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Dr David Sinclair: Can Aging Be Reversed? After 8 Weeks, Cells Appeared 75% Younger In Tests!

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Dr David Sinclair: Can Aging Be Reversed? After 8 Weeks, Cells Appeared 75% Younger In Tests!

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4037 segments

0:00

This is very

0:02

>> It's bad, right?

0:02

>> It's hard. Yeah.

0:03

>> That's what it's like to be old. And for

0:05

far too long, we've [music] ignored it

0:06

or accepted it as natural. And I reject

0:09

the idea that aging just because it's

0:11

natural is acceptable. Dying at 80 is

0:14

not inevitable. Absolutely, that can be

0:16

changed. So, if you're skeptical, I am a

0:18

Harvard professor who has been studying

0:20

aging, longevity, and age reversal for

0:22

30 years. And I've seen enough from my

0:24

lab showing that we can literally now

0:26

reverse the aging process. And it's not

0:28

a question of if, [music] it's a

0:29

question of when this is going to

0:30

happen. And everyone should stick around

0:31

cuz I'm going to tell you some of the

0:32

major things that people should be

0:34

doing. They can lengthen your life by a

0:35

decade. Hey, you're not taking that off,

0:37

Stephen. You got 10 minutes for that.

0:39

So, you can accelerate aging by smoking,

0:41

getting an X-ray, ultrarocessed foods,

0:43

excessive drinking, flying a lot.

0:45

>> I fly all the time.

0:46

>> That's probably accelerating your aging

0:48

process.

0:50

Even going to a rock concert and

0:52

blasting your eardrums because your ear

0:54

hair cells are [music] getting older

0:55

faster. And so I look at the body like

0:57

it's a computer and we can reinstall the

1:00

software. And what's [music] interesting

1:01

is when you reverse aging, diseases like

1:03

Alzheimer's, cancer, heart disease go

1:05

away [music] or are cured because what's

1:07

driving a lot of those diseases is

1:10

aging. And so my lab is like Willy

1:12

Wonka's chocolate factory. They are

1:13

making discoveries that blow me away

1:15

every week. And I think we're at a

1:16

turning point in human history [music]

1:18

where you're probably going to live into

1:19

the 22nd century if you do all the right

1:21

things.

1:22

>> And we're going to dig into all of those

1:23

in great detail. But what are the

1:24

unintended consequences of such a world

1:27

where we all live longer? And also, do

1:28

you think it's going to be possible in

1:30

the next 50 years for us to live

1:32

forever? And then, what's the best

1:33

treatment you've discovered for hair

1:34

loss?

1:35

>> This is why I love your podcast,

1:36

Stephen. You asked the right questions.

1:38

So, first,

1:39

>> this is super interesting to me. My team

1:41

given me this report to show me how many

1:42

of you that watch this show subscribe.

1:44

And some of you have told us according

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to this that you are unsubscribed from

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the channel randomly. So, favor to ask

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all of you. Please could you check right

1:51

now if you've hit the subscribe button

1:52

if you are a regular viewer of the show

1:54

and you like what we do here. We're

1:55

approaching quite a significant landmark

1:57

on this show in terms of a subscriber

1:59

number. So, if there was one simple free

2:01

thing that you could do to help us, my

2:03

team, everyone here to keep this show

2:05

free, to keep it improving year over

2:07

year and week over week, it is just to

2:09

hit that subscribe button and to double

2:10

check if you've hit it. Only thing I'll

2:11

ever ask of you, do we have a deal? If

2:14

you do it, I'll tell you what I'll do.

2:15

I'll make sure every single week, every

2:18

single month, we fight harder and harder

2:19

and harder and harder to bring you the

2:20

guests and conversations that you want

2:21

to hear. I've stayed true to that

2:23

promise since the very beginning of the

2:24

Dio and I will not let you down. Please

2:27

help us. Really appreciate it. Let's get

2:29

on with the show.

2:31

[music]

2:34

Dr. David Sinclair, I have waited many

2:37

years to speak to you and I've been so

2:40

keen to speak to you for so many years

2:41

because so much of the research and the

2:45

information I've consumed on the

2:46

subjects we're going to talk about today

2:48

comes from you directly from research

2:50

you've done and from theories and ideas

2:52

and hypotheses that you formed. I think

2:56

the place that this conversation should

2:57

start is is probably with this picture

3:01

because it appears to be incredibly

3:02

formative

3:04

in your journey. Oh yes, that is an

3:08

important picture. True. This is a

3:11

picture of my grandmother and me when I

3:14

was in my early 20s. I'm now 56 if

3:17

you're wondering. And uh my grandmother

3:20

has played a major role in my life. Uh,

3:22

I'm gonna have to be careful not to get

3:24

too emotional because, uh, she's now

3:25

passed pass passed away, but she's

3:27

inspired me to do the best I can to

3:31

leave the world a better place than, uh,

3:33

I found it.

3:34

>> And there's this particular book here

3:36

called Now We Are Six.

3:39

>> It is. Anyone who's read my book, uh,

3:41

lifespan knows that this book is very

3:44

important to me. And I didn't realize

3:45

it, of course, when I was a kid, that

3:47

this was going to change my whole life.

3:51

And there's a poem at the back there

3:53

that my grandmother Vera used to read

3:55

me. When I was six, and it goes like

3:59

this. When I was one, I had just begun.

4:02

When I was two, I was nearly new. When I

4:05

was three, I was hardly me. When I was

4:08

four, I was not much more. When I was

4:11

five, I was just alive. But now I am

4:14

six. I'm as clever as clever. So I think

4:18

I'll be six now forever and ever.

4:22

I'm getting chills reading this again

4:25

and hearing this poem again because the

4:27

impact on me was the following that

4:29

subconsciously my grandmother was saying

4:32

you you don't want to grow up adults can

4:34

be evil. She grew up after World War II.

4:37

There was horrendous uh impact on her

4:39

and her family in Hungary.

4:42

and she thought that a child is innocent

4:45

and people shouldn't grow up. But what

4:48

actually happened was I realized why do

4:50

people grow old? That's a terrible thing

4:53

to happen. And so I've spent my life

4:56

trying to figure out why do we get old?

4:57

Why do we grow up? Why do we get frail?

5:00

Because I also think that if we can

5:02

solve that, understand it, slow it, even

5:05

reverse it now, we will have the biggest

5:08

impact on human health in history. Am I

5:10

right in thinking your grandmother told

5:12

you at that young age that she was going

5:14

to die, that you were going to die, that

5:16

your parents were going to die?

5:17

>> Yes. Uh she did tell me that. I remember

5:20

it very clearly actually. I was on the

5:22

floor and she was crouching down and I

5:24

said, "Vera, I didn't call her grandma."

5:27

She didn't want to be called grandma.

5:28

She wanted to be young like a kid, too.

5:30

I said, "Vera, will will you always be

5:32

here to protect me? Will you always be

5:34

around?" And she said, "No, I'm going to

5:35

die." I'm like, "What do you mean?" She

5:37

goes, "Every everything dies. I'm going

5:39

to be gone. Your parents will be gone.

5:41

Your pet cat will be dead pretty soon.

5:44

And you yourself will be dead one day.

5:46

At age, you know, four or five. That

5:49

that's that's heart-wrenching, right?

5:51

We've all gone through this realization

5:53

around that age that the world that we

5:56

believe in and see will one day all be

5:59

gone. That moment, I remember it so

6:01

clearly because I thought that's not

6:03

fair. Why would any species be made or

6:07

created that knew that fact? That's

6:10

cruel. It's better to either not know or

6:13

to not exist. But to know that that's

6:15

what's going to happen is really cruel.

6:18

And so I I I vowed actually legitimately

6:22

around the age of 18 to get a PhD to go

6:26

to the United States and develop a

6:29

research lab to try and do something

6:31

about it. The preservation of health and

6:33

life is the most important thing that we

6:35

can do as human beings. We do it with

6:38

some drugs to treat that disease and the

6:40

other disease, cancer, heart disease,

6:42

Alzheimer's.

6:44

But what's underlying that? What's

6:45

really causing about 150 to 200,000

6:48

people every day to die is the

6:51

underlying universal process we call

6:52

aging. And for far too long, we've

6:55

ignored it or accepted it as natural,

6:58

therefore acceptable. And I I I

7:00

fundamentally reject the idea that aging

7:03

just because it's natural is acceptable.

7:06

There will be a day when we look back at

7:08

today and think how medieval were were

7:10

our medicines and how sad it was that we

7:13

accepted that we became frail before

7:15

100.

7:17

If someone has just clicked on this

7:19

conversation now and they deep in their

7:21

core

7:23

believe that they're probably going to

7:24

live to 80 years old and that we all are

7:26

and that we're never going to be able to

7:27

do anything about it cuz that's just the

7:29

way that it is. People get old and then

7:30

they die and aging is a fact of life as

7:32

the phrase goes and you just have to

7:35

accept it.

7:37

If that's their sort of core belief,

7:39

what is the what is the most persuasive

7:41

sort of topline argument to that person

7:43

to convince them that in the next two

7:45

hours when we have this conversation,

7:48

we will do a job of both reversing that

7:51

belief or at least challenging it in

7:52

some way and then also presenting them

7:54

with a set of possible solutions.

7:56

>> Yeah. All right. So, first of all, who

7:58

am I? Um, I'm a Harvard professor. I've

8:00

been studying aging longevity and age

8:03

reversal for 30 years. The technology

8:06

now that we have in my lab that is used

8:07

every day by my students literally

8:10

reverses the age of tissues in animals

8:12

in human tissue that we grow in the lab.

8:15

And the first human trials to test this

8:18

are going to be performed in about a

8:21

month from now. And if it works, it'll

8:23

transform human history. It means that

8:25

we're on a path to finally being able to

8:28

reset the age of the human body. Not by

8:30

a year, not by 10 years, but even more

8:32

than that. And what happens when you do

8:34

that? What we're finding in animals,

8:36

that includes primates, is that we can

8:39

cure things that have previously been

8:41

impossible, including blindness, by the

8:44

way. And so, if you're listening and

8:46

you're skeptical,

8:47

I'm not some hack. I am a Harvard

8:50

professor who is telling the world and

8:53

has written a book about it and every

8:55

day spends my life researching with a

8:57

team of the best scientists I can gather

8:59

around the world showing that we can

9:01

literally now reverse the aging process

9:03

and reset how old the body is in

9:06

animals. Yes, but potentially this year

9:09

showing it can work in the human body as

9:12

well. So you're doing the first ever

9:15

trial of this type in humans to reverse

9:18

aging

9:20

next month.

9:21

>> Yes. So we've submitted a form to the

9:25

you know the FDA in the US to get

9:27

approval to treat blindness couple of

9:29

types of blindness in people

9:32

um as early if all goes well as next

9:34

month.

9:35

>> And what what exactly is happening

9:37

there? cuz there's many ways one might

9:39

fix blindness,

9:42

>> you know. What is it you're doing to the

9:45

eyeball that is a precursor of our

9:49

potential ability to reverse aging

9:50

generally?

9:51

>> Yeah. Well, we chose the eye not because

9:54

it was going to work well, but because

9:56

it's a it's a nice system to study age

9:58

reversal. The eye is an enclosed space,

10:01

and so it's much safer than trying to

10:03

initially reverse the age of the whole

10:05

body. Now in mice we reverse the age of

10:06

the whole body and the effect is

10:08

longevity rejuvenation the skin gets

10:10

better all parts of the animal get get

10:13

healthier and younger but in humans you

10:15

you don't want to go straight to

10:17

rejuvenation uh because in case

10:19

something goes wrong it could set us way

10:21

back and we have to make sure we don't

10:23

have any safety mishaps. So we're being

10:26

a little cautious in humans in mice it's

10:29

a little different. So, in the human

10:31

eye,

10:31

>> just for those that aren't watching the

10:33

video, there is a an eye on the table.

10:34

>> Well, a plastic eye. It's a it's a

10:36

larger version of an eye, but yes, uh

10:38

Steven's right. What we're doing, we're

10:40

going to look at the back of the eye,

10:41

which is your retina, and that's where

10:43

the light hits. And at that point, there

10:47

are a lot of nerves that coalesce into

10:50

the optic nerve that runs to the brain

10:53

by just a few millimeters. So, the brain

10:55

is here. The eye is actually part of the

10:57

brain. A lot of people don't know that

10:59

you can touch your brain if you touch

11:00

your eye.

11:01

>> Um,

11:01

>> so the optic nerve gets old and what

11:03

we've discovered if it gets damaged or

11:05

gets old, it's not working. But the

11:07

nerves for most the most part if you're

11:09

old are still there. They just forget

11:11

how to work. And that's aging. And later

11:15

everyone should stick around because I'm

11:17

going to tell you why it is we get old

11:19

and how it is we reverse it. But but for

11:21

this this model, what we're doing is

11:23

we're introducing a set of three genes

11:27

into this optic nerve at the back of the

11:30

eye and turning them on for 6 to 8

11:34

weeks.

11:36

And those three genes are what we now

11:38

know reset safely, apparently safely,

11:42

reset the age of cells, including

11:45

nerves, by about 75% and then stop. They

11:48

don't go more than that, which is good.

11:50

We don't want to go back to zero. I

11:52

don't think anyone wants to go back to

11:54

high school.

11:55

>> But this is the way it works. And we

11:57

chose the optic nerve because it's a

11:59

safe enclosed system, not because it

12:00

should work better in optic nerves. In

12:02

fact, we've now done it in mice in my

12:04

lab for the brain. Uh we're doing

12:07

hearing. We've done skin. Uh we did

12:09

multiple scerosis. Uh we're now doing

12:11

motor neuron disease and seeing great

12:13

effects. So it's important to know I'm

12:16

not an eye specialist. I didn't choose

12:17

the eye cuz I love the eye. I chose it

12:19

because that's a good place to start for

12:21

age reversal in humans this year.

12:24

>> You mentioned a second ago you've been

12:25

able to extend the life of mice in your

12:28

laboratory.

12:30

How and by how much? Is it the same

12:31

process and by how much?

12:33

>> Right. Well, the the study that that I

12:35

was referring to was done using our

12:37

technology in an independent lab, which

12:40

is you might argue even better than

12:42

having done it in my lab. Instead of

12:44

putting the three reversal genes into

12:46

the eye, they injected into the vein of

12:48

the mouse, the old mice, uh, and turned

12:51

it on in these really old mice. These

12:52

mice would be the equivalent of about 80

12:55

to 85 years. So, they're really old

12:57

mice. They're really frail. And just any

13:00

any extension in their lifespan and

13:02

health would be bet would be a great

13:03

thing. And they got an additional 100%

13:06

lifespan extension. Additional. So,

13:09

>> that would be like an 80-year-old living

13:11

to 160. Well, the remaining life of an

13:13

80-year-old isn't long.

13:15

>> Oh, okay.

13:16

>> Right. So, let's let's say if you're

13:17

give it to a 70-year-old on average,

13:19

they'd have another 10 years to go. Give

13:22

them 20 years. So, it's that

13:23

calculation. Um, but that was not an

13:26

optimized study. They just did a Hail

13:27

Mary injection, turn it on, see what

13:29

would happen.

13:30

>> And I I heard when we did a bit of a

13:32

research call, you say, "The world

13:34

doesn't know how close we are." The

13:37

world doesn't know how close we are to

13:39

what? to being able to safely reverse

13:42

the age of the human body.

13:45

>> How can you be so sure?

13:47

>> I'm not sure. But I'm confident that the

13:50

science is solid, right? That the the

13:53

biology of aging is is understood. I

13:57

believe in concept. My theory called the

14:01

information theory of aging has so far

14:04

been not disproven, which is important

14:06

for a scientist. And that has allowed us

14:11

to succeed really for the first time to

14:14

safely reverse aging. And I now believe

14:17

and though I didn't 10 years ago, I now

14:19

believe in my lifetime I'm going to see

14:22

medicines on the market that reset the

14:24

age or at least reverse in a large part

14:27

uh the age of the body. And that that

14:30

initially won't be to make us just look

14:33

better and feel better, although that's

14:35

what a lot of us want. It's going to be

14:37

used to cure, certainly prevent, but

14:40

definitely cure diseases that are

14:42

currently incurable. So, we're I think

14:44

we're at a turning point, dare I say, in

14:47

human history. It's not a question of

14:49

if, it's a question of when this is

14:50

going to happen.

14:51

>> I want to get into your theory of aging,

14:53

which we talked about there. Um, but you

14:55

did have a prediction before I get to

14:56

there about

14:59

how you think we'll be potentially

15:01

taking a pill in 10 years time every

15:05

couple of weeks that will make us

15:06

younger. Can you explain to me that

15:07

prediction? What is what is the

15:09

prediction?

15:09

>> I I do believe that I and you're about

15:13

20 something years younger than me.

15:14

You're going to see this for sure that

15:17

there will be a pill. So you might say,

15:18

"Well, my critics might say, "Well,

15:20

David, that's exaggerating, right?

15:22

You're still trying to get this gene

15:24

these genes to work. How's it going to

15:25

be a pill? But this is where my lab

15:28

comes in. My lab is like Willy Wonka's

15:30

chocolate factory if you visit. It's

15:32

magical. And the students that I teach

15:34

and the trainees who are sometimes in

15:36

their 30s and even 40s who are, you

15:38

know, brilliant scientists. Uh there's

15:40

about 25 of us. They are making

15:43

discoveries that blow me away every

15:46

week. It's not a pill cuz you can't give

15:47

a mouse a pill. They won't chew it. But

15:50

we give them a liquid down their throat.

15:52

It's a drink. And within four weeks, we

15:54

can rejuvenate them. Not with this this

15:57

these genes anymore that we're giving

15:58

humans. That's the old older technology.

16:01

The new technology is something you can

16:04

swallow

16:06

in a mouse and rejuvenate them in 4

16:07

weeks. It's normal for my students to

16:09

say, "Oh yeah, we just rejuvenated the

16:12

ear. We just rejuvenated the skin. uh we

16:15

just cured ALS, motor neuron disease in

16:18

these animals. By the way, speed and

16:20

Stephen, this isn't just each disease

16:22

doesn't get a different medicine. Each

16:24

disease doesn't get a different set of

16:26

genes. It's the same set of genes, the

16:28

same molecules that treat cure multiple

16:32

scerosis as the same one that cures

16:34

blindness in mice.

16:36

So, let that sink in. The same drug that

16:40

we're using in the eye will be used to

16:41

treat other diseases in the body, even

16:43

liver disease. So if if your predictions

16:45

are correct and your timeline is

16:47

correct,

16:49

what does this mean for the way that I

16:52

should be living my life right now?

16:54

>> Most people look at their parents and

16:56

their grandparents and think that's what

16:57

my life will be like. I'm going to be

16:59

frail in my 80s. That's not true for us.

17:02

I like the Wright brothers analogy. It'd

17:04

be like in 1900 saying we're always

17:06

going to travel as fast as a horse.

17:08

That's not true, right? The 20th century

17:11

saw that we could go tens of thousands

17:14

of kilometers. They went to the moon,

17:15

right? That's what our generation is

17:18

when it comes to biology and aging.

17:21

Previous generations are no guide to

17:23

what our lifespan is going to be like.

17:24

You're going to potentially live to the

17:26

22nd century. If you do all the right

17:29

things, technology keeps increasing,

17:31

right? What kind of technologies will we

17:32

have in 50 years?

17:33

>> You'll be around in 50 years.

17:35

>> Hope so.

17:36

>> You're a healthy guy. I know you are.

17:38

All right. So in 50 years, what kind of

17:39

things will you be able to do?

17:41

>> Gosh,

17:42

>> this is what most people forget is that

17:44

technology isn't static. When you're

17:47

old, you will not be using today's

17:48

technology. You'll be using technology

17:51

of 2070, 2080, right?

