July 2, 2024 • 40 mins
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/
Mark as Played
Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:20):
Hello, I'm Angela Young and away Macular
degeneration.
Hello, I'm Angela Young and Ihave macular degeneration.
This podcast aims to look intoa condition which affects more
than 700,000 people in the UKand is the biggest cause of
sight loss in the country.
You'll probably hear it calledAMD or age-related macular
(00:42):
degeneration, a term I don'tlike.
Now, while it affects almostexclusively people over 55, I
think the danger is that maculardegeneration is then
categorised as an old person'sproblem.
I've no evidence for this, butit could explain why there's
been so little progress infinding a cure or at least a
treatment.
It doesn't cause totalblindness, but it can make
(01:04):
things like reading andrecognising faces difficult.
I have difficultydistinguishing between grey and
green.
I complimented my niece'shusband on his wedding day on
his green waistcoat and helooked bemused, as it was grey.
On a more serious note, I findit hard to see where an unmarked
road meets the verge, and I'vefallen off my beloved bike
(01:25):
because of this.
In fact, that's how I was firstdiagnosed in 2017.
It might also explain why Ihave offended people when I
don't remember who they are, asI can't recognise their face.
If you're listening to this andhave AMD, you'll have your own
difficulties.
I'm really afraid of concretesteps with no colour edging on
(01:45):
them, in case I fall headfirstdown them.
My most recent eye test at mylocal opticians wasn't a happy
experience.
You know the chart with theletters Well.
My left eye could managereasonably well.
My right eye struggled to seethe outline of one massive
letter blown up to fit one pageof A4.
There's a large bit missing inmy central vision, called
(02:06):
geographic atrophy.
You can go on several websitesto see what this looks like.
They usually show a grey cloudhovering over the middle of an
image.
That's actually not what it'slike.
For me it's more as thoughsomeone has edited out a central
bit of a picture and joined theoutsides together.
Anyway, come to SpectacularOpticians with me and meet
(02:26):
senior optometrist Stuart Gibson.
Speaker 2 (02:30):
To give you some indication there has been
significant you know, asignificant drop off in the
level of vision in the right eyeand because of the macular
degeneration you know, it israpidly, rapidly progressing.
Some people get it much earlierthan others and unfortunately,
in this instance that's what thecase is.
(02:50):
So just to try and quantify itfrom your point of view, if you
look up there, you've got botheyes open yeah last time with
glasses, we could get you to seethe bottom line.
Yes, there, um, in your righteye, okay, yeah, now today, we
(03:12):
can't even achieve this level ofvision in that right eye.
So that is the degree of.
So that's gone from 6 over 48to 6 over 200.
Speaker 1 (03:30):
Now, if you go onto an NHS website, it will tell you
without treatment, your visionmay get worse.
On the next page, it informsyou that there is no treatment
for dry AMD.
Now, just an aside here if youhave wet AMD, there are
treatments which this podcastwon't go into.
I'm a former BBC Radio Newseditor and I like to question
(03:52):
the status quo.
I also thought that if I made apodcast about AMD, I could be a
voice for other people with thecondition and ask questions on
their behalf.
So talking about degenerationwas born.
Originally, it set out to be aninvestigation into what, if any,
treatments were being developed.
I started with the MacularSociety, whose aim is to beat
(04:13):
the fear and isolation ofmacular disease with world-class
research and the best adviceand support.
They produce a monthly webinarwhich provides invaluable advice
.
I listened to the webinar onthe changing landscape of
treatment for AMD by JamesNeffendorf, consultant
ophthalmologist at King'sCollege Hospital in London,
(04:33):
specialising in the retina, withan interest in AMD.
Later I caught up with himone-to-one.
I started by asking him toexplain what AMD actually is
Age-related macular degeneration, which is what we're really
talking about today.
Speaker 4 (04:45):
I started by asking him to explain what AMD actually
is.
Age-related maculardegeneration, which is what
we're really talking about today, is an incredibly common
condition and it's thought toaffect probably somewhere
between 10% and 20% of the over65s.
Now that's in varying degrees,of course.
Some people have almostsubclinical changes which you
(05:07):
wouldn't necessarily know aboutand other people are essentially
registered blind from thecondition.
So there's a huge spectrum ofthe condition and, broadly
speaking, this is where themacula is not working as well
and it starts to affect yourcentral vision.
And there are two broad typesof macular degeneration.
(05:27):
We have what we call dry maculardegeneration and wet macular
degeneration.
Now, dry you can think of as awear and tear type of macular
degeneration.
That is, and the way thedistinction is made is a little
bit crude, because traditionallypeople used to say well, if you
get the wet type, it was verybad news.
If you have the dry type, itwas very slow, slightly
(05:49):
progressive, but actually withinthe two subsets there are
severity of disease themselves.
So somebody with dry maculardegeneration, which is the more
common type, probably affecting,you know, 80 to 90 percent of
those with macular degenerationthey, you know, they can either
just have some changes that wecall drusen, which are these
(06:11):
little deposits under the retina, or actually, as the disease
gets more advanced, they canstart to lose some of the tissue
at the back of the eye and theycan have these punched out
lesions when we, when we look atthe retina and that's called
atrophic change and then werefer to that as geographic
atrophy.
So, and you know, a few drusencan still be compatible with
(06:32):
completely normal vision andthen, as you get to atrophic
change, if the area of atrophyis not right at the center you
can be fairly asymptomatic.
But if the area of loss ofretinal and RPE tissue is
involving your fovea, so thevery central part of the macula,
then of course your sight canbe very severely affected.
(06:53):
So that's dry maculardegeneration and then wet
macular degeneration, as thename implies, is where there's
been leakage of a fluid, eitherblood or just a general sort of
fluid which is like having wateron the film as the camera.
Unfortunately, dry maculardegeneration has lagged behind a
little bit, even though it'smore common, and that is a sad
(07:17):
situation that we're in.
However, I think the currentsort of scope of what's out
there is lending itself for alot of potential benefit for
these patients and I think we'renot maybe at the crest of the
wave, but we're approaching itin the next few years whereby we
(07:38):
might have some treatmentsavailable for patients with dry
AMD that we can really use andmake a difference to people.
Speaker 1 (07:46):
So what are some of those treatments not only on the
horizon, but actually available?
Speaker 4 (07:52):
There's a more non-invasive option which is the
light therapy which some peoplemay have heard about, and this
is the Valeda system made byLumathera, and that's the people
more at the earliest stage ofmacular degeneration and there's
potentially some mild visualbenefit and possibly some
reduction in the progressionwith with that treatment.
(08:13):
And then you get to slightlymore cutting edge research which
are things like gene therapy orcell-based treatments, so stem
cells, and that's obviously verymuch in its infancy, but
actually these things are closerthan we might think to clinical
(08:33):
practice.
So that gives you a bit of anoverview of what's out there.
Speaker 1 (08:38):
I had signed up for a trial of one of the latter two
gene therapy but it turned out Iwasn't eligible and I was
feeling quite despondent.
The Macular Society hadpreviously provided another
webinar on red light therapy byGlenn Jeffery, professor of
Neuroscience at the Institute ofOphthalmology at University
College in London, so I went totalk to him too.
(08:59):
He explained that red lighttargets something called
mitochondria.
Speaker 5 (09:05):
Mitochondria are the body's batteries.
You've got thousands ofmitochondria in each of your
cells.
They make energy and as you getold, the energy level declines.
That's why it's a little bitharder to swing your legs out of
bed in the morning and it'salso why your vision declines.
Mitochondria are the keybatteries, but mitochondria are
(09:29):
influenced by light, so we canuse different wavelengths of
light to either charge thebattery, give you a bit more
energy, or to discharge thebattery, and the consequences of
which are that you suffer fromvisual decline, also caused by
light.
Yeah, light is, if you thinkabout about it.
(09:50):
For millions of years you'veevolved 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 dothat in evolution.
You should probably be dead inyour 40s um.
So your batteries are beingtested by your increased
(10:10):
longevity.
Your batteries are also beingtested because you are in light
environments.
