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Anti-Aging Expert: Missing This Vitamin Is As Bad As Smoking! The Truth About Creatine!

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FULL TRANSCRIPT

0:00

Why do people not know that vitamin D

0:01

deficiency can increase dementia risk by

0:03

80%. Why do people not know that having

0:06

a lack of this mineral is affecting

0:08

their long-term risk of cancer? Why do

0:10

people not know that having a low

0:11

omega-3 index is as bad for you in terms

0:13

of mortality as smoking? And as a

0:16

scientist, I've seen firsthand that 70%

0:19

of the way you're aging is actually due

0:20

to your lifestyle. And all these things

0:22

are so easy to do. So for example, as we

0:24

age, certain areas of the brain which is

0:26

involved in learning and memory starts

0:28

to shrink by about 1 to 2% per year. The

0:31

good news is studies show that people

0:33

being part of an exercise protocol, not

0:35

only did they not have their hippocampus

0:37

shrink, it actually grew by 1 to 2%. And

0:40

there's more. There are other things

0:42

that don't even require as much effort

0:43

as exercise, like supplements. And it's

0:46

been shown study after study that if you

0:47

take someone and you sleep deprive them

0:49

for 21 hours and give them 25 to 30

0:52

grams of creatine, not only does it

0:54

negate the cognitive deficits of sleep

0:56

deprivation, it makes people function

0:58

better than if they were well rested.

1:00

And then there's magnesium. There have

1:01

been studies showing that people with

1:02

the highest magnesium levels have a 40%

1:05

lower all-c cause mortality. And over

1:07

300 different enzymes in your body need

1:09

it to help with short-term survival. And

1:11

yet 50% of the population in the United

1:13

States does not have adequate levels of

1:15

magnesium. And there's still more.

1:18

There's saunas, red light therapy,

1:19

ketogenic diets, blueberries,

1:21

electrolytes. We can talk about all of

1:23

them.

1:23

>> Please.

1:24

>> Okay. So, I found when you go into this

1:26

sauna, something happens. That's

1:28

incredible. So,

1:31

I see messages all the time in the

1:32

comments section that some of you didn't

1:34

realize you didn't subscribe. So, if you

1:36

could do me a favor and double check if

1:37

you're a subscriber to this channel,

1:39

that would be tremendously appreciated.

1:40

It's the simple, it's the free thing

1:42

that anybody that watches this show

1:44

frequently can do to help us here to

1:45

keep everything going in this show in

1:47

the trajectory it's on. So, please do

1:49

double check if you've subscribed and uh

1:51

thank you so much because in a strange

1:52

way you are you're part of our history

1:55

and you're on this journey with us and I

1:56

appreciate you for that. So, yeah, thank

1:58

you.

2:02

>> Dr. Ronda Patrick, you strike me as a

2:06

fairly obsessed person.

2:09

What is it you're obsessed about and why

2:11

are you obsessed about it? Because I can

2:13

see from speaking to you previously how

2:15

passionate you are about the subjects

2:17

we're going to talk to about today. And

2:19

so I was I was um I was wondering what

2:22

it is about these subjects that is

2:24

driving you and what what you're trying

2:26

to accomplish.

2:28

>> I've learned through my experience. So I

2:30

have a PhD in biomedical science. I've

2:32

done research on aging, on cancer, on

2:35

metabolism, nutrition, neuroscience, a

2:37

lot of different fields, very

2:38

cross-disciplinary.

2:40

And I've realized over, you know, the

2:42

decades of doing research that there are

2:44

many different small changes that can be

2:46

made that have a really big impact on

2:48

our health, what's called our health

2:50

span. So, this is essentially being

2:53

disease-free uh throughout our life,

2:56

being healthy, feeling good. And I'm

3:00

sort of obsessed with trying to optimize

3:03

that and find a protocol to optimize it

3:05

and then share that information with the

3:06

world. And it's funny because, you know,

3:09

we live in a time now where we've got

3:11

access to so much information,

3:13

overwhelming amount of information. But

3:16

the reality is is that simple important

3:20

tools that people can do in their life

3:22

right now to drastically improve the way

3:26

they age are still not known to the

3:28

general population. And so my mission is

3:30

to get that knowledge to people so that

3:33

they can make these simple changes and

3:35

live healthier and feel better.

3:37

>> And what will be the impact on their

3:38

lives if they understand that

3:40

information and start to implement their

3:41

that information on a real sort of

3:43

specific practical

3:45

in a real specific practical sense.

3:48

>> Well, there are things that people are

3:50

deficient in, for example, that they

3:52

could simply take a supplement. Vitamin

3:55

D is a is a good example that could

3:57

affect their disease risk, their

4:00

dementia risk. I mean, so you're talking

4:02

about quality of life improvement

4:05

right now and also later. So, it affects

4:08

mood, it affects depression, and it

4:10

affects your neurodeenerative disease

4:11

risk risk like dementia and Alzheimer's

4:13

disease. So there are lowhanging fruits,

4:15

things that are simple that you can just

4:17

basically fill these gaps. I mean there

4:19

are things that are also a little more

4:20

effortful and this is where exercise

4:22

comes in where you put in this effort

4:25

and it just if you could pill up what

4:28

exercise does in a pill, I mean it would

4:31

be be the biggest blockbuster miracle

4:32

drug out there. I mean it blow ozic out

4:35

of the water. It'd be I mean just no

4:37

comparison. So, um I think I think that

4:41

you know again that it's it's these

4:43

little things that you can do that is

4:45

going to help with depression, help with

4:47

mood right now, make you feel better

4:48

right now, give you more energy, help

4:51

you be more focused, help you be more

4:53

motivated, but also affect your

4:55

long-term disease risk so that you know

4:58

when you're older in life, you're not

4:59

demented. And that affects you, it

5:01

affects your family. So I think I think

5:03

it's it's just an important it's so

5:06

important because there are easy things

5:07

that can be done that people just don't

5:09

know about.

5:09

>> Is there a psychological element to this

5:11

where we kind of see aging as an

5:14

inevitability so we don't fight it

5:15

because we only seem to interfere with

5:18

and fight and are motivated by things in

5:20

life there where we feel like we've got

5:22

an element of control and we see we see

5:24

everybody get old and we see everybody

5:26

start to you know lean over a little bit

5:28

and struggle to walk and get a little

5:30

bit more frail. So I think because we've

5:33

observed that so much over the last

5:34

couple of decades. I'm 30 years just

5:36

over 30 years old. I assume that will

5:38

happen to me. So I've seen my dad, you

5:41

know, get older, get a little bit more

5:44

large, lose his lean muscle. So I think,

5:47

well, I'm like my dad. I've got the some

5:49

of the same genetics. That's inevitable

5:51

for me.

5:52

>> So genetics does play a role in the way

5:54

you age, but it's a small role. In fact,

5:57

70% or more of the way you're aging is

6:01

actually due to your lifestyle. Let's

6:03

just imagine two 70ish year old men,

6:07

okay? John and Rob. And John, you know,

6:11

he's razor sharp. He can carry groceries

6:14

to his car. He doesn't get out of

6:16

breath. You know, I mean, he's he's

6:18

feeling healthy. He's be able to he can

6:21

walk efficiently, right? And then

6:23

there's Rob. And Rob is

6:28

forgetting his words. You know, he's not

6:30

cognitively sharp. He's out of breath

6:32

just from walking to his car. He has a

6:34

really hard time carrying groceries.

6:36

Genetics only plays a small role in in

6:39

those two different outcomes for those

6:41

two men. The biggest, I would say, thing

6:44

that's dictating the way these two men

6:46

age is their lifestyle, with a huge part

6:48

of that actually being exercise. Mhm.

6:51

>> And you know, I know we've all heard it

6:53

from our mother or grandmother,

6:55

great-grandmother. You know, exercise is

6:57

is good for you. If you eat healthy and

6:59

you exercise, you're going to you're

7:01

going to be healthier. And that's like a

7:02

general statement, but the reality is it

7:05

is so true that exercise affects

7:08

everything, you know, down to the

7:10

molecular level in terms of like the way

7:12

you're aging. So, um, no, it's not just

7:16

dictated by genetics and it's not

7:18

inevitable and there are things that you

7:20

can do to dramatically age better.

7:23

>> So, let's play a little a little game

7:25

here. So, imagine that I listened to

7:28

your advice and the things that you know

7:30

about health, longevity, aging, um, and

7:32

I followed all of them, which is very

7:34

hard to do because, you know,

7:35

implementation is is not the same thing

7:37

as knowledge. So, imagine that's person

7:39

A, that's Steve A, and then there's

7:41

Steve B. I do the exact opposite. Based

7:44

on what you know about the science and

7:46

about outcomes and expected outcomes,

7:49

how would Steve A that followed your

7:50

advice

7:52

live his uh live his life as he ages?

7:55

And how would Steve's B, how would his

7:58

outcomes be as he ages? Like what would

8:00

you if you had to obviously this is like

8:01

super you're forecasting here and it's

8:03

hypothetical, but what do you think the

8:05

variance in these two people's lives

8:07

would be? Well, if you're talking about

8:09

the extreme ends, like if Steve B was

8:12

like eating sugar and smoking and

8:14

drinking and just obese and sedentary,

8:17

everything that you don't want to,

8:19

>> which is like a lot of the population.

8:20

>> I mean, then you're talking like a

8:22

14-year difference in life expectancy,

8:25

which is pretty big. But not just life

8:28

expectancy,

8:30

the way your your independence, right,

8:33

your your mind, so you'd be forgetful. I

8:37

mean, it would just be it would it would

8:38

be a terrible quality of life, right?

8:41

So, it's not only are you going to die

8:42

earlier, you're not you're just not

8:44

going to live a good quality of life.

8:46

So, so Steve A might be into his 90s and

8:49

out surfing, you know, because you're

8:53

you've exercised, you've you've given

8:55

your body like the right nutrients that

8:57

it needs, you've gotten good sleep,

9:00

you're not overweight, you're not eating

9:01

a lot of refined sugar, all these things

9:03

that sort of accelerate the aging

9:05

process. And we can talk about different

9:07

components of this and how they do

9:08

affect the way we age and our disease

9:11

risk, but I mean there's there's studies

9:14

that show even like a 14-year difference

9:16

in life expectancy for like someone

9:18

who's morbidly obese versus lean.

9:21

>> So Steve A could be out surfing at 90

9:23

and Steve B would be potentially dying

9:26

at 75, but also his quality of life

9:30

would his health span would diminish

9:32

probably in his 40s and 50s,

9:34

>> right?

9:35

So it's really it's a 14year reduction

9:38

in lifespan but potentially a 30 40 year

9:41

reduction in health span

9:42

>> in quality of life and health span being

9:45

able to be functionally independent

9:47

being able to be cognitively sharp feel

9:50

good right and your mood I mean all

9:51

these things are affected

9:53

>> you must be sitting on some some crazy

9:55

ideas because as a biomedical science

9:57

you can kind of see as a biomedical

9:59

scientist you can see some of the

10:01

research and technology that's coming

10:03

down the pipe so I'm wondering Before we

10:05

get into the the conversation, are there

10:07

any big ideas about the future of aging

10:10

and longevity that are in your mind that

10:13

you think about that are actually really

10:15

important to know because as Brian

10:18

Johnson has often said to me,

10:21

you want to live to to see these

10:23

breakthroughs.

10:25

>> Yes. Yes. I am excited about some gene

10:28

therapies and being able to sort of

10:32

reprogram our our cells to be more

10:35

youthful. So, you know, this is this is

10:37

something that was pioneered back in

10:40

2006 by Shinya Yamanaka from Japan and

10:44

he actually won the Nobel Prize. Why his

10:46

research was so important for the field

10:48

of aging wasn't really known at that

10:50

time. What he had shown is that you

10:52

could take a cell that's old and it

10:55

could be a any cell. It could be from an

10:58

85year-old person with Parkinson's

11:00

disease, for example, and you get it.

11:02

You know, we're constantly getting skin

11:04

cells and sloing them off every day. You

11:06

can take one of those cells and add four

11:09

different proteins to them. They're

11:11

called transcription factors.

11:12

Essentially, all that means is they're

11:14

kind of like master orchestrators of

11:17

many different genes in your body and

11:19

how genes are activated and turned on

11:21

and doing what they're supposed to or

11:22

they're turned off and quiet for the

11:24

time that they're supposed to be quiet.

11:27

And it's you you add those four proteins

11:30

and you can take that 85year-old cell

11:32

skin cell from a person with Parkinson

11:34

disease and you can make it into what's

11:36

called an embryionic stem cell. And it

11:39

does that by sort of wiping out the

11:42

what's called epiggenome. So people are

11:45

familiar with their DNA, right? Well,

11:47

the epiggenome is something that sort of

11:50

sits on top of your DNA and it

11:53

regulates, you know, how your genes are

11:54

being expressed or turned on and off,

11:56

right? And it sort of brings it back,

11:58

reprograms it to this youthful state

12:00

where it becomes an embryionic stem

12:02

cell. And then that embryionic stem cell

12:04

can then form any type of cell in the

12:06

body. you can form a heart cell or a

12:08

liver cell or a brain cell or a cell

12:10

from your eye and so this is called

12:12

induced pur potent stem cells and this

12:15

was a breakthrough at the time because

12:17

it's it was so import it's important for

12:19

cell regenerative therapies okay let's

12:20

say someone does have Parkinson's

12:22

disease and you want you know

12:24

Parkinson's disease people are losing

12:27

dopamineergic neurons and their

12:29

substantia so these are dopamine

12:31

producing neurons and dopamine is

12:33

important for motivation and it plays a

12:36

role in our, you know, cognitive

12:38

function, but it's also important for

12:39

movement, right? So, um, people with

12:42

Parkinson's disease are losing those at

12:43

a rapid rate and they lose control of

12:46

their motor capabilities. And so, you

12:48

want to be able to take an old skin cell

12:50

from someone, reprogram it to become a

12:53

dopamine neuron and then inject it into

12:55

that person, right? It's their own cell,

12:57

so they're not going to reject it,

12:58

right? So, that was like the big thought

13:00

at the time. Fast forward, you know, a

13:03

decade or so and a a whole handful of

13:08

brilliant aging scientists have

13:10

discovered that instead of taking these

13:13

old cells and putting these four

13:15

proteins on it to become this sort of

13:17

stem cell, they can pulse it. Just a

13:20

quick little pulse.

