New Approach to Treating Floaters

Dr. Chris Wolfe: [00:00:00] Hello and welcome to this whole podcast on I Code Media. Today I’m excited to have a great conversation with Dr. John Nolan, who we’ve had on the podcast before. And, you know, you should know that, uh, Mac Health is a, uh, is a sponsor of the podcast. But what I really like about, uh, Dr. John Nolan is he allows me to ask him the questions, whatever question I want to ask him.

So, as a, a podcast sponsor, they have not tried to influence my approach to, uh, to asking questions. Uh, they’re always about the evidence and I want to dig into the evidence behind Vitreous Health today. Uh, I think it’s pretty compelling. I’ve got some questions that I think, uh, are probably challenge questions.

They’re probably the common questions people might ask. And so we’re gonna get into that. And, um, as always, be sure to subscribe to the podcast, write a review, share it with your friends, and support those. Who support us. So today I wanna talk about the, my day multifocal for just a second. It has been a really great thing in our practice for our patients [00:01:00] who are presbyopes of all areas.

But you know, those tricky presbyopes are always the ones that are kind of emerging where they don’t want to give up any of their far away vision, but they’re having some struggles up close. And so what, uh, the MyDay multifocal has been able to do for us is to allow those patients to transition into a multifocal more easily.

And then as we have those patients progress into other levels where they need more ad powers, it’s been a nice smooth transition. So the ultimate hurdle that we’ve seen in our practice before the day multifocal. We’d have patients who would resist any transition to a multifocal lens because of that distance blur.

We just haven’t seen that. So if you haven’t started using Mida multifocal in your practice, I would encourage you to start check it out. Uh, contact, reach out to your Cooper reps for those trial lenses, uh, and commit to mighta multifocal for your patients. I think they’re gonna like it. If you haven’t checked out macia Health yet for your patients in category one through category four, I think there’s a lot of [00:02:00] evidence that you should be considering.

The first is, if we just look at a Reds two and what they, they talk about MAC Health is a, So for patients in category three and category four, um, AMD Macia Health is a great option for them that follows that entire, um, that entire protocol. And it also add. Meso Z is anthing to the mix, which if you look at some of the evidence, I believe, shows me that it’s going to thicken the macular pigment better than without meso zanine.

It also uses the A correct a Reds two dose of zinc, uh, at 25 milligrams. And so you don’t have to worry so much about the potential side effects of zinc. The other thing to to think about, and it’s beyond the scope of this, although you’ve probably heard me talk on other podcasts, is that in patients in category one and two, there may be some additional benefit, uh, to supplementing them with something that may be a little bit less than the A res two, so you don’t have to add as much to it.

And that’s where I use the MEChA Health LMC three. And so I think if you haven’t done this yet, I’d consider Mai Health in your practice and for your patients, [00:03:00] and it’s been great for my patients and um, and we really feel like we can have the ability to, uh, help those patients in all categories of macular degeneration.

So Professor Nolan, thanks for doing this again. This is the third time I’ve had John. Uh, and um, and I’m excited because, you know, about five months ago we, we, uh, had the fly study come out and we were able to have, uh, an assessment of doing something else for the vitreous, uh, for patients. So actually I’m kind of getting right into it, but actually I don’t wanna do that yet.

I want to, I wanna talk to you about your running. I saw a picture of you running, were you running a marathon or a half marathon or what? 

Professor John Nolan: Yeah. Yeah. Great. I was pacing a half marathon and um, so I use, I used raced half marathons and I still, still can race them, but um, yeah, it’s just so good to get back with people on the running line to get to see people kind of run towards.

I think that’s the beauty of running by the way. You know, you don’t have to be the best [00:04:00] at it, to have the best experience. Um, so that’s why I like pacing cuz I see people kind of aim for their targets and. Some of them get it, some of them fall short. But we had a great day. Yeah. I was at, I was pacing a half marathon in Waterford on our beautiful Greenway.

So 

Dr. Chris Wolfe: yeah. What’s your pace? What’s your, what pacer were you? What schedule or what pace? 

Professor John Nolan: Uh, that was a one 40 half marathon. I’m typically, uh, a one 30 pacer. But um, they needed someone to do the one 40. I actually You’re fat man. Yeah, well I had the pleasure of racing in New York, believe or not the half marathon.

And I did a sub 80 half Martin. That’s my pb my personal best in, in New York. That was a very 

Dr. Chris Wolfe: special, a sub 80. So you were under one 20? Yeah. 

Sub 

Professor John Nolan: pretty good sub six minute miles. Yeah, just around six minute mine. 

Dr. Chris Wolfe: That’s fast man. And so I think, I think my fastest is one 30 is my fastest. You and I are gonna have to, um, one time that you’re in the United States, uh, we’re gonna have to work out [00:05:00] together sometime.

I didn’t realize that until I saw you in, um, Well, where were we? This, Was it Houston? It was Houston. Houston, yeah. Yeah, yeah. And so I didn’t realize that until you and I had a chance to sit down and chat a bit and I was like, Oh, what you’re, And then. ? No, it was Washington DC It was Washington, DC Washington.

Professor John Nolan: That’s right. I’m thinking cause I actually went on that lovely run down by the, by the, 

Dr. Chris Wolfe: Yeah. Okay. We gotta plan that. That’s gonna have to be on, on a, on on my list of things to do with John Nolan . Plus, you know what happens when you run, and I’ve said this before, but your brain sort of opens up, especially when you get those long distances.

Like, like I, there’s, there’s some kind of key ti points in time where I’ve built fellowship with guys that I can distinctly remember that mile marker that we crossed when we were done with the bs. We weren’t just like having these sort of like, you know, uh, conversations that were like, Hey, how’s your day going and how’s your wife and family doing?

Which are important. Yeah. But we got beyond that. And so there’s a [00:06:00] couple of them where I remember that and it’s like, you know, five, six miles, boom, six miles, there you go. And now we’re having a real conversation about things that are impacting their lives, like things that are, and, and there’s something about those kind of hard moments, um, that.

That put, it’s probably women too, but put men in a place that they can, um, you know, sort of exercise whatever’s on their mind. I don’t know. It’s weird. What do you think 

Professor John Nolan: about that? I, I, I agree and I think as we, as we get that little bit older, that becomes more important. I mean, I know I always, I look up to you with your family and how, you know, I can’t remember how many kids you have, but I know you have a lot of kids, Right?

Um, nine, you deserve men. Nine. You deserve men. And Cause 

Dr. Chris Wolfe: my wife, my wife gets all the eol. I 

Professor John Nolan: absolutely, I, I have two and I’m exhausted. Um, but I, I agree with you. Oh, I have this, you know, this group that we run with on a Sunday, um, and it’s kind of men typically around my age and we, we do all that nicety stuff, as you say, [00:07:00] but you do go into you, It’s really, really, like my wife kind of makes sure I do it.

Jane makes sure I do it because she knows how important it is for me to be able to kind of just talk about stuff that men are not good at talking about. And I think you get into that comfort zone where you, you can do that. And, and you know, when I was younger, actually when I was training, I was kind of around the time where we were writing the major grants.