You shouldn't be in, likeinside buildings with led
lighting.
So it's a challenge.
It is a challenge, but it is adisease extension of living too
(10:44):
long.
Speaker 1 (10:44):
So what does red light therapy do and how can it
help and how can it be used?
Speaker 5 (10:50):
Red light therapy recharges the battery, the
mitochondria, like putting atoothbrush back on the stand.
It's extremely simple.
Critically, it's very safebecause the wavelengths of light
we're giving you are thewavelengths of light you get in
sunlight.
Ok, so it is the red componentof sunlight.
(11:13):
So far we have found absolutelyno downside whatsoever for
using red light and we shouldn'tdo.
We're using energies that arewithin reach of sunlight and it
is a component of sunlight.
Speaker 1 (11:23):
So can you tell me about what you know about
current trials or completedtrials using red?
Speaker 5 (11:28):
light therapy.
Okay, so this is.
This is where the breaking edgeof the wave is currently.
At the moment, red light isgreat at catching an early
disease that has energy basedall right.
So there are now some studiescoming out which look for
macular degeneration lookextremely positive.
(11:50):
I must admit they do lookpositive, but the key thing is
it's safe.
I have two elderly aunts andI've been running them on red
light for quite a while and Iprobably use red light twice a
week and most of my lab do.
Speaker 1 (12:05):
In what form?
Speaker 5 (12:07):
We bounce it off the walls in a from a big lamp, um,
so you can buy big lamps thatgive off, uh, near infrared, and
um, they're relatively cheapand, yeah, you just bounce it
off a wall.
Now, in in the olden days, asit were, when we had
incandescent light bulbs, we hada large amount of infrared
(12:31):
light in them, so there was adegree of protection.
Now we have LED lights andthere is no infrared light in
them.
So what we're doing is we'redriving the aging process a
little bit by using lights thatdon't have infrared light in
them and and sadly, lights havegot a lot of blue in them and
(12:51):
that blue is discharging yourbattery.
Speaker 1 (12:55):
so bad news in an aging population if we're not
you and don't have a lamp tobounce off walls, what are our
options?
Speaker 5 (13:06):
well, the best option on the planet is go for a walk.
Go for a walk outside.
There is loads of infraredlight outside.
There is nothing supercomplicated about this.
So all of the studies that wehave done we have done with
relatively simple devices thatcost relatively little.
Speaker 1 (13:26):
So, for example, there is a pair of glasses
available from a company basedjust outside Bath, I think
they're £60 for a pair ofglasses that you charge with a
USB charger and sit in bed forthree minutes once a week.
Is that comparable to theeffects of something?
Speaker 5 (13:42):
like Valida.
Well, in terms of what it does,biologically they would not
agree with me, but I see nodifference.
Um, I I don't have a commercialinterest.
However, I've tested those andthey do what they as they say.
They do what they say on thepacket and they are perfectly
safe.
So I only tested them becauseif people come and ask me, I
(14:03):
want to be able to say well,there is something out there
there.
If you go on the web, you willfind hundreds of devices.
Most of them are not safe.
Most of them are relativelyuntested.
Most of them will fall apart ina few months.
Most of them will not do whatthey say they do.
Speaker 1 (14:19):
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 (14:27):
I've always been interested in science technology
, so I always keep an eye onwhat's going out in the academic
press.
I sort of look at various newsfeeds and science articles and I
saw one that really sort ofcaught my eye and I could see a
degree of synergy because, asthe director of a lighting
(14:48):
company, could see a degree ofsynergy because, as the director
of a lighting company, I sawthe work by Professor Glenn
Jeffrey of UCL, who justpublished a paper on the use of
red light to help with reducingthe ageing of the eye.
I thought aha, brilliant, nicesynergy here.
I know everything aboutlighting, he knows everything
(15:09):
about eyes, so let's have aconversation.
He was very, very supportiveand suggested I went away and
did my research and he wouldsort of provide help and advice
where he could, so effectively.
That's what happened.
I went away and started to domy research.
Speaker 1 (15:28):
And what was the product you came up with?
Speaker 6 (15:31):
We called it the iPower.
Because it shines out red light, it's called the iPower Red.
We looked at various designsinitially.
Some would make you laugh.
I mean they're almost out ofStar Trek.
In fact, the very first designI did was almost like a half
(15:52):
face mask with sort of full eyegoggles, which looked horrible.
In hindsight I still have a 3Dprint down in the workshop and I
look back at it now and thinkwhat was I thinking?
But in the end it sort ofslimmed down and with a bit of
advice from Glenn and from hiscolleague Chris Hogg, we sort of
(16:15):
focused on more of a sort ofsubstitute for glasses rather
than goggles themselves.
Speaker 1 (16:22):
So tell me how does it work and what does the user
have to do?
Speaker 6 (16:25):
We've tried to make it as simple as possible for the
user, because we appreciatethat we're trying to attract a
very wide demographic here.
So the whole strategy was tohave something that somebody
could take out the box, just puton as they would a normal pair
of glasses and with just thepress of of the button, actually
(16:48):
activate and complete a singlesession.
So that's what we've built intothe glasses, so you simply put
them on.
There's a little button at thebottom, a little clear plastic
button which you push.
As soon as you push that, itactivates the light.
It goes through a littletwo-stage process which we built
(17:09):
into it.
So for three seconds it comeson at half brightness just to
make somebody aware that thesession is about to start.
Then, after the three seconds,it goes to full brightness and
you then get a full three minutesession of 670 nanometer red
light.
Speaker 1 (17:27):
Stephen sent me a pair of glasses and I've been
using them once a week on aSaturday morning.
It actually feels as though I'mlying on a sunbed for those
three minutes.
It was around this time that anarticle appeared in the press
about a private eye hospitalwhich was offering what was
hailed as the first treatmentfor AMD in the UK, based on the
results of the LightSight 3study which James Neffendorf
(17:50):
referred to.
It was the trial in the US ofred light therapy, or
photobiomodulation, which hadsome very promising results, the
Daily Telegraph reported.
Speaker 7 (18:01):
Patients with a degenerative eye condition could
keep their sight for longer,thanks to the development of the
first treatment of thecondition After successful
trials in the US, a lighttherapy treatment that claims to
help patients maintain orimprove their vision.
It went on at the back of theeye.
A randomized control trial ofthe technology in the US found
dry AMD patients who had thelight therapy delivered through
(18:32):
a device called Valedaexperienced almost double the
improvements in their visionafter 13 months of treatment
compared to those treated withthe dummy device.
The patients, who were all over50, received a cycle of nine
sessions of five-minutetreatments over three to five
weeks, repeated once every fourmonths.
At the end of the study,patients treated with Valeda
(18:55):
were able to read 5.4 moreletters on a site chart.
Treated patients also had lessof a type of swelling within the
eye which can indicate thedisease is progressing, compared
with those treated with a dummydevice.
The study published last monthin the journal Retina was led by
the technology's manufacturerLumathera and tested on a small
group of 100 patients.
Its effectiveness is currentlybeing assessed in clinical
trials and it is yet to beconsidered by the National
(19:17):
Institute for Health and CareExcellence in England and Wales
for use in the NHS, but it hasbeen approved for sale in Europe
.
The technology is now availableat a handful of private clinics
in the UK and has just beenlaunched by the Optegra Eye
Hospital Group, the first chainto take it on.
The company is trialling itsdevice at its Manchester
hospital before rolling it outnationally.
Speaker 1 (19:38):
I wanted to look into these claims in a bit more
detail, so I asked JamesNeffendorf to explain how red
light therapy works.
Like Glenn, he says it's allabout the mitochondria.
Speaker 4 (19:47):
We've known for many years that light actually can
damage the retina and for thatreason, as you know, places like
the Macula Society advocatesunglasses or wearing a cap if
you're out in sunny conditions.
But it's probably to do with thetype of light, the type of
exposure and how that's done andthe wavelength, which is what
(20:07):
you're referring to.
And this Valeda system usesthree different wavelengths that
are shown at the eye one in theinfrared range of the light
spectrum and two within thevisual spectrum and these
wavelengths are thought tostimulate the cells and
specifically the mitochondriainside the cells.