13:20

>> What is a pulse? Like an electronic

13:22

shock?

13:22

>> No, what I mean is it's just not

13:25

incubated for as long of a time period.

13:28

So, it's a shorter time interval that

13:30

you're putting these four different

13:32

transcription factors on top of the cell

13:35

that reprogram it, right? And the reason

13:37

for the shorter time is that you don't

13:39

want it to lose its cellular identity.

13:42

So, let's say it was a skin cell. You

13:44

want it to stay a skin cell, not become

13:46

an embryionic stem cell, but you want it

13:48

to be a skin cell from a one-year-old,

13:51

not an 85y old.

13:53

>> So, the way to do that is what's called

13:56

partial reprogramming. And so they

13:58

basically researchers have found that

14:00

you can just sort of what I call pulse.

14:03

It's partial reprogramming. You're kind

14:05

of putting it on for like a shorter

14:06

period of time and then that cell keeps

14:09

its identity but it's youthful. It wipes

14:12

out all the damage, everything that's

14:14

accumulated over those those 85 years.

14:16

And this has been shown in animal

14:18

studies in rodents that if you if you

14:21

add these four different transcription

14:23

factors and you give them to mice, you

14:25

can rejuvenate many of the different

14:27

organs. So essentially turning back the

14:29

aging clock in different organs in these

14:31

mice. Now this obviously has to be

14:34

translated to humans, but I think it's

14:36

super exciting and I do think it's the

14:38

future in terms of solving aging and

14:43

rejuvenation, rejuvenating our organs.

14:45

And so it's something that I'm pretty

14:47

excited about and following closely.

14:50

>> And are they then living longer?

14:53

>> Some of these studies were done in

14:54

animals that are what's called

14:56

accelerated aging. So yes, they were

14:59

living longer in that background of

15:01

accelerated aging. Um the question is,

15:04

you know, can they live longer if it's

15:07

just a normal mouse that's not like an

15:08

accelerated aging model? And and these

15:10

are things that are all being done right

15:11

now. These sorts of studies are in

15:13

progress.

15:15

Where do you think is the most important

15:17

place for us to start this conversation

15:19

based on everything you know and maybe

15:21

some of the presumably there's some like

15:23

foundational stuff, right?

15:24

>> I do. I think the important place to

15:28

start would be we're talking about we

15:31

were talking about aging as a disease

15:33

and I think being sedentary is a disease

15:37

and I think that's a good place to

15:38

start. What I mean by being sedentary is

15:41

not physically active. someone who

15:44

doesn't engage in any type of physical

15:47

activity.

15:48

>> And what is the spectrum there of, you

15:50

know, someone who doesn't move at all

15:52

for, you know, 24 hours a day versus

15:54

you've got obviously someone that's

15:55

constantly running marathons and doing

15:57

crazy stuff, but where is where are most

15:58

of us on that scale? And are we moving

16:00

enough?

16:01

>> Most of us are not moving on that

16:04

enough. And most of us are, if you're

16:06

talking about globally, we're on that

16:07

sedentary scale where we're just not

16:10

physically active. we sit at our

16:12

computer or our desk or our cubicle, you

16:14

know, all day and we're not we're not

16:17

actually moving around a lot. Um, and I

16:20

say I say sedentaryism

16:22

is a disease because it's actually been

16:25

shown to

16:27

increase the risk of early mortality

16:30

even more than diseases that we know of

16:32

like type two diabetes, cardiovascular

16:35

disease, or even terrible habits like

16:37

smoking. So being sedentary actually

16:40

could predict early mortality even more

16:43

than those diseases. But it it it's

16:46

let's take a step back. It's even bigger

16:48

than that. There there's this amazing

16:50

study. It's called the Dallas bed rest

16:52

study. And the study started back in the

16:55

1960s. And this is done by probably the

16:58

world's most talented cardiovascular

17:02

exercise physiologists.

17:04

And so Ben Saltine, uh, Jerry Mitchell

17:06

were involved in this early study in the

17:08

1960s. And what they did was they took

17:11

five men, they were college students and

17:13

they put them on bed rest. And this is

17:16

like 3 weeks of legitimate bed rest.

17:18

We're talking they couldn't get up to go

17:20

to the bathroom, so they had catheter in

17:22

them. They did not move for three week.

17:25

The researchers wanted to find out what

17:26

happens to your cardiovascular system if

17:29

you are not moving around for three

17:31

weeks. And now if you think about it,

17:32

you know, there's a lot of people that

17:34

are undergoing surgery or they have some

17:37

sort of bad illness, influenza or

17:40

something that keeps them bedridden for

17:43

it's not unusual to be 3 weeks to be

17:46

honest. So it's not completely

17:48

irrelevant.

17:50

And what was found is after that 3

17:51

weeks, you know, their cardiovascular

17:53

system was just tanked. And one of the

17:56

major they they were probably the some

17:57

of the most wellstied men at the time.

18:00

And um one of the biggest factors that

18:02

was measured was their cardiorespiratory

18:04

fitness. This is often called V2 max.

18:07

And essentially it's the maximum amount

18:08

of oxygen that you can breathe in and

18:11

your lungs then breathe that oxygen to

18:14

your muscles. And it's measured during

18:16

maximal exercise. You're putting in a

18:18

maximum effort and that's called your

18:20

cardiorespiratory fitness. And we can

18:22

talk a little bit more about that. But

18:23

their cardiorespir respiratory fitness

18:25

tank. And now I mentioned this was in

18:28

the 1960s. About 30 years later, and

18:31

this is where uh Ben Lavine came into

18:33

the study. He's at the UT Southwestern

18:35

in Dallas. He's also very one of the

18:37

most famous, you know, cardiovascular

18:40

exercise physiologists out there right

18:42

now. They found these five men from 30

18:45

years earlier and they measured their

18:48

cardiorespiratory fitness and a variety

18:50

of other parameters that they had

18:51

measured at the time. And what they

18:54

found was that three weeks of bed rest

18:57

was worse on their cardiorespiratory

18:59

fitness than 30 years of aging. So

19:02

essentially their cardiorespiratory

19:04

fitness was no worse 30 years later than

19:08

it was after their 3 weeks of bed rest

19:12

which is kind of amazing because you

19:14

would think that the 30 years of aging

19:16

would be worse on your cardiorespiratory

19:18

fitness than the three weeks of bed

19:19

rest. And it's the same the same

19:21

individuals,

19:22

>> the same individuals, the same five men.

19:24

Um, now after the three weeks of bed

19:26

rest, you know, back back in the 1960s,

19:29

they were able to get their

19:30

cardiorespiratory fitness back up again

19:32

once they started exercising and moving

19:34

around and it took a while. But when you

19:36

look at their baseline levels, their

19:38

baseline cardiorespiratory fitness and

19:40

you compare it to their

19:41

cardiorespiratory fitness baseline 30

19:43

years later, it wasn't worse than what

19:46

happened when they they compared it to

19:48

the 3 weeks of bed rest. And you might

19:50

go, well,

19:52

why is that so significant? The

19:54

cardiorespiratory fitness dropping. We

19:56

know that cardiorespiratory fitness is

19:58

one of the best predictors of longevity.

20:01

So there are studies that have shown

20:02

that people with a high

20:04

cardiorespiratory fitness

20:07

live five years longer than people with

20:09

a low cardiorespiratory fitness. That's,

20:12

you know, pretty big difference. They're

20:14

they're basically 80% less likely to die

20:17

of many different causes of of death. So

20:19

cardiovascular disease, cancer,

20:21

respiratory disease, things like that

20:24

than people with a low cardiorespiratory

20:26

fitness. So you're really getting, you

20:28

know, a five-year increased life

20:30

expectancy. You're sort of pushing and

20:32

delaying those age related diseases like

20:34

cardiovascular disease, you know, like

20:37

cancer, for example, you're pushing them

20:39

down later in life. So you're not you're

20:41

not dying from them sooner. And we do

20:43

know that really

20:46

just going getting anywhere out of that

20:48

low cardiorespiratory fitness. So people

20:50

with the low cardiorespiratory fitness

20:52

are people that are sedentary. And if

20:54

you just move anywhere above that, even

20:56

if you're going low from low bad to like

20:59

low normal, you're gaining about two

21:01

years increase in life expectancy. And

21:04

that's not really that hard to do. But

21:07

if you think about cardiorespiratory

21:09

fitness, like right here, just having

21:11

this conversation, actually even just

21:13

sitting quietly, it takes about three

21:16

milliliters of oxygen per minute per

21:18

kilogram body weight to do that. to

21:22

carry groceries to your car, it takes

21:24

about 11 milliliters of oxygen per

21:27

minute per body weight, per kilogram

21:28

body weight.

21:29

>> And so as you're aging, you're kind of

21:32

heading towards this cliff, right?

21:34

Because your cardiorespiratory fitness

21:35

goes down with age. It does. That's what

21:38

happens naturally. If you're at the

21:40

point where you don't work on your

21:41

cardiorespiratory fitness, if you're not

21:43

being physically active, and there are

21:45

certain exercises that are better at

21:46

improving cardiorespiratory fitness than

21:48

other others, if you're not trying to

21:51

improve it, you're going to be heading

21:52

towards that cliff faster. And then

21:54

everything becomes a maximal effort.

21:56

You're out of breath just talking.

21:58

You're out of breath carrying groceries

21:59

to your car. Everything is a maximal

22:02

effort. And you don't want to be there.

22:04

You don't that that quality of life is

22:06

not good. It's not good. Right. And then

22:09

on top of that, you're also going to die

22:11

sooner. So you're talking about two

22:13

things here. You're talking about

22:14

decreased health span and decreased

22:16

lifespan.

22:17

>> So yeah, we should be moving more,

22:19

>> right? And the question is, well, how do

22:21

you improve your cardior fitness? Right.

22:23

Yeah. I mean,

22:24

>> do you lift weights? Do you go for runs?

22:28

Do you bike? What is it that is really

22:31

good at improving cardior fitness? And

22:34

that's the question that a lot of

22:35

exercise physiologists have answered

22:37

over the last couple of decades. You

22:40

want to do and engage in what's called

22:42

vigorous intensity exercise. So this is

22:45

the kind of exercise where you're not

22:48

able to have a conversation when you're

22:49

engaged in it. Right? So so your heart

22:52

rate is going up to about 80% your max

22:55

heart rate. You're not able to really

22:56

talk. And it's I would say you know it's

22:59

something that can be done in intervals.

23:01

So you can do highintensity interval

23:03

training. So you have these intervals

23:04

where you're getting your heart rate up,

23:06

you're doing vigorous exercise, and then

23:08

you have recovery periods where you're

23:09

kind of resting. You're you're lowering

23:11

your heart rate. You're not doing that

23:13

max that maximal sort of exercise. And I

23:15

say this because

23:18

there have been studies, multiple

23:19

studies that have shown people that

23:22

engage in moderate intensity exercise.

23:25

So this is the kind of exercise when you

23:26

can you're breathy, but you can still

23:28

kind of have somewhat of a conversation

23:30

while you're doing it.

23:31

>> Like the stair master. like the

23:32

stairmaster. Yeah, exactly. Um, even

23:36

people that are engaging in that type of

23:37

exercise for two and a half hours a

23:39

week, so this is following the physical

23:41

activity guidelines, 40% of those people

23:44

can't improve their cardiorespiratory

23:46

fitness.

23:47

And it's like, well, I don't know about

23:49

you, but like I don't want it to be a

23:51

coin toss in terms of like if I'm doing

23:54

that kind of exercise, well, if I have a

23:55

50% chance of not improving my

23:57

cardiorespiratory fitness if I'm doing

23:58

this. I want the sure thing. And the

24:00

short thing is you take those people and

24:03

then you have them engage in

24:05

highintensity interval training and

24:07

they're able to improve their

24:08

cardiorespiratory fitness. And that's

24:10

because

24:11

you you're putting a stronger stress on

24:13

your cardiovascular system. And so the

24:16

adaptations are greater. And part of the

24:18

adaptations are you're able to bring in

24:20

more oxygen, carry it to your muscles,

24:22

carry it to your your you know other

24:24

other tissues better. And so that's your

24:27

cardiorespiratory fitness. Uh and so and

24:29

so that's that's really I would say um

24:32

the bottom line here is engaging in even

24:34

just once or twice a week. And I would I

24:37

would say the the most wellressearched

24:40

protocol for that would be something

24:42

called the Norwegian 4x4.

24:44

And that is where you're doing a longer

24:47

interval. It's a 4-minute interval and

24:50

it's best done on either a stationary

24:52

bike or maybe a rowing machine. And

24:55

you're going as hard as you can and

24:57

maintain that intensity for four

24:59

minutes. And then you're going to go

25:02

down to light exercise and recover for

25:04

four minutes and let your heart rate go

25:06

down. And you do that four times. So

25:08

it's a four by four. And that is

25:11

probably one of the most robust ways to

25:13

improve cardiorespiratory fitness. But

25:15

there are other ways even doing you know

25:18

one minute on one minute off. So you do

25:20

one minute as hard as you can go again

25:22

for that entire minute. not going all

25:23

out, but as hard as you can and maintain

25:25

that for the entire minute. And then you

25:27

rest a minute and you do that, you know,

25:29

10 times. So, it's a 20-minute workout.

25:32

>> So, for the several million people that

25:35

are listening right now, if you had to

25:36

prescribe them all something to do and

25:39

it was the minimum they had to do.

25:42

Tell me what exactly the workout would

25:44

look like and how frequent it would be

25:46

on a weekly basis.

25:48

>> I would say the minimum effective dose

25:50

would be once a week. Okay.

25:53

>> And it would probably be

25:57

the one minute on, one minute off. If

26:00

you want like the upper end robust

26:03

effects of improving cardiorespiratory

26:04

fitness, you can still improve it with

26:07

something like a Tabata.

26:08

>> What's a Tabata?

