TransVision Madrid 2025 Summit: Longevity March, Omniscope, Gil Rodas, Steve Horvath, Michael Ringel

Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:00):
Greetings and welcome to the United States Transhumanist Party Virtual
Enlightenment Salon. My name is Jannati stolier Off the second
and I am the Chairman of the US Transhumanist Party.
Here we hold conversations with some of the world's leading
thinkers in longevity, science, technology, philosophy, and politics. Like the

(00:21):
philosophers of the Age of Enlightenment, we aim to connect
every field of human endeavor and arrive at new insights
to achieve longer lives, greater rationality and the progress of
our civilization.

Speaker 2 (01:05):
At Madrid Madrid.

Speaker 3 (01:14):
And you got it like me and the president Madrid Rugby,
I've no great Bocaboland Intermedia and DA Madrid and.

Speaker 2 (01:27):
Baracio Lesidlis go rock at boys may be the.

Speaker 4 (01:35):
Monday. Yeah, I'm a ruther.

Speaker 2 (01:42):
Clara Feld Mama about an insurer, then a Clarafield.

Speaker 5 (01:52):
I'm gonna say, what.

Speaker 6 (01:56):
What whe.

Speaker 7 (02:05):
On?

Speaker 8 (02:05):
That is the river the river driver.

Speaker 4 (02:12):
He needs to help you not now.

Speaker 8 (02:18):
Seen seen.

Speaker 4 (02:22):
We love it about your paddle.

Speaker 9 (02:30):
You're not You're not half be.

Speaker 4 (02:34):
Okay, I wanna go.

Speaker 2 (02:38):
I think gonna field them. I'm very forgive me that
your PM Nothingada, It's a concrete so I got it, Okay,
I want a concretely the.

Speaker 4 (02:59):
Count.

Speaker 2 (03:00):
They puts a man though it's not the man.

Speaker 4 (03:05):
Though it's not that never made.

Speaker 9 (03:41):
Welcome my heir acro.

Speaker 10 (03:45):
I'm bullying for bully for president.

Speaker 11 (03:47):
You know your opinion.

Speaker 4 (03:48):
You want to look about it. I don't thin anything down.

Speaker 2 (04:21):
Petrea Forti sire more time pretty in the hotel.

Speaker 9 (04:27):
Say years.

Speaker 4 (04:30):
And night, amyn A.

Speaker 12 (04:42):
Mre down Lbarda mr Da Edborda Edbarda, Mrda ed moretborn Morena.

Speaker 4 (05:01):
Where the party is no prey. You know there are
partial politicos.

Speaker 13 (05:20):
Okay, points humanist alias afo tourista. We must prepare partidos umanista.

Speaker 8 (05:28):
He said it you're not be heard.

Speaker 13 (05:30):
The mud dorstrsnamos na la lucha in three partinos.

Speaker 4 (05:35):
The recall canamos.

Speaker 8 (05:38):
That thro they say, they say, they say fuego dess loo.

Speaker 9 (05:42):
He said, yeah. The long man in us a cover not.

Speaker 13 (05:45):
Called the Marti Park, said Pip.

Speaker 4 (05:49):
With a toll of people, that says amos.

Speaker 13 (05:53):
He says to Manila one he said, directly endo dido
ela in forma field, yeo investing as your sable, investing,
your ivesting her has I say a point of the TODs.

Speaker 9 (06:11):
But I stay talk.

Speaker 13 (06:15):
For sequesto boro and get the money at money that
that's all a lot of money. That nothing okay, pretty.

Speaker 2 (06:31):
There's a stay that where.

Speaker 8 (06:33):
The guy where the okay?

Speaker 4 (06:41):
There where the birthday day? More day? Yeah, let's.

Speaker 14 (07:04):
Mother there when ware?

Speaker 4 (07:10):
What water the water? Yeah? What are the one there
was there? Yea bag?

Speaker 7 (07:30):
Stop age stop hey stop aging stop.

Speaker 15 (07:34):
Baby stop age stop agies stay.

Speaker 4 (07:38):
Stop asy stop age stock and stop he go and
stop he leans up it's up enable and stop dle
ever get.

Speaker 16 (07:57):
L e.

Speaker 6 (08:05):
He up.

Speaker 4 (08:20):
It is age up saying ay ag ag age maybe.

Speaker 17 (08:31):
Age stop stop age stop aging stop aging stop agent
stop Asian stop Asian stop stop.

Speaker 4 (08:45):
It stop. It's not you, it's.

Speaker 2 (08:51):
It's stop and it's stop behind without here listen, that's.

Speaker 14 (08:58):
Not listen.

Speaker 4 (09:04):
You know. Never let's speaks.

Speaker 7 (09:44):
Not a.

Speaker 4 (09:46):
Stop never.

Speaker 14 (10:00):
About about.

Speaker 4 (10:16):
Black brown, blacking bum.

Speaker 14 (10:21):
Lad brown, black um.

Speaker 16 (10:25):
Sound brown, black uma land crown las um what is
la brown black uno la fold black bull la found

(10:45):
black um um found black bum wound.

Speaker 4 (10:56):
Mm hm mm hm.

Speaker 14 (11:01):
Mm hmmmm.

Speaker 4 (11:06):
Mmm mm hmmm. You know j j Zy.

Speaker 7 (11:19):
You you young, he get you off. Let's all the
ever get it off. Let's all them hens get it off.
That's all he's off. That's all right, that's all he's hale.

Speaker 4 (11:39):
That's lend. No, that's a never after yet no, it's all.
There's no leave ye.

Speaker 14 (11:52):
Leave you leave up.

Speaker 5 (11:57):
He is Dramasaki form of the October.

Speaker 4 (12:05):
Yes, thea in the pa la vida, la vida.

Speaker 2 (12:12):
Da todos lavida, la la vida maas woman davida maslaga
da vida nas last.

Speaker 4 (12:19):
Parados if a whoi.

Speaker 2 (12:23):
Aki fred Magrid and then paras sivees nimos unto mr
maas livir mahone bastiepo limir masado rivera vida yad va
my great Vania Espana s and price bastro quemo. Then

(12:47):
repair in my breve is lasil bast from heeva. Then
to repair or chain, I says told annual le v
beam was Plania pavia a burday, but better than con

(13:09):
He said that Sammy and Stub was again bad. Birthday
birthday day, birthday birthday birthdays.

Speaker 14 (13:27):
On Morday word.

Speaker 4 (13:30):
Borday Monday morning.

Speaker 18 (13:33):
Nor Morday people of be the what a Morday.

Speaker 5 (13:52):
Bepleastania birthday bday.

Speaker 19 (13:58):
Mama a birthday birthday the birthday came Peter the Monday. Yeah,
gonna give you the picture on Monday, can't Dina.

Speaker 5 (14:10):
He so so so it's worth Monday Morday free menders
of cover it.

Speaker 4 (14:27):
They are in the Okay, this that was again horn.

Speaker 12 (14:32):
Of meam me.

Speaker 14 (14:37):
Monday.

Speaker 4 (14:41):
N I came more day.

Speaker 2 (14:46):
Monday days to get down.

Speaker 9 (15:00):
I forget them.

Speaker 4 (15:01):
It's not to get it's not I get no paso

(15:48):
hang out, pick up. Okay.

Speaker 20 (16:10):
Aging is a natural process, but it's a process which
helps our health and well being.

Speaker 10 (16:17):
We are lucky to have longevity researchers developing rejuvenation therapies.

(16:47):
Welcome to Transvision twenty twenty five.

Speaker 20 (16:57):
So longevity is of course not just a theory, it's
a biology. And in our next session, we're going to
explore the cellular model of age, really decoding how exercise,
immune resistance, and epigenetics really shape our health span or lifespan.
And we're going to hear from leaders who are really
mapping aging from the molecule to the system level and

(17:20):
what it means for interventions today. So we're going to
have speakers are going to talk twenty minutes each and
then at the end we're going to have a, Q
and A, so make sure either if you send in
your questions your SLIDO or that you have some questions
prepped afterwards. And first up, we have Vijai Vasvani, co
founder and CEO of Omniscope, together with Holger Hayne, co

(17:42):
founder and CSO of omniscope, and they are both innovators
in single cell and multi omnix building maps of how
aging manifests in our biology. Really on a mission to
crack the so called immune code. So Omniscope just shortly
is decoded the immune system and using AI to scalably

(18:03):
develop diagnostics and accelerate therapeutics, building the world's largest immune
data banks. So please give it up for vj and Holger.

Speaker 8 (18:25):
You are made of cells. All of you are made
of cells. Not all cells are created equal. Your immune cells.
We are defending you and protecting you from disease right now.
They are both the detectors and the very living medicine

(18:47):
that allows you to live along in healthy life.

Speaker 21 (18:52):
In the end, it's our immune system that keeps us healthy.

Speaker 22 (18:54):
Especially here in Madrid, people live healthy along our lives
and we want to figure out why it is so.
In age, specifically, the immune system is losing its function,
so we lose protection from viruses, but we also lose
protection from deadly diseases such as cancer. Immune sets also
lose their self control, and here they attack our healthy

(19:15):
tissue and really make us suffer diseases such as out immune,
our new inflammatory diseases.

Speaker 21 (19:22):
So it only go we're reading the immune system.

Speaker 22 (19:25):
We implement a technology that reads the immune system one
cell at a time, and that now, over the years,
really allowed us to generate a data bank really to
understand the holistic immune system and how it acts in
the healthy context, but also to use that as a
reference to quantify what's going wrong in disease and what's
going wrong while.

Speaker 21 (19:46):
We age or suffer age related diseases.

Speaker 8 (19:50):
Indeed, when you think about the fundamental mechanisms that rule
our biology, you could think of the brain as a
central command system and the immune system as your distributed
cellular sol Now, decoding the immune system is not a
small feat. It is an incredibly complex system, and there
is not much utility in only being able to understand

(20:12):
something if you cannot act. So not only does only
Scope read the immune system at millions and millions of cells,
it rights the immune system. We write your immune system
so that you can use your own immune system as
a living medicine. And this is not science fiction. We've

(20:32):
actually done this.