(20:28):
So the mitochondria like thepowerhouses, the energy building
blocks, and they produce ATPand this drives the energy and
the ability for the cell to work.
And we also know that if youactivate the mitochondria with
red light, you potentiallyimprove their function.
(20:50):
You reduce the inflammation,because it reduces the cytokine
release, and we knowinflammation is implicated in
macular degeneration and alsothey release nitric oxide, which
is a molecule that's involvedin the dilation of blood vessels
, or they help stimulate thatrelease.
So there are various aspects ofwhy red light might be
(21:15):
protective or support the backof the eye.
Speaker 1 (21:18):
The Macular Society then produced another webinar
exploring the Valida systempresented by Tim Jackson,
consultant ophthalmologist andprofessor of retinal research at
King's College Hospital.
In the webinar he explained theresults of the trial.
It had 100 patients.
Speaker 8 (21:36):
Some patients had treatment in both eyes.
So 100 patients and 148 eyesPatients are randomised to
active or sham treatment.
By sham I mean sort of fake orplacebo treatment, so the
patient wouldn't necessarilyknow.
It was designed not to let themknow whether or not the
treatment was real or not.
Whenever you design a clinicaltrial, it's very, very important
(21:57):
that the patients who have thetreatment were the same as the
patients that were on the trial,Because if you're not comparing
like with like, then you reallydon't know whether or not the
technology is safe and whetheror not it works.
So the patients had to have dryAMD.
The vision had to be between2032 and 2100.
Those are US metrics, but Ithink it's the closest that
(22:20):
anybody's familiar with theso-called 2020 phase phrase.
So 2020 doesn't mean perfectvision, it means normal vision.
So 2030 is sort of moderatelyreduced vision.
Still be good enough to drivethe drusen, which are these
little yellow deposits in theback of the eye.
They're a telltale sign of AMD.
(22:41):
Now lots of people have a smallnumber of very tiny drusen.
The patients on this clinicaltrial had medium-sized drusen,
so it's important that youconfirm that you have drusen of
this size before considering thetechnology.
Patients could also get ontothe trial though, if they
instead, or also, hadnon-central geographic atrophy
(23:03):
Now by that I mean an area inthe back of the eye where the
cells have died away.
But the patients were eligibleif they had some GA, as it's
called, but not if it involvedthe very center of the eye, the
fovea, where the light comes tofocus.
Because if you have GA in thecenter of the fovea, where the
light comes to focus, then thevision is usually poor and maybe
irretrievable, sadly, at thatstage.
(23:25):
So these are looking forpatients who have GA, but not
involving the foveal center.
So, looking at the results ofthe trial, so the main outcome
that was pre-specified wasvision.
This is main outcome is atmonth 13, but the trial does
continue to month 21.
So if we look at the activegroup, these are the patients
who had the real treatment.
(23:46):
They gained 5.4 letters.
Now, 5.4 letters is a measureof visual function and a greater
gain is a better vision, butthese are relatively small
numbers.
So to put this into context,these five letters, if any of
you have had your vision testedon an eye chart, the sort of
normal eye chart that you mightsee if you go to the optician or
if you're attending an eyeclinic in hospital.
(24:07):
One five letters is the same asone line on the eye chart.
So if you looked at the eyechart and you could read the
letters at one line, if yourvision improved by five letters,
it would mean that you couldget down to the next line on the
chart and see the second row ofsmaller letters.
One of the things that makes thetrial more difficult to
interpret is that the sham groupthose that didn't get the
(24:30):
active treatment that may havethought they did gained three
letters as well.
Maybe that's just a chancefinding it's not real.
Well, maybe perhaps they gotbetter at doing the vision test.
Now, of course, you've got totake off that result in the sham
group, because if the patientwould have naturally got better
anyway, that 5.4 letter gainisn't 5.4 letters.
What we look at is thedifference between the two
(24:50):
groups of the trial and what wesee.
If we look at the differencebetween the two, which is just
simple subtraction, then therewas a difference of 2.4 letters
between the active group and thesham group.
Now the question then is is 2.4letters going to make a
difference to somebody havingthe treatment?
Would they notice it and 2.4letters probably isn't something
the patient would necessarilynotice.
(25:14):
One of the things that's beensort of made some noise about
within the trial is that theactive group of participants
developed were less likely todevelop geographic atrophy.
So that's potentially of realinterest because expanding
geographic atrophy if thisexpanding geographic atrophy
expands to take in the fovea,then the vision will drop, and
(25:36):
often quite substantially.
So we like to avoid geographicatrophy.
Now the trial looked atgeographic atrophy.
From what I've been able todelineate, the trial set out to
work out whether or not thistreatment would reduce the
expansion of geographic atrophy.
It looked at the size of thegeographic atrophy and the
statistical tests suggested itdidn't make a difference.
So in terms of the conclusions,I think LightSight 3 was a
(26:01):
well-designed trial.
It ticked a number of importantboxes.
It was randomized and shamcontrolled and those are two of
the most important things intrying to maintain objectivity
of a clinical trial.
So we like that.
But compared to the drug trialsit's tiny, very, very small
study and this is an importantdisease.
If you were studying a veryrare disease then 100 patients
(26:23):
would be a big trial, but thisis no stretch that this could
possibly be imagined as a raredisease.
It's not.
It's an extremely commondisease and in that setting we
need to have a much higherburden of proof.
We need to have studies thatgive us real certainty, because
if we're going to roll this outand use it in thousands, tens of
thousands, even hundreds ofthousands of patients, then we
(26:43):
need to have huge certainty thatactually it does work.
Speaker 1 (26:47):
By now.
I wanted to speak to mybrilliant executive producer,
vince Hunt, an analyticalMancunian with a messianic zeal
for seeing through pressreleases.
Now he happens to live in thearea of Manchester where the
Optegra Hospital, which isoffering the Valida system, is
based.
So I gave him a ring.
Hi, vince, it's Angela.
Hi, angela, how are you?
(27:08):
Yeah, not bad, thank you, youlive in.
Manchester, don't you?
Speaker 10 (27:13):
I do.
Speaker 1 (27:14):
Can you visit the Optegra Hospital I don't think
it's far from you and do arecording for me.
Speaker 10 (27:20):
Yeah, sure, yeah, it isn't far away.
Speaker 1 (27:21):
No, Well, they've just introduced something called
red light therapy for maculardegeneration.
It is actually the only placeoffering it at the moment and
it's only being availableprivately.
(27:42):
And it's quite expensive.
Speaker 10 (27:42):
It's about 1500 pounds for a round of treatment
and they're suggesting three ayear, so I'm wondering if you
can go and find out a bit moreabout it.
Yeah, sure, sounds interesting.
Sounds expensive, but very muchworth looking into for the
purposes of your programme.
I'm on my way.
Speaker 1 (27:54):
Thanks, Vince.
Speaker 11 (27:55):
OK, this is Octegnodon and I've even managed
to find a parking space.
Let's go inside and meet Sarge.
Speaker 9 (28:03):
My name's Sir Stadler , I'm a consulting ethnologist
and I work primarily withOctober.
Speaker 11 (28:11):
It seems that you've identified an area for which
there was no treatment andyou've formulated a treatment.
Speaker 9 (28:21):
The dry metal generation things have been
tried over the years.
This is one therapy.
It was first tried around sevenyears ago.
It's called photobiomodulation.
It uses certain wavelengths oflight to stimulate the retina,
to stimulate the retina cellswhich are losing their function
(28:42):
in the context of biomethodegeneration, and so I've been
watching the development of thatover the last seven years or so
.
Other things that are indevelopment of biomethode
generation are actually eyeinjections similar to injections
for that of dry method ofgeneration are actually are
injections similar to injectionsfor that or given methods of
generation, and that's still notavailable and that comes with
(29:03):
potential issues that we need tobe discussing with.
But what I was interested inwas the obvious stages of dry
method of generation in placesthat have puncture and vision
but and they're looking for sometreatment.
Now I didn't rush into openpresence and the treatment.
