David Sinclair on AI Longevity, Reprogramming and Daily Protocols

Name: "We Grew Human Brains in a Lab, Gave Them Alzheimer's, & Reversed It" Dr. David Sinclair A.O., Ph.D.
Uploaded: 2026-04-16T13:01:39+00:00
Duration: 2 h 18 min 36 s
Channel: Tom Bilyeu
Description: Summary and key takeaways on David Sinclair on AI Longevity, Reprogramming and Daily Protocols, covering AI and the Future of Longevity Artificial intelligence
Tom Bilyeu
Apr 16, 2026
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138 min video
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2 min read
YouTube video ID: tMYoiHSYgWw
Source: YouTube video by Tom Bilyeu — Watch original video
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Artificial intelligence now screens roughly eight billion virtual chemicals, a task that would otherwise require about 160 years. By training models on cellular images, AI distinguishes “young” from “old” cells and proposes novel hypotheses for reversing age. This capability democratizes expensive gene‑based therapies, slashing both cost and development timelines for anti‑aging drugs.
The Information Theory of Aging

Aging is framed as an information‑integrity problem: cells lose the ability to read their original, youthful genetic instructions. Methyl groups misplaced on DNA act as “scratches” that corrupt the epigenetic backup copy, turning the biological clock into a malfunctioning read‑out. Sirtuin proteins, which normally regulate gene expression, become distracted by DNA‑repair duties, further accelerating the loss of epigenetic fidelity.
Cellular Reprogramming Breakthroughs

Introducing the three genes Oct4, Sox2 and Klf4—collectively called OSK—can reset cellular age without erasing cell identity. In mice and monkeys, toggling OSK drives aging forward or backward at will. Four weeks of OSK treatment restores strength, memory and balance in mice, while monkeys with optic‑nerve damage achieve a 100 % functional recovery after reprogramming.
Regenerative Applications

De‑aging protocols have regenerated optic nerves, restored vision, and produced mini‑brain organoids that model Alzheimer’s for drug testing. Glaucoma is reinterpreted as a nerve‑function disorder rather than merely a pressure issue, highlighting the broader potential to treat neurodegenerative diseases and infertility with rejuvenated cells.
Daily Longevity Protocols

A practical regimen centers on NMN (1 g daily) and Resveratrol (1 g daily, taken with fat for five‑fold better absorption). Berberine replaces Metformin for glucose control, while nattokinase supports cardiovascular health. Managing elevated LP(a) with statins, practicing box‑breathing, and ensuring deep sleep help clear beta‑amyloid. The diet is roughly 95 % plant‑based calories, with strict sugar avoidance.
Looking Ahead: Clinical Translation

NAD⁺ IV therapy shows early promise in improving egg quality, pointing toward fertility applications. The long‑term goal is to compress the three‑gene/three‑chemical cocktail into a single pill. Ongoing human trials will test safety and efficacy, and the next two decades may see organs of 86‑year‑olds functioning like those of middle‑aged adults.
Takeaways

AI can virtually screen eight billion molecules in a fraction of a century, dramatically accelerating anti‑aging drug discovery.
The information theory of aging describes epigenetic loss as a corrupted backup copy that sirtuins fail to maintain when occupied with DNA repair.
Introducing the OSK gene trio reprograms cells to a younger state without losing identity, reversing age in mice, monkeys and optic‑nerve injuries.
Daily protocols of NMN, fat‑soluble Resveratrol, berberine, nattokinase and a 95 % plant‑based diet aim to preserve epigenetic fidelity and cardiovascular health.
Human trials are moving toward single‑pill solutions, with the prospect of restoring organ function in the elderly within the next twenty years.
Frequently Asked Questions

How does AI accelerate drug discovery for aging?

AI evaluates billions of virtual chemicals in weeks instead of centuries, using trained image models to spot youthful cellular signatures. This rapid virtual screening narrows candidates to those most likely to reverse age‑related damage, cutting both cost and development time.
What is the information theory of aging?

The theory views aging as loss of epigenetic information: methylation errors scratch the cell’s backup copy of youthful instructions, preventing proper gene expression. Sirtuins become preoccupied with DNA repair, leaving the epigenetic clock unchecked and accelerating decline.
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Helpful resources related to this video

If you want to practice or explore the concepts discussed in the video, these commonly used tools may help.
Continuous Glucose Monitor For Health Tracking Recommended
Tracks blood glucose levels in real-time to help manage metabolic health and avoid glycation, which the guest identifies as a key driver of aging.
Amazon →
Digital Blood Pressure Monitor For Home
Allows for regular monitoring of cardiovascular health, which is essential for managing risks like LP(a) and arterial health mentioned in the protocol.
Amazon →
High Quality Organic Extra Virgin Olive Oil
The guest specifically recommends mixing fat-soluble supplements like Resveratrol with healthy fats like olive oil to increase absorption by five-fold.
Amazon →
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Full Transcript YouTube

You are at the intersection of my
absolute fascination with health, which
is where it's intersecting right now
with AI. I've heard you say that AI is
making things possible in human
longevity that previously weren't. So,
what specifically has AI put on the
table that wasn't possible before?
>> Well, so the the big thing is the speed
that we can do things. Um, we currently
have technology that can reverse aging
in animals, and we'll find out this year
if it works in people, but it's it's an
expensive technology. it uses genes and
we have to introduce genes into the body
or the eye in this case. Um that that's
potentially hundreds of thousands of
dollars to do that. So what we wanted to
do in my lab was democratize this
technology. So how do you do that? Well
AI is helping. We've now screened
probably about 8 billion virtual
chemicals for one that will reverse
aging so that instead of introducing
genes which is expensive, we could take
a pill or rub it on our hair or our
skin. And I asked one of the AI uh
sites, how long do you think this would
have taken uh in a normal world uh pre
AI and it estimated it would have uh
taken about 160 years for my team to
have finished that experiment and the
cost would have been in the many
billions of dollars.
>> Why is that? Is AI just is is it
crunching numbers, pattern recognition?
What is it that makes AI able to shorten
the timeline?
>> Yeah. Yeah. Well, a big one was we we
need to thank uh Demis Hassabus for his
uh and his team, of course, uh for
elucidating the structure of all of the
proteins in the body. We didn't have
that until uh what was about four or
five years ago.
>> And now that we have those structures of
those proteins, we can virtually dock
billions of molecules into each of one
of each of those proteins and find ones
that modulate those proteins either. Is
this based on shape or
>> mostly and charge?
>> So we know the behavior of atoms and
small molecules and now we know proteins
and proteins are vibrating. So it's a
little complicated.
>> And you say we know. So one of the
things I want to know about AI is AI
getting to the point where it
understands the fundamental rules that
govern biology or is it just learning
all of the patterns in the literature?
>> Oh, it's it's more than in the
literature. It's understanding the
patterns in biology and how to
extrapolate from atoms to molecules to
proteins. That's a big jump. We couldn't
do that uh more than 5 years ago. And
now AI is really using that. I mean it
it's partly AI, it's partly brute force,
you know, just uh mathematics. Uh but on
top of that you can add now intelligent
agents that can take the results from
those screens as we call them and we
typically get hundreds of thousands of
hits as they're called and
>> the hit is this shape matches this shape
>> and allows the chemical reaction to
transpire.
>> Exactly. And we in in this case what
we're doing is
>> is virtually impossible. Uh at least 5
years ago it was impossible. And that is
that we're trying to find one chemical
that does the work of three that we
currently have. So when we reverse aging
in a mouse, we give it a cocktail uh
down its throat of three chemicals. And
in drug development, finding one better
chemical can cost hundreds of millions
of dollars and years of work. And I'm
asking my team and and our
collaborators, find one molecule that
does what those three do and even
better. And then once you found those
hundreds of thousands, which ones are
most likely to work? Cuz in in the lab,
it's not that easy and it's very
expensive to order and synthesize
thousands and especially hundreds of
thousands of molecules.
>> Order meaning online. Like I need to get
some of these molecules in the lab so I
can get the mouse to eat it. Well, we
don't test it on a mouse initially. That
would be prohibitively expensive.
>> Uh cells, and that's also where AI comes
in. We've got an AI system we developed.
It's machine learning um with a layer of
AI that can look at cells from humans
that we grow in the lab and we paint
them. So, they've got colors and so we
can see different shapes and things that
are happening inside the cells live
>> or we kill them and stain them. And then
the visual, we use visualization to say
is that cell from a 92 year old going
back to look more like the 20-year-old
cells from a 20-year-old. And we've been
working for about three and a half, four
years on that.
>> Did you guys have to train your own
model or
>> We absolutely did. So we got the cells
from these people who were young and
old.
>> Yeah. And we trained the model and it
took a long time to get that right.
>> And it was just like this cell young,
this cell old, this cell young, this
cell old. And then it gets to the point
where it's like you don't have to tell
it anything. It just looks at it. It
knows the patterns and it says, "Ah,
that's an old cell, young cell,
whatever." Yeah.
Fascinating. Okay. How much So when
people talk about um large language
models, they're talking about billions
of parameters. How many cells did you
guys have to feed it in order to get it
to be able to discern a cell?
>> Uh we looked at millions. Um but these
days we can actually train very quickly
at the the models have gotten better at
at learning.
>> Who's doing the underlying models?
uh my lab at Harvard.
>> You guys are starting from scratch.
Yeah.
>> Damn.
>> That's why it took a few years, but
we're there. We're there now. So, my
team used to be just biologists who
wrangled a ye cell and now a mouse, but
um I've had to build up my team with uh
real bionformatics and AI expertise.
>> Okay, you just gave me the chills. Uh
so, here's the thing. I'm trying to get
people to understand that we're living
through the weirdest moment in human
history ever. and that when we think
about the direction of travel, and I'll
press you on timelines, but I know
they're going to be wrong. Don't worry
about that. I just want people to
understand that things are moving faster
than they realize. Um, I did not realize
that individual labs were able to train
this from the ground up, which uh is
utterly fascinating. But, okay, so I'm
going to lay out, so I've done a bunch
of research on you, obviously. Uh, I'm
going to lay out what I think are the
presuppositions that will make this
interview make sense to people. I want
them to understand the perceived
direction of travel as of today. Of
course, it's going to be wrong in the
fullness of time. I understand that. I'm
sure you understand that. But it gives
people a direction of travel. So, I'll
give you what I think you're saying. If
any of this is wrong, let's correct it
now so that as we go through the
interview, people can understand what
you're actually trying to achieve. Okay?
So, this is me trying to channel what I
think you're saying in a very simple
direct uh way. So biology abides by a
set of rules which means that AI is
going to be able to understand it. So
like the laws of physics we may not know
what they are but there are rules. Those
rules are ultimately going to be
knowable. So same thing with biology. Uh
AI is ridiculously good at identifying
the patterns inherent to these rules
giving AI predictive powers over
biology. So ah if you fold a protein
this way then it will do this. Okay. Uh,
next is aging is a disease caused by
information degradation over time, but
cells store the original healthy
information in a kind of backup. So far
so good. Yes. Uh, with a with a little
footnote which is that's the theory that
my lab works on
>> that we came up with. It's not
universally agreed upon that there that
there there is a backup copy, but it has
to be there because we use it every day
to achieve what we do in the lab.
>> Okay. Uh so that one may be a little bit
controversial, but this is the point of
science is we're going to find out.
Okay. Uh
so next any disease tied to a breakdown
in information integrity theoretically
can be effectively treated if you can
get the cell to start reading this
somewhat controversial healthy backup
data again.
>> That's correct.
>> Okay.
>> Therefore AI is going to dramatically
accelerate the effective treatment of
many if not all information related
diseases including aging.
Um, I would say that's as close to a
fact as we could get right now. Th
>> this is the the presuppositions that
you're operating on. So presumably in
time some of this will end up being
true, some of this will need to be
modified, whatever. But these are the
things that give you the courage and
momentum to go down this path.
>> Yes. And and it even if some of it isn't
100% true, we're still going to achieve
the goal because we can do it. We're
just trying to figure out how how the
heck it's working because we're getting
results that
>> are nearly unbelievable
>> and we have to figure out how is that
possible.
>> And so the nuances we'll argue probably
for the next 50 years, but doesn't
change the fact that we're doing it.
>> Yeah, that makes sense to me. I have a
>> I'm haunted by and I can't remember if
it was Max Planck who said it, but
whoever said the quote that science
advances not one insight at a time, but
one funeral at a time, that winds me up.
It drives me absolutely crazy that
people cannot go, "Well, there's
obviously something I don't understand.
I'll figure it out." This is the whole
point of the scientific method in
business. I literally teach this. I call
it the physics of progress. The physics
of progress is make your best guess.
You're going to be wrong to some degree.
Run the experiments, figure out in what
way you are wrong, adapt, get a little
bit better, and then you just run that
cycle over and over and over. So, I
presume that's what you're doing as you
march down this path.
>> Yes.
>> Yes. with the scientific method, which
is
>> fail, fail, fail, and then something
works.
>> Okay, so we know what we believe and
what we're pursuing. It's the things
that I just ran through. What would be
the falsification? How would we know if
we're like, oh, we just proved that this
doesn't work?
>> Well, we we've been doing those
experiments trying to disprove our
theory. That's what we do as scientists.
Very
>> What's the What would be the kill shot,
though?
>> There are two main tests. One is if we
degrade the information in the cell in
an animal for instance or take a mouse
and the mouse gets sick and dies but it
doesn't get old then that's not aging
that's just sick. But we did that
experiment and the mouse got old
>> and we published in 2023
that information loss is a cause of
aging in mammals in us.
>> Then the next test is can you reverse
that process? Can you bring back the
information like my hypothesis says we
should be able to do even if we don't
know where it's stored? Um, and in 2020
on the cover of Nature magazine, which
is as as good as you can get as a
scientist, we published that we could do
that. That we could get back that
information somehow using three genes
that embryos usually use to reset their
own age from their parents age. And so
those th if they had failed, if we
couldn't reset age, if we couldn't age a
mouse forwards, uh then okay, we'll move
on, we'll do something else. But the
fact is now, Tom, that in my lab, we can
drive aging in either direction at will
using the technologies that we've
developed and it's only going to get
better.
>> Okay. In mice,
>> in mice and we've done it in monkeys, um
we've cured as effectively or is that
more complicated?
Um, it's actually not that not more
complicated uh, in a monkey. If you want
to get into the details, it's there's a
there's a membrane in the monkey that
the mouse doesn't have that might have
inhibited the genes getting into the
back of the eye, the retina, but it
worked fine. And the monkeys they got
their electrical signals back in the
optic nerve. And we believe that that is
good enough signal to go into humans to
treat blindness, couple of diseases in
humans. And if all goes well, we'll get
ready to start the trial.
>> We'll get back to the show in a second.
But first, let me brag about someone on
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show. Okay. Uh so membrane was a concern
but just didn't end up in practice being
a problem,
>> right? Um, but the fact that it worked
in monkeys where a lot of things in mice
don't translate into primates was a big
deal. And so that raised my confidence
level from 50% to about 80 90%.
>> Okay. But the big question mark right
now is you're reaching into a black box
that we don't quite understand why it's
working because you're you know the
effect is that using those three
chemicals.
>> Genes. Well, we we've got three genes
and three chemicals.
>> Okay. Um, I don't know why it's three,
but that's just what turned out.