Speaker 21 (20:35):
So we have the entire system virtually integrated.

Speaker 22 (20:38):
We're we're reading the immune system and specifically immune system
dynamics when, for example, we ate or when patients respond
to treatment, for example, immune moderating drag immune therapy can
serve accids. And here we also implement a system where
we biobank healthy cells and to use those for future
autoovis therapy. But what you see here in the screen

(20:58):
is actually the next phase writing the immune system. In
this case, we are writing the immune system of a
half a year old child that was suffering from a
pediotric tumor.

Speaker 21 (21:08):
So we are working with her over the years.

Speaker 22 (21:10):
Now she's on complete mission because she responded to immunotherapy
the drug that is activating the immune system. And as
in company, we were following that process and we were
identifying those cells that were killing the tumor cells and
that we're protecting the patient from the tumor coming back.

(21:35):
So it is and it was the immune system that
prevented her cancer to come back. She's still in complete
remission now after three years. But as a company, we
kind of took the language of the immune system. We
took her own T cells and we engineered the T
cells to recognize the tumor. And this is something that
in the end is a living dug a drug and
will protect herd tumor for coming back in the future.

Speaker 8 (21:58):
So it's really the ability to use your own biology
scalably and scale is very important. You see, engineering your
own immune system the way we've done here using mr
Anda technologies was not only fast, it was incredibly cost effective,
and it was cost effective for a public health system
and an omniscope. We believe that healthcare is for everyone.

(22:24):
This key point moving from immune engineering to the fact
that in order to engineer the immune system and to
bring health care for everyone everywhere, you need to represent
everybody's cell by cell. That's billions and trillions. You yourself
have over two kilos of T cell dry weight within

(22:45):
your body up to ten to the sixteen unique combinations,
and Omniscope really understands that in order to use data
actionably and sustainably, we need to.

Speaker 9 (22:58):
Represent all of you.

Speaker 8 (23:00):
Is why we've spent five years building the world's largest
immune databank.

Speaker 22 (23:07):
So having sequenced millions of cells from thousands of individuals
in the end really allowed us to work with the
drug companies to develop better drug to increase the drug
development cycle, to make it faster. We were working in
areas of cancer mainly immune oncology, infectious disease, but auto
autoimmune diseases really where we could make an impact by

(23:30):
reading the immune system, sometimes in real time, working with
clinical researchers in clinical trials. But what about aging? What
about being healthy? So having sequenced thousands of samples from
newborns to centenarians really allowed us to understand the process
of aging and to use our system as a biomarker

(23:52):
to quantify the process why we age, or to quantify
the process why we respond, for example, to geotherripeutic agents.

Speaker 8 (24:02):
And as by esteemed compatriot doctor Mahmultkan alluded, this is
not about a single nation or a single individual or
an act of heroism. This is about really all of humanity.
So we not only looked at different age ranges from
newborns to centenarians, we also looked at different HLA types

(24:22):
and ethnicities. We also ensured that our models are equally
representative from a sex perspective, because whilst our biologies as
humans are similar, our sexual morphologies and differences do mean
that we react to age differently. It's really this database
that really allows us to have a foundational model of

(24:46):
the immune system and really moving forward. It is only
by building a model that you can truly act. You
can only act on what you know, and you cann
only de risk and intervene if you can predict and
model what may happen. Thus, by building a complete model

(25:09):
of human aging at a cell by cell basis, not
only do we bring that to you so that you
can live longer, healthier lives, we bring it to our
esteemed colleagues developing therapeutics as well, so that they can
use these models to test and accelerate the ability to

(25:31):
enhance human lifespan and quality of life.

Speaker 22 (25:35):
So during the next days in this conference, we will
hear a lot about the hallmarks of aging, but in
the end, it is the immune system that is either
the root course or extra consequence of these hallmarks. So
as a company, we put together a model of age
that is incorporating our own proprietary sequencing methods, our proprietary

(25:56):
machine learning models, for example related to mun age or
the inflammating process. But we also paired that up with
already existing with accepted markers biomarkers of aging, for examples
in essence TeleMe length or the DNA methilation clock. And
I'm obviously very proud to have Steve Forward in this session,
who was the pioneer looking at methylation and the prediction

(26:20):
of biological age.

Speaker 8 (26:23):
And it is also an honor for us to use
some of the technology which doctor Hobart has designed in science.
We genuinely mean it when we stay, we stand on
the shoulders of giants. And I do want to take
a second to thank you for being such a major
contributed to a field.

Speaker 9 (26:44):
Thank you.

Speaker 8 (26:57):
Thus we build a model of age with respect to
what has come before us scientifically, but also moving the
field forward with all of the tremendous advances. How do
we use this model of age? You see, now that
you have a model, you can genuinely from a public

(27:18):
health and epidemiology perspective, look at age as a disease. Now,
you know, we often look at aging and say, well,
all the bad stuff happens to us when we age
from a incidence perspective, as we age, cancer, cardiovascular disease,
susceptibility to infection all become more and more prevalent. And

(27:42):
one of the fundamental reasons for that is an aging
immune system. But I also want to take a step back.
Being mortal isn't all that horrible. Other good things happen
to you when you age. You become a little bit smarter,
You have families, you can enjoy your wealth, you can
give your wealth to better causes, you can use that

(28:04):
knowledge to make a better world. So for us, from
a humanistic point of view, we want to extend your
health span so you can do more good and not
just get a lot sicker. So aging as a disease
is something which we show in our next slide that
is not always entirely bad news. You see, I am

(28:29):
interested in you, but I'm going to take a moment
to talk about me. My name is Vija, and I'm
the CEO and co founder of Omniscope. This is my
cellular avatar. This is my actual, real cellular avatar being

(28:51):
updated right now with my wearables and is a digital
model and representation of my own biology with millions and
millions and millions of cells. It is as personalized as
personalized gets.

Speaker 21 (29:10):
So my name is Horgahina.

Speaker 22 (29:11):
I'm chief scientific officer and co founder of omsco together
with VJ and Lynette who's hearing the audience, and this
is my cellular avertar. And my question is being here
in a blue zone, how this cellular avatar is actually
changing during the next days of the conference. And as
you can see by VJ and my own avatars, they

(29:32):
look very different. And we explain in the next light
what that different actually means and how we challenge each
other to get younger or older related to inflammating or
the aging process channel.

Speaker 8 (29:45):
So let's do the riskiest thing that you can possibly
do at a conference. Let's go for a live demo
of always Lifetime, which actually allows us to look at
my own immune system. So going to the live demo
of OS Lifetime, which my colleague Nina is just about

(30:08):
to switch over to OS Lifetime is really designed for
you and for science based longevity clinics.

Speaker 9 (30:19):
We believe in a.

Speaker 8 (30:20):
World where AI and software have a physician at their helm. Anina,
if you could move to the demo. If not, I'll
admit defeat at my only chance at doing the Steve jobs.
But I guess I'm not going to do that, am I.
One of my major issues that I faced, which you

(30:43):
can see in my previous slide, is whilst my date
of birth is forty two, my immune age is actually sixty.
Whilst I have practiced sports at a semi professional level
for many many is one of the things that I
unfortunately suffer from a crisis quite acutely. I inherited this

(31:07):
as a gift from my father, although he gave me
a lot more good things than just crisis. And the
issue that I've had is that my inflammation at one stage,
when I compared it to what we had in our database,
was actually as high as a cancer patient. Now for

(31:29):
a CEO trying to spend their life helping other people,
that was not necessarily the best message I got. So
what you can really see here is that now my
inflammating is back to normal. Indeed, if I actually go

(31:50):
to my actual inflammating, you can actually see.

Speaker 9 (31:55):
How bad this got.

Speaker 8 (31:57):
The peaks and truffs that you see going up and
down are my crisis flares, and the reason that they
go down is because of administration of corticoids, which are
a synthetic form of cortisol. The stress common, which has
both pron inflammatory and anti inflammatory effects. Unfortunately, like many patients,
after over a decade of use, I have resistance to

(32:21):
this therapy and it doesn't really work. And crisis doesn't
just attack your dermis, your skin, it can get to
your bones. That's not the end which I wish for myself,
and for this reason, I actually then also realized as
we scroll down that not only was my inflammation of

(32:43):
the charts, my cellular damage was off the charts. And
not only am I shorter than Holger, my telomers are
shorter than Holger as well, and my telomers are what
allow myself to constantly actually replicate, and as they get shorter,
the ability for me to regenerate my cellular populations is impaired.

(33:03):
I can also see that, aside from my immune age,
my methylation clock also shows signs of accumulated accelerated aging.
But let's move for a second to the presentation where
I can show you very briefly what I did to
reduce my inflammation. You see, I decided to use non

(33:28):
pharmaceutical interventions. Why because I wanted to contribute as an
end of one to society and show you that you
don't always need access to expensive medical care to actually
change your biology. I did stuff which is quite free.
I slept, I worked out thanks to football club Barcelona.

(33:50):
I changed the way I work out, and we'll talk
more about that, because as you age, you need to exercise,
but you need to change the way you do it.
And I took supplements which are generic and cheap, fish oil, melotonin, HI, those,
vitamin C. I'm publishing the entire thing and it's completely free.
Don't do it without medical advice. But here's what happened

(34:11):
to me. You see in the next slide you can
actually see quite clearly that.

Speaker 15 (34:18):
In just a few weeks I went from cancer patient
inflammating to athlete fit inflammating.

Speaker 8 (34:30):
And this was a major, major benefit to me. I
want to make sure that using OS lifetime you have
the same benefit. If you can see it, track it,
you can do something about it.

