#198 - Eye health—everything you need to know | Steven Dell, M.D.

Hey everyone. Welcome to the Drive Podcast. I'm your host Peter Attia. This podcast, my website and my weekly newsletter all focus on the goal of translating the science of longevity into something accessible for everyone. Our goal is to provide the best content in health and wellness, full stop, and we've assembled a great team of analysts to make this happen. If you enjoy this podcast, we've created a membership program that brings you far more in depth content. If you want to take your knowledge of this space to the next level, at the end of this episode, I'll explain what those benefits are. Or if you want to learn more now, head over to peterattiamd.com subscribe Now without further delay. Here's today's episode. My guest this week is Stephen Dell. Stephen is an internationally recognized leader in refractive eye surgery, special specializing in LASIK surgery, cataract surgery, and refractive lens exchange. He's also the Chief Medical Editor of the journal Cataracts and Refractive Surgery. Today he's the Emeritus Chair and President Emeritus of the American European Congress of Ophthalmologic Surgery. He's a principal investigator on a variety of FDA clinical trials in the field of eye surgery. He is the inventor of several surgical instruments and devices and holds over 20 US and international patents in the field of eye surgery. He is also the author of numerous textbook chapters and peer review reviewed journal articles in this episode we talk about all things related to the eye, and I'm pretty open in the outset of this in explaining that of all the things that one would learn in medical school, there are none that I know less about than the eye. In fact, I come into this episode truly knowing as little as a layperson would know about the eye. And I think at the outset of the interview I explain the extent to what I know about the eye. And while it may be slightly more than you will know, I promise you that within about 15 minutes of this episode we are all going to be at the same level. So this for me was just a fascinating discussion and I treated it almost like the discussion I would have with Steven if we were at a cocktail party, really picking his brain about kind of the anatomy of the eye, why it's relevant, how it factors into the natural processes of aging, and how those kind of differ from some of the pathologic processes that also tend to increase with aging, but are not necessarily related to aging per se. We get into just the really simple fundamentals of what is nearsightedness, what is farsightedness, what is presbyopia, which by the way, I used to think was farsightedness till I did this interview. We talk, of course, about what the treatments look like for these things and basically get into a very nuanced discussion about how the different treatments might be beneficial to some people versus others. So we talk obviously about Lasik eye surgery, but we also talk about a procedure that came along slightly before that called prk. We talk a little bit about a procedure that is just coming online today called Smile. All three of these are similar, but they differ in fundamental ways. And that can be an important thing to consider if you are in the market for one of these procedures. We also talk about eye health. What are the things that we can do? And for many of us listening to this, it's what can we do for our kids to maximize eye health? We talk about some of the real epidemics that are going on in myopia, that is to say, kids that are requiring glasses earlier and earlier, what that might be about and what we can do in our kids to prevent those things and also in ourselves, what we can be doing. So, anyway, there's a lot of stuff that's covered in here. This is really kind of the everything you need to know about the I episode, and I hope you enjoy it as much as I did. So without further delay, please enjoy my conversation with Dr. Stephen Dell. Hey, Stephen, thank you so much for coming over. As we were talking about. I don't really do many of these in person anymore, often just out of sheer laziness, but I do enjoy it a lot more. So the fact that I know it was a bit of a hassle, you had to probably change clinic or something today. But anyway, really appreciate you coming out. And this is a topic that I think everybody has questions on this topic, and everybody, myself included, is comically ignorant on this topic. I mentioned to you a few minutes ago the extent of my knowledge from medical school. I remember there's an optic nerve. I remember it's a cranial nerve. I think it's even the second cranial.

There you go. You're ahead of the game.

I remember something called a fovea. And I know there's a blind spot, but I've kind of forgotten why. So it's safe to say my knowledge of this topic right now is probably at par with everybody's. Right.

Well, that's not rare, frankly, because the eye is so literally compartmentalized, we just don't interact that much with other specialties. So it's not rare for people who are in other specialties. To be very ignorant of the eyeballs. And that's fine because I think it'll help us keep the level of discussion at an approachable level for everyone.

Has there ever been a discussion about suggesting that ophthalmologists don't need to do the 4 year MD degree? Like how much of what you learned in medical school became relevant in your residency?

Actually, quite a lot, honestly. Yeah, because you think about it, the eyeball, there's really nothing specifically magical about the eyeball. It's got neurological tissue in the back, actual brain tissue in the back. It's got a vascular supply. There are a lot of crossovers to other medical disciplines. All of the cellular processes are the same. We operate adjacent to the eye. I think it's important for us to have a general sense of medical knowledge, particularly because so many systemic diseases manifest as eye problems. There is a discipline of medical training or of visual training, basically optometry, which deals with the eye, but not all of the surgical stuff. So we work in a collaborative fashion with optometrists and those are the folks who are fitting glasses, they're screening for eye disease, they're handling preoperative and postoperative care. In many cases, they're treating some diseases that are specific to the eye, like glaucoma, for example. And we work in a collaborative fashion with them.

Does everyone in an ophthalmology residency spend time operating? There's no non surgical discipline to this, right? It doesn't bifurcate in the training?

Well, it does, actually. There are non surgical ophthalmologists, but I think they all start out as surgeons. To become an ophthalmologist, you're really training to become an eye surgeon. But there are, for example, neuro ophthalmologists, which are really more neurologists than eye surgeons. In fact, it's typical that they don't do eye surgery. So there are some ophthalmologists who don't do eye surgery.

One of my sort of lasting memories from residency was stealing suture from the ophthalmology or at Hopkins, because I guess for people who don't know, the number of the suture, of course, gets larger, the suture gets smaller. So an O suture is like, you can see how thick it is. It's like a piece of rope. 102030. By the time you're at 4.0, it's actually quite thin.

Right. We use 11 0.

Exactly. In cardiac surgery, you're using a 7, 0. Occasionally there's some guys that would sew the distal end of a coronary artery with an 8. 0. And at that level, it's already very thin. I mean, just the slightest tug too much and it breaks. But then in ophthalmology, you guys wrote 11 0. And so I used to steal 11. 0 constantly. Every night I was on call and practice suturing with 11. 0. The thinking being, if you can tie an 110 with your hands and not tear it, that 7. 0, which normally is like a piece of hair, is going to feel like a piece of rope. So I used it to help me develop a good feel for fine suture. And then I also realized I'm kind of being a schmuck here. I bet this 11.0 stuff's really expensive, and I'm just stealing it. Like there's. Taking it to the call room all night.

More likely. It was probably 10. Oh. But yes, our tools are little, tiny tools. And I can remember our operating room when I was in training was sort of near the orthopedic surgery, the exact area. And you hear this Black and Decker stuff going on over there. And our little tiny tools are very. It's just a totally.

Do you. Is everything you do under a microscope operationally, like, you don't operate with a naked eye.

Right, right. It's all under a microscope. Just to put it in a visual for people who may not be familiar, we have a binocular microscope. So I'm looking through both eyes, and this is either mounted from the ceiling and has controlled by my feet. So the X, Y, and Z and the zoom focus are controlled by a foot pedal. And that either comes from the ceiling or it's on a really large stand. So I'm sort of sitting. I'm looking straight ahead, so the image is here, but I'm operating down here. And it's interesting because sometimes my wife will kid me, I'll come home from a day of surgery exhausted. But she says something like, well, I don't really get it. You're just sitting in a chair, sort of making these little tiny movements, and there's soft music playing. It all seems very, very sedate. It's incredibly stressful and exhausting.

Although I will say, in your wife's defense, she has it harder because of the kids.

Yeah, that's true for sure. Let there be no misunderstanding about that. It's way easier.

Well, actually, I didn't realize. I never really thought about that. But the other advantage you have is you don't have that cervical flexion problem that most surgeons have when they're in an open. I mean, nowadays with more robotic and laparoscopic surgery, you can be in an advantage neck position.

We have a different problem though, and that is that people tend to, and I don't want to mess up the sound and microphone, but they tend to hyper extend, they tend to bring their head forward to come up to the oculars.

Yeah, yeah, yeah.

And that creates a whole other set of problems. So there are ergonomic challenges, for sure. And I remember early on in my career I was, I was coached very carefully on how to sit, how to have your spine arranged. Don't crane your neck forward and make sure that your shoulders are down. It's interesting because when you train surgeons and you look at them, they're all sort of raising their shoulders up and they're terrified that they're going to do something wrong. So they're in a very, very compromised and stressful position. And then they tend to lift their hands up so they're actually, and again, I mentioned earlier that these are little tiny movements, so very small positional changes can have a huge impact on the outcome of the surgery.

Yeah. I have a number of friends, two in particular from residency, who have had multiple neck surgeries, including one that required such a significant extent of fusion that he could no longer operate. So he trained as a cardiac surgeon and now does cardiac critical care. So still a great career, but, you know, after 10 years of training as a cardiac surgeon, can't operate anymore.

Yeah, I mean, surgery, it takes a toll on the surgeon for sure.

So when you went to medical school, did you know you wanted to do ophthalmology?

Not really. I think I knew I wanted to do something surgical. I wanted to do something with my hands. I'd kind of always been good with my hands and I could draw reasonably well. And, and, and you get, as you kind of know, you get feedback early on in your medical career, if you demonstrate that you're decent with your hands, people say, hey, you're pretty good with your hands. You should think about something surgical or maybe not. They say, have you thought about radiolog? Something along those lines. And so I kind of knew that I wanted to be a surgeon, but really didn't know what type. And I remember a Eureka moment where the first time I looked through what we refer to as a slit lamp, which is basically like a microscope to look into the eye, the very first time I looked through that instrument at an eyeball, I was hooked. I knew this is what I wanted to do.

And that was something you did during an ophthalmology rotation or were you doing an ER rotation and somebody came in with something stuck in their eye?

It was during an ophthalmology rotation. And I'd had some exposure to ophthalmology because a friend of mine's father was an ophthalmologist, quite a famous one. And I'd had a background in photography when I was a little kid, so I kind of understood optics well. But that was during one of those one week. Do a little ophthalmology, do a little ear, nose and throat, do a little bit of whatever it is. And that was. That was the nice thing about medicine is that you kind of get to taste a little bit of everything before you decide you're going down a particular pathway.

It's funny, I didn't really overlap with ophthalmologists. So you guys didn't do a general surgery internship, I'm guessing, right?

Some of us do that. I did what is referred to as a transitional residence internship, where you do a little bit of everything. You do general surgery, internal medicine, you do a little bit of everything. That's very helpful. And the general surgery part, I will confess, that was rough. I mean, as you well know. But it was nice to have exposure to a little bit of everything.

It's probably a four year residency, I'm.

Guessing, when you include the internship.

That's right, yeah. Back in the day, when you did it, what was the bread and butter? You always kind of judge a discipline by what the bread and butter is of the era. So general surgery, if you did it in the 1960s and 1970s, the bread and butter would have been Bill Roberts procedures and things like that, where the most common thing you were doing was cutting out half of the stomach because of peptic ulcer disease and things like that. By the time I got to residency, I never did one of those. Right. Because H2 blockers and PPIs basically eliminated the need to surgically remove part of the stomach for gastric or peptic ulcers. So at the time you went through your training, where did 80% of the volume come from? What type of cases?

Yeah, still cataracts. Cataract surgery and then retinal disease, the scourge of essentially diabetes, where you had these very, very complex retinal problems. So those were really the two main ones.

So this is probably a good moment to sort of take a step back and get into some of the anatomy and get me up to speed and everybody else, by extension, on what it is we are talking about here, because even the word retina cornea. These are like. I kind of know the retinas at the back of the eye that like. It's just embarrassing, Steven, how much of a Luddite I am when it comes to this part of the body. So I can say this literally talk to me like I'm a four year old. Okay, explain the eye to me.

That's good. That'll work for both of us. So it's funny you mentioned that because I don't typically see kids in my practice, but there is one disease state where I do see kids and that's because we did some research in that area that anyway allows me to see kids. And when you explain the eye to a kid and you say, well, the eye is like a camera and the film in the back, that's the retina. And they look over at their parents like, what is this camera? What is this guy talking about?

Isn't a camera the thing on your phone?

What is he talking about? Film? What is that? You know, a 50 year old understands that. But literally the eye is kind of built like a camera, where in the very front you have the cornea, which is kind of like the covering on the front of a watch. That's the thing that a contact lens would sit on. And then the next thing you encounter is the pupil, which is the hole in the iris. Behind that is the lens. We refer to it as the lens, but it's really one of the, a couple of different lenses inside the eye. But the lens behind the pupil, then you have the vitreous cavity and then in the very back, the retina, which attaches to the optic nerve. And that's what goes to the brain. So images come in, they're bent by the cornea first, then bent again by the lens, and then they focus hopefully on the retina. So in a perfectly sized eye and someone who doesn't need spectacles to see, images come from say, optical infinity, which is, for the purposes of our discussion, about 20ft or beyond, where light rays come in parallel and they're bent so that they fall perfectly on the retina.

And what does that mean, fall perfectly on the retina? Meaning if you think about the back of the eye here, what fraction of the back of this sphere is considered retina?

All of it.

Everything?

Yeah, all of it. The whole back of the eye is coated essentially by retina. But there is the fovea you mentioned earlier. That's the point where you cast your gaze. So the image, that of the thing you're looking at falls on the fovea which is the very center, the bullseye, literally, of the retina. So when I'm looking at you, images from you are falling on the fovea of both of my retinas. Now, if someone is nearsighted, those images come into focus in a point that is not exactly on the retina, and so that can become a problem.

And nearsighted again, the way I used to remember this, because this is literally how little I know. Nearsighted means you see things near.

Well, yes, that's right.

And that those are people like me who need either glasses or contact lenses to see things at a distance.

Correct. So this is typical cocktail party banter. Someone will say, I think I'm nearsighted. Or maybe I'm both nearsighted and farsighted. So nearsighted means you see better up close. Farsighted is a little trickier because farsighted people see better at far. But their far might also be kind of blurry. It's just that the near vision is even worse.

So that person who says, I'm neither I'm near and farsighted could be. That's an accurate statement. That's a plausible.

No, it's actually probably that they're what we refer to as presbyopic, which is that they see well, far away, but their focusing ability is compromised, typically through age, and they can't see up close. And we'll get into that.

I want to get to that in detail because I experienced that a few years ago in a manner that rocked my world. Because it didn't happen gradually. Yeah, that seemed to happen overnight.