>> Sure.
>> The three genes have a name. Um, Oct 4,
socks 2, KO4, OSK we call them.
>> And they were, we can talk about how
they were found, but essentially those
three genes, then we mimic those with
three chemicals and hopefully, as we
discussed, get down to one pill that we
can take. Okay, we'll get to the pill in
a second, but uh so we administer the
genes and the chemicals, which we don't
have to get too specific. I think people
will uh not be able to track, but we've
got those things. We get them into the
system somehow some way, whether it's
injecting pill later, whatever,
whatever. But we get them into the
system where they need to be.
>> Y
>> but we don't know exactly
how we're then able to get the cell to
deage. I don't know if we're comfortable
with that word, but we know that it
happens. And so your best guess is that
there is somewhere in there the storage
of the youthful healthy cell like a
backup
>> and that is somehow getting the cell to
reread off of that versus the
>> I might be jumping ahead here, but the
methylated cell that's sort of gotten
the scratches on the CD of the DNA, if
you will, right,
>> over time, which is causing it to Again,
I worry about getting too far ahead, but
I'm going to say it anyway. The cells
begin to differentiate. So, an eye cell
stops being just an eye cell. Maybe it's
a little bit of a skin cell or a brain
cell or whatever. And so, it starts
getting confused.
>> Yeah.
>> Uh,
how'd we do so far?
>> Brilliantly. Uh, yeah. I couldn't have
said it better myself.
>> You can and have, but that's very
generous. Uh, okay. But we now at least
hopefully people following along at home
understand what we're trying to do when
we say that we want to take this we want
to take a view of aging that it is an
information integrity problem that there
is something akin to a backup copy of
what the cell should look like but aging
is basically oh we stop checking the
original work and we just start going
off of like the repaired house if you
will and it's like, well, the repair
starts to get weird unto itself, and so
now it's we're not replicating properly.
Okay, you guys have a mechanism to
somehow someway get it to build as if it
were a young cell again.
>> Well, build isn't the right word. It's
to read the right genes at the right
time.
>> Why do you say build isn't the right
word?
>> Well, when you reinstall software, I
guess you could call that a build, but I
don't mean it's not physically building.
>> The cell is being built, which is why I
think of it as building. Oh, well,
you're you're putting together two
theories. My theory is that the cell and
aging is information. And the old theory
is that the cells just break down, wear
out
>> and so you're thinking rebuilding that
repair, right? Restore.
>> Interesting. The way I'm thinking of it,
which is probably um messy because I've
not thought about it like you have, uh
goes something like this. I I'm not
playing a song. I'm building a house.
And so the cell is physical. So when the
DNA gets uh we're going to have to
explain methylation. Um do you want to
give people a quick primer on exactly
what is breaking down like what
methylation is the tight winding all
that?
>> Uh and then we can get back to why I say
building.
>> Sure. And I I think where you're going
is that when we restore the information,
the cell can now rebuild itself in a
youthful way. cell when it builds the
next one will build it better and it
will be a truly differentiated cellul
>> not just the next one itself we we
restore the health and the youth of
nerve cells in the eye and elsewhere
that don't divide the cell itself gets
healthy doesn't need to even grow it can
just reinstall the software then it
makes new proteins makes new lipids
makes new
>> uh I didn't come by there were cells
that didn't divide so There are cells
that don't divide. Full stop.
>> Oh, yeah. Your heart, your brain mostly.
That's the same cells you had when you
were a teenager.
>> That is wild. Okay. Didn't know that.
Thank you.
>> Yeah.
>> Okay. So, sorry. Uh, explain to people
the methylation just real fast.
>> Yep. All right. So, that we've got six
feet of DNA in our cells. Every cell
gets wrapped up. Um, and there are
20,000 genes, but not every gene gets
turned on in every cell. The cell
wouldn't function. So, we need a certain
set, let's say 10,000 nerves, nerve
genes, and then a different set for
skins, skin genes. So, it's like a
piano. You got lots of keys. Every piano
has the same set of keys, but how you
play them makes the difference to the
music.
>> The cell works the same way. Same genes
play them differently. You get different
cell types. You get a different
>> What is the play just to not be analogy?
Is it um the creation of proteins?
>> Mostly. Mostly, not all genes make
proteins. Some of them make other things
like RNA. Um, but yes, mostly it's we're
talking about those proteins that become
enzymes that do the work of living and
repairing.
>> Okay. So, we are even in a cell that
isn't dividing. So, I was wrong about
necessarily what is being built, but the
thing that we're fixing is the building
mechanism itself. So, we're building
enzymes, which by the I had to look all
this stuff up. Uh, enzymes like do a
thing. They like move around. They're
machines for sure. They're really super
interesting machines. They all there's
tens of thousands of different ones.
Yeah. And they do cool stuff.
>> That's so wild.
>> Including reading the genes themselves.
>> So the DNA is a is a string of
chemicals, right? And the cell has to
open up the DNA strand. It's double
stranded. It's a helix like a think of
it like a um a spiral staircase. It
looks like that. But to read it, you
have to open up the stairs. Each stair
splits in half and the cell can read
that half of the of the stair. And a
gene is about a thousand or more of
those steps. It'll read that and and the
a set of three of those steps determines
which amino acid goes next in the
protein. There's a what's called a start
set start codon and it always starts
with the amino uh methionine. So every
protein has a methionine. Almost every
protein has a methionine. But what comes
next is dependent on those three steps
in the rung of that staircase. Or in
this case, the letters on the DNA, A, T,
C, or G. Now, that's a gene, right? A
thousand of those steps in that
chemical. And there are 20,000 sets of
those that are all encoding proteins at
the amino acid level. That's your
blueprint. But the problem with aging is
the cell forgets which genes to read. it
actually turns off some genes and for
the most part turns on other genes. And
now instead of having skin genes turned
on, it's some skin genes and some nerve
cell genes and kidney genes start to
look more like liver genes that are
coming on. And that inability to read
the right music of the cell, I think, is
the major reason why we get sick and get
old. And that that's reversible. These
methals are little chemicals that get
attached to the rungs of the staircase,
the the steps. And if you have lots of
them on the steps, the cell doesn't read
the gene anymore. Shuts it down and you
don't make protein. So that's why a
nerve cell isn't turning on skin cells
genes because they've got a lot of these
methyl chemicals on the ladder uh on the
steps.
>> They basically say stop reading or only
read this.
>> Yeah. Don't read this one. Go and read
the one you need to go read. But those
methals, including more complicated
structures, larger structures, um, are
what determines when we're developing in
an embryo, go over here and make some
skin, but go over here in the skull and
make some more brain cells.
>> Okay. And the methylation has to be
redone every time a cell divides or
takes damage.
>> Yes. Um, every time a cell divides, you
should be getting an identical
methylation pattern between the daughter
and the parent cell.
>> Uh, and there are copying mechanisms. We
understand how that works. Um, it
changes during development, of course,
because we're starting from one cell
that has to become hundreds of different
types. The problem is as we get older
through things that we believe are uh
largely due to cell damage and stress in
the cell, those chemicals on the ladder,
on the stairs, they get misplaced. They
get taken off where they shouldn't be
and put on where they shouldn't be.
>> And now the cell doesn't know what to
do. It's reading the wrong music. And uh
it's a complete disaster. We get gray
hair, we get wrinkled skin, we get
disease, we die.
>> Do you have a hypothesis as to what is
making the methylation be imperfectly
um replicated?
>> We do. Um and the the history is not
well known. Um when I came to the United
States, you probably noticed I don't
have a strong American accent. Not yet.
Um, I went to MIT and the goal was to
figure out why the do yeast cells that
make things like beer, vegeomite, um,
which I really like. Tom, I'm going to
get you some. The ve the uh, the yeast
cells, they're microscopic, but they
have chromosomes just like we do. And so
I figured if we if we can't figure it
out for yeast cells, we'll never figure
it out for humans. So for four years, I
worked under the tutelage of a professor
who deserves a lot of credit, Lenny
Genti, and we worked together. he and I
and a team and we put out a paper he and
I just on on my first big paper in my
life um the cause of aging in yeast
cells and that was the blueprint excuse
the pun for the rest of my career
including the information theory of
aging which we're talking about now and
in that I said that what's largely
changing these patterns of gene
expression what we just called the
process of aging is that protein that
should be turning genes on and off. We
call them regulators, protein regulators
of genes. They get distracted by doing
other things. And there's one set of
enzymes and proteins that I've worked on
my whole career that came from these
studies called certuins
um based on the gene called siru in
yeast. Sertuins, they actually go to the
DNA and they tell the cell shut this
gene off. They they see the methals.
They see those chemicals and those
chemicals are really simple by the way.
They're just a hydro uh carbon with
three hydrogens. These methals are
recognized by the sertuins. They and
these proteins go in and help shut off
the gene and stop the cell from
accidentally reading it. They bundle it
up. They actually bundle up the DNA like
a little package
>> um versus a big loop of open DNA that
gets read. So it's a bundling sertuan.
And there were a few breakthroughs. One
was that uh the sertuins get distracted
and one of the major distractions that
they have is broken chromosomes. They
hate broken chromosomes. Yeast cells and
our cells they can die if they don't
repair a broken chromosome
>> or in our case you get you can get
cancer. So a cell panics when there's
even one break on a chromosome and it
often happens when cells are dividing
and they're trying to separate the
chromosomes. They get caught, tangled
up, break. Now you're screwed if you
don't fix it. So the sertuins have an
have two roles. One is to control these
methyl patterns and genes, but they also
go repair DNA
>> and they'll prioritize repairing the
DNA.
>> They do. Otherwise, there's no cell.
>> Okay? And so, if you're doing something
that breaks your DNA frequently, you're
going to age fast presumably because
it's going to be so distracted repairing
that that it's not doing its job with
the methylation.
>> Yes. And remember how I said there was a
test of the theory, which was if we
cause aging,
>> do we get an old mouse?
>> So, you just go [ __ ] up their DNA.
basically to cause the certuins to run
over to have to fix it.
>> Well, we didn't I wouldn't use the word
F
because we were very precise. We were
surgical about it. We we found an enzyme
that is in a slime mold found in the the
forests around here. And there turns out
there's there's an enzyme that cuts DNA
rarely in mouse and human cells.
>> Um
>> yeah,
>> a dozen or so sites, maybe a couple of
dozen, but not thousands. and because
you'd kill the mouse. So, we surgically
uh inserted that slime mold DNA into the
mouse itself at the stem cell stage and
then we turn that stem cell into a mouse
which is standard procedure for students
these days in my lab.
>> Damn.
>> And that mouse now we could turn on this
cutting enzyme from the slime mold and
surgically create a few of these broken
chromosomes.
uh not a lot, not enough to kill the
mouse, but just enough to distract the
sertuins from their normal job, make the
cells panic and see what would happen.
And we did that for three weeks in these
young mice and nothing happened. It's
like, oh goodness, the the experiment is
not going to work. Nothing happened. But
then I thought, you know, when you get
an X-ray, you get a lot of broken DNA,
but you don't feel it.
>> So, let's just wait to see what happens.
>> And I went to Australia, uh, and this
was the year 2012.
and I got a photo on my old iPhone and
it was a photo of a sick mouse and the
text was should we kill the mouse cuz
it's looking really sick and I said tell
me which is this mouse and they said oh
that's the one we treated with the slime
mold cutting enzyme
>> and I said that that's not a sick mouse
that's an old mouse right there so that
was the first evidence that by
distracting the sertuins to broken
chromosomes it leads to an acceleration
of aging and we published that it took
another decade to publish and this was
this uh big paper I mentioned was in the
um in the journal cell which again is
pretty hard to get into
>> and this was the one that said uh that
the change in information loss of
information was the cause of uh aging in
mammals.
>> What's the difference in phenotypical
expression between something that's
naturally old and something that ages
due to the breaking of the DNA?
>> Nothing.
>> Nothing. You wouldn't be able to tell.
>> Right. That was the cool part except
that they were 50% older and we can
measure
>> and we did we measured the methals
across the chromosomes
>> and we can use those changes as a clock
>> u and in fact you probably know you can
get a DNA methylation clock done
>> these days commercially.
>> So we did did it on the mice and the
mice were 50% older. Those methyl
changes
>> were the same as an old mouse just
happening 50% faster.
>> Yeah. Okay. Wild. So that sets us up
well for understanding the thing that
we're chasing.
Now
one thing I've heard you say about AI is
just the timeline speed up that we get
here. So what is the where are you
injecting AI into this process? Is it
simulating biology and simulating cells
and just like running thousands of
experiments in the amount of time that
we can normally run one or where's the
real advantage?
Uh it's
simulating experiments. So normally we
would in the case of finding chemicals
have to get make the chemicals which can
take weeks for each one. Imagine trying
to do seven billion or 8 billion.
>> U so we don't have to make them anymore.
We can actually we're now at the point
and this is this is new news I think
everyone would be interested in hearing.
We started doing 8 billion which we
thought 2 years ago mind-blowing 8
billion. Normally a pharmaceutical
company might screen a couple of million
right that's physically
we can now do an infinite number of
molecules. We believe that we're going
to cover all possible chemicals.
>> Wow.
>> Which is an orders of magnitude bigger
than what we've been doing. And that's
that's only happened in the last year
that we could do that. Um, but what's
what's speeding it up is the ability to
turn physical world into synthetic
virtual
>> and instead of it taking a year to
figure something out like it can be
milliseconds in some cases.
>> And what's the most complex thing we can
simulate? Is it the cell? Can we
simulate a liver? Like
>> no. Biology is so much more complicated
than most engineers understand.
um we're we still probably only know
about 3% of biology. So trying to trying
to model it is pretty hard. And then the
complexity I mentioned that it took all
of Deep Mind and uh and those guys until
recently to figure out how to just model
a protein of a thousand amino acids,
even 20 amino acids was a challenge.
Trying to model a cell is going to take
a lot more work.
>> It's not impossible because you will
make assumptions. But there's there's no
way in my lifetime that I I believe that
a cell can be modeled from the ground up
looking at every molecule
>> really in your lifetime.
>> Right. And I'm an optimistic guy.
>> I was going to say you don't plan to die
too early. That's wild. So you're saying
we're what more than 50 years away?
That's crazy
>> to model a cell with every molecule. No,
I mean you can make assumption. You can
say okay
>> generally these proteins are around in
this cell and these proteins around in
that cell. But to say
to if if you're right, well, if if they
can do that, what they should be able to
do one day is to take an egg
>> and the genome
>> and what we call the epigenome, those
methyl marks, and predict what the human
looks like.
>> Yes, we'll get back to the show in a
second, but first, let's talk about the
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And now, let's get back to the show. I
suppose this is where I confess my base
assumptions. My base assumption is that
our current um quest for intelligence
shows no signs of asmtoing. So, it's
going to keep getting better. And so as
we come up with more efficient
algorithms, as we're able to make bigger
and bigger data centers that AI will get
smarter and smarter, uh if you can
believe that in very narrow ways, we've
had AI achieve something like 147 IQ. Uh
and that's I mean what are we you know
50 years into like real AI development.