Speaker 22 (34:46):
And as initially introduced, so our technology is reading single cells,
reading single immune cells, so we can look switching to
the next slide really to look at the root course,
what is behind what's a mechanism behind the improved inflammation score.
So here we're looking at very specific parts of the
immune system. CD four and cdat cells, but those can

(35:06):
also produce inflammatory markers. They're not only helping us defending
us against pathogens, but they can be pro inflammatory and
produce inflammatory markets that we measure in the blood and
that causes systematic damage of organs. So we've seen then
with correlation of the reduction of the inflammatory scores and inflammating,

(35:30):
those immune cells also going down, and this is something
obviously we are tracking now over time. Going to the
next slide, let me introduce to my own cellular avatar.
So here you can see in one single view inflammating
immune age protection score and what you can see from
my immune age that although I'm forty sixty year old,

(35:54):
my immunage is actually thirty seven. So this is very
good news and this is something follow up I will
try to keep improving. Bad news though, is that my
inflammation inflammating is very high. But the good news again
is something actionable. Right together with my protection score displayed
by the rings around around the sphere points to the

(36:16):
fact I have a solid protection. But again, protection is
cellular defense against pathogens, and that's something actionable for example
using vaccination.

Speaker 9 (36:25):
Next likely.

Speaker 22 (36:27):
So here today I will walk you through starting with
a view today. It's why how my immune age and
inflammation looks like to take you back in time, and
how the evolution of the immune age has been over
the last almost two years. So you see kind of
a constant gradient, consistent profile over the last one and
a half years. But then at the end of twenty

(36:48):
twenty five, I was facing a disease called limes disease,
which is introduced through a tick bike then bacteria causing inflammation.
It can have a systemic fact so you see the
actually the drop in my immune age. You see through
the integration of my variables, the drop in view two mugs,
and all this together was a warning signal. Then quickly

(37:12):
the disease was resolved using high dose doxicycline, and you
see actually both immune age viewing to bugs going back
to baseline. Now, thinking about it, it's a bit counterintuitive, right,
So I'm facing a disease still my immune age is decreasing,
so I'm actually desiderating I'm getting younger. But if you
think about it from the other angle, from the kind
of defense by immune biology anger, it is really through

(37:38):
a disease that is quickly resolved, we're training the immune system.
It's a little bit like a vaccine, right, So we're
training the immune system. We make it younger, we make
it better, we make it defending us better in the future.

Speaker 21 (37:49):
And this is what has happening.

Speaker 22 (37:52):
And again looking at the immune age model as a general,
we can then look at specific populations again identifying CD
for T cells that are very much correlating while my
immune system is getting longer, a younger, and I'm responding
back to baseline. These CD four T helper cells, so

(38:12):
those cells that are building a stable memory in this
case against the times disease puthogen are going back to baseline.
But then having the full model of age, we can
look at other biomarkers of age. So next slide please
so here biomarkers in essence, So zombie cells that cause
chronic inflammation are actually behaving the opposite way. So during limes,

(38:35):
disease in essence is speaking and then it's decreasing while
I recover and my immune age is going back to baseline.
Next slid please slide before please. One important thing to
mention is, and it's where many aging clock fail is

(38:57):
a reproducibility. So if I send a set I measured
three times, it should give three times the same result.
And this is what you see on the slide on
the on the right hand side, where we measured multiple,
multiple samples repeated times and it gave you can kind
of see that by the low standard deviations gave it
gave repeat it repeatedly the same result. But then we

(39:17):
also looked at biological replications. So samples that you see
in the circles last like place that you see in
the circles where I've been giving blood repeatedly over weeks,
So these are samples taking only weeks apart.

Speaker 21 (39:32):
And here the immunage.

Speaker 22 (39:34):
Prediction is really following the evolution of my immuneage over
time while I was recovering from Lymes disease. What you
see here is really then now not only VJ and myself,
but we now are testing many individuals for years now,
and you see the consistent evolution of immuneage over time.
But in specifications for example myself suffering from diseases, you

(39:58):
see in active training for example VJ, you see active
peaks where his crisis flares are really acting against the
immune AGD cock.

Speaker 8 (40:10):
So really the message here is that we've been very
very rigorous at understanding aging as a process across thousands
of individuals from different age gradients, different nationalities, healthy affected
by disease in a reproducible manner to really measure the

(40:31):
way our age changes go to infection to disease, but
also very important to therapeutics as well as other interventions.
But ultimately we also need to understand how do we compare.
A model allows you to compare yourself to other people,
It allows you to compare yourself to your aspiration. In

(40:52):
the next slide we really go into what is it
that we can learn from long lived centenarians. Omniscope has
invested a significant amount of resources, thanks to our investors
who are here in the audience today, to really understand that.
And one of the things which jose has mentioned, which

(41:15):
I'm entirely aligned with, is that Spain itself is also
quite a special country. It's a country where many long
lived individuals do live. What can we learn from these individuals?
What can we learn from centenarians Walker.

Speaker 22 (41:34):
It's centenarians or in this case even super centenarians. So
what you see on the screen is the study that
was published about a week ago. It's a mighty omic
profile that basically means there are different layers of information,
looking at the microbiome, looking at immuneage clocks, looking at
DNA infanation clocks.

Speaker 21 (41:50):
So everything kind of summed up with.

Speaker 22 (41:52):
A holistic profile how a super centenarian was managing to
live that long. This is obviously our north star, and
this is something what we implement in those lifetimes, so
you and myself I can do today already I can
track how might specific biomarkers of age are on track

(42:13):
to be a centenarian or potentially super centenary in the future.

Speaker 8 (42:17):
And that's what we are all after, right, So centenarians
are non star, but we also have to have an
idea of where do we want to get to? Right,
So for a lot of us as we age, we
want to retain our functionality. We want to be able
to play, we want to be able to move, we

(42:37):
want to be independent. These are the whole marks of
vigor and of leading a complete life. Do you know
which population has all of this vigor if you think
of it, If you think of the individuals, you know
who are most most functional in our next slide, it's athletes.

(43:04):
Athletes represent arguably a paradigm in what it means to
be fully functional, fully vigorous, they have less sickness, they
have more activity, they keep more muscle mass, they suffer
less sarcopinia, They keep cognitive vigor. They are engaged with
their communities and their teams. They are brimming, simply brimming

(43:29):
with life. And we live in a world where centenarians
are running one hundred meters and competing in incredible athletic events.
If there's one common sense thing that we ought to do,
it is to learn the secrets of athletes. And it

(43:50):
is with great privilege that we have doctor Jill Rodas
from Football Club Barcelona, who is going to share with
us the secrets of athletes.

Speaker 9 (44:11):
Thank you very much. First of all, I would like
to talk with a microphone. Is this possible? Oh, it's here.
I'm sorry I didn't see cola ola. Ah, fantastic.

Speaker 23 (44:28):
Well, first of all, I would like to say thank
you very much to the organizers for this great event
and especially of course to Omnisko. Why I am here
from Football Club Barcelona in Madrid. Well, I am a

(44:48):
privilege because I am working on probably one of the
best football clubs in the world. But at the same
time I am a privilege because I am working also
in one of the best, one of the best hospitals
in Europe, that is hospital Clinic and hospitals joined the
deal of Barcelona for this is nice in order to

(45:10):
share this double vision from a sports to the health,
often to the health to the sports. Okay, I am
a sports decision and now I believe that you are
a little bit tired, because after one hour and a
half or two hour, sit down. Please, I think that
it will be fantastic if you want to stand up

(45:32):
and move a little bit.

Speaker 20 (45:34):
Yes, fantastic.

Speaker 23 (45:39):
How many people are suffering low back pain now because
I no, thank you, thank you, thank you very much.

Speaker 9 (45:45):
Okay, sit down please, well next slide. Why why we
are here?

Speaker 23 (45:56):
It's true that during many years I have been researching
with these guys, with these athletes. No no, and these
athletes are really different. Sincerely, I have the privilege to
be their sports physician during many years from Messi, Iniesta

(46:23):
and Ronaldina, and believe me, they are different. They have
some special things that we need to know, not only
in terms of the genes, if not in terms that
how they adapt depending on the epigenetic factors. And this
is a great secret that I tend the possibility to

(46:47):
know it not just only in terms that to help
football club Barcelona to be greater than real Merit or
letic the Merit, but also for the future for the
general population. And this is a question for you and
I hope that you answer me at the end of
this is small, this short speech. What do you believe

(47:11):
is I say that these athletes probably will have longer
life span and better health span than all of you.

Speaker 7 (47:22):
Do you.

Speaker 9 (47:24):
Believe that this is true? Or no?

Speaker 23 (47:26):
Please wait a minute, I have the answer, that scientific answer,
but please that is true that everyone in the world
things think that this is not good? Well, next is
like please of course, the cancer in the world of

(47:46):
sports is injuries. Yesterday run merit and analytic the medrid
one that is fantastic, But as you know, there are
many many players that has for very different kinds of injuries,
and our cancer are injuries. Our players are constantly in
an inflammation process.

Speaker 9 (48:05):
All the players that play yesterday today have inflammation.

Speaker 23 (48:10):
And you can imagine that this during twenty years, twenty
five years of your life, every day you have suffering
an inflammation. For the reason when we as a doctor's
we need to know more about the health of our
players and to find a good bio markers in order

(48:33):
to help the health of my players and at the
same time increase the performance of my main players. I
found omniscope because it's the first time that I see
something that can help me in order to know the emological.

Speaker 9 (48:48):
Status of my players next life. Please, this is a
dream or no is a dream.

Speaker 23 (48:57):
Today we create thanks to this partners, a good avatars
of every of my players. Why because I need to
anticipate when this player we will suffer another injury or
when this player will suffer increase or a decrease of
his performance. For this reason, today we have the possibility

(49:20):
to create this avatar using the Digital Twins technology. Repeat,
this is not the future. I'm sorry, this is the present.
Next like please, In terms of that is in difficult.
Sometimes we need.

Speaker 9 (49:37):
Big data of every of our players.

Speaker 23 (49:41):
In terms of from omics, we are talking about the genes,
transcriptomic meta programic, metabolomic epigenetics, also immunologic profile.

Speaker 9 (49:55):
But we also we can incorporate an integrate radium mix.

Speaker 23 (50:01):
GPS because we have the possibility to know exactly the
load of our players during all their career. Load is
very important because they need to adaptate every day to
the training. You can imagine it today to talk with
the players of the real madit and say how are you?
I am tighter because yesterday I play and how is

(50:23):
your muscle? It's okay, you heard, how is your immunity profile?

Speaker 9 (50:27):
Now we need to know this.

