Talking 'Bout Degeneration
An in depth look at the treatments available for the eye condition Age related Macular Degenration (AMD), or lack of. It is also a personal journey for presenter and journalist Angela Young, who has the condition.
Talking 'Bout Degeneration
Episode 1: New Horizons in AMD Treatment
Imagine living with a condition that makes recognizing faces and navigating simple steps a daily challenge. Join us as Angela Young bravely shares her personal story of living with macular degeneration, a condition affecting over 700,000 people in the UK. We follow Angela to Spectacular Opticians for a revealing eye test and later hear from a consultant ophthalmologist James Neffendorf, who breaks down the complexities of AMD and dispels the myth that it’s just an “old person’s disease.”
Curious about how red light therapy could revolutionize eye health? Discover the promising advances brought by innovative devices like the Valeda System. Listen to firsthand accounts and research insights, including a significant US trial demonstrating vision improvements, and learn how red light therapy is providing hope for many.
Hear about real patient experiences, clinical trial results, and the potential for these therapies to change lives. Join us for an episode filled with cutting-edge research and inspiring stories of hope and resilience.
The executive producer is Vince Hunt
http://www.vincenthunt.co.uk/
The Voice over artist is Richard Westgate
https://www.linkedin.com/in/richard-westgate-186a1795/recent-activity/all/
Music performed by Mike Udin
https://www.facebook.com/profile.php?id=61558974233544
For information about red light therapy in the UK and where it will be offered next, contact Optegra:
https://www.optegra.com/dry-amd-treatment/
To find out about trials in Canada, visit Erie Retina Research https://erieretinaresearch.com/contact/
The Executive producer is Vince Hunt
http://www.vincenthunt.co.uk/
Music performed by Mike Udin
https://www.facebook.com/mike.udin.9
The statement from Clark Tedford was voiced by Dr Sean Lang https://expertfile.com/experts/sean.lang/sean-lang
Presenter Angela Young is the founder of Cambridge Podcasts https://cambridgepodcasts.co.uk/
Hello, I'm Angela Young and away Macular degeneration. Hello, I'm Angela Young and I have macular degeneration. This podcast aims to look into a condition which affects more than 700,000 people in the UK and is the biggest cause of sight loss in the country. You'll probably hear it called AMD or age-related macular degeneration, a term I don't like. Now, while it affects almost exclusively people over 55, I think the danger is that macular degeneration is then categorised as an old person's problem.
Speaker 1:I've no evidence for this, but it could explain why there's been so little progress in finding a cure or at least a treatment. It doesn't cause total blindness, but it can make things like reading and recognising faces difficult. I have difficulty distinguishing between grey and green. I complimented my niece's husband on his wedding day on his green waistcoat and he looked bemused, as it was grey. On a more serious note, I find it hard to see where an unmarked road meets the verge, and I've fallen off my beloved bike because of this. In fact, that's how I was first diagnosed in 2017. It might also explain why I have offended people when I don't remember who they are, as I can't recognise their face. If you're listening to this and have AMD, you'll have your own difficulties. I'm really afraid of concrete steps with no colour edging on them, in case I fall headfirst down them.
Speaker 1:My most recent eye test at my local opticians wasn't a happy experience. You know the chart with the letters Well. My left eye could manage reasonably well. My right eye struggled to see the outline of one massive letter blown up to fit one page of A4. There's a large bit missing in my central vision, called geographic atrophy. You can go on several websites to see what this looks like. They usually show a grey cloud hovering over the middle of an image. That's actually not what it's like. For me it's more as though someone has edited out a central bit of a picture and joined the outsides together. Anyway, come to Spectacular Opticians with me and meet senior optometrist Stuart Gibson.
Speaker 2:To give you some indication there has been significant you know, a significant drop off in the level of vision in the right eye and because of the macular degeneration you know, it is rapidly, rapidly progressing. Some people get it much earlier than others and unfortunately, in this instance that's what the case is. So just to try and quantify it from your point of view, if you look up there, you've got both eyes open yeah last time with glasses, we could get you to see the bottom line.
Speaker 2:Yes, there, um, in your right eye, okay, yeah, now today, we can't even achieve this level of vision in that right eye. So that is the degree of. So that's gone from 6 over 48 to 6 over 200.