So it's like in the next 50 years given
where we're at, no way. like you will oh
this is going to be ignorant and wrong
but it will give people certainly how I
view this um 10 years I can't fathom a
universe in which 10 years we don't hit
artificial general intelligence Ray
Kerszswall who's been right with his
predictions I think 87% of the time uh
says 2030 that's four years for anybody
keeping score he says we'll hit AGI the
question becomes is artificial general
intelligence given that at that point it
will be able to improve itself health uh
is artificial super intelligence four
years and one day like or does it take
longer? But I don't I cannot fathom a
universe in which we don't hit
artificial super intelligence in 50
years.
>> I agree.
>> But you just said that we won't be able
to map a cell. And so what I'm saying is
you'll get into an upward spiral of
intelligence where we can't imagine
doing it now because being locked into
in my case very low IQ in your case
better. But like as you start pushing
this into the I mean what does uh the
smartest guy ever clocked I think is
like 225 IQ or something but I've seen
his tweets. I don't buy it. Uh so 250
300 400 5 a,000 IQ like what does that
start looking like? Well, it's not IQ
that's the problem.
>> The the problem is the compute. Now,
maybe with quantum computing, we're
going to get there, but using
traditional computers to model the
interactions in a cell, even for a
millisecond, would be more calculations
than have ever been performed in a
computer to this point?
>> Yes.
>> Um,
>> so you don't believe you think that um
advancements in computation are going to
stall out? Um, even if they don't,
it probably would take more molecules
than exists in the universe to without
quantum computing to calculate what
happens in a cell within 1 second.
>> It's that complex. It's it's
mindboggling how complex a cell is. Um
and so we can model one molecule hitting
another and we can even model uh I can
imagine modeling
uh a million molecules but molecu
modeling an entire cell with the quantum
effects that happen a lot of it's
unknowable without going in and
disturbing it as well. So that's another
issue.
>> But what what I'm not saying is that we
can't model a cell. I think that we will
be able to model a cell and I know very
smart people who are doing that or
trying to do that right now. It's just
that we don't know enough about biology
yet to make an absolute model from the
ground up. There's a lot of assumptions.
We know the fundamentals. We know that
there's DNA and these methals and we
know the proteins get folded.
>> Uh but I can tell you from work in my
lab, there's a whole area of biology
that we've been missing that uh will
hopefully allow us to figure out where
this backup copy is. And without knowing
that
>> is there describe the black box into
which you're appearing right now. What
do you mean? There's a whole area of
biology that we don't know.
>> Uh well, one of one of the problems with
science is we don't know what we don't
know usually.
>> And that's the tough part. But one of
the big questions in biology right now
is how does a cell deage? I I do like
that word. And we we know that it ages,
not just from work in my lab and others
like mine,
but we know that you can take a skin
cell. I could take your skin cell. I
could take the DNA out of your cell.
It's going to be old. Not too old.
>> How dare you?
>> It's going to be older than a baby. And
I could inject that into an into a a an
egg. Uh, and theoretically, um,
actually, it's not even theoretical. I
could turn that into a sperm and turn it
into an egg. Now, I could fertilize you
and make a clone out of you. This has
been done with with simpler organisms,
but we can do it with humans, uh,
eventually. I think that's how IVF one
day may be done. If people want to have
children, if they don't produce eggs, we
can.
>> Chinese doctor that went to jail. I
forget his name, but follow him on
Twitter. Shout out. Uh, he cloned
humans, right?
>> No, he genetically modified a baby,
>> right? Gotcha. Gotcha.
>> To be resistant to HIV. Um, but his goal
is to and and he's he's doing this
offshore from us, of course. But there
there is the technology to do that. But
let's just say,
>> but we haven't cloned humans. That's the
punch line.
>> No, no, but we've cloned monkeys. Okay.
So, let's just stick to monkeys. So,
it's not controversial.
>> Although, even that's controversial. Uh,
how about we talk about Barbara
Stryand's dogs. She's cloned those. Or
Tom Brady recently got Okay.
>> All right. So, we can do that. That was
done with old DNA. the DNA gets reset.
>> The information can be reset in that
cell. The other thing we know is that if
you have parents who are 30 years old
and they have a baby, for the first week
of life, that embryo is 30 years old.
>> What?
>> Yeah. We We're not always young when
we're alive. Babies would be born if
there wasn't a reset switch.
>> Uhhuh.
>> So
>> So wait, at what point are you saying
this is like we know this that embryos
are
>> people have measured it? Yeah. wild.
Okay.
>> It's a fairly new discovery, which is
why
>> it's shocking, but it will be known one
day. At some point post um conception,
>> day seven to day nine, we know that.
>> Whoa.
>> And the baby goes back to being age zero
again.
>> Whoa.
>> All of us. We were once the age of our
parents. So I was my parents were about
about 30. I was 30 years old twice in my
life. When I was conceived and when I
hit 30.
>> That is wild. Okay. Didn't know that new
info.
>> And then the same the same mechanisms we
believe the same mechanisms what are
what we're using to reset the age of
human tissue and monkeys and hopefully
>> Okay. So we got on to this because
there's certain things we don't know.
You're saying we don't know why those
reset.
>> We don't know how it resets. How does
the cell know what it was 30 years ago?
>> And does this feel like it falls into a
category of the unknowable or just we
don't know yet? Um, we have a pretty
good idea in my lab, but we haven't told
the world yet.
>> Okay.
>> Um, I I do text my student often and
walk into the lab and say, "Have you
figured it out? Have you proven it yet?"
Um, but we are doing
>> to hack your phone.
>> Uh, no, they shouldn't, but you probably
could with your team out there. Um, but
yeah, so so Chris Petty deserves great
credit. his PhD is on finding what we
call the observer, which is what Claude
Shannon in at MIT in the 1940s called
the backup copy.
>> Um, so what we imagine and are testing
is whether there are structures that get
laid down when we're very young during
our youth that can be accessed
later in time in a 60-year-old, 70-y old
to reset the age. Not we don't want to
go back to zero. That was the
breakthrough we had in 2020. You don't
want to go back to zero. I mean, first
of all, who wants to do high school
again? But you'd probably get cancer.
So, we don't do that. So, we figured out
a way using those three genes, OSK, to
go back 75, 80% and stop.
>> How does that happen? We think there are
little messages with new biology,
structures, chemicals that are new to
biology that AI may not have figured out
or will not figure out easily. Maybe
they would,
but that's where we're at now. If we
probably in the next few months, we'll
know if we're right. And uh I've been
saying that for about a year now, but
we're close. We one one way we do this
as scientists is we look for necessity
and sufficiency, right?
>> Necessity from an evolutionary
standpoint.
>> No, from a genetic standpoint. What we
do as scientists, geneticists, is if we
change something,
>> let's say if we knock out a gene,
>> is that gene necessary for the reversal
of aging? Mhm.
>> Is that process necessary?
>> And then if we force it
>> to turn on and now we we trigger that
event, is that
>> sufficient in itself to make the change?
>> And when you get necessary and
sufficiently satisfied, you're really on
to something. And it was similar with
that mouse, right? We knew that uh it
was necessary
uh
that uh these methylation changes could
rewind aging, but also we knew that was
sufficient to change those methyl
chemicals to cause aging. And that's why
I'm so certain that the information
theory of aging is correct.
>> Okay. Uh this brings me back to
something I asked you earlier, but I
want to push on it a little bit. So when
you interface with AI, I've always said
if AI can come to understand the
fundamental laws of physics, it will be
able to make novel breakthroughs and all
bets are off, technological singularity,
the world is unknowable to us. um as
you're approaching it, has AI made any
novel discoveries, novel insights that
aren't already in the literature, or is
it just doing a really good job of
recognizing patterns in like what we
already know about a cell? We in my lab
collaborated with another group uh out
of Stanford who developed an agentic
system with multiple agents about a
dozen agents that did different things
and we fed it our data. Interestingly,
it's the data that map those chemicals
on the DNA that change with time. And we
did mouse. We've looked at tissues from
mouse at very young age, middle age, uh
about our age, and then even older
equivalent. And uh the the what happened
was the the agents went to work and and
about a month later and there was some
iterations, right? It probably didn't
take a month, but we got the data back
from this group we're collaborating with
at Stanford out of Stanford. And what
was incredible was it didn't just come
up with validating what the field the
smartest people in my field had done
over the last 10 years which which by
the way would have been oh yes you can
make a clock out of DNA methylation
using these parameters and this you know
markoff modeling and and uh you all all
sorts of of what was already known in
the literature which is what I was
expecting. What happened was it came
back and said, "Hey, did you guys ever
think of this before?" And came up with
a completely new way of looking at the
data
>> and making a new model to predict
biological age out of the data we gave
it. Not only that, it it proofed the
data. It did the statistics. It wrote
the paper up for us and presented us
with the finished product, which sucked
because we want to be co-authors, too.
So, we changed a few words. But now I'm
a co-author with an AI system.
>> Damn. that we have. It's up online but
it's not published yet but you can you
can find it on bioarchchive if you know
if you do Sinclair Agentic uh biological
>> what was that like was it like holy [ __ ]
this has just had a novel insight and
how fast are we going to improve or
>> it it was a holy [ __ ] because I thought
that my job was not at stake
>> the arrogance was I've got all this
knowledge and experience and gut feeling
and I'm really creative
But here I'm seeing the beginnings of
creativity that can be super creativity
in the future. And I I think most people
who are not like us at the forefront of
technology
like discussions with my father who's
86, AI can never be creative. That's
just human arrogance. They definitely
are already creative and it'll only get
better.
Yeah, that's uh that's encouraging in
terms of its capabilities if it's
actually able to understand the
fundamental rule set and then say, "Hey,
what about this?" Okay, so we you guys
have created in your lab a um model that
is able to actually gain real creative
insights based on what it understands
about biology and all the cells that
it's seen and all of that. So, where is
this pointing? If you don't have
conviction that we'll be able to
simulate a cell in your lifetime,
is it that you don't think we require
the understanding or the sophistication
in order to profoundly deage the body?
Because the body is the very complex
system that you don't think that we can
fully understand. But yet you seem
optimistic that we'll be able to
influence these incredibly complicated
processes in a way that is both knowable
so we can do it repeatedly
um and advantageous
>> for age reversal.
>> Yes,
>> absolutely. We're doing it already.
There's no question about that.
>> Why?
>> We don't need to know every molecule.
>> Okay. So it's just as long as we
understand how to manipulate the output.
Nothing else matters. And knowing why it
works is the hard part. Manipulating it
to give us a predictable outcome is hard
for sure, but far easier.
>> Oh yeah.
>> Than the simulation.
>> Yeah. Yeah. My students, I mean, they're
in their 20s. They have regular tools.
They can do it.
>> You I could set you up with the lab. You
could do it. It's not that difficult now
that
>> we have this hypothesis that appears to
be true.
>> In the same way, I often refer to the
Wright brothers because this is this is
our right brothers moment for humanity
when it comes to aging. And there were
skeptics like in 1904 people were saying
in fact the New York Times published
that it would take a million years or
more to figure out how to fly. Uh and
then it was like three weeks later
Wright brothers
>> that's how I feel when you say that a
cell won't be replicated but you know
it's all right.
>> Yeah. Uh well the we don't need to know
and we still don't know how every
molecule in an airplane functions.
>> Yeah. Fair.
>> We don't need to model that. We we can
make assumptions. We can make
generalizations about wind flow and wing
structure and metals. Same with the
cell,
>> but you still need to know what's the
metal,
>> what's the wind, how how does air work?
And there's still a few missing pieces
when it comes to biology to be able to
simulate an entire cell. But when it
comes to aging, I think the big
breakthrough was understanding that
aging is information and that it can be
reset. So, how far are you going to be
able to push that though? So, I'll give
up. Doesn't matter. We're not going to
be able to simulate the cell. Doesn't
seem like it's relevant to be honest. So
now we've got uh we're showing great
signs that we can improve eyes.
Um I want to feel as good as I did when
I was 25. I want to look as good as I
did when I was 25. Like how realistic is
it that we can go in and influence
multiple systems in the body in
coordination with each other and not end
up with whatever catastrophe looks like.
So I imagine the catastrophic fail here
which you've already mentioned is
cancer. That would be one catastrophic
fail state where you go back too far
>> and it just all hell breaks loose or um
getting into some sort of decoherence
where it's like
>> uh we are telling the cell to move in a
direction and we can't stop it or
whatever and so it just basically
becomes a pur potent mess. Um so how far
can we take this?
>> Yeah. Well pur potent is a good word.
will just explain it that that's a cell
that can become any other cell type. So
age zero uh and that won the Nobel
Prize. Uh Shina Yamanaka deserved the
Nobel Prize for figuring out that using
his Yamanaka genes of which we use a
subset can take cells back to being pur
potent.
>> It's incredible.
>> And that's how you make a clone by the
way. But that doesn't work for for human
health because as you said if your cells
lose their identity and become age zero,
you're not going to live very long.
>> Um and even if you do it in a few cells,
you could get cancer. So that was the
tough part.
>> I love the way you always whisper
cancer.
>> Yes.
>> Well, I I will say uh cancer's been in
my family, so it's not
>> I just had skin cancer, so I feel
anyone's pain.
>> Yeah. Well, the the good news is we find
that when we reprogram cancer cells, the
majority of them slow down or die. So
deaging cancer doesn't make it worse. It
actually makes it die and shrink. So
that's good. I'm not so I'm not worried
actually about cancer anymore.
the the observer.
>> I need to follow up on that in a minute,
but keep going.
>> The the I'm going to call it the
observer, the backup copy, because
that's what we call it in the lab.
>> The observer has a way of stopping the
reversal at about 75%.
And it works in every tissue that we've
tested it in. We started with the eye
and human skin cells. Um, really not
because the eye is easy, it's because
it's really hard. But it's an enclosed
system and safer to deliver to humans
than giving it IV.
>> Interesting.
>> But it worked in the eye. And that was
>> because you can keep it uh localized.
>> Yes. Got it.
>> Exactly. Okay. So putting genes into the
human body
is is you know done but it's the FDA
here in the United States
>> is much more comfortable treating the
eye because it's it's done every week in
in patients.
>> So we started with the eye and it was a
hailmary experiment. My student one
chang who uh at one point was ready to
give up because it was so difficult and
so challenging and things weren't
working. Um but he went for the eye. He
chose the eye. I let him go for the eye
even though I thought it was crazy to
try curing blindness but he did it and
the results were clear that we could
reverse the age of the eye the back of
the eye in particular which is the
problem for old
>> mice and monkeys
>> mice then monkeys um and then we we've
moved on since then. So the the mice
were in we were doing that in 2018 right
it was even pre-COVID we had some of
these results so now we're you know how
many years 7 years or so later we've
done a lot we've done whole mouse brain
we can reverse the age of the brain and
the results are that old mice get their
ability to learn and they even get we
think get some of their memory back from
their childhood.
>> Okay. Uhhuh. Yeah.
>> Yeah. Yeah.
>> And that's in an Alzheimer's context and
an old just old age
>> mouse.
>> Okay. A lot of people just sat up.
>> Yeah.
>> Uh Okay. So, obviously we haven't done
human trials yet, but does this give you
a level of optimism that we'll be able
to um positively impact things like
Alzheimer's?
>> Yes. Now, Alzheimer's is is a big
disease.
>> Yeah.
>> And it it would be
>> a little bit outrageous for me to say
>> it's going to be easy to cure
Alzheimer's. That's crazy.
