Article on NITM and accommodative buffer

This is no doubt related to active focus, ciliary spasm, etc. Let’s try to understand this together.



There’s a related one that might help, too:


And this, by a different author:

This quote is really important:

"Hyperopia of 0.50 to 0.75 diopters is the mean human refractive state. This low hyperopia is viewed as a desirable refractive state; it provides a buffer in the presence of exogenous and endogenous factors which influence autonomic balance and hence the accommodative system. Emmetropia is seen not as a normal, perfect, or ideal state, but rather as reflecting a loss of this buffer, signaling the likelihood of further adaptive change, frequently into myopia.

If low hyperopia is an optimal refractive state, the question is frequently raised, why not prescribe low minus lenses for emmetropes and over-correct myopes, to artificially create low hyperopia? Such solutions simulate hyperopia in terms of optical effect upon accommodative demand, but do not simulate the flexibility between effector systems or the behavioral attributes which permit the retention of natural low hyperopia. Indeed, application of minus to the individual with inadequate freedom between effector systems creates additional stress."


Now, let’s discuss it.

My take is that about a half diopter of hyperopia masks the NITM, so you don’t notice blur. This is probably why people who don’t need glasses can see better without taking time to focus in many cases. @hellothere

If I’m understanding it right, this also keeps you from having to move stuff closer as you develop NITM during the day, and moving stuff closer only increases visual stress and makes you more likely to develop myopia.

But at the same time, overcorrecting myopes is a bad idea, because the original focusing mechanism is already disrupted, and it will just cause more NITM.

Also, if your differentials are too weak, you lose your buffer and move too close and get more ciliary spasm.

Active focus is likely the ability to stimulate negative relative accommodation, and it helps give a clear image that the system can use to identify as a reference frame for the sign of the blur caused by NITM or uncorrected myopia. This tells the system which way to modulate eye growth to go toward a zero refraction over time. Probably being at the edge of blur and using active focus is the next best thing to having slight hyperopia/intact buffer.

So, the ideal lens power for distance is one that gives you mostly clear vision, and freedom from most fatigue, preserves as much buffer as possible, and allows use of active focus. Exactly what Jake discovered.

So, if you’re using a -0.50 D undercorrection to achieve that, you’ve eaten into about 0.50 D (or is it 1.0 D???) of your buffer. Maybe active focus that shifts the refraction by 0.25 to 0.50 D in the positive direction is actually compensating for that loss of the buffer, or restoring it.

At least that’s my very quick take on it. I may be totally wrong. I feel like I don’t understand very much of it at all, yet…it’s not easy reading.


I need to find some time to read and properly respond to this, could be a couple of days, no disinterest, just a little swamped right now, it’s bookmarked so I’ll get to it!

I’ve read the first two, but the big one is going to take me a little longer, stay tuned…:wink:

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That quote might be out of context. Perhaps age related? Been reading Borish’s Clinical Refraction which describes itself as the ancestor of the 1970 classic Clinical Refraction by IM Borish.
Unfortunately, nothing matches the above quote.

“Fusional vergence component is a buffer” Not sure what that means but the word ‘buffer’ got my attention. from - Lecture 5

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Maybe hyperopia and exophoria go together. 6 prism diopters of exophoria is supposed to buffer near vision. I take that to mean prevent ciliary spasm for a time period.

I don’t think Dr. Harris is talking about older people only. He’s one of the experts on this stuff. Few people understand it as he does (though I plan to, one day).

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From the second article about hyperopia:

Hysteresis is a dynamic lag between an input and an output that disappears if the input varies slower than the output. After accommodating at near for a sustained period and shifting back out to distance, there is a lag in how long it takes for accommodation to fully make its way back to baseline. It may undo 80% to 85% of the shift in a few minutes but can also take a few hours.1 The refraction doesn’t actually change from moment to moment, but the hysteresis effect can make it seem like the hyperopia is disappearing as the day goes on and explains why an emmetropic patient may complain of some intermittent distance blur later in the day.