Yeah. It's funny you say that. Some people wake up on their 40th birthday and they say, I just can't see up close anymore. And for others, it's a little more gradual process. But the reason that comes into play is that when we are young, when we're born, the lens of our eye is extremely elastic. It's like a gummy bear. And it can change shape to bring near objects into focus. But as we age, and this is universal, the elasticity of the lens goes down, and we're no longer able to sort of zoom focus in. And you have it have to start pushing things farther and farther away or get some sort of optical aid, like a pair of spectacles, to see up close. That process continues as the lens becomes less elastic and harder, eventually resulting in a cataract where it begins to lose its optical clarity. So now you have a lens that's stiff, hard, and starts to become opaque.

So A cataract is a disease of the lens.

Correct.

And it's a natural. I guess this is kind of a gray area. Do we consider this to be a natural product of aging, the way our skin wrinkles and the elasticity changes, or is it considered a pathology in the way that type 2 diabetes is a pathology, not necessarily a normal consequence of aging that can be avoided?

Yeah, that's a really good and interesting way to look at it. So I think that cataract formation is a universal component of doe days on earth. You know, just. I don't recall seeing many people in their 70s without some degree of cataract formation. It starts to become universal. However, there are things that can pathologically prematurely cause cataract formation. Some of them are sort of surprising. Like being electrocuted can actually cause premature cataract formation. But that's one sort of exotic, weird one. But trauma, head trauma can certainly do it.

Just head trauma, not necessarily eye trauma, Just one thing. Well, you know, the head, I mean, obviously they go hand in hand.

Typically the eye is in the head. And if the head receives trauma, there's going to be a certain amount of trauma in the eye itself. So.

Right. But point is, it doesn't have to be direct trauma to the eye. Simply the coup, counter coup forces of the brain are presumably also being reverberated through the vitreous fluid.

That's exactly right. So if you think about the eye as a fluid containing organ and when it receives trauma, and just as you mentioned, with coup and contre coup injuries of the brain inside the skull, I think those same forces come to bear on the eye itself. So I think it's more common when you do have direct eye trauma. But I think even head trauma alone can predispose someone to cataract formation. Certainly diabetes is a cause of premature cataract formation. Steroid use, corticosteroid use can lead to cataract formation.

So is the lens a vascular structure?

It is not. And the protein, if you think about the lens, it's kind of the shape and about the size of an M and M candy. Just like a plain.

The chocolate ones.

Yeah, the chocolate ones. Right. You know, just the ones without the nuts or pretzels or whatever they're putting inside MMS now. But the, you know, a plain M and M candy, and it's got a coating kind of like the candy shell. And the protein inside the chocolate is optically clear when you are a kid. And that protein does not turn over or exchange. But the membrane, the candy Coating the so called lens capsule can allow molecules to diffuse in and out. So a classic example of this is someone will point out, hey, my vision, my glasses prescription suddenly changed. I became much more nearsighted, or I became much more farsighted in the space of a month. And I went to the eye doctor and they said, wow, your glasses are totally wrong. And the first thing I think of is go get your blood sugar checked. Because glucose can diffuse into the lens, cause it to swell and that will change the shape of the lens. The lens becomes physically bigger. So it's like a thicker, more powerful lens.

So it's an osmotic change. Correct, Basically.

And the timeframe for that to happen is over a period of several weeks. So if the blood sugar goes up, there may be a lag of a month or two before the vision changes. And when the blood sugar goes down, same thing, it takes weeks for that to kind of go back to normal.

So again, I'm just so. I'm almost struggling to organize my thinking around this. But the other thing that comes to my mind when you think about an avascular structure is what is the immune system's behavior around the eye? Are these immune privilege sites, are they more or less susceptible to certain types of infections, systemic infections that is? Obviously, I know we'll probably talk a little bit about sort of local infections.

But yeah, I mean, the eye itself is certainly prone to damage from systemic infection. There is a blood retinal barrier in the same way that there's a blood brain barrier that protects that highly metabolically active brain retina from systemic disease. But the lens itself is relatively privileged from an immune standpoint. It's within that capsule and it's hard for large molecules to get across that. Small molecules can.

That's going to be important from a pharmacotherapy standpoint.

I'm sure it is. And for example, there is a technology, there's a medication that is a lipoic acid cholinester that is being examined as a way of softening the lens to maybe break some of the disulfide bonds that become a problem and become one of the reasons why the elasticity of the lens is lost.

So you're saying there might be a day when there's either a topical or injectable substrate that could go into the lens that could delay the onset of.

Farsightedness and the onset of cataract? That's the hope. This is sort of, at the moment, it's a little bit of a pipe dream because it's in the early Experimental phase, but human trials have begun to look at the lens softening properties of this particular compound. The trick is you've got to use it in a topical fashion. So putting in an eye drop, and that drop has to run the gauntlet of going through the cornea, which has lipid layers and water soluble layers. It's got to get through all that into the aqueous humor in the front and then through the lens capsule into the lens to actually do its work. And that's why that particular drug or compound is a choline ester, because that allows it to get through that, the lipid layer in the front, through the aqueous, through the water soluble portion of the cornea, and then hopefully into the lens itself. And that's not easy to do. So the lens is a relatively privileged area, both from an immunological but also a pharmacological standpoint.

And so that would helps it also stay clear.

Yeah, makes it hard to clear. You want the lens to be optically clear.

Let's go back to a little bit of the front of the eye. So the pupil we all recognize is the dark part. And we talk about the dilation and constriction of the pupil. Is the pupil itself actually changing in size or is it just that the iris is moving? The colored part of the eye dilation means it's actually moving back and constriction means it's actually closing.

That is correct. The physical aperture changes in size. It gets bigger, it gets smaller. So when you go to the eye doctor and they dilate your pupils, they are physically opening up the pupil pharmacologically. And that's mostly so we can see into the back of the eyes.

And you do that by forcing the iris to move out of the way.

Correct. The iris has a. It almost looks like the aperture of a camera. You can either constrict it or you can make it bigger. And interestingly, one of the big pharmacological, I think, frontiers that we're on the cusp of seeing are drugs that intentionally shrink the aperture in the pursuit of increased depth of focus. So students of photography will know that the, the smaller the aperture, the smaller the hole, the more stuff is in focus at the same time. So if you can make the pupil small pharmacologically and get it into the sweet spot, which is probably about 1.6 millimeters, you can suddenly see up close again because you've expanded the depth of focus.

Wait, this is, Let me make sure I understand this. You're saying that putting the lens aside for a moment, which is a great source of the pathology, the inability of the lens to move in and out, call it the Z axis, if we want to think of it that way. You now have another way to manipulate your ability to see things close up. If you could force the aperture to be in a position that isn't necessarily dictated by the availability of light.

That's exactly right. So imagine it's kind of like squinting. If you squint, you're reducing the aperture through which you're looking and you're filtering out optically. What's happening is you're filtering out all of the light rays that are not perfectly parallel. And if you can get rid of those scattering rays that make the image blurry and only use those parallel rays that happen to be coming parallel off of an object, you can actually resolve it. You can actually see it. And that's why pharmacologically, if you shrink the pupil, you could once again see up close.

Now this again is a little counterintuitive to me because anybody who's in my shoes, who's experiencing farsightedness, or actually I shouldn't say that, Presby. Presbyopia, Presbyopia knows that nothing makes it worse than darkness. There's two scenarios where it wreaks havoc. The first is one of my children has a train book. That why these guys wrote a book in like six point font that they know parents are going to read their kids in bed when it's kind of dark. It's beyond me. Like, there should be a mandatory 24 point font for nighttime books for little kids. But anyway, he's got this one book and he even tells me before he wants that book read, he's like, daddy, go get your glasses. And then the other place is the restaurant where it's usually poorly lit. But in both of those situations, isn't my aperture narrowed because. Oh, no, no, of course not. It's the opposite.

The opposite.

Oh, yeah.

So if you put the sun on something, you're going to be able to read it because your pupil.

So is that why light makes it different?

Some of it is just the. Absolutely. It's pupil effect alone.

I never thought.

Some of it is just the light. There's much more light energy available for you to resolve something. So yes, there are competing forces. When you reduce the size of the aperture, you're letting less light in, but the only light you're letting in are those rays that happen to be parallel. In perfect focus, you can actually see. So in the clinical trial that we performed to look at this, those competing forces were examined very closely, and we found that the aperture effect, the depth of focus, outweighed any loss of vision from loss of light.

And how long would these eye drops stay in effect? How long would they be able to maintain after you put them in?

I think about it depends a little bit upon eye color, believe it or not.

Because something I want to ask about in a moment. Yeah, glad you brought that up.

Yeah. Certain eye color, like light eyes, tend to react more to any given strength of dilating, drop or constricting, but about six to eight hours, maybe up to 10 hours. So this would be a once a day, maybe a twice a day eye drop.

And would this have any impact? Would it compromise your far vision?

Quite the contrary. What was really interesting is that when we looked at patients who had their pupil size reduced pharmacologically, their distance vision also gets better by the same principle because their depth of focus is so good. So in the same way that you can squint and make out a highway sign if you're a little bit nearsighted or a little bit farsighted or have astigmatism, which we haven't even talked about.

Yet, which I don't even know what that is, even though I have one.

That's right. And squinting makes that better. By the same token, the pharmacological manipulation of your pupil will do that as well. And by the way, I think you will see in early 2022, commercial availability of these. Of the first of these drugs.

So going back to the more complicated drug you were talking about, that has. It's complicated because it has to make its way into the lens. I can now see why that would be more about the cataract issue and not about the presbyopia issue, because this would be a much easier way to solve presbyopia because you only have to basically get onto the iris.

Yeah. Well, you're looking at a drug that shrinks the pupil and works in 15 minutes versus something that softens the lens that might work in 15 months. So I think it's. They're very different markets. And while that lipoic acid, Cholinester, is being pursued as a presbyopia near vision aid or something to reduce the effects of. I think their real goal is to reduce the incidence or delay the onset of cataract formation, which would be really cool.

Yeah. Is there any clear evolutionary explanation for why different eye colors have emerged? What's the advantage of brown iris versus blue?

Yeah, it's protection from UV light and from visible light in the same way that different skin tones have emerged. So typically you see dark eyed people closer to the equator, clustered closer to the equator because the visible light and UV light and infrared light or infrared radiation are really destructive. And as you might remember, this is one of the few things that people remember from medical school about the retina. But it's one of the most metabolically active tissues in the body, if not the most metabolically active tissue. And because it's constantly being bombarded with radiation, effectively it's prone to free radical formation. So the, what's called the retinal pigment epithelium, which is the pigmented layer behind the retina, underneath the retina that is responsible for shielding the vascular supply behind the retina from all of this radiation. Because that vascular network behind the retina has a very high oxygen tension and it would be prone to free radical formation if it were constantly being bombarded by UV light, infrared radiation, visible light. And that's why you see in people near the equator more pigment. And that's also true of the iris as well.

So the other thing I do remember vaguely from medical school is rods and cones. And of course I also remember a few other things now that we're talking about it, about which part of the brain actually does the signal process processing and stuff. So let's go back to the light hitting and what are the rods and cones and how are they processing that signal?

You might remember cones are primarily for your daytime vision and they're clustered in the center of your visual sphere, so near the center of the, what we refer to as the macula, which is the central portion of the retina. And the very center of the macula is the fobia. Right. So that's primarily where the cones are. The rods are in the periphery and they typically are responsible more for dim illumination vision, like night vision. And they're very good at picking up motion. So as predators, we want to make sure that we can hone in on where prey is. But as prey ourselves, we want to be able to detect, oh, that's some kind of a tiger over there. Something's moving in my periphery. I need to be aware of that. So that's primarily the difference in responsibility.

Is each rod and each cone, Is each one a single cell?

Yes, that's right. They're each highly specialized cells.

Obviously they have mitochondria. What distinguishes them? Do they have photoreceptors? Like what makes them unique?

They are photo, they refer to as photoreceptors and they have stacks of structures within them that are photosensitive, and that causes a depolarization.

So they work like channel opsins. Do they use a photon to create an action potential or.

Correct. Once the photon hits that particular cell photoreceptor, then there's a change in the membrane, and ions flow, and that's how a signal is generated.

Wow. Okay, so all of that ion flow ultimately makes its way to the optic nerve, correct?

That's right. And to the brain. And most of the visual processing is in the very back of your brain. And about half of the overall brain structure deals with vision in some capacity. And that's why, for example, when people have a stroke, there's almost always some component of visual involvement in a stroke. So you may have a droopy face on one side, and then a limb is droopy as well. But if you map out the visual sphere, you will detect some deficit in the visual sphere from most strokes.

Now, people who listen to this podcast on various episodes, we've got into the brain, and people understand that I think there's sort of the brain stem, the most primitive piece of our brain, that is basically responsible for autonomic function. You then have sort of this midbrain that sits on top of it that we call the sort of reptilian brain. A lot of emotion there. But of course, what in theory distinguishes us from all the other animals is this remarkable cortical piece that sits on top of it. And how much of the visual processing is in that neocortex? Is it virtually all done there? Is any part of it done in the midbrain?

Yeah, stuff like pupil responses, the autonomic stuff, the autonomic stuff, those are in the midbrain. But the visual processing and the actual mapping of the visual sphere, and even as hierarchical as parts of the brain that are specific to edge detection or moving. Edge detection or edges that move this way or that way, that's all been mapped quite elegantly, and it's in the cortex.

Is there a cross? Is the left doing the right and vice versa?

That's right. But remember, you send information from your left visual sphere to the right side of the brain, but you're getting information.

In other words, this is the trick.

Both eyes.

Yeah.

So both eyes.

Yeah. Explain how that works, because I remember in med school needing to draw this a few times.

How long do you have? The simplest way to think about something is that at the pituitary, there is something called the optic chiasm. You probably Remember where the. The.

The optic nerves cross?

Right. Some of the fiber half. About half the fibers cross. So if a visual deficit is in one eye only, we know that it is in front of the chiasm. Correct. And if it's behind that, it should affect both eyes. Maybe asymmetrically, but it should affect both eyes. And that could be very helpful in localizing where a particular problem is. Now, a lot of that's done through imaging, but it used to be there was quite an art to this clinical exam. To this clinical exam, which, sadly, we've lost a lot of.

Yeah. And I do remember both in neurology and probably neuroanatomy, kind of going into these really crazy tests that you'd see the patient performing the test and missing a certain thing, and you'd think they must be faking it. Like, there is no way you could produce such a bizarre deficit in this one part of this one visual field. But then, of course, you see. And look, there's a tumor. And it totally explains this. Once you understand how the nerves cross.

It kind of goes back to one of your earliest questions, which is, do you think that eye surgeons need to go to medical school? Yes. Because we diagnose brain tumors. We find things that are systemic diseases that have ocular manifestations.