Speaker 23 (50:29):
It's too that sometimes the players don't like that you
know everything about them because maybe yesterday after the match
they went.

Speaker 9 (50:39):
To the party.

Speaker 23 (50:40):
But repeat, we need to know this because probably this
we can when they play again, some of these players
will sufair injury.

Speaker 9 (50:49):
And then's when the coach say, hey, what's happened here?
What's happened? If you a load that these.

Speaker 23 (50:54):
Players play every three days, probably you will have injury.

Speaker 9 (50:58):
Well, thanks to this kind of.

Speaker 23 (51:02):
Universal the io medical, we have the possibility in terms
that to anticipate NEXTSS light.

Speaker 9 (51:09):
Thanks to a suppose we are creating.

Speaker 23 (51:12):
This, this is possible, and this is sometimes it's more
difficult to convince to the coach that this tool can
let him to have more information. Finally, the decision is
from the coach. The coach is the is the man
in the world of the sport world in the hospital
is a doctor. But in the sport is the coach.

(51:34):
Coach is the post. But coach needs to believe in
these kind of tools. But for the reason these do
need to be very rigorous. Nextest light, please we create
these profiles. We have these tools. Of course, the doctors
are very very happy with these tools. Repeat every day
we are increasing the information about every of our players.

Speaker 9 (51:58):
Next lights please, this is.

Speaker 23 (52:00):
Very interesting, but of course it's very necessary to be
very regulars in others, not to say not to send
no no, this is science. Nexts life please. We did
some research. Real Madrid probably is the best sports team
club in the world in terms to win European championships.

(52:26):
But sincely I believe that football persona probably today is
the leader in the sports team research because in the
last ten years we have been we have invested a
lot of time more than money in order to have
this research.

Speaker 6 (52:43):
You know that.

Speaker 9 (52:44):
And now to cand to show you this is an
that is.

Speaker 23 (52:47):
An example that we are doing now with the omni
score in terms that code change the immune age in
function about your position.

Speaker 9 (52:56):
NeXT's life.

Speaker 23 (52:56):
This is an example and this is a little bit
more that you like that whole Can you explain me
these last reserves that we are doing.

Speaker 21 (53:07):
Now for us.

Speaker 22 (53:07):
So what you see is the immune age evolution of
a player over the course of the season, and for us,
it was incredible to see that immune age now as
a metric of immune fitness or fitness in general, is
changing very rapidly, and it's not changing consistently across the
entire team, but there's actually correlation. So players that play

(53:28):
more matches, players that move more age faster. Strikers so
forwards age faster than midfielders or evenders. And what you've
see in this light is the very high resolution picture
where we correlate immune age together with GPS data. So
football players are probably the best profile players on the

(53:48):
world when it comes to movement, so movement in general,
but also impact and this is all represented by different
GPS metrics. You've seen on my slide that we have
wearables integrate it from the for example, from the Apple
Watch view to Marx hard right verability. So here this
is very different because we have much more different metrics

(54:09):
that we can correlate, and for us, it wasn't credible
to see that GPS data, So the external load is
translating to a very different internal load of a player
and the immune age has been our sensitive metrics to
quantify this.

Speaker 23 (54:23):
Thank you.

Speaker 9 (54:23):
Hold next lights please, and what about the genetics.

Speaker 23 (54:28):
Of course, we are genes and how we can adapt
to how we are sleeping, muticians, training, travels. Genetics of
course is very important and probably we need a good
balance between genetics and genetics.

Speaker 9 (54:46):
Please next the slide.

Speaker 23 (54:47):
But today we have the opportunity also to work in
terms of metilation, etc. In order to know these are
another accents how our players have adapted to that training
into the competition.

Speaker 9 (55:00):
And for this reason also we have some.

Speaker 23 (55:01):
Another partner that we are working on and researching in
terms of to know the genetic age clock, the telemetter
eletics clock.

Speaker 9 (55:08):
Maybe later you another speaker can talk about more of this.

Speaker 23 (55:13):
But it's interesting to know, for example that our players
for Jample have these specifically in male athletes in football
male they are a little bit older than the normal population.

Speaker 9 (55:28):
Two years more.

Speaker 23 (55:30):
But in female teams know and this is another message
we need more research in terms of female teams because
in terms of the female we don't know anything. When
we are looking for some biomarkers in terms of transcriptomic, protemic, metabolomic,
they are different bio markers for female and male and
for this reason we need to also remember to researching women.

(55:52):
Next is like please, and this is one of the
lightest studies that we are doing that we just only
we shown a genetic we have the opportunity to know
the relationship between the law and some biomarkets that can
help us in order to anticipate different injuries.

Speaker 9 (56:06):
Another's like please.

Speaker 23 (56:09):
For at the end understanding and athlete in money, a
genetic and genetic profile may help with personalized preventive strategics.

Speaker 9 (56:18):
This is the key.

Speaker 23 (56:20):
Sometimes the people send me the doctor, are you doing
a genetic and epigenetical test before higher contractor players? No,
but when we contract one player a player, a new player,
I need his permission in order to do this kind
of tests. But I think that this is good because no,

(56:43):
he knows and we know which are the risk factors
in different areas. And for the reason we can create
a specifical strategic preventive strategic for to help him in
terms of health and performance.

Speaker 9 (56:59):
And the last next light please, this is the coach.
Remember in the whole of the sport, this is the boss.

Speaker 23 (57:10):
But he believed in this and we try to explain
them to the coaches that the first step towards personalized
and position missing in the world of the.

Speaker 9 (57:19):
Sport is fundamental. Is fundamental. I think that this is
my last slife. Thank you very much for your attention. Doctors,

(57:40):
Thank you so much.

Speaker 8 (57:42):
I think we're uniquely privileged because we can learn the
secrets from these elite athletes, and with Football Club Barcelona,
we are working really, really closely to bring the best
type of science which already has accredited fIF A medical
center exists and put this all together.

Speaker 9 (58:05):
But you see, at the end of the day, I
am certainly not an athlete.

Speaker 8 (58:08):
So my question to you is when we look at athletes,
do they actually live longer, healthier lives compared to the
general population.

Speaker 9 (58:21):
Well, this was one of the meta analysis that.

Speaker 23 (58:26):
In part create evidence scientific evidence that this kind of guys,
these kind of athletes, of course have.

Speaker 9 (58:36):
Span span life longer than all of us. This is true.
For this reason, I think that we need to learn
about this kind of of special population. But it's true that.

Speaker 23 (58:52):
Maybe they will have more problemming in their niece or
in the hips, but in terms of less disease and
long and life span longer, this is the answer.

Speaker 8 (59:12):
Well, I guess the natural next question is you know
we see that with a free non medical intervention exercise
and sport, we can see scientifically that we lengthen life
and reduce the risk of many diseases, including cardiovascular and cancer.
But a lot of us in the audience and even

(59:33):
for what you saw on os lifetime using our wearable data,
we're not training like athletes every day, right, So do
in order to get the benefit to live a longer life?
Do you need to train eight ten hours a day
like an athlete?

Speaker 4 (59:51):
What do you need to do?

Speaker 9 (59:53):
No, but we need to do exercise, and there is
another question.

Speaker 23 (59:58):
Is the last question for you, h I would like
to know if you can do some exercise every week
every week? How from here, how many of you are
doing exercise at least three times per week?

Speaker 9 (01:00:18):
Thank you very much.

Speaker 23 (01:00:20):
You are really really well. But it's not necessary to
do ten, ten, or or twelve hours per day. No,
but that's fantastic, Thank you very much. I think that
this is a great population.

Speaker 9 (01:00:37):
Did you want to add a midle.

Speaker 21 (01:00:40):
Just a final announcement.

Speaker 22 (01:00:43):
So you have seen our both allse longevity profile, but
we also want to bring all longevity to you. So
that's why it's our honor to announce today our partnership
together with the Zand Clinic in Stockholm, Sweden. I've been
visiting stank Clinic for the last couple of weeks and

(01:01:05):
it is a perfect match where science meets clinics. So
I have been very impressed the implementation of jeroscience and
therapy diapeutics and moving forward, we want to see o's
lifetime being applied and sant Clinic is the perfect partner
and crime for us.

Speaker 8 (01:01:30):
So if you're if you're looking for science based longevity
care to increase your health spatter together with only scope technology.
Both the chief medical Officer and the CEO of Sant
Clinic are here and the audience with us today and
I personally think that it is one of the best
clinics around in a country which is very much health focused.

(01:01:56):
So why are we bringing this to you in the
spirit of public health. We don't just want another health tool.
We're not just here to take care of one or
two people. We want to make the world a better
place before we leave it, and the only way to
do that is to invest in yourselves. It's to invest

(01:02:17):
in your own lifetime to have a technology which allows
you to achieve your goals. And today as a thank you,
du Josse, we would like to give one full package
off OS Lifetime, which is the same technology which doctor
Rhodas presented to allow you to become part of this community.

(01:02:41):
So grab your phone, grab the QR code, because one
individual in this audience today will win your OS lifetime.
And on that note, I wish you a long and
healthy life.

Speaker 20 (01:02:56):
Thank you. I was just about to grab my phone
because I definitely want to win that, but I guess
I have to give it to the audience. But thank
you so much for great presentation. And it's quite synchronistic
because I know the suand clinic and I was actually thinking, hmm,
I think they need to meet Oi Scrope, and here
you are having a fusion, so I can definitely verify

(01:03:18):
it's it's actually one of the role model clinics. So
thank you so much, and hopefully have time for a
bit of a Q and A.

Speaker 9 (01:03:24):
I'm just going to.

Speaker 10 (01:03:24):
Deduce the next speaker of this session.

Speaker 24 (01:03:27):
Bam Wa bou bam bown b ba Wa b bam
bun b bam Wa ba bam bown b wam bound
bam bun bam whom bound bam brown down bad wam

(01:03:54):
bound bam bw bam Wow bud bam.