That’s curious, and helps explain why sometimes why I might see very well despite not taking breaks. If we take the view that there is a "buffer’ to be preserved, then perhaps your observation may be correct. Maintaining the edge of blur provides just enough stimulus without producing the dark effect. From Oxford,, the dark effect/dark focus is when:

A stable resting accommodation (1) of the eye’s crystalline lens, usually corresponding to a focal distance of about one metre, that the eye assumes when confronted with a stimulus lacking any features on which to focus, such as a completely enveloping blank screen resembling the inside of a giant ping-pong ball, or a blank screen viewed through a lens that makes it appear too close to focus on, or an isoluminant stimulus, or complete darkness. It produces a temporary condition of anomalous myopia.

Perhaps this also explains why active focus needs only a small amount of stimulus. If things are too blurry, you induce dark focus, which causes anomalous myopia. You can’t focus if the image in front of you has nothing to focus on. From the same Oxford dictionary, anomalous myopia,

A transient form of myopia caused by the temporary absence of adequate stimuli for accommodation (1). See also dark focus.

So what I’m getting then is that there are two forces at play:

  1. Taking breaks and properly using differentials preserves the hyperopic buffer
  2. Active focus from the edge of blur stimulates accommodation towards zero as a natural adaptive response, if we take Skeffinton’s model. That said, if you induce too much blur, your eyes undergo dark focus and cannot properly focus, which causes plateaus/lack of progress.

That’s what I gleaned from my quick skimming, but I’ll do a little more reading later :slight_smile:

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So, I finally found some time to read through it all and give you guys my take on this all. First of all, the third article is out of my league for sure. I’m not versed enough in the optical terminology to make sense of all these states and many tests they are referring to. So I’ll stick to what I could understand.

It seems to make perfect sense that the ideal scenario for our eyes is a small state of hyperopia (+0.5-+0.75). Like all the articles say, this will give you the ability to use your eyes for some close-up work and still be able to see clearly to infinity.

I don’t agree with the first one stating that prolonged close-up work will result in NITM. If you’re in a state of hyperopia, you can’t just jump to myopia. It should be called Near Induced Transient Emmetropia if you ask me. These hyperopes end up with some ciliary muscle spasm bringing their effective refractive state to emmetropia.

Interestingly enough this hyperopic state might have consequences for becoming presbyopic later in life. In a hyperopic state the ciliary muscle has to contract more to focus on something up close. If your lens is smooth enough, no problem, but if it stiffened up later in life, you are asking even more of you ciliary muscle to contract that eye lens and focus properly. This may prelude a greater necessity to get reading glasses as one ages. A more myopic state of the eyes will reduce this dependency somewhat.

All the articles seem to agree on overdoing work up close may very well result in becoming myopic. So it’s best to preserve the hyperopic buffer as much as possible. Alternatively, making sure that you stay out of ciliary muscle spasm will be even more preventive, because you won’t need that buffer. If you are used to good habits, emmetropia could even be more desirable because it takes less effort to focus up close.

These interesting articles (thanks @FMR) also give us a clue as to why some people with very poor close-up habits can just get away with it. If you are +0.75 by default and not very prone to axial elongation, you’ll reset quite quickly by unlocking your ciliary muscle and having your eyes return to their original state. A good night sleep after and all it good and well. This may very well be a key element as to why some people just don’t end up with distance glasses, although they should end up with some because of their bad habits.


I keep wondering: why is about +0.75 an equilibrium state?

Much of the discussion is about the effects or benefits. But it’s not obvious how an eye even gets to this number. Could it be because the emmetropization mechanism disregards NITM to some extent? Or could it be an offset from chromatic aberration?

And why can’t we use this buffer for improvement? If we were adapting toward having such a buffer, just using any reasonably reduced glasses for near work should lead to systematic improvement over time, well beyond the 20/20 mark for distance. But that is not what we observe. So the buffer either doesn’t come back once removed, or there is some ingredient missing to make it reappear.

Though there are occasional stories on here where eyes improve beyond the 20/20 mark on the glasses used. If there’s a way to make that happen on purpose, it could help us get rid of the excessive low-light blur after reductions.


Or maybe it’s the alternating hyperopia-myopia that allows the full range of ciliary focus, clarity signal on the retina, etc. In other words, maybe the short term NITM is actually protective against myopia.

This leads me to wonder if clear, comfortable vision with occasional periods of myopic focus are recalibrating the focus back to infinity each time, i.e. completing a full cycle of focus adjustment…


@Varakari, thinking a bit more…

Maybe the +0.75 just masks the defocus caused by NITM. Not sure how they can call that protective…what if you eat through it over time and become closer to emmetropia and then eventually myopis? Oh wait…this actually happens to people in real life and that’s the whole reason why this site exists, huh?