17:54

>> And then you'll be able to live into the

17:56

22nd century and take advantage of those

17:58

technologies. That's why people talk

18:00

about the singularity. The singularity

18:02

is this idea that if you can make it to

18:04

a certain point in human history, you

18:06

won't have to age anymore.

18:09

And that that's in the future, right?

18:10

But first steps first, let's show that

18:12

we can get this to cure blindness and

18:14

then get to the point where every year

18:17

that we get one year older, we can get

18:20

one year younger. When that happens,

18:22

it's a very interesting world, right?

18:23

You don't have to age anymore. That is a

18:26

future. I don't know when we're going to

18:27

get there,

18:29

but if you don't live 10 to 20 years

18:31

longer than your parents, something's

18:33

wrong

18:34

>> on that point of the singularity. So,

18:35

this is a particular moment in time

18:38

where we're going to be able to make

18:39

aging or age reversal, I guess, a

18:42

choice, right? So, the I guess the

18:44

thinking or the theory is that if you

18:45

can just make sure you survive up until

18:48

this particular date, then you have the

18:50

choice to live forever. Is that how is

18:52

that like the

18:53

>> Well, that's what they say. Yes. Uh

18:54

there are a lot of proponents of that,

18:56

but that that's an idea. And

18:58

>> isn't it logically true though? It's

18:59

like logically

19:00

>> it's an Yeah, it's an extension of what

19:02

I'm I'm talking about. Um but I don't

19:04

know when that's going to be. It's I

19:05

think Ray Curtzwell said it's coming

19:08

soon.

19:08

>> Did he have a prediction? I think

19:10

>> it was in the 2040s sometime.

19:11

>> So Ray Curtzwell is a famous futurist

19:13

that seems to predict the future really

19:14

well um across multiple disciplines. So

19:17

he said 2040.

19:19

>> Yeah, that's my recollection. It's

19:20

around there.

19:21

>> Do you believe that? because I'm going

19:24

to hang on till 2014. I'm

19:25

>> skeptical. I won't leave the house.

19:26

>> I mean, Ry is a smart guy, right? He

19:28

predicted AI and all that's happening.

19:31

So, it's it's it's dangerous to bet

19:32

against Ray's predictions. I I remain

19:35

skeptical. You know, as one of the

19:37

leaders in the field, I think we have a

19:38

lot still to do. That said, if this

19:41

trial works this year, we will be in new

19:44

territory. We will be on a path to age

19:46

reversal in the whole body. It's going

19:48

to happen. And you know, and right now

19:50

it's now 2026. We're talking

19:54

2040 is a number of years away. It could

19:56

be that we truly are able to multiply

19:59

reset the age of the body. That's that's

20:02

another thing that that's often missed.

20:04

We can re reverse the age of the eye not

20:07

just once, but seemingly as many times

20:09

as we want. In mice, we've done it at

20:12

least twice. We didn't do it a third

20:14

time because the mice actually just got

20:16

old and they died. But they died with

20:17

perfect eyesight. But the point is that

20:20

we we don't believe it's a one-shot

20:22

wander. You can keep reversing aging and

20:24

then you age out and then you reverse it

20:26

again and you just keep going. And if

20:29

that's true, then it is possible that we

20:31

will live dramatically longer. I don't

20:33

yet see any technology in the near

20:35

horizon that will make us live forever.

20:38

But I do see that we'll have a radical

20:40

change in how we treat diseases and how

20:42

long we can live.

20:43

>> So let's talk about what aging actually

20:46

is. And can you explain this to me like

20:47

I'm a total idiot because that will

20:49

help.

20:49

>> Well, that's difficult because you're

20:51

not a total idiot. But this is my theory

20:53

is that aging is not just wearing out.

20:56

It's not just that your body becomes old

20:59

and dysfunctional and you get pain, you

21:03

get inflammation, and you die from a

21:04

disease. I look at the body like it's a

21:07

a computer. It's software

21:10

and we can reinstall the software. In my

21:13

lab, we believe we've found the way to

21:15

do that and we see the evidence of that.

21:18

So, the body is a carrier of information

21:21

from our parents and what happened in

21:23

the womb. That information is intact.

21:27

Keeps our body functioning almost

21:30

perfectly in our teenage years, 20,

21:33

you're in your early 30s. You're

21:34

starting to lose that information and so

21:38

your body's not functioning perfectly

21:39

anymore.

21:40

>> Gray has

21:41

>> you've got some gray. Exactly. That's a

21:43

good example of cells that lose their

21:46

identity and stop making melanin, the

21:48

black pigment.

21:49

>> But it's going to get worse. I promise

21:51

you, unless you know, unless we we're

21:53

hurry up and uh gets lost. It gets

21:56

corrupted. But the beautiful thing is we

21:59

believe we found a backup copy of that

22:01

information from youth that we can

22:03

reinstall into cells, into tissues, into

22:05

the entire body of a mouse and hopefully

22:08

a human. That backup copy is in every

22:11

old person, I believe, and it can be

22:14

accessed. So when I see an old person

22:16

walking down the street now, I don't

22:17

think, oh, that person's just worn out,

22:18

frail, going to die. I just think that's

22:20

someone that needs a reset. And inside

22:23

that person is a young person waiting to

22:25

come out again. That's a totally

22:28

different way to think about old age.

22:30

And in the future, people will have a

22:32

choice to be rejuvenated or not.

22:35

>> Where is that backup copy that I need?

22:38

>> Well, we're working on that. And uh if I

22:41

if I told you, my student would kill me,

22:44

but we believe we've found

22:47

largely where that information is

22:49

stored. It's entirely new biology.

22:52

>> And it's currently a secret.

22:53

>> It's a secret.

22:54

>> Okay. So, you you you lead the way. Tell

22:56

me what we should we should talk about

22:57

next as it relates to aging.

22:59

>> Let's talk about information, right? We

23:00

live in the information age and biology

23:02

is becoming part of that information

23:04

age. And it started with the uh

23:08

elucidation of the structure of DNA.

23:11

Okay. And so I have I have a model of

23:12

DNA here. So for listeners who are not

23:14

watching this is a little plastic double

23:17

helix. My friend uh Jim Watson uh died

23:21

recently last month who he and his

23:24

colleague discovered that DNA the

23:26

information of life that we get from our

23:28

parents is a chemical that's about 6 ft

23:30

long in every cell and uh this model

23:33

here shows that DNA is a ladder and the

23:36

steps on the ladder are the information

23:38

of the DNA.

23:39

>> Okay.

23:40

>> Yeah. And you can pull this apart so

23:42

that each step becomes 50 50% ripped

23:46

apart. So that should come apart. Right.

23:48

So I ripped the rung of the ladder apart

23:51

and that is called a base on the DNA and

23:54

it always matches with its corresponding

23:56

chemical. So this short hand we call an

24:00

A. It always matches with a T. So an A

24:03

becomes a rung on the ladder. And down

24:06

here different color here I'm looking at

24:07

a red and a green step. Rip it apart.

24:11

This is a G and a C letter. G's and C's

24:13

come together. And actually when if you

24:15

if I rip this ladder into halves and

24:18

each step becomes half a ladder. Now you

24:20

can see that you can copy DNA because

24:23

the A has to match with the T wrong and

24:26

the G has to match with the C. So that's

24:28

basic DNA. That's how the information is

24:30

transferred from cell to cell from

24:33

mother to daughter parents to offspring.

24:37

There are about 20,000 genes. about

24:39

15,000 are turned on, but a different

24:42

set gets turned on in large part uh to

24:46

make a nerve cell compared to a liver

24:48

cell and a skin cell.

24:50

>> That's gene expression. And what

24:53

controls that gene expression is what's

24:55

called not not the genome, which is

24:57

what's in front of me here on the DNA

24:58

molecule. It's the epi genome. The

25:02

epiggenome is the information we get

25:05

transferred from cell to cell, from

25:07

parent to offspring that's not in this

25:09

molecule.

25:11

So where's this epigenetic information?

25:14

Well, it controls which genes are

25:16

switched on and off. And a major

25:18

regulator of that process

25:21

is the modification of these steps on

25:24

the DNA. these chemicals, the C,

25:27

particularly the C, which I'm showing

25:30

you here, uh, in this red part of the

25:32

the molecule, the C gets a little

25:34

chemical added to it called a methyl.

25:37

And a methyl is just, if you remember

25:39

from chemistry, high school, uh, it's a

25:42

carbon with three hydrogens. It's very

25:45

simple molecule. It gets stuck on that

25:47

piece of the the DNA molecule. That's

25:50

called DNA methylation. And that will

25:52

help determine that pattern of DNA

25:54

methylation determines whether this

25:57

particular gene will be switched on say

26:00

to make an optic nerve or switched off

26:02

so that it becomes a liver cell. And

26:05

that happens as we're in the womb and we

26:07

become an embryo. [snorts] And that's

26:10

the epiggenome. These chemicals that

26:12

turn genes on and off is the epigenome.

26:15

And the information theory of aging

26:18

states that the information that's in a

26:22

cell, which includes the DNA, but

26:25

actually more importantly for aging is

26:27

the control systems, the epiggenome that

26:31

is pristine when we're young, but as we

26:33

get older, we lose that epigenetic

26:35

information. The ability to tell a cell

26:38

to be a nerve cell versus a liver cell

26:40

versus a skin cell, it starts to get

26:42

erased. So it when we look at a mouse or

26:45

or an old tissue, if I took maybe not

26:47

your skin, but but my skin, my skin

26:50

cells are no longer as skin-like as they

26:53

once were. They've started to lose their

26:57

identity. They're starting actually to

26:58

to look more like nerve cells and nerve

27:00

cells starting to look more like skin

27:02

cells because the genes that were once

27:05

turned on correctly in my young cells

27:08

that that control system, these

27:10

chemicals on the DNA molecule, these

27:11

methals are getting erased.

27:13

>> So aging is an identity crisis of the

27:15

cells.

27:16

>> It absolutely is. Well put.

27:17

>> The cells forget what their job is.

27:21

>> Yes, the genes are still there in large

27:24

part. 99.999% of the genes are still

27:27

there. The molecule's intact,

27:29

but the control systems,

27:31

>> the label thing you mentioned,

27:32

>> the label to tell the cell that this

27:35

gene needs to be on, but this one should

27:37

always stay off. That gets erased over

27:39

time.

27:39

>> Why?

27:40

>> H we we did partially figure that out.

27:43

>> And how do you know?

27:45

>> Well, oh, even better.

27:47

>> This is this is why I love your podcast,

27:49

Stephen. You asked the right questions.

27:52

these there are enzymes that remove

27:54

these methyl groups um and put them back

27:57

on. So the cells controlling these

27:59

things they shouldn't change but they

28:00

do. And one of the things that messes

28:03

the system up is

28:06

major catastrophe in a cell. And when

28:08

the cell panics

28:11

it removes these structures to try and

28:13

adapt to the stress

28:15

>> the label

28:15

>> the label comes off in a desperate

28:18

attempt to survive. But then the cell

28:21

doesn't fully revert back to the

28:23

original state. Some of these chemicals

28:25

and some of the proteins that bind to

28:27

the DNA, which is also important for

28:28

this epiggenome, they don't all go back

28:30

to where they started. I've used the

28:33

analogy that uh it's like a pingpong or

28:36

a tennis match where the proteins that

28:38

control the genes, they they get

28:41

relocized to where the emergency is. and

28:44

an emergency. One, the one that we think

28:46

is most dangerous and a large c of cause

28:49

of aging is a broken chromosome. If you

28:52

have a broken chromosome, if you don't

28:53

fix that, you're either going to become

28:55

a cancer cell or you're going to die.

28:56

It's not good. Um, and so cells panic.

28:59

And in that panic of moving proteins

29:01

away and turning on these stress

29:03

response genes, uh, that's great in the

29:06

short term. The cell might survive, but

29:08

they don't fully reset. those proteins

29:10

don't all go back to where they once

29:11

were say 10 minutes ago when the stress

29:14

needed to be the disaster happened. And

29:17

if you do that time and time again and

29:19

every one of your cells has at least one

29:21

broken chromosome every day that's 20

29:24

trillion of these events every day in

29:26

your body over time tick tick tick you

29:31

get the aging process we believe.

29:34

>> So I I guess I've got two questions. Uh

29:36

I guess the first question if I was

29:38

thinking about the sequence of asking

29:39

these questions is

29:41

what is increasing that stress on my

29:45

cells? Therefore what is increasing

29:46

aging? And also like why didn't

29:48

evolution just come up with a solution

29:50

for this that stopped me aging then?

29:52

>> Like evolution is very smart. Couldn't

29:53

it just fix this?

29:54

>> Well before I get into that uh one of

29:56

the the reasons we know that this works

29:58

because you asked me how do we know

29:59

that's true is that we created this this

30:03

catastrophe in animals. We we took mice

30:06

and we we we broke their chromosomes in

30:09

a way that didn't cause [clears throat]

30:10

cancer or mutations.

30:12

If we're right, what should happen to

30:14

these mice?

30:15

>> They get old fast.

30:16

>> They get old fast.

30:17

>> Gray hair.

30:18

>> And they did. We call them the ice mice.

30:21

Ice stands for inducible changes to the

30:23

epiggenome. And we were able to induce

30:25

these changes. And we took bets in the

30:28

lab. This is going back now 12 years

30:30

ago. Uh I I bet that we would get aging.

30:34

Okay. But I was the only one in the lab

30:36

that thought that that would happen. We

30:38

had a lot of bets that the mice would

30:39

die, a lot of bets that the mice would

30:42

get cancer, and a few said nothing would

30:44

happen. But we got aging. In fact, I was

30:47

I was in Australia where where I'm from,

30:49

as you know, and I got a picture on my

30:51

old old style iPhone and it was a

30:54

picture of an old mouse. Uh well, it was

30:57

a sick-l looking mouse and the and the

30:58

the text was problem. We have a sick

31:01

mouse and I wrote back, "That's not a

31:02

sick mouse, that's an old mouse." And

31:04

that was the first time I realized that

31:06

we'd had evidence that our theory, the

31:10

information theory of aging is correct.

31:12

So what we did actually, and this might

31:14

satisfy your and your listeners

31:15

curiosity, we generated a mouse from

31:18

scratch using stem cells. And so we

31:22

start with a a mouse stem cell that we

31:23

grow in the lab in the dish. And we

31:26

changed the genetics of that stem cell

31:29

so that we could feed it a drug uh

31:32

tmoxifen which is used uh in in

31:35

chemotherapy. And that drug turned on

31:39

a gene from a slime mold, something you

31:41

might find in the forest that breaks DNA

31:44

of the mouse but does it in a way that

31:47

doesn't cause cancer or mutations. Just

31:49

cuts it and the cells put it back

31:50

together. So we could take a mouse and

31:53

for 3 weeks we turned on this slime mold

31:57

cutting protein and nothing happened to

32:00

the mouse at the time. It's like a you

32:02

don't feel an X-ray. You don't feel

32:05

different when you fly except for maybe

32:06

jet lag and dehydration. But you don't

32:08

get old suddenly. Same with the mice.

32:10

They were normal. They felt fine. And

32:13

that's why at first people said, "Oh,

32:14

nothing's going to happen to these

32:15

mice." After 3 weeks they were fine. But

32:18

we set in motion a cascade of

32:20

accelerated aging events that about 10

32:24

months later they were super gray and

32:26

super old and had all the diseases of

32:28

aging 50% faster than their twins that

32:31

we didn't treat.

32:32

>> And you've got photos of those we could

32:34

show.

32:34

>> Yeah. Yeah. Let's show those. So, if I

32:36

was to do the experiment in you, I might

32:38

have to engineer it a clone of you, but

32:41

I could do that. Uh, you know, I'm not

32:43

saying that it's ethically right, but

32:45

but theoretically we could make a clone

32:47

of you, put in that slime mold gene,

32:49

turn it on,

32:50

>> and your clone would be 50% older than

32:53

you are.

32:54

>> Can you translate this into the equival?

33:01

So, it would be like in me doing what

33:04

and then me getting old fast.

33:06

>> Yeah. Uh, well, we're exposed to to

33:08

things that cause DNA breaks all the

33:09

time. They happen naturally as the cells

33:11

try to copy their DNA. But you can

33:13

accelerate that by getting an X-ray, a

33:15

CT scan, flying a lot and cosmic rays

33:18

banging into your DNA. And

33:20

>> I fly all the time. I've had loads of CT

33:22

scans and X-rays.

33:23

>> Yeah. Uh and and though it's

33:26

imperceptible, I believe that that's

33:27

probably accelerating your aging

33:29

process.

33:29

>> What's flying doing to my So again, you

33:32

talked about flying being equival to

33:33

what you did to the mouse. In what way?

33:35

Well, every time you break your

33:37

chromosome, you're rearranging your

33:39

epiggenome in a catastrophic way that

33:42

doesn't fully reset and your cell will

33:44

lose its identity faster. I also believe

33:47

um and we have some evidence that even

33:48

going to a rock concert and have

33:50

blasting your eardrums is such a stress

33:53

on those cells in your ear that the

33:55

reason that you become deaf earlier is

33:57

because your ear hair cells are getting

33:59

older faster. You don't want to break

34:02

the DNA. You don't want to cause

34:04

catastrophe to your fragile cells in

34:06

your body because the recovery isn't

34:08

complete and aging ensues.

34:11

>> So, with this theory in mind, what are

34:13

the day-to-day things that we're all

34:15

doing that are accelerating our age?

34:17

Like, cuz I think what's really

34:19

interesting is I looked at my brother

34:21

Jason. He's a year older than me. He has

34:23

three kids that are like under the age

34:25

of seven or eight now. And this

34:28

Christmas time, cuz it's just been

34:29

Christmas, I looked at his hair to see

34:31

how many gray hairs he had versus me.

34:33

And I thought, "Okay, he has

34:34

considerably more.

34:36

>> He's a year older than me." And I was

34:38

thinking that's like a a proxy of aging

34:41

to some degree. What is it he's

34:43

potentially done on a day-to-day basis?

34:45

I know you don't know him, so this is

34:46

why it's not not an offensive uh answer

34:48

to give. What is it that someone who is

34:52

generally sort of genetically very

34:53

similar but is making different

34:54

lifestyle choices is doing to accelerate

34:57

that process of wrinkles or gray hairs

34:59

or well here's the good news that you

35:02

can have a big impact on your rate of

35:04

aging by changing your lifestyle. It

35:06

turns out your DNA is not your destiny.

35:08

It's the epiggenome. So that how you

35:10

live your life is really 80 to 90% of

35:13

your rate of aging.

35:15

That's good. It's in your hands. But it

35:16

also means that some people mess up

35:18

their lives. There are actually twin

35:20

studies from uh mostly from Denmark,

35:23

identical twins, one that goes and

35:25

smokes and gets obese and uh goes in the

35:28

sun and they are much older looking than

35:31

their identical twin. Essentially

35:34

proving that the DNA is not the reason

35:36

you age. First of all, they're going to

35:38

be people in the audience uh who are

35:39

listening or watching who have gray hair

35:41

saying, "Damn it, I'm not old." And

35:44

that's true. I mean, nobody died of gray

35:45

hair, right? And sometimes genetically,

35:48

you can get gray old uh but not be

35:51

physically old. What is true that's

35:53

often not comfortable is how old you

35:56

look is a very good representation of

35:57

how old you are in your organs as well.