>> But do I see a path to doing that? And
why would I think that my approach is
more effective than
>> the tens of thousands of scientists that
have come before me who are probably
>> kind of pissed with me if I say this
kind of stuff.
>> The reason is that we haven't addressed
Alzheimer's from an aging point of view.
Most of Alzheimer's is aging. You don't
get Alzheimer's typically when you're 12
because your brain can fight the
disease. Even if you have the genes for
Alzheimer's, APOE4 AI ill, you don't get
it till you're 60, 70, 80.
>> Why? Because the brain has to get old
first. And what we've discovered is if
you deage the brain, the disease goes
away.
>> Yo,
>> and that we find true for every disease
we've tackled so far.
How many diseases have you tackled so
far?
>> Let's let me try to list them. Um, and
uh just just in my lab, I'm not not the
only one working on this.
Um we've done multiple scerosis. All
right. So MS we've we've published that
that that is ailarated by deaging the
nerves. Uh we've done kidney liver
disease. Um a big one is ALS motor
neuron disease. Nothing you can do for
those patients really. That looks like
it's working um in my lab. And uh skin
deaging. We're now working on hair and
hearing.
Damn, man. Uh, okay. So, all of that is
incredibly encouraging. Uh, you said
some positive words about your reduction
in fear around cancer, but you haven't
tackled cancer yet. Uh, the diseases
that you all just mentioned all in mice
or all in mice and monkeys.
In monkeys, we've only done the eye.
>> Okay.
>> Okay. So, in mostly it's growing human
tissue from scratch. Uh well, there are
two ways we do it. We either grow flat
cell layers of human skin. So, if I took
a biopsy uh back to my lab from your
skin, I could grow a flat layer.
>> Old skin. Back to that.
>> You're uh almost middle-aged skin.
>> I hope I'm only middle-aged.
>> Yeah, you're you're a fair bit younger
than me, I think.
>> I don't think so.
I'm 49.
>> Yeah, you're a fair bit younger.
>> Yeah, I'm 56.
>> That makes me want to punch you. I'm
inspired.
>> Blame my parents.
>> It is. Well, I want to blame your
protocols. I'm secretly hoping that this
is all uh something I can learn to do
myself.
>> It's kind of you, Tom.
>> So, a lot of the testing that we're
doing in labs is basically on just
cells, correct?
>> So, we build the cells up. So, it's so
we have in theory tested on human cells.
>> We just grew them ourselves.
>> Yes.
>> Okay.
>> That's our standard. And human cancers
we grow in the lab. Lung, colon cancer,
melanoma, we grow those. But we go one
step better somewhere
towards a monkey. Even better in some
cases, we could we do and we could take
your cells instead of making them flat,
we could rediffiate them into organs or
tissues.
>> And we do that in my lab. We grow
miniature brains.
>> Get the [ __ ] out of here. You have
miniature brain. Human brains.
>> Yeah. And then we give them Alzheimer's.
We make them old.
>> What? And then we deage those with our
chemicals in our genes.
>> Do they look like brains?
>> Yeah, of course. Yeah.
>> What?
>> They look like if you cut them through,
they've got all the structures in the
brain.
>> If I look at it, am I do I feel like I'm
looking at a G.I. Joe brain that
actually has like all the structure of a
human brain? There's no way. They're
like little blobs,
>> right?
>> They're blobs but with the same
structures.
>> Do they look brain like a brain?
>> They look like
>> I need to know if they look like a thing
that is on the Systeine Chapel. It's got
the shape and all that. Like, is that
what we're talking about?
>> The cyine chopper.
>> Yeah. You know that God is sitting
inside of a thing that's a brain that's
been vivisected.
>> Surely.
>> I don't know that.
>> What? Okay. Anyway, so the brain has a
super recognizable shape. You're saying
it's in that shape.
>> This is wild.
Come
>> later today. This is crazy.
>> We Well, let's have someone from my lab
take a photo, send it over. And
sometimes they grow little black dots,
which are eyes that grow, too. You get
two little dots.
>> This is incredible. And you can measure
the brain waves.
>> Can I ask what are the ethics on this?
>> It's Are they conscious?
>> I don't know. But they have brain waves.
>> We don't We don't know what they're
thinking.
>> This is insane. Okay, now I'm totally
fascinated. We have to like put a pin
because I need I have to ask. Okay, so
you guys are able to replicate micro
brains. How do you make them small?
>> Well, we grow them from single cells. We
we turn them into stem cells.
>> Would they just keep growing and growing
and growing and growing if you fed them?
>> They reach a certain size where they
don't keep growing because they don't
have blood vessels.
>> Do they have a pituitary gland?
>> They don't have blood.
>> I don't know if they stay alive.
>> We shake them in liquid and the oxygen
diffuses through. But if they get too
big that the core becomes hypoxic and
doesn't grow well. But what we need to
do is to mix them with blood vessel
cells which people are working on and
then we could grow them really big.
>> This is so interesting. Oh my god.
>> And then you it's ethical questions
about if you can grow a brain from
scratch, should you teach it something?
Should you give it something to think
about?
>> Yes.
>> Anyway, it's a good model for aging,
>> dude. So wait, there are, it's my
understanding, AI that right now can do
like these really rough like this person
is thinking about this and it like shows
you like a horse and you're like it's
kind of a horse. It's just like sort of
blobby shapes. We need to apply
immediately this AI to these brains. I
need to know if these things are like
screaming out, I'm bored, bro. Like come
on, give me something to do. This is
wild. Okay, love everything about this.
Here's the other thing is
>> we see them get old, they lose their
firing, and we can look at them in real
time. They're actually you see these
sparks. It's like looking at fireworks.
>> When they get older, there's fewer fewer
sparks.
>> How are you monitoring the brains?
>> Uh, well, you put them under the
microscope and we can see calcium
changes. When calcium gets
>> the fireworks,
>> the nerve cells when they get calcium
>> Uhhuh. They
>> under the micro though, are they now
dying at this point?
>> No, they're living. We should put put
them back.
>> Wow. Okay.
>> So, we see the calcium changes and
wherever calcium comes in, which is
what's happening in our brains right
now.
>> Yeah.
>> With the firing, it lights up with a
die, not naturally. We have to give them
a dye that lights up. But you can see
that. And so, you see with the old
brains that are a year old, that's old
for a for a brain organoid.
>> Uhhuh. If we give them our genes or our
chemical cocktail, our three chemical
cocktail, the firing comes on again.
>> And we did that to a mouse as I
mentioned. And the mouse brain work on
like the human brain now.
>> Well, we we hope
>> how close
>> we hope to be testing this in humans.
>> Uhhuh.
>> For the brain as well.
>> Adult humans, you're saying?
>> Adult humans. Yeah.
>> I don't know that I want to leave the
baby brains yet, but Okay. So, adult
humans, uh, what condition would they
have to have to subject themselves to
this? cuz this sounds experimental.
>> Uh, well, the three chemicals are we're
getting permission to give them to
people in a clinical trial to see what
happens.
>> But people just like, "Hey, I'm Bob. I'm
doing fine, but hit me with the three
chemicals. Let me see what happens."
>> Yeah.
>> Wow.
>> Yeah,
>> people do that
>> all the time.
>> This is amazing.
>> It's called a phase one clinical trial.
>> Wow. Yes. Okay. Hey, cool.
>> That's amazing. All right. So, people
are gonna volunteer to have these. Are
How are you getting the chemicals into
their brain?
>> Oh, you just swallow it.
>> You can take it in a pill.
>> That's the goal.
>> That's wild. How does this survive
metabolism?
>> Well, it at least two of these molecules
have been taken by humans already. So,
we know maybe all three actually by now.
>> Wow.
>> We know that they're metabolized.
>> But we we need AI to make improve that
three chemical cocktail,
>> right?
>> So, that I don't think that's the
ultimate drug that I'm going to put on
the market. Uhhuh.
>> I think though if I mentioned those
three molecules, you could bet that
people will be out buying this stuff
already.
>> Yeah. Didn't you say them at the top?
>> No, I said the genes or something.
>> Those are OSK. Be
>> very careful. Smart.
>> I have to be. I mean, hopefully people
won't go and inject them with some sul.
>> Oh, it will. Apparently, they'll even
just sign up for a clinical trial cuz
why not?
>> I do know some people have injected
themselves with OSK already, which is
>> uh Okay, so people are injecting
themselves with this stuff. Fascinating.
because because they think this deaging
thing will work.
>> Yes.
>> Okay. Even though you're saying it's
there's more to it than just that.
>> Well, just to be clear, these are these
are not FDA sanctioned clinical trials.
The there is there's a fringe.
>> I think people should be able to do
their own body what they want. Do you
think
>> so? Then it's a few people in the world
that are willing to try anything not to
age. Um
>> but getting back to really mainstream
science and drug development. But I was
having so much fun with the baby brains.
And
>> we can go anywhere you want, Tom. It's
your show.
>> Yes.
>> The uh I do want to say though that we
we I'll just tick off um
>> the diseases that have worked well.
>> Yes, please.
>> No, I already did that.
>> You're talking about in the baby brain
though or I thought those were like thin
sheets.
>> Yeah, I know what I wanted to tell you.
That we don't just grow brains.
>> Oh, we grow other things
>> such as
>> Well, we're growing a uterus.
>> Why not? Are we impregnating said
uterus?
>> No.
>> Why a uterus? Why are we building a
uterus? Because
>> Oh, to see if you can reverse fertility
problems.
>> Yes.
>> Let's go.
>> Well, we just in in all public
disclosure, I have one X chromosome and
one Y chromosome. So, I'm a male.
>> Yes.
>> So, we males are fairly dominant when it
comes to female health.
>> Yes.
>> And my partner Serena is much more
expert in female fertility.
That said, I'm a scientist and so I want
to be able to help women have children
for longer and even have children after
they've gone through menopause.
>> Let's go.
>> And uh so we've we've already shown a
number of years back that using a
certuin, remember the sertuins?
>> I do.
>> Sertuin activating molecule that we
could reverse infertility in old very
old mice, female mice, and they could
produce fresh eggs and have children.
>> That we published. That's real.
But uh we I want something more potent
than that um that will truly reverse the
age of all parts of the female
reproductive system
>> uh including the uterus. And I have a
student uh Maria
>> is working on that. That's her project.
>> Damn.
>> So
>> this is wild. Okay. So we grow.
>> So give me give me just a quick timeline
for this stuff has to work its way
through the FDA. Like when are we
talking about a 65year-old woman deaging
her uterus
>> and having babies?
>> Well, you you don't actually fully have
to deage a uterus. Uh you can have a
surrogate. So I I I could hear people
screaming at us that we don't need to
fix the uterus. What we need is healthy
eggs and a healthy sperm.
>> That's
>> Wait, I'm not I'm not tracking the
caveat. So you just said you want to
help deage the uterus. Well, I do
because that's
>> now we're trying to soften it for the
screaming people, the chattering masses
in the comment section. Uh, but talk to
me about when So, got it. There are
other things that people can do right
now today. Yay. But I'm saying when are
we going to deage a woman who's 65,
she's been through menopause for a
decade. When are we going to get her
producing eggs again and a womb that can
like house a healthy baby to term?
>> Ballpark me.
>> The uterus is early stages. We're still
growing those in the lab and looking at
menstrual fluid and that kind of stuff.
>> Wild. Is this a full collect fluid?
>> This isn't This isn't flat cells. This
is like I would actually recognize the
uterus.
>> Yeah. We grow it from scratch and it's
threedimensional and it's in the dish.
Yes. Uh-huh.
>> And then we're going to age them and
hopefully deage them, obviously.
>> So, but what I I can predict with more
certainty because I can see where we're
going with more clarity that
>> this discovery that we made in the mice
is now being tested by others in humans
already.
>> So,
we have the certuin activator.
>> Okay. Um it was I think about eight
years ago we published that raising the
levels of a certain activator called NAD
>> that chemical which we make less of as
we get older by raising that the eggs
became produced and fresh again
>> just from NAD
>> in a month from raising NAD.
And just last week I saw a study testing
women who were
not very fertile
uh receiving for 10 weeks an IV each
week of NAD and if there's no placebo
>> egg count
>> of egg count egg quality embryo quality
>> very rigorous actually and although it's
the first of hopefully many studies it
was extremely promising there was a a
dramatic difference two three-fold
difference between those that got the
NADIV and those that didn't.
>> I have a feeling you want me to let go
on the timeline, but I'm not going to.
So, ballpark me knowing certainly I know
that whatever you say isn't going to be
accurate. It'll just be directional. But
if you had to swag me, if that was if
that study is true,
>> again, be cautious. It's one study.
>> Yeah.
>> But let's say it's true,
>> then I think it's likely that NA NADIVs
are going to help women who want to get
pregnant.
>> Yeah. Yeah. timeline. We're rejuvenating
utery here.
>> Well, the uterus is different. Uterus is
more challenging, but the egg story
>> 10 years, 20 years, 30 years already.
>> Okay. So, NAD for somebody that's sort
of on the cusp,
>> but I want to know when we're
>> when's a uterus.
>> Yeah, I'm talking I'm giving you the
very specific set of sounds like you
really need a fresh uterus.
>> No, but this is so interesting. Yeah.
that the so never did I think that
already on the sort of pipeline of
things to be tried would we be growing
brains actual mini brains in a lab
actual uterus in a lab like this is
thrilling exciting shocking but I just
this was not on my bingo card so uh now
I want to know because it's clearly
closer than I thought
>> um given that we have to get through all
the FDA and all that like are we talking
30 years are we talking 15 years. Like
what are we talking about?
>> All right. Well, there's there's
actually there's two options. One is the
FDA route, which is novel molecule. AI
gives it to us. We take that. I've got a
company, Life Biosciences, that's ready
to go. Um, and they're all set to go.
So, that usually takes 5 years to get
through the FDA with a small molecule
that's been showed to work in animals.
>> But, do we have 20 years of discovery
still on the deaging of the uterus, or
are we already pretty deep in that
process? Well, we're going parallel.
We're going AI to find the molecule. And
I said we've already done a lot of that.
And then we we're building the uter in
the dish right now. And we'll just put
those two together when they're ready.
>> This is so wild.
>> And then if that works and the mice
work, then we can apply to test this in
humans uh with, you know, adequate
safety studies.
>> Wow.
>> In animals. The safety studies take a
couple of years.
>> That's wild. All right. I want to go
back to the brain. The brain is my
thing. If ever there was something I
wanted a a fresh new one, it would be to
keep my brain healthy forever. So, there
are things that people do now. So,
you've got stuff like ketones.
I will take ketone supplements. I will
take uh caffeine, obviously, nicotine.
So, I do things to sharpen my brain.
Now, how does that stuff compare to what
you're talking about? Well, right now I
think stuff like ketones are are
excellent for the brain. Um, yeah, I
>> similar mechanism or totally unrelated.
>> We don't know. It's possible that
they're related because um beta
hydroxybutyrate can actually not just
affect energy in the brain and that's
why I drink uh actually there's a group
that I'm collaborating with
scientifically as well that are doing
good studies at ketone IQ. The science
looks really good. The brain is what I
use it for. I I chug it before I do
recording of the podcast that uh I'm
relaunching season two coming up.