You do have those kind of other moments as well where you get clarity on something. And, and what I can remember about that is that it might be something relating to, um, you know, uh, uh, um, Protocol design or something from an experiment that you don’t know kind of really how to go about it. And then you just get this clarity that comes in.

And I remember that I had, when I was writing the grant for your, the Crest uh, program, which was two years in the Macon, I ran every day at lunchtime. I just dropped tools, went out. I hadn’t fortunate, been a researcher, I can do that. I went and we have a lovely area here and that was really, I, [00:08:00] I truly believe that was one of the reasons.

And I remember some of the research saying to me like, You’re so busy, how do you get time to run? I said, I’m too busy not to. Yeah, that’s the point. I’m too busy not to find time to run because if you don’t, that’s where, that’s where it all falls down. And I think you can extend that then into kind of what we’re talking about life and wellness and, and particularly on the back end of, of what we’ve all come through with the, you know, the uncertainties around the pandemic and, um, all of, So yeah, I think, I think find it’s cliche, but finding that balance and that people have different balances.

For you and me, it might be, you know, getting a workout, going for a run. Um, I play a lot of tennis lately. I’ve kind of, not that I’ve stopped running so much, but I, I get the same type of enjoyment and endorphins from, from tennis, which I just started playing actually during, during the pandemic. And um, Can you 

Dr. Chris Wolfe: put a lot of English on the ball?

Pardon? Can you get a lot of spin on the ball ? 

Professor John Nolan: I think I can. Um, I’m getting much better . [00:09:00] Um, I’m very good. . 

Dr. Chris Wolfe: I like tennis. Sorry. You’re competitive. I I bet you are. Yeah. 

Professor John Nolan: I, I, yeah. I hate not winning. So when I play tennis, it, I, you know, I say this, I actually coach, um, uh, we have this game in Ireland called Harling in for, for the girls, it’s called Kamogi, and it’s basically like lacrosse.

um, mix between lacrosse and hockey. It’s a very fast field sport. And my daughter Penny plays, and I coach her team, you know, so , I can see all the mammies and dads looking at me because I’m kind of very serious, you know, I take it very serious. And I’m saying to them, you know, your mammies and dads are telling you, you know, it’s all about having fun, but I say them winning is fun,

So let’s figure out if we can win. So maybe that’s not the right approach, but anyway, you 

Dr. Chris Wolfe: know, I, no, I think, I think there’s something to that. I, I like to play tennis. I, I grew up my dad and I, um, I’d play tennis with my dad and he was always a good sport. You know, he could have always beat me, um, until I [00:10:00] got, you know, faster enough to be able to move the ball in different places.

But I do not like to lose, um, especially when it’s something that I think I’m really good at. You know, I don’t wanna lose. And one of my, one of my best friends from optometry school is named Scott Ackerman. He practices in Garden City, Kansas. Hopefully he is listening. Um, but if you are Scott, uh, Scott can beat you in any.

Anytime. Okay. No matter how good a shape you’re in, he will beat you. And tennis was no exception. And I always, I remember like playing with tennis with Scott when we were out time school and uh, you know, I can put a little spin in the ball here and there, but like, he’s a good player, like a really good player, and you’re sitting there and, and he would, he would serve up the ball to me and he’d put enough spin on it where I’d just be like, Do you want me to return this?

Or, or are we, are we just gonna have a serving contest for, for Scott Ackerman? And then he’d, he’d ease up a little bit, but just enough to like, let me return it. And then he’d, you know, it’s huge walk all over me. Yeah. As game. So anyway, Scott, if you’re listening, [00:11:00] you’ve bested me at, at too many sports.

Yeah. I think 

Professor John Nolan: it’s the science to tennis though, isn’t it? It’s the, you know, it’s the small things that you can do that make the big difference to the, you know, how you stand, you know how you hold rack, the follow through. Um, and it’s what I love about tenants, for me, it’s a game of patience. If you’re good enough, it can be just a game of patience.

You know, I, when I’m not playing well, I’m going for the win straight away. And you never get the win straight away. You have to earn the win. So unless you’re playing a really good player like your friend Scott, I’m sure he could probably 

Dr. Chris Wolfe: just, it’s, he doesn’t have to earn it with me. He doesn’t have to earn it.

Yeah. . Ok. Okay. So, um, sorry. So the 

Professor John Nolan: tennis is funny though. Go ahead. The tennis is funny, Chris, because, um, speaking about today’s topic, floaters, um, this is when I realized that I actually didn’t like having the, the floaters that I had. Mm. And so sample [00:12:00] size, is 

Dr. Chris Wolfe: that, what, was that one of the reasons that started the, the fly?

No, not, 

Professor John Nolan: not at all. Um, and because we were, the fly study is, is, you know, there’s 10 years work gone into the fly study in terms of the observational. That’s what people don’t realize. They look at, I know 

Dr. Chris Wolfe: this is why it’s fun to talk to you, is to unpack that. Cause I actually wanted to start there because, um, because first when I, when I was reading the fly study, uh, you have to, you basically start by, by how do you even get to knowing which supplements are potentially, uh, involved in reducing floaters.

So the biochemistry within the vitreous and what makes the vitreous sticky and what makes the collagen fibers o uh, opacified versus more, um, more integrated and better connected without obscuring, uh, light. So I was reading that and I’m like, I bet there is years of stuff that goes into that. So unpack that a little bit to me about where you start and how you get there from a, from a standpoint 

Professor John Nolan: of vitreous.

Yeah, I’ll do my best. I’ll do my best of course. And, and the first thing to [00:13:00] say is that, you know, , it wasn’t, you know, there were so many people that have contributed to this, to this idea, classically. I mean, if any of your kind of viewers or listeners, um, really want to do a deep dive into the vitreous, they need to kind of start getting comfortable with the works of, um, Dr.

Jerry Cak out of California. And, um, his, his big, his big piece of information from the work that he does, and he works with patients all day long, is that, you know, having vitreous floaters, um, somatic is a problem, you know, and it’s, it’s, it, it affects the health, it affects the quality of life of their patients.

So one of the first inter the, the, the kind of parallel universe of what Dr. Cach was doing and what we’ve been doing with or kind of macular work is that you. having bad visual function, ak, reduce contrast, sensitivity, glare, disabilities, all these are a problem and they really [00:14:00] affect the quality of your vision and we shouldn’t be okay with that.

Classic eye medicine ophthalmology is okay with that and even optometry to agree. It’s like they’re fine. Don’t worry about them. They don’t body it. But the first learnings in all of this are that they are a real problem for your patient. And we, we shouldn’t dismiss that. We should. And if you look at his work, his earlier works, he’s, he, he looks at these things called utility values, which is basically a medical way of quantifying the negative impact.

And like this is right up there with having diseases like macular degeneration, diabetic retinopathy in terms of how they affect quality of life. They’re a problem. The reason why, maybe we don’t, why we ignore that 80% of the. And this piece of the eye that gives you your optical system, we kind of just accept that it gets old and it, there’s liquid fraction and all.

