercises). There are people who have actually fully reversed their Myopia with the EndMyopia method, so to say that EndMyopia is fundamentally wrong just because it doesn’t consider EOMs is simply foolish. More so when you do not even fit the demographic that the entire EndMyopia premise rests on: healthy eyes capable of responding to given visual stimuli in a predictable manner!

Worse so when you start falling for unicorn farmers and start spewing nonsense like it’s the truth. Ortho C, when you’ve not even tested them yourself, when the theory is completely deficient and the actual user reviews unfavorable. Bates, that has been around for ever but I’ve not heard from a single real person who have succeeded on it. I had personally tried Bates too with no avail, and after studying eye anatomy and physiology, it is no wonder why it didn’t work. Look, it’s okay to look at alternatives, but do not confuse your hope for the truth.

While no one knows for sure if EOMs are implicated in Myopia (I don’t either, which is why I go through all the papers that are linked), there’s no evidence that it does so far. All the theories put out there are incomplete and untested. Even if EOMs are implicated for myopia, the EndMyopia method has no reason to deal with eye exercises because they are not habit forming like active focusing. Which means it has no place in the EndMyopia method, (cuz who has the time for it). EOMs and eye exercises are just pointless and a distraction to the actual method that works, active focus!

Just saying, if you stopped wasting time blaming the method, and focused on eye improvment, you might have found active focus already. Also if you start entertaining the possibility that you don’t know everything, you might actually learn something.

Good luck to your vision improvement journey.

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