36:00

So, doing the right things. So, what are

36:02

those things? Let's tick off some of the

36:03

major things that people should be doing

36:06

and they can have a big impact. They can

36:07

lengthen your life by a decade just by

36:09

doing some of the major things. So, we

36:11

know that on average people can live 14

36:13

years longer. This is based on a study

36:15

that came out from Harvard, a long-term

36:17

study of the lifespan of World War II

36:19

veterans. If you avoid smoking,

36:22

cigarette smoking, and really any type

36:24

of smoke in your lungs, smoking breaks

36:26

your DNA. It's going to accelerate aging

36:27

in your lungs, your whole body. Avoid

36:30

excessive drinking. We now know that

36:32

even more than one glass a day of

36:34

alcohol is bad. I've given up alcohol

36:37

for the most part for that reason. Eat

36:39

well. So, you want to eat healthy food.

36:41

We've got some healthy food here we're

36:43

going to talk about. Um, so make sure

36:45

you you don't uh overeat or eat

36:48

ultrarocessed foods. And the big one,

36:51

one of the best things you can do

36:52

besides all of that is exercise. Okay?

36:55

And exercise covers a lot of things. So,

36:57

we can drill into that as well. But the

36:59

fifth one is interesting. It may be

37:01

surprising, but actually good news for

37:03

you. Have a reliable partner.

37:05

>> I think you're going to say be a

37:06

podcaster. I was going to Okay.

37:08

>> Oh, [laughter] no. That probably

37:09

accelerates your age. Yes. So, um, if

37:11

you don't have a reliable partner, have

37:13

a pet because the human bond is

37:16

something that is shown to slow aging

37:19

and associates with people who live

37:22

longer than others that are lonely.

37:25

>> Interesting. We're going to dig into all

37:26

of those in great detail. Specifically,

37:28

very interested in in exercise, diet,

37:31

lifestyle, fasting, I know is a big

37:32

subject you speak about which I'm very,

37:34

very interested in. And actually, as I

37:35

was doing the research into this

37:36

conversation,

37:37

again, my the way that I'm going to

37:39

approach nutrition has shifted because

37:41

of some of the things I discovered

37:42

there.

37:43

>> I want to just tick off on this

37:44

evolution point,

37:45

>> right? Let's come back to that.

37:47

>> Yeah. I just want to get clear. Yeah.

37:48

Like, why didn't evolution fix it for

37:51

me? Because they talk about survival of

37:52

the fittest and that the very fact that

37:55

I'm here is because my my ancestors were

37:56

good at survival, but listen, my

37:58

ancestors all died at like 30, 40, 50,

38:00

60, 70, 80 years old. That's not very

38:01

good. Why? Why didn't they just live

38:03

longer?

38:04

>> Well, that's why. You just said the

38:06

answer yourself. Because your ancestors

38:08

didn't live beyond 40 or 50, even less,

38:11

right? Most men uh in prehistoric times

38:15

would die from [clears throat] famine,

38:17

disease, and actually a lot of them from

38:19

war. So, most people didn't make it 80.

38:21

Some people did, but very, very rarely.

38:25

So the the forces of natural selection

38:27

were on early survival and fast

38:31

breeding. Let's put it this way. If

38:33

there was someone who was born with a

38:35

mutation that allowed them to live a lot

38:38

longer to 90 in a prehistoric world,

38:41

that's useless because you're probably

38:43

going to die at 30 or 40 anyway and so

38:44

are your children. [clears throat] So

38:46

what you want to do is find genes that

38:47

allow you to become reproductively

38:50

successful early on in life. um and make

38:53

sure your children survive. And so we we

38:55

have children pretty early, but humans

38:58

for for various reasons have a long

39:01

developmental period including

39:02

education. So we don't we don't develop

39:05

very rapidly, right? We don't wake up

39:07

and we can walk and run like a lot of

39:08

other species and mammals. [gasps]

39:10

But we don't live a long time because

39:12

there was in the environment that we

39:14

evolved, the Serengeti plane is pretty

39:16

much agreed upon as that's one of the

39:18

places we evolved. Certainly uh Eastern

39:21

Africa that was extremely difficult and

39:24

dangerous place to live. You could get

39:27

eaten by an animal and if you didn't get

39:29

eaten by an animal you get killed by the

39:31

neighboring tribe. That's super

39:33

dangerous, right? And then so we we

39:35

evolved to live really at optimal to

39:38

about 30

39:41

but not much more than that. So after

39:43

30, as you might be experiencing with

39:46

with your body,

39:47

>> we're at the forces of entropy. So the

39:50

body starts to decay. The information

39:53

starts to get lost in the body.

39:56

But the the good news is that if you

39:58

take away predation and death from a

40:01

species, it evolves longer lifespans.

40:04

Now, it makes evolutionary sense to have

40:07

genes that allow you to put more effort

40:10

into building a strong body and slowing

40:12

down the aging process and preventing

40:14

DNA breaks, chromosomal breaks. We know

40:17

that this is true because if you put

40:19

species, say, on an island where there

40:22

are no predators, what happens to their

40:24

longevity?

40:26

They get longer lived naturally. It

40:28

takes 20, 30 generations, but only when

40:32

there's no predation, when you're not

40:34

under a lot of stress to uh breed

40:37

quickly, do you get longer lifespans

40:40

evolving. Given that humans don't have

40:42

predators anymore, we are slowly

40:44

evolving,

40:46

longer lifespans. But it's very slow and

40:48

it's not going to happen fast enough for

40:50

you and me.

40:50

>> And do the organisms that do live

40:53

really, really long have a small amount

40:56

of predators in nature? Absolutely.

40:58

Absolutely. Think about them.

41:01

>> The bristle cone pine.

41:02

>> What's that?

41:03

>> It's the longest lived tree in the

41:05

world. It can live many thousands of

41:07

years.

41:08

>> It's Are you jealous?

41:11

>> Not jealous. No. [laughter] No. They

41:13

live a tough life. Some of those trees

41:15

have been around since the pyramids.

41:17

>> Wow.

41:18

>> The reason they live can live for so

41:19

long and evolve to live so long is that

41:21

things don't eat them. They're totally

41:23

poisonous. You you don't want to eat a

41:24

bristle conine. The same for a whale,

41:27

right? The boowhead whales, some of

41:28

these very large animals, no predators.

41:30

So, they've evolved a strategy of

41:32

breeding slowly, but building very

41:36

powerful systems to stop epigenetic

41:39

changes. Their epigenetic control

41:41

systems are stable. They don't get

41:44

cancer and they they don't lose they

41:46

don't have this identity crisis until

41:48

hundreds of years. And we know that

41:50

people study the cells of whales in the

41:53

dish and those cells don't lose their

41:55

identity very quickly even when you

41:57

break their DNA.

41:58

>> So I I guess the place also to to go

42:01

next is talking about disease generally

42:04

and what disease is. So are these

42:08

diseases a function of aging? Does this

42:09

idea of reversing aging even matter if

42:12

cancer is going to take most of us out

42:13

anyway at some point? Is there a link

42:16

between aging and disease? This might be

42:18

the most important point that I make

42:20

today.

42:21

When you reverse aging, diseases of

42:24

aging go away or are cured. And in my

42:28

lab, including many types of cancer as

42:30

well.

42:32

The diseases that we try to treat

42:34

individually with different medicines

42:36

today that we think are unrelated,

42:38

Alzheimer's, cancer, heart disease, you

42:40

name them. Fundamentally, what's driving

42:43

a lot of those diseases is aging.

42:47

If you never got old, would you ever get

42:49

Alzheimer's even if you had the genes

42:51

that predispose you? No.

42:54

Right? And so what we see in my lab is

42:56

when we give an animal a disease and we

42:58

can do that. We can put in the human

43:00

genes for Alzheimer's into a mouse, it

43:03

becomes has dementia. When we reverse

43:06

the age of the brain of that animal,

43:08

we're not treating the disease. We're

43:10

treating aging. The disease goes away.

43:13

The body can heal itself when it's

43:15

young. So, it's the aging process that

43:18

reveals the disease that can be cured by

43:22

reversing.

43:22

>> Why does the aging process reveal a

43:24

disease? Why don't we get Alzheimer's at

43:27

15?

43:28

>> Because the cells are so healthy, they

43:30

can fix themselves. They can renew

43:32

themselves. The disease processes that

43:35

cause these problems for us don't exist

43:38

when we're young. Why is it that a

43:41

teenager rarely has a heart attack?

43:43

because their body prevents them. Why do

43:47

young people typically not get cancer?

43:49

Because the immune system finds cancer

43:52

cells and clears them out. You and I

43:54

have cancer cells in our body right now.

43:56

Why are we probably not going to die in

43:58

the next year? Cuz our immune system

44:00

will find them and kill them. But as we

44:02

get older, we're going to lose that

44:03

ability and we'll have a greater chance

44:05

of having cancer.

44:06

>> So, are you saying that if we cure

44:08

aging, we're probably going to by way of

44:10

that cure most of these diseases?

44:12

>> 100%.

44:13

We were talking about um

44:16

menopause quite a lot on this podcast

44:19

and fertility, menopause, women's

44:21

ovaries as um one of the first places

44:24

that ages. And I've heard you explain

44:26

that you think that evolution programmed

44:28

women to stop having children during

44:29

menopause because continuing

44:30

reproduction would drain energy needed

44:32

to raise existing children. So is

44:35

infertility something that could

44:36

theoretically be prevented? in mice,

44:39

which is where we live in my lab where

44:41

we work, it can be prevented and it can

44:44

be reversed.

44:45

>> I thought we'd run out of eggs. That's

44:47

like the

44:47

>> that's the current theory. The evidence

44:50

that we have from my lab and a lab that

44:52

I worked with in Australia

44:56

caused me to question that idea that we

44:58

run that women run out of eggs.

45:02

We have published and repeated many

45:04

times that if you treat old female mice

45:10

16 months of age, which is like a 65,

45:13

70year-old human that has long time

45:16

since given up having offspring,

45:20

we can treat the ovaries with a chemical

45:23

that rejuvenates the eggs that are in

45:26

the ovary, maybe even produces new ones.

45:29

We don't know for sure, but those

45:32

16-month-old mice that stopped having

45:34

kids a uh probably at least 6 months ago

45:38

now start producing healthy offspring

45:40

again. Their eggs look young, pristine,

45:44

compared to the terrible eggs that if

45:46

you try to harvest some eggs from a

45:47

mouse that old, it's hard to find any

45:50

that look normal. The chromosomes are

45:52

messed up, ripped apart. They're not

45:54

going to produce healthy babies. But we

45:56

can take those eggs or at least the

45:59

ovaries with those eggs in them and

46:01

cause them to be young again and make

46:03

fresh eggs that can produce healthy

46:05

offspring that live a normal lifespan.

46:08

The real question is will this work in

46:10

women? And that's something that I'm

46:12

keen on testing.

46:15

>> It must be really hard to test a lot of

46:17

these things in people, right? Because

46:18

we you've mentioned the word mice quite

46:20

a lot.

46:20

>> It's harder than you can imagine

46:22

actually. Um, and I've spent a lot of my

46:24

career since I was 35, um, aiming to

46:27

develop a medicine to treat diseases and

46:30

aging. And it can be it can go wrong in

46:34

many ways. Um, even if the science is

46:36

good and right. Um, and it it's there's

46:39

money, there's business, there's laws,

46:42

there's politics, there's business

46:45

strategies, there's change of

46:46

leaderships.

46:48

um all sorts of human introduced

46:52

variables that can get in the way.

46:54

There's patents and uh and then there's

46:57

there's competition and spite that also

46:59

gets into it. Um and I've had to deal

47:03

with all of those things. Um including

47:05

competing against some of the largest

47:06

pharmaceutical companies in the world

47:07

who really didn't want me to succeed.

47:10

But yeah, it's extremely difficult to

47:12

make a drug. But I do want to remind you

47:15

and everyone listening and watching that

47:18

we're beyond mice now for age reversal.

47:20

We've done this in monkeys. Monkeys that

47:22

are physically and almost genetically

47:25

identical to us. So it's not a big leap

47:28

from It is a pretty big leap from mouse

47:30

to human, but from a monkey to a human.

47:32

It's we're essentially, you know,

47:34

slightly smarter monkeys.

47:36

I just had a thought about how other

47:39

countries and other nations might be

47:42

conducting their own sort of secret

47:43

research and they might not have the

47:45

same bureaucratic political ethical

47:48

considerations that you have to contend

47:50

with. Do you think about this much that

47:52

some of the sort of geopolitical

47:54

adversaries might be doing secret

47:56

testing in some research lab somewhere

47:58

on humans?

47:59

>> I think about it um and in fact the

48:02

United States government thinks about it

48:03

too. a large investment into uh the com

48:06

one of the companies that I uh sit on

48:09

the board of was blocked because the US

48:12

government claimed that the technology

48:14

was too dangerous to be in the hands of

48:16

foreign companies and governments. So

48:19

there the US government at least in in

48:22

the previous administration was

48:23

extremely cautious about this technology

48:26

falling into the wrong hands.

48:29

>> Which technology

48:31

>> the ability to reverse aging? So the US

48:33

government blocked that technology

48:34

because they were scared that it might

48:36

fall into the wrong hands.

48:37

>> Well, they blocked the the very large

48:39

investment over $und00 million into the

48:41

company from a foreigner because they

48:43

would have more access to the

48:45

information and the progress.

48:47

>> Is it China?

48:48

>> Um I won't say more. It's sensitive.

48:51

>> Most I can say is that governments are

48:54

watching this technology very closely.

48:55

not just the US but around the world

48:58

because the winner will make not not

49:02

just a lot of economic benefit but there

49:04

will there will be potential for radical

49:07

change in the pharmaceutical industry in

49:09

healthcare um the amount of change

49:12

socially will be dramatic as well but

49:14

there are also uses that the government

49:16

has identified uh so-called super

49:20

soldier potential now I I don't agree

49:23

that that's a reason to slow down on the

49:25

research. Others claim that it was worth

49:28

it. But I do believe that the technology

49:31

is very powerful and we should start to

49:32

get ready for when this comes to

49:35

society. Cuz it's not an if, as I said,

49:38

it's a when.

49:39

>> The technology to do what?

49:41

>> To rejuvenate the human body.

49:44

>> Why do we need to get ready?

49:46

>> Well, because it'll be massive social

49:47

change. If you can choose how old you

49:50

want to be and people don't die as at 80

49:53

anymore, let's say they they can live

49:56

till 120 or beyond, there's big changes.

49:59

There's social security issues. There's

50:01

uh employment. Though I will say that

50:04

the the disaster scenario that often

50:07

comes to mind when I talk about this and

50:09

which I covered in in the last part of

50:11

my book, lifespan, it's actually

50:13

economically hugely advantageous to slow

50:16

aging and prevent diseases. A lot of the

50:18

US economy and most advanced economies

50:21

goes to healthcare and chronic disease.

50:24

A lot of people are sick for 5 to 10

50:25

years. That's where most of people's

50:27

savings and retirement and government

50:29

money goes in the most expensive years

50:31

of your life for the last 2 years. If

50:33

you can delay that, it's going to have

50:36

massively positive economic benefits to

50:39

a nation that adopts these medicines.

50:41

I've got a question for you that

50:42

actually came to mind yesterday when I

50:44

was I watched some I don't know some

50:46

video on social media and they asked a

50:47

question to a guy. Um David, if you were

50:50

a billionaire now at age 56, would you

50:53

give it all up

50:55

to be

50:57

my age again, 33?

51:00

>> Um I don't think you can put a price on

51:02

being young. Another way of of putting

51:04

it, and I've I've seen this on social

51:05

media, would you for a billion dollars

51:07

would you swap with Warren Buffett?

51:09

>> No. Absolutely not. Right? So there's no

51:11

money in the world that you want to be

51:12

old. Right? Uh

51:13

>> yeah,

51:14

>> it's not worth it.

51:15

>> In other words, youth is more valuable

51:17

than a billion dollars.

51:20

It may be the most valuable thing you

51:22

could ever have is your youth.

51:25

>> Is it's such an an interesting and

51:27

illuminating analogy or metaphor or

51:29

whatever because suddenly you do realize

51:32

that how much we value it. We value it

51:34

more than anything.

51:36

I would rather be 33 years old than be a

51:42

43y old billionaire. Even the 10 years I

51:44

value as a billion dollars.

51:46

>> Yeah, one year maybe, but not 10 years,

51:49

right? 10 years is super I I totally

51:51

agree with you. Um and the older you

51:54

get, the more valuable it becomes. It's

51:56

important to realize the the massive

51:59

impact that this technology can have not

52:02

just economically but on individual

52:04

lives of human beings across the planet.

52:06

The world when this becomes a reality.

52:10

Again, I'm speaking like it's a

52:11

certainty cuz I'm pretty convinced it's

52:13

going to happen. The that world is going

52:15

to be so different from the world we

52:17

live in. It's going to be as different

52:18

as the precomputer world and the

52:21

pre-eroplane world as today is. I'm

52:24

trying to imagine the world where we

52:27

could pick our age and maybe even, you

52:29

know, you talked about earlier being

52:30

able to continue to reset to that age.

52:33

>> Yeah.

52:33

>> Trying to imagine what the world would

52:35

be like if I could be 33 forever or if

52:38

you could be, you know, 33 forever

52:40

>> or even for another 100 years or

52:42

something.

52:43

>> Yeah.

52:43

>> Yeah.

52:44

>> I could stay 33 for 100 years. Do you

52:46

think that's the plausible outcome which

52:48

is we can kind of pick an age and stay

52:49

there for a hundred years like at that

52:52

particular age or is it just that I'm

52:53

going to be 150 in my physical form. I'm

52:57

going to be wrinkled and gray but I'm

52:59

just going to continue to live. Is it

53:02

looking young or is it just living

53:04

longer?

53:06

>> It's actually both.

53:07

>> It's the good news is it's both. And

53:10

we're doing a lot of work in my lab on

53:12

skin and hair uh hair loss, hair

53:14

graying.

53:15

>> Yeah. Please help me. Like if I

53:17

[laughter]

53:18

>> You don't have to worry just yet. Um you

53:20

know, we we'll help your brother first.

53:22

>> No, no, come on.

53:23

>> Yeah, we we will tell him to call me. Um

53:25

so we we we've seen that we can

53:27

rejuvenate the skin of again mice, but

53:29

still we also grow human skin in the lab

53:31

from scratch and we can put that human

53:33

skin on mice and the mice have human

53:36

skin. So we can now test age reversal in

53:38

that system. I'm very optimistic that

53:41

we'll be able to rejuvenate uh the the

53:44

external part of the body as well as the

53:45

internal. If we can cure blindness,

53:48

reversing the age of the skin is is a

53:50

piece of cake. What what does that world

53:52

look like? I'm trying to understand all

53:54

of the sort of unintended consequences

53:57

of such a world where we're all kind of

53:59

young and we all live longer. Is there

54:02

problems of meaning and purpose? Is this

54:05

what are the unintended consequences?

54:07

>> I've thought a lot about this. There's

54:09

this gut feeling that a lot of people

54:10

have, maybe you're feeling it now, is

54:12

that if I'm not worried about death, I'm

54:15

not going to strive as hard or I'm not

54:17

going to have as much meaning. I'm not

54:18

going to have agency.

54:21

I totally reject that view.

54:24

I believe that every moment is special.

54:26

I don't believe I would be enjoying this

54:28

conversation with you anymore

54:30

if I could live 200 years. I'm loving

54:33

the moment.

54:34

>> Mhm.

54:35

>> Right. And so I I believe that we get up

54:37

with purpose and that if I lived for a

54:40

thousand years, I'd still enjoy every

54:42

day that I lived. And even a thousand

54:45

years, one day may be seen as too short.

54:48

You know, it's 20 times my age, a little

54:50

bit less than 20. That's still not very

54:53

much in the grand scheme of, you know,

54:55

the age of uh geology and the earth. We

54:58

still are around like that. Uh and so I

55:01

think that we will still love life. Most

55:03

of us will still love life and enjoy

55:05

every moment, but we'll get more

55:06

opportunities. We can try multiple

55:08

careers. Maybe we we we will get

55:10

divorced and find have a whole new life.