And as I, and I’m a little embarrassed by the way, because as I started to [00:15:00] study it, it just became obvious to me then, you know, all these kind of really kind of site threatening, really impactful kind of retinal problems are in, in many ways connected to degeneration of the vitreous. You know, um, macular holes, uh, tears, detachments.

If you have a really healthy structured vitreous, the risk of those diseases is, is, is much more unlikely. So from a, from a classic medicine perspective, I think, um, that’s important. And so 

Dr. Chris Wolfe: I suppose we have, we have, Sarah’s gonna erupt, but I think that, to amplify your point, we, I think we’re trained largely in iCare to say, Well, that’s not, It, it may be a symptomatic problem for you, but it’s not really a problem problem, so you just have to deal with it.

But one of the things in the fly study in terms of the, I think it was in the background of that you brought up that I honestly, I never really thought about that much, um, was, you know, I know patients are bothered by [00:16:00] them, but when you quantify that, that discomfort, that visual discomfort, I think that you made reference to another paper that, that looked at patients would be willing to give 1.1 years of their life for 10.

What was, what was the actual number? So 1.1 years of 

Professor John Nolan: life for, for 10 years of their remaining life. That was from c a c, That was his work actually. Yeah. Um, you know, it’s just, . 

Dr. Chris Wolfe: So we just don’t think about that. You know, we just don’t think about it’s, this is so significant that if you put it to a patient, you know, you would give up 1.1 years of, of a 10 year time period in order to have life nine, 8.9 years without floaters, right?

Yeah. So that’s, that’s pretty significant when you really, because we always think like, well, people just always wanna live as long as they possibly can. And this is answering the question of like, what is the value of that symptom? 

Professor John Nolan: Yeah, agree. I, I think there’s two other kind of important misconceptions in here that kind of, this kind of, the platform of the [00:17:00] kickstart of all of this is that, you know, of course risk factors, we look at age op, diabetes, um, and so on, but age people, your patients that are, are suffering with this.

They’re not all necessarily, in fact, we know they’re not all old. If you look at, there’s, there was one online study on published proper study where they basically asked people to volunteer you. Um, if they had, um, issues with floaters and they, they reported data like the age, the mean age was 30 years of age.

So yes, vitreous degeneration is very much an age, but the vitreous floaters can start, um, affecting us very, uh, early in our lives. We know, you know, from age of 40 that, you know, we really see structural changes to the VITs that’s meaningful, you know, um, liquid fraction, and it just, it, it excels from, from here on in.

Um, so I think the other [00:18:00] big learning is that, you know, we may say in iCare, Oh, well, they go away. They might, they, they’ll probably go away. I think that data very much says that that’s not the case. People that are symptomatic. Their problem doesn’t go away. Um, in, in fact, we quantify that it gets significantly worse in a relatively short period of time.

Um, and again, if you quantify properly by looking at measure, the visual function, you know, that are connected to the presence of vires floaters, one of, So from our perspective, we, I was very reluctant to do this work, by the way. Um, there was, um, because I was uncomfortable with my knowledge on the vitreous, I had spent my whole life studying macular nutrition and visual functions.

And I was like, Well, why is no one talking about the vitreous? And, um, there was a guy from Germany, uh, Robert Kling, um, who spent his whole life working at Nutrition as well. He’s a veterinarian actually. And he, he, we, we knew Robert and his company Avega [00:19:00] Vision for many years. He, he would be a partner with our university.

And, um, so he kept telling me about, you know, Possibilities for the vitreous and what John, why have you not looked beyond the macula? You know? And, and I’m always very protective of being good at what we do. So I said, Okay, let’s reluctantly, I said, Let’s have a look. And he was showing me all the data that was coming from observational work done outta clinics in, in, in Heidelberg and Germany and so on.

And, and very good medical doctors that, that were working there. And it was really interesting. So I agreed. What we agreed to do, um, maybe six years ago from where we are now, um, was to build it from the bottom. You know, I was impressed by what, what the information we’ve been given, but we really wanted to build it from the bottom and have a command and an understanding.

So we set up a full PhD program on this. And there was a scientist, Emmanuel, who now, um, has, has passed his PhD vi, he’s now Dr. Emmanuel. [00:20:00] He’s an OD as well, actually, he’s an optometrist from Ghana. Who joined us many, many years ago, and he spent two years just studying the literature, um, to try and get a comprehension of the mechanisms that nutrition may be involved.

And, and he taught me, you know, and all these billion people taught me. Um, and we learned together in terms of like, you know, something else that your viewers, listeners may, may, may not be familiar with. The, you’re probably trained that the vitreous is a closed system and nothing gets in and nothing gets out.

And, you know, that’s not the case. You know, there is active and passive transfer of nutrition primarily. And, and remember, we know the composition of the vitreous is primarily water, of course, but you have your proteins, your collagen fiber is your hyn, but nutrition is a big part of that. So, really, You know, I couldn’t even tell you the, the amount of kind of, um, enzymatic, non enzymatic, uh, nutrients, um, antioxidants rather that, that are present cuz [00:21:00] there’s so many of them.

But what his work was able to do was really to kind of validate the formulations that, that, that were being put together by, um, a be Division Robert Kling in terms of putting them into, um, a formulation and ones that were naturally occurring, ones that had the properties, and let’s talk about them maybe in a minute.

You know, you’re antioxidant, anti location enzymatic. These are the three proposed mechanisms. So when you look at it, it’s, it’s, it’s classic micronutrients, like water soluble vitamin C, remember the vi, the vires being water. And, and then we had to really study vitamin C and there’s so much to actually learn about vitamin.

Um, and I wasn’t an expert in vitamin C, but you know, I, I, I correlated it with something that’s orange or yellow. And then I said, Well, why is the vitreous not orange or yellow? And when you look at it, you, you see it’s because vitamin C in the vitreous is not oxidized. It’s only orange when it’s oxidized.

So there’s all these little learnings along the way. But [00:22:00] long story short, um, you know, the basic goal here was that, is there a formulation that is regulatory approved, safe, allowed to be used? Could you put it together? And that’s what a bigger vision did, and that’s what we tested in, in, in part of the, the Flies trial.

Now, leading up to that, we had this major review published, which is a great read. If, if anyone has a long plane journey coming, you know, it would be a really deep dive on literature. Um, that was, and there, these are all on my website, these papers, published papers. Um, and we actually partnered, um, with Dr.

Jerry Syk. On that because there was so much we didn’t know, and he was the expert. So, uh, quite, quite cautiously and nervously we approached him to see if he’d help us because, you know, we were wondering what would he, what would a, a retinal doctor be? Think about nutrition? And I’ve, I, you know, thankfully he, he came to help us and, you know, very directly gave us some advice and was significantly involved in those [00:23:00] publications.