26:09

>> Where you're doing a 20 second interval

26:11

and you're going more all out because

26:12

it's shorter time and then you're

26:14

recovering for 10 seconds.

26:16

>> So, it's a 20 second on, 10 second off.

26:18

You do that eight times. And um if you

26:21

repeat that twice, so it's essentially a

26:23

10-minute workout, that's also something

26:25

that can improve cardiorespiratory

26:27

fitness. But I would say, and I'll tell

26:30

you I'll tell you why. There's the

26:32

minimum, right? So the one minute on,

26:34

one minute off. But I would say the

26:35

Norwegian 4x4 is the gold standard. And

26:39

that's because it's not only improving

26:41

cardiorespiratory fitness.

26:43

This is probably one of the most

26:45

exciting

26:46

pieces of evidence I've seen with

26:48

respect to, you know, exercise and

26:51

aging. And that is that being part of an

26:54

exercise protocol was shown to reverse

26:57

the structural changes that occur with

27:00

age in the heart by 20 years.

27:05

So what do I mean by that? I mean,

27:10

people that were 50 years old that were

27:13

sedentary, so they weren't really going

27:15

to the gym, they weren't engaging in any

27:18

sort of physical activity, but they

27:20

weren't, you know, they didn't have

27:22

diseases. They didn't have type two

27:24

diabetes, they didn't have

27:25

cardiovascular disease. I would argue

27:26

sedentary, being sedentary is a disease,

27:28

but putting that aside, they didn't have

27:30

any diseases, right? And they're 50, so

27:32

they're midlife.

27:34

And um this was again this was done by

27:36

Ben Lavine out of UT uh Southwest at in

27:39

Dallas. He took these you know

27:41

50-year-olds and put them on a pretty

27:43

intense exercise routine for two years

27:47

or a stretching routine. This was like

27:49

the the control.

27:51

And this type of exercise routine was

27:53

progressive. So they started out lighter

27:55

and sort of worked their way up, right?

27:56

Like you don't want to just start with a

27:57

Norwegian 4x4 people that never never

28:00

exercise. I mean that's going to be

28:01

tough. So it was a progressive sort of

28:04

building up to that. But um towards the

28:07

ends of about the first six months,

28:09

these people were exercising about 5 to

28:11

six hours a week and that included one

28:13

to two sessions of the Norwegian 4x4.

28:16

And it also included a lot of, you know,

28:19

they're they're doing moderate to

28:22

vigorous intensity cycling or running

28:25

and some some strength training as well.

28:27

And they did this for two years.

28:31

their hearts were looked at and so as we

28:33

age our hearts shrink and they get

28:36

stiffer and that plays a role in causing

28:39

cardiovascular disease. I mean that's

28:40

the number one killer in the United

28:41

States. It also affects

28:43

cardiorespiratory fitness right why does

28:46

the the heart you know stiffen with time

28:49

has a lot to do with actually being

28:51

exposed to a lot of glucose when you're

28:55

eating a lot of refined sugar and

28:56

refined carbohydrates you're having a

28:58

lot of glucose around in your system.

29:00

This causes a chemical reaction called

29:03

glycation. So you get these advanced

29:05

glycation end products that sort of

29:07

react with your collagen that's lining

29:10

your heart and your mocardium and it

29:12

causes it to stiffen and so now the

29:14

heart can't really respond to stress

29:17

well. It's stiff and that plays a role

29:19

in like heart attacks for example. So

29:22

exercise is one of the best things you

29:24

can do to

29:26

move glucose out of your vascular system

29:29

and get it to your muscles. And so

29:31

that's that's one of the things that it

29:32

does and helps with not causing that

29:34

stiffening of the heart. And so

29:37

essentially these 50-year-olds had

29:40

their their heart the structure so it

29:42

was bigger and less stiff after two

29:45

years of this you know exercise

29:47

protocol. It essentially made their

29:49

hearts look like 30 year olds. And I

29:51

mentioned they were 50 year olds. I

29:53

mean, that's amazing. That's incredible

29:54

that you can take someone midlife, put

29:57

them on a two-year training protocol,

29:58

and reverse the aging of their heart by

30:00

20 years.

30:01

>> So, on this Norwegian 4x4,

30:05

you've convinced me to give it a shot.

30:07

But specifically, how I how I do that.

30:10

So, it's it's I do my warmup and then I

30:13

do four minutes of hard exercise. I take

30:16

a break and the exercise I'm doing in

30:18

those four minutes can be any number of

30:21

things but I just have to get up to 85

30:23

80% of my exertion levels 80%

30:26

difficulty.

30:27

>> So the way it works is as they mentioned

30:30

it's it's best if you're doing a

30:31

cardiovascular type of exercise. So like

30:33

>> the assault bike

30:34

>> you could do assault bike. Yep. Assault

30:36

bike. You can do a rowing machine. You

30:38

could do uh stationary cycling machine

30:41

as well.

30:42

>> Could I run?

30:44

You can, but that is is it's definitely

30:47

um it's I think it's better on on doing

30:51

like maybe a bike or a salt bike or

30:52

something. Um but you can run like what

30:55

whatever it is that you like to do and

30:57

you are going as hard as you can for

30:58

that four minutes and maintain within

31:00

that four minutes. So it's not an allout

31:02

or it's far from all out, right? But

31:04

you're not really having a conversation

31:05

while you're doing it. And then the four

31:07

minutes of recovery, you're if you're

31:09

running, you kind of go down to walking.

31:12

If you're on the rowing machine or the

31:13

assault bike, you're just going very

31:15

slow. You're just really going slow and

31:18

you're letting your heart rate come

31:19

down. You're letting your muscles kind

31:21

of recover, your cardiorespiratory

31:23

fitness, you know, kind your your

31:25

cardiorespiratory fitness system recover

31:27

somewhat. And then after that 4-minute

31:29

recovery, you go back to the four

31:31

minutes of like intense again. And

31:34

you're doing that four times. It's not

31:36

easy, but you know, people can start

31:39

out, they don't I mean, even if you

31:41

start out with not going super super

31:44

hard in those four minutes where you

31:46

just maybe you can have a conversation,

31:48

but you're still going hard harder than

31:50

you're used to pushing yourself. And I

31:51

think for people that haven't really

31:54

engaged in any type of high-intensity

31:56

training before, that's a good idea

31:58

where you kind of you got you can't just

32:00

start doing it

32:01

>> right out the gate. You want to kind of

32:02

work your way up that. So doing the four

32:04

minutes do just try to put in as much

32:06

effort as you can right during those

32:08

four minutes and then you do your

32:10

recovery and you repeat that four times

32:13

but then work your way up as you as you

32:15

do it one week, two weeks, you know, a

32:17

month later, two months later and really

32:19

try then to get to that point where

32:21

during those four minutes you're

32:22

getting, you know, you're pushing

32:24

yourself hard where you're not really

32:26

able to have that conversation

32:28

>> and physiologically what is going on in

32:30

my body when I get to that 85 90% effort

32:33

range and I and I stay there for a

32:35

couple of minutes. That doesn't occur

32:37

when I'm doing my stair master.

32:40

>> I mean, so many things are are

32:42

happening. I mean, there's a lot of

32:44

different, I would say, physiological

32:46

responses that are

32:48

>> You've got a big smile on your face when

32:49

I ask.

32:49

>> Yes, I do because it's, you know, one of

32:51

my favorite things to talk about and it

32:54

has to do with when you're when you're

32:56

pushing yourself really hard, you need

32:59

you need to make energy, right? And the

33:01

way that most of our cells make energy,

33:03

like our muscles, is by using our

33:07

mitochondria, these are tiny organels

33:08

inside of our cells that produce energy,

33:10

but they need oxygen to do it. So that's

33:13

where the oxygen comes into play. When

33:16

you start to push yourself really hard,

33:18

you can't get the oxygen to your muscles

33:19

quick enough, but you need to make the

33:21

energy. And so your body decides to make

33:24

energy in the form of ATP without the

33:27

mitochondria, and it uses glucose to do

33:29

that.

33:30

and you're not making as many of those

33:33

ATP energy molecules, but you're still

33:36

making them and you're making them

33:37

quick. And that's what your your body

33:39

wants to do. And and so it's using

33:42

glucose to do that without the

33:43

mitochondria,

33:45

but as a byproduct, it's making

33:47

something called lactate. And this is

33:50

what gets me so excited because, you

33:52

know, for the longest time, lactate was

33:54

thought to be this just metabolic

33:56

byproduct of glucose metabolism. you

34:00

know where you're when you're pushing

34:01

yourself really hard anorobic it's

34:03

called anorobic by the way you're not

34:05

you're not only anorobic you're just

34:08

some somewhat anorobic you're still use

34:10

producing energy with your mitochondria

34:12

it's just you're also producing without

34:13

the mitochondria it's not like a a sort

34:15

of black black and white sort of thing

34:17

right it's a little bit gray

34:18

>> but the reality is you're producing

34:20

something called lactate and for the

34:22

longest time it was thought this lactate

34:24

oh it's just it's bad because you know

34:26

it can form lactic acid and that burns

34:28

forms that burn in your muscles. And you

34:31

know, this was, you know, decades ago.

34:33

And we now know from the work of George

34:35

Brooks out of UC Berkeley that lactate

34:38

itself isn't causing the burn. And not

34:41

only is it not causing the burn, it's

34:43

like a miracle molecule that's being

34:46

made. This metabolite lactate gets into

34:49

your circulation and it gets consumed by

34:52

your heart, by your brain, by your

34:55

liver, and it's used for energy. It's

34:58

very it's it's very much similar to beta

35:01

hydroxybutyrate that ketone body that

35:03

you always hear about people talk about

35:05

when they're fasting or doing a

35:07

ketogenic diet. It's actually very

35:09

similar to that. It gets used it gets

35:11

transported through the same transporter

35:13

and it's used like energy. Very similar

35:16

to that. Um but what's more exciting is

35:19

that lactate is a way for your muscles

35:21

to communicate with other organs like

35:23

the brain. And it's called a signaling

35:26

molecule. So, it's your muscles are

35:28

going, I'm working really hard. This is

35:30

really hard. We have to respond to this

35:32

work. We have to adapt. And so, your

35:35

body goes, okay, I got to like turn on

35:37

all this awesome stuff that I have

35:38

because I'm working so hard. I need to

35:41

respond to that so that like I'm I'm

35:43

good, right? And so, what happens is the

35:45

lactate, this has been shown, it gets

35:47

consumed a lot by the brain. And in the

35:50

brain, it it activates something called

35:52

brain drive neurotrphic factor, BDNF.

35:56

And this is kind of like a miracle grow

35:58

for your brain. So essentially, it's

36:00

able to increase the growth of new

36:03

neurons, which is amazing. It's called

36:06

neurogenesis. It increases the

36:09

connections between neurons. So it

36:11

improves memory, cognition, and then um

36:14

it's involved in what's called

36:15

neuroplasticity. So the ability of your

36:18

brain to adapt to a changing

36:20

environment. This is all from lactate.

36:22

Um, and it also increases

36:24

neurotransmitters like norepinephrine,

36:26

so focus and attention, serotonin, your

36:29

your mood, you're feeling better,

36:31

you're, you know, motivated. All these

36:33

things are happening because of lactate.

36:34

And there's been studies in humans

36:36

showing that people that are compared

36:38

working hard, working out hard, vigorous

36:40

exercise versus sort of moderate to

36:42

light exercise, they make more lactate.

36:45

And that lactate, you know, it's been

36:48

shown that high levels of lactate are

36:50

correlated with improved cognition

36:51

scores, uh, improved impulse control. So

36:54

serotonin plays a role in impulse

36:56

control. So you're able to not just go

36:58

on your impulse, right? You're you're

37:00

able to kind of like, which is great if

37:02

you want more focus and attention,

37:03

right? So this is this is all really

37:06

exciting stuff because it all comes down

37:07

to just it's it's like your muscles are

37:09

these little chemical pharmaceutical

37:11

factories and the way to make them make

37:14

these pharmaceuticals is to work them to

37:16

challenge them and that can be done with

37:18

an easy highintensity interval training

37:20

protocol. A variety of them Norwegian

37:23

4x4 can increase brain drive neurotrphic

37:25

factor that's been shown. The one minute

37:27

on one minute off protocol also has been

37:29

shown to increase that again through the

37:31

lactate. So that's one of the big sort

37:34

of I would say differences between

37:36

vigorous intensity exercise and more of

37:39

that moderate intensity or like low

37:41

intensity exercise. And I honestly

37:43

think, you know, I think the guidelines,

37:46

you know, everyone's sort of obsessed

37:48

with steps. I need to get my 10,000

37:49

steps in, my 10,000 steps. And they have

37:51

wear wearable devices, and I think

37:52

that's great, but I think we need to

37:55

change the 10,000 steps to at least 10

37:58

minutes of vigorous intensity exercise.

38:00

like you could do 10 minutes of, you

38:03

know, any type of exercise that's really

38:05

going to get your heart rate up and it's

38:07

going to be so much better. So, this is

38:10

a really dumb question, but it's the

38:12

question that I had in my mind, which is

38:13

if lactate is such a miracle

38:16

drug,

38:18

why can't I just drink it? Why can't I

38:20

just get get a shot of lactate versus

38:22

having to go through vigorous interval

38:24

training? It's a great question,

38:26

Stephen, because um there have been

38:29

studies that have been done looking at,

38:31

for example, traumatic brain injury

38:34

patients. So, people that have undergone

38:36

some sort of head trauma and they've

38:39

infused sodium lactate through like an

38:42

IV

38:43

into their, you know, system and the

38:45

lactate immediately gets consumed by the

38:46

brain and it's been shown to improve

38:49

their recovery. So, it's called the

38:51

Glasgow score. You may have heard of it,

38:52

but it's kind of essentially this

38:54

battery of tests that's done to sort of

38:56

assess how someone's recovering from

38:57

traumatic brain injury. And the sodium

38:59

lactate does improve that. So there are

39:03

you can find out there, you know,

39:05

different types of lactate that you can

39:07

consume.