55:13

So, there will be opportunities and it

55:15

will be a magnificent world. Not to

55:18

mention the productivity that humans can

55:20

provide with the the knowledge of a 50

55:24

or 80year-old, but with the body of a

55:26

30-year-old.

55:28

>> Do you think people will make different

55:30

decisions about having children? Well, I

55:32

think we have a problem already with the

55:34

decisions that a lot of couples are

55:36

making, which is leaving it too late.

55:38

Um, it's very clear with the fertility

55:40

rate and the rate of child birth that

55:44

basically we're going off a cliff. And I

55:46

I think that

55:48

it's going to be important to be able to

55:50

give couples and women especially the

55:53

choice to have children for longer. And

55:56

that's one of the reasons that I work on

55:57

this topic is that I think that the

55:58

world with all of the the training that

56:00

we need to do and the pressures on

56:02

finding a mate and being happily married

56:05

or or at least being partnered up that

56:08

can take decades to get the right

56:09

person. You don't want to rush into it

56:10

like people used to. And being able to

56:13

have children in your 50s and 60s, I

56:15

think would be a great gift to humanity.

56:18

That's my personal view. Some people

56:19

may, you know, for whatever reason

56:21

disagree with that. But I think that the

56:22

pressures to have children before 35

56:25

typically are just extreme and and

56:28

unfair. But also that it'll help us

56:31

maintain the human population cuz by

56:33

2050, we're going to start going in a

56:36

bad decline and earlier in many western

56:38

countries. And without humans, you know,

56:41

absent android robots everywhere, we're

56:43

going to have a deficiency of human

56:46

capital and human productivity. And this

56:48

is I would argue with Elon that this is

56:51

the best solution to that uh lack of

56:54

humans is just keep people healthy and

56:56

alive and productive for longer.

57:03

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The deal applies sitewide. New year

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59:02

You mentioned uh cancer earlier on is

59:04

something that you're working on in your

59:06

laboratory. What progress have you made

59:08

in your laboratory? What has that taught

59:09

you about what the nature of cancer, but

59:11

also how we might prevent and cure it

59:13

someday? Cuz I I was reading that in

59:15

your laboratory, you have been able to

59:18

slow the growth of certain cancer cells

59:20

and kill those cancer cells completely.

59:22

>> Yeah. Uh so my my wonderful student

59:25

Nalat uh is is doing her PhD on this and

59:29

what we've hypothesized and now tested

59:32

is the idea again based on the

59:34

information theory of aging is that

59:36

cancer is

59:38

expressing those genes differently in

59:41

the same way that aging is is a cellular

59:44

identity crisis. Cancer is a cellular

59:47

identity crisis and that if we can

59:50

rejuvenate an old cell to be normal and

59:52

turn on the right genes again, we should

59:55

be able to do that for a cancer cell

59:57

>> and either make it normal or if it tries

60:01

to be normal and wakes up from its

60:03

zombie-like state, it might even kill

60:05

itself. And that's what we're finding in

60:08

my lab. Nut's work has shown that a

60:11

majority of cancers that we've grown in

60:13

the lab will die and shrink in an animal

60:17

if you try to reverse their age

60:20

>> through the injection

60:23

>> that you were referring to earlier on.

60:24

>> Yeah, we can do it a couple of ways. One

60:26

is using those three genes that

60:28

rejuvenate the epiggenome and make cells

60:31

young again.

60:32

>> Yeah,

60:32

>> the one for the eye. The same technology

60:35

for the eye we're using in cancer cells.

60:37

But we also have this chemical drink

60:39

that we can give to animals or to put on

60:42

the cells and that also wakes the cancer

60:45

cells up tries to they try to become

60:47

more normal. They turn on the original

60:49

set of genes that they might have had on

60:52

30 40 years ago. Some of these cancer

60:54

cells that we grow in the lab were from

60:56

the 20th century. We rejuvenate them. We

60:59

turn on those those genes that were

61:02

originally in the normal tissue and the

61:04

cells kill themselves. And so I believe

61:06

that we may not be able to cure all

61:09

cancer using this. That would be crazy

61:11

to even say that. But I do believe that

61:14

if we're successful rejuvenating the

61:16

human body, cancer is not

61:19

going to be a risk. And that's just a

61:22

nice side effect of what our original

61:25

mission was, which was to treat aging.

61:28

>> So from this we can start to try and

61:30

understand what we think is causing

61:32

cancer. And I guess this goes back to

61:34

the a lot of the carcogenic behavior

61:36

that you described earlier, things like

61:38

smoking, anything that's applying stress

61:40

on the DNA. Is that like a

61:42

>> Yeah, you have to break the DNA.

61:44

>> Um that's the cat a catastrophe is

61:47

really broken DNA, but you can do other

61:48

things that catastrophes like overheat

61:51

the cells. Um even mechanical stress,

61:55

you know, too many hits on the brain in

61:58

football will will do that. So yes,

62:00

that's exactly right. And that drives

62:03

aging. And aging drives cancer. By the

62:05

way, one of my theories called the

62:07

Goncoenesis hypothesis. Terrible name,

62:10

but nevertheless, Goncoenesis it is.

62:14

It's the idea that as we age, we're

62:16

becoming more cancer-like as as a as a

62:18

human. Our metabolism when we're old is

62:22

closer to heading towards what a cancer

62:24

cell's metabolism is like. So that when

62:27

we actually do get cancer, the cancer

62:29

cells grow better in an old person than

62:31

when you're young. And so by

62:33

rejuvenating those cancer cells, giving

62:35

them the the ability to be young again,

62:39

they actually either slow down in their

62:41

growth or, as I said, kill themselves in

62:43

response.

62:44

>> I've got a bit of a a prop here, which

62:47

might be useful for the the context of

62:49

>> goodness.

62:50

There are people here that may not know

62:52

what I'm holding in my hands, but uh for

62:54

those of you who don't know and who are

62:56

just listening, I'm holding a record uh

63:00

in my hands, a vinyl record uh that

63:02

Steven just handed me. So the the

63:05

information theory of aging, uh the

63:07

analogy that I used is that it disrupts

63:10

information. And so this record, this

63:12

album has information on it. It's music.

63:16

And just like DNA, it's information. So

63:19

instead of the DNA information, the

63:21

control of the DNA bit getting messed

63:22

up. It in the album, it's like

63:25

scratching this album. So I'm literally

63:28

going to scratch this album. Is that

63:29

okay with you?

63:29

>> Of course you can.

63:30

>> All right. I'm not sure I can fix it, by

63:32

the way. It may be a one-way thing, but

63:35

I've never done this before, but

63:38

that's painful.

63:41

Maybe you can hear that happening. So,

63:43

if we were to play this on a record

63:45

player with a needle, it's going to jump

63:48

around and it's going to read the wrong

63:49

songs or it's it's going to certainly

63:51

not sound very good. So, that's that's

63:54

now the equivalent of an old cell. The

63:57

information, the beautiful music is

64:00

there, but the ability to read it has

64:01

been messed up in the same way that old

64:04

age, the information is in the DNA, but

64:06

you the cells don't read it correctly.

64:08

And what our technology is is to get rid

64:11

of those scratches. and so we can play

64:13

the beautiful music of our youth again.

64:17

>> Um, I have got this uh you told me to to

64:19

bring my weighted vest and this neck

64:22

brace.

64:23

>> Oh my goodness. Uh,

64:24

>> I think I put on the wrong way. Okay,

64:26

>> any anyone listening, Steven's putting

64:28

on a very heavy jacket right now with

64:30

lead weights and a strap around his neck

64:32

to limit his neck movement.

64:34

>> Oh, wow.

64:36

That's a lot. Listen, so I'm I just put

64:38

on a 20 I think it's 20 kg. My son's

64:42

weak now. Um, jacket and a neck brace.

64:47

And ahead of this conversation, my team

64:49

told me to get one of these. What is the

64:51

analogy here that you're you're

64:52

creating? This is very hell.

64:55

>> It's bad, right?

64:56

>> It's hard. Yeah.

64:57

>> Right. Imagine

64:59

feeling like that for a decade. That's

65:01

old age. You feeling tired, weak. You

65:04

can barely hold your body up. You can

65:06

barely move your neck. It would be

65:08

painful. You're not in pain yet. No. But

65:10

most people in their 80s have some sort

65:12

of disease and aches and pains.

65:15

Try doing that for another 10 minutes

65:18

maybe. How long can you keep that on?

65:20

>> I'll keep it on for another 10 minutes.

65:21

But so why is this? Cuz it just it's

65:23

weight and im immobility. I can't move

65:26

my neck the same. My shoulders feel

65:29

heavier.

65:30

How How is this a relevant analogy to

65:32

aging? Because it just kind of feels

65:34

like immobility and weight. Uh, well, I

65:36

have to come over there and use this

65:38

pair of scissors to be stabbing you as

65:40

well. So, you can feel pain as you move

65:42

as well. That's part of old age. It is

65:45

not a fun thing being old. And most old

65:48

people, the reason that they don't love

65:50

life anymore is because they feel like

65:52

you do or worse. Not to mention the fact

65:56

that there you need to put Vaseline on

65:58

your eyes, earplugs in your ears if you

66:01

want to know what it's like being old.

66:03

>> Oh god, it's not nice. Mm- or even

66:06

worse, shut your eyes and you can never

66:08

open them again.

66:10

That's what it's like for those patients

66:11

that we hope to cure a blindness in.

66:14

>> If if I'm going to ask you a really

66:15

tough question, which is if I put a

66:17

calculator in front of you right now and

66:19

you had to hit a number on that

66:20

calculator and then hit enter

66:22

>> and that was the age that you were going

66:24

to live to and you had to make that

66:26

decision now.

66:26

>> Yeah.

66:27

>> What number would you hit on that

66:30

calculator?

66:31

>> Infinity.

66:32

>> Really? So you No, no, no. There's no

66:34

day if you're healthy where you want to

66:36

die. Even if you're 100, 120, if you

66:39

have friends, family, loved ones, you're

66:41

healthy, would you say, "Okay, tomorrow

66:44

I'm ready to die."

66:45

>> No, it's not happen unless there was

66:47

some kind of psychic issue or something.

66:48

>> Exactly. Right. So, that's my point is

66:51

when people say, "Oh, when I'm 80, kill

66:53

me." That is That's Excuse my

66:55

language. Am I allowed to swear on this?

66:57

>> No question.

66:58

>> Um,

66:58

>> sorry. I'm going to have to beep it for

67:00

the kids. I guess

67:00

>> it's it's only when you're sick or you

67:03

have depression that you want to leave

67:05

the leave this world. Otherwise, life is

67:08

a joy for most people on in the world.

67:10

Not everybody and we have to fix that as

67:12

well, but for most of us,

67:15

being alive is is the greatest gift of

67:17

any, you know, collection of atoms.

67:21

Consciousness is even greater. And why

67:24

would you want that to end?

67:26

who would choose that if they had the

67:28

alternative to be with family and

67:30

friends.

67:31

>> Interesting. I say that's interesting

67:33

because I have always assumed that I

67:36

wouldn't want to live forever. But the

67:38

when when you asked me if I was healthy

67:42

and I had my friends and family and I

67:44

was [clears throat] doing things that I

67:45

loved professionally, would there come a

67:47

day where I would choose to go now? No,

67:50

there wouldn't. Just like there hasn't

67:52

come a day in the last 33 years where

67:54

I've chosen to go now.

67:57

>> Exactly.

67:58

>> Do you think it's it's going to be

68:00

possible in the next 50 years for us to

68:02

live forever?

68:04

>> I'd be shocked if that happened, but

68:07

I've been shocked my whole career at how

68:09

fast this technology is moving. And now

68:10

with AI, things are going so fast. My

68:12

head's spinning.

68:14

So, I'd be happy to be proven wrong. But

68:16

I'm I'm skeptical that we could live

68:18

forever in my lifetime at least. But as

68:22

I said, you're pro you're probably going

68:23

to live you are going to live into the

68:25

22nd century. We can't imagine what the

68:28

world's going to be like then.

68:29

>> And AI has really changed this equation.

68:32

>> Oh, absolutely. We're we're doing things

68:34

in my lab that would have taken 160

68:36

years before and and quite literally

68:39

billions of dollars on a 10 $10,000

68:42

budget.

68:43

>> Well, I guess I better make it to 2040.

68:46

Um, so let's talk about fasting and food

68:49

and nutrition and get go a little bit

68:51

deeper on that. I've had so so many

68:53

conversations over the years about this

68:54

subject of fasting. But, um, as I was

68:57

reading your research, you really do

68:59

feel that fasting, just eating less

69:02

often

69:04

is one of the most important things that

69:05

we can all do for longevity.

69:07

>> I I do. I do and I practice it as much

69:09

as I can, though it's challenging in a

69:11

world that's full of abundant food. But

69:14

yes, we've known for thousands of years,

69:16

the ancients are not dummies. They they

69:18

could witness what happens when you

69:20

fast. Uh clarity of mind, long-term

69:23

health. They could observe the

69:25

difference between the glutton and the

69:26

people that fasted for religious

69:28

reasons. It's obvious, but there's

69:30

certain ways to do it. Fasting doesn't

69:31

include malnutrition. You have to do it

69:34

with abundant, you know, vitamins,

69:35

minerals. You want to make sure that

69:37

you're you you have adequate nutrition.

69:40

But I think three meals a day is is

69:42

craziness. It turns out this idea

69:44

breakfast is the most important meal of

69:46

the day is marketing from the early 20th

69:48

century by companies I will not name,

69:51

but it was breakfast cereal. Breakfast

69:53

is not the most important meal of the

69:54

day for most people, especially adults,

69:57

especially if you're not hungry when you

69:58

wake up. There's no point in eating if

70:00

you're not hungry in the morning. I'm

70:02

one of those people. So, I've skipped

70:04

breakfast. How about you?

70:05

>> Yeah, I'm the same. I'm the same. I

70:06

don't eat. My first meal today was 300

70:08

p.m. because I had a podcast until, you

70:10

know, 2 2 p.m. So, which is typical for

70:12

me. I just don't get hungry in the

70:13

mornings now because of the marketing

70:15

though for breakfast sometime I've

70:17

sometimes I've said to myself you should

70:18

eat and I'll make myself eat but it's

70:21

very very rare I'm notoriously people

70:23

know that I'm notoriously

70:25

um a late eater 4 p.m. sometimes 5 p.m.

70:28

How are you feeling with that heavy?

70:30

>> It's it's heavy, David. I'm going to be

70:31

honest. It's not I'm finding myself like

70:33

trying to find a comfortable position.

70:35

>> Yeah, it it's tough being old and by the

70:37

end of it, you will be so convinced that

70:40

this research is important because to

70:42

live like that

70:44

>> in most people life is not worth living.

70:46

>> I put a suit, a very heavy suit like

70:48

that, but on the arms as well, not just

70:50

the body. And he had the the ear muffs

70:52

and the the eyes. This was the uh the

70:55

governor of Massachusetts 15 minutes in

70:58

that bodysuit and he was crying not

71:01

because he was in pain because he as he

71:04

said on stage it was the first time in

71:06

his life he understood how his father

71:08

feels and could be empathetic. We young

71:12

people I'm relatively young 56 you're

71:14

very young 33. We have no idea what it's

71:16

like to be old. It can be horrific. So

71:20

why wouldn't we do the right things like

71:23

fasting, exercising [clears throat]

71:25

so we can get an extra 10 years, 20

71:27

years, maybe longer of healthy life?

71:30

>> It does also give me a lot of empathy

71:31

for people that um have a bit more

71:34

weight on them as well because of you

71:36

know if I was if I weighed that much I

71:39

don't know if I'd be very active to be

71:41

completely honest with you.

71:42

>> Exactly. And you're in pain too. Don't

71:44

forget every joint can be hurting. How

71:46

do you feel taking that off?

71:47

>> Much better. right?

71:48

>> Free like I want to jump.

71:49

>> So let's

71:52

hope, pray, wish that these technologies

71:56

that I'm talking about today work cuz

71:58

that could be what it feels like to be

72:01

rejuvenated when you're 80.

72:03

>> I hope [clears throat] so. Um to close

72:05

off on this point of of fasting, why why

72:07

does it help extend my life? Yeah. Just

72:09

eating less.

72:10

>> Part of it came out of research in my

72:12

lab, but of course many others I need to

72:14

give credit to. But in my lab

72:16

specifically, what we worked on in

72:17

initially when I started, we studied

72:19

yeast cells, little uh microscopic cells

72:23

that as everyone knows we used to make

72:25

beer and bread and champagne. These

72:27

yeast cells live about 10 days and then

72:29

they die. And we used yeast as a model

72:31

for aging. And what we discovered with

72:33

yeast cells, which turns out to be true

72:35

in our bodies, is that adversity, as

72:38

long as it's not killing these cells, is

72:41

good for you. It's called hormesis. It's

72:44

the technical term for what doesn't kill

72:45

you makes you stronger and live longer.

72:48

Adversity mode is what we're aiming for.

72:51

The opposite is abundance mode, which is

72:54

what modern life is all about. Popcorn,

72:57

movies, wheels on your suitcase, sitting

73:00

down all day.

73:02

It's we're in an abundance world. So

73:05

adversity is something we don't often

73:06

feel. We have to work at it. Fasting is

73:09

adversity. Exercise is adversity. cold

73:12

plunges, sauners, adversity. Adversity

73:15

mimics. They're not really threatening

73:17

your life. What happens at the cellular

73:19

cellular level is that those cells, they

73:22

get freaked out. They're worried that

73:25

these times of adversity could kill us.

73:28

So, they fight back. They turn on repair

73:30

systems. They turn on recycling systems.

73:34

They turn on DNA repair systems that

73:36

help slow down aging. So in this modern

73:39

world, we when we have total abundance,

73:40

we don't have to exercise, we don't we

73:42

eat three meals a day, we get

73:44

overweight, we don't sleep much, we have

73:46

air conditioning in summer, we're

73:49

actually aging faster than we need to

73:50

cuz our bodies are not fighting aging

73:53

like they do when they feel adversity.

73:56

>> Your team discovered I can't say the

73:58

word seratunis.

74:00

>> Oh well, I was one of many scientists in

74:03

the 1990s. Uh I was part of a team

74:05

called Sertuins. Yeah. So twins.

74:08

>> Yeah. Yeah. In yeast, actually. That's

74:11

right. Uh that's a good story. I went to

74:14

the US to figure out why we get old. But

74:18

I didn't choose to study humans cuz I

74:20

figured if we can't figure it out for

74:23

little yeast cells, we'll never figure

74:24

it out for humans. So I went to MIT. My

74:27

professor was Lenny Garenti. I went to

74:30

his lab and I said, "I'm I'm not going.

74:31

I'm not leaving." The goal was to in my

74:34

mind was to figure out are there

74:36

longevity genes. At that time most

74:38

people thought that there were aging

74:40

genes that caused aging death genes.

74:43

That doesn't make any sense to me. Our

74:44

bodies would have longevity genes that

74:46

give life. So in yeast I went searching

74:49

for them. And out of that work came two

74:51

things. The first is Lenny and I my

74:54

professor and I published in the journal

74:56

cell which was a massive big deal in

74:58

those days still is but it was my first

75:00

time. the first evidence for a cause of

75:04

aging for any species. We figured out

75:06

why yeast cells get old. Do you want to

75:08

guess?

75:10

>> Why do yeast cells get old?

75:13

>> Have you been paying attention? What

75:14

does the information theory of aging

75:16

say?

75:16

>> I was going to say they have an identity

75:17

crisis, but

75:18

>> they do.