Speaker 1:Now, if you go onto an NHS website, it will tell you without treatment, your vision may get worse. On the next page, it informs you that there is no treatment for dry AMD. Now, just an aside here if you have wet AMD, there are treatments which this podcast won't go into. I'm a former BBC Radio News editor and I like to question the status quo. I also thought that if I made a podcast about AMD, I could be a voice for other people with the condition and ask questions on their behalf. So talking about degeneration was born.
Speaker 1:Originally, it set out to be an investigation into what, if any, treatments were being developed. I started with the Macular Society, whose aim is to beat the fear and isolation of macular disease with world-class research and the best advice and support. They produce a monthly webinar which provides invaluable advice. I listened to the webinar on the changing landscape of treatment for AMD by James Neffendorf, consultant ophthalmologist at King's College Hospital in London, specialising in the retina, with an interest in AMD. Later I caught up with him one-to-one. I started by asking him to explain what AMD actually is Age-related macular degeneration, which is what we're really talking about today.
Speaker 4:I started by asking him to explain what AMD actually is. Age-related macular degeneration, which is what we're really talking about today, is an incredibly common condition and it's thought to affect probably somewhere between 10% and 20% of the over 65s. Now that's in varying degrees, of course. Some people have almost subclinical changes which you wouldn't necessarily know about and other people are essentially registered blind from the condition. So there's a huge spectrum of the condition and, broadly speaking, this is where the macula is not working as well and it starts to affect your central vision. And there are two broad types of macular degeneration.
Speaker 4:We have what we call dry macular degeneration and wet macular degeneration. Now, dry you can think of as a wear and tear type of macular degeneration. That is, and the way the distinction is made is a little bit crude, because traditionally people used to say well, if you get the wet type, it was very bad news. If you have the dry type, it was very slow, slightly progressive, but actually within the two subsets there are severity of disease themselves. So somebody with dry macular degeneration, which is the more common type, probably affecting, you know, 80 to 90 percent of those with macular degeneration they, you know, they can either just have some changes that we call drusen, which are these little deposits under the retina, or actually, as the disease gets more advanced, they can start to lose some of the tissue at the back of the eye and they can have these punched out lesions when we, when we look at the retina and that's called atrophic change and then we refer to that as geographic atrophy. So, and you know, a few drusen can still be compatible with completely normal vision and then, as you get to atrophic change, if the area of atrophy is not right at the center you can be fairly asymptomatic.
Speaker 4:But if the area of loss of retinal and RPE tissue is involving your fovea, so the very central part of the macula, then of course your sight can be very severely affected. So that's dry macular degeneration and then wet macular degeneration, as the name implies, is where there's been leakage of a fluid, either blood or just a general sort of fluid which is like having water on the film as the camera. Unfortunately, dry macular degeneration has lagged behind a little bit, even though it's more common, and that is a sad situation that we're in. However, I think the current sort of scope of what's out there is lending itself for a lot of potential benefit for these patients and I think we're not maybe at the crest of the wave, but we're approaching it in the next few years whereby we might have some treatments available for patients with dry AMD that we can really use and make a difference to people.
Speaker 1:So what are some of those treatments not only on the horizon, but actually available?
Speaker 4:There's a more non-invasive option which is the light therapy which some people may have heard about, and this is the Valeda system made by Lumathera, and that's the people more at the earliest stage of macular degeneration and there's potentially some mild visual benefit and possibly some reduction in the progression with with that treatment. And then you get to slightly more cutting edge research which are things like gene therapy or cell-based treatments, so stem cells, and that's obviously very much in its infancy, but actually these things are closer than we might think to clinical practice. So that gives you a bit of an overview of what's out there.
Speaker 1:I had signed up for a trial of one of the latter two gene therapy but it turned out I wasn't eligible and I was feeling quite despondent. The Macular Society had previously provided another webinar on red light therapy by Glenn Jeffery, professor of Neuroscience at the Institute of Ophthalmology at University College in London, so I went to talk to him too. He explained that red light targets something called mitochondria.
Speaker 5:Mitochondria are the body's batteries. You've got thousands of mitochondria in each of your cells. They make energy and as you get old, the energy level declines. That's why it's a little bit harder to swing your legs out of bed in the morning and it's also why your vision declines. Mitochondria are the key batteries, but mitochondria are influenced by light, so we can use different wavelengths of light to either charge the battery, give you a bit more energy, or to discharge the battery, and the consequences of which are that you suffer from visual decline, also caused by light.