39:08

>> And theoretically, it should help, but

39:11

what happens is when you consume the

39:13

lactate,

39:14

>> lactate actually gets used by the gut.

39:17

So a lot of it's going into the gut

39:18

cells before it gets into your

39:20

circulation. There's always a trade-off

39:21

with these bloody things whenever you

39:23

try and trick the system or shortcut the

39:26

system by like drinking something. I

39:28

feel like there's a trade-off which

39:29

people don't talk about a lot.

39:31

>> Well, the thing is is that I it is good

39:32

for the gut. In fact, a former colleague

39:34

of mine, Mark Chanaga, has shown that

39:37

lactate is really beneficial for for uh

39:40

the gut epithelial cells. In fact, if

39:41

you think about it, all these sort of

39:43

beneficial probiotic bacteria like

39:46

bifido bacterium for example, they're

39:48

producing lactic acid and that lactic

39:51

acid does get converted into lactate.

39:54

It's sort of like this physiological

39:56

homeostasis where you have uh the

39:59

difference of just a hydrogen atom. So

40:00

you're having lactic acid and lactate

40:02

sort of in this equilibrium so to speak.

40:06

But um those those bacteria in your gut

40:08

are making lactate essentially. And the

40:10

reason it's so good is because it is an

40:14

very e easily utilizable source of

40:16

energy for the gut cells. So, not to

40:19

like go off on a tangent here, yes,

40:20

there is always a tradeoff, especially

40:22

for doing something orally, but when it

40:24

comes to exercise,

40:26

there's so like I mentioned when we

40:28

first started talking about exercise, if

40:29

you could pill up what exercise does,

40:32

I mean, it's so many things, right? It's

40:34

not just the lactate.

40:35

>> Yeah.

40:36

>> So many different things, so many

40:37

different adaptations that occur. I mean

40:39

it would be a miracle drug. So there's

40:41

you're not just getting the lactate,

40:42

you're getting the, you know, the

40:44

improvement in cardiorespiratory

40:45

fitness. You're getting the muscular

40:46

response, right? The adaptations to your

40:48

muscle. Um you're you're increasing

40:50

stress response genes like heat shock

40:53

proteins that are important for

40:54

preventing neurodeenerative disease.

40:56

You're making antioxidants because the

40:57

inflammation that you're generating

40:59

while you're exercising. There's

41:01

hundreds and hundreds of things that are

41:02

happening all in concert from exercise

41:05

and you just can't you can't pill it up.

41:09

>> I have another really silly question

41:10

which is if lactate and these other

41:12

things even like creatine and you know

41:14

all these other things are so good for

41:16

me why doesn't my body just make more of

41:18

it?

41:19

>> I mean your body does make it. The the

41:22

problem is is that you know as we're

41:24

aging everything becomes less efficient.

41:27

everything doesn't do what it used to do

41:30

as well as it did when it was younger.

41:32

Um, and it and also in the in the case

41:34

of creatine, which we can talk about,

41:36

you know, later if you're interested,

41:38

then um, you know, your body only makes

41:40

so much of it. And

41:42

>> why doesn't it make more?

41:44

>> I don't, you know,

41:45

>> maybe I'm not giving it the the minerals

41:47

or the environment it needs naturally to

41:49

make more.

41:50

>> I don't know.

41:50

>> You you get it from your food, too.

41:52

Creatine is found in meat, in poultry,

41:56

and fish. So, probably that's why your

41:59

body doesn't make more of it because it

42:01

knows you're going to be getting it from

42:02

your diet as well.

42:04

>> And so, that is another way to get

42:06

creatine.

42:07

>> Okay.

42:08

>> Of course, the vegans and the

42:09

vegetarians, that's a whole other

42:11

ballgame because they aren't eating meat

42:13

and so they're really essentially only

42:15

relying on what their body can make.

42:17

>> We'll definitely talk about that later.

42:19

Um on this point of the brain then if if

42:21

I I don't want to be an older person who

42:26

can't remember things and stutters over

42:28

my words and falls into cognitive

42:30

decline. And I'm I'm 32 now. So I'm I

42:33

feel like I'm at a moment in time where

42:35

I can really make decisions now that

42:37

have a really big impact on my

42:39

90-year-old brain and my ability to

42:40

think straight and clearly and remember

42:42

things. Are there things that I can be

42:44

doing now that will have a profound

42:45

impact on my cognitive performance at

42:47

90?

42:48

>> Yes. And what are those things?

42:49

>> Absolutely. Well, first of all, just to

42:51

kind of wrap up the exercise story

42:53

because I think this study is so

42:55

profound and in fact it wasn't done in

42:58

32 year olds. It was done in older

43:00

adults. So, we're talking 60 year olds

43:02

or a little bit older. And these

43:04

individuals were put on a aerobic

43:07

exercise training program for one year

43:10

that was more of like a 70 to 75% max

43:13

heart rate. It wasn't so vigorous, but

43:16

it was pretty pretty vigorous for them,

43:18

right? And um the the basis of this

43:21

study was to look at brain aging. As we

43:24

age, I mentioned our heart aging, right?

43:26

It gets stiffer and shrinks with age.

43:28

Our brain also shrinks with age. It's

43:30

called atrophy. And as we age,

43:32

especially starting in midlife, so

43:34

around the age of 50, your your brain

43:37

and certain areas of the brain like the

43:39

hippocampus, which is involved in

43:40

learning and memory, starts to shrink by

43:43

about 1 to 2% per year.

43:45

>> I don't want that to happen.

43:46

>> Same. Same. The good news is um in this

43:50

study, after a year of this sort of

43:53

aerobic exercise training program, they

43:55

were doing three times a week about 30

43:57

minutes a day. Really not even that

43:59

intense. these individuals and then

44:02

there was a control group that was kind

44:03

of the stretching they like to use the

44:05

stretching as the control group. So that

44:08

let's talk about the the control group,

44:10

the stretching group. They did lose

44:12

about 1 to 2% in terms of the size of

44:14

their hippocampus, it shrunk one to 2%

44:17

after that year, which is what you would

44:19

expect normally. However, the group that

44:22

was training, not only did they not have

44:25

their hippocampus shrink by 1 to 2%, it

44:29

actually grew by 1 to 2%. which comes

44:32

down to that neurogenesis, that growth

44:35

of new neurons, the brain drive

44:36

neurotrphic factor that's able to do

44:39

that. You're actually able to grow new

44:41

neurons even when you're in the age of

44:43

50, which is amazing. It's incredible.

44:46

So, that study I love because a couple

44:50

of reasons. one, it shows that it's

44:52

possible to not only stave off, you

44:56

know, some of the components of brain

44:58

aging, but to reverse it and increase

45:01

it, right, through exercise. And number

45:04

two, I love it because it's never too

45:07

late. Like, you can start this, you

45:10

know, in your 60s and still have a

45:13

benefit, right? you're you're talking

45:14

about being in your 30s, but you know,

45:16

some people watching this show,

45:19

listening to the show, may already be in

45:20

their 50s or 60s, right? So, it's never

45:22

too late.

45:23

>> Um, likewise, you know, we're talking

45:26

about being cognitively sharp and not

45:27

getting dementia. There's also studies

45:29

showing that people like women that were

45:32

brought into the lab, they had their

45:34

cardiorespiratory fitness measured,

45:37

those women with the highest

45:38

cardiorespiratory fitness were 80% less

45:41

likely to come down with dementia over

45:42

the follow-up period of time. So it

45:45

again, I think exercise is one of the

45:47

big ones when it comes to brain aging.

45:49

But you asked an important question. and

45:51

you say, "What can I be doing now that's

45:54

going to affect the way my brain ages,

45:56

you know, for the subsequent decades of

45:58

my life?" And there are other things

45:59

that can also be done that don't even

46:02

require as much effort as exercise.

46:05

Exercise is the gold standard because I

46:08

mean, being able to not only, you know,

46:10

stave off atrophy of the of the brain,

46:13

but to like regrow some of it is

46:16

incredible, right? I mean, that's just

46:18

mind-blowing. Have they ever taken

46:20

people with dementia, Alzheimer's, and

46:22

put them on an exercise program and

46:24

monitored the decline of their cognitive

46:27

abilities on an exercise program?

46:30

>> Yes. I mean, it's it's much harder when

46:32

you already have someone who

46:35

is in that pathological state because

46:37

things just really snowball and

46:39

accelerate. And there are some benefits.

46:42

I mean,

46:43

>> but it's not it's not prevention is

46:45

always the best. Prevention is always

46:47

the best. And so, you know, I I think

46:50

that if there's any sort of take-home

46:52

here, it's that like let's let's try to

46:55

do what we can now so that we don't get

46:57

to that point

46:58

>> before we get into the the the easier

47:00

ways of staving off cognitive decline.

47:05

Do do we know what causes dementia and

47:06

Alzheimer's yet? Do do we have any

47:08

ideas? Because we can when they do the

47:10

brain imaging, they can kind of see

47:12

these plaques on the brain, they say.

47:13

that

47:14

>> I mean there's a lot of different it's

47:16

multiffactorial which means there's a

47:18

lot of different causes of dementia and

47:20

Alzheimer's disease so I would say you

47:22

mentioned plaques amaloid beta plaques

47:25

what happens is you know that's the

47:27

aggregation of a protein in our brain

47:29

called amalloid that typically is

47:32

cleared from our brain and um what

47:35

happens is this abnormal

47:38

you know thing happens where you're not

47:39

clearing the amaloid and so it starts to

47:41

kind of form these clumps and aggregates

47:44

with the amaloid proteins that are not

47:46

being cleared. And that essentially is

47:49

happening outside of your neurons, but

47:52

it's happening where the synapses are

47:53

formed between neurons. And so what

47:55

happens is it kind of disrupts the

47:57

synaptic connection between neurons,

47:59

which is essentially forming a memory.

48:01

And so when you start to disrupt that

48:03

connection, you lose not only the the

48:06

memories start to go away, but the whole

48:09

purpose of the neuron is to kind of I

48:11

mean one of the purposes is to to form a

48:14

memory. And so you start to like neurons

48:16

start to die, right? When they start to

48:18

lose their purpose. Amaloid aggregation

48:21

is linked to a lot of things. So, for

48:23

example, I mentioned it being cleared

48:25

when we sleep, particularly when we're

48:27

in our deep sleep stage, slowwave sleep.

48:30

That is um something happens that's kind

48:32

of incredible. It's called activation of

48:35

the glimpmphatic system. So, you've

48:37

heard of the lymphatic system. Well, the

48:39

glimpmphatic system is essentially this

48:41

series of like networks and like almost

48:45

like these like highways and essentially

48:48

roads and stuff all like throughout the

48:50

brain where you're squirting this

48:52

cerebral spinal fluid throughout the

48:54

brain and it's clearing away all the

48:57

garbage things like proteins that didn't

49:00

get cleared and it's sort of squirting

49:02

them out and clearing them out through

49:03

this lymphatic system. that lymphatic

49:05

system is activated during sleep and

49:07

it's one of the reasons why people that

49:09

don't get good sleep over the course of

49:12

decades have a higher risk of

49:14

Alzheimer's disease is because they're

49:16

getting these amaloid plaques built up

49:18

in their brains but there's other causes

49:20

as well so for example glucose

49:22

metabolism is disrupted in the brains of

49:25

Alzheimer's disease you need glucose

49:27

your neurons need glucose and so you

49:30

know the essentially um your your brain

49:32

isn't able to make energy correctly

49:34

without the glucose getting into your

49:36

brain. And so that's another sort of

49:39

metabolic underlying cause of

49:41

Alzheimer's disease where you're

49:43

essentially I mean it's thought to be

49:45

where you're eating a lot of refined

49:47

carbohydrates, refined sugars and you're

49:49

not exercising and essentially you're

49:52

you're disrupting the glucose metabolism

49:55

in the brain as well as the whole body.

49:58

Right? So the brain and body are

49:59

connected but um there's also genetic

50:03

causes as well and you know some people

50:06

have genes that can increase the risk of

50:08

Alzheimer's disease because they're not

50:10

able to clear amaloid as well because

50:13

they're not able to repair damage as

50:15

well. So the the bloodb brain barrier

50:18

which is really important for filtering

50:19

out toxic things from getting into the

50:21

brain

50:23

it starts to break down and that's one

50:25

of the I would say early early signs of

50:27

Alzheimer's disease is that breakdown of

50:28

the bloodb brain barrier and that

50:30

happens in people that have a genetic

50:32

risk factor called APOE4. You may have

50:34

heard of this but this is probably one

50:36

of the biggest

50:38

genetic risk factors for Alzheimer's

50:39

disease. About 25% of the population has

50:42

one copy of this gene. That increases

50:45

the risk of Alzheimer's disease by

50:46

twofold. If you have two copies of it,

50:49

it increases the risk of Alzheimer's

50:51

disease by tenfold.

50:53

>> So twofold being 200%.

50:55

>> Twofold being twice twice as much. Yeah.

50:58

200%. And 10fold being a,000%. Right.

51:01

You're you're you're basically I mean

51:04

it's it's pretty bad. And it's not like

51:07

a

51:09

it's not your destiny to get the

51:10

Alzheimer's disease if you have those

51:11

genes. You can do things in your

51:13

lifestyle that can sort of turn the

51:15

table. So you're not you're not

51:17

necessarily going to be getting that

51:18

that Alzheimer's disease and a lot of

51:20

different lifestyle factors like getting

51:22

good sleep, like exercising, avoiding

51:23

alcohol, avoiding smoking, not being

51:25

overweight and obese. Like those affect

51:27

your Alzheimer's disease risk.

51:30

More importantly, if you have one of

51:31

those genes, then you really have to be

51:33

cognizant of those things because if you

51:36

have one of those, you know, ApoE4

51:38

genes, then then essentially your

51:41

lifestyle matters even more than people

51:43

that don't.

51:44

>> And you can do a test to figure out if

51:45

you have those genes.

51:46

>> Yes. Yes. There's a a variety of genetic

51:48

testing services that can be done.

51:50

pretty much all the ones that are out

51:52

there on on the market, you know,

51:53

ancestry DNA. I mean, depending on where

51:56

you live and what there's so many out

51:57

there right now that that will test for

51:59

that.