75:19

>> How would we know if they have they're

75:21

having an identity crisis?

75:22

>> Oh, you can measure the identity of

75:23

yeast cells. They have an identity. It's

75:26

called their mating type. The main

75:27

identity of a yeast cell is they are

75:29

either a type or alpha type, male,

75:33

female.

75:34

And the hallmark of a yeast cell that's

75:37

old is it loses its A and alpha identity

75:42

and gets an identity crisis. It doesn't

75:45

know what sex it is and it doesn't mate

75:47

anymore, becomes sterile. So when I

75:49

arrived at MIT in 1995, we knew that the

75:53

hallmark of an old yeast cell besides it

75:55

being a bit slow and bigger is that it

75:58

became sterile. It had an identity

76:00

crisis. So we figured out that broken

76:02

chromosomes

76:04

distract the sertuan defenses

76:07

and that causes aging in a yeast cell.

76:10

But we didn't know in the '90s that that

76:12

was going to be true for us as well. It

76:14

took another decade or two to figure

76:16

that out. And how does this link to

76:17

eating all the time?

76:19

>> Yeah. So, sertuins are proteins that

76:22

actually are attracted to DNA. They

76:25

actually associate with it and they

76:27

protect uh the DNA from getting damaged.

76:30

>> Okay. Like bodyguards.

76:32

>> Yeah. And they repair broken

76:33

chromosomes, right? It's all coming

76:35

together now. But they also get

76:37

distracted. So look, a sertuan's normal

76:40

job if there's no crisis is that they

76:42

turn genes on and off. They are

76:44

epigenetic regulators. They control the

76:47

epiggenome. They tell a cell what type

76:49

it is. Nerve cell, skin cell, right?

76:51

>> Like a conductor.

76:52

>> Thank you. Conductor. Exactly.

76:55

But the conductor

76:57

becomes demented over time. What happens

77:00

is when you have a chromosomal break,

77:03

the sertuins panic. They leave the DNA,

77:06

what they're supposed to be doing,

77:07

controlling the cell's identity, and

77:10

they go and they repair the DNA. That's

77:11

their other job. They have two jobs,

77:13

identity and repair. So when you have

77:15

this break, the Suins go away. They

77:17

repair the problem, but they don't all

77:19

go back in the next few minutes. It's

77:22

very quick. They don't all go back to

77:23

where they started. So you've got like

77:25

this tennis match that the sertuins are

77:27

the balls and they get hit over to the

77:30

break, then hit back. Most of them find

77:32

the genes that they should go back to,

77:34

but they don't all do that. And that

77:36

total game of tennis or ping pong, if

77:38

you like, is what I believe causes the

77:40

identity crisis. than aging itself

77:43

causes aging in yeast cells. It's why

77:45

yeast cells don't live longer than 10

77:46

days. And I believe it's why we struggle

77:48

to live beyond 80 or 90.

77:50

>> So if I'm eating all the time, then

77:52

those sertuins, they're not going to be

77:54

doing their job as the um the conductor

77:57

making sure I know the identity of my

77:59

cells. They're going to be doing repair

78:01

stuff. So I'm going to age faster.

78:05

>> Yes. And the breakthrough happened in

78:07

the lab as I was just leaving to go to

78:08

Harvard. I got a job at Harvard when I

78:11

was 29, super excited. And just as I was

78:14

leaving, there was a big breakthrough

78:15

that they actually kept it secret from

78:17

me cuz I they were worried I was going

78:19

to work on it when I left. And in fact,

78:21

my professor tried to prevent me from

78:23

working on it when I left on Sertuins in

78:26

general. crazy to think about. But what

78:28

they discovered was that there's a a

78:31

metabolite, a molecule that goes up and

78:35

down with food and up and down with

78:37

sleep called NAD. We have lots of it.

78:40

There's grams of it in our body. It's

78:42

one of the most abundant molecules in

78:43

the body. It's very ancient. It's in

78:44

yeast. It's in us. And what they found

78:47

was that sertuins

78:49

to control genes and to repair DNA

78:52

that's broken, they don't do it unless

78:54

there's NAD. It's the catalyst. It's the

78:57

fuel for their reaction. They need NAD.

79:00

And when we're young, we have lots of

79:02

NAD. So, it works well. The satuans

79:05

control the information on the genes and

79:07

they repair the DNA very well because

79:09

they've got lots of NAD to carry out

79:11

their their work. These are enzymes.

79:13

They work. They do things. As we get

79:16

older, by the time you're 50, about my

79:18

age, you have half the levels of this

79:20

NAD molecule. my body is making less NAD

79:24

and it's also destroying the NAD faster

79:26

than when I was 20. That's a problem.

79:29

And so what we found was that when we

79:31

fast the yeast or we fast a human, NAD

79:35

levels go up again. So fasting raises

79:38

NAD and makes the certuins young again

79:41

essentially and that preserves the

79:43

epiggenome and it also repairs the DNA

79:45

better.

79:46

>> So can I just drink NAD?

79:47

>> Uh you can drink NAD and not much would

79:50

>> how? How do I take NAD?

79:52

>> Uh, so NAD can be taken as a supplement

79:54

which is a prec precursor to NAD. It's

79:57

better to take the precursors.

79:58

>> A precursor meaning something that

80:00

creates it naturally.

80:01

>> Exactly. There's one called NN, not to

80:03

be confused with M&M's, which will

80:05

probably not make you live longer. And

80:07

there's another one called NR. NN is

80:09

directly converted into NAD. You put two

80:11

NAMNS together, you get NAD in the cell.

80:13

We know this for a fact. This isn't

80:14

isn't speculation. When you give a human

80:16

NMN by swallowing it, a gram of it, you

80:20

can t you typically double the amount of

80:22

NAD in your body. And we believe and we

80:24

have some evidence now in human clinical

80:26

trials that the Sertuins are imparting

80:29

health benefits, reestablishing the

80:31

epiggenome, lowering body weight, uh

80:34

improving inflammation, uh and even

80:37

changing cholesterol levels in a

80:38

positive way in humans.

80:40

>> So, I mean, I'm assuming you take NN.

80:43

I've been taking an amen and admitting

80:45

that publicly uh for a while now and my

80:48

father who is uh an even more advanced

80:52

uh experiment at 86.

80:55

So yes, we've been taking it for over a

80:57

decade now and we're still alive. So so

80:59

far so good.

81:00

>> So far so good. I do want to get into

81:01

and I will ask you in a second about the

81:03

the supplement stack that you would

81:04

recommend for the average person. Um but

81:06

that's good to know. But just to close

81:07

off on this point of fasting, is there a

81:10

particular type of fasting method that

81:13

you would recommend for someone who's

81:16

trying to, you know, improve their

81:17

longevity?

81:18

>> Because there's so many that I hear 16

81:20

hours, 5 days.

81:21

>> I'm a scientist, so I go with what's

81:22

proven. I'm not selling anything. So,

81:25

what the science says, first of all, is

81:27

that there isn't one sizefits-all for

81:29

everybody. Um, it it often depends on

81:32

what you can do personally. It's

81:35

challenging to do this, right? you'll

81:36

feel hungry for the first two weeks you

81:38

try it. So I I would suggest the way I

81:42

do it is I start by skipping one and

81:45

then maybe one and a half meals uh like

81:49

what you do. Try to go without a meal

81:52

until 3 4:00 if you can. Maybe not the

81:55

first day, right? If you do that the

81:57

first day, you'll say this is crazy. I'm

81:58

I'm going to grab a snack and you won't

82:00

do it. So go slowly, build up to it. So

82:03

the first day I would say just don't eat

82:05

breakfast and maybe have a snack midm

82:08

morning. A week later try to go without

82:10

breakfast completely until lunch and

82:13

eventually work up to what you do and I

82:14

do which is eat a very late lunch if not

82:17

go to dinner. What you get with that is

82:19

obviously not eating in bed hopefully.

82:22

So you've got that the night fast

82:24

starting what would it be 7:00 p.m.

82:26

roughly. When do you finish dinner?

82:28

>> Oh god. No comment.

82:30

>> Okay.

82:30

>> It's usually pretty late. Last night it

82:31

was, you know, it was, this is probably

82:33

why I don't eat very early the next day.

82:35

Last night would have been about, I'm

82:37

going to say 1000 p.m.

82:39

>> Okay,

82:39

>> it was super late. It was, that's an

82:41

extraordinary example. Usually, it would

82:42

be 8 or 9:00 p.m.

82:46

>> Okay, but but you've got at least 13, 14

82:48

hours, which is good. Try to aim for 14

82:50

hours. Some people go 16 hours, but

82:53

that's a good start for fasting. And

82:55

hopefully you can do that most days, 5

82:57

days a week. That's great cuz that means

82:59

that you're turning on your stratuins,

83:00

raising your NAD. You're exercise as

83:03

well. So that's also added into it. One

83:06

thing that I've started doing is fasting

83:09

for longer than just 14 16 hours. I try

83:14

maybe once a month to go for 3 days

83:16

without eating.

83:16

>> Why?

83:17

>> Because there's a type of cellular

83:19

recycling that doesn't happen within the

83:22

first 16 hours. Um you will enter

83:25

ketosis. So you'll your body will start

83:26

to change its metabolism produce what's

83:28

called ketone bodies. But the true real

83:32

deep clean cleansing of old proteins and

83:35

damage damaged proteins happens after 2

83:39

and 1 half to 3 days and it's called

83:41

chaperone mediated autophagy.

83:43

>> Autophagy.

83:44

>> Autophagy is the word for auto self-eing

83:49

and it really kicks in for with an

83:51

extended fast.

83:52

>> What's the evolutionary reason for that?

83:54

What's going on there? Why does it take

83:55

me 2 and 1/2 days for this deep clean to

83:57

happen?

83:57

>> Uh cuz your body doesn't want to uh do

84:00

it. It costs a lot of energy and having

84:02

to remake body parts is energy

84:04

expensive. And our body tries to

84:06

conserve energy as much as possible. Uh

84:09

when you're fasting, what it'll it needs

84:11

to do is to use your body as fuel. So

84:14

it'll start breaking down proteins for

84:16

fuel that you need. So first of all,

84:18

what'll happen is in the first few

84:20

hours, you use glycogen from your your

84:21

liver. Your liver makes glucose. You'll

84:23

feel a little bit hungry, but you'll

84:25

eventually be fine. Then once you run

84:27

run out of glycogen, then you're going

84:29

to start breaking down fat and making

84:31

ketones. Uh that's when you start to get

84:33

a bit of bad breath from from that. And

84:36

you but you feel great. When you're in a

84:38

between about 15 hours and 24 hours,

84:42

that's when you get a lot of ketones and

84:43

your brain uses those for fuel. So

84:45

you'll have sharp mind, can remember

84:47

things, you can focus on work if you

84:50

ever get there. beyond that you need to

84:52

break down fat and uh that is uh when

84:57

your body is starting to do that but

84:59

ultimately what what what happens after

85:01

3 days is your body says hey I'm going

85:04

to start breaking down protein as well

85:06

and uh I wouldn't do that often because

85:09

I don't want to break down a lot of

85:10

protein but your body will start to turn

85:12

over old proteins preferentially and a

85:14

little bit of that that's why I do it

85:16

maybe once a month has been shown at

85:18

least in animals to be not just healthy

85:20

but life extending.

85:23

>> On that point of ketosis,

85:26

um, I like being in a state of ketosis.

85:30

I kind of cycle in and out of it during

85:32

the year because I get so many of the

85:34

like cognitive benefits. I'm more

85:36

articulate on the podcast. I can think

85:37

better. I feel better. I feel more

85:40

focused and more attentive.

85:42

Is ketosis

85:44

is the ketone diet the keto diet a

85:47

healthy diet in your view? Is it what

85:49

are the benefits of it? Is it something

85:51

that you think is natural to be

85:52

recommended?

85:53

>> Well, I don't mind being controversial,

85:54

but I do speak the truth. Um, there's

85:57

not a lot of evidence that long-term the

85:59

ketogenic diet is healthy.

86:01

>> Certainly doesn't correlate or associate

86:03

with uh longevity.

86:05

Short-term, okay, it does help people

86:07

lose weight, no question. Uh but I am

86:10

rather concerned for people that don't

86:11

have a balanced diet with an input of

86:15

plant material which has molecules that

86:18

are unique to plants and you won't find

86:20

in high processed foods or meat. The

86:24

evidence speaking as a scientist is that

86:27

the long-term ketogenic diets are not

86:30

going to be longevity inducing. The

86:33

evidence is more having a lean diet with

86:37

a focus on plants that are not

86:38

overcooked and not ultrarocessed.

86:41

That one is undoubtedly the healthiest

86:44

if you can do it.

86:45

>> Do you eat meat?

86:46

>> I do eat meat, but not like I used to. I

86:50

used to think that a meal was not a meal

86:52

unless I had a piece of meat there and

86:54

then the vegetables were the decoration

86:56

and I'd begrudgingly eat the green

86:58

stuff. I've been flipped totally. Um

87:01

Serena, my partner Serena Pune is not

87:04

just a nutritionist but a longevity

87:06

expert for the last 26 years. And so she

87:09

came to my apartment uh which is now our

87:12

apartment and she just cleared out all

87:13

the food that I had. Pretty much

87:15

everything was either toxic or uh or

87:18

just not healthy. It was ultrarocessed.

87:20

She said, "What are you eating that kind

87:22

of peanut butter, you know, full of

87:24

sugar?" So she she's taught me how to

87:26

live healthy. And so now I rarely eat

87:29

meat. I rarely drink alcohol. I focus on

87:33

really fresh, high quality uh preferably

87:36

organic foods because I don't want

87:38

pesticides and I don't want other

87:39

contaminants.

87:41

But I do know organic can be more more

87:43

expensive.

87:44

>> Why not meat?

87:46

So animals unfortunately don't make what

87:48

are called polyphenols which are a type

87:51

of molecule that uh I believe uh and

87:54

have evidence turns on the certuins and

87:58

other pathways biochemical reactions

88:01

that delay aging. So certuins are just

88:04

one of a few enzymes that control aging.

88:08

We know this. There's certuins. There's

88:10

mTor which responds to aminos and

88:13

another one called. So those three

88:16

pathways are altered in just the right

88:19

way by molecules found only in plants

88:23

well and a small extent in fungi but not

88:26

in meat. So if you're not eating a lot

88:28

of vegetables or fruits, you're not

88:30

getting these molecules. They're like

88:32

medicine as food. So right here, I hope

88:36

you don't mind me mentioning that there

88:38

are some some food in front of us. And

88:40

I'm looking at blueberries here.

88:41

Blueberries are packed with polyphenols.

88:44

One of the reasons they have purple

88:45

color is the polyphenols have the color.

88:47

And as Serena would tell you, eat the

88:50

rainbow. I call it xenomormmesis, which

88:52

is not as attractive, but xenomormis is

88:55

the same idea as eat the rainbow. that

88:57

by eating plants that have a lot of

88:59

these molecules that are often produced

89:01

by stressed plants.

89:04

>> Stressed plants.

89:05

>> So plants will be stressed just like we

89:07

are. If you don't give them enough

89:08

water, food, too much sunlight, not not

89:11

enough sunlight. They in their defense

89:14

they make polyphenols.

89:16

There's a whole bunch of them.

89:17

Resveratrol, physitan, coretin, there's

89:20

there's hundreds. Uh this one has um

89:23

anthocyanidins. That's the color. These

89:25

activate these adversity responses in

89:29

our cells. The sertuins will get

89:32

activated by molecules in this

89:35

blueberry.

89:35

>> So if I eat this blueberry,

89:38

those conductors that conduct some of

89:41

the aging process you talked about

89:43

making sure my cells don't have an

89:44

identity crisis, fixing the the the

89:48

negative stress that's going on in my um

89:51

in my cells. they will be

89:54

benefited by me eating this blueberry.

89:57

>> Yeah. It's it's like a a free hack,

89:59

right? You can eat something that's

90:00

yummy, but you're also getting the

90:03

benefits by mimicking fasting and

90:06

exercise in your food as well. The

90:08

certuins don't just need NAD. That's the

90:11

gas pedal. That's the petrol for those

90:13

of you in the British world and

90:15

Commonwealth. The fuel for certuins is

90:19

NAD. The accelerator pedal are the

90:22

polyphenols in fruits and vegetables

90:25

like resveratrol coretin which we know

90:29

when you give them to sertuins they get

90:31

hyperactivated

90:32

>> and when you say eat the rainbow you

90:34

mean eat colorful looking food

90:37

>> because that's an an easy way to

90:39

remember how to eat foods that have the

90:41

most polyphenols. I'll give you a really

90:43

good example, Stephen. Serena put me on

90:46

to green tea matcha, right? So, matcha

90:49

tea. If you haven't tried it, uh I'm

90:51

sure you've tried it, but those of you

90:52

who haven't tried it, I highly recommend

90:54

it. It It tastes great. The reason for

90:56

it switching from coffee mainly to

90:59

matcha in the morning for me is that

91:02

it's full of polyphenols. Why is it full

91:05

of polyphenols? It's not just because

91:07

it's green tea, which is not naturally

91:08

healthy, but the growers of those plants

91:11

in Japan typically they shade the plants

91:14

before they harvest. Shading the plants

91:17

stresses them out. Plants need light.

91:20

So, they don't just make more

91:21

chlorophyll, which produces the deep

91:23

green color in the tea. But the

91:25

polyphenols are super high. And through

91:28

trial and error over thousands of years,

91:29

the Japanese figured out that by shading

91:32

the plants, giving them this mild

91:34

hormetic stress, it makes them not just

91:37

extra tasty, but extra healthy. Same

91:40

with red wine, by the way. But the

91:41

alcohol can be an issue. But absent

91:44

alcohol, red wine is very good for you.

91:49

>> Okay. Without the alcohol,

91:51

>> it's unfortunate. You know, I I one of

91:53

my papers in 1996 caused red wine cells

91:56

to go up 30% and stayed up. I apologized

91:59

for saying that red wine every day was

92:02

healthy. Doctors were recommending it.

92:03

Remember?

92:04

>> Yeah.

92:04

>> But I now changed my mind. I have to say

92:08

that I no longer believed having one

92:10

glass of red wine every day is healthy

92:13

in my opinion. And I've stopped drinking

92:15

red wine every day. Instead, I take

92:17

polyphenols from red wine and from

92:20

vegetables either in a pill or in my

92:22

food as a substitute because the

92:25

evidence for alcohol is rather damning.

92:27

There's a UK bioank study and the UK

92:29

looked at thousands of people's MRI scan

92:31

of their brain who were drinking one

92:33

glass of alcohol a day and there was a

92:36

statistical difference between people

92:38

that were drinking one glass a day and

92:39

were not in terms of brain size and gray

92:41

matter. Of course, the gray matter was

92:43

tended to be smaller in those that drank

92:45

even slightly.

92:47

>> Yeah, I do. [clears throat] Um I

92:48

actually have a matcher company. It's um

92:50

it was this year voted the fastest

92:52

growing company in the UK. Um it's by

92:55

some founders that I invested in um

92:57

Levi, Teddy, and Marissa from Dragon's

93:00

Den. And it's been an absolute

93:03

unbelievable in business. Unbelievable.

93:05

>> So tell us where where do I get it?

93:08

>> Japan. You get the matcha from Japan,

93:09

but the company is called Perfect.

93:10

People know about it. Um cuz I've talked

93:12

about it before, but I didn't realize

93:14

when I made the investment that matcha

93:16

was considered by many to also be very

93:19

healthy, especially a health alternative

93:20

to certain energy products on the market

93:22

that you get in cans that give you um I

93:27

shan get sued. [laughter]

93:29

>> But the other thing that um other

93:30

company I invested in is this one here

93:32

called uh Ketone IQ. I'm a coowner of

93:35

this company as well. And

93:37

>> yeah, I love that uh love that company.