(29:33):
I've been looking at the studiesthat are ongoing over the last
seven years or so in thistreatment for
photobiomagnetization and that'sbeen for a number of things.
I've had the largest trialreported last year and the
products are the light typestudies and so the third
industrial study was reportedlast year and I was given
(29:55):
additional reassurance becausethe studies are done in lab,
very representative centres.
There's some university centresin the United States with data
also objectively andindependently within it.
If the imaging gets that, welook at the change in the scan
(30:15):
and things that we do and thatis independently reduced by the
reading center.
So I thought the trial that wefound was of sufficient quality
and the data, the fracturing,the data that's showing the
patient could be obviously dieover with macular degeneration,
(30:35):
a slow bolization and an averageof a little bit of improvement
in living, but more importantly,the disease process being slow
down and less to the function.
What we look at in the case ofdry ovary with macular
degeneration, the early showingthat the cells are losing
(30:57):
function, is that suddenly thepresence of the problem is
losing better, sign that thecell's own function is well.
And so we saw in the studiesthat patients who were
under-treated versus those whoweren't showed a showed less
accumulation of this material,indicating that cell paints are
(31:18):
having teeth.
And also what we see with drymetal generation is a
progression from the oldeststages, where some species have
lesions and some milder thanthat, to more severe than that.
We call that the light stage orthe ectopic stage and present
on treatment, there was asignificant reduction in the
(31:41):
percentage of patients that wenton to the light phase of the
method of generation.
So in the studies, patientswithout treatment, that could be
10% of them and the other twothat went on to the most severe
light phase and that was reducedabout 5-6% in people who were
in treatment A big reduction.
So, given that there was apotential legal benefit and also
(32:04):
some effective evidence ofindependently reviewed evidence
of the disease processbenefiting, I felt the data was
strong enough to start to offerthe treatment myself of the
disease process benefiting.
I felt the data was strongenough to start the treatment
myself.
And I didn't you know I wasinto it but the machine's been
around for most of the idea forabout five years and it's been
(32:25):
the first baby.
But I go to them saying thedata was strong enough and I
would say, from my thinking, thedata was strong enough that if
I remember what I got to buy,I'd be happy to have the
treatment available.
Speaker 11 (32:47):
Having had a chat in the consulting room with Sarge,
I then moved across thecorridor to see how this
treatment actually works, and Isat in on the session with John.
Speaker 12 (32:58):
I'm going to bring that down a little bit Now, up
or down.
Speaker 3 (33:04):
Probably up.
Speaker 12 (33:05):
Up a little bit, a bit more.
No, that's about right, that'sit Right, and we are doing both
eyes.
Speaker 9 (33:13):
We are.
Speaker 12 (33:15):
And can I have your date of birth?
Speaker 3 (33:16):
18 to the 5th 1948.
Speaker 12 (33:19):
Yeah, make sure it's you.
I know it's you, but we'll makesure it's you.
Right, just bear with me.
Let me sort the machine out foryou and we'll start with your
right eye.
Speaker 8 (33:32):
Yep.
Speaker 12 (33:35):
And I'll line you up .
First one 30 seconds and youreyes are open.
Okay, Are you ready to go?
Yeah, Off, we go 30 seconds 30seconds.
Speaker 3 (33:54):
18 months ago at the optician's, when I was on a
routine eye check, they told meat the end of it that I'd got
muscular degeneration.
And I knew that I'd hadmuscular degeneration.
So it sparked a fear straightaway.
I'd observed that I wasstruggling reading, but then I
thought, well, I want to dosomething with opinion.
(34:15):
So I asked if I could go to thehospital in Manchester.
The doctor sorted that out andthey needed to transfer me over
into an NHS term at the time.
So I came down there, had a fewtests and they confirmed yeah,
matthew is a Dermatologist.
Dermatologist, my time was donethere macular degeneration,
where light-time was from theleft.
(34:37):
And then it was promising forme actually, because I asked
about is there something goingon in America?
And with that they said yeah,there is, and there could be
something that you know thewhole plant scene would have
considered Well, we haven't gota lot of chance with macular
degeneration, you can't standstill.
So I said yes, I would considerit Fully, appreciating that it
(35:00):
was going to be private, itwould not be a mention of that.
And then the second bout ofmain treatment.
They've had the first one andthen the third one of the second
one and they are picking upimprovements from my test.
Speaker 11 (35:18):
You've just come out from the treatment room.
Speaker 3 (35:23):
How do you think?
I noticed after about six orseven of the processes from the
first round that I was startingto pick things up on the
television, on the screen, whereI couldn't read things on the
screen.
I was starting to read thingson the screen, not all of it,
but enough to make me think, oh,there was some improvement
(35:45):
there.
When I came back and did thebenchmarking, before we started
the second process, the secondround, we did a benchmark test
to go back against the first andstraight away the doctor said
to me we've got subjectiveevidence that you're improving.
I said and I'm not feelingsubjective he said that you've
(36:09):
also got other evidence, clearevidence, scientific evidence,
and there's photographs andstuff that were taken at the
back of the island.
But things are improving now.
It's a miss, it's quite earlybecause we'd expect to see this
into the second phase, notstraight after the first one.
And the thing with this isabout hope.
I think, yeah, there's got tobe.
(36:33):
That hasn't there.
You know, if you weren'tploughing this furrow, you'd be
sat at home just thinking thisis slowly going downhill.
It's going nowhere, at leastwith this.
Whether you're touching itstraws or not remains to be seen
.
I'll accept that you know a lotof this is in its early days,
but it does give you hope andthat is a big thing, I think you
(36:55):
know.
You know put that against clownshows and clowns, and I can't
spend it when I'm in the shower,can I?
So you know, let's get on withit and see what happens.
Speaker 1 (37:09):
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 (37:18):
Yeah, really good thanks.
Look, I'm at Optegra and I'mreally, really impressed with
what's going on here, so Ithought I'd call you straight
away and tell you what's beengoing on.
I've been talking to theconsultant, ophthalmologist
Sarge Mahmood, and he's reallyconfident about this treatment
(37:39):
and they have a lot of peoplesigning up and I've spoken to
one or two of them and thethings that they are saying.
I really think that you oughtto be considering this treatment
yourself.
Speaker 1 (37:52):
Really.
Speaker 10 (37:54):
Well, you know, Manchester's not that far away.
However, they are talking aboutrolling it out in London and of
course, that's an hour fromwhere you are.
Speaker 1 (38:05):
Why are you so convinced?
Speaker 10 (38:07):
Well, it comes really from the testimony of
people who have been having thistreatment.
I mean, obviously it's betterif you live close to the Optegra
hospital, but some of theresults, some of the short-term
results from the first cycle areshowing better results than
they had expected and this isreally really encouraging.
(38:29):
And what that's doing is it'sgiving the people with AMD a
much more positive outlook.
It's giving them hope and Ithink in this case, as somebody
who's short-sighted, if youreyesight starts to go, that can
be really really frightening andit completely affects your
(38:52):
philosophy, your perspective onlife, your mobility and
everything.
So you know, if this issomething that you're looking
into, I would say it definitelybears further investigation.
Speaker 1 (39:05):
Wow, I think I'd better ring Optegra Well.
Thanks very much, Vince.
Speaker 10 (39:10):
No problem, Angela.
Speaker 1 (39:13):
I have to say I contemplated moving to
Manchester, but then I heardthat Optegra was going to start
offering Valida in London and Isigned up for an assessment to
see if I'm eligible.
So this podcast has now taken anew turn and it will follow my
Valida journey.
I'm not sure if I will beeligible, but I'm certainly
going to get assessed.
I hope you'll stay with me forthe second episode of Talking
(39:36):
About Degeneration.
Huge thanks to executiveproducer Vince Hunt and the
Optegra Eye Hospital, manchester, to voiceover artist Richard
Westgate who recorded thenewspaper article, and to
musician Mike Udin who recordedour special new version of the
(40:00):
who classic Talking About myGeneration.
Links to their websites andbios are on the show notes.
Bye for now.
This has been a CambridgePodcast production written and
(40:24):
produced by me, angela Young.