Speaker 5:Yeah, light is, if you think about about it. For millions of years you've evolved under sunlight, which has a very wide spectrum. Um, as you get, we're now, people are now making it to 82 83. Very happily, you shouldn't do that in evolution. You should probably be dead in your 40s um. So your batteries are being tested by your increased longevity. Your batteries are also being tested because you are in light environments. You shouldn't be in, like inside buildings with led lighting. So it's a challenge. It is a challenge, but it is a disease extension of living too long.
Speaker 1:So what does red light therapy do and how can it help and how can it be used?
Speaker 5:Red light therapy recharges the battery, the mitochondria, like putting a toothbrush back on the stand. It's extremely simple. Critically, it's very safe because the wavelengths of light we're giving you are the wavelengths of light you get in sunlight. Ok, so it is the red component of sunlight. So far we have found absolutely no downside whatsoever for using red light and we shouldn't do. We're using energies that are within reach of sunlight and it is a component of sunlight.
Speaker 1:So can you tell me about what you know about current trials or completed trials using red?
Speaker 5:light therapy. Okay, so this is. This is where the breaking edge of the wave is currently. At the moment, red light is great at catching an early disease that has energy based all right. So there are now some studies coming out which look for macular degeneration look extremely positive. I must admit they do look positive, but the key thing is it's safe. I have two elderly aunts and I've been running them on red light for quite a while and I probably use red light twice a week and most of my lab do.
Speaker 1:In what form?
Speaker 5:We bounce it off the walls in a from a big lamp, um, so you can buy big lamps that give off, uh, near infrared, and um, they're relatively cheap and, yeah, you just bounce it off a wall. Now, in in the olden days, as it were, when we had incandescent light bulbs, we had a large amount of infrared light in them, so there was a degree of protection. Now we have LED lights and there is no infrared light in them. So what we're doing is we're driving the aging process a little bit by using lights that don't have infrared light in them and and sadly, lights have got a lot of blue in them and that blue is discharging your battery.
Speaker 1:so bad news in an aging population if we're not you and don't have a lamp to bounce off walls, what are our options?
Speaker 5:well, the best option on the planet is go for a walk. Go for a walk outside. There is loads of infrared light outside. There is nothing super complicated about this. So all of the studies that we have done we have done with relatively simple devices that cost relatively little.
Speaker 1:So, for example, there is a pair of glasses available from a company based just outside Bath, I think they're £60 for a pair of glasses that you charge with a USB charger and sit in bed for three minutes once a week. Is that comparable to the effects of something?
Speaker 5:like Valida. Well, in terms of what it does, biologically they would not agree with me, but I see no difference. Um, I I don't have a commercial interest. However, I've tested those and they do what they as they say. They do what they say on the packet and they are perfectly safe. So I only tested them because if people come and ask me, I want to be able to say well, there is something out there there. If you go on the web, you will find hundreds of devices. Most of them are not safe. Most of them are relatively untested. Most of them will fall apart in a few months. Most of them will not do what they say they do.
Speaker 1:I tracked down the man who had designed the glasses Stephen Allen. He's not an ophthalmologist, but the director of a lighting company.
Speaker 6:I've always been interested in science technology, so I always keep an eye on what's going out in the academic press. I sort of look at various news feeds and science articles and I saw one that really sort of caught my eye and I could see a degree of synergy because, as the director of a lighting company, could see a degree of synergy because, as the director of a lighting company, I saw the work by Professor Glenn Jeffrey of UCL, who just published a paper on the use of red light to help with reducing the ageing of the eye.
Speaker 6:I thought aha, brilliant, nice synergy here. I know everything about lighting, he knows everything about eyes, so let's have a conversation. He was very, very supportive and suggested I went away and did my research and he would sort of provide help and advice where he could, so effectively. That's what happened. I went away and started to do my research.
Speaker 1:And what was the product you came up with?
Speaker 6:We called it the iPower. Because it shines out red light, it's called the iPower Red. We looked at various designs initially. Some would make you laugh. I mean they're almost out of Star Trek. In fact, the very first design I did was almost like a half face mask with sort of full eye goggles, which looked horrible. In hindsight I still have a 3D print down in the workshop and I look back at it now and think what was I thinking? But in the end it sort of slimmed down and with a bit of advice from Glenn and from his colleague Chris Hogg, we sort of focused on more of a sort of substitute for glasses rather than goggles themselves.