>> But yeah, I I find that when I'm I'm
stressed and I'm having to basically
take 15 pages and and remember it in a
few minutes, then I need that extra
fuel. And we know that ketones are very
good for the brain. But you're asking me
is it related to my work? What's
interesting is that these ketones um and
one is is one that's related to related
molecules. Um they're kind of related to
vinegar. These molecules actually go in
and they change the structure of how the
DNA is packaged to help with the
methals. It's so acute though. It's not
like I can take one shot of ketones and
my brain is better for a month. It's
very, at least for me, very short
acting. Yeah. So that's that's yeah
there so that's probably two things
happening. The first is the ketones are
good fuel for your brain. So what we
know is when we fasted for let's say
about over 15 hours ketone levels will
go up because we run out of glycogen
from the liver.
>> Uh and then the clarity mental clarity.
You might be a little angry because
you're hungry but the clarity is there.
We all we we've probably all done this.
If if we
>> if we study and we're not eating a lot
we can focus. Yeah, I know. I need that.
I get distracted by every little bug
around me.
>> But the the so the focus is there and
the ketones really help with the focus
and I can mimic fasting and I can even
enhance my fasting. I try to do
intermittent fasting um as best I can
and some of these ketones if you take it
with fasting can actually improve your
ketosis.
>> Those sound like separate mechanisms to
me. one feels very acute and is a hey
there's this molecule that you put into
your brain I'm fumbling for the
mechanism here and it's essentially like
giving it food to run its processes
faster. The other is reaching into this
black box and finding these magical
um the observer
and getting that to work its magic.
>> Yeah.
Let's let's just take a take a pause on
you are what you eat and it's not just
energy. It actually does modify the DNA
and the structures that package the DNA.
So let's just get back
>> the ketone or
>> well the ketones like beta
hydroxybutyrate these molecules actually
get attached. So let me briefly explain
to you how is DNA packaged in the cell
because that determines whether a gene
is on or off. We talked about these
methals. When it's methyl, it's blocked.
But it's not just a string with
chemicals on it. It's actually wrapped
up tightly in proteins that are like
balls, tennis balls. And the tennis
balls come together. So now you got this
big structure. If you look at them, it's
called a chromosome. So these balls,
they aren't just tennis balls. They
actually have flags on them. Imagine a
tennis ball with little flags that say,
"Read me or ignore me."
Some of these flags are methyl as well.
on the DNA and on the bowls, the protein
bowls called histones. But there are
other things, there's a whole semaphore
of flags that tells the cell what to do
at that point in the genome. And two of
those chemicals, one is butyrate that
gets attached to the ball. The other is
acetate attached to the ball on amino
acids, lysines usually. And these
histones have tails. So it's a tennis
ball with a a tail, protein amino acid
tail. And it's that tail that accepts
these little flags. So when we know this
for a fact that if you drink acetate or
butyrate or molecules like we're talking
about these ketones, you can change the
pattern on these little flags in ways
that are healthy. So that's another
reason why fasting may give you a buzz
or focus for a while, but long term, if
you do it for months, you will actually
change your gene expression and slow
down I I believe slow down the rate of
aging as well.
>> Okay. Preserve the
>> So we have reason to believe that's true
through fasting. Can you supplement your
way there? We don't know. But there's no
reason to believe that that wouldn't
work because what we're drinking in
these bottles um like the 13 butin dial
is that is naturally there in our body
anyway. We're just giving it the body
more of it. These are breakdown products
of fat, right? So after 15 hours of
fasting, we get these fatty acids out of
our fat. That's how the body uses fat.
Turns them into these ketones that give
fuel but also change the regulation of
genes. some temporarily, some long term.
>> Okay. Uh so that's the exogenous stuff
that may or may not have long-term sort
of stacking effects, but what you guys
are doing now on the brain, the brain is
insanely complicated. I've always
assumed that part of the problem with
Alzheimer's, not that the amaloid plaque
is the cause, but that you would have
built up so much plaque. I don't see how
you start unwinding that if you're not
clearing the plaque out. Do you think
the plaque is um the brain knows how to
get around it or uh does it get cleared
in some way? Like how how would this
look?
>> That's a a really great question and one
that we are addressing. The reason I
don't know the answer yet and I can tell
you what I think is going on based on
other experiments in different tissues
which do clear out proteins like beta
amaloid but we don't know in the eye
sorry in the brain for sure and the
reason we don't know is
we don't get a lot of plaque in the
mouse model
>> we get all these other problems there's
a protein called tow phosphottow we do
see that and we turn that on in the
brain but we don't know for sure yet if
the plaque goes away or if the brain
just can handle it better.
>> What about all of our little mini
brains? We haven't run the same.
>> No, the mini brains are not getting
plaque. They just get dysfunctional with
the APOE4
>> because you're um like racing forward.
They're aging so much.
>> Well, it's partly that, but also the
ApoE4 is producing this APOE protein,
which can cause problems inside the
cell. You don't need to have these
collections, these crystal crystals
outside the cell to be defective.
>> But doesn't that tell you that there's
something different going on? So, if
Alzheimer's were just pure aging and
part of the the phenotypical expression,
which fancy word for what does it look
and act like? Um if the expression of
aging is the some damage occurs that
causes the buildup of amaloid plaque if
you art artificially I'll put that in
air quotes but if you artificially age
it and it does not build up amaloid
plaques and we know there's some
different mechanism happening
>> for sure not everybody gets Alzheimer's
but we all get old.
>> Yes. So the Alzheimer's is accelerating
the aging of the cell
>> um and causing it to be dysfunctional.
>> But what we know is that we don't need
to be clearing any plaque for the
animals to get better memory and it may
not be necessary in humans as well.
>> But just to really beat this to death
and maybe this is what you were just
about to say, but um h how do you
interpret the I get two different
results? When I age up my mini brain, it
does not build up plaque.
>> Right. human life seems to build up
plaque.
>> You might be right that the mini brains
don't age 80 years, which is what humans
do. Maybe we're only aging them to 40.
>> You know, we don't get there. It's not a
perfect mim direction to travel. But
>> yeah, I mean, every model in the lab has
its caveats. You got to take what you
can get. And right now, the state of the
art is mini brains getting old but not
getting plaque. But we do put those
genes in there and they do get
dysfunctional quicker.
Um I I think it's it's an interesting to
point out that the the age reversal may
clear out the plaque and the reason that
I I'm optimistic that it would in humans
is because we've done this in other
tissues. The eye for instance builds up
proteins lipoposcin uh causes macular
degeneration. And to my surprise, when
we reversed the age of the retina in a
mouse that had those protein inclusions,
they went away and the retina regrrew
and became flat and nice and functional
again. So there what we're finding is
it's not just reversing aging, it's
actually rebuilding the body to be young
again.
>> And the the best test of that was
>> we actually pinched optic nerves and
destroyed them. That's one way to test
this. And what we found was the optic
nerve regrow back to the brain. So even
something as bad as crushing nerves
causes them to regrow like they were
embryos again.
>> Whoa. Hold on. For uh my whole life, I
believed that nerves don't regrow.
They don't. So this really is like if
this ends up being predictably um
repeatable, this would be huge.
>> Well, that's why in part it got the
cover of nature, which was oh my god,
we're able to regrow nerves again. And
it's huge not just for the eye, of
course, anyone who's broken or or could
>> What about like spinal injuries? Yeah.
Yeah,
>> that's right. That's that's low hanging
fruit as well.
>> Huh. Are there people right now because
let me tell you, if I was a
quadripollegic, I'd be like, "Yes, I'm
first in your trial. Inject the life out
of me. Give me whatever you need to give
me." Um, do we have people lining up for
that one? And is there a reason that
we're not already doing that?
>> It's regulation that's stopping us from
doing it because we need to make sure
it's safe. Are you by any chance
connected? You must be. You know so many
of the same people. Are you connected to
Elon Musk?
>> No.
>> I'll be I I don't know him at all, but
uh I know Peter D. Mandis knows him
well. I know you know Peter well just
because obviously what they're doing
with trying to sort of bypass all that
stuff and maybe they wouldn't care.
Maybe it's even contrary to their
business model. But
>> um
being able to fix somebody who broke
their back would be obviously massive.
>> Yeah. I mean, it's not technology that's
holding us. It's safety and rigor and
regulations. I think we're we're there.
It probably would work because the eye
is no different than
>> How profoundly is the nerve regrowing?
>> Well, you're right. Looms don't regrow.
And there have been some small advances
over the years.
>> Other labs have regrown nerves maybe
5%.
We got 100%.
>> What the [ __ ] man? This is one of those
uh
there's there's always such a big gap
between what works in the lab and what
works in real life. So, I'm aware of
that. But this is this is very
interesting. If you're able to So, my
wife's grandmother um I think she
actually died from cancer, but she had
Alzheimer's for the last god knows how
many years of her life. Absolutely
tragic. My great fear is losing my
brain. Um the thought of being paralyzed
has always been so hopeless my entire
life. The thought that you can regrow
nerves is absolutely wild.
>> Yeah.
>> And for a disease like ALS where the
nerves that are holding on to your
muscle are retreating, degrading,
regressing, we're finding that we can
regrow those. One of the reasons people
have falls and can't control themselves
physically when they're older and
maintain balance is that problem. The
nerve muscle junction
>> get retraction. These nerves go away.
>> We've got images in my lab when we treat
with our chemical cocktail. Those nerves
then regrow for the first time ever in
biology to go back to where they came
from.
>> What's going to stop this from being
real?
>> Like this. When something seems to be
too good to be true, it is too good. So
what's the what's the catch in all this?
There there are making a drug period
whether it reverses aging or not is is
hugely challenging from bench to bedside
as they say. There are
uh biological issues. So you might be
wrong about the theory. Don't think
that's the case. It may not be relevant
to humans. It could just be in rodents
or mice. Don't think that's true because
it's working in monkeys already.
>> Um there could be safety issues, right?
But we've ticked all those off so far.
So what's left? Well, uh there's
funding. You need hundreds of millions
of dollars. So I spend fair amount of my
time traveling with Serena around the
world to raise money to do these trials.
And thank you to all the investors that
have come in to help us with that. And
uh that's the company's called Life
Biosciences, which I'm chairman of the
board of. That company um has a great
team. You got to have a great team
because you can mess up a clinical trial
and not get great results.
you got to do it the right way with the
right controls. Um, and then I don't
know, I think that's that's pretty much
it. And and then it does it works or it
doesn't. And if you're wondering what's
the chance now, I've I've pegged it at
at least 80% given that it's worked well
in the monkeys multiple times
>> in that you're clamping down on the
nerve effectively killing it and then
regrowing it. What nerve are you
clamping down on?
>> Uh, the entire optic nerve.
>> Okay. So, you make them blind and then
unblind them. Yeah. Then they can see
again.
>> That is wild.
Uh, okay. So,
>> by the way, that that's that's required
by law. It's not something I want to do.
>> What do you mean?
>> Well, the the the government makes us
drug developers do these safety studies
in animals before we can touch a human.
>> Meaning they force you to blind and
unblind the monkey.
>> Yeah.
>> I wouldn't want to do that, but that's
what we've done. And fortunately, it
worked. It cured them. They're all good.
And uh That's wild.
>> Yeah.
>> Okay. And so, uh, are you just clamping
the nerve and the pressure is what makes
them blind and just unclamping it by any
chance?
>> No, it was done differently than a clamp
because it's harder to do with a clamp.
>> Uh, it was done with a bright light.
>> So, you burn the nerve essentially.
>> I don't know if you word choices.
>> It's not really burning, but it is
bright enough.
>> Permanently damaged. They're not going
to see again unless we treat them.
>> Okay. Are you doing it just by shining a
light into their eye?
>> It's a laser.
>> Interesting. Okay. Uh Okay. So, we are
overloading frying whatever word feels
accurate. Uh the optic nerve and then
you're able to regrow it. That is crazy.
Okay. So,
oh, let me say in humans we're not
treating
laser induced blindness. We're treating
glaucoma which is the leading cause of
blindness in the world of
>> nerve related.
>> Oh yeah.
>> Interesting.
>> People think it's the pressure but it's
it's actually the pressure that's just
disrupting the function of the nerves at
the back of the eye
>> which we can
>> don't you have to alleviate the pressure
first or do you just have to keep doing
this? like the pressure takes time to
crush the nerve again and
>> well the pressure may come back but
there are good drugs already to lower
pressure but even if you lower the
pressure the nerves are still not going
to work
>> wild
do you have a guess as to why nerves
don't regrow understood that like so
many other things in the body do but
it's like oh you broke your back sorry
done
>> yeah well that's unfortunately the
cruelty of evolution if it's not 100% ne
necess necessary for a person to
>> survive
And it's rare enough,
>> pretty necessary.
>> If if all of us in in on the savas of
Africa were getting back damage, we
would have figured out how to regrow.
But it was so rare.
>> By the time you broke your back, you
were getting eaten. So
>> that one of us is expendable.
>> But you got to keep the children coming.
Um and uh it was mostly men who were
getting broken backs anyway, probably
>> from war and whatever.
>> We're expandable.
>> So wild.
>> Yeah. But there are some species that do
regrow their nerves and grow regrow arms
even uh salamanders.
>> Yeah. Yeah. I thought you were saying
for humans for a second. I was like,
"Wait,
>> I wish."
>> Not yet. But we know that it's possible
in biology. And we actually have
evidence that what we're tapping into to
regrow the optic nerve and fix the liver
and skin is the same process as
>> lizards and salamanders use to regrow
limbs.
>> Interesting. Okay. So, what's the
approach with skin? How do we Same idea.
It doesn't matter the cell type. we're
going to get these three. So, wait, can
you then if it's not an injection and we
do turn this into a pill, is it just
everything that can't be positively
impacted by this will be? How will that
work in terms of um flash me forward?
It's 10 or 15 years from now. We've
identified the single molecule or the
best combination of these.
>> And are we do you see this as a targeted
thing where we go in and say, "Okay,
this is the optic nerve treatment. This
is the broken back treatment. This is
the liver treatment. Or is it just like
take this thing and it goes and deages
all your cells?
Yes. Is the answer. What I mean by that
is um I talked about two paths. The
first path is FDA which takes a decade
or more.
>> Uh fortunately, you know, we're in the
clinic this this next quarter. So, we've
come a long way.
That's on its way. But there's another
path to getting this technology to
everybody and democratizing it and
making it cheaper and available. And
that's the non-FDA path, which is going
down the consumer product route
>> and just making it what? Like a
supplement.
>> It could be a supplement, could be a
cream, could be a spray, it could be
even an IV. Um I guess that's not to
consumer but but it's there are some IVs
that are uh if it's a natural molecule
um you can get deliver like a
supplement. So where where we're at now
is so we formed a company to spin out
the molecules that we're finding. We
have a patent already uh that's been
filed and spun out uh Paradigm 88 with
Serena uh who's the CEO, my partner. And
we are developing consumer products that
we hope that will not be 10 years. that
may be a lot less pretty soon that we
have natural safe versions of the super
drugs that we're developing that will be
available much sooner and cheaper and it
could be something for the hair, for the
skin, could be a drink, could be
something like that. I won't reveal what
it is. We're developing the product
right now.
>> My base assumption is that if it can be
delivered in that sort of
over-the-counter fashion that it's like
some [ __ ] that it's not like the
real deal. How is it possible that it
could be so effective to regrow a nerve
and yet be over the counter in an IV
bag?