Thank you.
Hello, I'm Angela Young and away Macular
degeneration.
Hello, I'm Angela Young and Ihave macular degeneration.
This podcast aims to look intoa condition which affects more
than 700,000 people in the UKand is the biggest cause of
sight loss in the country.
You'll probably hear it calledAMD or age-related macular
(00:42):
degeneration, a term I don'tlike.
Now, while it affects almostexclusively people over 55, I
think the danger is that maculardegeneration is then
categorised as an old person'sproblem.
I've no evidence for this, butit could explain why there's
been so little progress infinding a cure or at least a
treatment.
It doesn't cause totalblindness, but it can make
(01:04):
things like reading andrecognising faces difficult.
I have difficultydistinguishing between grey and
green.
I complimented my niece'shusband on his wedding day on
his green waistcoat and helooked bemused, as it was grey.
On a more serious note, I findit hard to see where an unmarked
road meets the verge, and I'vefallen off my beloved bike
(01:25):
because of this.
In fact, that's how I was firstdiagnosed in 2017.
It might also explain why Ihave offended people when I
don't remember who they are, asI can't recognise their face.
If you're listening to this andhave AMD, you'll have your own
difficulties.
I'm really afraid of concretesteps with no colour edging on
(01:45):
them, in case I fall headfirstdown them.
My most recent eye test at mylocal opticians wasn't a happy
experience.
You know the chart with theletters Well.
My left eye could managereasonably well.
My right eye struggled to seethe outline of one massive
letter blown up to fit one pageof A4.
There's a large bit missing inmy central vision, called
(02:06):
geographic atrophy.
You can go on several websitesto see what this looks like.
They usually show a grey cloudhovering over the middle of an
image.
That's actually not what it'slike.
For me it's more as thoughsomeone has edited out a central
bit of a picture and joined theoutsides together.
Anyway, come to SpectacularOpticians with me and meet
(02:26):
senior optometrist Stuart Gibson.
Speaker 2 (02:30):
To give you some indication there has been
significant you know, asignificant drop off in the
level of vision in the right eyeand because of the macular
degeneration you know, it israpidly, rapidly progressing.
Some people get it much earlierthan others and unfortunately,
in this instance that's what thecase is.
(02:50):
So just to try and quantify itfrom your point of view, if you
look up there, you've got botheyes open yeah last time with
glasses, we could get you to seethe bottom line.
Yes, there, um, in your righteye, okay, yeah, now today, we
(03:12):
can't even achieve this level ofvision in that right eye.
So that is the degree of.
So that's gone from 6 over 48to 6 over 200.
Speaker 1 (03:30):
Now, if you go onto an NHS website, it will tell you
without treatment, your visionmay get worse.
On the next page, it informsyou that there is no treatment
for dry AMD.
Now, just an aside here if youhave wet AMD, there are
treatments which this podcastwon't go into.
I'm a former BBC Radio Newseditor and I like to question
(03:52):
the status quo.
I also thought that if I made apodcast about AMD, I could be a
voice for other people with thecondition and ask questions on
their behalf.
So talking about degenerationwas born.
Originally, it set out to be aninvestigation into what, if any,
treatments were being developed.
I started with the MacularSociety, whose aim is to beat
(04:13):
the fear and isolation ofmacular disease with world-class
research and the best adviceand support.
They produce a monthly webinarwhich provides invaluable advice
.
I listened to the webinar onthe changing landscape of
treatment for AMD by JamesNeffendorf, consultant
ophthalmologist at King'sCollege Hospital in London,
(04:33):
specialising in the retina, withan interest in AMD.
Later I caught up with himone-to-one.
I started by asking him toexplain what AMD actually is
Age-related macular degeneration, which is what we're really
talking about today.
Speaker 4 (04:45):
I started by asking him to explain what AMD actually
is.
Age-related maculardegeneration, which is what
we're really talking about today, is an incredibly common
condition and it's thought toaffect probably somewhere
between 10% and 20% of the over65s.
Now that's in varying degrees,of course.
Some people have almostsubclinical changes which you
(05:07):
wouldn't necessarily know aboutand other people are essentially
registered blind from thecondition.
So there's a huge spectrum ofthe condition and, broadly
speaking, this is where themacula is not working as well
and it starts to affect yourcentral vision.
And there are two broad typesof macular degeneration.
(05:27):
We have what we call dry maculardegeneration and wet macular
degeneration.
Now, dry you can think of as awear and tear type of macular
degeneration.
That is, and the way thedistinction is made is a little
bit crude, because traditionallypeople used to say well, if you
get the wet type, it was verybad news.
If you have the dry type, itwas very slow, slightly
(05:49):
progressive, but actually withinthe two subsets there are
severity of disease themselves.
So somebody with dry maculardegeneration, which is the more
common type, probably affecting,you know, 80 to 90 percent of
those with macular degenerationthey, you know, they can either
just have some changes that wecall drusen, which are these
(06:11):
little deposits under the retina, or actually, as the disease
gets more advanced, they canstart to lose some of the tissue
at the back of the eye and theycan have these punched out
lesions when we, when we look atthe retina and that's called
atrophic change and then werefer to that as geographic
atrophy.
So, and you know, a few drusencan still be compatible with
(06:32):
completely normal vision andthen, as you get to atrophic
change, if the area of atrophyis not right at the center you
can be fairly asymptomatic.
But if the area of loss ofretinal and RPE tissue is
involving your fovea, so thevery central part of the macula,
then of course your sight canbe very severely affected.
(06:53):
So that's dry maculardegeneration and then wet
macular degeneration, as thename implies, is where there's
been leakage of a fluid, eitherblood or just a general sort of
fluid which is like having wateron the film as the camera.
Unfortunately, dry maculardegeneration has lagged behind a
little bit, even though it'smore common, and that is a sad
(07:17):
situation that we're in.
However, I think the currentsort of scope of what's out
there is lending itself for alot of potential benefit for
these patients and I think we'renot maybe at the crest of the
wave, but we're approaching itin the next few years whereby we
(07:38):
might have some treatmentsavailable for patients with dry
AMD that we can really use andmake a difference to people.
Speaker 1 (07:46):
So what are some of those treatments not only on the
horizon, but actually available?
Speaker 4 (07:52):
There's a more non-invasive option which is the
light therapy which some peoplemay have heard about, and this
is the Valeda system made byLumathera, and that's the people
more at the earliest stage ofmacular degeneration and there's
potentially some mild visualbenefit and possibly some
reduction in the progressionwith with that treatment.
(08:13):
And then you get to slightlymore cutting edge research which
are things like gene therapy orcell-based treatments, so stem
cells, and that's obviously verymuch in its infancy, but
actually these things are closerthan we might think to clinical
(08:33):
practice.
So that gives you a bit of anoverview of what's out there.
Speaker 1 (08:38):
I had signed up for a trial of one of the latter two
gene therapy but it turned out Iwasn't eligible and I was
feeling quite despondent.
The Macular Society hadpreviously provided another
webinar on red light therapy byGlenn Jeffery, professor of
Neuroscience at the Institute ofOphthalmology at University
College in London, so I went totalk to him too.
(08:59):
He explained that red lighttargets something called
mitochondria.
Speaker 5 (09:05):
Mitochondria are the body's batteries.
You've got thousands ofmitochondria in each of your
cells.
They make energy and as you getold, the energy level declines.
That's why it's a little bitharder to swing your legs out of
bed in the morning and it'salso why your vision declines.
Mitochondria are the keybatteries, but mitochondria are
(09:29):
influenced by light, so we canuse different wavelengths of
light to either charge thebattery, give you a bit more
energy, or to discharge thebattery, and the consequences of
which are that you suffer fromvisual decline, also caused by
light.
Yeah, light is, if you thinkabout about it.
(09:50):
For millions of years you'veevolved 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 dothat in evolution.
You should probably be dead inyour 40s um.
So your batteries are beingtested by your increased
(10:10):
longevity.
Your batteries are also beingtested because you are in light
environments.
You shouldn't be in, likeinside buildings with led
lighting.