Speaker 1:So tell me how does it work and what does the user have to do?
Speaker 6:We've tried to make it as simple as possible for the user, because we appreciate that we're trying to attract a very wide demographic here. So the whole strategy was to have something that somebody could take out the box, just put on as they would a normal pair of glasses and with just the press of of the button, actually activate and complete a single session. So that's what we've built into the glasses, so you simply put them on. There's a little button at the bottom, a little clear plastic button which you push. As soon as you push that, it activates the light. It goes through a little two-stage process which we built into it. So for three seconds it comes on at half brightness just to make somebody aware that the session is about to start. Then, after the three seconds, it goes to full brightness and you then get a full three minute session of 670 nanometer red light.
Speaker 1:Stephen sent me a pair of glasses and I've been using them once a week on a Saturday morning. It actually feels as though I'm lying on a sunbed for those three minutes. It was around this time that an article appeared in the press about a private eye hospital which was offering what was hailed as the first treatment for AMD in the UK, based on the results of the LightSight 3 study which James Neffendorf referred to. It was the trial in the US of red light therapy, or photobiomodulation, which had some very promising results, the Daily Telegraph reported.
Speaker 7:Patients with a degenerative eye condition could keep their sight for longer, thanks to the development of the first treatment of the condition After successful trials in the US, a light therapy treatment that claims to help patients maintain or improve their vision. It went on at the back of the eye.
Speaker 7:A randomized control trial of the technology in the US found dry AMD patients who had the light therapy delivered through a device called Valeda experienced almost double the improvements in their vision after 13 months of treatment compared to those treated with the dummy device.
Speaker 7:The patients, who were all over 50, received a cycle of nine sessions of five-minute treatments over three to five weeks, repeated once every four months. At the end of the study, patients treated with Valeda were able to read 5.4 more letters on a site chart. Treated patients also had less of a type of swelling within the eye which can indicate the disease is progressing, compared with those treated with a dummy device. The study published last month in the journal Retina was led by the technology's manufacturer Lumathera and tested on a small group of 100 patients. Its effectiveness is currently being assessed in clinical trials and it is yet to be considered by the National Institute for Health and Care Excellence in England and Wales for use in the NHS, but it has been approved for sale in Europe. The technology is now available at a handful of private clinics in the UK and has just been launched by the Optegra Eye Hospital Group, the first chain to take it on. The company is trialling its device at its Manchester hospital before rolling it out nationally.
Speaker 1:I wanted to look into these claims in a bit more detail, so I asked James Neffendorf to explain how red light therapy works. Like Glenn, he says it's all about the mitochondria.
Speaker 4:We've known for many years that light actually can damage the retina and for that reason, as you know, places like the Macula Society advocate sunglasses or wearing a cap if you're out in sunny conditions.
Speaker 4:But it's probably to do with the type of light, the type of exposure and how that's done and the wavelength, which is what you're referring to. And this Valeda system uses three different wavelengths that are shown at the eye one in the infrared range of the light spectrum and two within the visual spectrum and these wavelengths are thought to stimulate the cells and specifically the mitochondria inside the cells. So the mitochondria like the powerhouses, the energy building blocks, and they produce ATP and this drives the energy and the ability for the cell to work. And we also know that if you activate the mitochondria with red light, you potentially improve their function. You reduce the inflammation, because it reduces the cytokine release, and we know inflammation is implicated in macular degeneration and also they release nitric oxide, which is a molecule that's involved in the dilation of blood vessels, or they help stimulate that release. So there are various aspects of why red light might be protective or support the back of the eye.
Speaker 1:The Macular Society then produced another webinar exploring the Valida system presented by Tim Jackson, consultant ophthalmologist and professor of retinal research at King's College Hospital. In the webinar he explained the results of the trial. It had 100 patients.
Speaker 8:Some patients had treatment in both eyes. So 100 patients and 148 eyes Patients are randomised to active or sham treatment. By sham I mean sort of fake or placebo treatment, so the patient wouldn't necessarily know. It was designed not to let them know whether or not the treatment was real or not. Whenever you design a clinical trial, it's very, very important that the patients who have the treatment were the same as the patients that were on the trial, Because if you're not comparing like with like, then you really don't know whether or not the technology is safe and whether or not it works.