And he’s gonna remain involved hopefully, as we kind of get ready for kind of phase two of research, which I’ll talk about maybe in a minute. But, um, Well, 

Dr. Chris Wolfe: yeah, go ahead. Sorry. No, no. I was gonna, I was gonna ask you, you know, one of the things that strikes me in all of this is that with all the complexities of, of the oxidation, the enzymatic transport and, and the nutrients, you know, My view as a clinician of the, of the vitreous has always been that it’s just sort of a remnant from development and, and it’s just sort of a, a necessary evil that is just left over from the scaffolding that is required to, to supply a blood flow to the anterior portion of the, of the eyes.

But, well, I guess, uh, the lens of the eye. Yeah. And so, and so it’s just sort of like left over. I haven’t really given it much more thought than that, but, but it strikes me now as you’re talking that there’s probably some additional benefits, um, that we are not typically thinking of. Are, are there any that, that come to your mind?[00:24:00] 

Yeah, 

Professor John Nolan: absolutely. Great question. I, I mean, the first one is it provides the optical system for the eye to the, for the eye to work. It allows for a fra without a, without a vitreous, you have no optical system to do business. So that’s one. It provides that system. Um, it, it, it, it is your, as you know, it provides a protective mechanism, a shock absorber, if you like, for, for everything that happens when we’re run, when we’re moving.

It’s that it’s protective in that way. Hmm. Um, the way I explain it to people that ask me to talk about, you know, how, you know, the collagen fibers and where the floaters come from, is that I, I, I talk about, you know, the, you made reference to the structural system, and if you think of the various types of proteins, the various types of collagen that’s present, you have your classic ones that are very long and extend throughout the vitreous.

And then I, I describe it like a ladder. And then you have these kind of cross links, which are the steps in the ladder. And what we believe is that, you know, the, the [00:25:00] cross links can. Are oxidized. And when they’re oxidized, they slightly change their shape. And then you have these conglomerates and these can mm-hmm.

present themselves in the form of these kind of cob webs or annoying, um, disturbances. Um, so yeah, all of those, um, it also is likely to be servicing, um, other tissues and cells across the retina that we don’t know about the, the, the very fact that the high nutrient content there, but there’s a lot of unknowns around that.

So there’s a lot more research to do to your question. 

Dr. Chris Wolfe: That’s the thing that over, Yeah. Yeah. I think that’s the, the thing that strikes me, the more you talk about that, is that we think clinically as a leftover, but if it’s doing all that other stuff, you know, there’s, there’s no reason that from a, from a developmental standpoint, that.

You couldn’t have other blood vessels that feed that system that, [00:26:00] uh, don’t have to use a scaffolding to, to do that. I mean, you know, it would probably be a lot easier for retinal vessels to span that distance and have a support structure on the retina. So there’s probably some other reason for vitreous.

And, and the one that, that is most interesting to me, and the one that you made a, a reference to, which again, I don’t have any knowledge of per se, but it would make sense that if it holds all these nutrients and requires all this additional input, um, and has the potential for other, you know, problems with clarity with time, then there has to be some additional advantage in terms of structural support or enzymatic support or, you know, nutrient support to the rest of the retina or other, you know, posterior segment tissues.

Professor John Nolan: So it’s just interesting. No, I think so. I think it’s very, and Jerry Sak has these two great expressions, which I think maybe your doctors will use in clinic if they’re ever talking about the vitreous in this context. . The vitreous is invisible by design. So , we don’t really look at the vitreous until we have [00:27:00] to, until we have a problem with it.

It, it’s invisible. So I like that. And he also says in one of these papers, we need to look at the vitreous and not just truth. Mm-hmm. . And I think, I think that really sets, sets the tone for, for kind of exciting research in this area. I think the other points before we moved into the interventional works were to really, to confirm, and we published this as well in another paper, so there’s a, there’s a bunch of papers on this, but Emanuel also published work where he quantified the visual function loss as assessed again with photo topic contrast sensitivity.

Um, and we see that there’s reduction about 65%, so six 65% reduced. So that has a massive effect on vision related. Quality of life. Um, and c a CAC did the very same, um, same, same piece. And he’s also done kind of, um, extraction. He’s vitamin C. He’s looked at, he’s done a lot of work with vitamin C. And you see that in people at risk of [00:28:00] vitreal degeneration or with vire floaters, that these basic antioxidants are significantly reduced.

So that kind of localization of them is different and the amount. And so understanding why that is, is, is, is, is something, um, for the future, I think, 

Dr. Chris Wolfe: Well, the contrast sensitivity one too is interesting because, you know, it’s something that again, our patients are gonna be bothered by, but they don’t know exactly how to articulate it.

Yeah. Uh, and we. Generally measure it. Uh, most of us, I know Harvey Hanlon has a really good kind of quick, uh, and dirty assessment of, of contrast sensitivity, but it is not something that by and large we’re saying, Oh, a patient has floaters. I wonder how their contrast sensitivity is impacted. It’s like, I, I’ll tell you that it’s not entering in my mind and not just because of, of me, but I talk to doctors all the time.

It’s just not entering into their mind in terms of contrast sensitivity with floaters. But it’s an interesting point and, and it, and it, uh, shows you how it can additionally impact quality of quality of life. [00:29:00] 

Professor John Nolan: Yeah. The contrast sensitivity discussion is going around in circles, isn’t it? In, in, in, in optometry.

Um, and, and thankfully, and, and America is doing great here. You know, it’s, it’s, it’s leading the way. I, my printer decided to

opt in terms of caring about, you know, other ways to look at visual function. And, um, I, I think that’s really important. And I think the issue with contrast sensitivity, Chris, is standardization. The standardization of how we do it because, you know, Lumin, all of these things can have a great impact on, you know, the data that you get.

And I think, I think that’s what’s missing. And we see all the companies now trying to say that they have new ways to assess visual function and it’s a race to the finish line. Maybe, you know, I know the MNS system in, in the us which is, which is, um, we use their systems for research. Very, very [00:30:00] good system.

Um, we use in our research and standardization of that is good, but you know, is how clinic friendly is. It then becomes the question I think. Yes, exactly. Maybe a VR headset, maybe something like this. But I don’t think the technologies are ready yet, um, to, to, to help ods. Quickly they’ll come and people are working on ’em.

But right now, today, if you ask me what would you get to measure contrast, you know, you probably all have them in whatever visual systems you’re using. You just need to probably turn them on and standardize them yourself. A little bit of work. 

Dr. Chris Wolfe: So that’s the hard part. Yeah, it’s the hard part for the individual clinician is to know what to do with that and then how often and how you know you’re gonna check on it.

Are you gonna check for it to improve? And then it, it opens up this whole other can of worms of. You know, what is visual, like what’s required for visual function testing and is, And then the other can of worms that opens up is like, how much, how [00:31:00] far do you push this in terms of micromanaging the problem?

I mean, I would say that if a patient is symptomatic from it and you can do something to intervene to improve it, and you, you do want to have some way to measure it. And if you can measure that and to know, one, it reinforces to the patient that you’ve improved it. And two, you’re, you know, all the other things that can come from contrast sensitivity.

