Active Focus as a result of astigmatism decompensation

In my opinion, Active Focus (AF) has something to do with the mechanism of natural compensation by crystalline lens for corneal astigmatism (let me guess 90% of population have corneal astigmatism near 0.50 D). When Active Focus is “ON”, the SPHERE slightly decreases (up to 0.50) and CYLINDER slightly increases (up to 1.00). At the seconds it is “OFF”, all goes the opposite: you see without CYLINDER, but at the cost of higher SPHERE. But thanks to the lower SPHERE you have when you turn AF “ON”, your axial length thus myopia decreases.

For example in 2011 I’ve had R -2.00/-1.00 or -2.25/-0.25 and L -2.75/-0.75 or -3.00/0.00, as seen in the photo:


The fog in this theory is why some people claim they can clear up even 0.50 or 0.75 of SPHERE.

And other fog is AF as much as 1.50 - this can be shined out by assuming they have ciliary spasm or lens stuck in the near mode or “bulged” mode.

I have no astigmatism in my right eye and a hint (0.25D) in my left. I can active focus at least 0.5D, and if I do eye exercises for a month or so, push that to 0.75D, all sphere correction.

A few months ago I was at the opto and they dilated my pupils. That also numbed my ciliary muscle, and I lost any ability to accommodate closer than my relaxed distance. Essentially, the front part of my eye was paralyzed. But active focus was unaffected! It was the clearest time I’d ever had playing with AF.

So while I personally believe that the cornea plays a major role in active focus (and myopia), I’m not convinced that AF is a result of astigmatism corneal relaxation.


Supposedly 10 minutes of meditation can reduce astigmatism up to 0.4D if people are tested and then retested again 10 minutes later. I’ve read journal articles from surgeons talking about changes of up to half a diopter CYL difference between sitting and lying down which causes problems with eye surgery when people are measured sittting and then the surgery is performed while they are lying down. I would guess that besides the cilliary muscle there are a lot of other little muscles around the eye and in your face that actually squeeze and pull and change the shape of the eyeball. Supposedly people with access to testing equipment can consciously induce several diopters of astigmatism, so I would guess that there’s a lot more complexity to accommodation and active focus than just one cilliary muscle.


You also suppose that myopia and/or astigmatism could born outside of the eye and/or brain - and that’s a brilliant idea I ended up my research with.

Don’t get me wrong - that does not mean the stimulus and reponse don’t work.
But another idea if axial elongation is from muscle action is that eye, just like every part of body can compensate and then it gets stuck in a pattern. Why? Because some muscles are shorter and some are longer due to deformed skull - and every time eye gets muscle work (accommodation), every time it reinforces that pattern. Bates’ exercises were all about getting out of the pattern. EndMyopia is about retraining the neuromuscular system to fire properly, the question is why the eye, while being incomparably lighter than a bone takes too long to change by a negligible amount. And seeking the faster improvement, even than 1.25 D/year is not any shortcut, no matter how much the myopia is. It’s enough for the tecnique to be cause-addressing, and I aimed with passion for EM to show non-folky science, in years of heavy enough funding, isn’t the time @jakey :slight_smile: ? It was all about reverting the eye back to its premyopic shape, and the community would wonder even about the possibility of this - definitely the lack of materials proving that.

Digging into the relationship about EOMs and myopia, EOM paths and skull deformities is a great field in occupation in eye research. But I am happy with what I have (also things besides EM) and rather let someone other will do that job. Becuase the treatment would differ, depending on which kind of cause is behing axial elongation - neuromuscular/biomechanical or metabolical/biochemical.

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Is EOMs early onset myopia? Or myopes?

Extraocular muscles - the muscles that move the eyeball around.



Thank you! I had an article open and they’re using the EOM acronym for Early Onset Myopes so I was scratching my head.


Yes, we should be careful when using acronyms. :smile:


Interesting, could you place your full autorefractor readings here (including cornea astigmatism if possible)?

I bet there could be more than 0.25 D of astigmatism on at least one trial. It’s the average what you write.

This one is doubtful IMO: I played with my eyes so much and can’t either increase or decrease the astigmatism… It seems my eyes are steel stable.

But I had an episode with astigmatism increased to -3.25 and -2.25 with a decrease of sphere. Though I attribute it to autorefractor outage, and different keratometers show different data, like the right cornea astigmatism is from -2.00 to -2.50 and left cornea astigmatism is from -1.37 to -2.00. The cornea is often fairly astigmatic yet people receive corrections without cylinder… Like -0.75, -1.00 or -1.50 cornea astigmatism could be 0.00 if it’s compensated by the lens. Your case is most likely a ciliary spasm - if you get rid of it, your astigmatism should go away also. You might have too short eye and the natural state is hyperopia, so ciliary could spasm. Or some postural issues - look at the teeth.

By the way, J. Yee also intentionally increased his astigmatism to over -2.00 both eyes - he did a lot of central fixation by Bates, also cutting off peripheral vision. To people getting irritated I talk too much about J. Yee I could say he is the one I found really doing some more serious research about myopia and his mind is not locked that axial myopia could not be reversed and all we can do is to prevent or blah blah. I am still waiting for some more real science about EM and could estimate the bridge in uniting these two researches with predicting the best outcome.