Speaker 8:So the patients had to have dry AMD. The vision had to be between 2032 and 2100. Those are US metrics, but I think it's the closest that anybody's familiar with the so-called 2020 phase phrase. So 2020 doesn't mean perfect vision, it means normal vision. So 2030 is sort of moderately reduced vision. Still be good enough to drive the drusen, which are these little yellow deposits in the back of the eye. They're a telltale sign of AMD. Now lots of people have a small number of very tiny drusen. The patients on this clinical trial had medium-sized drusen, so it's important that you confirm that you have drusen of this size before considering the technology. Patients could also get onto the trial though, if they instead, or also, had non-central geographic atrophy Now by that I mean an area in the back of the eye where the cells have died away. But the patients were eligible if they had some GA, as it's called, but not if it involved the very center of the eye, the fovea, where the light comes to focus. Because if you have GA in the center of the fovea, where the light comes to focus, then the vision is usually poor and maybe irretrievable, sadly, at that stage. So these are looking for patients who have GA, but not involving the foveal center. So, looking at the results of the trial, so the main outcome that was pre-specified was vision. This is main outcome is at month 13, but the trial does continue to month 21.
Speaker 8:So if we look at the active group, these are the patients who had the real treatment. They gained 5.4 letters. Now, 5.4 letters is a measure of visual function and a greater gain is a better vision, but these are relatively small numbers. So to put this into context, these five letters, if any of you have had your vision tested on an eye chart, the sort of normal eye chart that you might see if you go to the optician or if you're attending an eye clinic in hospital. One five letters is the same as one line on the eye chart. So if you looked at the eye chart and you could read the letters at one line, if your vision improved by five letters, it would mean that you could get down to the next line on the chart and see the second row of smaller letters.
Speaker 8:One of the things that makes the trial more difficult to interpret is that the sham group those that didn't get the active treatment that may have thought they did gained three letters as well. Maybe that's just a chance finding it's not real. Well, maybe perhaps they got better at doing the vision test. Now, of course, you've got to take off that result in the sham group, because if the patient would have naturally got better anyway, that 5.4 letter gain isn't 5.4 letters. What we look at is the difference between the two groups of the trial and what we see. If we look at the difference between the two, which is just simple subtraction, then there was a difference of 2.4 letters between the active group and the sham group. Now the question then is is 2.4 letters going to make a difference to somebody having the treatment? Would they notice it and 2.4 letters probably isn't something the patient would necessarily notice.
Speaker 8:One of the things that's been sort of made some noise about within the trial is that the active group of participants developed were less likely to develop geographic atrophy. So that's potentially of real interest because expanding geographic atrophy if this expanding geographic atrophy expands to take in the fovea, then the vision will drop, and often quite substantially. So we like to avoid geographic atrophy. Now the trial looked at geographic atrophy. From what I've been able to delineate, the trial set out to work out whether or not this treatment would reduce the expansion of geographic atrophy. It looked at the size of the geographic atrophy and the statistical tests suggested it didn't make a difference. So in terms of the conclusions, I think LightSight 3 was a well-designed trial.
Speaker 8:It ticked a number of important boxes. It was randomized and sham controlled and those are two of the most important things in trying to maintain objectivity of a clinical trial. So we like that. But compared to the drug trials it's tiny, very, very small study and this is an important disease. If you were studying a very rare disease then 100 patients would be a big trial, but this is no stretch that this could possibly be imagined as a rare disease. It's not. It's an extremely common disease and in that setting we need to have a much higher burden of proof. We need to have studies that give us real certainty, because if we're going to roll this out and use it in thousands, tens of thousands, even hundreds of thousands of patients, then we need to have huge certainty that actually it does work.
Speaker 1:By now. I wanted to speak to my brilliant executive producer, vince Hunt, an analytical Mancunian with a messianic zeal for seeing through press releases. Now he happens to live in the area of Manchester where the Optegra Hospital, which is offering the Valida system, is based. So I gave him a ring. Hi, vince, it's Angela. Hi, angela, how are you? Yeah, not bad, thank you, you live in. Manchester, don't you?
Speaker 10:I do.
Speaker 1:Can you visit the Optegra Hospital I don't think it's far from you and do a recording for me.