93:39

and the CEO, uh, Michael, good guy.

93:42

>> What's your thoughts on exogenous

93:43

ketones, like drinking ketones?

93:46

>> I do it in fact that I drink ketone IQ

93:49

before I do a podcast.

93:51

>> Why?

93:52

>> It improves my clarity. I find um I also

93:56

believe the science and there have been

93:58

multiple studies now in people in some

94:01

of the the science comes out of ketone

94:02

IQ but also independent studies have

94:05

shown that it's extremely healthy for

94:07

the heart and uh there's new studies

94:09

that show for the brain as well it can

94:11

be healthy the brain uses ketones like

94:13

beta hydroxybutyrate or in that one it's

94:15

13b butin dial um just a shot of that

94:18

will give the brain food that it needs

94:20

rather than the body having to make it

94:22

um and you get I and I feel it. I get

94:25

the clarity of fasting without being in

94:27

a fasted state, but I also drink it when

94:29

I'm fasting to give it the body the

94:31

extra boost that it needs.

94:33

>> And on this point of diet, one of the

94:35

things that I was told by my doctor when

94:37

I did a like one of those blood tests

94:39

was he cautioned me about bad

94:41

cholesterol.

94:42

He said to me something along the lines

94:44

that I need to be careful about the bad

94:46

cholesterol. And there's been lots of

94:48

conversation about cholesterol, good,

94:50

bad. What's your perspective on this

94:53

conversation around bad cholesterol

94:54

which has been thought to increase um

94:57

certain foods have been thought to

94:58

increase bad cholesterol um which is

95:00

very very detrimental to our health.

95:03

>> I didn't realize there was a debate at

95:05

least in my world there is no debate um

95:08

if you're referring to do you want to

95:10

get your LDL cholesterol as low as

95:13

possible.

95:14

>> Yeah

95:15

>> definitely.

95:15

>> Oh really? Okay. So it's

95:17

>> yeah I mean the science is irrefutable.

95:18

thousands of people in studies. Now, I

95:21

think I know what you were you were

95:22

talking about. There there are some

95:24

stories that you need cholesterol in

95:27

your brain and if you inhibit it, you

95:30

might affect your brain function. Um,

95:32

you also need it for repair of arteries.

95:35

But there's no evidence that that's a

95:37

problem. In fact, it's it's a little

95:38

known fact that the brain doesn't use

95:41

the cholesterol from the bloodstream. It

95:43

makes its own. So, I've actually been on

95:45

a statin to lower my LDL since I was 30.

95:48

>> Really?

95:49

>> Well, I had high cholesterol. It's in my

95:51

family, but I went to my doctor and I

95:55

said, "I want to go on these new drugs

95:56

at the time, statins." And he said,

95:58

"Why? You don't have heart disease yet."

96:01

And I said, "Why would I wait? Get me on

96:04

it. I want to be on it." And in those

96:06

days, it was very weird to give someone

96:08

a statin at age 30 with no evidence of

96:11

heart disease. But as you know, I'm of

96:14

the opinion that we shouldn't wait till

96:17

we get diseases to treat them. We should

96:19

preempt that and start early in life.

96:22

And so, yeah, I insisted with my doctor

96:24

initially with statins, but on all of

96:26

these things, I go in and I say, "I need

96:28

you to prescribe me this test. I need

96:30

this medicine." And eventually after

96:33

talking it over with him, he typically

96:35

prescribes me something or gets me a

96:37

test. But I've been fighting the system

96:40

and my doctor's at Harvard, so he's a

96:42

good doctor but conservative. The old

96:44

way of doing medicine is if you're not

96:46

sick, we're not going to give you a

96:47

medicine. Certainly not if you're young

96:49

and healthy. Uh but that has to change.

96:52

>> So you saying that I should be on

96:53

statins potentially?

96:53

>> Well, what's your LDL level?

96:55

>> Not I don't think it's great. I think I

96:56

ate too much bacon or something.

96:58

>> Well, we can talk about food and

97:00

cholesterol cuz it depends whether you

97:02

absorb still or not. We can test for

97:04

that. But if you do absorb cholesterol

97:07

more than most, I would say that you may

97:09

want to change your diet at a minimum.

97:11

>> On this plate here in front of us, I

97:14

have the

97:16

top five foods that I believe you think

97:19

are great for reversing aging. Am I

97:21

correct? Is that does that

97:22

>> these are great choices. Yeah.

97:24

>> So, what are these and why? So, we've

97:25

already done the blueberries and we've

97:26

you've explained to me about polyphenols

97:28

and they're rich in them, which I

97:29

understand.

97:30

>> Mhm.

97:30

>> And they're low in sugar, right?

97:33

Well, they're not low in sugar, so don't

97:35

eat a ton of them. A handful is fine um

97:39

as a snack. It's also known that having

97:41

too much sugar is bad for longevity.

97:43

>> Keep your blood sugar levels steady and

97:45

low, as much as you can. So, don't eat

97:47

too many of those. A better choice than

97:49

blueberries would be something like

97:51

matcha, which is not full of sugar. In

97:53

fact, if you go to some of these chains

97:55

that sell matcha and it tastes really

97:57

sweet, you're going to reverse the

98:00

effects of any polyphenols by drinking

98:01

that much sugar. So, I always have

98:03

unsweetened matcha. Okay. So, now we've

98:05

got avocados here.

98:06

>> Yeah.

98:06

>> Yep. Avocados.

98:08

>> Um, they're not so much known for their

98:10

polyphenols, though they do have them.

98:12

It's the type of fats, the

98:13

polyunsaturated fats. They help with

98:16

satiety, so you're not going to be as

98:18

hungry. Uh, so if you put that on your

98:20

sandwich at lunch, you're not going to

98:21

feel peckish and they're highly

98:24

anti-inflammatory as well. The molecules

98:25

are in there and the fats are very good

98:27

for you.

98:29

>> Extra virgin olive oil.

98:30

>> Oh yeah. Excellent. So the type of uh

98:34

oils that are in there are very healthy.

98:36

There's omega 9 which is also known to

98:39

activate certuins and again if you have

98:41

the right uh grower and this has been

98:45

cold pressed not too processed and

98:48

stressed before harvesting you'll have

98:50

huge amounts of polyphenols as well.

98:52

>> I really hope that this is what the team

98:55

said it was. [laughter] This has

98:57

happened before where I tried something

98:59

and I thought it was something else but

99:01

it it was some basically it was a white

99:03

powder and it was labeled with something

99:05

for

99:06

>> a yellowine yellow liquid

99:08

>> urine or something.

99:09

>> Oh urine urine. No, I'm joking. It's

99:11

not. [laughter] I can

99:13

>> I don't think drinking urine uh is is

99:15

longevity but yeah on and off I I do

99:18

take a teaspoon of olive oil in the

99:20

morning and mix it with rveratrol

99:22

polyphenol.

99:24

>> Oh okay. Interesting.

99:26

>> Okay. Okay. So, extravirgin good.

99:29

>> And there's a lot of evidence, not just

99:30

molecular like me, but

99:32

epidemiologically, people that that have

99:34

a lot of olive oil in their diet tend to

99:36

have low inflammation and less disease.

99:39

>> And we've got some nuts.

99:41

>> Yep. Nuts are good for many reasons.

99:42

They're full of vitamins and minerals.

99:45

Uh if there's a Brazil nut, you want to

99:46

have one of those every day for the

99:48

selenium, which is a very rare element

99:51

in our food supply. And there's a recent

99:53

study just last month showing that a

99:56

lack of selenium um can be very

99:59

delotterious. So nuts are great as a

100:01

snack. Be careful. They're full of

100:03

calories though. So if you're trying to

100:05

lose weight and you're not exercising a

100:07

lot, don't overeat on the nuts.

100:10

And what? Oh, my least favorite food,

100:14

but nevertheless, I will eat them. This

100:16

is a Brussels sprout.

100:19

Um when I was a kid, Brussels sprouts

100:20

tasted a lot more a lot worse. bitter.

100:22

[clears throat]

100:23

>> Those are good u because they have

100:26

polyphenols, but there's also another

100:27

molecule in them called sulfurophane.

100:30

It's actually the reason they taste

100:31

terrible and smell terrible.

100:33

Sulfurophane is what it sounds. It has a

100:36

sulfur atom in it and that gives it that

100:40

rotten egg smell. But sulfurophane

100:42

activates these hormesis pathways.

100:45

There's one called NRF and that is a

100:48

stress response

100:50

protein that sulfurophane activates. So

100:52

you actually by eating preferably

100:55

relatively steamed not fried to death

100:58

Brussels sprouts, you'll get

100:59

sulforophane. You can also take

101:01

sulforophane as a supplement if you

101:02

don't like Brussels sprouts.

101:04

>> You've used this word pulsing before. Uh

101:06

you believe that the body should go

101:07

through cycles of stress and recovery

101:09

rather than receiving constant daily

101:11

inputs. When you say pulsing, what do

101:13

you mean? What? Give me an example of

101:14

pulsing and why I need to do that.

101:16

>> Well, there's there's a few examples.

101:18

The first time I came across this result

101:21

as a scientist was resveratrol. So,

101:23

resveratrol is found in red wine among

101:25

other things.

101:26

>> And uh it's thought to give the the

101:28

health benefits of red wine. And we fed

101:30

it to mice, fat mice, skinny mice, old

101:33

mice, and it worked very well in the fat

101:35

mice. It made them thinner. It made them

101:38

live longer. It cured most of their

101:41

diseases. They lived about I think it

101:43

was 15 20% longer. Then we gave it to

101:46

normal mice every day and they lived a

101:50

little bit longer but not significantly.

101:52

>> Resveratrol.

101:52

>> Resveratrol. What we found to my

101:54

surprise what does when we gave old mice

101:56

rveratrol not every day but every second

101:59

day then they lived significantly

102:02

longer. So then I thought well maybe

102:05

giving them a foreign substance every

102:08

day is not good. Maybe there's some side

102:10

effect that's counteracting the benefit.

102:13

The other thing I want to mention, I

102:14

said there's a few examples. Another

102:15

good one is metformin. Metformin has

102:18

been shown to make athletes and

102:20

bodybuilders and people who go to the

102:22

gym, weightlifterss, um, do less

102:25

repetitions and as a result, their

102:27

muscles are about 5% less compared to

102:29

those that don't take metformin in size.

102:33

I don't think it's molecular. I think

102:34

it's because you feel a little bit

102:36

weaker with metformin because it's

102:38

actually interfering with your body's

102:39

ability to make energy through

102:40

mitochondria.

102:42

Mitochondria, I think most people have

102:44

heard of the little power packs living

102:46

in our cells originally bacteria that

102:48

came into our bodies. The point is that

102:51

by pulsing metformin, I think that's a

102:53

better way to do it for longevity.

102:55

>> You mean cycling it? So like doing it

102:57

every other day or

102:58

>> Yeah. Yeah. Okay. Yeah. [clears throat]

102:59

I don't take if I take metformin or the

103:01

natural equivalent which is bourberine.

103:04

If you don't want to take the drug, you

103:05

can take bourberine. Um, that also

103:07

activates this AMPK, this other so to

103:11

and like pathway. Taking it every other

103:14

day, I think is better. And particularly

103:16

if you like to work out, don't take the

103:18

metformin a few hours before you work

103:20

out. Take it after or maybe skip it that

103:23

day. I think that's a better approach.

103:26

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103:27

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be in touch. We talked about exercise

105:17

earlier. On page 102 of your book, you

105:20

talk about how there's a CDC funded

105:23

study that found people who exercise

105:25

regularly, about 30 minutes of jogging 5

105:27

days a week, have telomeres that look 10

105:31

years younger than sedentary people,

105:33

people that just sit around all day and

105:35

do don't do much exercise,

105:38

which is pretty remarkable.

105:40

How do we know it's the exercise and not

105:41

something else? Like how are we able to

105:43

establish causation there?

105:44

>> Yeah, we don't. We don't. Unfortunately,

105:46

all of these association studies just

105:48

lead to a need to do placeboc controlled

105:51

or at least controlled trials in people.

105:54

So, we don't know for sure speaking like

105:56

a scientist, but there have been studies

105:59

where people are told to do exercise and

106:02

those that are told to sit and then you

106:03

can compare tum length and that has been

106:05

shown. So, that's a much better evidence

106:07

of causation. But you're right. When you

106:10

see an association, it could be that

106:11

people who do exercise also eat

106:14

>> well and drink matcha,

106:15

>> sleep better and

106:16

>> Exactly. So, you have to be careful

106:18

interpreting these association studies

106:19

always. But when you've got a placebo

106:22

control trial or you know these these

106:25

studies that are called uh prospective,

106:27

not retrospective studies, then they're

106:30

better. So, tieumirs are the ends of

106:33

chromosomes that get shorter as you as

106:34

you get older. Um, we used to use them

106:37

really as a good indicator of age,

106:39

biological age. Now we use the

106:41

epiggenome and the DNA methylation

106:42

chemicals as a better clock.

106:44

>> And then cold plunges and sauners.

106:46

>> Yeah, let's get to those.

106:47

>> I've got a sauna in the house, but I

106:49

never use it to be honest.

106:50

>> You should.

106:51

>> But if you if you tell me I should maybe

106:53

we should actually jump in there after

106:54

this.

106:54

>> Well, your girlfriend's still here,

106:55

David. So,

106:56

>> she can come [laughter] too. Uh, so

106:59

sauners are in my mind it it's not even

107:02

a question. They are proven to be

107:03

beneficial for multiple reasons. Heart

107:06

disease and even long-term mortality.

107:09

>> What's going on in the sauna in the

107:10

heat?

107:11

>> Anyone who says they know is lying. We

107:13

don't know. But one theory that I like

107:16

and it also goes back to yeast cells.

107:18

There are what are called heat shock

107:19

proteins that come on and defend the

107:21

cell when they the cell senses heat. And

107:25

it may be that these heat shock defense

107:27

proteins called HSC, HSPS

107:30

uh come on when we breathe in this moist

107:33

hot air, the moisture actually seems to

107:35

help as well. And in many studies,

107:38

mostly on Finnish men, businessmen, uh

107:41

those that go into their home sauners,

107:43

and the majority of homes in Finland do

107:46

have sauners, so they can do these

107:48

studies pretty easily. The bottom line

107:51

is that those that didn't do regular

107:53

quote unquote sauna bathing uh tended to

107:56

die earlier uh in particular from heart

107:58

disease and cardiovascular events than

108:00

than those that did regular sauna

108:02

bathing. So I'm I'm a big advocate of

108:05

sauna. I don't have one in my house, but

108:07

I do have a really hot steam shower

108:09

which I use regularly every day.

108:11

>> And is there a difference between the

108:12

steam room and the sauna in terms of the

108:14

impact here?

108:15

>> I think a sauna is better cuz it gets

108:17

hotter. Yeah. And I I would have a sauna

108:19

if I had my choice.

108:20

>> And the cold plunge,

108:22

>> not a lot of data, but there's a lot of

108:24

theory that again hormesis adversity,

108:28

feeling better. There's there's some

108:30

evidence that it can actually help with

108:31

muscle repair after workouts. But I

108:34

think we need a lot more research in

108:36

that regard. But then nevertheless, I

108:38

used to do it um before I was so busy

108:41

and traveling the world. Um and I

108:43

certainly feel better. So, even if I

108:44

don't didn't live longer because of it,

108:46

I I definitely had more mental clarity

108:48

and I felt better in general.

108:50

>> But but if you were if you were

108:52

prioritizing all of the things we've

108:53

talked about so far and you had to pick

108:55

one,

108:56

>> do I have to pick one? Cuz you need more

108:58

than one. But

108:59

>> in terms of like the most important one,

109:02

that's maybe the first domino.

109:03

>> Yeah. I I would say that the a

109:07

combination of what the easiest biggest

109:09

impact you can have combine that that

109:11

would be skipping meals. skipping meals.

109:14

>> Skipping meals. And then a close second

109:15

would be exercise that includes losing

109:19

your breath for at least five minutes

109:22

three times a week. So what do I mean by

109:24

losing your breath for 5 minutes when

109:26

you couldn't carry out a conversation

109:28

easily that you're panting? If you're

109:30

not panting and you're just lifting

109:32

weights, that's not going to have the

109:33

the kind of benefit.

109:35

>> Why?

109:36

>> We don't know. But it's been shown that

109:38

the health benefits and those that live

109:41

long

109:43

tend to do a lot more aerobic exercise,

109:45

not just weights. But both are important

109:48

for mobility, strength, falling in older

109:52

age, and hormones like testosterone,

109:54

>> red light therapy, um the red light

109:56

masks.

109:58

>> Yeah. Um

109:59

>> red light sauners.

110:00

>> At first, I was skeptical. Uh but I've

110:02

done the research on the research. Um,

110:05

and it looks reasonable. I I use a red

110:08

light cap on my head to preserve my

110:11

hairline. And uh there's some now good

110:13

evidence that the mitochondria, which

110:15

are the power packs, and a lot of, you

110:18

know, good things come from

110:19

mitochondria. They actually are

110:21

rejuvenated, either rejuvenated or

110:24

enhanced by this certain wavelengths of

110:26

red light. You have to get the

110:27

wavelength right. But, uh, it's not BS.

110:30

It sounds like BS, right? how you shine

110:32

light on your skin and it gets better or

110:34

you get your hair. But, uh, I think that

110:36

there's good evidence now that that it's

110:38

not BS.

110:39

>> And in terms of the supplement stack

110:41

that you take every day.

110:43

>> Mhm.

110:44

>> If I was to look at the on a if on a

110:47

great week where you just did everything

110:50

right, what would your supplement stack

110:52

look like? And I know this evolves over

110:53

time, so I'm very keen to hear what it

110:55

is right now.

110:56

>> Yeah. Well, that that would be another

110:57

podcast uh to go through each one of the

110:59

things. And well, I I I travel with

111:02

Serena with with a a little little case.

111:04

>> Have you got it?

111:05

>> I've got it here.

111:06

>> Can I see it?

111:07

>> Well, no, it's not in it's not in the

111:09

studio. Oh,

111:09

>> okay.

111:10

>> I didn't bring it with me.

111:10

>> Can you send me a photo?

111:12

>> Sure. Uh, I couldn't publicly share it

111:15

because it would be posted all over the

111:17

internet. Would things would go crazy,

111:18

but I can tell you the the main things.

111:20

>> Why would it go crazy on the internet,

111:22

would you think? Cuz it's cuz it's

111:23

because there's a lot in there.

111:25

Well, some of the things are

111:26

experimental and I wouldn't want people

111:29

>> to

111:30

>> to go nuts about it because it's still

111:31

experimental.

111:32

>> I'm okay experimenting on myself. I'm

111:35

not okay advocating for things that are

111:37

not yet proven or known to be absolutely

111:39

safe.

111:40

>> Okay. So, give me the ones that you know

111:41

to be safe.

111:42

>> Uh well, the enemy we've covered. Yeah.

111:46

>> Resveratrol

111:48

and either metformin or bourberine.

111:51

>> Yeah.

111:52

>> Okay. Spermadine. Spermadine.

111:55

>> Yeah. And the quantities are either on

111:57

the screen or in my book if you want to

111:58

know exactly.

111:59

>> Is that what it sounds like?

112:00

>> Uh, yes. [laughter] Yes. But you get it

112:04

these days not from sperm or semen, but

112:07

you get it from wheat germ typically

112:09

plants.

112:10

>> It used to come from sperm.

112:12

>> Well, that's how it was discovered. It

112:13

was crystallized by, I believe, Anthony

112:16

von Lewan Hook, the one of the first

112:17

microscopists and microbiologists.