So it's a challenge.
It is a challenge, but it is adisease extension of living too
(10:44):
long.
Speaker 1 (10:44):
So what does red light therapy do and how can it
help and how can it be used?
Speaker 5 (10:50):
Red light therapy recharges the battery, the
mitochondria, like putting atoothbrush back on the stand.
It's extremely simple.
Critically, it's very safebecause the wavelengths of light
we're giving you are thewavelengths of light you get in
sunlight.
Ok, so it is the red componentof sunlight.
(11:13):
So far we have found absolutelyno downside whatsoever for
using red light and we shouldn'tdo.
We're using energies that arewithin reach of sunlight and it
is a component of sunlight.
Speaker 1 (11:23):
So can you tell me about what you know about
current trials or completedtrials using red?
Speaker 5 (11:28):
light therapy.
Okay, so this is.
This is where the breaking edgeof the wave is currently.
At the moment, red light isgreat at catching an early
disease that has energy basedall right.
So there are now some studiescoming out which look for
macular degeneration lookextremely positive.
(11:50):
I must admit they do lookpositive, but the key thing is
it's safe.
I have two elderly aunts andI've been running them on red
light for quite a while and Iprobably use red light twice a
week and most of my lab do.
Speaker 1 (12:05):
In what form?
Speaker 5 (12:07):
We bounce it off the walls in a from a big lamp, um,
so you can buy big lamps thatgive off, uh, near infrared, and
um, they're relatively cheapand, yeah, you just bounce it
off a wall.
Now, in in the olden days, asit were, when we had
incandescent light bulbs, we hada large amount of infrared
(12:31):
light in them, so there was adegree of protection.
Now we have LED lights andthere is no infrared light in
them.
So what we're doing is we'redriving the aging process a
little bit by using lights thatdon't have infrared light in
them and and sadly, lights havegot a lot of blue in them and
(12:51):
that blue is discharging yourbattery.
Speaker 1 (12:55):
so bad news in an aging population if we're not
you and don't have a lamp tobounce off walls, what are our
options?
Speaker 5 (13:06):
well, the best option on the planet is go for a walk.
Go for a walk outside.
There is loads of infraredlight outside.
There is nothing supercomplicated about this.
So all of the studies that wehave done we have done with
relatively simple devices thatcost relatively little.
Speaker 1 (13:26):
So, for example, there is a pair of glasses
available from a company basedjust outside Bath, I think
they're £60 for a pair ofglasses that you charge with a
USB charger and sit in bed forthree minutes once a week.
Is that comparable to theeffects of something?
Speaker 5 (13:42):
like Valida.
Well, in terms of what it does,biologically they would not
agree with me, but I see nodifference.
Um, I I don't have a commercialinterest.
However, I've tested those andthey do what they as they say.
They do what they say on thepacket and they are perfectly
safe.
So I only tested them becauseif people come and ask me, I
(14:03):
want to be able to say well,there is something out there
there.
If you go on the web, you willfind hundreds of devices.
Most of them are not safe.
Most of them are relativelyuntested.
Most of them will fall apart ina few months.
Most of them will not do whatthey say they do.
Speaker 1 (14:19):
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 (14:27):
I've always been interested in science technology
, so I always keep an eye onwhat's going out in the academic
press.
I sort of look at various newsfeeds and science articles and I
saw one that really sort ofcaught my eye and I could see a
degree of synergy because, asthe director of a lighting
(14:48):
company, could see a degree ofsynergy because, as the director
of a lighting company, I sawthe work by Professor Glenn
Jeffrey of UCL, who justpublished a paper on the use of
red light to help with reducingthe ageing of the eye.
I thought aha, brilliant, nicesynergy here.
I know everything aboutlighting, he knows everything
(15:09):
about eyes, so let's have aconversation.
He was very, very supportiveand suggested I went away and
did my research and he wouldsort of provide help and advice
where he could, so effectively.
That's what happened.
I went away and started to domy research.
Speaker 1 (15:28):
And what was the product you came up with?
Speaker 6 (15:31):
We called it the iPower.
Because it shines out red light, it's called the iPower Red.
We looked at various designsinitially.
Some would make you laugh.
I mean they're almost out ofStar Trek.
In fact, the very first designI did was almost like a half
(15:52):
face mask with sort of full eyegoggles, which looked horrible.
In hindsight I still have a 3Dprint down in the workshop and I
look back at it now and thinkwhat was I thinking?
But in the end it sort ofslimmed down and with a bit of
advice from Glenn and from hiscolleague Chris Hogg, we sort of
(16:15):
focused on more of a sort ofsubstitute for glasses rather
than goggles themselves.
Speaker 1 (16:22):
So tell me how does it work and what does the user
have to do?
Speaker 6 (16:25):
We've tried to make it as simple as possible for the
user, because we appreciatethat we're trying to attract a
very wide demographic here.
So the whole strategy was tohave something that somebody
could take out the box, just puton as they would a normal pair
of glasses and with just thepress of of the button, actually
(16:48):
activate and complete a singlesession.
So that's what we've built intothe glasses, so you simply put
them on.
There's a little button at thebottom, a little clear plastic
button which you push.
As soon as you push that, itactivates the light.
It goes through a littletwo-stage process which we built
(17:09):
into it.
So for three seconds it comeson at half brightness just to
make somebody aware that thesession is about to start.
Then, after the three seconds,it goes to full brightness and
you then get a full three minutesession of 670 nanometer red
light.
Speaker 1 (17:27):
Stephen sent me a pair of glasses and I've been
using them once a week on aSaturday morning.
It actually feels as though I'mlying on a sunbed for those
three minutes.
It was around this time that anarticle appeared in the press
about a private eye hospitalwhich was offering what was
hailed as the first treatmentfor AMD in the UK, based on the
results of the LightSight 3study which James Neffendorf
(17:50):
referred to.
It was the trial in the US ofred light therapy, or
photobiomodulation, which hadsome very promising results, the
Daily Telegraph reported.
Speaker 7 (18:01):
Patients with a degenerative eye condition could
keep their sight for longer,thanks to the development of the
first treatment of thecondition After successful
trials in the US, a lighttherapy treatment that claims to
help patients maintain orimprove their vision.
It went on at the back of theeye.
A randomized control trial ofthe technology in the US found
dry AMD patients who had thelight therapy delivered through
(18:32):
a device called Valedaexperienced almost double the
improvements in their visionafter 13 months of treatment
compared to those treated withthe dummy device.
The patients, who were all over50, received a cycle of nine
sessions of five-minutetreatments over three to five
weeks, repeated once every fourmonths.
At the end of the study,patients treated with Valeda
(18:55):
were able to read 5.4 moreletters on a site chart.
Treated patients also had lessof a type of swelling within the
eye which can indicate thedisease is progressing, compared
with those treated with a dummydevice.
The study published last monthin the journal Retina was led by
the technology's manufacturerLumathera and tested on a small
group of 100 patients.
Its effectiveness is currentlybeing assessed in clinical
trials and it is yet to beconsidered by the National
(19:17):
Institute for Health and CareExcellence in England and Wales
for use in the NHS, but it hasbeen approved for sale in Europe
.
The technology is now availableat a handful of private clinics
in the UK and has just beenlaunched by the Optegra Eye
Hospital Group, the first chainto take it on.
The company is trialling itsdevice at its Manchester
hospital before rolling it outnationally.
Speaker 1 (19:38):
I wanted to look into these claims in a bit more
detail, so I asked JamesNeffendorf to explain how red
light therapy works.
Like Glenn, he says it's allabout the mitochondria.
Speaker 4 (19:47):
We've known for many years that light actually can
damage the retina and for thatreason, as you know, places like
the Macula Society advocatesunglasses or wearing a cap if
you're out in sunny conditions.
But it's probably to do with thetype of light, the type of
exposure and how that's done andthe wavelength, which is what
(20:07):
you're referring to.
And this Valeda system usesthree different wavelengths that
are shown at the eye one in theinfrared range of the light
spectrum and two within thevisual spectrum and these
wavelengths are thought tostimulate the cells and
specifically the mitochondriainside the cells.