Speaker 10:Yeah, sure, yeah, it isn't far away.
Speaker 1:No, Well, they've just introduced something called red light therapy for macular degeneration. It is actually the only place offering it at the moment and it's only being available privately. And it's quite expensive.
Speaker 10:It's about 1500 pounds for a round of treatment and they're suggesting three a year, so I'm wondering if you can go and find out a bit more about it. Yeah, sure, sounds interesting. Sounds expensive, but very much worth looking into for the purposes of your programme. I'm on my way.
Speaker 1:Thanks, Vince.
Speaker 11:OK, this is Octegnodon and I've even managed to find a parking space. Let's go inside and meet Sarge.
Speaker 9:My name's Sir Stadler, I'm a consulting ethnologist and I work primarily with October.
Speaker 11:It seems that you've identified an area for which there was no treatment and you've formulated a treatment.
Speaker 9:The dry metal generation things have been tried over the years. This is one therapy. It was first tried around seven years ago. It's called photobiomodulation. It uses certain wavelengths of light to stimulate the retina, to stimulate the retina cells which are losing their function in the context of biomethode generation, and so I've been watching the development of that over the last seven years or so. Other things that are in development of biomethode generation are actually eye injections similar to injections for that of dry method of generation are actually are injections similar to injections for that or given methods of generation, and that's still not available and that comes with potential issues that we need to be discussing with. But what I was interested in was the obvious stages of dry method of generation in places that have puncture and vision but and they're looking for some treatment. Now I didn't rush into open presence and the treatment.
Speaker 9:I've been looking at the studies that are ongoing over the last seven years or so in this treatment for photobiomagnetization and that's been for a number of things. I've had the largest trial reported last year and the products are the light type studies and so the third industrial study was reported last year and I was given additional reassurance because the studies are done in lab, very representative centres. There's some university centres in the United States with data also objectively and independently within it. If the imaging gets that, we look at the change in the scan and things that we do and that is independently reduced by the reading center. So I thought the trial that we found was of sufficient quality and the data, the fracturing, the data that's showing the patient could be obviously die over with macular degeneration, a slow bolization and an average of a little bit of improvement in living, but more importantly, the disease process being slow down and less to the function.
Speaker 9:What we look at in the case of dry ovary with macular degeneration, the early showing that the cells are losing function, is that suddenly the presence of the problem is losing better, sign that the cell's own function is well. And so we saw in the studies that patients who were under-treated versus those who weren't showed a showed less accumulation of this material, indicating that cell paints are having teeth. And also what we see with dry metal generation is a progression from the oldest stages, where some species have lesions and some milder than that, to more severe than that. We call that the light stage or the ectopic stage and present on treatment, there was a significant reduction in the percentage of patients that went on to the light phase of the method of generation. So in the studies, patients without treatment, that could be 10% of them and the other two that went on to the most severe light phase and that was reduced about 5-6% in people who were in treatment A big reduction.
Speaker 9:So, given that there was a potential legal benefit and also some effective evidence of independently reviewed evidence of the disease process benefiting, I felt the data was strong enough to start to offer the treatment myself of the disease process benefiting. I felt the data was strong enough to start the treatment myself. And I didn't you know I was into it but the machine's been around for most of the idea for about five years and it's been the first baby. But I go to them saying the data was strong enough and I would say, from my thinking, the data was strong enough that if I remember what I got to buy, I'd be happy to have the treatment available.
Speaker 11:Having had a chat in the consulting room with Sarge, I then moved across the corridor to see how this treatment actually works, and I sat in on the session with John.
Speaker 12:I'm going to bring that down a little bit Now, up or down.
Speaker 3:Probably up.
Speaker 12:Up a little bit, a bit more. No, that's about right, that's it Right, and we are doing both eyes.
Speaker 9:We are.
Speaker 12:And can I have your date of birth?
Speaker 3:18 to the 5th 1948.
Speaker 12:Yeah, make sure it's you. I know it's you, but we'll make sure it's you. Right, just bear with me. Let me sort the machine out for you and we'll start with your right eye.
Speaker 8:Yep.
Speaker 12:And I'll line you up. First one 30 seconds and your eyes are open. Okay, Are you ready to go? Yeah, Off, we go 30 seconds 30 seconds.