52:00

>> Mortified if I found out I had two of

52:01

those genes.

52:03

>> Two of them is less common. When I

52:05

mentioned the 25% of the population

52:06

having it, it's usually one alil.

52:08

Alcohol essentially can really increase

52:12

the risk of Alzheimer's disease if you

52:14

have one of those genes. And I think

52:15

that there's really no safe amount of

52:17

alcohol that can be consumed for people

52:19

that have APOE4. if you're concerned

52:21

about dementia and Alzheimer's disease.

52:22

The other thing is contact sports and

52:24

traumatic brain injury. people that have

52:27

any of the, you know, any one or two of

52:29

the APOE4 genes, if they have that, then

52:33

if they get a TBI, like if they're

52:35

playing American football or they're

52:37

playing soccer or MMA or boxing,

52:40

whatever,

52:41

>> then you talk about like going up to a

52:43

10-fold risk for Alzheimer's disease

52:45

when you get like an injury because

52:47

people with those genes don't repair

52:49

damage as well.

52:50

>> So, it affects their their brain's

52:52

ability to repair damage. And so that's

52:54

also really important to consider.

52:56

>> So moving back then to this the simple

52:58

things that we can do to improve our

53:00

cognitive performance as we age, the

53:01

things that are simpler than doing the

53:03

vigorous hit training.

53:04

>> There's actually quite a few. And first

53:06

and foremost, the one I love the most is

53:09

a simple multivitamin.

53:11

And the reason I love this is because

53:15

I don't know it was about 10 years ago

53:17

there was a a huge study that was

53:19

published and it was published in the

53:22

Annals of Internal Medicine and it was

53:23

called Enough is Enough. Multivitamins

53:26

are not only useless, they're harmful

53:28

and it was essentially looking at a

53:30

variety of studies and arguing that

53:32

multivitamins are expensive urine.

53:35

You're just not really doing anything.

53:38

And in fact, if you take a multivitamin,

53:40

you might even be increasing the risk of

53:42

disease.

53:44

That study was terrible. And I 10 years

53:48

ago went and just broke it down and, you

53:50

know, pulled it apart piece by piece.

53:53

But here we are 10 years later. Three

53:57

large clinical trials have been done.

53:58

And these are randomized control trials

54:00

where older adults were given either a

54:03

multivitamin and this was just your

54:04

standard run-of-the-mill multivitamin

54:06

Centrum silver or they were given a

54:08

placebo and they were given this for a

54:10

couple of years.

54:12

And what three different studies showed

54:15

was that a multivitamin improved

54:17

cognition, improved processing speed, it

54:20

improved what's called episodic memory.

54:23

So the kind of memory where you're

54:25

remembering experiences and you can

54:27

recall events, things like that. And not

54:30

only did it improve it, it improved it

54:31

so much that it was equivalent to

54:34

reducing the aging of the episodic

54:37

memory by 5 years. So a simple

54:41

multivitamin and why is that important?

54:43

Because you know multivitamins have a

54:45

variety of these vitamins and minerals

54:47

that we're not getting from our diet

54:50

that are important for everything. for

54:53

metabolism, for the way our

54:54

neurotransmitters are firing, for

54:56

reducing damage that's causing, you

54:59

know, oxidative stress, right? So, a

55:02

simple multivitamin, how much easier can

55:04

it be than taking a simple multivitamin?

55:06

And the fact of the matter is that we're

55:08

talking about a randomized control

55:10

trial. This is showing cause, right?

55:12

This isn't just an association. This is

55:14

showing that you took a multivitamin for

55:17

a couple of years and improved your

55:19

cognition more than a placebo. So, I

55:22

think that's pretty incredible and it's

55:24

one of the examples that I like.

55:27

But, um, diving deeper into some of the

55:30

the nutrients, this is this is an area,

55:33

you know, I started out as a scientist.

55:37

I started out as a chemist actually. But

55:39

when I first got into biology,

55:42

I was working in an aging lab and

55:44

studying aging. It was very interesting

55:46

to me because I essentially with my own

55:50

experiments with my own two hands could

55:52

could manipulate these like tiny little

55:54

worms. They're called sea elegance and

55:57

their whole genome was sequenced at the

55:58

time and this was like in the early

55:59

2000s and um they have a lot of genes

56:02

that are similar to humans. It's called

56:04

homology and one of the genes is the

56:07

insulin signaling pathway and the IGF-1

56:10

pathway. So insulin signaling would be

56:12

something that's activated with glucose.

56:15

You're eating a lot of sugar, right? And

56:17

I could take these worms and I could

56:19

genetically decrease their insulin

56:22

signaling. So it kind of, if you think

56:24

about a parallel to that, that would be,

56:26

okay, we're not going to be eating as

56:27

much sugar, right? We're not going to be

56:29

activating that pathway so much. Mhm.

56:32

>> And I could do that in this worm that

56:34

has a life expectancy of about 15 days

56:37

and I could extend its life expectancy

56:39

to 30 days, right? So you're increasing

56:42

its life expectancy by pretty much, you

56:45

know, 100%. Right? Well, not only did

56:49

they, you know, live longer, they were

56:51

healthier and youthful, and you could

56:52

see that visually, they're moving around

56:54

and they were just youthful worms. And

56:56

so I was very excited about this, you

56:58

know, in my 20s because I was like,

57:01

"Wow, this is very relevant. We have

57:03

this gene and we know lifestyle factors

57:06

that affect it, right? Sugar." So the

57:09

takehome for me was

57:11

lifestyle matters, you know? Yeah,

57:13

genetics, maybe that'll be something one

57:14

day where we're decreasing the insulin

57:15

signal. But I was looking for the now,

57:17

not the future technology. And so the

57:19

now to me was wow, like I don't want to

57:22

be constantly activating my, you know,

57:24

insulin signaling pathway. like look

57:25

what happens to these worms if you

57:27

reduce it. I mean it's amazing. They're

57:28

youthful and they live longer. And so I

57:32

started to kind of get into diet and

57:34

lifestyle sort of just out of curiosity

57:38

and sort of reading in the literature

57:40

and I came across some studies from my

57:43

mentor Dr. Bruce Ames where he was

57:45

showing that not getting enough

57:48

nutrients like for example folate.

57:50

Folate is found in dark leafy greens

57:52

like kale. You know, folate if you if

57:55

you if you decrease folate and make

57:57

someone deficient in it, it essentially

58:00

causes doublestranded breaks in your DNA

58:04

that essentially is like being under

58:08

ionizing radiation. And that experiment

58:10

was done like you could take a mouse

58:12

make it like put low folate in the in

58:14

you know the mouse's food and then take

58:17

another mouse and put it under an

58:19

ionizing radiation machine and the

58:21

amount of double stranded breaks in

58:23

their DNA which cause cancer which

58:25

accelerate aging which affect every

58:27

every you know how how your your cells

58:30

are functioning it was the same. So, it

58:33

was like, wow.

58:35

Not having a certain nutrient in your

58:37

diet was like standing under a radiating

58:39

machine, ionizing radiation. No one's

58:41

going to want to stand under an ionizing

58:42

radiation machine, but no one's thinking

58:44

about how your diet can do the same

58:46

thing. Um, and that was kind of I got

58:49

into a lot of Bruce's Bruce's research

58:52

at the time. So, Bruce,

58:54

he anyone in the in the science field

58:56

knows Dr. Bruce Ames. actually came up

58:57

with the Ames carcinogen test and that

59:01

essentially was a way of cheaply looking

59:03

at and identifying whether something's a

59:05

carcinogen and he got into sort of

59:07

nutrition as he started to figure things

59:08

like folate basically being lack of

59:11

folate being a carcinogen essentially

59:13

right like ionizing radiation is a

59:14

carcinogen

59:16

and then he started to go on to other

59:18

nutrients as well like magnesium and B

59:21

vitamins but I think for me the aha

59:23

moment was

59:25

micronutrients and these vitamins and

59:26

minerals are affecting the way we age,

59:30

are affecting our health on a similar

59:33

level as these toxic things that we're

59:35

worried about like ionizing radiation.

59:37

>> And nobody's thinking about it like

59:39

that.

59:40

>> So, I'll give you an example. Vitamin D,

59:43

you talked about dementia, what's going

59:45

to help prevent dementia. Vitamin D is,

59:48

it's actually more than a vitamin.

59:49

Vitamin D gets converted into a steroid

59:52

hormone. So, a steroid hormone

59:55

essentially what it does is it goes into

59:58

the nucleus of a cell where all your DNA

60:01

is and it it's activating genes and

60:04

deactivating them. It's affecting your

60:06

genome and it's actually over 5% of your

60:10

your your genome is being affected by

60:12

vitamin D. Why is that important?

60:15

Because

60:17

70% of the US population has

60:19

insufficient levels of vitamin D. The

60:22

reason for that is because vitamin D3 is

60:25

actually made in the skin from UVB

60:28

radiation from the sun. And so if you're

60:31

not outside, then you're not really

60:33

making a lot of vitamin D3 in your skin.

60:36

And vitamin D3 then gets converted into

60:38

this steroid hormone that regulates

60:40

everything, right? And so um you know

60:43

modern day society, you know, we're

60:45

inside all the time. We're working.

60:47

We're not outside. And even if you were

60:50

outside, there's so many other factors

60:52

that affect it. So, anything that blocks

60:53

out UVB radiation blocks out the

60:56

availability of your body to make

60:57

vitamin D3. So, sunscreen, right? That's

61:00

a big one. Melanin, the the darker

61:03

pigmentation that acts as a natural

61:05

sunscreen. And then latitude, depending

61:07

on where you live, also. So, you know, a

61:10

good number of months out of the year,

61:12

if you're in a more northern latitude

61:14

like England, like Wales, like Chicago

61:18

or Sweden, you're not UVB radiation is

61:21

not even hitting the atmosphere, you

61:23

know, for several months out of the

61:24

year. Combine that with sunscreen or

61:28

melanin, and you got like this disaster,

61:32

right? In fact, there was a study out of

61:33

the University of Chicago that looked at

61:37

African-Americans and Caucasians

61:40

and their ability white people.

61:42

>> Yeah, exactly. Their ability to make

61:44

vitamin D3 from UVB radiation

61:47

>> from the sun. Yeah.

61:48

>> And as I mentioned, you know, melanin is

61:51

a natural sunscreen. And you know,

61:53

people that are, you know, either, you

61:55

know, from African origin or South

61:58

American or Southeast Asian, right?

62:00

People that are closer to the equator

62:02

usually have more melanin. It's an it's

62:03

an adaptation to prevent you from

62:05

burning from the UV rays of the sun.

62:08

Well, um, this University of Chicago

62:10

study found that, um, you know, people

62:12

that are African-American had to stay in

62:14

the sun six to 10 times longer than

62:17

people with fair skin, the Caucasians,

62:19

to make the same amount of vitamin D3.

62:21

And so, as a consequence, if you take

62:23

someone who like yourself, well, you're

62:25

you're you got a little bit more mel

62:26

melanin mixed

62:27

>> a little bit. Yeah, you've got a little

62:29

bit more melanin. But let's say you take

62:30

someone who, you know, has a

62:32

>> like my mom, she's Nigerian.

62:34

>> Okay. Your mom from Yeah. Nigerian. And

62:36

let's say your mom moves to Chicago,

62:38

>> right?

62:38

>> Well, she's moved to bloody England.

62:40

>> Or she moved to England, right? Exactly.

62:42

Then you're talking about a recipe for

62:44

disaster in terms of vitamin D because

62:48

you're not only not making it several

62:51

months out of the year, I forgot how

62:52

many months out of the year, maybe four

62:54

or five or something like that where the

62:55

UVB radiation is not even hitting the

62:57

atmosphere, but you have this natural

62:58

sunscreen. What's the consequences of

63:00

that in terms of symptoms?

63:02

>> Well, it's it's kind it's not like an

63:04

acute thing where you kind of just look

63:06

in the mirror and you're like,

63:08

>> what is the causation then in terms of

63:10

>> Right. Right. Yeah. So, the reason I say

63:11

this is because people always think of

63:13

like, well, I'm not getting enough

63:14

vitamin C and I have scurvy and you can

63:16

look in the mirror and your gums are

63:17

falling apart. Right. It's easy to

63:19

identify this. Vitamin D deficiency or

63:22

insufficiency is more insidious. It's

63:24

kind of this damage that accumulates

63:26

over time. it's something that isn't,

63:29

you know, quite noticeable or maybe

63:32

maybe you're feeling, you know, m maybe

63:34

you're feeling like lethargic or you

63:36

don't have enough energy, things like

63:37

that, but you don't really really know

63:38

quite why. So, vitamin D insufficiency

63:41

and deficiency, there are acute effects

63:43

where like if it's severe, it can cause

63:44

ricketetts and like bone mal forations

63:47

and stuff, especially if it's happening

63:48

early in life. But um what we now know

63:52

is that being

63:54

deficient or insufficient in vitamin D

63:57

can increase dementia risk by 80%. And

63:59

that's been shown in multiple studies.

64:02

The converse is also true. So people

64:05

that supplement with vitamin D3, and

64:06

this is where a simple solution comes

64:08

in, right? So you're not making it from

64:10

your skin, but you can take a

64:12

supplement. People that supplement with

64:14

vitamin D3 have a 40% reduced risk of

64:16

dementia. So in other words, they're

64:18

avoiding deficiency, which is very

64:20

common, and avoiding that deficiency

64:22

then is reducing their dementia risk.

64:25

And there's actually even been studies

64:26

in people with dementia, in people with

64:28

Alzheimer's disease that were giving a

64:30

vitamin D supplement or a placebo

64:32

control. And those individuals given the

64:35

vitamin D supplement had improved

64:37

cognition. They had um lower markers of

64:39

amaloid plaques. So those were this will

64:42

those were also measured as well. So

64:44

vitamin D is doing a lot of things. It's

64:46

it's regulating 5% of your protein

64:49

encoding human genome.

64:51

>> If I want to increase my probability of

64:52

getting dementia, then I've got to stay

64:54

out of the sun. I've got to avoid um

64:57

vitamin D. I've got to drink alcohol,

64:59

smoke, be sedentary, and I've got to

65:02

sleep really badly.