So you're obviously well aware that your brother and I are close friends, and he's become pretty obsessed with hunting now. And I'll take full responsibility, at least for the part.

I did not see this one coming.

Yeah, well, you'll see where this is going. Right. So he's become super obsessed with hunting. And one of the things that hunting teaches you is how we stack up to wild animals. So if you're out hunting an elk or an Axis deer or one of these remarkable creatures, especially with a bow and arrow.

Yeah, I was going to say, how much technology do we have access to in this hypothetical scenario?

So. So, no, let's talk about bow and arrow hunting, where you really. I mean, if you really want to reduce the margin of error, you want to be inside of 50 yards to be able to take that shot. So the way I always talk about this is animals have superpowers, and we just have to decide, as do we. We have superpowers, our greatest one being our intelligence, which allowed us to make the bow. But I generally think of the three big senses, which is the sense of vision, the sense of smell, the sense of hearing. And there's simply no comparison in sense of smell. We basically can't smell. We're effectively Useless creatures.

Ingredient.

If they're downwind of us, they can smell us a mile away. Literally one mile away. If the wind moves from you to them, they're gone. You'll never get close to them. It turns out that the closest sense we have to our prey is vision. It's the only thing where we're almost on par with them. Now there are some animals that can see better than us. You know, there are certain types of rams that if you break skyline within two miles of them, they'll see it.

And birds.

Yeah. But for the most part, this is the one sense that we have that rivals the best. Is that because we both had to, as you said, be hunters and be hunted for such a large part of our revolution? I mean, this is sort of teleologic explanation I'm looking for.

Well, I think so, but just think about this for a moment. Imagine you are in the desert and there is a single candle a mile away from you and it's pitch black, there's no moon, you can see that. But at high noon in that same desert where there may be 200,000 lux illumination, you can still function and see well. So many, many, many, many, many orders of magnitude of change of illumination. Like it's astonishing that you can function in both of those environments.

Well, that's actually interesting that you make that point because as it gets darker we do tend to have an advantage over some of the animals. Now it turns out to be very short lived. There's a very narrow window at dusk and dawn where I think we can outsee them. And maybe that's the benefit we have in that we evolved slightly better to have this greater range, if you will. But I've always been amazed at like why did we not develop a sense of smell that. I mean, because we effectively can't smell compared to animals. I mean it's really absurd how different it is and I don't know why evolution didn't push that harder.

And even our hearing I think is, you know, we're not even nothing compared to them. Yeah, but vision, you know, and if you ask, it's very common for patients to grab my arm as we're going into surgery and they'll say, Dr. Dell, you don't understand. My vision is really important to me. I've got to see, I've got to see. And I get that, you know, it's, it's the one sense that if you asked people which sense they'd be most willing to give up or least.

That's right. This is the last One. And in Covid, we saw many people, at least transiently, lose a sense of smell and a sense of taste. And of course it's inconvenient, but it's totally survival.

Yeah, it's hard to function in the world as a blind person. And, you know, it's a fear that many of us have. So it's a sense that we value very highly. And also evolutionarily, it's valued highly just owing to the fact that so much of our brain is devoted to vision.

Yeah, this is a little bit off track, but maybe good for a psa. When I was a kid, we did so many dumb things without ever any concern for our eyes. I just don't think our parents knew enough and we didn't think about it. So I'd be out in the backyard chucking things around, cutting wood, smashing rocks. Never a thought to put on safety goggles. And now my kids, who are both completely obsessed with cutting down trees and, like, just. They're always. They're very active outdoors. I mean, they just know, like, you're wearing your safety goggles if you do that stuff, because I'm totally paranoid they're going to, you know, have one of these tragic accidents. Do you see much of that stuff?

For sure. And you see a lot of eye injuries. I think injuries are one of the main causes of devastating visual loss in young people. If we take visual loss in general, almost all of the big causes and movers of visual loss are senescence related. They're age related. But in terms of vision loss in young people, it's a lot of trauma.

And what are the most common traumas that you see? Like, is it object flying into eye or is it more.

I think it's more blunt trauma, frankly.

Wow.

Yeah, more blunt trauma. The eye is pretty well protected with the brow and the cheek. But, you know, there are certain things that can get in there and can directly impact the eye. And so I think, you know, in a young person, trauma is something you have to certainly watch out for.

What is the velocity at which we can't outblink it? Because the other day my son was smashing beads and he didn't want to put his safety goggles on. And I was like, look, buddy, you got to get these things on. And he goes, no, dad. And he's like, why? And I said, because you're hitting sharp objects with the sharp object. If one of them flies up and hits your eye, he goes, I would see it and I would close my eyes. No, you wouldn't, buddy.

Yeah, let's just put it this way. Those objects are flying at supersonic speed and you can't blink that fast.

So do we have a sense of, like, what our reaction time is to blink?

That is known, but I've long since forgotten what that is because you get.

The sense, like, if somebody's throwing you a ball and you misjudge it, you're going to blink. Like that's slow enough that you can catch it. But yeah, but then there's other objects where you can't.

Interestingly, you know, I've operated on a number of Major League baseball players, and for them, seeing the laces on the ball as hitters is enormous.

It's their career.

It is their career, and it's the difference between them hitting well or average. And some of these players that we've operated on have been 2020 before they had surgery, but they wanted to be 2015 or 2010. And what that means is, again, here's another nomenclature issue. What is 2020 vision? 2020 simply means that you can see at 20ft what a quote unquote, normal person can see at 20ft. If you're 2010, you can see at 20ft what a normal person has to get 10ft up to in order to see. So 2010 is better than 2020. So some of these guys want to be 2010 or 20, you know, whatever it is, 2015, we've been able to achieve that with modern forms of laser vision correction.

Because wait a minute, how isn't this now getting into the performance enhancing side of things? Isn't this kind of amazing? You know, I never even thought of it.

Yeah, for sure. And, and I had a discussion yesterday with a guy who owns a soccer team, and I said, have you ever had your players tested for their vision? And he sort of froze and turned white. Turned white for a second. He just said, it's so crazy you say that because we put them through this barrage of tests physically to see what? Their heart, their lungs, their kidneys, all that stuff. We didn't check their vision. And there are ways to boost human performance beyond 2020. The theoretical limit of how well you could see is defined by essentially the pixelation of your retina, the spacing of the cells of those photoreceptors that we talked about earlier.

Does that vary from person to person?

It has to, but it's somewhere in the vicinity of about 2008 or so. So if you can have a sharp enough image, you could theoretically see better than 2010. And the only way you can really achieve that is to remove some of the optical irregularities that we are all born with and somehow neutralize them along with the glasses prescription. And we can actually do that with laser vision correction currently.

So why would it be beneficial? I guess we'll talk about laser surgery and maybe you'll want to park this question until then. Why would it be beneficial to an athlete who for understandable reasons, needs the best vision possible to undergo laser corrective surgery versus just using contact lenses to accomplish the same thing? Is that possible?

Yeah. So if you think about contact lenses, anyone who's ever worn contact lenses knows that when you put in a brand new pair of contact lenses, you can see pretty well with them. And then you begin to regard that contact lens as a foreign object. So your body just begins to attack it, coat it with all sorts of immunological debris. You are susceptible to pollen, dust, whatever it is that coats this formerly pristine object. And let's say there is correction for astigmatism in that contact lens where its orientation is important. Every time you blink, that contact lens moves a little bit. All of those factors contribute to optical performance that is less than what you could achieve with spectacles or laser vision correction. Particularly soft contact lenses do a very, very good job, but they don't give you superhuman vision performance typically.

You know, it's funny, I experimented two years ago with a stronger prescription than normal to get me to 2015 in my dominant eye for archery.

Sure goofed up your near though.

That's the problem. I just abandoned it immediately after like six months of suffering because it made my presbyopia worse.

Yes, goofs.

So I was just like, ah, this just isn't worth it.

Yeah, that's right. That's the challenge. When you pull the image farther and farther away, you're doing the same thing with the near image as well.

Let's now talk about how to correct these. Oh, I guess let's define an astigmatism since I don't know what that is yet.

Yeah, I mean, it's when the eye is shaped like a football instead of a basketball.

And when you say the eye, which part of the eye specifically?

The cornea. The very front part of the eye, typically.

And how thick is the cornea, by the way?

It's about as thick as a credit card. Like 500 microns? Yeah, yeah, like 550 microns. Something like that.

So half a millimeter.

Yeah, exactly right. So half a millimeter. And typically that is the location of astigmatism. There can be astigmatism in the lens itself, the lens behind the pupil.

You probably don't remember which one I have, do you?

I do.

Which one do I have?

You have corneal astigmatism.

That's the. So that would be normal.

Yeah. It's very pedestrian. You're very boring patient.

But so, meaning just to be clear.

Yeah.

I'm not perfectly shaped around here. I'm a bit oblong.

That's right. Shaped like an egg or a football. An American football. So if you're walking along the laces of the football, you would encounter a fairly gradual curve. But if you took a right turn and walked, it gets perpendicular. It would be very steep.

Okay.

And so that means that the power differs by meridian. So you need a different glasses prescription in this meridian versus this meridian.

What's the prevalence of this?

It's very high. I think 60 some odd percent of patients with glasses prescription have some significant degree of astigmatism.

Why has poor vision or I was going to say why has poor vision been allowed to evolve? I was going to offer that maybe really poor vision hasn't. Right. Vision that would impair your ability to survive through reproductive age probably didn't evolve. Maybe there was a day when the genetic variability of eyes was broad enough that a subset of people had really poor vision. The type of people today who maybe we don't encounter.

Right. This is a super interesting topic and it shows you how plastic, the evolutionary or actually the adaptive component of the eyeball is itself. So the length of the eye is really what determines whether you are nearsighted or farsighted.

When you say length, you mean distance.

From front to back. So anterior, posterior, length of the eyeball, primarily, that is the main driver as to whether you are nearsighted or farsighted. Those who are in the know and are watching this or listening to it also realize that sometimes it's the curvature of the cornea that contributes to whether someone is nearsighted or farsighted. But let's say for the purposes of this discussion that it's the length of the eyeball that is the main reason why someone is nearsighted or not or farsighted. So a very nearsighted person has a very long eyeball.

Let me make sure I understand that. Very long AP axis. You're going to have a real hard time seeing things far away. And is that because the further something is, the harder you have a time focusing all that light?

Well, let's talk about the genesis of this. So if most of your work, most of Your visual environment is close, then the light rays from that close object are diverging, so they are falling behind the retina of someone who's perfectly targeted for distance. So your eyeball is really smart and it says, okay, so you're telling me everything is here, close up, I know I'll just grow longer so that these near objects are in perfect focus. And that is exactly what happens over what time scale? Over a period of months. So if you take a young person and you exclusively have them perform near tasks, their eye will grow longer so that those near objects are in perfect focus.

So if you could do an awful experiment, it's been done. Take a child and not put them in a white room where there's nothing that they can see that's far away and just have them play with close objects that they can reach. And you would put that kid into glasses as a child.

That's called society in 2021 is children looking at screens near objects for hours on end and not going outside. There are two drivers of nearsightedness in the plastic developing human number one, deprivation from outdoor light and number two, near work. So, for example, there have been cohorts of children. These, most of these studies have been done in Asia, where there is an epidemic right now of myopia of astonishing proportions. I'm talking about 90% of the population is now nearsighted in certain southeastern Asian cities. When that becomes such a dominant phenotype, something is really oddly off. Wow.

So this really transcends evolution because you can change, if you can change something.

In years or months, it's not evolutionary, it's adaptive within the eyeball itself. So if you take a group of children and this has been done 7 to 11 year old children, and you send half of them outside for 80 minutes during the school day for recess, and half of them stay inside in an indoor environment for their recess, the risk of, or the incidence of nearsightedness is half in the group that went outside. So you cut your risk in half.

By going outside without any instruction to go and look at things far away, but just by the very fact that if you're outside, there's so much more to see and you're going to be looking further out.

Right. And this has been further studied in terms of is it just being outside or is it the light? It's actually both. But the light is really the most important driver of protection from nearsightedness. So if you are outside on a bright sunny day, you're releasing a fair bit of dopamine from your retina. And dopamine inhibits the growth of the eye. So the worst thing you could do is stay inside in a dimly lit room and perform near tasks. That raises your risk of nearsightedness 16 fold compared to kids who go outside.

I'm sure there's epidemiology that would suggest that the further you are from the equator, does that imply that you have a greater risk of nearsightedness just based based on the light part of this argument?

Yes, there is some data to look at that that shows that. And not only that they've taken children and given them equal intervals of outdoor activity, but the ones who had noontime outdoor activity did better than the ones who were outdoors at 8am where there was less illumination. And we know from animal models that it is illumination that is critical in this dopamine release. So does that mean we need more skylights in classrooms or more windows? We need more natural light. Could we artificially mimic some of the sunlight by making these rooms brighter and prevent some of this myopia epidemic?

Is a photon a photon? A photon? I mean, does it.

I mean, I don't think that it's known, frankly, Peter, whether that's the case because there's a whole spectrum of light. So is the blue light more important? This is tangential and we'll talk about this. I know, but blue light, you hear all this negativity about blue light. Blue light is critical for wakefulness, for attention, for, I think, for preventing myopia. And by the way, when we say myopia nearsightedness, it's not just the inconvenience of wearing glasses or contact lenses or having laser vision Correction when you're 23 years years old. There are pathologies that are much more common in very nearsighted patients compared to the general population. It's much more common to see cataract formation in myopic patients. They get something called myopic macular degeneration. They're at risk for glaucoma, they're at risk for tears and detachments of the retina. So it's not just the inconvenience of spectacles. These are disease associated conditions.

So going back to my evolutionary question, it's quite possible that over hundreds of millions of years, any deficit in vision that would have prevented you from reproducing or impaired your ability to escape a prey would have taken that out. So from a genetic standpoint, our vision should be very good.

And in non literate societies it typically was. So if you look at hunter Gatherer tribes. There is no nearsighted. There are no Kalahari Bushmen with spectacles. It just doesn't happen.

This is amazing. This suggests that because my parents wore glasses, I should wear glasses. Is not true.

Well, there is.

Or is there an epigenetic part of this where you can.

Well, both. There is a genetic component, and if you look at siblings of individuals who wear spectacles, there is a higher incidence of myopia or hyperopia.

But that could be susceptibility, right?

It could be susceptibility.

And then the environmental trigger is what's going to do it in anyone.

And we don't know whether parents of reading children were reading children themselves. So, you know, it's hard to separate out the genetic component. But there does seem to be a genetic component as well. But the environmental component seems to be way stronger and more powerful. So if you take parents who don't wear spectacles and you put their child in a dark room and give them an electronic device or a book or whatever it is, and have that child focus it near for hours on end, odds are they're much more at risk for developing nearsightedness.