>> Yeah. Well, we're not developing
something to cure blindness. That's
super potent gene therapy currently.
Gene gene manipulation.
>> What we're talking about here or gene
introduction. We're not manipulating
anybody's genes.
>> What we're talking about here is
something that
undoubtedly will be less potent. But you
don't need to cure blindness just to
regrow hair or make your skin look
better or to feel better. So, we're
going to have something we believe
available that will show by clinical
trials. I'm not going to put something
out there that isn't proven to work um
that will rejuvenate the body over time
that uh we'll turn on the same
mechanisms that we're currently working
on. And I believe it's possible because
we already have three molecules. Some of
those are already natural that we can
get it to work and it works within four
weeks. And what do we get in the mice?
Might be people want to know what the
heck do you see in the mouse? Well, we
don't know about the hair yet cuz we
were we were the mice weren't bald, but
we did see and this was a year ago. We
gave it to the mice down their throats
for 4 weeks and what we saw was
rejuvenation. So they they were better
on tests of strength, memory, um
balance. We have a we have a whole set
of tests about 20 of them that tell us
whether a mouse is young or not.
>> And based on those parameters, the mouse
was deaged in four weeks.
>> Okay. So your job right now is basically
to tell the AI, hey, here's what we've
got in the industrial strength version.
I need you to find a natural coralate
that I can do over the counter that will
work and build the
>> already done. Um we're at the stage of
testing, but yes, we have those natural
molecules that list.
>> Okay. And are you already taking these
bad boys?
>> Some of them.
>> Interesting.
Interesting. Well, I gotta say up close
and personal, you look good.
>> Hey, thank you.
>> You look good, man. Uh, keep me posted
on when these become available. So,
skin, hair,
>> those are the ones that we're focusing
on right now.
>> Uh, well, and whole body for because
it's working as a drink in the animal.
We'll we'll see if we can make a drink.
>> Gotcha. So, you'll feel better, but skin
and hair you'll be able to see,
>> right?
>> You either have less gray hair or you
don't. That one, the hair is probably
the most like non placebo zone one that
you're going to get.
>> Yes. And and it's by popular demand.
Everywhere I go, it's like, David, what
am I going to do for my hair? Because it
>> will help people regrow hair or just go
from gray to color?
We
we still have to prove it out, but we've
deageded the skin, so we know that the
skin gets younger. The hair is next. And
the way we're testing that is one of the
tissues that we grow in the lab besides
brain and and the placenta, not
placenta, the the the woundus.
>> Urus is uh we're growing skin, human
skin from scratch.
>> And you age it and then deage it.
>> Yeah.
>> Wild.
>> Yeah. And it it's pretty cool
>> to see the the hair
anything like that of this stuff?
>> Yeah, I could get permission. I mean, my
employer, Harvard University, isn't that
keen on sharing pictures of mice growing
human hair on their backs, but maybe we
could.
>> I mean, if you want to talk about a
great marketing campaign, brother, like,
if you're able to show like here we are
aging it up, here we are aging it back
down. Like, people go crazy. Now,
needless to say, people are going to
come out of the woodwork and be like,
"Yeah, it's all good at first and then
you're gonna Benjamin Button or
whatever." I guess he was the opposite
direction that there's going to be some
complication that only manifests itself
10 years down the road.
>> Uh, and the immediate one is going to
be, well, if the catastrophic fail state
is cancer, how do I know this isn't
going to give me cancer in 10 years?
Well, that's why we we don't rush into
these things and why I think it's too
early to be trying this uh systemically
in our whole body. We'll start with the
eye and see how that goes.
>> You said you're already taking some of
this stuff.
>> Oh, the natural molecules. Yeah. And the
some of these molecules have been in
ancient medicine for a while. So, I'm
not too worried. The safety is known.
>> I'm not taking anything where
>> So, you're saying there's sort of two
grades of this stuff. There's the um
hardcore stuff. Is it the hardcore stuff
that's going to degrade your hair or is
it the over-the-counter ancient herbal
Chinese medicine that's going to degrade
the hair? My expectation is that we'll
find natural versions in the tens of
thousands of molecules that have been in
the human food supply that the right
combination of those or maybe one will
be sufficient to fix hair because in
skin it's working beautifully. Does the
wrinkles go away? the thin skin gets
thicker.
>> What's the I mean, I guess you're saying
we're reaching into the black box and
we're just getting it to solve the
information problem. This isn't like,
oh, it's collagen,
>> right? It's a lot more powerful than
that. You you hit a good point just
there.
>> The approach with disease and of
cosmetics up until this point is let's
fix one thing that's missing or overrou
produced. We're fixing everything. We're
going in and changing the biology back
to what it was when it was young, which
affects tens of thousands of processes
with a single treatment.
>> It's crazy.
>> It's crazy that it works.
>> It's crazy that it's so far safe.
>> I mean, it's a gift to humanity. Maybe
that's the best proof that we're in a
simulation that this stuff is actually
happening.
>> Cuz in a in the real world, you're like,
what's the chance that you get AI and
you get age reversal? Come on. But it's
happening. So, whoever's watching and
making this happen, maybe uh they're
having fun.
>> It's bananas. Uh did your dad age as
well as you?
>> He's aging better than me.
>> Um but I'm saying like before you came
up with all this stuff, like cuz if dad
looked like you at whatever 50ish
>> you are. Yeah.
>> Then okay, you just have good [ __ ]
jeans. But if this is dad look like a
normal 55year-old,
uh there's yeah more hope.
Well, my my mother was would did better
off though. She died of cancer, but uh
lung cancer. She had good skin and uh
and not a lot of gray. But my father uh
yeah, he he looks like
when he was my age, 56, he looked like a
56 year old,
>> right?
uh though it's slowed down. Anyone who's
seen the photos out there, he's slowed
down over the last 20 years.
>> His aging because of working with
protocols that you've been advising him
on or
>> Well, I'm not experimenting on my dad.
He's a scientist as well.
>> Uh but he he listens and he takes a few
of the things that I do, about five of
them. And uh he's he physically doesn't
look like he's aging. And at at 86, he's
in better health than he has been in
decades.
>> Uh no aches or pains. He's if you see
him walk, he doesn't he doesn't walk
like an 86y old. We just climbed the
Harbor Bridge in Sydney, which is a
massive thing for anybody. And for him,
it's no big deal. Actually, Serena and
I, we did like 20,000 steps around the
city before we climbed the bridge.
>> And at 86, most men are in in the ground
or
>> Yeah.
>> gone. Um, and my father's run out of
friends uh his age that he can hang out
with and go for walks because they're
all very frail. And he's like, "What's
the what's the big deal? I got nothing
wrong with me and I'm going out every
night."
>> So, you know, it might be coincidence.
It's a N of one, which is basically you
can't draw any conclusions.
>> Sure.
>> But like you say, he was old at my age
looking. He'd lost his hair. It was all
gray in his 50s, 60s, but physically he
hasn't changed since then. since he
started working on it, which is about 25
years of work.
>> Yeah.
>> Well, if it if you can regrow hair,
you've got a monster hit. If you can
degra hair, you've got a hit. Uh and
man, if you can make especially women's
skin look younger. Oo, buddy.
>> I'm really optimistic that we will have
a new approach to cosmetics, right? What
products out there, they all say they
deh skin, but which ones like
permanently deh skin? None.
And you might
>> understand you're saying it permanently
dees if you keep using it because my
understanding was uh that you have to
pulse this stuff so that as you use it
it dees but then it starts aging again
then you use it again
>> right but it's not like uh collagen or
or moisturizer where a week later you
don't see it or Botox which is gone in
months or whatever. What we see in our
studies is in the case of the mouse, we
cured its glaucoma. It could see again
and then it wasn't for another third of
its life that it lost its sight again.
But the good news is we could turn it
back on again. So the timeline for us is
you you treat and then you treat maybe 5
10 years later and you just keep
treating. And the treatment is
interesting that we've engineered it so
that you don't need to get an injection
every time. You just take a drug to turn
on the genes and deage the eye or deage
the body. Um, and that's a proprietary
system and it's we used a molecule
doxycyc. Um, it's used to treat Lyme
disease, but we're using it over a
matter of a few weeks or really six
weeks to turn on those three genes OSK.
And uh so really the deaging comes down
to one shot and then antibiotic
treatment for as often as you need it.
>> And is that uh an altered variation of
the antibiotic or literally if you want
to DH go take lime medication?
>> Yeah, it it is the drug and we chose it
because it was well established as a
gene inducer the way it was engineered.
Ideally, we want to change that and get
away from an antibiotic because there of
course, you know, you want your gut
bacteria.
>> Yeah. I was going to say my wife has
been hammered from too many antibiotics.
>> Yeah. That said, um it was the most
reliable system and if it works, we will
engineer a new system, but we know we
need to make sure it works. If it fails,
we're going to set the field back by
years.
>> So, we got to make sure it works. Then
we can use something else to turn it on
besides doxycyc.
That said, you know, if if you're a
paraplegic or you've lost your eyesight,
you'll take some probiotics, right, to
restore your gut.
>> Yeah. Yeah. Wild. Okay. Um, talk to me
about personal protocols.
>> When I take a molecule, I see what
happens to me before I take something
else. I'm very scientific about it. So
it's taken me 25 30 years to get to the
point where I'm taking a set core set of
things and I know what each one does and
in combination taking a lot more
simultaneously and when you do that it's
impossible to know exactly what the
interactions are what's affecting what
exactly right so it's it's different and
so it's hard to figure out if you take
something what is the effect of that
molecule alone which is the way science
is generally
Now, do you trust that? Like, if I could
run a similar protocol in terms of being
able to afford it, if I were to go that
crazy, are you like, "Yeah, if you're
taking 80 things, but you're looking at
these 36 biomarkers or whatever, if
those biomarkers are going in the right
direction, I can't tell you which one of
the 80 things is actually doing the work
or what combination, but yeah, those are
the biomarkers. Go for it."
>> Well, I I want to be cautious because
there could be long-term negative
consequences that you can't see with a
blood test. So, first of all, it's
it's not for everybody. It does require
do doctor supervision and testing.
Otherwise, if you start taking that
stuff, you could react very badly. Uh
you can measure the rate of aging by
looking at how these methals change over
time. And um it's called a DNA
methylation clock if you want to look it
up. I would say that there's not one
clock to rule them all. U but we also
it's still an association. We the
association is never conclusive in
science. The association though mostly
from my good friend Steve Horvath who
developed these clocks originally. He
found that people with slower rates of
of change in those clocks or had less
age in those clocks tended to live
longer and have fewer diseases. That's
pretty good. But we don't know if
changing the rate of your clock midlife
makes a difference. Probably. Right.
>> But that's I got to you know you're
you're very rigorous in what's [ __ ]
and what's not. So, I'm being very
careful about delineating what we know
and what we don't.
>> His major assertion is, I'm slowing my
aging down because I believe that AI on
a long enough timeline is going to uh
make it so that humans can live forever.
Do do you see a stopper in biology that
will make that impossible? Obviously,
nobody knows how to do it yet, but do
you see anything where it's like because
of that, there's no way we're going to
be able to do this. Or to you, is it
just I don't know. It's in between. And
now
I'm not a kind of guy that that I'm not
stupid. I don't want to bet against Ray
Kurtzwell too much. He's been right a
lot. And he's talking about sing
Singularity. Do you remember the day?
It's in the mid uh 2045, I think.
>> Yeah. Something like that. Now, I'd be
the happiest person on the planet if if
our stuff works and we can live forever.
That's that's not a bad day. But I but I
think that
being at the the forefront of this
change, there is something that concerns
me that may prevent us within that time
frame of becoming, you know, living for
a thousand years at least. Immortality,
I think, is is so far out there. I think
it's better to talk about is there going
to be a small change of 5 years or is it
going to be hundreds of years or
thousand and one of the problems with
aging is that there are two types of
information.
There's the methals which is the
epigenetic information and I know how to
reverse that 75% multiple times.
Probably eventually
it'll you know we'll lose information
eventually. There's there's no way it's
100% re you know pure reversal. So
there's noise in the system even if I
reverse it. Um but where we're not very
good at reversing is the genetic
information loss. Right? Epigenetic is
cool. There's a backup copy. We found
that. But there if you've lost both
copies of the gene for X in a cell,
there's no backup. All right? And so
trying to do that for those cells is
very difficult right now. We do know how
to edit genes. We can fix genes. But
doing that on a cellby- cell basis is
beyond current imagination and
technology, even imagining technology to
do that.
>> Well, you can't just flood the body with
stem cells or whatever.
>> Not currently. No, cuz the stem cells
that people inject, they stick around,
but they don't find their niche. Um, you
know, you can't yet cure gray hair, as
far as I know, by injecting stem cells.
And the reason is you have to get them
into that very small m almost
microscopic niche hole where they sit.
>> So no, not yet.
>> But hopefully someone will come up with
either a type of stem cell or a type of
gene therapy that can go into a cell,
figure out what's missing or broken and
correct the genome and then you know my
stuff will come along and reverse the
epiggenome and then I can imagine living
thousands of years because I can imagine
it. People say thousand years that's
crazy. The reason that I think it's
doable is there are already living
things that last that long. Why? Because
they have very stable information.
There's a plant in the Nabib Desert that
lasts for it's been around since the
pyramids. Some of these plants
>> Whoa. And when you look at their genome,
they have a very special genome that
protects the information and preserves
it for thousands of years. We lose our
information pretty fast. we kind of lost
a lot of our information by age 80.
Whereas these plants and somewhere in
between a whale preserves information
even better than we do.
>> It's incredible. Okay, give me one um
prognostication. Where do you think this
goes in the call it near-term? So, what
are we looking at? What changes will we
actively experience in the next three
years? And then um I'll really give you
some wiggle room and tell me what it
looks like 20 years from now. The next
few months are critical. Um, I'm going
to find out
if this gene therapy, I shouldn't call
it gene therapy, it's more of a a gene
introduction, the age reversal
technology, if it works in people. Um,
the world will probably find out
a year from now. I'm going to be sworn
to secrecy. I'm not even going to be
able to wink. It's that important. But
I'm going to know in a few months if
this works. Wow.
>> Okay. But anyway, let's say a year from
now, everyone knows that that it works.
This is best case scenario. And again,
it's I think 80 90% chance. Then the
world goes nuts. That's a chat GPT
moment for biology for aging
>> because we've got it to work in humans.
Now the question is now what do you do
with that technology? There's going to
be a a gold rush already. There are
billions of dollars um spread across my
company and others competitors. Sam
Alman's company, uh Brian Armstrong, uh
even uh Jeff Bezos is in this.
>> There's going to be a massive gold rush
to try and catch up to break my patterns
to get around them and to treat other
things besides vision. And just like AI
is now, uh what is it? It's only three
years since Chip came.
>> Yeah,
>> it's crazy.
>> Crazy. So there's going to be that kind
of a momentum if this works where the
world will just be listening to every
result, every pundit on this topic.
That's my prediction for the short term.
In 20 years, I think that whether I'm
successful or not, we're still going to
have somebody achieve what I'm talking
about.
>> Um, and it could be age reversal for
many organs. And again, there's billions
of dollars put to this. So it's
>> Does everyone just look 25? Like what
what does that actually look like?
It's possible that my father who looks
86
could look like us after treating
himself for a few months.