65:03

>> Yes. And eat a lot of refined sugar.

65:06

>> Yeah.

65:07

>> Yes. Yes. Exactly. Okay.

65:08

>> Exactly. Now, you might go, "Well, how

65:10

much vitamin D?" Right? I'm talking

65:12

about deficiency and insufficiency and

65:13

you really want to get a blood test to

65:16

know what your levels are. There have

65:17

been I don't know 30 plus studies that

65:20

have looked at vitamin D levels and all

65:24

cause mortality. So that would be again

65:27

you know how you know dying from a

65:29

variety of different diseases

65:30

cardiovascular disease respiratory

65:32

disease cancer and people that have

65:34

blood levels of vitamin D between 40 60

65:37

maybe 80 nanogs per milliliter have the

65:40

lowest all-c cause mortality so these

65:41

people are not deficient not

65:43

insufficient insufficiency happens at

65:46

about 30 nanogs per milliliter below

65:48

that deficiency is 20 nanogs per mill

65:52

milliliter and below and so um there

65:55

have been a variety of studies that have

65:56

looked at for example the brain and the

65:58

aging brain and vitamin D levels and

66:00

it's been shown that for every you know

66:03

10 nanimal per liter decrease in vitamin

66:06

D blood levels there's an increase in

66:09

brain damage it's called white matter

66:11

hyperintensities it's basically damage

66:13

to the white matter in your brain and

66:15

the white matter in your brain is myelin

66:18

that's how your brain's communicating

66:19

and and like how you know it electrical

66:22

impulses are being you know moved so

66:24

that you can think and talk and all

66:26

that. Exactly.

66:27

>> Yeah. I hadn't had one today, so I feel

66:29

like you you've persuaded me.

66:32

>> Most people that are deficient can

66:33

increase their blood levels to a normal

66:35

sufficient level by about 4,000 IUs of

66:38

vitamin D per day. So, not and that's

66:41

been done that's been shown in multiple

66:42

studies. Not it's not it's not that hard

66:44

to take. In fact, vitamin D supplements

66:46

are probably the cheapest supplement out

66:47

there. It's like 10 cents per pill. When

66:49

you talked about these,

66:50

>> I was really surprised to hear that they

66:52

have cancer preventing chemicals in

66:55

them. And then um I was looking at some

66:57

of the research and it does say exactly

66:59

as you said, things like kale, broccoli,

67:00

Brussels sprouts linked to a reduction

67:02

in breast cancerous prostate, lung, and

67:05

colarctyl cancers. According to the

67:07

World Cancer Research Fund and PubMed,

67:11

most of us don't eat enough of this

67:13

stuff cuz it's not the tastiest stuff.

67:15

And you talked about sugar as well. It

67:18

it makes me think about the diet that

67:20

I'm currently on, which is the ketogenic

67:21

diet, and whether that is an optimal

67:24

diet in terms of all of the things we've

67:26

discussed earlier, dementia, longevity,

67:28

aging. What is your views on the

67:30

ketogenic diet? I think there's there's

67:34

the extreme ketogenic diet, like the

67:36

classical ketogenic diet, and then

67:38

there's modified sort of low carb

67:40

ketogenic diets that do allow for I

67:43

mean, there's yes, these are leafy

67:45

greens that are carbohydrate, but

67:47

they're high in fiber and they're low

67:49

glycemic index. And so, you can actually

67:51

eat leafy greens on a ketogenic diet and

67:54

still be in ketosis. So I the ketogenic

67:58

diet is very I'm very interested in it

68:00

because I do think that beta

68:03

hydroxybutyrate which is the ke major

68:06

circulating ketone body that's produced

68:08

when you're in ketosis is highly

68:10

beneficial much like lactate it can

68:13

actually do a lot of what lactate can

68:14

do. It gets into the brain and it's an e

68:18

easily utilizable source of energy by

68:20

neurons. These are ketones, which is

68:22

what your body makes when you

68:25

>> abstain from carbohydrates and sugars.

68:27

Yes. It eventually shifts into ketosis

68:29

where you're running on keto.

68:31

>> You're in ketosis and you're running on

68:32

ketones.

68:33

>> Yes. It's what you're measuring when

68:34

you're doing your when you're measuring

68:36

your finger prick that it's beta

68:37

hydroxybutyrate. That's the major

68:39

circulating one

68:40

>> that you're measuring. And that's

68:42

actually a signaling molecule. It's

68:44

activating brain drive neurotrphic

68:46

factor in the brain. And so it's very

68:49

interesting because it's it's almost

68:51

like having lactate in your body but

68:53

having it constantly. So I'm super

68:56

interested in a ketogenic diet

68:58

particularly for people that respond

68:59

well. I mean some people their

69:02

triglycerides go really high, their

69:03

cholesterol goes really high and there's

69:06

sort of an I would say individual

69:07

variation in terms of how you respond.

69:09

And so it's good to always measure

69:11

everything right to make sure that

69:13

you're responding well to ketogenic diet

69:14

or to maybe cycle it. I've been very

69:17

interested in cycling it for brain

69:18

benefits as well because of the beta

69:22

hydroxybutyrate where it's it's just so

69:24

beneficial for the brain. You know, it's

69:26

been shown that you know beta

69:29

hydroxybutyrate. So what happens is when

69:31

you have this ketone like beta

69:34

hydroxybutyrate get into the brain, it's

69:36

able to be used as energy instead of

69:38

glucose. I feel like we should take a

69:40

step back and explain what keto is for

69:43

for the for the listener who maybe has

69:46

never really heard or understood it

69:47

before. And I know that there's a large

69:49

proportion of people that don't know

69:50

what it what it is because I spend a lot

69:52

of time at dinner parties trying to talk

69:54

about it. And it's super surprising to

69:57

me that the average person actually

69:59

doesn't really know what what keto or

70:00

ketosis is.

70:02

>> So, I think that's great. Yeah, we can

70:04

talk about ketosis. Um, essentially if

70:07

we if we kind of take a a thousand mile

70:09

high view of it without getting so

70:11

technical,

70:12

>> yeah,

70:13

>> I would say the best way to think about

70:15

being in ketosis is your body is using

70:19

fatty acids as energy and not much

70:23

glucose. You'll still use a little bit

70:25

of glucose. You need to use glucose

70:27

because your red blood cells, for

70:29

example, don't have any mitochondria.

70:31

They need glucose, but you're mostly

70:33

using fatty acids as energy that are

70:36

being produced from they're being

70:38

released from fat stored in atapost

70:41

tissue,

70:41

>> which is like my belly,

70:42

>> which is like your belly, visceral fat,

70:45

um, subcutaneous fat.

70:46

>> So, this sounds great. My body's going

70:48

to use burn the fat instead of burn, you

70:51

know, burning glucose, which I've got

70:52

from eating bread or something. So, I'm

70:54

going to get skinny.

70:55

>> People do lose weight on a ketogenic

70:57

diet.

70:57

>> My dad has lost so much weight, it's

70:59

ridiculous. It's like shocking. on a

71:00

ketogenic diet.

71:01

>> Yeah, it's crazy. He was quite a big man

71:04

if I say so myself. Very big belly. And

71:07

he sent me this screenshot the other day

71:08

after a couple of months on the

71:09

ketogenic diet.

71:11

>> And he's like 13. He's just for the

71:14

first time ever been 13 stone since

71:15

since he was in his teens. He's now 13

71:18

stone. So he's lost what the equivalent

71:20

of about four four or five stone in

71:22

weight in a couple of months. And he

71:25

just looks completely different. Now,

71:26

I'm not, you know, I'm not necessarily

71:27

saying to stay on that diet forever, but

71:29

the the speed in which one can lose

71:32

weight on a ketogenic diet is

71:34

remarkable,

71:35

>> right? And so, you're you're basically

71:37

the food that you're eating is

71:38

predominantly

71:40

fat, right? So, you're you're basically

71:42

not only using the fat that your body

71:44

already has stored, but you're also

71:45

fueling yourself. You're feeding

71:46

yourself more fat, right? So, you're

71:48

basically using the fat as energy and

71:51

through a whole bunch of biochemical

71:53

reactions, you produce ketone bodies as

71:56

a byproduct of of that. It doesn't

71:59

necessarily have to be just ketogenic

72:01

diet. Like, you can when you're fasting,

72:04

you go into ketosis, right? Because if

72:06

you think about it, you're you're not

72:09

giving yourself food. Instead, you're

72:11

relying on what your body already has as

72:13

a source of energy. And you only have so

72:15

much glucose stored as glycogen right in

72:18

your liver. And that I would say after

72:21

there's individual variation, but after

72:23

about 12 hours of not giving your body

72:26

food, you sort of deplete all your

72:28

glycogen stores and then so you start to

72:30

shift to lipolysis, which means the

72:32

breakdown of fat. So fasting is another

72:34

way to go to get into ketosis. Another

72:37

way would be intense exercise. So, like,

72:39

you know, these endurance athletes that

72:41

are doing long duration types of

72:43

exercise also can go into ketosis,

72:46

right? Because they're depleting their

72:47

glycogen stores much quicker and they're

72:49

also using all this energy that they've

72:52

they've fueled themselves with because

72:54

it's it's so intense, right? Long

72:56

duration type of exercise. And so, and

72:58

you can combine these things as well,

72:59

right? You can do endurance exercise

73:02

with the ketogenic diet and you really

73:03

kind of can get into ketosis quicker. Is

73:06

it like a switch?

73:08

>> So there is something called metabolic

73:11

flexibility which essentially means that

73:14

your body is able to

73:17

switch between burning glucose and using

73:19

glucose as energy but also using fatty

73:21

acids as making you know as energy and

73:24

then producing ketones as well. And the

73:28

more I would say the more um if you've

73:30

done ketosis or if you exercise a lot

73:33

like frequently or you do any form of

73:36

fasting or what's called timerestricted

73:37

eating. So let's say you eat all your

73:39

food within an eight hour window and

73:42

then for 16 hours you're not eating

73:43

food. Your body is used to switching to

73:46

fatty acid metabolism to to using fatty

73:48

acids as energy. So you're really

73:50

metabolically flexible. And um not

73:53

everyone's able to do that because most

73:56

people actually they think they eat

73:57

within a 12-h hour period, but they

73:59

there's been studies that have been done

74:01

that have shown that actually they eat

74:02

more like within a 15 to 16 hour period,

74:05

not not even a 12-h hour period.

74:07

Certainly not a 10 or eight hour period.

74:09

So there's, as I mentioned, it takes

74:11

about 12 hours on average to deplete all

74:14

your glycogen levels. Now, you can

74:16

accelerate that, if you're doing a lot

74:17

of physical activity, but once you

74:19

deplete that liver glycogen, that is

74:22

when you shift into burning fatty acids

74:24

and then eventually ketosis, right?

74:26

>> In terms of longevity, have they ever

74:28

done any studies where they've put

74:29

someone on the ketogenic diet or like a

74:31

mouse or a rat on a ketogenic diet

74:33

versus the the average diet and then

74:35

monitored how long they live?

74:38

>> There have been studies by uh Dr. Eric

74:40

Verden out of the uh Buck Institute for

74:43

Aging in Novado, California. And I mean

74:46

this was several years ago. He's done

74:47

these studies probably almost 10 years

74:49

ago, maybe about 2018 or 2017 these

74:51

studies were published. But um he he did

74:54

do some of these studies with a

74:56

ketogenic diet in rodents and it did

74:59

seem to extend life expectancy but more

75:02

importantly the health span. So

75:04

particularly in the brain. So it's like

75:06

their brain had aged much much better.

75:09

they had less of the all of the

75:12

pathological features of Alzheimer's

75:14

disease. And again, I do think like I

75:17

mentioned, I I'm I'm super interested in

75:20

beta hydroxybutyrate

75:22

in particular. I mean, there's it's

75:23

multiffactorial because on the one hand,

75:25

you're not eating as much glucose,

75:27

right? And that in in and of itself is

75:29

important because glucose can be so

75:32

damaging particularly if you're not

75:35

physically active because it's not if

75:36

you if you're physically active and

75:38

you're eating some amount of glucose

75:39

that's going into your muscle.

75:40

>> It's not damaging the vascular system.

75:42

>> The vas the cardio the vascular system

75:44

is very much related to the brain,

75:45

right? So when you start to stiffen your

75:47

blood vessels and stiffen everything, I

75:49

mean that's that's affecting blood flow

75:51

to the brain. It's you know it's causing

75:53

hypertension. That all affects brain

75:55

aging as well. So, I think just, you

75:58

know, and then the the the damage that

76:00

the glucose does in and of itself, like

76:02

I mean there's studies, it's really

76:04

interesting. There's studies showing

76:05

that people even on the high end of

76:08

normal in terms of their blood glucose

76:10

levels. So, they're normal, but they're

76:12

kind of on the high end of normal. They

76:14

had more brain atrophy than people on

76:17

the low end of normal.

76:20

>> By brain atrophy, you mean their brain

76:22

was

76:23

>> shrinking.

76:23

>> Shrinking.

76:24

>> Shrinking. And it was the hippocampus,

76:25

by the way. again that

76:26

>> that part of the brain that's involved

76:28

in learning and memory. So the glucose

76:30

itself has this effect on you causing

76:34

damage and accelerating the aging

76:36

process. But then there's this other

76:38

very interesting effect of these

76:40

chemicals that are made as a byproduct

76:42

of being in ketosis and that is the beta

76:45

hydroxybutyrate that ketone body gets

76:47

into the brain. It's transported across

76:49

the brain through an MCT transporter.

76:52

And when it gets into the brain, it can

76:54

be used as energy. And you your neurons

76:56

don't need to use glucose. And it can do

76:58

that. So your your neurons can use

77:01

glucose as energy, but it takes energy

77:03

to use that glucose to make energy. When

77:06

you use the ketone, the beta

77:08

hydroxybutyrate, it takes less energy to

77:10

you to make that energy. So it's

77:12

energetically favorable to actually use

77:14

that ketone, that beta hydroxybutyrate.