So when I just think about this through the lens of my kids, so my wife has perfect vision. I don't. What is my diopter? I think I'm minus three and minus four.

That's about right. Yeah.

So what does that mean in terms of the 20 scale? I'm 20.

You're probably like. It depends on how much you squint and look at the eye chart. We honestly don't really attach a lot of significance to the 2100 or 2080, whatever it is. You're probably in that ballpark. 2100, maybe.

But I'm clearly at the point where without contacts, I can't drive, I can't do anything. I mean, I know some people who, you know, or a minus 15. They literally can't. They have to put glasses near the bedside. I'll spend the first hour of the day without contact.

That's right, because you could probably, you know, things are very well.

It's easier for me to read without my contacts.

Very things for you are very well in focus at a typical normal reading distance. So your eyes have been tuned, like postnatally for near work. That's in your development. You must have spent a lot of time reading or doing near tasks.

Well, that's the thing I was thinking about. It's like I grew up in Canada, so from a light perspective, it wasn't so great. You had two months of no light whatsoever. But I didn't watch TV much as a kid, maybe 30 minutes a day. I was mostly outdoors, so I don't know how much of it. But I also didn't. I'll tell you, this is funny. I didn't need my first pair of glasses till college. So it could also be that this happened later in my life as a result of more bookwork, for sure.

So the classic example is we see law students who have great vision when they enter law school, and then they read for 12 hours a day, and then they come in and they say, you know, I think my vision's going. And you look at them and sure enough, they've become nearsighted. And that's not rare in many graduate school situations where there's just, you know, grinding reading for hours on end.

So when I think about our kids, because now I just think, well, what can I. It's too late for me. Right?

But, but so get them outside.

So they are. So fortunately they live outside, but when they're inside, they're obsessed with like playing with Legos and trains and trucks and I mean, that's near, right? So is it that, hey, there's nothing wrong with that, but you just have to make sure they're spending a couple hours outside a day.

I think the data would suggest that good illumination would be helpful as opposed to poor illumination. But, you know, you don't want to discourage near activities because those are really important development.

That was the flip. True. So you mentioned that hunter gatherers or illiterate societies who are out by definition outside all the time, there's no such thing as nearsightedness in them. Do they develop farsightedness?

Not really. I think that they are fairly well tuned, if we want to use that term, to distance vision, to prey hunting and things like that. So distance vision is very well tuned. Now, there's a whole host of other problems that come into play. Once you've outlived your genetic usefulness, you've reproduced and you've imparted your knowledge onto the next generation. You can go ahead and get cataracts because you're done genetically useful, you're utility.

So the cataract is sort of like atherosclerosis, functionally, which is it really? It's the one thing that really has no bearing on your reproductive capacity, but is otherwise inevitable to our species.

It seems to be fairly inevitable to our species. And I've, as I mentioned earlier, I just haven't seen patients in their 70s. Typically that don't have some cataract formation. Now, there are patients who are 80 that are still functioning with cataracts, but the optical clarity of their lenses has degraded to the point that it's not the way it was when they were 20. Maybe their visual needs are significantly reduced at that age. But if you took an 80 year old lens and you put it in a 20 year old person, they would be shocked at how poor their vision is.

That's really interesting. Now, earlier you mentioned that we think that senescent cells, or at least the soluble secretory products of senescent cells are probably playing a role in this.

Well, I think in the lens, it's mostly that the lens proteins are degrading or becoming damaged over time, maybe with UV light, because we know light exposure is certainly related to cataract, as are some of the other things that I mentioned, like glucose going into the lens, corticosteroid use. We don't know what it is specifically about trauma that causes a premature loss of clarity of the lens proteins.

The trauma ones get me worried because I boxed for so long. I took way too many hits to the head. I hope that doesn't come back to. I mean, I've already been. I'm worried about that for other reasons.

Let's put it this way, the cataract would be the easiest thing to fix.

Yeah, yeah, yeah.

You know, that's, you know, cataract surgery today is like a four or five minute procedure and it's astonishingly effective.

How often does one need to repeat that surgery?

Cataract surgery typically is not repeated. It's a once in a lifetime deal.

And what you're noticing is like you're wearing glasses that are dirty. Is that effectively what the patient with cataract is experiencing?

I think the first thing they notice is probably changes in their night vision. Glare, halos, streaks off of lights at night, problems with contrast sensitivity. For those who can appreciate that loss of contrast, those are really early signs of cataract formation.

So then the patient comes to you, they're 74 years old. Or let's say it's sooner they're 70 years old.

More like 64 or 54. Yeah.

Okay. And you're telling them, hey, Billy, you've got cataracts. We're going to just ride this out until you tell me you've had enough.

Typically, we let the patient decide when it's the right time for them to have the surgery. Once we determine that the cataract is visually significant, there are people who elect to have Their cataracts removed earlier than they really need them removed as a means of getting rid of their glasses prescription. Because now the lenses, the implant lenses that we put in to replace the cataract have advanced in function to the point that they can fix the near vision as well as the distance vision, as the astigmatism, the nearsightedness, the farsightedness, the presbyopia, all those things that we've been talking about, they're all correctable with artificial lenses that we put in the eye to replace the cataract. Wow.

But earlier when you talked about during your residency, one of the pieces of bread and butter of your practice would have been cataract surgery that didn't involve intraocular lenses. No, it did.

It did. And there's a fascinating history about the evolution of intraocular lenses. But back in those days, the implant lenses that were put in were simply designed to give the patient good vision with spectacles, just to replace the cloudy lens with something that was in the ballpark of good distance vision.

Sorry, I need to take a step back because I'm actually kind of confused.

Right.

Does all cataract surgery involve the placement of an extra lens?

Yes, that's correct. There are exceptions to nitpickers who will listen to this, but virtually every cataract surgery that we perform involves the removal of the cataract and replacing it with an artificial lens.

Again, you'll have to pardon my ignorance. Does that mean removing the entire lens or removing a diseased part of the lens that has a cataract?

Do you remember our analogy of the M and M candy?

Yes.

So we leave. We leave the shell, Right. We open a hole in the front of the shell, we take out all the chocolate, and then we. Now we have kind of like a flattened bowl. Looks like a Japanese teapot flattened. And we put the implant lens in that bowl, and that holds the implant in place.

And is it a viscous fluid that gets hardened, or is it a hard object that goes directly in?

It's actually a bendable plastic object. And the bendability of it is what.

Allows it to get in, allows us.

To fold it up and put it through a tiny incision, and then it opens up. So that was a very big advancement.

When did that happen?

1980S was when that began to become.

What happened before this.

So this is a really amazing series of stories, but I'll abbreviate them in the interests of time. But in the ancient world, if you had cataracts, the way they dealt with it, is that they would just poke the lens of the eye backward and it would drop down into the bottom of the eye so that you now had a clear optical pathway again to let light in. And this took someone who was functionally blind and allowed them to see shapes. So that was better than right, because.

You don't have a lens, so there's no way you can focus.

You can't focus. All you can see are shapes.

But it's basically like taking someone who has no light transmission and saying, we're going to let unfocused light go through.

Right. So some light's better than no light. So that's what happened in, you know, Hammurabi time.

I'm always amazed. We look at that now and we say that's barbaric. The fact that they knew enough to do that is kind of amazing.

Well, they probably tried everything else first.

You know, they probably dissected cadaveric lenses and tried to figure this out, I would assume.

And there have been artifacts uncovered that I think a lot of them were made out of gold. But they would take a gold needle and poke it through the cornea, and then it was called couching the procedure. They would just poke the lens and it would detach from its ligamentous attachments and then drop down into the bottom of the cavity of the eye. And you see some of these artifacts from Egypt. This was done in China. It was certainly done in ancient Greece. That was how you dealt with cataracts back then, by the way.

It's just worth pausing for a moment to reflect. If you're talking about the pharaohs, you're talking about, what, 5,000 years ago, right. This is not in an evolutionary timescale. That's a pittance.

Right. My profession is an old one.

And you think it would be better to be the poorest person on Earth today than to be the pharaoh of Egypt 5,000 years ago?

I think in many ways, or certainly.

It was, it would be better to be in the bottom 10 percentile economically today than the top 10 percentile 5,000 years ago. If the best you have to your cataracts is some guy sticking a hot poker in your eye.

That's right. Then you fast forward to right after World War II. And there's an ophthalmologist in the UK named Harold Ridley, and he notices that some of the RAF fighters would have fragments of their canopy, their Plexiglas canopy, shatter when they were fired upon. And these things would actually get inside the eyeballs. Shards of plexiglass essentially would be inside the eyeball. And the dilemma was, well, what do we do with this? And he learned very early on that these fragments were biologically inert, that the eye was perfectly happy and people could walk around the rest of their lives with plexiglass inside their eyeball. And that's a shard of sharp plexiglass.

And this is in part because the lens is so immune privileged.

Well, this is a foreign object that has now entered the eye, not necessarily in the human lens. It might even be in the vitreous cavity or in the front of the eye.

So there was something about sharp plexiglass that did.

It's something about plexiglass. So the light bulb goes off that, wait, you can put plexiglass, which is essentially polymethyl methacrylate. You can put that in the eye and the body doesn't really care that it's there, doesn't mount an immune response. So in Ridley's book, which I've read, it's really amazing, but some intern asked him, well, when you take this cataract out, are you going to replace it with a new lens? And he looked at this young intern in a very British fashion, I'm assuming, and just said, you know, that's the stupidest question I've ever heard. And then he went home and thought, wait a minute, that's brilliant. We should replace it. And then they lathed a lens from some spectacle maker that was about the size and shape of the human lens. And they actually threw eight of these in patients. And there's amazing footage of, I think one of the first operations, they dropped the lens on the floor and of course, it's the only one they had. So they pick it up and rinse it off and they, it's fine. They put it in. And these patients did, like, shockingly well. And this was viewed as heresy. And there was, you know, 20 years of, you're blinding people. But eventually the technology won out and became.

So there were bad outcomes, presumably, I.

Think in the early days, for sure. There must have been for sure. And there were. But like any new technology, the first iteration of it is probably terrible and maybe just a little bit less terrible than the alternative. And now it's a ubiquitously used.

So I never thought, because basically, I didn't realize until you said it, that polymethyl methacrylate is all over the body in terms of joints. Like when you replace a knee joint, the tibial plateau, I think, is made out of polymethyl methacrylate. So presumably there's something about it that is just. Just invisible to the immune system.

Well, we don't. And we don't use that material anymore because it's stiff. It is not deformable. So you had to. You had to. In the old days, you had to make a fairly large incision to get.

The cataract, to get this thing in.

First of all, to get the cataract out and then to get the implant lens in. Two converging technologies made that go away. The number one was we were able to take the cataract out through a tiny incision because you break it in situ. We break it up, we emulsify it, essentially with ultrasound. Now we even sometimes use a femtosecond laser to break up parts of it. But the bottom line is that we can remove the cataract through about a 2 something millimeter incision, which is very small, like the thickness of a pencil lead, basically. And we can now take these implant lenses and fold them up and put them through that same tiny incision, and then they can open up and be exactly where you want them to be. Now, why is it important for the incision to be small? Well, if you make a big incision, obviously it takes longer to heal, but it induces astigmatism. So you want the incision to be tiny.

So does the. Using your M and M analogy, does the coating on the surface of the M and M grow back?

No, it does not.

So it's fixed. Whatever hole you put in there, they're stuck with.

Yeah, it's fixed. Now, sometimes the coating, the M and M candy shell, can begin to opacify after surgery, and we can treat that in the office with a laser where we can just disrupt that coating.

So this has got to be like my mom. Actually, my mom's 72nd birthday is today. I don't know if she's had any issues with cataracts, but if not, she's due for them. My dad has. He's 83. I'm trying to think. He must have had surgery then by now, right? There's no way.

Yeah, odds are.

So. I can't believe I've never really talked about this with him. But it must be a game changer for a patient to come out of the clinic or the. Or whenever, wherever these. Do you do this in your. Well, you have an or in your office?

We do, but cataract surgery? We do in an ambulatory surgery center. But it may be that your dad didn't talk about it because it was such a non event. You know, you go in for cataract surgery and the next day you're kind of back to your regular.

Right. But wouldn't it have been a big event in terms of his ability to see?

For sure. Especially now that the implant lenses can correct the near vision and the distance vision. So that in addition to the added clarity from just removing the cataract, they patients typically have this benefit of not needing.

So this is a procedure we should all be looking forward to when it comes to. Like you're going to get.

I don't know if I would go that far. I mean, it's still surgery. There are risks associated with it.

What are the biggest risks?

No, I think that the number one thing we think about is infection. But it's extraordinarily unusual to see an infection less than 1 in 10,000 cases where you'll see a serious infection. It's like any other surgery in the body. You look for bleeding, damage to the inside of the eye. You have to keep tabs on the pressure. It's basically everything that you would look for for if you were taking out an appendix. You're also dealing with in the eye.

What fraction of patients do not have a material improvement in their vision or have some deterioration of even another subset of vision? So, yes, you've taken away my cataract. I can see better in the sense of clarity, but oh my God. I became abjectly nearsighted as a result of it.

Yeah, I think that's pretty unusual because the science behind getting the prescription correct or very close to correct is pretty advanced.

And tell me what that entails. So if I came in and right now and I had a cataract, what are you assessing microscopically to make it? So I'm getting the impression not everybody gets the same lens.

No, they do not. And some of these lenses are expensive and they involve the patient having to pay some extra money to get.

And more money gets you what?

I mean, I think the more money people pay, the more spectacle independence they get. In terms of optical quality, all the lenses are.

How much does a lens cost? Or pair? I guess since you're doing both.

I mean, I'm the wrong person to ask. Honestly, I don't even know.

But directionally, like, if somebody has to pay out of pocket for one of.

These, if they're getting just like regular cataract surgery and there is no attempt to get rid of spectacles, it's probably going to be completely covered by their health insurance.

And if they're saying, I want to go premium all the way, get rid of my.

It could be thousands of dollars out of pocket if they want to get rid of all their spectacle dependence. And what patients will tell us is they'll say, well, what else do I use every waking moment of my life forever? They could go on a vacation for a week or two and spend that money, and then the vacation is over. But we find that patients value, as we pointed out earlier, their vision. They value it pretty highly. And their independence, I think, is really what they're trying to preserve.

This is amazing. I had no idea that when. Look at how much. I didn't know. I didn't know you were. I literally. This is how dumb I am. I thought cataract surgery is literally removing the sort of crud that's in the lens. And I don't know. I just naively assumed it would, like, the good stuff would grow back. I never knew you were putting another lens in, let alone that you could actually use the new lens as a way to correct other visual defects.

