Let’s go all straight science today. No fluff, no saucer eyes. Title of today’s science exhibit:
Imposed Peripheral Myopic Defocus Can Prevent the Development of Lens–Induced Myopia
Brought to us courtesy of IOVS, the Investigative Ophthalmology and Vision Science Journal.
Wait, wait. Don’t click out, don’t fall into a narcoleptic slumber. I’ll give you a bit of easy to understand background, to make sense (and even enjoy) this one. It’s worth it, I promise!
Ready? Here we go:
The core argument of your darling friend Jake’s method is that the eye is a stimulus response system. That’s to say that the development of the eye, and changes of focal plane in the eye, are created by your visual environment. Changes in the eye are stimulus based, not created by genetics or the boogey man, or some unknown quantity.
In other words, whether you find yourself farsighted, or nearsighted, you need to look at your visual environment, not some cause outside of your control.
This is actually an argument rather than universally accepted fact, believe it or not.
There are more than a few (or basically most) optometry professionals out there who don’t subscribe to this premise that the eye is dynamic. This is the case despite the wealth of science clearly demonstrating that the eye is a dynamic system (that link, the motherload of science). This is one of the core reasons that prevention and reversal of myopia isn’t discussed. If the eye is “broken”, there’s no point considering anything besides symptom management.
So that’s why I often bring up these medical journal articles, to give you insights into what we know about myopia, rather than what you might be told at the optic shop.
Back to the topic at hand.
If your eyes are in fact healthy, and simply responding to stimulus, then what is stimulus?
Simply put, stimulus is whatever you see around you. It’s how the light hits the retina in the back of your eye. That’s where the incoming light gets sent on to the visual cortex in your brain, and things are interpreted into what you perceive as your vision.
Vision actually happens in your *brain*.
We talk quite a bit about stimulus, all over the blog. Stimulus is what creates healthy vision in babies, human and otherwise.
Glasses are stimulus, too. In particular, glasses change the focal plane. Glasses change where light focuses inside your eyeball. And this is what causes your eyeball to elongate (or shorten). This is where a lot of mainstream optometry falls into a tizzy, if you dare to suggest that axial elongation is a response to lens based stimulus. This is akin to heresy, and you might as well be a Martian space alien asking for directions to the mall, for all the considered discussion you’ll get if you bring it up.
Glasses change the focal plane – where light focuses inside your eye.
You know what’s veird though, yaaaa?
Axial elongation of your eyeball, based on lens stimulus created focal plane change? That’s a thing. Science says so.
Not just science. Ophthalmology science. Ophthalmology science medical journals.
So much for the whole setting up the study here. Hopefully that made it worth reading through this, dry as it might be. Read this stuff, understand the very core argument of which we are on one side of, and a lot of mainstream optometry is on the other side.
Purpose: : To determine whether myopic defocus imposed on theperipheral retina is able to prevent the development of lens–inducedmyopia (LIM), and to determine the minimum time of exposureto myopic defocus to prevent otherwise constant stimulationof eye growth.
Methods: : PMMA contact lenses were obtained from Australian ContactLenses (Doveton, Victoria), and were fitted over the eyes of5 day–old chickens, using Velcro mounts glued to the feathersaround the eyes. Positive lenses were custom–made in 3configurations – full +10D, and +10D with 3mm or 5 mmplano central zones (PCZ). The effects of the positive lenseswere assessed after 7 days of constant wear. LIM was inducedwith –5D lenses for 7 days, and its development was interruptedby replacement of the –5D lenses with positive lensesfor 1h, 30 or 15 minutes each day at noon. Axial lengths weremeasured by ultrasonography using a Mentor A–scan ultrasound,and inter–ocular differences (IOD) were calculated.
Results: : After 7 days of constant wear, +10D lenses with 3mmPCZ were as effective as full +10D lenses in slowing axial elongation,with experimental eyes significantly shorter than control eyes(p<0.01). +10D lenses with 5 mm PCZ were ineffective (p=0.76).Both full +10D lenses and +10D lenses with 3mm PCZ were ableto block axial elongation induced by –5D lenses, witha minimum exposure of 30 minutes per day to both full +10D and+10D with 3 mm PCZ required to substantially counter the increasedaxial elongation induced by otherwise constant wearing of –5Dlenses.
Conclusions: : These results show that +10D contact lenses with 3mm plano central zones are as effective as full +10D lenses in suppressing normal eye growth, and excessive eye growth induced by –5D lenses. The results suggest that imposed peripheral myopic defocus may be able to be used to control on–axis axial elongation, even with normal central vision.
Still with me on this one?
Yes, this particular article goes beyond the basic premise of the impact of lenses on axial length. Why? Since that’s been discussed ad nauseam for decades and a lot of research now looks for nuances in how variations in lens use can affect axial change.
Why’d I used this article, rather than re-hashing the old minus-lenses-make-your-eyes-longer topic? It serves well to make the point that lens induced myopia is old news. More recent exploration gets into how even partial exposure to focal plane changes can affect the length of your eyeball.
Meanwhile though, we still have the mainstream blissfully unaware of the impact of minus lenses on your vision health.
Minus lenses move the focal plane further back in your eye. That’s the long and short of this story. That change in stimulus (yea?) incentivizes the eyeball to grow longer. A longer eyeball is a (you got this one already?) more myopic eyeball.
That’s why sometimes this kind of myopia is called “axial myopia”.
Plus lenses move the focal plane further towards the front of your eye. Again here, change in stimulus, axial change going the opposite way. Less myopic eyeball (or eventually, hyperopic / shortsighted).
There are a quadrazillion medical journal published studies, reviews, analyses, on this topic. So why do you still get the professionals telling you about myopia being just “a thing”, something you can’t control in any way?
Who knows. I’m no psychic, kittehs.
Though if I was …
The one counter argument you’ll get on this, is that the study in question was using chicken eyes, rather than human eyes. Which, if you want to see me hyperventilate and then go into cardiac arrest, just use that as counter argument. Especially if you’re an ophthalmology PhD, in which case hide your diploma, lest I straight up set that thing on fire.
Chicken eye, same reason we test medication on animals first. How hard do you think it would be to get a green light on inducing severe myopia in a human test subject?
Right. You might as well forget about it.
The chicken eye isn’t the same as the human eye. I’ll concede that it’s not even going to respond the same as the human eye to stimulus. Not to the same extent, not at the same rate. But here’s the thing: Chickens are used in these studies, because the eye is very, very similar. You are going to get similar outcomes. It’ll have to do until the government says it’s all right to induce human myopia (which, all the irony in this statement).
Just for a quick visual, here’s chicken vs. human eye:
Left human, right chicken. Reasonably not-so-different.
Want to know more about the chicken eye? Check out Mike, the chicken vet.
Keep up with the Twitter, eh?