Speaker 3:18 months ago at the optician's, when I was on a routine eye check, they told me at the end of it that I'd got muscular degeneration. And I knew that I'd had muscular degeneration. So it sparked a fear straight away. I'd observed that I was struggling reading, but then I thought, well, I want to do something with opinion. So I asked if I could go to the hospital in Manchester. The doctor sorted that out and they needed to transfer me over into an NHS term at the time. So I came down there, had a few tests and they confirmed yeah, matthew is a Dermatologist.
Speaker 3:Dermatologist, my time was done there macular degeneration, where light-time was from the left. And then it was promising for me actually, because I asked about is there something going on in America? And with that they said yeah, there is, and there could be something that you know the whole plant scene would have considered Well, we haven't got a lot of chance with macular degeneration, you can't stand still. So I said yes, I would consider it Fully, appreciating that it was going to be private, it would not be a mention of that. And then the second bout of main treatment. They've had the first one and then the third one of the second one and they are picking up improvements from my test.
Speaker 11:You've just come out from the treatment room.
Speaker 3:How do you think? I noticed after about six or seven of the processes from the first round that I was starting to pick things up on the television, on the screen, where I couldn't read things on the screen. I was starting to read things on the screen, not all of it, but enough to make me think, oh, there was some improvement there. When I came back and did the benchmarking, before we started the second process, the second round, we did a benchmark test to go back against the first and straight away the doctor said to me we've got subjective evidence that you're improving. I said and I'm not feeling subjective he said that you've also got other evidence, clear evidence, scientific evidence, and there's photographs and stuff that were taken at the back of the island. But things are improving now.
Speaker 3:It's a miss, it's quite early because we'd expect to see this into the second phase, not straight after the first one. And the thing with this is about hope. I think, yeah, there's got to be. That hasn't there. You know, if you weren't ploughing this furrow, you'd be sat at home just thinking this is slowly going downhill. It's going nowhere, at least with this. Whether you're touching it straws or not remains to be seen. I'll accept that you know a lot of this is in its early days, but it does give you hope and that is a big thing, I think you know. You know put that against clown shows and clowns, and I can't spend it when I'm in the shower, can I? So you know, let's get on with it and see what happens.
Speaker 1:As soon as Vince came out of the Octepra hospital, a funny thing happened. He called me Angela. Hi Vince, how did you get on?
Speaker 10:Yeah, really good thanks. Look, I'm at Optegra and I'm really, really impressed with what's going on here, so I thought I'd call you straight away and tell you what's been going on. I've been talking to the consultant, ophthalmologist Sarge Mahmood, and he's really confident about this treatment and they have a lot of people signing up and I've spoken to one or two of them and the things that they are saying. I really think that you ought to be considering this treatment yourself.
Speaker 1:Really.
Speaker 10:Well, you know, Manchester's not that far away. However, they are talking about rolling it out in London and of course, that's an hour from where you are.
Speaker 1:Why are you so convinced?
Speaker 10:Well, it comes really from the testimony of people who have been having this treatment. I mean, obviously it's better if you live close to the Optegra hospital, but some of the results, some of the short-term results from the first cycle are showing better results than they had expected and this is really really encouraging. And what that's doing is it's giving the people with AMD a much more positive outlook. It's giving them hope and I think in this case, as somebody who's short-sighted, if your eyesight starts to go, that can be really really frightening and it completely affects your philosophy, your perspective on life, your mobility and everything. So you know, if this is something that you're looking into, I would say it definitely bears further investigation.
Speaker 1:Wow, I think I'd better ring Optegra Well. Thanks very much, Vince.
Speaker 10:No problem, Angela.
Speaker 1:I have to say I contemplated moving to Manchester, but then I heard that Optegra was going to start offering Valida in London and I signed up for an assessment to see if I'm eligible. So this podcast has now taken a new turn and it will follow my Valida journey. I'm not sure if I will be eligible, but I'm certainly going to get assessed. I hope you'll stay with me for the second episode of Talking About Degeneration. Huge thanks to executive producer Vince Hunt and the Optegra Eye Hospital, manchester, to voiceover artist Richard Westgate who recorded the newspaper article, and to musician Mike Udin who recorded our special new version of the who classic Talking About my Generation. Links to their websites and bios are on the show notes. Bye for now. This has been a Cambridge Podcast production written and produced by me, angela Young. Thank you.