Speaker 20 (01:04:03):
I'm just going to deduce the next speaker of this session,
and we wouldn't actually be able to maybe measure different
biomarkers in our body if we didn't have what the
next speaker has given us. He is principal investigator at
ALSOCE Labs and the scientist and genius who gave us
the epigenetic clock, redefining how we measure biological age and

(01:04:26):
made the seminal discovery of the Horvat clock and epigenetic
clock based on DNA methylation. Please around welcome of applause
for steam Horvats.

Speaker 25 (01:04:45):
Yeah, thank you so much, Jose for this invitation. It's
been an honor to speak after Mamood Khan, who has
done so much for the rejuvenation field with evolution. I
was very impressed by the omniscope technology. I will talk
about epigenetic clocks and also immunity. I think some of

(01:05:08):
my material matches their previous talk. So there are many biomarkers.
By now, there are broadly three categories molecular biomarkers, such
as methylation, and so then there are these physiological biomarkers
functional performance, and of course we are now in the

(01:05:30):
era of weariables, various trackers of step counts, and so
much more. And I will really focus mostly on these
O mix measures, in particular methylation and epigenetics. Here I
show you a short history of biomarkers of aging, and

(01:05:51):
it goes all the way back to the nineteen thirties. Actually,
with these foundational experiments that caloric strains in the rad
can slow aging as measured by lifespan extension. You calorical
restrict a rodent, it will probably live longer. By now

(01:06:13):
we know that caloric restriction is very much a gold
standard intervention for slowing methylation clocks. And what this timeline
shows in red boxes are epigenetic clocks. Interestingly, when people
compiled this history of biomarkers of aging, they listed many,

(01:06:36):
many methylation clocks. And the question is why, And the
answer is obvious. Methylation contains a huge signal for aging.
That's why it was easy to do, you know. So
in twenty eleven we published the very first epigenetic clock
based on saliva, and we were of course hoping that

(01:06:58):
the saliva methylation measures would be useful. And later, if
I have the chance, I'll talk about how we measured
saliva methylation in a soccer team Premier League in Germany.
Maybe not as good as the football club in Barcelona,
but still very good. But anyways, then the multitissue clock,

(01:07:21):
and now we are in the era of next generation
epigenetic clocks that predict mortality risk. So I was always
interested in how to measure biologic age in people who
do follow the perfect lifestyle. Here I'll show you a
well known body weight athletes, bodybuilder, and he, of course

(01:07:45):
has tremendous muscle strength, but probably he wouldn't be able
to fool many molecular biomarkers of aging. Our best mortality
risk predictor is called grim age. It's named after the
Grim Reaper. It does not predict your calendar age. Rather,

(01:08:07):
it predicts your in certain ways, your risk of dropping
dead in the coming year. That's kind of what it
measures the mortality risk estimator. So the field has developed
many mortality risk predictors and epigenetic clocks and their comparisons.
Here I show you a comparison of a dozen epigenetic

(01:08:31):
clocks and grim age still stands out as the most
significant predictor of mortality risk, which surprises me because this
was developed in twenty nineteen and many years have passed.
I'm hoping for more powerful epigenetic biomarkers. An early criticism

(01:08:52):
of epigenetic clocks was that we don't understand the mechanism
what exactly do methyl lation clocks measure, But we now
have learned quite a lot. After twelve thirteen years of
tremendous effort by the whole aging community, we now know
many factors that accelerate aging. In short, methylation clocks are integrators.

(01:09:18):
They integrate a lot of various stressors and damage accumulation,
but one important aspect of what they measure is changes
in cell type composition. For example, the previous speakers talked
about the immune system, and I now want to talk
about really this relationship between age related changes in the

(01:09:43):
immune cell composition and epigenetic age in blood. Of course,
so Andrew Heschendorf recently published a wonderful paper, very large
scale study, where he accumulated a dozen different large co
to ask the question, well, what cell types correlate with

(01:10:07):
various epigenetic biomarkers and Here I show you the results
for GrimAge. One insight is people who have a high
abundance of naive T cells CD four T cells or
naive CD eight T cells, so naive these are in
essence young T cells. Sure enough, their grim age is reduced. Conversely,

(01:10:33):
people who have a high abundance of so called monocytes
of adult monocytes, their GrimAge is accelerated. So these results
very much match some of the material from omniscope, who
of course track different immune cells. But yes, so that's

(01:10:54):
all expected to some extent. What this slide shows is
that epigel getic age relates both to the adaptive immune
system T cell biology, but also the innate immune system monocytes.
For example, so when you go to the doctor, the

(01:11:14):
doctor will sometimes measure a complete blood count and with
flow cytometry or related technology. But interestingly, we can really
deconvolute blood cell composition just using methylation. We measure your
methylation and we can estimate the abundance of many different

(01:11:36):
cell types. Here I show you the reader of nineteen
different cell types, and now you can ask, well, which
of these cell types actually predict your mortality risk, your
time to death. And interestingly, one of the top hits. Again,
these naive CD four T cells. If you have a

(01:11:57):
high abundance of naive cdaight T cells will live longer.
But now there's a question. Okay, we can measure methylation,
and we can measure blood cell composition. Do the clocks
measure anything beyond just blood cell composition? And here I
show you briefly the answer. So here we predict time

(01:12:18):
to death even after adjusting for nineteen different immune cell types.
In other words, we remove the confounding effect of blood
cell composition, regress it out, and what you can see
is these epigenetic clocks are still highly predictive of all
cause mortality, even after you regress out anything you can.

(01:12:42):
Here I show you that epigenetic clocks predict cancer specific death.
Will you die of cancer or of course cardiovascular death,
even after regressing out the immune cell composition. So the
conclusion of this very life, large scale and comprehensive study
is that, yes, epigenetic clocks reflect the innate and adaptive

(01:13:07):
changes of the immune system. But this is really not
the whole story of epigenetic clocks. Rather, epigenetic clocks capture
deeper layers of biologic aging as well. We sometimes call
it innate aging. Now I want to come to this
topic that was briefly discussed by doctor Khan young plasma.

(01:13:30):
Should you expose should you get young blood plasma? There
have been studies in rodents, the so called parabiosis experiments,
where people have shown that if you connect an old
mouse to a young mouse, then you get benefits in

(01:13:52):
the old mouse. And Vadim Gladyshev and Bohan Zang and
their labs have shown that sure enough, epigene age is
reduced if you expose the old mouse to young blood.
So conversely, Jesse Puganik and Vadim Gladyschev showed the opposite phenomenon.

(01:14:12):
You take a young mouse, you connect it to an
old mouse. Suddenly the young mouse ages faster and epigenetic
age is increased in the young mouse. And that of
course leads to an insight or an idea. Well, maybe
the old blood plasma contains factors that made you age faster,

(01:14:39):
and therefore you should remove or filter out these old
pro aging factors. And here I show you the results
from a human clinical trial that evaluated plasma poresis. So,
plasma poresis is a procedure where all blood plasma was removed,

(01:15:02):
and in this particular study, Pavel did not replace the
removed plasma by anything else, just removed it.

Speaker 9 (01:15:11):
I think of it like an.

Speaker 25 (01:15:12):
Oil change, get rid of the old oil or the
old plasma. We were, of course, hoping that this procedure
would lead to rejuvenation of epigenetic clocks, and we looked
at multiple epigenetic clocks and there was a frustrating result.
It was the opposite of what we expected. Actually, the

(01:15:35):
number of plasma foresis sessions was associated with increased epigenetic
age according to multiple clocks, so it was disappointing. Now,
these investigators were very thorough and they looked at many
clinical markers for example lipid levels or red blood cell

(01:15:57):
distribution and so on, and the these results were mixed.
So the finding was that, for example, this plasma phoresis
yes led to lower total cholesterol, but conversely it made
things worse when it comes to red cell distribution, width
and other biomarkers. So overall we couldn't see any benefit

(01:16:21):
of using this plasma phoresis for rejuvenating these individuals. Now,
I want to come to another important topic metabolic stress.
For example, due to obesity so everyone has heard perhaps
of semaglutide or these GLP one receptor agonists. These are

(01:16:42):
miracle drugs for helping you to lose weight, and of
course the longevity field has been very interested in the
question whether GLP one agonists receptor agonists would lower epigenetic age.
Here I'll show you the results from a preprint. I
was not involved, but I thought it was a very

(01:17:03):
nice study and pretty large scale, forty five treated versus
about thirty nine controls. And I do want to highlight
that this population was not particularly healthy, so all of
these people were HIV positive, but more than that they
suffered from obesity body mass index thirty two. However, the

(01:17:27):
striking result was that the GLP one receptor a semi
glutite treatment once a week for thirty two weeks very
much was associated with reductions of grim age and all
other epigenetic clocks after you regressed out, for example, markers

(01:17:49):
of inflammation, body mass index, and other confounders. So here
I show you the results for different epigenetic clocks from
that paper. You see the negative values. All of these
indicate rejuvenation based on this compound, but there are many
open questions. So would GLP one receptor orgonists show similar

(01:18:13):
effects in healthy, non obese people, so, in other words,
people who do not have HIV and also of cause
the mechanism, So this remains to be seen. I want
to now talk about viral stress and doctor Cahn mentioned
earlier happetitis. See I talk now about HIV. So we

(01:18:34):
now know that HIV positive individuals who take this so
called anti retroviral therapy for repressing the HIV virus, that
their epigenetic age gets.

Speaker 21 (01:18:48):
Reduced by quite a lot.

Speaker 25 (01:18:50):
So this is a wonderful study from Ragarf se Gal
and Albert Higgins from Yale University where they looked at
fifty two different and interventions and they ranked these interventions
by which ones had the strongest anti aging effect. And
as I mentioned, the top hit was anti retroviral therapy.

(01:19:13):
The second hit is anti TNF alpha. So some people
who have high levels of inflammation autoimmune diseases, they need
to take anti TNF alpha. Another oldie bud goodie that
showed up is Mett Foreman, well known in the longevity field.
And the other thing that surprised me that also showed

(01:19:34):
up is the so called hyperbariatric oxygen therapy. So these
therapies seemed to have an effect on epigenetic age. I
want to briefly talk about exercise, because the previous talk
was very much about athletes. So here I collaborated with
Zoltra Dak from Budapest University and he analyzed Olympic medalists

(01:19:58):
and champions, and he found that people who had won
an Olympic medal less than ten years ago fairly recently, yes,
their GrimAge was slightly reduced, so they were younger than
the average population. However, if an athlete had won the

(01:20:19):
medal more than ten years ago, there was no difference
to the average person. And I show these results because
they make an important point that we see over and
over again, which is rejuvenating interventions sometimes have a transient effect.
You know you're an athlete, your epigenetic age is reduced.