That's right. And the technology has evolved to the point where you can actually correct those spectacle requirements. Now, many of our patients don't really care about spectacle independence. They just want to see well. And that's easy to achieve as well. But as these lenses have gotten better, our capabilities have gotten better.

If I needed cataract surgery today, knowing my diopter, the minus 4, minus 3 business with the slight astigmatism, although I still haven't figured out how that's impacting my vision, I guess I sort of have it just. But we'll come back to that. If you were going to swap out my lens, would you be able to correct the deficit of my magnitude?

We could, yes. Yeah. Now, the problem with a lot of these eyes is they are attached quite firmly to people. And sometimes the patient's set of expectations can be unrealistic in terms of what we can deliver. And so we have to really carefully educate them on, well, what can these lenses actually do? Am I going to see, like, a perfect hunter at dusk while still being able to read up close? And maybe the answer is yes, maybe the answer is no.

And can you tune it? Like, for example, if I said, stephen, look, I don't care if I have to keep wearing contacts. I would love to not have to wear reading glasses. Because if I'm going to be honest with you, the reading glasses are a way bigger pain in my butt than contacts, because I just put my contacts in in the morning and Take them out at night. It really doesn't faze me. The reading glasses annoy the hell out of me because I never remember to bring them to rest restaurants ever. So I'm shining a phone light at my menu and putting it out here. Or I'll be reading the book to my kid at night, and I'm like, oh, hang on, buddy, I gotta go get my glasses. Like, that's actually more of an imposition on my life.

Yeah. It's not an unusual request where we can intentionally set your vision for near or leave it for near. You can certainly do that. It's just an optical calculation to set the point of focus where you want it to be. You asked earlier about, well, what happens if I come into the clinic? What gets measured? Well, one of the first things that we have to do is make sure that the surface of the cornea is tuned up from a dry eye standpoint. Because those dry eye patients, the surface of their corneas, it's not optically pristine. It's a little distorted.

Do contact lenses make that better or worse?

It makes it a lot worse. And it can throw off our measurements, which can throw off our calculations. Because it's kind of pretty simple Newtonian physics. Right. If you know the length of the eyeball and you know the curvature of the front of the eye and you know the index of refraction of the stuff that's inside the eyeball, how bendy the material is light bendy the material is. You can correct for as long as you know where the implant lens is going to reside, you can correct for placing that image on the retina.

So the more perfect the shape of the cornea, the better that calculation.

That's right. And that is probably the weak link in the set of measurements that we take, because we can measure the length of the eye from front to back very accurately with lasers. So we can sort of. It's almost like a sonar, but with light. We can bounce a beam off of the back of the retina, and we know exactly how long the retina, how long the eyeball is, and we know roughly where the implant lens is going to rest when we put it in. And if we know some other dimensions of the eye and use the front curvature as one of our pieces of data, we can predict what power implant lens to put in.

Wow. Okay, so is there anything left on the IOL front or is there another huge step function of technology that's going to be coming there? Because it doesn't. I. It already sounds pretty remarkable.

Well, in the mid-2000s, I started getting involved in product design for a type of implant lens that could actually zoom focus front to back. Not a bifocal or a trifocal, where you had different zones of focus, but a lens that could actually move or change its shape. And I developed an implant that we put in humans in multiple clinical trials outside the United States. And we found that we could zoom, focus, kind of like the human lens would. But the multifocals, which are the lenses we've been talking about, like bifocals, trifocal implants surpassed the capability of what we could achieve with the lenses that I designed. And until someone comes out with a focusing implant lens that can zoom focus with the same degree of power as the bifocal and trifocal implants, it's not going to be successful. But if we had a lens that could change its shape or change its position and zoom focus seamlessly from near to far, that would be a game changer.

I assume that there's no. You don't take the lens from a young person who's passed away and ever try to implant that into. No, it doesn't work the way a cornea does, for example.

That's right. That's right. In fact, if you violate that capsule of the lens, the lens immediately becomes cloudy. So here's an example. Let's say that you talked about trauma. So a typical scenario is somebody is working with a weed eater or whatever, a weed whacker, and a shard of rock or glass or something goes through the cornea and embeds itself in the lens. And it might even be an optically unimportant part of the lens. Maybe it's off to the side. But once that capsule has been pierced, inevitably lens protein starts leaking out. Inflammatory cells become.

Yeah, you violated the privileged site.

It's no longer privileged. And within days, you start to see a cataract.

And they need a new lens.

They need a new lens for sure.

Do they need a new cornea, by the way?

Well, they sometimes do, but oddly enough, sometimes an object will pass through the cornea, and because it's traveling at such a high velocity, it's usually sterile. And it'll go through the cornea and embed itself in the lens or the iris or wherever. And some of these objects can be left alone. But if the cornea has been damaged sufficiently that it's no longer able to transmit a clear image, then it has to be replaced.

Wow. So let's talk a little bit about corneal pathology. So everyone's probably heard about corneal abrasions. That's a very important reason I remember. It's one of the few things I remember right. In surgery, you always tape the patient's eyes shut because you don't want an eyelid flipping open in the middle of surgery and nobody's paying attention and a drape is running over the eye and scraping the cornea. Is that the biggest insult that we think about for the cornea?

I mean, that's probably one of the more common ones. If you think about that eye that's being left open in surgery while a patient is asleep and not blinking, that's sort of the extreme version of dry eye where the cornea has completely dried out. And even if you didn't abrade the cornea, those epithelial cells would be so damaged by exposure, just by not being continuously bathed in tears, that they would be severely damaged. So dry eye is intimately related to corneal abrasion because you lack the lubrication that normally takes place to prevent that type of thing.

And how much of an issue is that in our dry society? Yeah.

Oh, it's enormous. It's. I mean, it's. If you think about the things that.

Cause dry eye, I mean, there's obviously lots of medications that do it through cholinergic side effects.

Absolutely. But think about all the antihistamines. Hormonal influences are profound in terms of dry eye. Anything that causes dry mouth can also cause dry eye. In that sense, autoimmune conditions can cause dry eye. So Sjogren's, rheumatoid arthritis, all of the connective tissue diseases have a dry eye component to them. Perturbations of thyroid metabolism cause dry eye. But a lot of women suffer from dry eye because I think it's mostly the influence of, honestly, a lack of testosterone that is probably most intimately linked to dry eye. But we see women on hormone replacement therapy that have miserable dry eye.

So you think the addition of estrogen and progesterone postmenopause could be an issue, or do you think it's still just the lack of testosterone that you.

I think it's the lack of testosterone.

Why do you think that?

I think it has to do with the health of the epithelial cells on the conjunctiva. But there may be also influences on the secretion of tears from the lacrimal gland as well. But dry eye is. I mean, it's. I don't want to say it's universal in patients who are over a certain age, but it's Extremely common.

What type of eye drops should we be using? How do we apply them?

Well, it really depends on the type of dry eye that you have, believe it or not, because there are. We think of tears as just salt water, but that's really not what it is. It's really an emulsion of lipids and mucin and all sorts of immune modulators and antibodies and all sorts of things in this soup. Some of it is just what we refer to as the aqueous component of tears, really just the salt water. But the sebaceous glands that are in the eyelids, we call them meibomian glands. At the little where the lashes come out of the skin, the secretions of those meibomian glands can become dysfunctional. And that means that the tears have a hard time gliding over the surface of the cornea, and that can lead to dry eye. So all sorts of things that cause meibomian gland dysfunction. Some of that relates to diet, and some people believe that a diet high in saturated fats is more likely to cause meibomian gland dysfunction. Certainly colder weather, like the sebaceous glands in your skin respond better to sunlight, to heat. In a cold environment, those can become plugged up, and bacteria can build up along the eyelid margin, causing inflammation. And when there's inflammation, the lacrimal gland shuts down even more. So dry eye is really multi. It's got a number of different causes.

Now, when I think about eye drops, I think about sort of the dropper that you try to get in your eye, and you can never get it. At least I can never get it in my eye, but. Because I end up blinking all the time. So then I. You try and drop it into your.

Into the corner.

Yeah, the corner. And then let it sit. But then I've also seen, like, the mist. Right. So tell me about the different ways that one even applies.

Yeah, I think those are really the main ones. I mean, eye drops work pretty well for most people, and. But there are some mist sprays that, believe it or not, you can spray some of these. There's one hypochlorous acid compound that you spray on the lids, and it sort of migrates into the eye and actually is very good for reducing the bacterial counts at the lid margin, which is part of that inflammation cycle that is so critical in dry eye. But most artificial tears come in the form of an eye drop.

And that's okay.

That's fine.

And it's okay if you can't manage to keep your eye open, or should you force it and hold your eye open.

I mean it's you, you gotta, at some point you gotta get it in the eyeball. But that's one of just a whole bunch of strategies that we use for treating dry eye. We add artificial tears, but we think that there's a very significant benefit from supplementing with omega 3 fatty acids. Especially high doses of omega 3 fatty acids and omega 6. Certain types of omega 6.

Yeah. Which omega 6 is it again?

That's what you'd find in blackcurrant seed oil or borage oil or evening primrose oil. That's the GLA gamma linoleic acid. So that is very helpful in dry eye. And interestingly, there was a very large randomized clinical trial looking at omega 3 supplementation in pretty high doses.

Do you remember how high?

3 grams.

Wow. Of actual of EPA NDA tract.

Correct. Yes. And the placebo arm was olive oil, which is presumed not to have a benefit in dry eye. And it showed no superiority of omega 3 compared to olive oil. However, there's been a lot of criticism of this study. It's called the dream study. It was put on by the National Eye Institute. It turns out that if you bring people into the eye doctor four times a year, everybody gets better. Their compliance with artificial tears gets better.

And were they using artificial tears?

They were. They were able to use whatever they would normally use to treat their dry eye. So I guess like in the same way that if you go to the dentist four times a year, all of a sudden you're flossing before you go to the dentist. Both arms of the study got better. But it is our very strong clinical impression that omega 3s in high doses help with dry eye primarily from I think an anti inflammatory standpoint.

Let's go back to light for a minute. So I've got some friends who are so fanatical about the importance of light that they never wear sunglasses. And I'm kind of. There's a part of me that thinks light is. Wow, it's got to be really important. I think about all the time I get outside in the light. It's great. It's great. But I also like wearing sunglasses because there's a part of me that's sort of afraid that too much UV light is damaging. So what's the balance of sunglasses versus not? And I want to talk about polarized glasses. Do they matter and all that kind of stuff.

Yeah, I mean, clearly there's a dose related phenomenon here. Too much light is bad, too little light is bad. What's the right amount. I tend to recommend sunglasses for our patients. Let's start with just the most obvious one. The most common site of skin cancer, the lower lid. Lots of basal cell squamous cell carcinomas. Sunglasses certainly reduce the incidence of that. Then we look at the photo aging of the lens itself. I think it's not a bad thing to delay the onset of cataract and then the retina macular degeneration. I think there's pretty clear evidence that UV exposure, particularly of the magnitude that you can get outside, is associated with an elevated risk of age related macular degeneration.

Now, do we see this in hunter gatherers who have otherwise amazing habits and therefore tend to be relatively privileged from optical pathology?

So the confounding variable there is that northern European ancestry is a risk factor for macular degeneration, probably because of the lack of pigment, because that pigment is protecting that very vulnerable vascularized component of the back of the eye.

Oh, wait. So the darker your eye, the more protected you are?

Absolutely. In the same way that your skin is more protected with more melanin. So light eyed patients have more light getting in from the front of the eye.

So their iris literally blocks less light hitting the lens.

Yes. And the retina has less pigment behind it. And so the vascular supply to the retina is more exposed to, to UV light. And that's the way it's evolved because they've been in environments that don't have as much light available. But if you live near the equator or your ancestry is from that area, then you're going to have more pigment from an evolutionary standpoint. But I understand the fanaticism about wanting to have lots of blue light or bright light, but I think that it probably is fanaticism. I don't think that, you know, at least if your goal is to reproduce, teach your children until they're 15 and then die, then get all the light you want. But if your goal is longevity or the postponement of senescence, certainly ocular senescence, I think it makes sense to protect your eyes from UV light.

So, for example, like let's. So you, you came over here today where it's middle of the day in Austin. It's a typical Austin, beautiful sunny day. You're driving with sunglasses for sure?

Absolutely, 100%.

Okay. You're in sunglasses when you're outside after what time in the morning?

If I'm outside and the, and my vision is better with sunglasses, it's not worse with sunglasses than I'm going to wear sunglasses. I Don't wear them at night and I don't wear them, you know, if it's very early in the morning. But if conditions allow, I'm going to wear them.

We talk about with sunscreen the importance of you're still susceptible to sunburn in the clouds. Right. If you're at the beach all day and it's kind of an overcast day, you can still. Do you recommend people still wear sunglasses even if it's not a clear blue day?

For sure. And sometimes, you know, this kind of came up during the recent eclipse because, you know, people were saying, okay, I'll look at the eclipse, this one was a few years ago, I'll just use sunglasses. Well, that's actually much, much, much, much worse because your increasing the aperture of your pupil because everything is dim, but you're letting through all this very damaging light.

Because no amount of sunglasses could block a straight shot looking at the sun.

Correct. So I think even on a cloudy day, I do recommend that people wear sunglasses.

Okay, what are polarized glasses doing?

As you know, polarized lenses are essentially, it's a lens that has a bunch of lines drawn in it all in the same direction so that some of the light is blocked. But in one meridian, all the light effectively is let through, but perpendicular to that, none of the light gets through. And polarized lenses have some pluses and minuses. One of the big minuses I found is that a lot of the displays in your cars now you get this really messed up cross polarized effect where the light coming off of the screen is polarized. And if you look at it through polarized glasses, if you tilt your head, it gets.

You can actually not see it.

You cannot see it. And by the same token, many of the windows or winds, I don't know if it's the windshield or the side windows, but I've noticed wearing polarized lenses, which I only wear for fly fishing now, that I would get these very weird effects by tilting my head because of the cross polarized effect. Essentially you have two different polarized filters and it's letting through variable amounts of light bending depending upon the orientation of your head and your eye and the spectacles.

I have found myself more comfortable in non polarized lenses. Unless I'm on water.

Yeah, I think the issue there is that the light bouncing off the water, or theoretically a highway, it's all. Pretty much a lot of it is polarized in one direction. That's the rationale behind polarized lenses. And for seeing a fish, if you're a fly fisherman, for sure, that's helpful.

I fly fish for the first time last month and I could see getting into that. That is an art.