77:17

On top of that, this is what's so

77:18

interesting, it frees up glucose. So,

77:21

the neurons aren't using the glucose.

77:22

Where does the glucose go? Right?

77:24

Because it's there. It's it it sort of

77:26

shunts it into this other pathway that's

77:29

called the pentos phosphate pathway. I

77:30

don't want to, you know, burden people

77:32

with all the technical details, but

77:34

let's get to the important part of that

77:35

is that it shunts glucose into this

77:37

pathway that makes essentially its

77:40

precursors that make what's called

77:41

glutathione, the major antioxidant in

77:44

the brain. And so you're making more

77:47

glutathione day after day after day.

77:50

That is huge because oxidation in the

77:54

brain, inflammation, this is a huge

77:56

cause of brain aging and Alzheimer's

77:58

disease, dementia. We now know

77:59

neuroinflammation is one of the major

78:01

causes of it. And so if you have more

78:04

glutathione in your brain, you are going

78:06

to basically sequester that damage

78:09

that's causing, you know, that's that's

78:12

aging the brain essentially. And so the

78:15

glucose now is not being used for

78:16

energy. It's being used to make an

78:18

antioxidant in the brain. Okay, that's

78:20

also

78:21

really cool. And there's more. There's

78:24

more. Okay, so then the beta

78:25

hydroxybutyrate itself is a signaling

78:27

molecule like lactate.

78:28

>> The ketone,

78:29

>> the ketone itself is a signaling

78:31

molecule where it's basically, you know,

78:33

it's a little bit of a stressed state,

78:35

right? So when you're in ketosis, it's

78:37

you're stressing the body. It's either

78:39

exercise or you're fasting or you're on

78:41

this ketogenic diet. And so your body

78:43

again is responding to that stress by

78:46

making like a bunch of awesome resilient

78:49

stress response things that are

78:51

basically gonna improve the way you age.

78:53

And so the ketone beta hydroxybutyrate

78:56

then activates brain drive neurotrphic

78:58

factor. This miracle growth for your

79:00

brain, right? It's involved in growing

79:01

new neurons. It's involved in increasing

79:03

the connection between neurons. It's

79:04

involved in neuroplasticity. All those

79:06

things. And so you get this multi-level

79:09

benefit not getting not having the glue

79:11

glucose causing the damage. You have um

79:13

basically the glucose now being used.

79:16

Not only is it not going causing damage,

79:18

it's being used to make an antioxidant.

79:19

And then you have the whole ketone, you

79:22

know, aspect where you're you're

79:23

essentially um making and activating all

79:26

these beneficial pathways in the brain

79:28

that reduces aging. And what's going on

79:31

when we take

79:33

exogenous ketones, external ketones via

79:36

a drink or something like that?

79:37

>> Yeah. So, what's happening is you're

79:39

essentially giving your body the beta

79:44

hydroxybutyrate ketone that it would

79:46

make normally if you were undergoing

79:48

ketosis and using fatty acids only as

79:51

energy. You're giving your body a big

79:53

boost of it. So, you're kind of

79:55

bypassing the the way that your body

79:57

would make it itself and giving it to

79:59

your body. And it's great for people

80:01

that

80:02

have a hard time with doing a ketogenic

80:05

diet, for example. Maybe they just can't

80:07

stick with it or maybe they don't

80:08

respond very well to it in terms of

80:10

other biomarkers. They're going to get a

80:13

lot of the benefit, but it's only going

80:14

to last, you know, one to three hours,

80:16

right?

80:16

>> Yeah. Until it flushes out, right?

80:17

>> Until until you use it up. Yeah. And so

80:20

it's in addition to just people that

80:21

want to get that focus and attention,

80:23

which is what both you and I have

80:25

experienced when we've taken these, you

80:27

know, supplements, this exogenous

80:29

ketone.

80:30

There's also some potential therapeutic

80:33

effects. So people that have mild

80:37

cognitive decline, maybe like the first

80:39

stages of dementia or Alzheimer's

80:41

disease can kind of perk up and um

80:45

perform better when they have when

80:47

they're given an exogenous ketone, this

80:50

supplemental ketone beta

80:51

hydroxybutyrate. There's not a lot of

80:53

studies on it, but there's like a few

80:56

case studies where

80:57

>> case studies being like a single person

80:59

is given it and they're followed and

81:02

looked at, you know,

81:03

>> and it's very interesting.

81:05

>> I actually know that they're doing

81:06

studies on exactly that at the moment.

81:08

Um because I've spoken to a few of these

81:10

companies and a few scientists that are

81:12

in this field over the last couple of

81:14

over the last couple of weeks in fact

81:16

and they were saying that we're

81:17

currently in the process of doing

81:18

studies to see that if exogenous ketones

81:20

which are these ketone drinks or ketone

81:22

shots can repair your cognitive faculty

81:25

faculties and is that via the process

81:27

that you describe where glucose is

81:29

pushed into this other pathway?

81:32

>> Yes. So, um, I think I'm aware of the

81:35

same study because I've I've looked it

81:37

up in the clinical trial and what's

81:39

what's being looked at after giving this

81:42

exogenous beta hydroxybutyrate, this

81:44

supplemental ketone in people with

81:47

Alzheimer's disease, you can repair

81:50

damage because again you are activating

81:54

brain drive neurotrphic factor which can

81:56

it can repair damage. It can grow new

81:58

neurons. It can help with brain atrophy.

82:01

it can strengthen connection between

82:02

neurons and then the glucose now is

82:04

being shunted into that repair pathway

82:06

that glutathione is being activated and

82:09

and that's able to you know repair

82:11

damage as well. So I I'm excited to see

82:15

the public like that that study

82:17

published.

82:18

>> I would hypothesize that there's going

82:20

to be beneficial effects and it's going

82:21

to be pretty exciting particularly

82:23

because it is hard for older adults some

82:27

older adults to do a ketogenic diet.

82:29

It's not the easiest thing to follow. I

82:31

mean, you do have to be pretty

82:32

disciplined.

82:34

So, this alternative to being able to

82:36

supplement with something that can sort

82:39

of at least for the course of a couple

82:40

of hours do what being on a ketogenic

82:44

diet can do is very exciting. Right.

82:46

>> When you took the keto shot that you had

82:49

at home, what did you experience? You

82:51

said it was potent. It was powerful.

82:54

>> Yeah. It was like a neutropic effect

82:57

where when I mean neutropic effect, it's

82:59

it's the kind of effect where you you

83:02

feel

83:04

focused, your attention, your alertness

83:06

is enhanced, you're sort of filtering

83:09

out all the background noise in your

83:10

brain that sort of those little thoughts

83:12

that pop in and distract you. And so,

83:15

uh, you're more productive. And, um,

83:18

that was very noticeable. In fact, there

83:20

was a time when I was like before any

83:21

podcast, I would take a shot of it. I

83:23

would do it and um it's kind kind of

83:28

expensive, but it is I there's a lot of

83:30

people that are that are using it now.

83:32

And I think it's I think it's a better

83:34

alternative to some other neutropics

83:37

that are common right now, like

83:38

nicotine, for example, which can really

83:40

have a negative trade-off, but can do

83:43

something similar. Whereas this is like

83:45

not only gives you that sort of

83:47

cognitive enhancement, that brain pump,

83:50

it also has like benefits for brain

83:52

aging. Right.

83:54

>> What are your superfoods? There must be

83:56

foods of yours. Um olive oil has become

83:59

one of my superfoods. Just a food that I

84:01

love to just put on as many things as I

84:03

can because everybody tells me about

84:04

these polyphenols which are apparently

84:05

amazing for you. But what are some of

84:07

the your sort of favorite superfoods

84:08

that you try and consume that most

84:10

people might not think of? So we talked

84:12

about leafy greens. I guess that's one

84:13

of them.

84:14

>> It is leafy greens. Um they have they're

84:16

high in magnesium and you know magnesium

84:19

is at the center of a chlorophyll

84:20

molecule. Chlorophyll give plants their

84:22

green color. Magnesium is very important

84:24

for preventing damage to DNA DNA and

84:28

cancer. And you know half half the US

84:31

population doesn't get enough of it.

84:32

They're high in a lot of different

84:34

compounds. I mean they're folate,

84:36

vitamin K one. So you're getting a lot

84:38

of these micronutrients that are

84:39

important. So I do like re dark leafy

84:42

greens. I particularly like kale and

84:44

broccoli because of something called

84:45

sulfurophane

84:47

which is sulurophane itself is not in

84:50

them but a precursor when you break the

84:53

plant or you chew it um it makes

84:55

sulfurophane. So there's an enzyme that

84:57

gets activated that converts a precursor

84:59

in these plants called glucaraphin into

85:02

sulurophane. Sulfurophane is also

85:04

increases glutathione in the brain. It

85:06

helps detoxify pollutants like benzene,

85:09

um, bisphenol A, BPA as well. So, I do

85:13

like dark leafy greens of the

85:14

cruciferous family of vegetables. Again,

85:16

that would be kale, broccoli. Um, those

85:19

are those are the cruciferous family.

85:21

>> I also like blueberries. Blueberries are

85:23

a source of polyphenols. You mentioned

85:25

olive oil as a polyphenol. If you're on

85:26

a ketogenic diet, olive oil is like the

85:28

great, right? Because you need fat. And

85:31

olive oil is so great because it also

85:33

has those polyphenols that are

85:34

beneficial. has been shown even in

85:36

studies to improve cognition and memory

85:39

and uh lower even marker markers of um

85:43

bad cardiovascular disease like Apo B

85:45

for example lower that. So blueberries I

85:49

like because blueberries have also been

85:50

shown even a cup of blueberries a day

85:52

has been shown to improve cognition. So

85:54

I like the polyphenols. It increases

85:56

blood flow to the brain. I also like

86:00

salmon and I think that would be

86:02

something that most people would think

86:04

is healthy. I like it because it's high

86:06

in the omega-3 fatty acids which I'm

86:09

very very it's I think it's very very

86:12

important to get enough omega-3 fatty

86:15

acids. I also supplement with them

86:16

because there's a lot of research out

86:18

there and if you want to get into that

86:19

we can but um the superfood would be the

86:22

the salmon because it is a fatty source

86:25

of fish that is high in omega-3 fatty

86:28

acids EPA and DHA which are found in

86:30

marine sources not plant sources of

86:32

omega-3.

86:33

>> I found it really interesting when I was

86:34

looking at omega-3 that it has an impact

86:36

on mental health and depression and

86:38

things like that.

86:38

>> Yeah, it does. It's it's it resolves

86:41

inflammation. It's sort of an

86:43

anti-inflammatory

86:45

and inflammation plays a role in

86:46

depression. A big role. In fact, we we

86:48

know that um people that are injected

86:51

with inflammatory molecules like

86:54

something that's made in our gut from

86:55

the bacteria in our gut called

86:57

lipopolysaccharide.

86:58

If you inject them with that it or a

87:01

placebo control, which is saline, it

87:03

causes depression. But if you give them

87:04

an omega-3 fatty acid supplement, EPA,

87:07

it blunts the depressive symptoms. So,

87:09

in other words, if you're causing the

87:11

inflammation by injecting something that

87:14

causes inflammation in people, it causes

87:16

depression. But if you give those same

87:18

people something that blunts that

87:19

inflammation, omega-3 fatty acids, it

87:22

doesn't cause the depression, which is

87:23

kind of amazing. And there's a ton of

87:25

other evidence out there. But, um,

87:27

omega-3 fatty acids are

87:30

they're so important. And what's

87:32

interesting was there's a study out of

87:33

Harvard that identified the marine

87:36

source. So, I talked about salmon, EPA,

87:40

DHA, and then there's the plant source,

87:42

ALA. And I say marine source because

87:44

it's really those are the important ones

87:46

that you really want

87:47

>> from the ocean,

87:49

>> from fish, seafood. So, this Harvard

87:53

study identified not eating enough

87:55

seafood as one of the top six

87:58

preventable causes of death up there

88:01

with not having hypertension, not

88:04

smoking. So essentially not getting

88:07

enough omega-3 from seafood was so

88:11

important for preventing early death

88:14

that it was comparable to people having

88:15

high blood pressure, having

88:17

cardiovascular disease, for example. And

88:19

again, it's one of those things where

88:21

people just don't think about what

88:22

they're not eating, what they're not

88:24

getting. And um you there's so much

88:26

research that have been done even since

88:28

that that study that was published in

88:30

like 2009 looking at omega-3 fatty acid

88:34

levels in our blood cells, red blood

88:36

cells. This is called the omega-3 index.

88:39

O it's really an important marker of our

88:42

long-term omega-3 because our our red

88:45

blood cells stay around in our system

88:47

for like 120 days. So it's a long-term

88:51

marker of your omega-3 intake. And

88:54

there's been a variety of studies um

88:56

done from Dr. Bill Harris out of the

88:58

fatty acid research institute. So I'm an

89:00

associate a scientist there showing that

89:03

people with what's called a high omega-3

89:06

index

89:07

>> which is a lot of omega-3

89:08

>> a lot of omega-3 their omega-3 index

89:10

would be 8% or higher that's considered

89:13

high compared to a low omega-3 index.

89:16

That would be 4% or lower. The average

89:19

omega-3 index in the United States is

89:21

about 5%. So, it's on the low low range.

89:24

People that had the high omega-3 index,

89:26

in other words, they were either eating

89:28

a lot of fish like salmon and or

89:31

supplementing with fish oil or

89:34

microalgae oil, which is another a

89:37

marine source of these omega-3 fatty

89:38

acids. They had a five-year increased

89:42

life expectancy compared to people with

89:44

a low omega-3 index. Pretty big

89:46

difference there. All all you have to do

89:49

is essentially either eat enough seafood

89:51

and or supplement with a fish oil

89:54

supplement. But what was so fascinating

89:56

about this study was that Bill and his

90:00

colleagues not only looked at the

90:01

omega-3 index, they looked at people

90:04

that also smoked and they said, "Okay,

90:07

we know smoking is terrible for your

90:09

heart. We know it's causes early

90:11

mortality, cancer, and all that, right?