112:20

Spermadine. The reason that I take it is

112:22

that it extends the lifespan of every

112:24

animal that it's been given to from

112:27

worms to to mice. And it's a very safe

112:29

molecule. So that I always weigh up the

112:31

downsides versus the upsides. And if

112:34

there's no downsides and I can afford

112:36

it, which you know, I work really hard

112:38

that so I can afford it and I prioritize

112:40

my health, then I take it. And if you're

112:44

wondering how it works, it seems to

112:46

stimulate autophagy, recycling of

112:48

proteins. It helps with the fasting. Uh

112:51

but I also have some evidence uh that it

112:54

delays the epigenetic information loss.

112:57

So it's slowing down the scratching of

112:58

the record.

113:00

>> Spermadine.

113:01

>> All right. So um I'm also um keen on

113:04

glycine. Glycine is a very safe

113:07

substance. It's an amino acid, one of

113:09

the 20 amino acids that makes proteins.

113:12

And I actually did a PhD on glycine. I

113:15

was one of the first people to perhaps

113:17

the first person to clone genes that

113:19

process glycine. So I know know it well.

113:22

For some reason when you give animals

113:24

and for instance mice grams of glycine

113:28

so I take about 5 g of glycine most days

113:31

uh they live longer though it's still

113:33

speculation as to why. What I think is

113:36

going on is that glycine controls what's

113:39

called one carbon metabolism. And not

113:42

wanting to bore the heck out of everyone

113:44

who's listening to me, glycine and one

113:47

carbon metabolism controls methylation

113:50

of DNA. Getting back to the little

113:52

chemicals that are on this DNA molecule

113:54

that control the information.

113:57

I wouldn't be surprised if by eating a

114:00

lot of glycine every day, I'm slowing

114:03

down this identity crisis you called it.

114:06

Nevertheless, it's very safe and again

114:08

falls into the same category as

114:09

spermadine. No downside. Can't afford

114:13

it. Why not?

114:15

>> Is there anything else?

114:18

>> Yeah, there's a lot. Um because I love

114:20

you and your listeners. Uh let's see. I

114:23

I'll I'll I'll reveal one more. Um there

114:27

are there are some basics that I do

114:28

there are if you're not doing them I

114:30

think is is where very wise make sure

114:32

you're not deficient in vitamin D

114:34

obviously we just mentioned one of the

114:36

reasons why [snorts]

114:38

it's also if you're lacking vitamin D

114:39

you can be uh susceptible to certain

114:41

cancers so I take a vitamin D supplement

114:44

Serena actually I take Serena's

114:46

supplement because her vitamin D has

114:48

vitamin K2 as well and K2 is another

114:51

vitamin that's important for longevity I

114:53

believe because it keeps calcium out of

114:55

your arteries which causes plaque

114:57

>> and tends to make your body put it into

114:59

where it belongs which is your bones.

115:01

>> What about aspirin? I read that

115:03

somewhere.

115:04

>> Yeah, that that that could be a whole

115:05

podcast actually. But the briefly I take

115:09

a baby aspirin every day even though

115:12

some doctors um and some institutions of

115:15

doctors say don't take it anymore even

115:17

though it used to be prescribed and

115:19

recommended. Why?

115:21

A large study looked at the risks versus

115:23

benefits. So the known benefits are you

115:26

inh inhibit platelets, you get less

115:29

clotting, you get less potentially

115:31

uh stroke and heart attack. But there

115:34

are also some downsides in some people.

115:36

You can have more bleeding in the

115:37

stomach. And when the doctor's

115:40

association weighed up those risks

115:42

versus benefit, they said, "Oopsy, we're

115:45

not going to recommend aspirin anymore."

115:47

But that's for the average person.

115:50

Someone like me, I believe it makes

115:52

perfect sense to take aspirin

115:54

every day, most days at least when I

115:57

remember. And that's because I have a

115:59

high risk of cardiovascular disease. I

116:02

don't just have high cholesterol

116:03

naturally. I have high levels of

116:05

something called LP little A, capital

116:07

LP, parentheses little A. And this is a

116:11

molecule that's just as important as

116:12

cholesterol, LDL. um LP little A is a

116:16

protein that inserts itself into

116:17

cholesterol particles that circulate

116:19

your blood and gets in helps insert into

116:21

plaque. So I naturally genetically

116:24

having an ancestry of um Judaism in

116:28

going back to my great ancestors which

116:30

by the way I traced back a thousand

116:32

years during during Christmas. Those

116:34

people that I descended from have this

116:36

LP little A gene that makes a lot of it.

116:40

And so I try to bring LP little A levels

116:42

down. Most people should test for it.

116:44

Ask your doctor about LP little A and

116:47

get it tested high levels like me 30 40

116:52

uh you want to bring it down because it

116:53

it's actually very important for

116:55

longevity. Uh normal levels of around 10

116:58

or so or less then a doctor wouldn't

117:01

panic. So LP little a uh get it tested.

117:05

The way I'm bringing it down, just a

117:07

little uh tidbit again because I love

117:09

you, Stephen, is I'm taking highdose

117:14

vitamin B3 or nascin.

117:16

Now, it can be uncomfortable for some

117:18

people to take it because it gives

117:20

flushing. You get little tingling in

117:21

your skin. And if you're not used to it

117:24

or you don't take it with an aspirin,

117:25

you'll feel hot almost like menopause

117:28

apparently. And so, I I I take it. I

117:30

built up to it. I'm taking half a gram.

117:32

Some people take a gram. And that's one

117:34

of the few things that's been known to

117:36

bring down the levels of LP little A.

117:39

There are drugs that are in development,

117:40

even in phase three, that look

117:42

promising, but until they're on the

117:43

market, I'm taking Nison instead.

117:45

>> What's the best uh treatment you've

117:47

discovered for hair loss? Hair loss,

117:49

hair graying, that kind of thing.

117:51

>> Yeah. So, my father went bald before 30,

117:54

like completely bald, right? And

117:56

completely almost completely gray by the

117:58

time he was 40. So, I'm super lucky,

118:01

right? I thought I'd be bold at 30. I

118:02

was pretty worried about it. So, I've

118:05

been doing the right things

118:07

intentionally. So, what I do is this red

118:10

light cap when I can. I don't travel

118:12

with it, but uh when I can, that's for 6

118:15

minutes. Stick it on there.

118:17

>> Proven? Is it?

118:18

>> Yeah. Proven. It's proven to slow. It

118:20

doesn't necessarily give you your hair

118:22

back. But when it comes to hair loss,

118:24

don't wait till you see the hair loss.

118:27

That can be too late.

118:29

>> Okay. You're you're good.

118:30

>> I'm okay.

118:30

>> You're good. But I know a lot of men are

118:32

are concerned. It's understandable.

118:35

I'm taking a hormone mimedic to stop uh

118:39

DHT, which is the form of testosterone

118:42

that leads to men related hair loss.

118:46

Right. So, one of the reasons that women

118:47

don't lose hair as much as men is this

118:49

DHT. So, I'm I'm blocking that.

118:52

>> So, so let me get that straight. You're

118:53

not taking testosterone?

118:55

>> No.

118:56

>> Because that's going to accelerate your

118:58

hair loss. Well, it can if it raises

119:01

DHT. The best way to raise testosterone

119:03

naturally is to build up muscle,

119:05

especially your legs, your back, big

119:06

muscles. That's another reason to work

119:08

out and maintain muscle mass, which I

119:10

need to do more of. You look like you're

119:12

in good shape already. But yeah, anyone

119:14

who is losing testosterone is is below a

119:16

level of about 400, highly recommend

119:18

hitting the gym. It'll go back up.

119:21

>> Do you recommend men taking testosterone

119:23

replacement? Um, well, I'm a scientist,

119:26

so I don't recommend drugs, but um, I

119:28

don't think it's necessary for most men.

119:30

I would start with, uh, reducing stress,

119:33

sleeping well, exercising, building up

119:35

muscle mass. Uh, and then if that

119:37

doesn't work, yeah, talk to your

119:39

physician. There there's not a big

119:40

downside. There's not a risk of cancer

119:42

to taking testosterone. I'm one of my

119:45

good friends has done many clinical

119:47

trials with testosterone. So, I think

119:49

there's a use of use for it, but it

119:51

doesn't lead to longevity. That was very

119:54

clear. So for for health reasons, yes,

119:57

for longevity, no need. What are the

120:01

what are some of the um you know when I

120:02

started watching your your videos many

120:04

years ago listening to your podcast and

120:06

following you on Twitter I I wondered

120:08

you know there's so much information you

120:10

can put out there because you're a

120:11

scientist and scientists are very

120:12

rigorous but you also must have a set of

120:15

really

120:17

interesting predictions or visions of

120:20

the what the future looks like that you

120:22

don't probably always talk about because

120:24

they're not scientific. They're not

120:25

based on anything. now maybe first

120:27

principles in your own mind that formed

120:29

where you go actually I think the world

120:31

might look like this and I think it

120:32

might happen then I'd love to hear about

120:33

some of these

120:36

>> and I understand they're not rigorous

120:37

>> I'm happy to what happens to me because

120:40

I'm a scientist and you know I'm part of

120:42

this ivory tower at Harvard where we can

120:46

only stick to facts and if you go beyond

120:48

that it's it's a it's a crime and I've

120:51

been criticized for that um but I think

120:53

you know as humans life's interesting

120:55

when it comes to predicting the future

120:58

and like you I'm very curious where is

121:00

humanity headed

121:02

I see a future as different from this

121:04

world as our world is from 200 years ago

121:08

and that will happen in our lifetime

121:11

different in that 100 years ago or more

121:13

if you had an infected splinter there's

121:15

a reasonable chance you could die

121:18

childirth you could die smallpox these

121:21

are things that we don't generally worry

121:23

about anymore and the idea would be

121:25

abhorrent.

121:27

In the future, hopefully within our

121:29

lifetimes, there will be a time when we

121:31

look back at today's medicine when you

121:33

could go blind and there was nothing you

121:35

could do. You could break your back and

121:37

never walk again. We will look back at

121:40

today and say, "How did those people get

121:43

through life? What a horrible world they

121:45

lived in." That I believe is is the

121:47

future that humanity is headed for and

121:50

way faster than most people realize is

121:53

coming. The kind of breakthroughs that

121:54

we've discussed today, most people have

121:56

never heard about the fact that we are

121:58

aiming and already do cure blindness in

122:00

monkeys like pure blindness. This isn't

122:03

just, oh, I can't see a little bit.

122:05

These are completely blind animals. Um,

122:09

and that they can see again in a matter

122:11

of 6 weeks. This is remarkable stuff,

122:14

right? And if it works this year in

122:17

people, it's going to be a really big

122:20

deal because for the first time, we we

122:22

have we'll have shown in humans that the

122:25

body can be reset safely.

122:28

And the eye is just the beginning,

122:29

right? The future looks like we can

122:32

rejuvenate potentially any tissue. If

122:35

you have a bad liver, we'll make it

122:37

young again. Bad brain, you've lost your

122:39

memory, we'll give you those memories

122:41

back again. We do this in mice in my lab

122:43

all the time. It's not even a big deal

122:45

in my lab anymore to reverse the age of

122:48

tissues and anal in an animal in a

122:51

matter of weeks. That is coming for

122:53

humanity hopefully initially this year.

122:57

But even if that doesn't work, it's only

122:58

a technical issue. We'll solve that. You

123:01

might be wondering how do we get the

123:03

rejuvenative genes into the body? And

123:06

what we do is we use a package that uh

123:10

is able to get into cells. And this is a

123:13

package that uh resembles a virus. It's

123:16

not a virus. It doesn't cause disease.

123:18

It's not infectious. But we package our

123:20

three genes inside the virus

123:23

uh virus like uh substance. And we close

123:27

it up. We just made a bunch of this in

123:29

Europe for the clinical trial that's

123:31

going to begin. Just making this is

123:34

difficult. It took us about a year to

123:36

make it and was about I think it was $10

123:40

million.

123:42

Right now it's expensive to do this.

123:44

Eventually it will be cheap and

123:45

eventually it will be a cheap pill.

123:47

Hopefully we have trillions of these

123:50

molecules, these delivery vehicles that

123:53

will go. So you can pass me the eye.

123:56

We're gaining back this eye model. These

123:59

delivery vehicles with our three genes

124:01

will be delivered. Obviously these are

124:03

microscopic. They go in through the eye

124:06

with a with a quick jab. All right. It

124:09

sounds horrible, but a quick jab into

124:11

the eye. If you're blind, who cares?

124:13

>> Yeah,

124:13

>> it's 2 seconds of discomfort. Now,

124:15

you've got the little virus,

124:18

which I'm going to break off the stand

124:19

here. The little virus, there's billions

124:21

of them, trillions of them in the eye.

124:23

Now, they infect specifically the nerves

124:25

at the back of the eye in the retina.

124:27

>> How do they know what to infect? Because

124:29

these little balls on the on the package

124:32

direct it specifically by design, by our

124:34

lab's design just to those nerves at the

124:37

back of the eye. If we change these

124:39

little proteins on the surface, we can

124:41

send it to the liver or to the brain.

124:44

This is the zip code, the post code for

124:47

where we want to send our three genes.

124:48

>> Mhm.

124:50

>> But this one's designed for the eye.

124:52

It's called an AAV2.

124:55

Um, long story short, these are ready to

124:58

go into humans. We're just waiting for

125:00

FDA approval to inject it into a blind

125:03

patient to see what happens.

125:05

>> And then inside there is the protein

125:07

which is going to fix the

125:10

[clears throat]

125:11

>> Well, actually, not the protein. What

125:14

actually happens is when this goes in

125:16

the eye, this what I'm So, what I'm

125:18

holding up looks like a little ball with

125:19

red dots on it. Um, it looks like a

125:22

virus, but it's not. It's a package. Now

125:25

what happens is these trillions of

125:27

little packages go into the fluid. Now

125:30

they they dock with the cells at the

125:32

back of the eye. They get inside the

125:34

cell and they open up and out comes this

125:37

little package that we've made.

125:40

This is a protein package. Each one of

125:43

these little dots on this little soccer

125:46

ball is a protein that's now inside the

125:50

cell. This is a little spaceship that

125:53

opens up and out of that

125:58

comes the DNA. This is a loop of DNA

126:02

just here. These are this is the DNA

126:04

package that we put in there. Trillions

126:06

of them. One of them gets into one cell

126:10

and now stays in that cell forever. So

126:12

that person or the monkey or the mouse

126:15

that we've treated becomes a transgenic

126:18

person with genes that we've put in

126:22

permanently into the back of the eye,

126:24

but they don't do anything until we tell

126:26

them to. That's now just sitting there.

126:30

We've engineered it uniquely and

126:32

patented the ability to turn on those

126:35

three genes whenever we want and turn

126:37

them off again whenever we want.

126:39

>> How? We give them doxycyc. It's used for

126:44

malaria. It's used for Lyme disease. And

126:46

we're using it in this case to turn

126:48

these genes on. So the patients will get

126:51

their doxycycline.

126:53

uh we'll give them some probiotics to

126:54

restore hopefully we'll we'll restore

126:56

their microbiome of course but the idea

127:00

is that this doxycycl will turn on these

127:03

three genes for about 8 weeks and the

127:07

doctor in charge of the clinical trial

127:09

one of them's at Harvard a good friend

127:11

of mine he'll measure the vision of the

127:13

first patient before the treatment and

127:15

of course regular intervals and if all

127:18

goes well because we're treating

127:20

patients not healthy volunteers in the

127:22

first trial trial, we should know within

127:24

a either one or two patients if it works

127:28

because we're not drawing a graph. It's

127:31

either going to work or it isn't.

127:32

>> Mhm.

127:32

>> The patient gets better eyesight or it

127:34

does or they don't. So by this time next

127:37

year, we will know if it works or not.

127:40

Maybe even sooner. But publicly, we may

127:43

know if this works. And if it works, the

127:46

eye is just the beginning. So the first

127:48

disease to treat is glaucoma, pressure

127:50

in the eye. There's also a stroke in the

127:52

eye which is becoming more prevalent in

127:54

the world because of the ampic and other

127:56

weight loss drugs and people go blind

127:58

overnight and there's nothing that you

128:00

can do for those patients. They're blind

128:02

and their other eye cannot can go a few

128:04

months later. It's very scary for them.

128:06

These are young people. A friend of mine

128:08

had it happen. It's pretty common these

128:09

days about 30,000 people each year in

128:11

the US alone. But these two diseases are

128:14

the beginning. If they work then we go

128:16

on to macular degeneration which is the

128:18

largest cause of blindness besides

128:19

glaucoma. Then we'll go on to liver then

128:23

maybe the lung the skin and we'll keep

128:26

going from there. We'll make different

128:29

packages for different organs and

128:31

ultimately we want to rejuvenate the

128:34

entire body. The company um people might

128:36

want to know it's called life

128:37

biosciences. It's a private company but

128:40

life biosciences I'm very proud of the

128:41

scientists who are doing this work. big

128:43

goal is to really make the world's first

128:46

age reversal medicine as a pill and

128:48

we're working with them using AI to find

128:51

that molecule.

128:52

>> And when do you think you might have it

128:54

if you had to forecast?

128:56

>> Uh

128:56

>> the world's first age reversal molecule.

128:59

That's

129:00

>> Well, we have right now we're down to

129:03

three molecules that work and we're

129:05

using AI to make all of those three in

129:08

one and we're we're in the middle of it.

129:11

We screened about 8 billion candidates

129:14

using AI and right now we're doing the

129:17

bench lab work to see if one of them or

129:20

more works. And for us to put that in

129:23

humans is still a number of years away.

129:26

But we should know within a year or two

129:29

uh if we're right because we'll we'll

129:32

put them into mice and if they get

129:34

younger and live longer then we're

129:36

really on to something important. And

129:38

the reason that I want to make a pill um

129:41

is is important for the planet. These

129:44

drugs are expensive. I mentioned 10

129:46

million bucks to do a clinical trial.

129:48

These are expensive. They could cost

129:50

over $100,000 per treatment. That's not

129:53

going to be for everybody. It's worth it

129:55

if you're blind. It's worth it for the

129:57

country to cure blindness. But what if

130:00

it could be instead of $100,000,

130:03

$100? That's what I'm working for. I

130:05

want to democratize this technology so

130:07

anyone even in Kenya can take these

130:10

medicines.

130:12

>> David, what's the most important thing

130:13

we haven't talked about that we should

130:14

have talked about as it relates to

130:17

>> the future longevity

130:20

and these adjacent subjects?

130:22

>> There's a lot of things and there's

130:23

there's push back. There's philosophical

130:25

push back from

130:27

>> religious folks who don't believe that

130:29

we should play God. And I would I would

130:31

argue to them that we've been doing that

130:34

as a species for thousands of years,

130:36

changing our biology, taking medicines,

130:39

plant medicines originally.

130:41

What about this room is natural?

130:44

>> Right? We change our world as species.

130:46

Aging is no different. In fact, it's

130:48

crazy that we haven't worked on it

130:49

sooner.

130:50

>> Do you believe in God?

130:52

So the the the the short answer is I

130:55

believe that there is something beyond

131:00

reality as we see it. You know I study

131:03

physics. Physics is so weird and anyone

131:06

who says they understand the quantum

131:08

world or quantum mechanics is I think is

131:10

also lying there. It's so bizarre.

131:13

Quantum entanglement simulation theory.

131:16

So I believe that that this this is not

131:19

a solid desk. I believe that there are

131:21

multiple versions of it. Maybe infinite

131:23

number of versions of this desk.

131:25

>> We've got four.

131:27

>> You do?

131:27

>> We've got four of them.