So somebody probably does need to, um, to pay for that. Right. That might, that’s not something that you’re thinking about, but I think what, when we think about like, okay, if I’m gonna have a patient back on a supplement and I’m gonna see them back, you know, is it medically necessary for me to see them back?

Uh, well, I think in the one hand you would see those patients back at some interval for floaters. You could probably, um, combine that, that assessment within that interval. Order it as a additional test that you might do and see if you can improve that. And if it’s a, it is an a measurable improvement, it’s one other indicator for the patient to adhere to their treatment.

Uh, and also just to understand the, the potential benefits or drawbacks [00:32:00] of, of their vision currently. So, yeah, uh, anyway, those are just thoughts that I’m having where I think that Laura would be a resistance to measuring that. I think the main one is standardization, uh, and making it simple in the practice.

And the other one is like, am I really gonna add another test that I’m not gonna get paid for? And you know, like, well, yes, if it’s easy to do and it, it can be combined with some other visits, uh, that you’re doing. So anyway, uh, those are the thoughts that kind of go through my clinician brain. Uh, that’s important in terms of 

Professor John Nolan: incorporating it in, you know, we can do all the science in the world and if it doesn’t get translated to people like you and people that you work with and, and your colleagues, you know, it’s, it’s kind of pointless.

So, Scientists have to listen to your problems and, and find ways to, you know, maybe provide some, answer some. So I think that the point with, with symptomatic vitreous floaters is, is, is an easier one than all our work on macular nutrition because sometimes it’s hard to demonstrate the benefits. You know, when you look how successful MA Health has been in our [00:33:00] trials and how, how the, you know, I was at, of, uh, some shows recently and you know, for me, brilliant validation of the science in MA health nutrition is, is the amount of doctors that genuinely came up and said, Yeah, this has been great.

So we’re kind of getting that clinic validation now. Um, in terms of vitreous health and vitreous floaters, it’s actually, there’s no hiding behind the fact that it’s either going to help the, the patients or it’s not. And you know, the comfort I would give your listeners on this is that yet this is one main study.

Um, if you look at all the data that’s available, we’re probably at about 600 reports, uh, of people, um, that have been on this treatment over a 10 year period. So it’s relatively large sample. The, the fly saw itself was a very select sample of, and we might talk about that in a minute in terms of what we actually did 

Dr. Chris Wolfe: and what we actually, actually that’s a great place to go cuz I think, I think to, to start right, when [00:34:00] we think about the pyramid, you and I have talked about this, but the pyramid of evidence right now we’ve got the fly study is so critical because it aggregates all those other studies underneath it and then learnings from them.

But then you, you be, you can kind of now do it in a randomized controlled trial, placebo controlled tribal that is masked. Uh, now your sample size is, is still, uh, the end I think is still high enough, Right? You’re 60. What is 61? Yeah. 

Professor John Nolan: I dunno if power to answer a question for 

Dr. Chris Wolfe: sure. Yeah, exactly. So, so let, let’s get right into that then.

So, um, So I, I think it’s, um, we, we’ve kind of gone through the background, we’ve gone through the nutrients, and that’s where we get into that 10 year period of data. Mm-hmm. . And then you decide, you design the study. So tell me how that study’s powered. Tell me the things that you’re, you are looking at in terms of symptoms and in terms of, uh, vitreous float or size.

Yeah. Those sorts 

Professor John Nolan: of things. Thank you. So we, we needed all the help in the world and we worked with, um, a Vitra retinal surgeon here in, in Waterford, Ireland. Um, Dr. Eugene Ning, [00:35:00] um, runs a massive Vitra retinal clinic, and his classic treatment for vitreous floaters would’ve been, um, uh, some vitrectomies, but, uh, laser as well.

He, he used both, so he would be the atypical surgeon that would try and treat these. Okay. Um, but he was very interested to be involved in something that was kind of a micronutrient based. And, um, so we spent a, we worked with, um, a statistician, Dr. Jim Stack. , who was a brilliant, uh, statistician. And we explained just like we would always do an experiment, what we were trying to do.

And then we looked at the questionnaires that were available. Um, we looked at Dr. Sach’s work, how we assessed it and others. And, um, essentially to, to kind of summarize it quickly, what we decided to do was power the study based on subjective assessment. So how do the patients feel today in terms of how the, the floaters affect their daily quality of life?

So kind of scaling it from not bothersome at all to really troublesome [00:36:00] to the point that I can’t live with these. Um, so there’s this kind of scale of assessment and there was a separate piece to this, which was, can we assess, um, The, how it impacts over the previous six months. So we kind of were looking at it from two subjective perspectives there.

Um, and so actually we, when we, when we were getting full design on the protocol, we were really leading with just subjective, which we know in its own, it doesn’t tell you the whole picture. So we wanted to quantify visual functions and everything. . Um, and what we did was we, we collaborated with local optometry and in addition to the vire retinal, uh, clinic, and we recruited patients who were essentially referred in to that clinic.

So they were there because they didn’t like having the floaters. They were of all ages. Um, and really they weren’t suitable or had decided not to have any of these treatments that the, the clinic would, would classically do. So we were able to get a recruitment that way. Um, around the [00:37:00] same time, and thankfully we were able to work with our O C T system, the Heidelberg Spectras system, um, and the manual worked with kind of, uh, software developers as well to, to basically use an approach where we could quantify the floaters because we felt it really important in addition to just like getting self reports and these questionnaire reports to actually quantify them.

So now we had something objective to marry with it. And um, so we ran the experiment. It was a six month intervention, placebo control, classic design. As you say, with something like this, you always get a subtle placebo effect. Um, and uh, we, we saw a small placebo effect as well. But the difference, you know, the, the, the strong effect in the active group was, was, was consistent.

Consistent in so far as our subjective reports were really impressive. People got better. Their, their wellness got better, Their vision related quality of life got better. But what was really essential here was that [00:38:00] that married up brilliantly well with our quantification of the size of the floaters. So on, on average, I think, you know, we see that about 70% of people on the active group at six months report an improvement, and that marries up with the quantification of the size of their floaters at the end of the, we didn’t get rid of all the floaters, but you’re kind of taking them more than half down in terms of how we quantify them to the point that the problem for some people is going away, where the, where they report floaters not bothersome at.

Yeah. 

Dr. Chris Wolfe: So I think that’s, that’s a compelling one, right? If as a clinician, if I wanna say something to my patients that continue to complain of floaters, there’s, there’s two things. The first one is, you know, and this has been my impression of it, and I could be completely wrong, but I actually am not suggesting it to my patients or prescribing it to my patients early on in their symptomatic PVDs.

So what I don’t want to do is say, this is gonna take care of that. I don’t, I don’t want to know about any new things. So my, my thought, if you look at our clinical practice guidelines, depending on the type of PVD and the [00:39:00] clinical findings we’d have, we’d see them on the initial visit, and then between two and four weeks and then six months, well then at that six month follow up, up, I’ve gotten there with my patients and there’s still complaining of them.