For sure, it is. But in terms of polarization, there's no evidence that I've seen that polarization versus non polarization in sunglasses helps. It's really the UV filter that is helpful for what we're doing. In terms of protection of eye health, you could wear clear spectacles as long as they had UV protection and still achieve the benefit of sunglasses.

Yeah, that's an important point, right?

It's not the tint.

It's not the tint, it's the ultraviolet protection. And it's the same as true in a car, right? I mean, the glass of the car is, assuming you don't have tinted windows, is still getting rid of most of the UV light.

Most of the uv, but not all. So you will see, and dermatologists tell us this, that in truck drivers who are in North America, they see more UV damage to the left side of their face than the right side of their face by far. And in the UK it's exactly the opposite. So even car and truck windows let some UV light in.

Okay, so let's now go back to the standard situation of nearsightedness. So person comes in, they're nearsighted. Decision one is, I'm going to correct this with glasses versus contacts. We'll start to talk about corrective surgery in a moment. Do you nudge people one way or the other? I mean, I wore glasses for the first four years that I needed corrective lenses. So that meant basically college, trying to think in med school. I think by med school I was wearing contacts. By residency I went back to glasses because the call, you just couldn't be predictable about when you were going to put them in. So I did all of residency in glasses. And then since that time I've been 100% contacts.

Yeah, it's funny because we'll see residents or fellows or whatever, and they come in and on their one day off and they're seeing one of our optometrists. And when did you last have your contacts out? And they're like, I think it was June 30, right before my internship started four months ago, that sort of thing. And so as you know, residents are notoriously bad about their own health hygiene because you're so busy. But to answer your question more directly, I don't really see patients for regular eye exams myself. So the people who see me are seeking surgery already. But in terms of, hey, I'm at a cocktail party and someone says, should I wear glasses or contact lenses or spectacles? Like. Well, you know, the safest thing you can do is wear spectacles. For sure.

Wait, do you use glasses and spectacles interchangeably, that term?

Yes. When I say spectacles, that's why I thought so.

Yeah.

Referring to glasses to distinguish them from stuff you drink water out of. So, yeah, spectacles is the term of art for glasses. Yeah. Yeah. You were thinking it's some sort of exotic type of.

Yes, I was like, oh, there must.

Be mounted spectacles, but then there's a spectacle down at Ye Olde Spectacle Shoppie, something like that.

Anytime my wife talks about pushing the gas pedal, I'm like, throttle.

It's a throttle.

Throttle application.

We need some gas. No, we need petrol. Okay, right.

It's gasoline or petrol. It's not gas. Gas refers to natural gas. When you push that thing, it's throttle application. Yes. Okay.

No, yeah. We're hard to live with, aren't we?

Yes, yes.

Okay. So spectacles and glasses are synonymous. That's the safest thing you can do. They're going to work every time and there's essentially no risk associated with them. There's a big debate about what the next safest thing is. Is it contact Lens wear for 10 years where you might be susceptible to infection, or is it laser vision correction? But I tend to say, if you're doing fine with spectacles or contact lenses, do that.

I was kind of hoping you were going to tell me get laser eye surgery, because there's a part of me that just wants to do it for the sake of doing it and getting rid of contacts once and for all. But you were very much in the camp of you asked me a bunch of questions and at the end your conclusion was, these don't seem to be an inconvenience for you. You've never once had an eye infection. You tolerate them really well. They don't seem to bug you.

Right. And you like your near vision. Yeah, yeah. And so if you were to correct your distance vision with laser vision correction and set both of your eyes for distance, you would lose that near vision.

Until maybe I get my cataracts fixed.

That's right.

Then we can tweak it.

That's a whole other. That's a whole other story.

Right. So let's talk about the advent of laser eye surgery. So I think everybody listening to this has heard of lasik. Most people probably haven't heard of prk, which we'll talk about. When did PRK Came along first?

Yeah, a little bit earlier. Yes.

And that was when. In the 90s.

Right. So the approvals for PRK and LASIK were in the mid-90s, 1995, 1996. The first procedures were actually done in. And the first procedure was prk, and it was done in New Orleans. And I happened to be in training there in New Orleans. And this was performed by a physician called Marguerite McDonald, and she did the very first treatment on a human eye. The way this came about was that excimer lasers, which are the kind of lasers we use in LASIK and in prk, which stands for photorefractive keratectomy. Excimer lasers are and were used to etch microchips. And an engineer at IBM realized that you could change the curvature or you could make cuts in human tissue. And because of the nature of this ultraviolet laser, there was essentially no bystander trauma to the adjacent tissue, so the tissue could be etched or cut. And because it generated no heat, there was no immune response generated, typically, so that these incisions, or whatever it was, they would heal without scarring. And I can remember vividly looking at the very first patients that were in an FDA clinical trial that had prk, and I was astonished that you could look at them under a microscope and you could not detect that surgery had been done. That was really a revelation for me where I just saw these eyes that looked like normal eyes, and the only difference was the patients could see. So the first eyes were treated in 89, and then that led to FDA approval in 95.

And the treatment in 89 is part of clinical trials. I'm assuming for sure it was part of a clinical trial. So let's explain what PRK does before lasik.

Yeah. So the way it works is that you have the cornea again, like the glass on a watch, the thing a contact lens would sit on. And let's say that the person is nearsighted. The cornea in that person is a little bit too steep to focus the light perfectly on their retina. Another way of looking at it is.

And again, the cornea is about 2 millimeters thick. No, the cornea is about half a.

Half a millimeter thick. It's about 500 microns, maybe a little more. So either the cornea is a little too steep or the eyeball is a little too long, probably a little of both. We can't change the length of the eye.

By the way, the length of the eye is the one that we talked about being somewhat malleable during development.

That's right.

And is the corneal shape hereditary? Is that the hereditary component of vision?

The corneal shape doesn't seem to change that much throughout life. It's the length of the eye that changes, unless there's a pathological condition that changes the cornea. So since we can't change the length of the eye, what we can change is the curvature of the front of the eye. And if you think about it, you don't have to change the curvature that much. Think about how thin a contact lens is.

How thin is a. I mean, I know I can feel it, but I don't know what that. Is that also about half a mil?

No, it's less. I honestly don't know. I don't work in that world. But it's pretty thin. I mean, it's like a little piece of cellophane. If you think about like an ACU.

View disposal, it probably just feels thicker because of all the goo on it.

Yeah, it's. So I don't. I'm sure someone will correct me and say, you should know how thick a contact lens is. I don't. But it's thin, right? It's pretty thin.

Yeah.

So it's just that little curvature that needs to change in order to focus the light on the rev.

And just to use an extreme example, so you take somebody who has a very minimalist degree of nearsightedness. So let's say their diopter is minus one. And then you contrast the lens that they would wear to the lens that someone who's near blind at like a minus 10. Is the minus one creating more of a bend or less of a bend? Meaning is it a bigger curve or a smaller curve?

So the person who's minus one, their cornea is less potent in bending light than the minus 10 person. Is that minus 10 means their eye is 10 units too strong. And we need to reduce the power of the eye. So how would you fix that with a laser? Well.

Well, first of all, how do you fix that with the contact? So their lens has to look.

The curvature of their. Of their lens, of their contact has to be effectively flatter than their eyeball. So you need a larger radius of curvature or a flatter eye.

I got it. Okay. So you would actually build up the outside of the lens.

Exactly right.

Okay.

So it's even easier to explain with laser vision correction. So let's take a crude analogy, which is that the cornea is made out of wood. And I have some sandpaper I can sand down the center of the wooden Cornea and take the plant off and I'm removing some sawdust. Goes away now that that is flatter and so it's less powerful in bending the light. And I can focus that on the retina. So in your minus one example, we would remove about 20 microns of tissue. That's not a lot. You figure a human. Human hair is about 50 microns, so like less than half of one human hair's thickness.

And PRK does that directly with an.

Excimer laser on the very front part of the cornea. So we. The way we do it is that the very front coating of the cornea is called the epithelium. It's a very thin layer, kind of.

Like how thick is the epithelium there?

It's about. Again, about 50 microns, something like that. 50, 55 microns. So it's got a basement membrane, but it's about. Call it 50 microns. So we remove that layer of cells with. The way I do it is with a solution of some eyedrops of alcohol and it just sloughs right off and it grows back.

Just like isopropyl alcohol.

Yeah, you could use that or ethanol.

You've anesthetized the eye before doing that, obviously.

That's a practice builder. Yeah, thank you for that tip.

How do we get the. Repeat this. Why?

No, the eye first. That'd be really good.

Yeah.

So you anesthetize the eye and then you put some alcohol solution on the front of the cornea. You remove that epithelial layer which is going to grow back in the same configuration. And then you use a very carefully calibrated laser to change the shape of the cornea.

Again, dumb question. The laser's coming at what angle?

It's essentially effectively perpendicular to the cornea. So the patient's laying down flat, they're.

On their back, and you put something into. Why are their eyes open?

We're holding their lid apart.

Are they sedated?

I mean, I honestly give people Valium because it's just sort of an intimidating minute. You know, it only takes a minute.

Here's what my fear would be in doing it is like my desire to blink would be so overwhelming. I'd break the little eye barrier. Of course, I wouldn't, but I'd end up moving my head and you'd zap the wrong part of my eye and I'd be blown away.

That's everyone's fear. You know, it turns out Valium is undefeated. It's just a question of how much it's a very good drug. But to address what you, you brought up several things there. First is a lot of patients fear that they'll do something to goof up the surgery. And there are a number of reasons why that really can't happen. But let's go through the procedure from the beginning. Long before this patient ever laid down on this gurney to have this laser treatment done, their eye was digitally mapped using what we refer to as a wavefront sensing device. So think about this. We send in a very narrow beam of light with a laser, and we look at how it bounces back from the cornea. It bounces back in a distorted fashion. So we send an ideal ray of light in or multiple rays of light in, and they bounce back in a distorted fashion. The amount of that distortion allows us to map.

So you do a topo.

It's much more than a topographical map. It's the entire optical pathway of the eye, from the retina to the back, all the way to the back and front. So we look at the entire distortion pathway and there's more than one way to do this. By the way, there is a topography based way to do this as well, which is very effective. But the one I'm describing to you is sort of the easiest one to think of. We send in a known uniform beam of light and look at how it bounces back from the back of the eye. That tells us what are the distortions present in this eye, how much nearsightedness, how much farsightedness. But also all of these physics terms.

Of we didn't do this in me, right? You only do this in someone who's going to be a candidate.

We may have done it in you just for grins. We diagnostically, this is part of our workup for laser vision correction. And we look at how this particular eyeball, Peter Attia's right eye, distorts light as it goes through the optical pathway. This technology was developed for telescopes that have to contend with atmospheric distortion. So the way this works is that telescopes, and I'm talking about like Keck and the best ones in the world, they send up a diagnostic laser into the atmosphere. And the distortion that that laser is encountering is adjusted for in real time with a deformable mirror, a very thin mirror, and that allows them to essentially correct for the distortions of the atmosphere in real time. And those are constantly changing. We have the benefit of not having to deal with real time evolving distortion. But we can take a snapshot of what are the distortions of Peter's Right eye. And then we can build them into the laser vision correction that we do on Peter's right eye. Part of doing that means that we have to be able to track your eye. So we have to lock onto and register your eye with the equipment and any movement that you make. Part of your fear was, I'm going to mess it up. Well, the laser can track far more rapidly than you can move your eye.

So while you're doing this patient's eyes can be moving.

They can.

And it doesn't matter because the laser is moving.

I mean, it's sort of annoying when they, you know. So we tell. We coach them, hey, look at the flashing light. But that's really just to keep them in the ballpark of where the tracker can lock onto them.

But I like knowing I'm not the only one that has this ridiculous fear.

It's not a ridiculous fear. Blinding himself, first of all, not a ridiculous fear. Secondly, it's universal. When I say to patients, hey, I'm not going to let you do anything to mess this up, they're like, thank you. Thank you for saying that. That was the thing I was worried about, because you don't want someone to laser your eye. And you looked off to the side. Oh, disaster.

Not only are you blind, we also gave you a brain tumor.

That's right. So the laser will not fire unless you are within its range of tracking, and it will move faster than you can move.

So PRK is. I like your analogy. Basically changing the shape of this via the mechanism of, like, it's not sanding it off, but it is.

It's vaporizing the tissue.

It's vaporizing the tissue.

And it's a laser that's sort of scanning around the cornea where it does a little treatment here. And then we know thermally that we don't want to do another shot right next to that one. So we move over here, and we want to let the tissue cool down for a few milliseconds. And then we go over here. So the laser dances around.

How many minutes approximately does it take? Does it take longer? The worse the prescription is? Yeah, more to shave.

So like minus two, it might be 15 seconds, you know, that's it. Yeah.

So minus 10 would be how long?

Like a minute or so, you know, Depends on the laser. It depends on the overall treatment size. How much astigmatism.

Oh, you're fixing the astigmatism as well.

And all the little distortions. How much coma trefoil. These are physics terms that I didn't really think I would become fluent in, but all these little optical distortions that optical physicists are very familiar with, we measure and do our very best to eliminate with laser vision correction.

So the whole procedure is what, half an hour by the time you put this thing in the eye. Put this thing in the eye, give them their volume for prk, two or.

Three minutes plus the Valium time.

So take your Valium an hour before.

Or maybe it's. Yeah, it's like half an hour. We have them chew it up, and then it works pretty quickly.

Okay, so talk about the recovery from prk, because one of the things I remember you saying when I was sort of humming and hawing about this was the biggest drawback of PRK is the recovery takes longer. But you otherwise, I think, really talked about PRK as the gold standard.

The only reason I might have said gold standard was that it came first. It was the first procedure. And if you look at PRK and lasik, which we'll get to in a bit, if you look at those procedures, say 30 days later, they're indistinguishable in terms of results, but the LASIK patients get there way quicker. So prk. Now I've removed your epithelium. So now you have this, let's say it's a 7 or 8 millimeter diameter area of your central cornea that has no epithelium. No epithelium. That's like having a big corneal abrasion, essentially. Luckily, we have drugs, drops that can reduce the feeling of the foreign body sensation dramatically. So we put those drops on the cornea, put a contact lens over the eye, like a band aid. It's really like a. Like a, just a regular soft contact lens. And then the epithelium begins to heal from the outside in.

That takes 30 days?

No, that takes about four days. But here's the thing. It's like if you were to have a cut on your arm, it would heal over, but you'd still be able to detect where that cut was because those cells have not fully remodeled themselves. So the cut heals over, or the defect in the epithelium heals over in about four days, maybe less.