(20:28):
So the mitochondria like thepowerhouses, the energy building
blocks, and they produce ATPand this drives the energy and
the ability for the cell to work.
And we also know that if youactivate the mitochondria with
red light, you potentiallyimprove their function.
(20:50):
You reduce the inflammation,because it reduces the cytokine
release, and we knowinflammation is implicated in
macular degeneration and alsothey release nitric oxide, which
is a molecule that's involvedin the dilation of blood vessels
, or they help stimulate thatrelease.
So there are various aspects ofwhy red light might be
(21:15):
protective or support the backof the eye.
Speaker 1 (21:18):
The Macular Society then produced another webinar
exploring the Valida systempresented by Tim Jackson,
consultant ophthalmologist andprofessor of retinal research at
King's College Hospital.
In the webinar he explained theresults of the trial.
It had 100 patients.
Speaker 8 (21:36):
Some patients had treatment in both eyes.
So 100 patients and 148 eyesPatients are randomised to
active or sham treatment.
By sham I mean sort of fake orplacebo treatment, so the
patient wouldn't necessarilyknow.
It was designed not to let themknow whether or not the
treatment was real or not.
Whenever you design a clinicaltrial, it's very, very important
(21:57):
that the patients who have thetreatment were the same as the
patients that were on the trial,Because if you're not comparing
like with like, then you reallydon't know whether or not the
technology is safe and whetheror not it works.
So the patients had to have dryAMD.
The vision had to be between2032 and 2100.
Those are US metrics, but Ithink it's the closest that
(22:20):
anybody's familiar with theso-called 2020 phase phrase.
So 2020 doesn't mean perfectvision, it means normal vision.
So 2030 is sort of moderatelyreduced vision.
Still be good enough to drivethe drusen, which are these
little yellow deposits in theback of the eye.
They're a telltale sign of AMD.
(22:41):
Now lots of people have a smallnumber of very tiny drusen.
The patients on this clinicaltrial had medium-sized drusen,
so it's important that youconfirm that you have drusen of
this size before considering thetechnology.
Patients could also get ontothe trial though, if they
instead, or also, hadnon-central geographic atrophy
(23:03):
Now by that I mean an area inthe back of the eye where the
cells have died away.
But the patients were eligibleif they had some GA, as it's
called, but not if it involvedthe very center of the eye, the
fovea, where the light comes tofocus.
Because if you have GA in thecenter of the fovea, where the
light comes to focus, then thevision is usually poor and maybe
irretrievable, sadly, at thatstage.
(23:25):
So these are looking forpatients who have GA, but not
involving the foveal center.
So, looking at the results ofthe trial, so the main outcome
that was pre-specified wasvision.
This is main outcome is atmonth 13, but the trial does
continue to month 21.
So if we look at the activegroup, these are the patients
who had the real treatment.
(23:46):
They gained 5.4 letters.
Now, 5.4 letters is a measureof visual function and a greater
gain is a better vision, butthese are relatively small
numbers.
So to put this into context,these five letters, if any of
you have had your vision testedon an eye chart, the sort of
normal eye chart that you mightsee if you go to the optician or
if you're attending an eyeclinic in hospital.
(24:07):
One five letters is the same asone line on the eye chart.
So if you looked at the eyechart and you could read the
letters at one line, if yourvision improved by five letters,
it would mean that you couldget down to the next line on the
chart and see the second row ofsmaller letters.
One of the things that makes thetrial more difficult to
interpret is that the sham groupthose that didn't get the
(24:30):
active treatment that may havethought they did gained three
letters as well.
Maybe that's just a chancefinding it's not real.
Well, maybe perhaps they gotbetter at doing the vision test.
Now, of course, you've got totake off that result in the sham
group, because if the patientwould have naturally got better
anyway, that 5.4 letter gainisn't 5.4 letters.
What we look at is thedifference between the two
(24:50):
groups of the trial and what wesee.
If we look at the differencebetween the two, which is just
simple subtraction, then therewas a difference of 2.4 letters
between the active group and thesham group.
Now the question then is is 2.4letters going to make a
difference to somebody havingthe treatment?
Would they notice it and 2.4letters probably isn't something
the patient would necessarilynotice.
(25:14):
One of the things that's beensort of made some noise about
within the trial is that theactive group of participants
developed were less likely todevelop geographic atrophy.
So that's potentially of realinterest because expanding
geographic atrophy if thisexpanding geographic atrophy
expands to take in the fovea,then the vision will drop, and
(25:36):
often quite substantially.
So we like to avoid geographicatrophy.
Now the trial looked atgeographic atrophy.
From what I've been able todelineate, the trial set out to
work out whether or not thistreatment would reduce the
expansion of geographic atrophy.
It looked at the size of thegeographic atrophy and the
statistical tests suggested itdidn't make a difference.
So in terms of the conclusions,I think LightSight 3 was a
(26:01):
well-designed trial.
It ticked a number of importantboxes.
It was randomized and shamcontrolled and those are two of
the most important things intrying to maintain objectivity
of a clinical trial.
So we like that.
But compared to the drug trialsit's tiny, very, very small
study and this is an importantdisease.
If you were studying a veryrare disease then 100 patients
(26:23):
would be a big trial, but thisis no stretch that this could
possibly be imagined as a raredisease.
It's not.
It's an extremely commondisease and in that setting we
need to have a much higherburden of proof.
We need to have studies thatgive us real certainty, because
if we're going to roll this outand use it in thousands, tens of
thousands, even hundreds ofthousands of patients, then we
(26:43):
need to have huge certainty thatactually it does work.
Speaker 1 (26:47):
By now.
I wanted to speak to mybrilliant executive producer,
vince Hunt, an analyticalMancunian with a messianic zeal
for seeing through pressreleases.
Now he happens to live in thearea of Manchester where the
Optegra Hospital, which isoffering the Valida system, is
based.
So I gave him a ring.
Hi, vince, it's Angela.
Hi, angela, how are you?
(27:08):
Yeah, not bad, thank you, youlive in.
Manchester, don't you?
Speaker 10 (27:13):
I do.
Speaker 1 (27:14):
Can you visit the Optegra Hospital I don't think
it's far from you and do arecording for me.
Speaker 10 (27:20):
Yeah, sure, yeah, it isn't far away.
Speaker 1 (27:21):
No, Well, they've just introduced something called
red light therapy for maculardegeneration.
It is actually the only placeoffering it at the moment and
it's only being availableprivately.
(27:42):
And it's quite expensive.
Speaker 10 (27:42):
It's about 1500 pounds for a round of treatment
and they're suggesting three ayear, so I'm wondering if you
can go and find out a bit moreabout it.
Yeah, sure, sounds interesting.
Sounds expensive, but very muchworth looking into for the
purposes of your programme.
I'm on my way.
Speaker 1 (27:54):
Thanks, Vince.
Speaker 11 (27:55):
OK, this is Octegnodon and I've even managed
to find a parking space.
Let's go inside and meet Sarge.
Speaker 9 (28:03):
My name's Sir Stadler , I'm a consulting ethnologist
and I work primarily withOctober.
Speaker 11 (28:11):
It seems that you've identified an area for which
there was no treatment andyou've formulated a treatment.
Speaker 9 (28:21):
The dry metal generation things have been
tried over the years.
This is one therapy.
It was first tried around sevenyears ago.
It's called photobiomodulation.
It uses certain wavelengths oflight to stimulate the retina,
to stimulate the retina cellswhich are losing their function
(28:42):
in the context of biomethodegeneration, and so I've been
watching the development of thatover the last seven years or so
.
Other things that are indevelopment of biomethode
generation are actually eyeinjections similar to injections
for that of dry method ofgeneration are actually are
injections similar to injectionsfor that or given methods of
generation, and that's still notavailable and that comes with
(29:03):
potential issues that we need tobe discussing with.
But what I was interested inwas the obvious stages of dry
method of generation in placesthat have puncture and vision
but and they're looking for sometreatment.
Now I didn't rush into openpresence and the treatment.