Now I’m saying, Look, I just don’t want to plant the seed. Like take this supplement and then you don’t have to worry about any new symptoms, right? So I’m trying to remove that away from them. That could be wrong, but I’m trying to remove that away from them. And then I’m also trying to say, we know that over the, for first six months, that these things are probably gonna improve somewhat.

So I’m saying, Okay, now if you’re gonna continue to complain about these things, now we’ve got another solution. And then, and then within that, I’ve got hundreds of patients over the years that are saying, Well, Chris, I’m still bothered by these floaters. You know, Dr. Wolf, I’m still bothered by these floaters and I know it’s not a problem because my retina looks okay, but it’s still bothering me.

They bring it up to me every single time I see them. Well, those are again, okay, fi Now we’ve got something for you. And, and I’ve got no retina surgeons in Omaha that are gonna do a vitrectomy for a patient with floaters. They’re just not gonna do it. [00:40:00] Um, and, uh, and most of the, I, I think none of them will use a laser for them either.

So anyway, my point is, is that now it in my hands, that’s where I’m using it, is, is the longer term solution where patients are still symptomatic as you’re suggesting. So then I want to know, um, talk a little bit about the placebo effect. You said there was always a placebo effect, so we get this 70% improvement in symptoms with, uh, with the treatment group, but what was the placebo effect?

Professor John Nolan: It, it was, I don’t have the exact date off top, but you see a small, small percentage of, of subjects on the placebo group reporting improvements as well. This was just on the questionnaire based data, not on the quantification. And that is why you need to have that placebo control design, right? Because with our statistics, our research question is not, does it get better in this group?

Is does it get significantly better in this group compared to this group, the placebo group? And that that’s really why you need that placebo control design to [00:41:00] address, to address that question. I mean, looking at it in basic terms, Um, I think you’re looking at about less than 11% of people on the placebo may have 

Dr. Chris Wolfe: reported.

So that’s the number that I want, because essentially what that tells me, and, and this again for, for the listeners, the power of this, Okay, so here’s the thing. If we can have a 70% improvement of, of symptoms in the treatment arm, and I’m, I’m trying to think what, what was compelling to me was that 11%, about about 10% was what I recall in the placebo arm.

That difference between your, your, uh, treatment arm and your control. Now you’ve got a 60% improve improvement, which basically then if you’re gonna invert that your number needed to treat of patients who are gonna have symptomatic benefit from this is not that many. It’s it’s less than two. And so, In my thought process, one of the things that detracts clinicians from saying, Well try this, is the, is the concern that this might not be effective for that patient?

Yeah. But when, then when I think about like the quality of life [00:42:00] improvement of willing to, you know, that 1.1 years, um, And I think Okay, well, is, if it were, it’s not, but if it were a hundred dollars per bottle or a hundred dollars per month, it’s not that that much Right. The patient. But if it were, you could say $600.

Right. If it were, if it were $600, would a patient be willing to trade those floaters, a 70% reduction in those floaters, floater symptoms? Um, would that be worth $600? Yeah, For most people it probably would. And, and most people, when they’re bothered by it enough, even if it doesn’t have the effect that they think that they, they want, it’s still worth the, the, the trial.

Right. So that’s the kind of power of the, of understanding the data and then understanding the benefit and the cost of that benefit becomes really pretty, a pretty easy answer to be able to offer it for patients. 

Professor John Nolan: Yeah, and what I’m learning actually is like when I speak to doctors about this, I’m kind of sensitive to the, to, to the data.

And what I mean [00:43:00] by that is there, there was this 30% group. In our experiment, we’re only active and they didn’t get any win. But the doctors are saying to me that if they can help some of the patients, even if it was a 50%, like the data suggests it’s higher now we’re at 70% in terms of people getting a win from, from doing this.

I think they’re really good odds. And I think, you know, to our earlier point, the patient will become their own experiment. Uh, if they’re really feeling that this is benefiting, they’re gonna tell you, and we’re seeing this already. I, I mean, I can show you emails, letters, people from across the world who have been on this now who are genuine.

And that’s not science. That’s just kind of people’s observations and people’s appreciation. And it’s, it’s, it’s a bit weird when you get those letters, but unlike anything I’ve ever seen, , that is the, the, the patient satisfaction [00:44:00] and the patient appreciation of, of the sciences, the research, the fact that there’s people working to, to really, you know, draw a line between the whole narrative that food supplements are snake oil and da da da.

You know, a lot of food supplements are low quality and that’s why what’s really important here, and I’ve always said this to, to you and to, to your colleagues when I, when I lecture on any of these topics, is, you know, if, if we go there that we, that we want to use evidence based and we want to just provide the information and prescribe in some cases to patients that there’s opportunities here to reduce your risk of macular degeneration or, or vit degeneration, or reduce vitreous floaters, that the quality piece is.

And the quality piece for me is twofold. It’s, it’s nutrients and interventions that have an evidence based, a akd being tested in terms of effectiveness, effect, [00:45:00] efficacy, but also the quality in terms of the stability. You know, these, when you look at, when you look at the, the micronutrients used in, in vitreous health, there’s nothing, there’s no big nutrient that we’ve discovered that we said, this is something, it’s, it’s, these are nutrients that exist naturally in the vitreous.

These are nutrients that can be sourced and quantified that we, we know about, uh, you know, zinc or lyin or vitamin C. We know about that. We know about their properties, but, but it’s, it’s getting ’em into a formulation that, that, that, that provides a potential solution for the patients as something. So I suppose my waffle there is that, look, science is one thing and evidence is brilliant.

And quality is essential. But with, with, with this particular. Effort, the, the patients themselves will, will really drive home how successful this is. And what I’m telling you is what we’ve seen now from Europe, from Germany and now in Ireland, across Ireland and, and Europe, and now thankfully in the us [00:46:00] um, patients that are trying this are really starting to already see the benefit.

And I might be wrong, you know, and I’ve come back if this, if I’ll come back on your, on your podcast, Chris, if, if if the, if the clinic and if the, the patients tell a different story. But all evidence so far is that people that have a problem with this are getting some reward from enhancing the safe and targeted micronutrients of the vitreous.

And it’s their decision to do. Yeah. 

Dr. Chris Wolfe: And I think, I think, um, the other part of that, which you just briefly touched on was the objective, uh, the objective measures, right? Yeah. So we can be, you know, within, within the evidence, we’re not just looking for the subjective measures, we’re looking for the objective measures.

And then we have the, the, the kind of case studies that you’re talking about that support the, uh, the research studies, which is, you know, how we think about evidence-based medicine where you have, you know, sort of patient preference, you have, uh, clinical research or research studies, and then [00:47:00] you have kind of clinical intuition and they all marry together to, to meet that patient, uh, where they’re at.

And, um, and so I, I do want to discuss a little bit because I, you and I had have talked about this briefly. Uh, it wasn’t until I read the paper that I understood how they were quantifying the size of those floaters, but one of the things that I was curious about was, okay, how are you taking the image and, and what the way they took the image was.