131:28

>> Yeah. But it's four times infinity. Um I

131:32

also I also believe that consciousness

131:35

is the ultimate goal of the universe

131:39

that consciousness creates reality. We

131:41

know that from particle physics. The

131:44

observation of particles changes their

131:46

reality even retrospectively in time.

131:49

Apparently,

131:50

>> when you look at them,

131:51

>> when you observe them, you can use a

131:52

camera or you can use your eyes.

131:54

Usually, it's a detector, but the the

131:58

detection and then conscious

132:00

interpretation of a particle's behavior

132:02

changes how it acts.

132:06

So, does does this mean that there's

132:08

something behind this wall unless we

132:10

look at it? Maybe, maybe, maybe

132:12

observation creates reality. We know it

132:14

influences reality. So, I don't know if

132:17

I would call it God, but I'm definitely

132:20

spiritual in a scientific way.

132:22

>> Has it ever dawned on you that actually

132:25

you might be the only real person here?

132:29

And actually, we only we all render when

132:31

you walked in, David,

132:32

>> I wasn't here before.

132:34

>> Yeah. Uh, well, that's even plausible,

132:37

but that would be very narcissistic to

132:39

you. [laughter]

132:42

>> I I actually I just rendered when you

132:44

walked in the house today. I I I've I

132:47

don't exist. [clears throat]

132:47

>> Well, there's no way of proving it right

132:49

or wrong, actually. Um I think most kids

132:52

think that initially, [laughter] but

132:53

then you then you realize it's probably

132:55

the least likely explanation for the

132:57

world, but there is some there is some

133:00

truth to that uh in terms of physics. Um

133:03

>> do you think we're in a simulation?

133:05

>> I think there's a better than 50% chance

133:08

that this is simulated.

133:13

>> So, you think it's probably a

133:14

simulation? That's another way. I think

133:15

it's probably a simulation.

133:17

Certainly, the world that we think it is

133:19

is not the world we think it is.

133:21

>> How can you be so sure?

133:22

>> Because when you get down to measuring

133:24

it at the fundamental level, reality

133:26

doesn't exist the way we think it does.

133:31

Things are created, things change just

133:34

by human observation.

133:36

That is the weirdest thing that you

133:37

could ever find in science. I don't know

133:39

why we aren't talking about it more.

133:42

This reality cannot be true if me

133:45

looking at this DNA molecule here

133:48

affects the the actual particles inside

133:50

it.

133:51

>> So I'm I might be sort of projecting it.

133:54

>> Yeah. You create realities of particles

133:57

at least maybe even macroscopic things

134:01

just by existing and having

134:03

consciousness

134:04

and having eyes and sensing it.

134:09

How does the particle know that you've

134:11

seen it?

134:14

>> How do we know that that's true? How do

134:15

we know that particles change based on

134:17

observation?

134:18

>> There's a classic uh double slit

134:20

experiment uh it's formerly called um

134:22

that was done I believe in the mid 20th

134:24

century maybe earlier. If you fire two

134:27

particles through two slits in a board,

134:30

the board blocks the particles. So you

134:32

can fire electrons is a good example.

134:35

Electrons, if you're observing them,

134:37

will go straight through the slits and

134:38

hit a backboard that detects it. Can be

134:40

film, can be a detector, and it'll get

134:43

two slits behind. Makes sense, right?

134:46

That's our reality. Two slits, particles

134:49

go through. If they hit the board, they

134:50

don't go to the detector. If they go

134:52

through one slit, they'll land on the

134:53

left. If they go through the right slit,

134:55

they'll land on the right.

134:56

>> Yeah,

134:57

>> that's our reality.

134:57

>> I'll put a picture on the screen for

134:59

anyone that's following.

135:00

>> Yeah. If you don't look at it, the

135:03

particles can behave

135:05

differently. They now behave not like a

135:07

particle but by a wave as a wave. And

135:10

they interact with each other. And they

135:13

don't make two slits. They make multiple

135:14

lines on the detector. Most of them are

135:17

in the middle. So the heaviest bands are

135:20

in the middle, but they also form other

135:22

bands. The bands go on essentially in

135:25

infinite, but most of it's, you know,

135:26

within a range. Why? because they're

135:29

they're interfering with each other like

135:31

waves. But here's the thing,

135:34

the mere act of looking at where they

135:37

landed, if you are detecting that,

135:40

you'll get two slits at the back, two

135:43

two lines. If you're not detecting it,

135:46

it'll form the pattern.

135:48

>> I'm so confused because

135:50

how would you know unless you were

135:51

looking at both?

135:54

Do you know what I mean? Do does that

135:55

does that question make sense?

135:56

>> Yeah. Well, you can obs observe it in

135:59

real time and you can observe it

136:00

retroactively. Yeah.

136:02

>> Oh, okay. So, if you look at it after

136:04

>> it it generally is not affected, but

136:09

they've done experiments where there is

136:11

some element seemingly of retroactive,

136:13

but generally we're not going back in

136:15

time. In fact, people debate whether

136:17

that's truly measuring back in time. So,

136:19

let's leave retroactive aside. If you

136:22

measure it in real time, you'll see two.

136:26

So the world knows you're looking at it.

136:27

The particles know you're looking at it

136:29

>> with an eye or with can you do it like a

136:31

camera or is it

136:32

>> Yeah, camera eye.

136:33

>> It just knows it's being observed.

136:35

>> Yeah. But if you develop the film later

136:37

and you weren't watching it at the time,

136:39

it's going to have affected the world in

136:41

stripes,

136:44

multiple stripes.

136:46

>> So from that we conclude that we know

136:49

nothing about reality,

136:50

>> right?

136:53

Because everything I'm observing is

136:55

changing by the mere fact that I've

136:57

observed it.

136:58

>> Yeah. And so does an octopus observe?

137:01

Does it affect? Somebody should do that.

137:03

Put an an octopus in there.

137:06

>> Yeah. I think octopi if they are

137:09

conscious it probably would also affect

137:11

reality.

137:13

And I they they'd be conscious. They

137:14

they they'd know they're detecting lines

137:16

on a page.

137:17

>> So what is all this stuff?

137:20

That is one of the biggest questions of

137:22

all time. What is the world made of? Why

137:25

are we here? I think the next big

137:27

question is, do we have to age? And I

137:31

think that other species around the

137:32

universe have figured this out before we

137:34

have. There have got to be other

137:36

species, type of life forms that have

137:39

figured this out. I think it's the goal

137:40

of every living form that's conscious to

137:43

work on this. We've just been a little

137:45

slow to figure it out.

137:47

>> And do you believe in aliens?

137:49

I don't believe in them but I believe in

137:51

mathematical probabilities and

137:54

you know knowing uh the odds and the

137:57

number of planets that are out there in

137:59

the trillions and a lot of them are

138:01

habitable for life and that the stuff of

138:04

DNA and proteins are all over meteorites

138:06

and planets. It'd be crazy to say there

138:09

isn't other life. Now is it a

138:11

civilization? Is it conscious? We don't

138:13

know that. But definitely there's life

138:16

out there. it it it's got to be all over

138:18

the universe.

138:20

>> This question about longevity and living

138:23

forever, it always comes back to this

138:25

point of like meaning and like what is

138:27

the point? And when we think about I

138:29

think there's an alien a million light

138:31

years away on some planet like what is

138:33

the point of their life? What is or am I

138:35

is this like a null and void question

138:37

that we always pursue this point of like

138:39

what's the meaning of life? Is it just

138:41

to have a good time and have, you know,

138:43

I don't know, have sex and have kids and

138:45

or I don't know,

138:48

enjoy ourselves and experience it.

138:51

>> This is the existential crisis of

138:53

conscious beings. We all need to find

138:55

purpose for sure. If you don't find one

138:58

cuz that's a key to longevity. People

139:00

with purpose live longer.

139:03

I think the purpose of the universe

139:05

existing is to allow consciousness to

139:09

emerge through biology. It may be by

139:12

design. It may just be coincidence with

139:14

infinite numbers of universes. But this

139:17

universe is set up for life and

139:18

consciousness. There are some uh small

139:22

changes you can make to physics that

139:24

would make this universe completely

139:27

impossible and life impossible. So this

139:28

this is a life consciousness producing

139:31

universe.

139:33

Does that mean there's meaning to us

139:35

existing?

139:37

No.

139:38

But I do know that consciousness is the

139:41

most interesting and important thing

139:43

that the universe will ever produce

139:46

and that it's worth preserving. So I'm a

139:49

lot like Elon Musk where humans are

139:51

amazing but cruel creatures, but

139:54

consciousness should be preserved.

139:56

>> What is consciousness in this regard?

139:58

Consciousness is the ability to know

140:00

that you're thinking and to be able to

140:02

be reflective, self-reflective.

140:04

>> So, is my dog conscious

140:06

>> partially,

140:07

>> but not in the same way?

140:08

>> No, they don't reflect. They don't think

140:10

about the past in the same way that we

140:12

do, and they're not aware of their

140:13

themselves the way we are, but but

140:15

they're semi-conscious, you know, they

140:17

think. They can predict the future. They

140:20

they know how you're feeling. They have

140:23

empathy. That's that's a form of

140:24

consciousness in my view. Of course,

140:26

it's up for debate. But so there's

140:28

levels of consciousness and and about a

140:31

million years ago, humans crossed that

140:33

threshold into pure consciousness.

140:36

>> Well,

140:36

>> maybe not pure.

140:37

>> I was going to say I was just thinking

140:38

about this. I was like, actually, maybe

140:40

consciousness is just a spectrum and

140:42

maybe there's another organism that I'm

140:44

currently inside the belly of and it's

140:46

going Steven thinks he's conscious. He

140:48

has no idea.

140:50

>> Well, you bring up a good point. Not not

140:53

about being in the stomach of, but we

140:55

are not the ultimate consciousness.

140:56

There are other levels of consciousness.

140:58

Serena Pune, my partner, is definitely

141:00

more conscious than I am. I am like a

141:02

gorilla to her. She exists on other

141:04

planes of consciousness. And you, if

141:07

you're wondering what what do I mean by

141:08

different levels.

141:10

>> No, I've got a girlfriend. Well, a

141:11

fiance, so I know as well.

141:12

>> Well, [laughter]

141:13

females in general, don't kill me. I

141:16

know there there are some some men that

141:17

don't like me saying this. In fact, I

141:19

got a death threat for saying females

141:21

are superior to men in my book. U they

141:23

said they were going to come and break

141:24

my legs, but I'm going to say it anyway.

141:27

Females are at a higher level of

141:29

consciousness than us men for for some

141:31

things. They certainly have much more

141:32

EQ. [gasps] So a higher level of

141:34

consciousness is the ability to have

141:37

extra perception including the ability

141:40

to see yourself thinking. And then my my

141:43

belief is that higher levels of

141:45

consciousness are the ability to see

141:48

yourself seeing yourself seeing yourself

141:50

thinking.

141:54

I couldn't get there. I tried.

141:56

>> Right. Do you do you know you're

141:57

thinking right now?

142:00

>> Yes.

142:00

>> Yeah. Do you have the ability to see the

142:03

events that know

142:06

that you're thinking?

142:14

>> Not. Not really.

142:15

>> It's hard, right?

142:15

>> Yeah. I tried.

142:16

>> It's hard. But I That's what I think

142:19

extra consciousness is. And you could

142:22

maybe have pure consciousness, which is

142:24

you you can you can basically be free of

142:28

anything but thoughts and the ability to

142:32

really be inside your own your own mind

142:35

and it's pure interesting thought is I

142:40

believe AI will be conscious

142:42

and not only that will be more conscious

142:45

than we are

142:48

eventually. There's no reason why they

142:50

can't evolve billions of times faster

142:53

than we do.

142:54

>> Are you somewhat concerned about AI?

142:56

Like, are you concerned that there's

142:58

going to be this intelligent life

142:59

amongst us that might um decide that

143:01

we're not important?

143:03

>> I think that there are risks to AI, but

143:06

but different than what the mainstream

143:08

media talks about. Um, we already see

143:12

that there are elements of self analysis

143:14

and early forms of dog like

143:16

consciousness in AI. And it's just the

143:18

early days, so it's coming.

143:20

Imagine when we stick on eyeballs and

143:23

hearing and legs and arms onto these AI,

143:26

they're going to learn. They're going to

143:27

read. They've already read every book on

143:29

the planet. They're going to learn from

143:30

experience. They're going to be

143:31

conscious. They're going to know they

143:32

exist. I'm not worried about those

143:35

creatures. I think that they will have

143:37

empathy. They will be kind. Not all of

143:39

them. There will be some cruel ones just

143:41

like in humanity. We'll need to have

143:44

rules. Misbehavior uh is a problem. The

143:48

where I I get nervous is that the use of

143:53

AI teaming up with

143:56

a million android robots

143:59

on ships invading a country all under

144:01

the control of you. One person

144:04

recruiting home robots into an army. Why

144:07

wouldn't you have conscription for your

144:09

android robot at home reprogramming that

144:12

millions of them will exist one day?

144:14

They can be put to work, not just

144:16

emptying a dishwasher. These are highly

144:19

intelligent, much more physical,

144:21

stronger creatures than we are. So, I'm

144:24

more worried about what bad humans will

144:27

use AI and robots for for evil purposes.

144:32

your um you have a podcast that's um

144:36

coming back.

144:37

>> Exactly. Yeah. Excited. Yeah.

144:39

>> Yeah. So, Lifespan uh the podcast um I

144:43

did the podcast because uh there was so

144:46

much new information that needs

144:48

interpretation by scientists. There's a

144:50

lot of speculation out there and new

144:52

news that I want to

144:55

filter and and and interpret for

144:58

everybody who is interested in living

145:00

longer. So, the podcast um went to

145:02

basically went to number one in in

145:04

health when I started it. Um I took a

145:06

pause cuz I I worked on drug development

145:09

and I did some other things, but I've

145:11

realized there's such a demand. Wherever

145:13

I go, people say, "David, when when's

145:14

the next series?" So, we're going to be

145:17

launching it uh imminently. If not,

145:20

we've just launched it

145:22

>> and uh it's called Lifespan. Check it

145:24

out. And it's all about the kind of

145:26

things we've talked about today, but

145:29

a lot more about digging in deeper into,

145:32

you know, biohacking, supplements,

145:34

exercise, the kind of things we didn't

145:35

have time to talk about today. But we

145:37

covered a lot. Um, I've loved the

145:40

conversation, but lifespan.com is also

145:42

the website. What I'm also doing,

145:44

Stephen, I don't think I told you this.

145:46

I'm I'm aiming to build the world's

145:49

largest longevity community online for

145:52

the benefit of the members who want to

145:55

be part of this to learn from each other

145:57

not just from me. Um I call it the three

146:00

C's with credibility which is what I

146:02

bring cuz I'm a scientist content which

146:05

is my podcast and other written

146:07

material. And then there's the

146:09

community. And that way, I think with

146:11

millions of people together, we can

146:12

learn faster and make advances. And the

146:16

majority of the profits from membership

146:18

will go to science and clinical trials.

146:22

>> Where where do we find that? On your

146:23

website,

146:24

>> lifespan.com.

146:26

>> We have a closing tradition on this

146:27

podcast where the last guest leaves a

146:28

question for the next, not knowing who

146:30

they're leaving it for. And I have a

146:32

funny feeling that I

146:36

h I basically asked you this question

146:38

already.

146:40

[sighs]

146:41

The question is, what do you believe is

146:44

the purpose of life?

146:47

>> Well, I'm going to give a different

146:48

answer because there are multiple ways

146:49

to answer it.

146:52

I think the purpose of life is to do

146:55

your best with the skills that you've

146:58

been given.

147:01

every day to make the world a better

147:03

place for future generations. And that's

147:06

how I live my life every day.

147:09

Thank you. Thank you for doing all that

147:11

you do. You really are pushing the

147:12

frontier forward and uh trailblazers.

147:17

Being a trailblazer comes with a cost, a

147:20

cost many people wouldn't want to pay. I

147:21

mean, you you have to be wrong a lot in

147:22

terms of running experiments and studies

147:25

and them not going to plan. And then you

147:26

get the opportunity to be right probably

147:28

less often I guess with your research

147:30

and experiments because that's the

147:31

nature of being a scientist. Um but also

147:35

you have to spend a lot of money and

147:36

energy and time on creating these

147:39

discoveries which we all ultimately

147:40

therefore benefit from. And you've done

147:42

a fantastic job of convincing and

147:45

educating people like me on some of the

147:47

basics of exactly what your book says,

147:50

why we age and why we don't have to. and

147:54

many of the the accessible lifestyle

147:56

factors that everybody listening now can

147:58

can use to live a longer, happier,

148:00

healthier life for them and their loved

148:02

ones. And I highly recommend people go

148:04

and get your book. It's it was a smash

148:05

hit New York Times bestseller for very

148:07

very good reason. And you the great

148:09

thing about this book is you don't have

148:11

to be a scientist to fly through it. Um,

148:14

and often times when you're looking at

148:16

sort of PubMed and some of these

148:17

scientific journals, they're incredibly

148:19

inaccessible. They're very, very

148:22

complicated. Um, but I also recommend

148:23

people go follow you on social media.

148:25

That's where I see so so many of your

148:26

updates, especially on X. That's kind of

148:27

where I've you continually come up on my

148:29

timeline when you're talking about new

148:30

research and things you're interested

148:31

in. Um, and go to your website. I'm

148:33

going to link all of that below for

148:35

everybody who's interested in more. And

148:37

also, I'm going to link your podcast

148:38

below so people can go and check it out

148:40

when it relaunches shortly. Might have

148:42

relaunched already, but just go look in

148:43

the comments se in the description

148:44

below. David, thank you.

148:46

>> Thank you, Stephen. I really enjoyed it.

148:48

Thank you. YouTube have this new crazy

148:50

algorithm where they know exactly what

148:52

video you would like to watch next based

148:54

on AI and all of your viewing behavior.

148:56

And the algorithm says that this video

148:59

is the perfect video for you. It's

149:02

different for everybody looking right

149:03

now. Check this video out and I bet you

149:05

you might love it.

Interactive Summary

The video discusses the science of aging and age reversal with Dr. David Sinclair, a Harvard professor. He explains that aging is not inevitable and can be reversed, drawing parallels to computer software that can be reinstalled. Accelerators of aging include smoking, processed foods, excessive drinking, and flying. Reversing aging can potentially cure diseases like Alzheimer's, cancer, and heart disease because aging is a primary driver. Sinclair's lab is making significant discoveries, and he predicts people may live into the 22nd century if they adopt healthy practices. The conversation delves into the information theory of aging, where cells lose their identity and function over time, akin to an identity crisis. Factors like DNA breaks from stress, environmental factors, and lifestyle choices accelerate this process. Sinclair highlights the importance of lifestyle changes, emphasizing that DNA is not destiny and the epigenome plays a crucial role. He discusses practical advice such as avoiding smoking, excessive drinking, eating healthy, exercising, and maintaining social connections. The video also touches upon the potential of future technologies like pills to reverse aging, the concept of the singularity, and the role of AI in accelerating scientific discovery. Sinclair explains his theory of aging as information loss and the potential to 'reinstall' youthful information. He discusses the role of sirtuins, NAD levels, and the benefits of fasting and certain plant-based foods like blueberries and matcha. The discussion extends to the science behind red light therapy, cold plunges, and saunas, and their potential health benefits. Sinclair also shares his personal supplement stack, including NMN, resveratrol, and spermidine, and discusses the importance of managing LDL cholesterol and Lp(a) levels. He addresses hair loss, the benefits of exercise, and the impact of sauna use on longevity. The conversation touches upon the philosophical and existential aspects of extended lifespans, the nature of consciousness, the possibility of living in a simulation, and the future of AI. Finally, Sinclair promotes his book 'Lifespan' and his online longevity community, emphasizing the importance of purpose and making the world a better place for future generations.

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