(01:20:41):
If you don't keep it up, it will bounce back.
Here I show you a very rigorous study from Germany
where the investigators used a wearable to track the step
counts in three thousand, six hundred German participants, and sure
enough they found that step count was associated with lower

(01:21:06):
grim age. So yes, walking around had an effect. However,
as a biostatistician, I looked at the results and to
be honest, I was disappointed in.

Speaker 9 (01:21:18):
The very weak effect.

Speaker 25 (01:21:20):
So for the experts, the p value was point zero
zero five in three six hundred people. To me, that's
a very weak effect. Some people talked about supplements. I
want to draw your attention to a very rigorous study
conducted by a Swiss professor called Heiker Bishop Ferrari, who

(01:21:42):
studied seven hundred older participants. Everyone was fairly healthy seventy
one years or older, average age seventy five, and they
received various supplements and then they were followed for three
years and supplement The most noteworthy finding was that omega three.

(01:22:06):
One gram of omega three was associated with lower grim age.
Now I liked the study because it was so rigorous.
It was a randomized controlled trial. Everyone was completely blinded,
so it's really a result one can trust. I of
course take omega three every morning, but not too much.

(01:22:28):
High dose of omega three may cause atrial fibrillation, so
be cautious. Now I want to come to the topic
how dynamic are changes in methylation? So what's the recommended
frequency for measuring methylation? Should you measure it? In a
continuous way, every week, every month, once a year, and

(01:22:51):
if you open a textbook, it will say methylation is
highly stable compared to any other read out. So textbook
knowledge would be measured once a year. But now I
want to show you the results from a study of
a German Premier League soccer team. This was a very
interesting study where they collected now saliva samples not blood

(01:23:16):
from players before the season, during the season, after the season,
before games, after over two hundred saliva samples from twenty
four members of the team. And here is the striking result.
Before the game, let's say, look at the left panel.
In athletes, the grimmage is roughly thirty years old. See

(01:23:38):
the young men. Right after the game, you see this drop,
So that really surprised me. And then after they rested,
the GrimAge bounced back. So that's already a very good hint.
That vigorous exercise really reduced the grimmage estimate by actually

(01:23:59):
a substantial amount, surprising to me. It was so surprising
that I didn't believe it. I thought this must be
an artifact. Now, the first thing I could think of
of an artifact would be that there's some blood collection problem.
But in this study, they also looked at the saliva
samples of the supporting staff, so people who didn't run

(01:24:21):
around for ninety minutes, and there there was no difference. Interestingly,
and here I show you the most controversial finding of
the whole study. So this is twenty four hours before
the game, they collect saliva.

Speaker 8 (01:24:38):
Right after the game they walk off the field.

Speaker 25 (01:24:40):
They collect saliva in these Bundesliga players, and then twenty
four hours later they again collect saliva and what you
see is a substantial decrease in the grim age in
the biologic age estimate. So this really puzzles me, this finding,
and I'm trying to understan than how that is possible.

(01:25:02):
So I think it reflects that the DNA in the saliva,
of course reflects the blood cells, and this very rigorous
exercise must have an effect on the DNA that makes
it into the saliva for whatever reason, you know, So
we see this transient rejuvenating effect. What it shows us

(01:25:24):
is when we use these epigenetic clocks in let's say,
human clinical trials, we need to be careful that these
people didn't just return from the gym, you know. We
need to standardize the collection of the DNA, you know,
in these athletes. I want to now talk about some

(01:25:45):
more futuristic ways of rejuvenating or slowing aging. There was
a wonderful study from Harvard by doctor Ratin and he
has a way to cool the body temperature of mice.
And how does it do it. There's certain neurons in
the brain and if you stimulate them, that leads to

(01:26:05):
a drastic reduction of body temperature in the mouse. And
the graph shows you how methylation age in these mice
relates to the age of the mice, how it changes.
The blue curve represents.

Speaker 21 (01:26:22):
The cooled mice.

Speaker 25 (01:26:24):
And the stunning finding is that the mice whose body
temperature was cooler, their methylation age was much lower.

Speaker 26 (01:26:34):
You know.

Speaker 9 (01:26:35):
Interesting.

Speaker 25 (01:26:35):
So there's clearly a connection to body temperature and epigenetic aging.

Speaker 9 (01:26:41):
I mentioned it.

Speaker 25 (01:26:42):
I show you here's some AI generated picture representing science fiction.
You know, in space travel they always put you in hibernation.
Maybe that type of intervention could slow epigenetic aging. It's
all science fiction. I looked at the effect of sex.
It turns out that women age a little bit more

(01:27:04):
slowly than men. And we recently looked at so called
Kleinfelter syndrome, and we found again a similar finding that
men who happened to have one extra X chromosome, their
grim age was lower than men that have only one
X chromosome. So it was kind of an interesting result

(01:27:26):
when it comes to sex differences. Yeah, here I show
you the grim age results for the so called x
x Y males versus x Y males. But we also
looked at many other dosages for sex chromosomes. So I
invite you to read the paper. Next slide, next slide,

(01:27:49):
next slide. I'm trying to make up for time. One
take home message is for you. There are many ways
of measuring biologic age, but they really capture different aspects
of aging. I like, of course, methylation because there's this
nice idea that the molecule that carries our genetic information

(01:28:11):
also keeps track of time of the organism. These methylation
clocks are ready for human clinical trials. People are already
using them in some clinical trials. They can be used
for studying rejuvenation in preclinical models. I've shown you the
study in mice. We have methylation clocks for all mammalian species.

(01:28:34):
I can measure methylation ag in dogs cats, pigs, anything.
Here's my acknowledgment and I'll stop here.

Speaker 9 (01:28:42):
Thank you so much, Thank you so much.

Speaker 20 (01:28:55):
Steve really giving us a deep insight into all the
different modalities when it comes to age clocks. I'd just
like to call down the other speakers so that we
can just have a quick You always run over time
when you're having fun and getting a lot of information,
So could I please have Jill Bijai. Are you all
here still?

Speaker 8 (01:29:14):
Holger, Jill you're here.

Speaker 20 (01:29:16):
That's good. So here, gentlemen, first of all, any questions.
I know it's been a long round a lot of information,
but this is actually correlating both to you as professionals,
but also I mean as human beings, because we all
I presume, check our biomarkers with different epigenetic clocks. Yes,
please if you can, just could someone just help me

(01:29:36):
run with the microphone please? Of course your career mage
is going down.

Speaker 9 (01:29:48):
Thank you, so all fantastic talks.

Speaker 6 (01:29:53):
This question is for a steven really great results and
really inspiring talk. I was wondering because we know now
that our organs can age at different rates, so then
to auderstand measure in the pigenetic clocks and all of
these tests can recapitulate if you do it from peripheral

(01:30:13):
samples or from the blood, salive or whatever. To what
the stand, They can recapitulate what is happening in the
in the organs. Do you think we need also organ
dependent tests or what is your opinion?

Speaker 21 (01:30:26):
Yeah?

Speaker 25 (01:30:26):
Yeah, So the dream is to take let's say a
blood sample, measure methylation, and then arrive at results for
the different organs you or anything kidney, lang, hard even grain.
And the really stunning result is, and I can say
this with great confidence, the blood methilation very much captures

(01:30:50):
that information. So there have been several publications out, some
as late as last week, but several publications describe now
ways of measuring what they call organ ages based on methylation.
You know, and I briefly talked about grim age. I
didn't mention it, but it's based actually on estimators or

(01:31:13):
for example, see reactive protein hemoglobin A one C. Many
traditional biomarkers of organ function can actually be estimated with methylation.
So many of the experts know proteomics has been used
to estimate organ ages. All I can say you can
do very similar things based on methylation. And my thoughts

(01:31:36):
are both readouts will really be needed to capture aging,
not just proteomics, not just methylation, really both.

Speaker 9 (01:31:45):
Thank you so much.

Speaker 20 (01:31:49):
I just want to mention we have around four hundred
people following us on YouTube, so we also have questions
from YouTube and they can vary from really scientific ones
to maybe more joy span ones. One before I take
your question was to omniscope, are you making sure that
FC is beating barsas beating Madrid or the other way around.

Speaker 8 (01:32:11):
I think that's a tremendous, tu cheeky question. I would
say that in the end, I think you know, we're
bringing science into sports and we work with a number
of teams, and the reason that we do that is
because science and sport.

Speaker 9 (01:32:30):
Is about all of us.

Speaker 8 (01:32:32):
It is literally these are two disciplines where the whole
world comes together and gets incredibly, incredibly passionate. And the
reason that we started our journey in Barcelona with Football
Club Barcelona is because we could not answer what health
meant at a cellular level.

Speaker 4 (01:32:51):
And it happened that Holmer and I were in our lab.

Speaker 8 (01:32:54):
Very late at night having a bit of a debate,
and we looked out of our window at the company
and we saw the players enter and we had our
Eureka moment.

Speaker 9 (01:33:04):
We said, that's what it means to be healthy.

Speaker 8 (01:33:06):
But I think actually you are all athletes because you
are all playing the beautiful game of life, whether you
are with FC Barcelona or Madrid or wherever you are.
And humanity has been practicing sports for as long as
we've existed, so there's complete impartiality from that point of view.

Speaker 20 (01:33:24):
Very well put in, very good answer and also really
interesting to really highlight this fact with science and sports
and how it can really catapult both innovation and also
incentivize hopefully humanity to step up and be maybe not athletes,
but athletes in their own arena.

Speaker 9 (01:33:41):
Yes. Please.