>> That's wild. So you think though it's
shave maybe 30 or 40% off your life.
It's not you go back to looking 25
because like fat storage, the type of
fat, where it's stored, all that stuff
matters. It's not just skin.
>> Exactly.
So, I'm I'm hedging my bets here, saying
that he's going to look middle-aged,
>> right? So, it's going to be far more
complicated. It's not like um you take
an ivy drip and like uh death becomes
her, like her boobs get perky again and
her ass tucks up and her skin changes.
It's not Yeah, it's not going to quite
be that horrible.
>> We don't know. We really don't know.
I've seen nothing to suggest that that
won't happen. It's just
>> we're at the beginning. We're at the
beginning. It'd be like asking again the
Wright brothers,
do you imagine that there'll be a
Concord jet that can fly around the
world? They're like, yeah, of course,
>> but we're still building the right flyer
right now.
>> So, it's coming. No question. We we
we've we've shown the biology is there
and we can do it,
>> but it's going to take some work to get
to that kind of a molecule. I think
>> we can take a pill and truly
>> regenerate our entire body back to being
20.
>> You know, that said, you do want to
stick around cuz this technology is
coming. And if you start early now,
eventually, imagine the the drug. Uh I
don't know if it'll ever be over the
counter, but imagine that it is. You can
go down to your local store and get this
stuff. It might be $5 a pill. I don't
know, something like that. And start
when you're 25.
And you just stay 25 for a while,
>> for a long while, right? Daging my
father from 86 is much more challenging
than starting at 25.
>> Yeah. Hurry, please. Uh, okay. So, given
that we've got to buy ourselves a little
bit of time while the technology gets
finalized, proven, all of that. Um, how
should people be approaching their
health with things that they can do
right now today? But I I want to start
by saying um I do some experimental
stuff and some regular stuff. Um so we
I'll tell you as much as I can tell
everybody. Um one of the reasons that
I'm starting restarting my podcast is
because every day literally on the
street people say, "When's your podcast
starting?"
>> Yeah, brother. It it is about time.
>> Yeah. Thanks. I've been busy working on
these drugs, but now that they're in the
clinic,
>> Yeah. Yeah.
>> I've got the time now.
>> You know, the future is set. It's going
to happen or not. So, I want to start ed
re-educating everybody about what have
we what's happened uh recently that
everyone needs to know about and uh so
that's coming. We're just editing now.
So, that's exciting. Very exciting.
>> And it's new and improved. So, you'll
see.
>> Um
also, I just want to remind everybody
that uh the stack that I had when my
book came out in Lifespan, the book
lifespan, is still
>> true. I'm still taking what's on page
304, but I've added a few things which
we can we'll talk about. All right, so
let's start with the fundamentals that
my father takes and I take and we've
been taking them for over a decade.
>> So far so good. I'm still alive. He's
still alive, which is good. When we
started taking them, by the way, people
said, "What are you taking that stuff
for? It's it's not known." Right. So now
10 years later, first one is NMN. NMN do
not confuse with N uh with M&M's, right?
that not making my dismay. Yeah.
>> Yeah. And I I heard your podcast about
sugar uh the other day about a fan.
>> Me neither. No.
>> Um and we should talk about what to
avoid actually. But what you should
consider taking uh what I've started
taking with my father is enaman and I
take a gram of that as capsules every
day. And uh you just want to make sure
it's really pure. Um it should either
taste slightly sour like a sour patch
kit if you're in the US. Um, or there's
a form of it that tastes a bit like
sweet popcorn.
>> Do you have Well, say more. Do you have
a brand that you can recommend or is
that weird given your position?
>> Yeah. You know what happens, Tom, is if
I mention a brand, it's all over the
internet now. I'm used to sell millions
of dollars of product.
>> Yeah.
>> That's not fair to to anybody. And even
if I don't mention it, my name is all
over the products as well.
So, I don't want to endorse product, but
I will guide people to say look for GMP
pure and you can look for it. It should
be pure white. If it's not pure white,
it's not pure. And uh and it should
taste like those two things. And that
that's the best thing. Uh but I won't
mention brands.
>> Um I I don't want to be lumped in
already. People think I sell supplements
for a living, which is BS, and I don't
want to make that worse. I'm I'm just a
scientist developing medicines.
>> Yeah. But you're you're on the internet.
Welcome. Well, yeah. You and I know how
AI is getting crazy, right?
>> It's wild. I can only imagine how many
AI David Sinclair's are out in the
world.
>> There there's a number and and the the
biggest one where there were millions of
views got taken down last week. Thank
God.
>> Thank God. Yeah.
>> Yeah. Um but that's a future. So,
everyone listening, be beware of fake
versions of me giving out health advice.
So, lifespan.com
and the lifespan podcast is the
original. It's going to be real. Uh so,
there's Enman. Next one is resveratrol.
That's the a staple of mine for 15
years. Resveratrol is that red wine
molecule,
>> but I don't drink red wine anymore.
Serena told me it's better not to drink
and I don't.
>> That's smart.
>> Yeah. And you don't drink alcohol
either. So, it is smart. Um I'm not as
funny as I used to be. But, but I do
have mental clarity like never before
since my 20s.
>> No, it's rough. I'd love alcohol. If it
was uh optimizing me, I would do it all
the time. It is very enjoyable. But
alas,
>> yeah. So, what you want to do is take
out the molecule without and take it
without the alcohol, which is what I do.
I take a a small spoonful. It's it's
about a gram of rveratrol. Again, look
for white or slightly gray. If it's
brown or brownish, throw it away. It's
contaminated with other stuff that can
give you diarrhea.
>> Fun.
>> Yeah. So, there's plenty of resveratrol
out on the supplement. And again, look
for 98 99% pure stuff. And I mix that
with something that dissolves it because
it if you put it into a cup of water,
it'll sink to the bottom and it will
just go straight through your tract.
Most of it you will not get absorbed.
You can increase that five-fold by
mixing it with either olive oil or a bit
of yogurt.
>> Um I I do either.
>> Is it fat soluble? Is that why?
>> Yeah.
>> It's like brick dust.
Yeah. So most people don't know that.
And even clinical trials that have been
done on resveratrol have failed because
they just gave it to them with water.
>> Interesting. Yeah. All these little
details matter.
>> Yeah. Okay.
>> The third thing is a glucose lowering
medicine.
>> Interesting.
>> Or a supplement.
>> Why not just eat low sugar?
>> That too. the combination because people
don't do it or even if like me my
glucose is low because I am
>> I'm a disciplined freak and if I decide
I'm not eating something that's that
>> uh so my glucose lives in the mid 80s um
you're saying even there I should take
something to push it down even more.
Um, well, mid to 80 is you you could go
slightly slower, lower, but um I mean if
it was uh fasting 80.
>> No, I don't fast at 80. If I'm fasted,
it's mid to low 60s.
>> I see. Okay, then you're good. It might
actually be,
you know, it might be too much for you
to take one of these things. You might
get hypoglycemia, though that's not
common. Um, I on the other hand have
diabetes in my family and without a very
strict diet and one of these medicines,
I'm I'm probably going to be about 100.
>> Really? What are you eating?
>> Um, and then fasted. It's
>> Wait, hold on. Cuz you're like super
veggie forward, right?
>> Yeah.
>> So, you're probably intaking a lot more
carbs than I am.
>> Yeah. Well, I don't know exactly your
diet, but I am taking a lot more
vegetables than I used to um for health
reasons, but I'm taking in the plants
because I want the polyphenols in the
plants as well as part of my diet, which
meat does not have.
>> Okay. Give me percentage of total
calories over a year, meat versus
vegetable matter.
>> 95 plants.
>> Wow. Okay.
>> Yeah. And I I changed to plants because
Serena is actually vegan. And I tried it
and within 30 days the inflammation in
my body came way down
>> and glucose came down actually.
>> So but I was I was I
>> measured by C reactive protein. What
were you measuring for the inflamation?
>> C reactive protein was the big one that
came down. But I'm also measuring things
like TNF alpha1 beta is 6.
>> Yeah. CRP is a good way to get it down
is to to cut out I cut out dairy uh and
I cut out uh meat for a while. I still
occasionally eat meat. I'm not total
vegan anymore.
>> Yeah. Yeah.
>> Um,
>> but 5% over a year, that's not a lot.
>> Okay, cool.
>> Uh, I will say that I'm I have an
advantage, which is that uh Serena is in
LA and I'm in LA a fair bit. It's great
food in this city. Boston, not so much.
Um, but I also I can afford good food,
so I buy the best quality foods, fresh,
organic, good restaurants that cook
don't overcook the food.
>> Listen, my wife and I eat from a vegan
restaurant routinely. I just put meat on
it. I'm not kidding. But their stuff is
so flavorful that I'm like,
>> "Give me more." Yeah.
>> But I gotta add meat.
>> Yeah. Uh so the drugs that the drug that
people typically take is metformin.
>> I think that's pretty wellnown and you
can get that online or from a doctor,
but it is prescription. You need to talk
to a doctor and you want to monitor your
blood glucose levels accordingly and
your liver.
>> Now from other podcasts, you you go on
and off metformin. You don't stay on
metformin. I I do a couple of things
that's worth that are worth noting. Uh
the metformin that I get in the US wres
havoc on my stomach. I'm one of the 40%
of people that have a stomach upset. The
stuff that um I don't get from the US,
let's put it that way. Um when I'm
acting like an Australian, for example,
their their version is coded and I don't
get that problem. So that's actually one
of the reasons that I I I change from
metformin to this other more natural or
totally natural form called bourberine.
>> Okay. Same idea though.
>> Yeah. Bourberine.
>> Bourberine over the counter.
>> Yeah. Yeah. I take Serena's supplement
um because I can trust her supplements
being pure
>> and um but yeah, bourberine has been
shown clinically to reduce blood glucose
very similar to what metformin does.
>> So those are the three big ones. Um you
good with those?
>> Yeah. Yeah. So, my father's on that. We
recently added a couple of things to my
father's regimen. Not we, he did. Uh,
one is nattokinise, which is an enzyme
that comes from fermented soybeans,
>> just like powder format.
>> Uh, it's a capsule powder. Yeah.
>> Okay.
>> I have cardiovascular disease in my
family.
>> Okay.
>> And my father also has cardiovascular
risk.
>> Do you have a marker that you look for?
Do you are you getting ultrasounds or
what?
>> I do. I'm getting uh and actually I want
to qualify. If you get really really low
uh LDLC, you can also reverse some
plaque. So, it's not the only thing, but
it's the most natural way. And uh yes,
so I get corateed ultrasounds and look
at the
>> um in IMT,
>> you know about that?
>> Yeah.
>> Um
>> not by that name. How about that?
>> Yeah. So, that that measures the
thickness of the wall of the
>> and the flexibility and all that. I've
had my arteries scanned before years
ago.
>> Uh how often do you do it? yearly.
>> Okay. And have you seen an improvement
or it just stays steady?
>> Not yet because I've not been on it for
a year.
>> Gotcha. Okay. Report back.
>> Yeah. Yeah, I will. Good. Um, so there's
nattokinise. I'm also taking um half a
gram of nascin, vitamin B3, these days
because I have high levels of something
that everybody should measure called LP
parenthesis little A.
>> Okay. What is it? It is a lipoprotein
that carries cholesterol in the
bloodstream and is thought to be
responsible for the deposition of
cholesterol and um inflammation in the
artery.
>> Oh okay.
>> And it was first found just by
association. Uh people had high levels
of this lipoprotein LP little A were
susceptible to cardiovascular disease. M
>> over the last 10 years, it's been
steadily showing that people with high
levels are really at risk in as much as
having high LDLC levels.
>> Interesting. Okay.
>> And uh so much so that there's a lot of
money being spent in the pharmaceutical
industry to make a drug that will lower
LP little A levels,
>> of course.
>> And there's one that's in phase three
that looks promising. Um, but I'm one of
the people that my father is because of
our Ashkanazi Jew heritage that we have
a version of the LP little A that is
highly expressed. So my levels were 34
and you'd want it to be more like 10 or
less.
>> Yo.
>> So I immediately increased the levels of
the statin. And I know there's pluses
and minuses for statins, but I've been
on a statin successfully since I was 29.
>> What?
>> My my grandmother had a stroke at 30.
Bro,
>> the fact that I'm still alive is is good
news.
>> Jesus.
>> Yeah.
>> Uh, was this like a stress induced was
she like in World War II? Like what are
we talking about?
>> Might be that.
>> Yeah,
>> cuz 30 is young.
>> She Well, she didn't have a very healthy
childhood cuz she grew up um after the
depression in Hungary. Then there was
the second world war where her
>> part of our family was wiped out.
>> Yeah. She Ashkenazi as well. No,
>> we haven't been Jewish for the last four
or so generations,
>> but I I recently did my uh family tree
and can could trace back a thousand
years.
>> Oh, snap.
>> So, I'm a a one of probably many
descendants of uh some of the most
famous rabbis uh from the Middle Ages.
>> Didn't know that till this this uh
season. But anyway, the the the point is
that gene coming from that line makes me
highly susceptible to heart disease and
I've had to fight it since I was 29.
Statin though, does it make your joints
hurt and stuff like that? Like I hear
horror stories about statins.
>> Not for me. No, I I of course make sure
that I'm okay on a particular drug
because we all react differently. And
for me, the statins being great.
>> It's not for everybody, of course. And
there are actually alternatives now that
are not statins. There's PCSK9
inhibitors which are really effective
for lowering LDL. And there's more to
come. The drugs that are getting there
for blood pressure, for cholesterol, uh,
and now for blood sugar are amazing. We
really shouldn't be dying from those
diseases anymore.
>> That's wild.
>> Yeah. And even cancer. The prevention
for cancer is getting to the point where
getting scans, getting DNA blood tests,
we're at a point where you have to be
really unlucky to get cancer. So,
>> I just got cancer. So, say more about
that. So,
>> uh, skin cancer. I have lived my whole
life with an abundance of caution around
the sun. Yeah. So, nobody I've been
clowned on by my wife for decades
because I stay out of the sun. I wear
hats. Like ridiculous hats.
>> Yes. I've never seen you with a tan,
>> bro.
>> Yeah.
>> So, uh
>> we barely need lights in here.
>> Yeah. So, what the [ __ ] Like, any
guesses?
>> Well, people can get lung cancer without
ever smoking there. There is
>> skin cancer. You get skin cancer without
overexposure to the sun. For real? like
>> it can happen
>> for real. For real. Like what what do I
>> how do we fight that fight? What's the
protocol?
>> Well, so the the the start is stay out
of the sun, which you've done
>> um your whole life,
>> bro. Well, first of all, I grew up in
Tacoma, Washington, so there is no sun.
>> And then uh here I've always stayed in
the shade now because my wife is Greek
and loves the sun more than anything in
this universe.
>> Uh there's no doubt that I'm sun
adjacent a lot. So, I'll be under the
umbrella while my wife suntans, but I I
can burn in the shade. Just to give you
an idea of where we're at here. So, uh
I've had to be paranoid because I will
burn so easily.
>> Do you have any family history?
>> My dad has had skin cancer multiple
times.
>> See, if I did your genome, have you have
you done your genome?
>> No.
>> See, cuz you could be susceptible in
some ways.
>> Well, apparently I am susceptible.