And then you take the contact lens off after four.

You can take the contact lens off then. But the vision is still not perfect yet because those cells have to reorient themselves like a bunch of orderly bricks in a brick wall. And when the cells first cover that defect, it's a very thin sort of disorganized layer of cells that have accomplished their mission of sealing the defect and preventing you from being susceptible to infection, which is their job, to quickly cover the defect. But then the body can turn its attention to reorganizing those cells in a.

So you do one eye at a time.

Obviously not with PRK or lasik. No, because the level of vision, typically we do both eyes on the same day, because the level of vision is probably about 2030 or 2040 within a day or two. So when I say the visual recovery takes a while, you get pretty good, pretty quickly, but that last little bit takes several days. So you probably could drive a couple, maybe two, three days later, but you wouldn't have 2020 vision at that point.

So, Lasik, the only thing I know about that is there's a flap involved. That's right. So presumably you're not shaving off the epithelium, you're cutting a flap. And how much of that tissue you take off determines the shape of the new cornea when the flap comes back.

Right. So the laser that does the vision correction, all the little distortions, the nearsightedness, the astigmatism, that's all the same laser. So that part of the procedure is identical. But instead of doing that on the surface of the eye, now we're using a step before that, where we create a flap in the cornea using a different type of laser. So we use a femtosecond laser to create about a, let's say 100 micron flap. So we are now under the epithelium.

So you've taken 20% of the cornea up.

That's right, about 20% of the cornea up. And now think of it as in our analogy, where you were sanding a wooden eye before. Now think of the cornea as a book. And in PRK, I'm removing the first 10 pages of the book.

Here are your.

Now I open it to page 100 and I'm taking out 100 through 110, and then I close the book. The beauty of LASIK is that because that tissue removal is sequestered under that flap, the body doesn't perceive that anything has been done. So it's very typical for patients who have lasik to be 20, 20 the next morning. And so that's the appeal of that procedure.

And that's why LASIK was developed post prk, presumably as a way to get around the healing process of prk.

Yeah, that was sort of a technological race, and the way it developed was interesting, and some of it was in pursuit of more rapid visual recovery.

So what percentage of corrective eye surgery in the United States today is PRK versus Lasik? I assume the lion's share is Lasik.

Yeah, I think it changes, but it's probably about 80 to 85% Lasik. And not to confuse things, there's another procedure called smile, which has a very small but perhaps growing segment of the market. And we can talk about that in a sec. But the lion's share of it is lasik, and there is but a significant chunk prk.

Are there more risks in LASIK than prk?

Well, the risks are different because the risks of infection with LASIK are lower because you don't have the.

You don't take the epithelium away.

That's right. But you introduce another step in the procedure where you now have a flap, and that flap can, you know, if it's not performed correctly, that can lead to problems. I think there is a little bit more dry eye issue with LASIK compared to PRK as well. Because when you create that flap, the way tearing works is that a signal from the front of the eye goes to the lacrimal gland, which then secretes tears. If you create a flap, you temporarily sever some of the nerves that are sending the signal, and eventually, over time, those nerves typically regrow back and you reestablish that feedback mechanism. But I think you get more dry eye with LASIK than with prk and for longer. That is a controversial statement. There are people who have data to show that they're equal, but I think they both result in temporary dry eye in most patients. Some patients have dry eye for really long periods of time after both procedures. But the majority of patients are kind of back to their baseline in about probably 60 to 90 days.

What about night vision or low light vision?

So that's fascinating. In the early days of lasik, nprk, the weakest part of vision was night vision. And that was because the shape of the treatment that we did and the diameter that we treated was limited. So we couldn't really treat the peripheral part of the cornea. That comes into play when your pupil gets big. So if you are treating a central part of the cornea that is smaller than a big pupil at night, you're going to see halos from that untreated peripheral part of the cornea. Over the last, like, I don't know, from the 90s to now, the treatment beam patterns have changed to address that issue and to treat that peripheral cornea differently. So now night vision complaints, we find to be pretty unusual with laser vision correction.

Is there a difference in the cost of these procedures for us?

No, but I'm sure there are some surgeons who charge more for one than the other. The added step of LASIK adds some cost, but PRK has more post operative care, frankly, because it requires more visits to see these folks. But we price them the same.

And how much does it cost, by the way? I mean, it's probably come down a lot in 20 years, right?

You know, I don't think that it has. I think it's been pretty stable. I think it's probably about a couple thousand dollars per eye is about the average in North America that you'll find.

What are the exclusion criteria? Like who is not a candidate for either one?

Yeah, there are certainly contraindications, some of them relative, but some of them are absolute. I'll give you an absolute one. There are conditions of the cornea where the cornea is biomechanically unstable, where the cornea is actually has a tendency to bow forward in a pathological state. And that means that the cornea, it's a moving target, essentially. So further biomechanically weakening the cornea makes no sense. And doing either procedure would do that. There are patients who have irregularities in their astigmatism that cannot be measured or corrected with any laser vision correction. There are patients that have certain autoimmune diseases that maybe render them as poor candidates for laser vision based on the.

Risk of healing or based on the.

Risk of healing or perhaps just the overall health of the eye. And that sort of extends to people who have other eye diseases like cataract or maybe glaucoma or retinal pathology. You are typically operating on healthy eyes when you're doing laser vision correction. So if there's some other issue involved, you might not be a candidate.

And is there anything that like. Well, I guess given the differences you've explained, why are 15% of people still opting for PRK?

Well, there are certain patients where that's a far better option. So we talked about how you're removing pages from a book. Well, what if you have a really deep treatment that you need to do and the book is sort of thin to start out with. Maybe it's better to begin on page one than to begin on page 100.

So the stronger the diopter and the thinner the cornea? That might move you more towards prk.

Sometimes the thickness of the cornea will dictate it. Sometimes it might be related to someone with pre existing dry Eye. And we're thinking, well, we have data that these two procedures are about the same in terms of dry eye. But our clinical impression is that LASIK makes them a little drier. So maybe let's do PRK on this particular individual. There are, There used to be some restrictions in branches of the military, and.

Remember that you couldn't have a flap in your eye if you were a pilot.

That all went away. So pretty much every. All the aviators and pilots can now have LASIK or prk. In fact, the military is one of the largest providers of laser vision correction now in the United States. But there are a couple of holdout Special Forces branches where they don't want you to be a. I think maybe an Army Ranger. And that has to do with getting poked in the eye and the possibility that a flap could be damaged. And some of this is sort of vestigial lore, and it's hard to change.

The military's rules, but they'll just say PRK or nothing thing.

Yeah, but that's. I'd say that the overwhelming majority of the branches of service allow either treatment, and certainly all the commercial airliners, they allow PRK or lasik, but with the caveat that you have to get to the point where you can pass the flight physical. So. And the same thing's true of people who want to be pilots or aviators. They, if they need to have 2020 uncorrected vision to be a pilot, they have to have 2020 vision after laser vision correction.

Is it pretty much a given that you can at least get someone to 2020 after laser corrective vision?

I mean, the way the lasers are built today, it's typically the case that you can get them to 2020 or better than 2020, as we were describing before.

And if you take them to 2015 and they have presbyopia to begin with, does it get any worse, or is it just that now they're. They're noticing it all the time because they never get a break from it. They never get to take their glasses off their spectacles, so to speak.

Well, you know, if you nail it perfectly so that their prescription is 0.00, I think their distance vision will be phenomenal and their near vision will be whatever it is, based upon their age. So if they're 50 years old, they're probably going to need some near correction, some spectacles for reading. If they're 41, 2, 3, 4, maybe even 45, they may not need glasses for close up.

And then you mentioned this smile procedure. I Haven't heard of that. What is that?

Yeah, it's an interesting procedure. It's using a single laser, a femtosecond laser. And this is. I want to go back to the book analogy where we opened the book to page 100. Well, imagine if you could somehow create a little tunnel down to page 160, snatch out pages 100 through 110 while keeping the incision really tiny and perform it through a very small keyhole procedure. That procedure has gained some traction outside the US and in the US it seems to be an effective procedure.

What problem is it solving? Given how effective LASIK is, I would.

Say the problem it was designed to solve was dry eye. But I think the problem it really solved, especially outside the United States, was needing two lasers versus one. So maintaining.

And although you could do one with.

Prk, you could do one with prk, but then you have the prolonged recovery time. So the idea was, could you get lasik, like velocity of return of vision.

With a single laser? With a single laser, and maybe along the way reduce dry eye?

Yes. There are pros and cons to Smile. The technology is evolving. I have not seen any data that shows that Smile is in any way better than lasik or even equal to lasik, frankly. But it seems to be a very good procedure.

Are you doing anymore?

I am not performing Smile and doesn't mean that I won't in the future. And there are a number of competing second and third generation versions of Smile that will come on board, and if one of them ever rises to the point where I think it's better than what we're doing, we'll offer that.

We didn't talk about glaucoma yet. I know every time I go to an optometrist or even when I came and saw you, is that the one where you blow the air at my eye?

Well, that's sort of a.

That's just an intraocular pressure test way.

Of measuring the intraocular pressure that we don't use. But it has the advantage of not requiring the patient to be touched with anything. So you can indent the cornea with a known amount of force from an air puff and look at how it optically deforms the disadvantage to the air puff. And it's not really considered a. I don't think a gold standard of measuring pressure is that if you blink really quickly and squeeze, then you can have a false reading with that type of air puff tonometry, and we typically don't use it.

So how do you measure intraocular.

We measure it with two ways, both of which indent the cornea. Physically indent the cornea.

So that's why you anesthetize the.

After you anesthetize the eye with a known amount of force, and then you look at the amount of force required to cause a certain amount of indentation.

And what's the definition of glaucoma?

Well, glaucoma is probably about a hundred different diseases, honestly. But they all share the final common pathway of damage to the optic nerve, the nerve in the back of the eyes, the cranial nerve that you mentioned at the beginning that is somehow related to pressure. So a pressure related optic neuropathy. Now what's odd about glaucoma is that there are people who have totally normal pressures with relation to the population, but that pressure is too high for them and they can develop damage to their optic nerve.

And the symptoms of glaucoma, are they all this? I mean, is it always some change in vision? Is that what would bring someone to attention if they weren't getting a screening test?

It's funny, you just sort of like triggered a memory of mine. I had a patient, I was, I was in training years ago and I was explaining to a patient that, you know, glaucoma is totally, has no symptoms at all. You wouldn't notice it at all. And yet if we don't find it, it could be really bad. And the patient said, well, if it has no symptoms, what do I care? Like, what's the point? What I should have said was that it has no symptoms until the very end. So what happens is that your peripheral vision is damaged and most people will not detect a slight reduction in their peripheral vision, particularly if it's segmental. There's just one little area off to the side that they can't see see, particularly if the other eye is covering for that area. But as glaucoma progresses, it can affect central vision and then it becomes symptomatic.

How much of a problem is this in the United States, first of all, and then in the rest of the world?

Well, luckily, glaucoma has become much more treatable. So the pharmacological management of glaucoma has gotten way better. And there are numerous laser procedures that can treat glaucoma and what are referred to as minimally invasive glaucoma procedures, or it stands for MIGs, minimally invasive. Basically, the management of this has gotten way, way better.

What's the 80, 20 of this? 80% of them are caused by what? Basically, yeah.

So 80% of them are caused by what we refer to as garden variety chronic open angle glaucoma, which means that the glaucoma is not a function of the anatomy of the front of the eye being too crowded where the fluid can't get out. It's more a problem of overproduction of fluid inside the eye. And the pressure is too high inside the eye as well.

The vitreous fluid?

No, it's the aqueous fluid.

And what causes that? Is that endocrine? Is that. Do we not know?

We do not know. I think this has a multifactorial pathogenesis. There are certainly family history components to this, where we see it run throughout families, but it's not like inheriting.

Does this run in parallel with diseases like type 2 diabetes or is it uncoupled completely?

No, it's not really. Coupled with diabetes, there's some relationship to hypertension, blood pressure, but ocular hypertension, we refer to eye pressure being too high. You see it in patients who are not hypertensive at all.

Wow. The lifelong incidence is what I think.

You got me there. I honestly don't know.

But it's common or uncommon?

It's very common. Every eye surgeon sees glaucoma patients daily, multiple glaucoma patients daily.

So presumably, like any neuropathy, if you catch it early enough, it's fully reversible. And if you catch it too late there, you. You damage it. Or is it because this is not a central. This is a central nerve, not a peripheral nerve?

Yeah, I think it's. It's. You can arrest the progression, but I don't think you can undo the damage that has occurred. So once there's been optic nerve damage.

So it's not like sciatica?

No, I don't think so. I think once there's been damage, we expect that damage to remain. So it's not unusual for a patient to have what we refer to as a visual thing, field defect. So a little area missing from their field of vision, and our goal becomes to prevent that defect from getting any bigger. And you can typically do that once you identify it.

At what age does it start to become enough of a concern that we should be screening for it?

Yeah, I mean, I think everybody, when they go to the eye doctor for a yearly exam, gets screened for glaucoma. The appearance of the optic nerve is examined as well as the pressure, and those are probably the two most important things to look for with.

So if you're screening annually, you're you're.

Being checked for it.

You're in good shape.

Yeah, you're being checked for it. The incidence does go up with age. So in the 50s, it's much more important to pay attention to glaucoma and beyond.

And presumably in the developing world, where people aren't going to get eye care, or even in the United States, if people don't choose to get eye care or can't afford to get eye care, it's a bigger risk because they'll only present when they have symptoms.

That's right. That's exactly right.

All right, so to summarize, again, we think about kind of the longevity of the eye as a pretty important thing. Right. If you want to figure out a way to live to 100, we spend a lot of time thinking about, well, you've got to really, really delay the onset of atherosclerosis. You have to have a very aggressive strategy around the mitigation of cancer, Alzheimer's disease and all these things. But it's these other things, teeth, ears and eyes, that I don't think get enough attention. Right. I mean, you don't want to get to be a hundred and have no teeth, and you don't want to get to be a hundred and be deaf, and you don't want to get to be 100 and be blind.

Yeah, those all sound bad.

Yeah. So, I mean, the things I'm picking up, unfortunately for many of us listening to this, we can't go back and change what we did as kids. We can certainly make a change in our kids so we can make sure that they are outside in natural sunlight. I don't put sunglasses on my kids. Should I be doing that?

Yeah, I mean, probably. It's trying to get a kid to wear sunglasses is tough.

We got to come up with better toys. My kids love trains. So if I could figure out a way to tell them that wearing sunglasses was train like this would be good.