To look up, look down, look to the right, look to the left, and capture that, uh, that floater in all of those different images. And then, uh, based on that location, they could say, Okay, well this isn’t just the, like a posterior of ous attachment that is, that is pushing anteriorly, thus creating a shadow on the retina that is inherently, uh, less dense but maybe larger in size.

Uh, it was actually qu able to quantify the actual size. So this idea that the question I had for you originally was, Well, John, is this just that time goes on and, and it, uh, you know, if a patient has a [00:48:00] post to your vitreous attachment, we’re just naturally gonna get less impact from the floaters. And you said no.

Uh, the, the way this study was designed is we were able to actually measure the floater size, which I thought until I read it, I wasn’t entirely sure how they did that, but that’s how they did it. And I think that’s really important. . 

Professor John Nolan: That’s right. And you know, obviously the floaters can move and if it’s, if it’s flow.

So the, that’s all kind of calculated in terms of the resolution, how they go and get to that image. It’s all controlled back. And, and, you know, for comfort, I can tell you that the, the repeatability of the assessment, we, we do what’s called icc interclass correlations. Um, it’s 0.9 99. It’s almost a hundred percent agreement.

If I do you now, I’ll do you tomorrow. I’ll do, I’m gonna get the same score on that, on that, uh, floater, um, that we bring, that we bring into picture. Um, so that was really statistically, and we were, we were really careful there. Um, it probably did most [00:49:00] work on, on the imaging in this entire experiment. Um, yeah.

Cause it was, it was pretty novel ground, you know, And Berger obviously delighted that we were able to use their system to do it as well. And. 

Dr. Chris Wolfe: I think it would be really interesting for H Board to use that, that technology that they’ve, I mean, could you imagine? I mean, it would, it would change our approach, uh, as clinicians to managing patients with, with vitreous floaters, if they could actually figure out an algorithm within that, that it would be easy, easily capturable and measurable over time, uh, where you could actually image that entire vitreous and then quantify that improvement just like we can with macular degeneration and drusen and, yeah, I mean, um, I’m sure they’re probably.

Wizards are thinking about that already. But I, That would be super cool. Like, if you’re thinking about what would be helpful for clinicians. Well, it would be really helpful when our signs and symptoms align and, and a patient comes back in and says, you know, why, you know, I, I am that 30% group and it’s not helping me at all.[00:50:00] 

And we could say, Yeah, it’s interesting. I can measure this. And it, it is shrinking. You know, we can, we can measure this. Here’s before, here’s after it’s shrinking. But why is this patient’s symptoms? And that leads me to another point. Were there any learnings? Cause there’s a whole bunch of other things that you guys looked for, um, in, in all of those patients.

Were there any learnings from the 30% that didn’t respond? Was there something about those patients? 

Professor John Nolan: A great question. We, we, we couldn’t see anything that was unique. So, you know, the, the first place we went to was like the, the stage of interest degeneration. Like, cuz you made, you’ve made reference to PVD a couple of times on this call, Rightly so.

The, the effect was great for more advanced, but it wasn’t significantly different. People were very early stage. Um, degeneration. So, So you didn’t have pvd, so at that very early stage. So they, they, they benefited as well, and so there was no, Maybe we didn’t have enough power really in the sample to do that, but we didn’t see anything.

To answer your question, we didn’t see anything, age or [00:51:00] nutrition or gender or even visual functions. 

Dr. Chris Wolfe: So you did look at nutrition too? I, I guess I, I must have, um, see how, how, I guess. It 

Professor John Nolan: may not have gone into the paper. Um, well it may not. Yeah, 

Dr. Chris Wolfe: I did, but I, but I may, it just may have skipped me when you um, I, I, I just don’t recall like how did you assess their nutrition?

That’s just another thing to think 

Professor John Nolan: about. I’m saying we made an out put to blame. We may not have put in the paper. Okay. Um, yeah, we, when we did, we did basic dietary assessment, um, and we, you know, lifestyle assessment, we also measure crot nights cuz that’s what I do for a living. Um, and um, we didn’t see anything that, that told us why the 30%, where the 30%.

And I think that’s probably something that we need to go. And the other question is like, does that 30% get less if we intervene for longer, For longer, longer presentation a few times now. And I’m asked all these really, you know, great [00:52:00] questions like what happens if we stop and I’m like, I don’t know, , what happens if we go for longer?

What happens if we double dose? There’s. , this is brilliant research and it’s time to be used. But I do think, you know, um, there’s, there’s a good bit more to do. We’re at the moment we’re planning a couple of new, uh, pieces of research related to the vitreous and, um, building upon this one of them is, um, and I’m in conversation with Dr.

Jerry around, He’s very interested to actually quantify vitreous micronutrition follow an intervention with vitreous health. So he wants, as a doctor, he wants to, he wants us to look at the vitreous itself and detect the magnitude of change. So that’s probably one experiment. The other experiment is the dose response.

Um, you know, what happens if we were to do more or slightly less? What happens if we go for longer? But it’s easy to say we’re going to do that. I mean, flies took, you know, five years from at the university from when we [00:53:00] started looking at the protocol to getting the scientists to do it, to doing, People don’t realize that it’s why, it’s why I get infuriated.

When it, it gets dismissed in medicine that it’s a small study because we’re not big pharma. You know, we’re, we’re academics at a university and we, we fight for our life to get grants and we work with organizations. You know, non exclusively across the world. Mac Health, uh, actually Mac Health, we’ve spoke about this before, they’ve never even supported financially any of the research we’ve done.

We, 

Dr. Chris Wolfe: I think that’s super important for, I, I know I’m brought it up at the beginning, but obviously Mac Health has, has allowed me to have access. Not that, I mean, I had access to you before Mac Health was a sponsor, but, um, but it becomes a little bit, uh, the connections with, with you and Jim and all those other sorts of things is what I really love about that, about that partnership is I can say, I can say, Hey, uh, Frederick, can I, can you put me in touch with this guy and that guy?

And he’s like, Yeah, let’s do it. And so that’s what what’s really one of the main values for, for the podcast, I think, is [00:54:00] it, it puts me in touch with, with people, uh, like yourself. Yeah. Um, but I, I think that you can’t overstate that point enough. Is, is this, there’s a thought that John Nolan is Mac Health and Yeah.

I want you to clarify that one more time. 

Professor John Nolan: Yeah. Okay. Thank you. Well, I’m employed by the university here, Southeast Technological University in Waterford. So, um, you know, I, I hold a chair here that’s funded by the Herd Foundation in uk. There are charity in the uk, but our, our research primarily has been supported by competitive grants.

So our, myself and my colleagues, we write research grants. So I would say about 90% of our funds have come from competitive research grants to do what we do. The easiest way to explain it is I look at macu Health or Vitreous Health, the formulations, as part of the methodology. So what do I mean by that?

If I measuring vision, I want to have the best technique to measure. Contrast are the best H P C in the chemistry lab to measure crot nines in the blood. [00:55:00] Part of our research is having a formula that’s stable and effective. Why wouldn’t I use. Mac’s intervention because we’ve, we’ve looked at them all.