(29:33):
I've been looking at the studiesthat are ongoing over the last
seven years or so in thistreatment for
photobiomagnetization and that'sbeen for a number of things.
I've had the largest trialreported last year and the
products are the light typestudies and so the third
industrial study was reportedlast year and I was given
(29:55):
additional reassurance becausethe studies are done in lab,
very representative centres.
There's some university centresin the United States with data
also objectively andindependently within it.
If the imaging gets that, welook at the change in the scan
(30:15):
and things that we do and thatis independently reduced by the
reading center.
So I thought the trial that wefound was of sufficient quality
and the data, the fracturing,the data that's showing the
patient could be obviously dieover with macular degeneration,
(30:35):
a slow bolization and an averageof a little bit of improvement
in living, but more importantly,the disease process being slow
down and less to the function.
What we look at in the case ofdry ovary with macular
degeneration, the early showingthat the cells are losing
(30:57):
function, is that suddenly thepresence of the problem is
losing better, sign that thecell's own function is well.
And so we saw in the studiesthat patients who were
under-treated versus those whoweren't showed a showed less
accumulation of this material,indicating that cell paints are
(31:18):
having teeth.
And also what we see with drymetal generation is a
progression from the oldeststages, where some species have
lesions and some milder thanthat, to more severe than that.
We call that the light stage orthe ectopic stage and present
on treatment, there was asignificant reduction in the
(31:41):
percentage of patients that wenton to the light phase of the
method of generation.
So in the studies, patientswithout treatment, that could be
10% of them and the other twothat went on to the most severe
light phase and that was reducedabout 5-6% in people who were
in treatment A big reduction.
So, given that there was apotential legal benefit and also
(32:04):
some effective evidence ofindependently reviewed evidence
of the disease processbenefiting, I felt the data was
strong enough to start to offerthe treatment myself of the
disease process benefiting.
I felt the data was strongenough to start the treatment
myself.
And I didn't you know I wasinto it but the machine's been
around for most of the idea forabout five years and it's been
(32:25):
the first baby.
But I go to them saying thedata was strong enough and I
would say, from my thinking, thedata was strong enough that if
I remember what I got to buy,I'd be happy to have the
treatment available.
Speaker 11 (32:47):
Having had a chat in the consulting room with Sarge,
I then moved across thecorridor to see how this
treatment actually works, and Isat in on the session with John.
Speaker 12 (32:58):
I'm going to bring that down a little bit Now, up
or down.
Speaker 3 (33:04):
Probably up.
Speaker 12 (33:05):
Up a little bit, a bit more.
No, that's about right, that'sit Right, and we are doing both
eyes.
Speaker 9 (33:13):
We are.
Speaker 12 (33:15):
And can I have your date of birth?
Speaker 3 (33:16):
18 to the 5th 1948.
Speaker 12 (33:19):
Yeah, make sure it's you.
I know it's you, but we'll makesure it's you.
Right, just bear with me.
Let me sort the machine out foryou and we'll start with your
right eye.
Speaker 8 (33:32):
Yep.
Speaker 12 (33:35):
And I'll line you up .
First one 30 seconds and youreyes are open.
Okay, Are you ready to go?
Yeah, Off, we go 30 seconds 30seconds.
Speaker 3 (33:54):
18 months ago at the optician's, when I was on a
routine eye check, they told meat the end of it that I'd got
muscular degeneration.
And I knew that I'd hadmuscular degeneration.
So it sparked a fear straightaway.
I'd observed that I wasstruggling reading, but then I
thought, well, I want to dosomething with opinion.
(34:15):
So I asked if I could go to thehospital in Manchester.
The doctor sorted that out andthey needed to transfer me over
into an NHS term at the time.
So I came down there, had a fewtests and they confirmed yeah,
matthew is a Dermatologist.
Dermatologist, my time was donethere macular degeneration,
where light-time was from theleft.
(34:37):
And then it was promising forme actually, because I asked
about is there something goingon in America?
And with that they said yeah,there is, and there could be
something that you know thewhole plant scene would have
considered Well, we haven't gota lot of chance with macular
degeneration, you can't standstill.
So I said yes, I would considerit Fully, appreciating that it
(35:00):
was going to be private, itwould not be a mention of that.
And then the second bout ofmain treatment.
They've had the first one andthen the third one of the second
one and they are picking upimprovements from my test.
Speaker 11 (35:18):
You've just come out from the treatment room.
Speaker 3 (35:23):
How do you think?
I noticed after about six orseven of the processes from the
first round that I was startingto pick things up on the
television, on the screen, whereI couldn't read things on the
screen.
I was starting to read thingson the screen, not all of it,
but enough to make me think, oh,there was some improvement
(35:45):
there.
When I came back and did thebenchmarking, before we started
the second process, the secondround, we did a benchmark test
to go back against the first andstraight away the doctor said
to me we've got subjectiveevidence that you're improving.
I said and I'm not feelingsubjective he said that you've
(36:09):
also got other evidence, clearevidence, scientific evidence,
and there's photographs andstuff that were taken at the
back of the island.
But things are improving now.
It's a miss, it's quite earlybecause we'd expect to see this
into the second phase, notstraight after the first one.
And the thing with this isabout hope.
I think, yeah, there's got tobe.
(36:33):
That hasn't there.
You know, if you weren'tploughing this furrow, you'd be
sat at home just thinking thisis slowly going downhill.
It's going nowhere, at leastwith this.
Whether you're touching itstraws or not remains to be seen
.
I'll accept that you know a lotof this is in its early days,
but it does give you hope andthat is a big thing, I think you
(36:55):
know.
You know put that against clownshows and clowns, and I can't
spend it when I'm in the shower,can I?
So you know, let's get on withit and see what happens.
Speaker 1 (37:09):
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 (37:18):
Yeah, really good thanks.
Look, I'm at Optegra and I'mreally, really impressed with
what's going on here, so Ithought I'd call you straight
away and tell you what's beengoing on.
I've been talking to theconsultant, ophthalmologist
Sarge Mahmood, and he's reallyconfident about this treatment
(37:39):
and they have a lot of peoplesigning up and I've spoken to
one or two of them and thethings that they are saying.
I really think that you oughtto be considering this treatment
yourself.
Speaker 1 (37:52):
Really.
Speaker 10 (37:54):
Well, you know, Manchester's not that far away.
However, they are talking aboutrolling it out in London and of
course, that's an hour fromwhere you are.
Speaker 1 (38:05):
Why are you so convinced?
Speaker 10 (38:07):
Well, it comes really from the testimony of
people who have been having thistreatment.
I mean, obviously it's betterif you live close to the Optegra
hospital, but some of theresults, some of the short-term
results from the first cycle areshowing better results than
they had expected and this isreally really encouraging.
(38:29):
And what that's doing is it'sgiving the people with AMD a
much more positive outlook.
It's giving them hope and Ithink in this case, as somebody
who's short-sighted, if youreyesight starts to go, that can
be really really frightening andit completely affects your
(38:52):
philosophy, your perspective onlife, your mobility and
everything.
So you know, if this issomething that you're looking
into, I would say it definitelybears further investigation.
Speaker 1 (39:05):
Wow, I think I'd better ring Optegra Well.
Thanks very much, Vince.
Speaker 10 (39:10):
No problem, Angela.
Speaker 1 (39:13):
I have to say I contemplated moving to
Manchester, but then I heardthat Optegra was going to start
offering Valida in London and Isigned up for an assessment to
see if I'm eligible.
So this podcast has now taken anew turn and it will follow my
Valida journey.
I'm not sure if I will beeligible, but I'm certainly
going to get assessed.
I hope you'll stay with me forthe second episode of Talking
(39:36):
About Degeneration.
Huge thanks to executiveproducer Vince Hunt and the
Optegra Eye Hospital, manchester, to voiceover artist Richard
Westgate who recorded thenewspaper article, and to
musician Mike Udin who recordedour special new version of the
(40:00):
who classic Talking About myGeneration.
Links to their websites andbios are on the show notes.
Bye for now.
This has been a CambridgePodcast production written and
(40:24):
produced by me, angela Young.
Thank you.
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