Yeah, it's tough. I mean, you see kids who are snow skiing, for example, and they should be wearing goggles because those have built in UV protection. So that typically works for that type of thing. But, gosh, when they're water skiing, they certainly can't wear glasses. If they're swimming, they can't wear sunglasses.

Although goggles these days are pretty good.

That's true. Yeah. It's hard to get my kids to wear goggles, but there's a certain amount of just UV exposure I don't think it's possible to avoid.

So the trade off is when in Doubt keep them out.

Yeah, Hats are important as well. We didn't really talk about that. That's a very good and effective way, but it's not enough because a certain amount of light bounces off and hits the bottom of your cheek and goes right into your eye.

So for those of us that are now adults, basically, we've kind of cast our lot with respect to that malleable period of changing the length.

Well, you know, we didn't really talk about what nutritional supplements might have some effect. And it's interesting because we know that with cataract that vitamin C deficiency is associated with an elevated risk of cataract. But it's been shown really conclusively that vitamin C supplementation to supranormal levels does not protect against cataract formation. And the things that have been looked at, I know A, C and E, basically antioxidants have been looked at. They've had no effect on cataract formation. There is a little bit of mixed weak evidence for lutein and zeaxanthine as possibly being protective for cataract also.

Antioxidants, right?

Yes, that's correct. And macular degeneration, we didn't really touch on that very much, but that's a huge problem. You may have seen in the drugstore they sell areds A R E D S formula for macular degeneration. That stands for the Age Related Eye Disease Study. That was again a National Eye Institute initiative. And first they looked at CE and beta carotene with zinc and a little copper. I guess they put the copper in because they were worried about copper deficiency with zinc supplementation. And then they got concerned about beta carotene. So they did another study where they took beta carotene out and put in lutein and zeaxanthine, powerful antioxidants. And what they showed was that you could delay or reduce the conversion of mild macular degeneration to severe. But it had no effect on severe disease. And it also, interestingly, had no effect on people who didn't have macular degeneration. It didn't prevent them from going on to get it. But I think most of us believe that there's something there. There's some signal embedded in that noise.

Is light also a big risk for macular degeneration?

It is, it is. So again, it's this dose thing. We want enough light so that you don't become nearsighted, but not so much that you're frying your retinas and giving yourselves cataracts. But I do Think that some form of broad spectrum antioxidant protection makes sense.

We didn't really talk explicitly about screen use. Yeah, I mean, you talked about it a little bit in that study in Asia where. But I don't know if that was specific to screen use or just could have been just as much reading.

Yeah, it was not specific.

Playing with Tinker toys.

Yeah, it wasn't specific to screen use.

So what do we know about phones specifically and computers?

Yeah. So, you know, this is a super interesting, obviously topic and everything from. People ask me about blue blocking glasses. They ask about am I damaging my eyes? Am I going to get macular degeneration because I'm looking at a computer screen for 10 hours a day. I'll start with the easy ones. The amount of UV radiation coming off of screens is sufficiently low that there has been no evidence at all that it's going to cause macular degeneration in the same way that you can't get a sunburn from a screen. I mean, the amount of blue light that you get from going outside is many, many, many orders of magnitude greater than what you can get from screens. But I do think that blue light can mess up your circadian rhythm. And if you take someone and expose them to blue light at noon, that's great. If you expose them to that at 11pm and then you try to go to sleep, that's messed up. It's almost like we're running this gigantic experiment with humans where think about like you have a turtle. Let's say you take a species of Turtle that spends 90% of its time in the water, 10% on land, and we take that and flip it. Now it's 10% in the water. And then we look at these turtles and we think there's something weird going on with these turtles. Yes, they're surviving, but we've got them in a very altered environment compared to what they were evolved to deal with. So giving people blue light from a screen that's bright at 10pm, 11pm and then asking them to go to sleep is a problem.

But there's not. It's not clear that it's damaging their eyes.

It's not damaging their retinas or they're giving them cataracts. But I think it's messing up circadian rhythms.

Although it is hard to disentangle that from the total amount of light that they're seeing, which is also unnatural and what comes with it, which is the stimulation. There seems to be a difference between watching TV and checking email before bed. Maybe Neither are ideal, but one seems demonstrably worse, at least for me.

Yeah, I think that's pretty universal. People feel that way, that passive watching a TV is different than I wonder where Winston Churchill is buried. You go down some wormhole and you're just seeking information that that takes you on these journeys. But one thing I do, I do have software embedded in all of my PCs that changes the color, temperature, like flux or something. I love flux. And flux is free, by the way, I think, for end users. And it will take the blue light sequentially out of your monitor as the day goes on, as the evening goes on, to the point that it's like super amber as you get ready to go to bed. I really think that's great.

Anything else we should be thinking about? I mean the big takeaways for me have been the importance of sunglasses, artificial tears, taking your contact lenses out as frequently as possible, so don't sleep in them and stuff like that. I know it's not your field, but do you have a point of view on daily versus the ones? I mean it just seems to me dailies, if you can afford them, make more sense than the two week ones that you have to wash every night. Yeah.

So, you know, I think the most important thing is that you just get them out of the eye. We really don't like extended wear contact lenses, so whatever type of contact that is. As eye surgeons we tend to see a selected sample of patients who are the problems? The people who have sight threatening infections from sleeping typically in contact lenses. So yes, I realize there are millions of people who sleep in their contacts and don't get infections, but the people who end up in my office have had problems and some of them quite devastating problems. So I'm not a big fan of sleeping in contact lenses in general, but if you're going to sleep in contact lenses, I'd rather they be a perfect pristine new pair every single time and get them out as quickly as you possibly can.

Talked about eye protection again, I think we're a little more aware of that now than when we were kids. The other takeaway for me is not to be so afraid of cataracts. They're inevitable and you can actually there's a potential silver lining which is not only the improvement of your vision, but potentially the correction of other age related visual changes.

It is interesting that once word got out in the community that this was something that could be done, you do see people coming in asking for cataract surgery. I think a little bit of sort sooner than they Otherwise would. Because they know that this added benefit is a. Is a potential possibility. You know, in the old days when we did not have intraocular lenses, or the generation, a couple eye surgeons before me did not have intraocular lenses, you'd have to wear these, what were called cataract glasses, these super thick lenses that were very, very powerful and magnified everything and didn't really work all that well optically. So in that context.

Wait, you wore those post cataract?

Post cataract, yeah. Because there were no implant lenses and your prescription was typically about a plus 10. So you know that a minus 10 is a very.

These people can't see without these glasses.

That's right.

And so these are like the Coke bottles. That's where glasses and spectacles meet.

Do people even know what Coke bottles are anymore? So the bottom of a Coke bottle is a really thick piece of glass. And this would magnify your eye eyes and make your eyeballs look enormous. And then you would have this, all sorts of optical distortions because it's very hard to make a super powerful magnifying.

Glass with a long enough focal length without peripheral distortion.

And so you, in that context, would put off cataract surgery as long as humanly possible. So that's really not the case.

Is cataract surgery one and done? I mean, you said it is. It should be. But do people ever need reoperations?

I mean, it's not unheard of where someone will have an implant lens put in that isn't functioning the way it should and that can be replaced.

Is it difficult to get the old lens out since you can't use the same technique to melt it away?

Not really. You can just fold it, pull it.

Out or so it doesn't get. Doesn't re. Epithelialize or the candy coating of the M and M doesn't stick to the new lens a little bit.

But you can free it up and take it out. You can swap out an implant lens. It's something that we don't do it. It's not like changing your shirt, but you can certainly do it. It's another operation.

One other question I had on the laser surgery, I forgot to ask was how stable does your prescription need to be? Because if I understood correctly, again, there's two things that are driving that, right? There's the length, which presumably that's the part that needs to be stable. You don't want the length to be changing, but the shape of the cornea you're actually fixing. So if there's anything that's changing there, do you care?

Well, there's really three variables if you think about it. There's the cornea, the retina, the length of the eye. I shouldn't say retina, but the length of the eye and the lens, the lens itself. So we know that the lens is going to continue to change throughout life, but typically not until you're in your 50s, 60s, 70s, when cataract formation will start to affect the light bending power of the lens. The cornea should not be changing.

So you just have to make sure this length is fixed.

That's right. And typically that, unless you're someone going back to law school or you're reading 30 hours a day, that is typically finished changing in the early 20s, like around 23, 24.

So does that mean our prescriptions shouldn't be worsening much as we age?

They really should not be worsening unless you're developing some cataract formation.

Okay, yeah. I think mine have been stable for about 15 or 20 years. So that means I'd be safe to have laser eye surgery. From the standpoint of stability of prescription.

From the standpoint of stability of the prescription. That's right. And then at some point in your future, and we tell patients this, at some point, you're going to start to develop some cataract formation and hopefully the boxing won't have any effect on that. UV exposure. You, you know, won't have any effect on that. Genetics will be in your favor. And, you know, but if you're a. I didn't mention radiation is another. You know, we see people who do fluoroscopy, like health professionals who are involved in exposed to ionizing radiation. I mean, if you are the, if.

You'Re the tech working, you're the ship.

Captain who smokes on a boat that's carrying nuclear waste and you're diabetic, you're going to get cataracts a lot sooner. A lot sooner. Yeah.

Yeah. So the last thing I want to talk about was, are we ever going to have a day when. Just as we look at hemoglobin A1C today, which is a pretty crude, unimpressive way to assess glycosylation. I've ranted on this elsewhere, so I won't waste your time with my rant on why I think hemoglobin A1C, he's not especially helpful outside of extremes, but I don't know why. I just think the eye is the most sensitive end organ to excessive glycosylated hemoglobin and it's also one of the few things you can look directly at. So I know when I was in your office, just for giggles, I wanted to have you do basically an angio of my eyes non invasively.

Non invasively.

And I thought that was really cool. I liked knowing that I had beautiful little vasculature back there.

Your capillary network was the envy of everyone in the office. Really, really good.

Like, what stands in. I mean, is there going to be a day when everybody's doing this every year and when we see changes there, we say, you know what, I don't care what your, your hemoglobin A1C might only be 5.5. You're quote, unquote normal, but that might actually reflect higher turnover of RBCs. And in reality there's a problem.

One of the really interesting things about the eyeballs, that it's a transparent organ, as you point out, so you can just sort of look in and see what they. The problem is it's not like, okay, there's belly pain, we need to do some testing.

Yeah, it's not like the spleen where you have to use more complicated tricks.

You can just look in and because, for example, we have a layer of brain tissue readily available for us to observe, including its capillary network. So we can look and see are these capillaries damaged, which is something you see in diabetics. Are they exudating fluid? Are they leaking fluid? And that's a very early sign of diabetic retinopathy. Could you, for example, image the lens and determine, is glucose leaching into this lens? Does it contain more glucose than you would expect a normal individual to have in their lens? Might that be a screening technique for diabetic disease? But I think probably yes. And what about the fact that diabetes manifests primarily as a microvascular disease in so many end organs, and we can actually directly visualize this microvascular disease occurring. So if it's in the eye, it's probably in the kidney, it's probably in the toes, and those are things that we can directly observe.

And again, it's not binary. Right? So it's not, you know, we make the diagnosis in a very binary fashion. When the hemoglobin A1C hits 6.5%, person has type 2 diabetes, but, you know, at 6% we just say they're pre diabetic and at 5.6% we say they're normal. But of course, if you understand everything we're talking about here, that couldn't be further from the truth. It's not like a person's going to be perfectly pristine and then they're going to be diabetic. This is a spectrum. And I just think that this, to me is a much more interesting way to go about gaining kind of a foothold in our understanding of a person's metabolic health is to sort of create this as now a new standard. Right. There's something I'm going to create as a standard for myself. Right. Which is I want to make sure that these nearly invisible arteries and capillaries are perfect. And when they cease to be, it's going to prompt investigation. Right. Whether it be lipids, whether it be glucose, whether it be any other thing that we can, you know, blood pressure. Right. I mean, all of the things that can damage a microvascular system, this becomes a beautiful window in which we can look at them. What is the cost of doing that test?

Yeah, it's super inexpensive to do. But I honestly believe that we would see perturbations in the glucose migration into the lens way sooner than we would see architectural changes in the retinal microvasculature.

And you measure that via pressure or shape as well.

So the technology to measure glucose in the lens doesn't exist commercially, although it's being studied. You could look at how the lens essentially reacts to light that you shine into the lens with a particular wavelength and determine how much glucose there is in that lens. And is that abnormal compared to a normal population? But looking at the retinal vasculature, we can do that with optical coherence tomography and we can image in a non invasive way the capillary network. But again, I think that's going to happen. The changes there would happen after.

But I bet you see a lot of damage there in people who are unaware of their metabolic state.

Right? You do, for sure.

But it's not the canary in the coal mine. You're saying the canary in the coal mine is actually going to be the lens distortion due to the osmotic effect.

Of glucose in initial diagnosis and screening. Yes. But what happens very commonly is that a diabetic will come into us and say, my sugar is well controlled. My doctor told me I'm under great control. And we look at their retina and there's no way they're under great control. They have fluid exudating into their retina. There are what we refer to as hard exudates. They're are microaneurysms in their capillary vasculature. These are signs that their Diabetes is out of control. And then we'll say, I'm glad that your A1C was normal. Would you mind going back to your doctor and mentioning that we see direct evidence of problems with your microvasculature and it's probably all over.

And how did the endocrinologist receive that news?

Typically, they will accept it. They'll say, okay, well, for this individual, that level of A1C is not acceptable. They've been typically very receptive because they know we can directly visualize.

I mean, look, this is sort of my soapbox, but I really think that ophthalmology should be more integrated into medicine than less, because you guys do in some ways operate sort of outside of what the surgeons and the internists and endocrinologists do. Obviously. Here's an example of where you're kind of saying, look, I'm seeing something and it's is important to your systemic health. I think there should be more of an integration of this. I think, again, you said it earlier and I think people might not have appreciated what you just said. You get to directly look at the brain. You get to directly look at the central nervous system in a way that a gastroenterologist can directly look at the colon. Right? That's why colon cancer screening is so freaking effective. You get to look with the naked eye directly at a polyp as it becomes cancerous.

That's one of the reasons I didn't become a gastroenterologist.

And we are thankful for them because of all they can save us from.

Absolutely no doubt. But it is amazing that we have the ability to directly observe brain and the vascular tree. And so that's very, very helpful.

Steven. This has been super interesting to me. I was a little intimidated coming into this one because I didn't have the amount of time I normally have to prepare. Prepare for this and try to get up to speed on the topic. So I came in blind and ignorant, but you did a masterful job of accommodating my ignorance. And I learned a hell of a lot and I'm sure everybody else did.

Well, thanks for having me, Peter. I really appreciate it.

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