>> Yeah. And that's another good reason for
getting your genome done if you can
afford it. Mhm.
>> Um, it can really make sure that you do
the right thing. Now, besides staying
out of the sun, you can also with your
diet, uh, maybe not prevent, but reduce
your chances of getting certain types of
cancer, including skin cancer.
>> Like,
>> I thought you'd ask,
>> are we in the avoid mechanism here now?
You said we should talk about what to
avoid.
>> For sure. Avoid. That's that's the easy
stuff.
>> Is that where we're headed with skin
cancer or
>> No, I was going to say what you can
take.
>> Say more. So the polyphenols in plants,
one of the reasons I take a lot of
plants, especially colored ones, Serena
says take eat the rainbow.
>> Isn't there a ton of polyphenols in um
olive oil?
>> Yes.
>> Okay.
>> So olive oil,
>> most olive oil ever
>> and green tea, matcha, the the thick
dark green stuff
>> with matcha, but maybe I should. Okay.
>> Those are highly anti-cancer.
>> And they're preventing DNA damage.
They're reducing inflammation that all
can drive cancer.
>> Interesting.
>> Yeah.
>> About to go hard on matcha then. So we
do Serena again you can tell Serena
played a big role in my life. the the
matcha we drink every morning at least
one and I don't drink coffee much
anymore instead
>> and then throughout the day I'm drinking
tea and eventually caffeine-free tea
after lunch but I'm always with liquids
and the matcha has been a great change
to my life and I don't own shares in any
matcha companies by the way
>> but I do love it and so the the kind of
foods I mean there are some good books
um about that about how to eat to
prevent cancer or treat cancer as well
um and if you do have cancer look into
it keep we talked about ketosis and
drinking ketones.
Those are
>> they have anti-cancer properties.
>> Yeah, there are certain types of
cancers.
>> So cancer loves sugar just like the
brain.
>> Um
>> but they don't just like the brain but
not like the brain they don't like
ketones.
>> So what often is recommended for someone
I'll give you an example. Uh my neighbor
developed prostate cancer.
>> Uh very common in men of course most of
us
>> my age we have something coming along.
We uh he went immediately and he was
he's an expert. I say was because he's
not around anymore.
>> O
>> but he specialized in oncology.
>> Oh god.
>> And he immediately went on a keto diet.
>> Yeah.
>> And took loads of metformin.
>> Yeah. Yeah. We studied this back at
Quest.
>> Yep.
>> Uhhuh. But he died. So the punchline
here is not great unless he was hit by a
bus and totally unrelated to the
prostate cancer.
>> He didn't die from cancer.
>> Really? What did he die from?
I don't know if I should say, but it it
>> I'm too curious now. You got to say
>> it was depression.
>> Really? Oh [ __ ] Okay. Yeah.
>> Secondary effect of the cancer though,
like the treatments grueling.
>> Yeah. What what happened to him? And of
course,
>> I haven't mentioned his name, so I think
it's okay to talk about it. Um, he was
on testosterone therapy,
anti-testosterone therapy, which for men
is uh is tough. And um he lost libido.
He lost will to live. It was the middle
of
>> in coming off of it.
>> No, while on the drug knocking down the
levels of his hormones so that the tumor
wouldn't thrive.
>> Right. Right. Right. Instead, he lost
his manhood.
>> Yeah.
>> And went into depression because of its
common
>> back.
>> Um and it was the middle of the pandemic
too.
>> Oh god.
>> So he didn't he didn't choose to stick
around.
>> Yo, that's rough. Okay.
So on that note, yeah, do what you can
to prevent cancer. Get yourself scanned.
Have you got that?
>> I Well, I've obviously now I get
visually scanned routinely. Um,
>> but no, I have not done the like full
body. I'm waiting for Peter Diamandis to
open his uh LA branch. He's been trying
to get me out to Florida or wherever the
other ones are, which now obviously when
I got the skin cancer, I was like, "Damn
it."
>> Uh,
>> we'll we'll get get that scan for sure.
MRI scans are good. Uh Serena and I get
one of those every year. Uh and that's
full body. It won't pick up melanoma
most likely because it's small.
>> So you do need to be visually scanned.
You can either get that done by your
physician or by
>> this wasn't melanoma. Melanoma I would
have been like this is a diet problem.
This was another one. I forget what it's
called. Uh but they say this is from sun
exposure. That
>> oh so it was on a place which is exposed
then.
>> Yeah. Yeah.
>> That's good. That's probably
>> that's good.
>> No no no
>> that's not good. Didn't I don't think I
said that's good. I said that makes
sense that uh it was on your if I said
that's good. I didn't mean that.
>> It's all right.
>> That's happy for my
>> no facial.
>> But it's gone now and I can't It's gone.
>> Yeah.
>> Now,
>> did you Is it okay if I ask you about
it?
>> Yeah. Go crazy.
>> Did you treat it with any cream?
>> Uh no. So we looked at that option and
it was going to be like three weeks of
open sore on my face and then may not
work and so they were saying listen you
should just get it removed and then I
was like I I don't trust you I need to
go get another opinion and so I went and
did like a deep dive on like what are
the pros and cons and given that it
itself can leave a scar because it's
basically like chemotherapy
topically
>> hydroxy. I was like,
>> so I said, let's just go to the one
that's like 98%.
Sorry.
>> So, I did that and
>> yeah,
>> so far so good. So,
>> okay, good. Yeah, this cream is is
tough. Um, yeah, it's it's probably five
floruracil which gets stuck in the
replicating strand of DNA and kills
cells that are dividing.
>> That's wild. Yeah, actually my father
recently for the same reason uh skin
cancer on his head, his bald head put
the cream on. Um so yeah, if you if you
are losing your hair,
>> did it go okay?
>> Be careful. Wear a hat.
>> Uh it went okay, but you peel and it's
you know it's not good.
>> Did it get rid of it?
>> Um he had a surgery as well.
>> Yeah. See, that's why I was like I don't
want to do the one-two punch. It's like
if I'm going to have the surgery, let's
just do the surgery.
>> Yeah. But he he also put the cream on
everywhere because
>> just in case to like get some early
stage.
>> That's what's often done.
>> Got it.
>> And a friend of mine did it all over his
face. Was like a burning your face. But
he had a few and just to try and get rid
of what's what's left. They do that in
case there's little ones that you can't
see.
>> But I'd recommend you do a blood test as
well.
>> I've done the blood test.
>> Yeah. And the great irony was like I
knew I all it had already been diagnosed
like I'd had the biopsy and so when I
got the blood test back and it's like
you're fine I was like well then I know
this thing isn't 100% cuz I actively
have it right now.
>> Yeah. Well that's that's also something
that everyone should know is that these
are adjuncts that these tests these
blood tests if they say you're cancer
free doesn't mean you're cancer free.
>> Means you don't have anything that we
know how to detect.
>> Yes.
>> Yeah.
>> And there's also false positives as
well. So,
>> I I use the test as a warning sign, not
as a diagnosis.
>> Very smart.
>> But still, if you can afford it and you
really want to put money into your
health rather than I don't know what
toys, then it's a good way to invest.
Get get the full body MRI and get a
blood test for cancer. And you may miss
something, but you may pick something up
as well. But there there are also
probably doctors who are listening to
this saying, "Great, everyone's going to
go out and get an MRI and find that
they've got some disease that isn't
real." There is some truth to that that
you on an MRI you can find things that
are not going to kill you and you might
want to investigate.
My personal view about that as a
scientist, not as a doctor, I'm a PhD,
is that more data is better in biology
in in health.
>> And that's why I science the [ __ ] out of
myself. Mhm.
>> And I'm also a guinea pig that I I want
to learn and educate,
>> but I don't want to shy away from
learning something even if I find a
false positive. You know, I'll I'd
rather not live in ignorance.
>> Yeah. No, I'm with you on that.
>> And then you get a baseline. So, my
baseline over the last few years has
been perfect health.
>> But if something changes, AI will the
doctor will detect it.
>> So, it's better to get a baseline before
you're sick in my view.
>> No doubt. All right. You just gave us a
bunch of stuff uh that we should do.
What about the things we should not do?
>> Uh well, the easy ones are if you smoke,
please quit. Uh my mother did not and
she is no longer with me and she would
be if she didn't smoke.
>> Do not deny. I know you don't smoke. I
never have.
>> But don't live in denial that you'll be
one of the lucky ones.
>> It's the best thing you can do for your
health is to not smoke.
>> You'll age prematurely, too, and you'll
look like [ __ ] at my age. Yeah.
>> Uh, drinking occasional drink, okay? But
don't drink consistently. I was drinking
red wine every day. That was too much.
>> We know that people who drink even just
one glass of alcohol a day tend to have
smaller brain size.
>> Oh, [ __ ] that.
>> Yeah, there's scatter in the plot. Not
everybody has this, but the trend line
is down with the more alcohol you drink.
And the more you drink, the smaller your
brain will be.
>> No thanks.
>> Yeah. So, skip alcohol smoking. um
sedentary behavior. We're all prone to
it. We're doing it right now.
>> Get a standing desk at a minimum.
>> Walk, take your stairs,
>> standing desk.
>> And if you if you if you can run, lose
your breath three times a week at least.
Um I don't care what kind of exercise
you're doing, right?
>> I can think of some fun ways to
>> There are fun ways. And you only need 10
minutes.
>> You don't need to be a marathon man.
>> Perfect.
>> Yeah. You're like, is is 2 minutes
enough?
But 10 minutes will be fine for us. And
uh you know even if it's a rowing sport,
it's all great but lose your breath
three times a week if you can. Uh I joke
that uh I my exercise is running to the
terminal uh to catch a plane.
>> It's kind of like that and that does
make it difficult but um got to move.
Got to move. Don't sit. And at at work
if you come I hope you come see me in
the lab. I'll be at a standing desk most
days
>> and people on Zoom think that I'm
floating in space because I'm doing this
but I don't. I'm not still throughout
the day. I even hold meetings while I'm
standing. I just pace around. They think
I'm crazy, but
>> sitting is is the new smoking as they
say.
>> So, those are the the big uh do nots. Um
>> you left out one that I think is musive,
which is sugar.
>> Thank you. Um I've for me it's just a
way of life. So, that's why I didn't
think of it. Um I avoid sugar like the
plague like you do. I think of it as a
toxin.
>> It's not really a toxin, but long term
it is. It will attach physically.
Glucose will attach to your proteins.
>> HBA1C, that's a prediction for diabetes,
right?
>> If you go, you probably know this. Not
everyone knows. HBA1C is what your
doctor tests for diabetes. That's
literally glucose attached to your
hemoglobin as a bellweather as a canary
in the coal mine for glucose attaching
to all the proteins in your body. You
don't want that.
>> Glucose attached to proteins will make
them dysfunctional. And who knows what
else is going wrong, but we know that
that causes diabetes.
Glucose also will uh give you a spike.
It'll give you a, you know, a real high
initially, but anyone who's worn a
glucose monitor will know the
consequences. You will have a crash,
brain fog, hunger, distraction. Whereas,
if you don't eat sugar, you got this
steady flow of glucose coming out of
your liver through gluconneogenesis,
which is the term for making glucose
naturally. Uh, and my liver is much
smarter than my mouth. It will make pure
minimal amounts of glucose that my body
needs and supplement that with ketones
by a drink and it's it's bliss. I power
through the day. I rarely get tired. If
your kids are eating a lot of candy,
please give them something else.
>> No joke.
>> Right? Because by the way, kids
epigenomes, the the methals on their
body on in their cells,
those marks are laid down during the
teenage years as well. And it's known
that kids that eat badly will have
consequences decades later because of
this memory in how the genes are turned
on and off.
>> Interesting.
>> And kids today are aging faster than
they used to.
>> That is not a surprise.
>> And I think it's because the diet.
>> Yeah. No doubt.
>> And it's no surprise that girls are
getting fertile more more earlier.
>> That one is distressing
>> because they're getting older earlier.
We are aging our children.
>> Interesting.
>> And it starts at birth is aging.
Actually, aging begins at the week,
second week of conception.
>> Yeah.
>> So, we we we're not immune. Even when
we're in our 20s and we eat pizza and
you know, a lot of us experiment with
drugs and alcohol, that's aging us and
you feel it at our age.
>> Thankfully, I didn't do drugs and
alcohol, but I did a lot of junk food.
>> I'll tell you that.
>> Yeah.
>> Woof. All right, man. Now that I've got
you, is there anything else? Any parting
shots you want to leave people with? the
super secret thing that they should be
doing or know about, pay attention to,
anything like that.
>> Um, there's there's sleep, but there's a
lot of experts on that. Make sure you
get good deep sleep. Deep sleep will
clear out the proteins in your brain
that you need to get rid of. Um,
including probably the Alzheimer's
protein, um, a beta. Uh, another thing
that would be important to mention would
be that stress in your life is a killer.
>> Yeah.
>> And it's difficult.
>> Shortening my life for sure.
>> High achievers are the worst. And if
you're high achiever, and I I am by
choice trying to be a high achiever, I
spent the first 50 years of my life on
edge almost every day. Even if I'd go
for a walk in the forest, I was thinking
about the mistakes that I'd made the day
before. That kind of guy in the shower,
I'm I'm swearing to myself, you're an
idiot.
>> All that is almost all of that is gone.
Again, Serena was a big influence. She
taught me how to calm my mind, not worry
about things so much. But it's hard.
super hard because we are by nature many
of us are driven
>> and we want to be perfect. We'll never
be perfect and we'll always have stress.
>> So try to think about life in the long
run. Treat it like a game. It's not that
serious. It may not even be real as we
discussed. So go for it. Have fun, but
don't worry too much. And get get sleep
because if you don't sleep enough or get
deep sleep, you will have a higher heart
rate. You will feel stressed throughout
the day. And I have times during the day
now that I I breathe. I shut my eyes. I
do box breathing. Um I've even even on
occasion set an alarm at 11:00. I'm
going to take time out to lower uh my
nervous system down again
>> and it's been great.
>> Very smart. All right. Well, you've got
the podcast rebooting. Where can people
follow along and engage with you?
>> Hey, thanks. Uh well, it's lifespan.com
and on social media you can find me. I'm
pretty prominent on most of those
platforms,
>> I would say.
>> Uh I do work at That's Fun. I like
educating, so I tell people about the
latest findings in science there and
what I'm doing. Um, and then I've got a
a Friends of Sinclair lab to fund my lab
now that all the government funding got
terminated. And uh, so if you're
interested, check out friends
friendsoflab.org.
>> Okay.
>> Friends of sinclair.org. You'll find me
there.
>> Love it, man. This is awesome. Thank you
so much for taking the time. It was
wonderful to sit across from you again
and I could not be more excited about
the things you're working on. Fingers
crossed that they get across the finish
line. Be incredible.
>> Cross your fingers for us really cuz uh
it's a it's a pivotal year for humanity
if it works.
>> No doubt.
>> Thanks a lot.
>> All right, everybody. If you haven't
already, be sure to subscribe and until
next time, my friends, be legendary.
Take care. Peace. If you like this
conversation, check out this episode to
learn more. From the year 2000 to today,
the average male's testosterone levels
have dropped by more than 25%.
And modern life is only making the
problem worse. Algorithms are now so
effective at hijacking the male brain's
dopamine
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May 19, 2026
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