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Great post from @card here:

Showdown Experiment: Will Enough Outdoor Vision Shorten My Eyes?

Now, what if active focus and other good habits are delaying or reducing accommodative lag? Makes some sense to me…

Could the buffer be produced by the front retinal cells? Like first they give clear flashes, then the pictures merge…and then a buffer? I might be way off here, but if that were true you wouldn’t have to be hyperopic in an axial length way to enjoy and use the buffer.

“Again, for this explanation we turn to the science of neuroplasticity. The retina is not single plane, but rather a tissue of some depth, consisting of multiple layers of sensitive photoreceptors cells (rods and cones) and intermediate conductive fibers. In fact, the photoreceptors perversely evolved for various reasons to be at the back of the retina, with the “wiring” actually in front of them. But the photoceptors are distributed over multiple layers. Presumably, the most active receptors are those which are usually stimulated by well-focused images. After all, those are the ones whose signals the brain can interpret, and they receive the most reinforcement. For a myope, these will tend to be the receptors in the focal plane of close objects, toward the back of the retina. Because the myope is doing a lot of close work and spends less time looking in the distance, the closer retinal cells get less stimulation and suffer from underuse. However, if these closer layers can gradually get more stimulation, or example by using plus lenses, they will adapt to increase in sensitivity and the strength of their signalling to the visual cortex will gain prominence. At some point, weak signals from this forward layer (on which there is a sharper image) will be sent simultaneously with the stronger signals form the backward layer (on which the images are blurred). During the period of adaptation, activation of multiple layers will be perceived as a double-image. Eventually, and with time, the sharper forward layer will dominate over the backward blurry layer. And as the overall shape of the eye is remodeled as the eye grows in response to focusing on distant objects, the focal “strain” on the eye will be reduced, and a new equilibrium shape will take hold. This hypothesis is unproven, but is consistent with known mechanisms, and could be tested experimentally.”


I’ve never read this explanation before, but the way the facts are put together makes sense. I do think this possibly explains both blur adaptation, and also the double images you get when you’re near full correction or emmetropia. @Laurens @Varakari

This also probably explains a few oddities about ciliary spasm…

-I’ve noticed weird, sharper vision at near during and following periods of ciliary spasm. I must be amplifying the activity of the near-centric photoreceptors during my bouts of too much closeup time. It could also be a choroid response I guess, but I think it’s more than that. The ciliary spam might be inducing a lo-pass effect on some of the receptors…?

-This also explains why my vision recovers best if I cease using glasses for about 24 hours, and then ease back in with differentials for short periods after that, and then short periods with normalized (removing them before the vision has a chance to blur up again).

It may not be just brain processing…but actual receptor chemical changes/changes in their relative activities. This may also have impact on high and low light condition or photoperiod influences on the vision and eye length (if eye length is related to the receptor stimulation pattern).

And remind me again…which of these receptors are the peripheral retina, where hyperopic defocus occurs?

I bet varakari will be the first to figure out some of these activation patterns one day. (Yes, that’s a motivational nudge).

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I like this explanation. Neuroplasticity is seen to account for more and more as neuroscience advances.


How thick is the highly photoreceptive part of the retina anyway? When I search for this, I get answers about cell thickness, but isn’t the real question the variance in depth at which light is sensed with enough acuity to determine the sign of defocus?

Numbers relating to the photoreceptive layer seem to turn out in the tens of micrometers, and I’d assume that significant thickness is needed to form an image, so the eye would get maybe half the thickness for comparing focus levels. And then everything is moving all the time and there’s chromatic aberration, with the continuous colors of a natural environment. So I’m not really sold on how the brain would reasonably single out photocensitive cells by depth in the retina, or what purpose that would serve.

Thanks for the encouragement FMR, but I’m not so confident. :sweat_smile: The eye is pretty damn complex, and I only have superficial knowledge of it. Fortunately, we only have to figure out the bottleneck changes that can influence eye shape in practice, so maybe there’s at least a chance.

BTW, on double vision: why would the sum of a focused image with defocused images give the appearance of two or more sharp-ish images? I still think that has to be from processing, not optics.

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