We’ve looked at their stability, we’ve looked at the optimal amounts. So I pick it because it’s, it’s something that has an existence that, that, that we’re able to use. So, uh, but to your question, I mean, you know, Jim Stringham and I, Jim was an academic, he’s now employed directly by Mac Health. Um, so I, I would have, I would’ve have an academic relationship with Jim.

We would coor on works. We work together as postdocs in Max Notley’s lab in Augusta, Georgia. Um, but yeah, I mean, I can use any formulation I want in, in, in the experiments we do, and we’ve used them all. I’ve used Bosch and lawn products. I’ve used, um, many different products from across the. And, um, the, the future is, you know, we work, we, we apply for funding to what’s called Horizon Europe.

It’s [00:56:00] European grant agencies. Um, it, the relation, one relationship that’s clearly pre present between macu Health and as you can say, John Nolan, is that I’m chair of the Bond conference, which is a conference that’s, that’s, um, run in Cambridge. And we have a big announcement coming about that soon. We hope to move it to, to the us and maced would be a sponsor of that conference.

So an unrestricted, uh, sponsorship for that conference. But that, that’s a non-for-profit conference. All the money goes into supporting the professors and the scientists to travel from across the world to go there. Um, it’s a, it’s a bon of fee day academic conference. So, but they, they do greatly and we appreciate their support and that of others as well.

You know, um, uh, bsf, um, uh, I don’t wanna forget anyone now, be Division Industrial Organic. Um, and we are open to work with any organization that want to, you know, get part of the scientific, uh, works that we do and support [00:57:00] people. Abbot Abbott are always part of it. So there is this connection between industry and academia.

There has to be in this new world. Yeah. You know, it’s, it’s, it’s, it’s how it works. We need to see, but we have to work through university policies, technology. Like, I don’t own any intellectual property on the work I’ve done full clarity. I don’t own anything. I’m an inventor on many of these, but the, the being an inventor and intellectual property are very different things.

People don’t understand that. Um, as a, as a scientist that works here, I assign all my discoveries to the university and they may partner with, uh, so it’s with, uh, industry and it’s safely managed that way. So, yeah. 

Dr. Chris Wolfe: That, that’s important. Yeah. So, No, I think I, I wanted to hit that point just cuz you, you brought it up again and, and, uh, and I wanted to make that disclosure cause I think it’s important.

But, but you brought up, and I think this might kind of round out our conversation because you brought [00:58:00] up the, the last, um, idea of, well, what’s next? What do I do? Uh, once we, you know, once, once that six month time period goes, and I think your answer is exactly right. We don’t know. We don’t know for sure.

Yeah. But, um, and I don’t know, I I, but as I think about this more, on the one hand I would say, well if it’s, if it’s improved that patient’s symptoms, uh, maybe we stop it. And see if symptoms return, you know, does it improve the patient’s symptoms? You stop and things get worse again. Or is it intuitive enough?

And this is where I’m thinking more about it, is if the vitreous is a, is a structure that’s supporting other things and yeah, you know, we talked about PVDs, but we also talked about floaters. And if the floaters are just a, uh, a clumping together and, and misalignment of those normally clear collagen fibers that have now, uh, become opacified because of their structural changes, then do we use it for longer?

Well, we can’t answer that with a study. Right. [00:59:00] But it might be intuitive to, we can’t answer it now with the study, but it might be intuitive to, to think that maybe it would, maybe it would be beneficial to support it longer. Maybe that 30% of patients did need a different dose, or they did need to carry out the, the treatment for longer.

Um, and so that’s where, what I think the beauty of being a clinician is, is that, is that, you know, evidence based medicine is, um, has. So long been thought and, and I’ve mis thought it as well that it is just pure research. It’s the pyramid of evidence, right? But, um, but remember that does that is important, Super important, but it’s also important to, to be able to apply that evidence to a specific patient population that may have been excluded from the evidence or included.

And then also being able to say, Well, what’s the logic behind that evidence? How does that logic actually make sense? And does it, does it mean that the e the study just wasn’t long enough to answer the question? But it doesn’t mean that it, it stops, right? It stops after six months, so, well, it’s no big deal.

We just [01:00:00] stop then, you know, Well, no, maybe we do keep going. Um, or maybe we stop and see if that patient’s symptoms come back and if they come back, you start again. I mean, it’s just an interesting thing to really think through. Um, and it’s kind of the unknown, right? You guys get to provide us with really good, uh, information about what we do know and what we can know.

And then we get to take what we can know and think, how would we apply this in a clinical situation? Thoughts. And that’s the beauty, 

Professor John Nolan: That’s the beauty of it. Because let’s just say I do a dose response or a 12 month intervention and we do phases. Like you answer all those questions and you create a whole other bunch of questions, , Which is fine.

Which is fine. I, I think the point I’m trying to make is sometimes you have to kind of work with the evidence that you have. Um, Exactly, exactly. You have to work with what we have. We can always look for the next piece. You know, the interesting thing about these nutrients, I think is relatively quick by which they get into the vitreous.

Now we need to determine that. Um, but’s, some evidence is like these are water soluble. The fat [01:01:00] soluble carotinoids that we use take time to affect the target tissues. I’m, I’m of the view that we can get these nutrients into the vitreous relatively quickly. And while we didn’t cut the experiment before six months, so I don’t, I can’t honestly tell you.

What would happen or what we know because that was the design and you’re not allowed to play with the design once you, once you publish what you’re gonna do. But what we’re seeing kind of clinically come back. You know, relatively quickly, you know, four weeks, five weeks, six people are starting to notice, um, difference.

And I’m one of those, you know, uh, here, here’s the supplement here. Now it’s, it’s, it’s the one I’ve never missed this since January of this year. And, and, and the reason being is I mentioned my tennis plane earlier. I was in Hawaii, I’m not sure if I told you this story, but I was in Hawaii at the island is conference I was presenting, um, with Frazier Horn and the group out of Pacific.

And um, I was doing my macular pig work and I had this really bad experience, unfortunately, where I was out [01:02:00] for my run. And I went swimming and I got into trouble in the ocean and I was basically saved by a teenager with a surfboard. My God. Wow. Yeah. So I’m lucky to be here. I was. I was. I was pretty much gone.

So yeah, remarkable experience. At seven 30 in the morning, this kid saved my life and I had to get on with my day. But the point is I felt following that, that my. Which I had became much more of a problem. Hmm. So I remember getting back to Ireland and I was playing tennis, um, one morning and I came back and I said to Jane, that was awful.

Jane would be my wife. That was awful. I said, I’m gonna have to take my own medicine here. So I, um, started taking, uh, Vitreous Health ViCAP that day and, um, Genuinely would not go without it. Now. That’s my experience. Wow. You know, so. 

Dr. Chris Wolfe: Wow. Let’s see. Well, I, I’m gonna have, I, it’s probably on a long run. I’m gonna have to explore that story about, [01:03:00] uh, about the surfer kid, but I’ll leave that for another, another day, our day.

Yeah. John Nolan, thanks so much for doing this again. It’s always so enlightening.

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