Speaker 11 (01:33:42):
So there are many things that we would like to
try that are being sold. There's a lot of blah blah,
but of course we need to test and usually things
are done in the kindle trials and it's expensive and
it's not available for old biohackers or the community to try,
yet it would be great. So the cheapest things are

(01:34:03):
things like grip strengths source peerometer, or some exercise at
home to step from a chair and count your heart
rate and things like that. Are these fine in order
for the community to stop establish I would say weak
signals or should we have a complimentary what is good
for what? That's my question, and maybe I would compliment
it isn't it all these in fact short term effects

(01:34:26):
on health? Shouldn't we have animal tests for seample have
a long term view? Or is it sufficient?

Speaker 20 (01:34:33):
Looking at a democratizing health level?

Speaker 9 (01:34:35):
What is sufficient?

Speaker 6 (01:34:36):
What is not?

Speaker 20 (01:34:37):
Steve as the first question.

Speaker 9 (01:34:39):
Yeah, I briefly mentioned it in my talk.

Speaker 25 (01:34:42):
These are so called functional tests such as walk and speed,
grip strength, and they are of utmost importance. They should
always be measured. You know, I would say it goes
without saying that. You would mention, for example, how often
you can get up and down from a chair in
let's say one minute. Everyone can do that at home.

(01:35:04):
That's a nice competition. So these are very important readouts.
They should be measured. It's rather the other way around.
Should you also add genomics which can be expensive And.

Speaker 20 (01:35:16):
There's so many questions to answer and time is running
out and we're talking about moving and this is really
looking at what is possible today, what is impossible today,
and what is plausible in the future. When it comes
to longevity, and we're going to start with Michael Ringle,
who is chief operating officer at Life Biosciences, a biotech

(01:35:37):
company focused on partial epigenetic reprogramming to reverse age related diseases.
So please give it up for Michael Ringdle.

Speaker 26 (01:35:51):
I'll use the handhad perfect Awesome, Hi everyone, Yeah, So
Michael Ringle, chief operating officer at Life Bio. That's David
Sinclair's company out of Harvard. I'm a biologist by training.
I actually spent twenty five years at a company called
Boston Consulting Group, which is one of the large consulting companies.
And that's really my origin story because I did a

(01:36:13):
project for a client who was interested in this space,
and I did a scan of all the technologies out
there and it just became convinced that partial epigenic for programming,
which I'll tell you about, is the philosopher's stone. It
has tremendous potential to address age related disease. So I
bet with my career, quit my job, jump to the company,

(01:36:34):
and I'm going to talk to you about why you
should also bet, maybe not with your career, although maybe,
but certainly with your time, with your capital, with your
intellect capabilities, with your heart and maybe all of the above.
So I'm going to talk about this in two chapters.
If you could click forward, I'll just say click, so
click click, yeah, and one more click.

Speaker 10 (01:36:58):
So two chapters. I'll spend a bit of time on
we'll see yeah, perfect, it's working, I'll spend a bit
of time on.

Speaker 26 (01:37:10):
Why we need a breakthrough, and then I'll probably spend
most of the time on why I think we've found it.
So a great starting point for why we need a
breakthrough is this slide. This is a survival curve in humans.
It's also called a Kapla Meyer curve. You can see
it starts at one hundred percent, it goes down to zero,
and it's shown here for four different cohorts. And actually,

(01:37:32):
there's been tremendous improvement in the last one hundred and
fifty years, largely due to sanitation, vaccination, and reduced in mortality.

Speaker 10 (01:37:43):
But there are two big gains that are missing.

Speaker 26 (01:37:46):
One of which is health span, which is the quality
of those years we can expect to spend maybe a
decade in ill health, which you know, obviously we would
like to address. And the second is that despite the
improvements in average life span, we have not improved maximum lifespan.
That's true no matter how much you spend. So here's

(01:38:08):
a chart of health adjusted life expectancy against healthcare spending
per capita. Each dot is a country, and you can
see there's something like an assump tote here. And whenever
you see something that looks like an assump tote, you
should ask the question, are we actually running up against
a limit? And the answer is yes, that is the limit.
Jay Olshansky and colleagues did a great piece of work

(01:38:29):
published in Science in nineteen ninety showing that if we
wanted to get to average and this is the US data,
but average lifespan of eighty five ninety one hundred and five,
we would have to reduce mortality by fifty five up
to ninety percent.

Speaker 10 (01:38:44):
And that's in the.

Speaker 26 (01:38:45):
Context that if you cured all major jitter disease, you
would only reduce mortality by seventy five percent. So they
looked at that data and said, the chance of us,
you know, radically improving is limited this point. And so
they made the conclusion you see on the right hand,
which is the period of rapid increase in life expectancy
has come to an end. They took a ton of

(01:39:06):
criticism for this, but they've been absolutely proven. Right. It's
leveled off throughout the developed world, and in fact, in
some places it's regressed largely due to obesity. But this
is not their actual quote. What they actually said was unless,
they said, unless we can address aging at the molecular basis,

(01:39:27):
and they go on to say that they're actually very
optimistic about that. So why is that so important? So
it's important because of something called the gerroscience hypothesis. So
the number one risk factor for more than ninety percent
of what kills us in the developed.

Speaker 10 (01:39:41):
World is age. You can see here shown.

Speaker 26 (01:39:45):
Our plotted cardiovascar disease, dementia, cancer, diabetes, really the scourges
of humanity, they all go up with age, and they
go up exponentially with age. We haven't thought of your
age as an intervention point for these diseases because historically
we thought you live one year, you age one year.
But if in fact it becomes possible to separate biological

(01:40:08):
age from chronological age and actually move where you are
on this X axis, a single intervention can address all
major degener disease simultaneously, exactly j O'shansky's challenge to us
and thereby extend both lifespan and health span simultaneously, and
there's a lot of evidence this is possible. We see

(01:40:30):
it in genetic variants. This is an example from worms.
This is another survival curve or kapamyer curve. Worms with
a single mutation and a gene called DAFT two in
this case live twice as long, and they're also healthier
all along the way. They move better, their diseases of
generation are moved out. We see it in pharmacological interventions.

(01:40:52):
This is an example from mice of the efficacy of rapamycin.
This is done by the National Institute on Aging. They
have something called the Intervention's Testing Program ITP, which test
is various interventions and you can see here another Kapa
Myer curve. The mice live longer, and again they're healthier.
Along the way, things like cancer is delayed, they're more

(01:41:14):
vibrant as they're living. And then lastly we see it
in epidemiological data. This is from humans, maybe most relevant
to us obviously, and this is different populations of Japanese,
from summer wrestlers to mainland to Okinawan's who are probably
the most famous blue zone along a grading of cloric restriction,
which is the really best validated intervention. In other mammals,

(01:41:37):
you can see they live longer and indeed again are
healthier all along the way.

Speaker 10 (01:41:45):
Great news.

Speaker 26 (01:41:45):
The problem is we really haven't advanced on the state
of the art in a long time. So the interventions
that have the best effect, largest effects size on lifestyle
is cloric restriction. We've known about this to some degree
since antiquity and certainly scientifically studied in the teens, twenties
and thirties. The most effective therapeutic in mammals and in

(01:42:09):
mice remains wrapped mice, and it was the first one
discovered and it's still the gold standard. Another way to
see this is to just compare modern advice to advice
from literally four hundred years ago. So there's this great
study on the left done by Win and colleagues at
the Veterans Affairs in the US, and it's actually a
really good study, so I don't mean to pick on it.

(01:42:31):
They identify the eight habits that are associated with living
twenty four years longer on average.

Speaker 10 (01:42:38):
In probably want to know what the eight habits are.

Speaker 26 (01:42:40):
So there's the holy trinity of diet, exercise, and sleep,
there's the three thou shalt knots, don't smoke, don't drink,
don't do drugs, don't have any fun, right, and then
the two around mental health, managing your social relationships and

(01:43:00):
managing your stress. But you can go back to Sir
Francis Bacon as I did, and literally find every single
one of these in his writings, and including some things
that you you know, might think of as as you know,
somewhat modern, like opioids. You know, he says, no poppy
juice will make the spirit curdle, or smoking right to bathom,
don't like poppy buzzle in trouble. But they're literally all

(01:43:24):
in there, including some things that we talk about now
is very you know, ultra modern, like this idea of
parabiosis and blood transfusion. No, he had an opinion on,
you know, four hundred years ago, and I thought it
wasn't going to work. Actually so which Steve Horvast data
actually supports. So to understand why we've stagnated with these interventions,

(01:43:47):
you have to actually understand why they work. And there
are various schools of thought on this, but I'm going
to tell you the correct one. I don't have time
to explain why it's the correct one.

Speaker 9 (01:43:56):
But it is.

Speaker 26 (01:43:58):
And the logic is based on evolutionary biology and it
goes as following. So energy and resources are not infinite,
so organisms have choices in how they deploy that across
a lot of different things. But you can kind of
grossly simplify that to growth and reproduction versus maintenance repair.

(01:44:20):
And when you're in a bad condition like coloric restriction,
why would starving and organism actually make it live longer? Right,
it seems paradoxical, and it's not just starving like any
many other stresses Steve showed you cold stress, heat stress, hypoxia,
lots of stresses cause organisms paradoxical that live longer. Well,

(01:44:40):
when they're in a bad situation so bad that offspring
are going to be challenged to survive or thrive, you
shouldn't invest in growth and reproduction.

Speaker 10 (01:44:49):
So even though your total resources.

Speaker 26 (01:44:51):
Have gone down a little bit during this famine, you
over reduce the amount that you putting growth and reproduct,
which means you have a little bit left to shift
to maintenance repair, to weigh out the bad conditions and
wait for.

Speaker 10 (01:45:08):
Another breeding opportunity.

Speaker 26 (01:45:09):
And you know, if you're a worm waiting for a
rain basically, you know a few extra days actually matters
a lot, or a fruit fly waiting for a fruit
to fall. You know, extra month matters a lot, or
a mouse one extra breeding season matters a lot. And
there's a lot of evidence that this is actually what's
going on, including many of the key genes involved are
actually what are called diapause genes daft too, which I

(01:45:30):
showed you we're kind of kicked off the field as.

Speaker 10 (01:45:33):
A diapause gene.

Speaker 26 (01:45:33):
It's involved in creating this quiescent state where organisms try
to weigh out bad conditions. So you can plot all
these known interventions against a master switch that exists for
this plasticity to shift between these states. So a switch
should be able to sense whether the conditions for growth

(01:45:54):
are ripe or not. So are the building blocks present?
Do I have oxygen? Do I have a ten puts
suitable for growth? Crucially, do I have energy? The switch exists,
It's called m tour. It integrates all these signals and
that switch to then turn on or off growth and reproduction.
I lost my screen down here, but I'll look back

(01:46:15):
up there. Or the maintenance and repair which are shown
in red so you've got turning on protein lipid nucleotide synthesis,
turning on mitochondria which put energy in a usable state,
turning off these repair and recycling pathways. And again you
see exactly that. And we can plot the known interventions

(01:46:35):
on this. So remember wrap mycein the intervention that had
the largest effects size ever shown in mammals, Well, it
sits right there. The next two in the IP that
have the largest effects size on maximum lifespan sit right there.
Everything else that's ever passed the ITP sits here, including

(01:46:56):
new information from just a week ago. And you know
there's a few others that people talk out, and you know,
if I've missed out your favorite one, like, I'm sure
there's a spot for it on here somewhere.

Speaker 10 (01:47:05):
But when you go back, when you have this.

Speaker 26 (01:47:08):
Understanding of what's going on, you go back to this slide,
you understand that this mechanism matters a lot more in
a short lived organism than a long lived organism. So
that fruit fly waiting for the fruit to fall, you know,
a month matters, But if you're already living eighty years,
you're actually averaging out a lot of this environmental variability
and the prediction is that coreic restriction and these other

(01:47:31):
insults and these other mechanisms matter more in short lived organisms.
That's exactly what we see empirically. It's a little bit
of a fanciful chart here. I've put it together from
a bunch of different sources. They've been done in different
methods and so on. But you can see this inverse
log linear relationship between how long the organism lives naturally

(01:47:51):
and how much benefit it gets from coloric restriction. And
you get down to humans and you you know, suspect
that in terms of maximum life span effect probably only
talking about a couple of years from a lifetime of
cloric restriction. It's also, by the way, supported by the
epidemiological data. Okinawans are pretty close to the limit of
what you could minimally eat, and yet you know they're

(01:48:12):
not living to one hundred and fifty. The implication here
is that the best interventions that we have right now
they're worth doing. Don't misunderstand me. You should do every
one of those eight healthy habits. They will make you
healthier in the years that you have. They will cut
out twenty four years of early mortality on average. They're
really worth doing, but they're not going to make you
live past one hundred and twenty. But there is a

(01:48:34):
different kind of biology that has the potential to reset
that because it taps into a totally different mechanism from
what I just showed you. It's the biology that makes
babies young. So there's a picture of my wife when
she was thirty seven and my youngest son at the
age of thirty seven, her excels were pretty old, and
even at you know, at eight eighteen, Right, she's an adult,

(01:48:56):
not an infant. When an adult has a baby, that
baby just comes from their own cells. They're old cells.
So there has to be a mechanism in nature that
takes an old cell and makes it young again.

Speaker 10 (01:49:11):
Which is a profound point.

Speaker 26 (01:49:12):
Right, we all know that, you know, babies happen, but
this idea somehow it just comes from our old cell. Well,
there must be a mechanism built in that makes them
young again. We actually now know what it is. Between
day seven and nine of ambiogenesis. The epigenic marks that
Steve Wrbrath talked about, these methyl marks as settle marks
on the DNA. On the histones the DNA is wrapped

(01:49:34):
around are just wiped clean, and the cell from that
point forward is told it's young again and behaves like
it's young again. So if the parent had Alzheimer's disease
or the parents had cardiovasc or disease, the parent had diabetes, the.

Speaker 10 (01:49:46):
Baby does not. I might have some second life from that.

Speaker 26 (01:49:50):
If the parent had a genetic disorder, it could be
passed on, But in general, the epigenic disorder.

Speaker 10 (01:49:54):
Is not passed on.

Speaker 26 (01:49:55):
The age itself is not passed on. That's been tapped
into artificially. Should Yamanaka won the Nobel Prize in twenty
twelve by showing that you could treat cells artificially with
just four small proteins abbreviated oskm.

Speaker 10 (01:50:10):
Jel peedue may talk about it a little bit.

Speaker 26 (01:50:12):
Those four small proteins take an old cell. I could
take a old skin cell from one of you and
turn it into a pluripotent stem cell. And in this
discovery people focused on the fact that these cells were pluripotent,
they could become anything.

Speaker 10 (01:50:27):
They no longer had an identity, they were no longer
a nerve cell and muscle cell. They could become anything.

Speaker 26 (01:50:32):
But hidden in that discovery was the fact that the
cells were completely rejuvenated. So if you grow a clone
from a cell that's gone through this process, the clone
is not born as an eight year old individual. The
clone is born as a baby. Now it's not ethical
to do that in humans, but in mice, for example,
this work has been done. So the thing that people

(01:50:54):
find conceptually hard to believe that we can actually dage
a cell, we actually already do. It's known tech, it's
routinely done. It's in the context of this reprogramming. Now,
the problem is you don't want to do that in
your own body because you don't want to take your
cells all the way back to flory potency.

Speaker 10 (01:51:09):
You would cease to function.

Speaker 26 (01:51:10):
If you do that in a mouse, you'll kill it
in about three days, because you know, your nerve cells
have to say nerve cells. Your muscle cells have to
say muscle cells, otherwise you stop functioning.

Speaker 10 (01:51:19):
There's also a risk of cancer.

Speaker 26 (01:51:21):
But the biggest insight that came out of the Sinclair
lab that was on the cover of Nature in twenty
twenty is that if you treat with just three of
the four factors or be OSK like, it's so simple, right,
just drop one of them.

Speaker 10 (01:51:32):
See what happens.

Speaker 26 (01:51:33):
Right, you take cells part way back, they get younger functionally,
they get younger transcriptionally, they get younger epigenetically, but they
don't go all the way back to flory potency.

Speaker 10 (01:51:42):
So it's safe.

Speaker 26 (01:51:43):
And this is the study they did that was on
the cover of Nature, which was in eyes and mice.
It's actually a picture of an eye with like a
clock going in reverse where they restored vision to blind mice.
So that's the technology that we want to take forward.
You could use that in any eight related disease theoretically,
And here's a list of just examples from the literature

(01:52:03):
showing different diseases associated with epigenetic changes. It's literally every
organ system. But you have to start somewhere. And so
our company Life Bio is taking David Sinclair's insight and
starting with the eye. Two major forms of blindness glaucoma
and nion. So the number one cause of blindness in

(01:52:24):
people over the age of sixty is glaucoma. The number
one acute cause of blindness is nion. There's really tremendous
on need here. If you catch glaucoma early, it's actually
pretty well treated, but unfortunately many people catch it too late.
There's actually three million people already blind, so a huge
amount of need that cannot be treated, and nion actually
has no treatment. We're taking our first molecule forward. There's

(01:52:47):
a tremendous pre clinical data package now showing that this
works not only in mice, which was the original work
done in the Sinclair lab, but now we've repeated that
in non human primates monkeys, showing the full logic chain
of what you would want to see. Drug is getting
to the right cells. It is actually shifting their epigenetic
state right back to youthful. It restores visual function, so

(01:53:08):
the electrical impulse that comes out of the nerves in
the eye goes from when we blind the animals becomes
flatline after treatment can go all the way back to a.

Speaker 10 (01:53:18):
Complete youthful signal.

Speaker 26 (01:53:19):
The fourth panel, there is actually a section of the
optic nerve showing the axons literally regrowing back down the nerve.
First time nerve regeneration has been shown. We show visual
improvement in the mice who can actually test in the primates,
but everything else suggests that we would see that in
the primates, and importantly in the studies that have been
done seen to be safe and they saw no nanog

(01:53:40):
which is a marker of going back to the pluripotency
in the mice work. They saw no increase in tumors,
and I'm happy to report we've now finished our GLP talx,
which is the preclinical work required by the FAA, and
had no serious adverse events. So we're going into humans
very shortly Q one. We'll be testing in and actual patients,

(01:54:01):
so even though it's a phase one study design for safety,
we'll get some efficacy data ideally by the end of
the next year. So it's going to be a huge
year for life bio. Obviously, it was actually a huge
year for the whole field because it'll be the first
time ever a rejuvenation agent has gone through clinical trials

(01:54:21):
and hopefully shows efficacy, So you know, watch this space
by the end of next year. We wanted to demonstrate
that this is not just an eye effect, so we've
been working on other organs. We haven't disclosed all of that,
but we've disclosed one which is liver, which is about
as different from the eye as you can imagine. So
the eye is compartmentalized, they're neurons, they're not dividing the

(01:54:42):
liver has a ton of cross talk with other organs.
It's one of the most regenerative organs, and yet the
same drug, the same underlying mechanism of action, addresses fatty
liver disease in these mice models. So you might ask,
why would a glaucoma drug work on fatty liver disease? Right,
that would be a paradigm that would make no sense

(01:55:03):
to a physician coming at this from kind of a
historic way of thinking about medicine. But when you understand, well,
if I rejuvenate the cells, they actually can heal themselves,
it becomes a very powerful tool to address all age
related disease. And now we've demonstrated that it works across
organs and diseases in.

Speaker 9 (01:55:20):
Mice so far.

Speaker 26 (01:55:23):
So that's just a snapshot. In the company, it has
this technology that can rejuvenate cells. You could address any
aid related disease with that, potentially aging itself. Perhaps we're
about to enter clinical trials expected a Q one of
next year for these opting thropathies. Many other diseases will
go after and we actually are in our series definancing.

(01:55:44):
We're a bit over halfway done with that. Anyone who's
interested in more information around that or you know, just
life by more generally obviously, here's QR code where you
can link with me and very happy to take questions.
But I think we're going to do that at the
end of the last session right now, No, we'll do
at the end the end, all right.

Speaker 20 (01:56:01):
Thank you very much, Michael, thank you, thank you so much, Michael,

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