90:14

What about people that smoke and their

90:17

omega-3 index? So, there was four groups

90:20

that were looked at. Smokers that have

90:22

either a high omega-3 index, so these

90:24

smokers were either supplementing or

90:26

they were eating a lot of seafood. And

90:28

then there were smokers with a low

90:30

omega-3 index. And they compared them to

90:33

non-smokers with a high omega-3 index

90:36

versus a low omega-3 index. And what was

90:38

so fascinating about this study was that

90:41

smoking was like as bad for you in terms

90:45

of mortality as having a low omega-3

90:47

index. So the smokers with a high

90:50

omega-3 index had the same mortality

90:53

risk as non-smokers with a low omega-3

90:56

index, which is fascinating because

90:59

everybody knows to avoid smoking.

91:01

Smoking, if you want to take years off

91:02

your life, if you want to decrease the

91:04

quality of your life, start smoking

91:06

right now.

91:08

But the same mortality risk was found in

91:11

non-smokers who did not have a high

91:14

omega-3 index. Right now, I say this,

91:18

I'll talk about this and smokers will

91:20

say, "Oh, great. Now all I have to do is

91:22

take fish oil and I'll have the same

91:23

life expectancy as a non-smoker with,

91:26

you know, a low omega-3 index." But of

91:28

course, the the take-home here is that

91:30

for those of us that are not smoking,

91:32

but we're not getting enough omega-3

91:35

from our diet, that's like smoking in

91:38

terms of mortality risk. So, super

91:41

important, and I like talking about this

91:43

because it really makes it again really

91:45

clear that not getting these essential

91:47

nutrients can be very detrimental to our

91:50

health. And it's easy to fix. You can

91:52

take a fish oil supplement. You can

91:53

increase the amount of salmon that

91:55

you're eating. And there have been

91:56

studies from Bill's group that have

91:58

shown people that supplement with

91:59

between 1 to two grams of fish oil per

92:02

day can go from a low omega-3 index to a

92:05

high omega-3 index, which is not hard to

92:07

do.

92:08

>> So, I guess two questions, which is, is

92:11

having these little omega capsules the

92:13

same as eating the salmon in terms of

92:15

the omega3 that I'm getting? And how

92:19

long do I have to take these little

92:20

omega capsules for to move from having a

92:23

low index to a high omega-3 index?

92:26

>> Well, these are great questions,

92:28

Stephen. So, essentially, this little

92:30

capsule here is not the same as eating

92:34

salmon. And there's a few reasons why.

92:36

So, for one, when you're eating a fish

92:39

that's high in omega-3, like salmon,

92:42

you have this omega-3 in what's called

92:45

triglyceride form. So the omega-3 is is

92:48

is bound to a glycerol backbone and

92:50

that's really important for the way you

92:52

absorb it. Some fish oil supplements

92:54

don't have that. They're they're aster

92:56

they're basically they're molecular

92:58

distilled and then they're put they have

93:00

an ethanol back backbone. So it's not

93:02

quite as bioavailable. But I think more

93:05

importantly is that these fish oil

93:07

supplements are

93:10

purified. So you're not getting mercury

93:14

or microplastics or things that are also

93:17

found in the whole fish.

93:18

>> So these are better.

93:21

>> Unfortunately, I think so. I do. Um, as

93:24

much as I think it's it's better, you

93:26

know, for the longest time I always I

93:28

was always a whole foods first approach.

93:31

Um, but we do have this environmental

93:33

pollution problem and fish have been

93:35

contaminated with heavy metals. They've

93:38

been contaminated with microplastics.

93:40

I would say that salmon is one of the

93:42

lowest fish that has the lowest amount

93:44

of mercury compared to other fish. So it

93:47

on a on a per gram basis, you're getting

93:50

less mercury per gram with salmon than

93:53

you would be with, you know, something

93:55

like swordfish, for example. But but you

93:59

also have microplastics unfortunately

94:01

that are now in fish. And it is

94:03

something that enters our body when we

94:06

eat the fish. And so I do think the fish

94:08

oil supplements are a good alternative

94:10

because you're getting those omega-3

94:11

fatty acids and you're not you're you're

94:13

not getting some of the other bad things

94:15

that are in the fish.

94:16

>> That's fascinating. I didn't really I

94:18

didn't really think of omega-3 as being

94:19

that important, especially as it relates

94:21

to longevity. I always thought about it

94:22

as being something that would help my

94:23

brain work better today. You know,

94:25

cognitive performance now.

94:27

>> Well, it does that and it also helps

94:29

prevent the cognitive decline later. And

94:31

also cardiovascular disease, that's a

94:32

big one. So there have been some really

94:34

large randomized control trials that

94:36

have actually given people with

94:38

cardiovascular disease that are on, you

94:40

know, some sort of standard of care

94:42

treatment like a statin and they've

94:44

given them four grams a day of a

94:46

purified form of omega-3 called EPA

94:49

versus a placebo. And the people given

94:52

the omega-3

94:53

had 25% less cardiovascular related

94:56

death or events like heart attacks and

94:58

strokes. So, it's not only like

95:01

preventing, you know, we talked about

95:03

all cause mortality and this association

95:05

where you live longer. It's also helping

95:07

people that already have cardiovascular

95:09

disease and reducing their risk of dying

95:10

from it.

95:12

>> Right guys, going to go get Steve. The

95:13

guest is here. Ready?

95:15

>> Come in.

95:16

>> Oh my god. Steve,

95:19

>> what are you doing?

95:20

>> This is uh the Bontage face mask. It's

95:22

good for blemishes, wrinkles, uh clears

95:25

up the skin. It's red light. Have you

95:26

not used it before?

95:28

>> No. I tried this before. It's um it's

95:30

really really good. It's shines red

95:32

light on your face which helps increase

95:34

and boost collagen production. Actually

95:36

found it out cuz the misses seen her

95:37

wearing it. She terrified me a couple of

95:39

nights in a row. Um I thought it was to

95:41

scare people with but actually it's

95:42

really really good for your skin. So

95:44

they are a sponsor of the podcast and uh

95:46

I've been using it every day for about a

95:48

year and a half now.

95:49

>> Wow.

95:50

>> Well, Steve is great.

95:52

>> Yes. And Bon Charge ships worldwide with

95:54

easy returns and a year-long warranty on

95:56

all of their products. So, visit

95:57

bondcharge.com/diary

95:59

for 25% off on any product sitewide. But

96:02

you have to order through that link.

96:04

That's boncharge.com/diary

96:07

with code diary.

96:09

When I asked you before this

96:10

conversation started rolling, what

96:12

you're really excited about at the

96:13

moment, your response to me was there

96:15

was a few things, but one of them which

96:16

lit up your face was creatine.

96:19

>> Yes. And it's funny because

96:22

>> it lit up your face again.

96:24

>> Yeah. It's it's funny because creatine

96:26

has been around for I mean ever for

96:28

decades and it's always been in my mind

96:30

it was like one of those Jim bro things.

96:32

I'm like I don't need to be swole.

96:35

>> Yeah.

96:35

>> I don't need creatine get get swole. And

96:38

you know this is this was the thought

96:39

for for many many years. And then over

96:42

the last five years or so

96:47

the effects of creatine on the brain

96:49

started to really get my interest.

96:50

anything that affects the brain I really

96:52

become interested in. And so that's kind

96:55

of what did get me the most excited

96:58

about about creatine, but also I started

97:00

doing a lot of resistance training. And

97:02

so I was like, "Okay, here I am now. I'm

97:05

like one of those gym guys. I'm doing

97:07

I'm doing the barbells. I'm doing the,

97:09

you know, the squats and the deadlifts

97:10

and all that." And so so why not give

97:13

myself some of the creatine? Well, what

97:14

is creatine, right? Why is it important?

97:18

You talked about earlier, you know, why

97:21

doesn't our body just make more of these

97:23

things that are so beneficial? We do

97:25

make creatine. We make about, I don't

97:27

know, our liver makes about 1 to three

97:29

grams a day of creatine and our brain

97:33

also makes creatine and those are the

97:34

two organs that make it. Creatine gets

97:38

consumed by other tissues like the

97:40

muscle is probably the one that's the

97:41

greediest because creatine is stored as

97:45

phosphocreatine but it's used to make

97:47

energy essentially. So it can increase

97:50

muscle mass, it can increase muscle

97:52

strength in combination with resistance

97:55

training because you're able to

97:57

regenerate and make energy faster. So,

98:00

for example, I became interested in it

98:03

after reading studies where people that

98:05

supplemented with creatine that were

98:07

engaged in resistance training were able

98:10

to gain more lean body mass. They were

98:12

able to gain more strength. It was

98:14

increasing their training volume. So,

98:16

you can do one to two more reps, right,

98:19

of of whatever exercise you're doing.

98:22

And it seems to decrease the recovery

98:24

time between those those sets as well.

98:26

So, you're able to increase your

98:27

training volume. Well, anything that's

98:29

going to in increase your training

98:30

volume is going to then have the

98:33

downstream effect of, you know,

98:34

increasing the adaptations like

98:36

increased muscle mass or increased

98:38

muscle strength. I started supplementing

98:40

with creatine about a year ago and I

98:43

started supplementing with it for that

98:45

reason, for the my training and I was

98:47

doing about five grams a day because

98:49

that was really what was shown to to be

98:52

beneficial for muscle health in

98:54

combination with resistance training.

98:56

And it's important for people to realize

98:57

that supplementing with creatine by

99:00

itself, without any type of resistance

99:02

training, isn't going to grow your

99:04

muscle. It's not going to make you

99:05

stronger. You have to put in the effort

99:08

because what creatine is doing, it's

99:10

helping you make the energy quicker,

99:13

right? And that and then being able to

99:15

make that energy quicker means that

99:16

you're able to then do that exercise

99:18

better, um, harder, more of it, right?

99:21

So, um, it's sort of sup supercharging

99:24

your exercise routine.

99:26

and five grams a day was like, "Okay,

99:28

perfect. That's what I'm doing. I'm

99:29

doing five grams a day." And definitely

99:32

noticed an effect on my training volume

99:34

where I was, you know, doing more more

99:36

reps. So that was like, okay, a year

99:38

ago, I had already been aware of the

99:42

effects on the brain. I thought maybe

99:43

the five grams a day would do that. So

99:45

what are the effects on the brain? Well,

99:46

your brain also consumes a lot of

99:48

energy, you know, needs a lot of energy.

99:51

So it does make its own creatine. But it

99:54

turns out if you can if you can give

99:56

your brain more of that creatine

100:00

particularly under a period of anything

100:02

that's causing stress. So let's say lack

100:06

of sleep or let's say emotional

100:10

psychological stress or in my case high

100:15

cognitive load where you're just every

100:18

day learning concepts, complex things.

100:21

you're trying to remember them. You're

100:23

putting ideas together and coming up

100:25

with new hypotheses and you know, you're

100:28

just you're just you're studying a lot

100:29

and it's very cognitively demanding and

100:32

it's it's a type of stress on your

100:34

brain. That's like my life, right? Um

100:37

under this condition of stress,

100:39

depression is another one. That's a

100:40

stress on your brain or neurodeenerative

100:43

disease. That's a stress on your brain.

100:44

So any kind of stressful condition,

100:48

that's where creatine shines in the

100:50

brain. I would argue that I mean all of

100:53

us who who has the perfect amount of

100:55

sleep never has stress nobody right

100:57

there's always some sort of stress in

100:59

the background. So um that's when I was

101:02

like okay so if you're the perfect

101:05

person you have no stress you get the

101:07

perfect amount of sleep every night your

101:08

brain makes enough creatine to kind of

101:11

do what it needs to do. I know that I'm

101:13

constantly under stress. So um I'm like

101:16

okay well I think I need a boost. And

101:18

this is where a lot of very interesting

101:20

studies have come out of many different

101:22

labs. Um, some out of Germany that

101:24

looked at the dose of creatine and how

101:27

it increases creatine levels in the

101:29

brain. And this is why I now supplement

101:32

with 10 grams a day. So the study out of

101:34

Germany

101:35

found that five grams a day of creatine,

101:38

if you're supplementing with five grams

101:39

a day, your muscles are greedily

101:41

consuming it. Particularly if you're

101:42

working out, they want it. They want it.

101:45

after about five grams a day, especially

101:47

over a few months, like you're you're

101:49

saturating your muscle and that's

101:50

enough, right? Anything above that kind

101:53

of spills over to the brain. And so they

101:56

what this German study found was that 10

101:58

grams of creatine increased creatine

102:01

levels in several different regions of

102:02

the brain. And that was probably the

102:04

most exciting, you know, I would say

102:06

evidence that supplementing higher than

102:07

five grams a day was actually doing

102:09

something in terms of getting creatine

102:11

into the brain.

102:13

There have now been a variety of studies

102:14

that have looked at different outcomes,

102:17

right? So, if you supplement with 10

102:20

grams of creatine or even go higher than

102:21

that, like 20 grams of creatine, how

102:23

does that affect cognitive function,

102:25

right? And so, um some of these studies

102:27

have been been done by uh Dr. Darren

102:29

Kandow. He's um at the University of

102:31

Regina in Canada and it's looked they've

102:35

looked at things like sleep deprivation

102:37

and it's been found that if you take

102:39

someone and you sleep deprive them for

102:42

21 hours and give them about 25 to 30

102:47

grams of creatine, it completely negates

102:50

the cognitive deficits of sleep

102:53

deprivation. Actually, not only does it

102:55

negate the cognitive deficits of sleep

102:57

deprivation, it makes people function

103:00

better than if they were well-rested.

103:04

That's where I was like, wait a minute,

103:07

there's many times when I'm traveling,

103:09

I'm jet-lagged. Uh lots of times when

103:11

I'm sleep deprived and I have to be

103:13

doing a podcast or a presentation,

103:14

whatever. And in those situations, I go

103:19

up from my 10 grams to more like 20

103:21

grams. Like today for example, I wasn't

103:24

really sleepdeprived, but you know,

103:27

there was a lot of high cognitive

103:29

demand. This is a long podcast. There's

103:31

all that stuff. And so I went up to 20

103:33

grams today on my creatine. And I Well,

103:36

I will say even at the 10 grams for me,

103:39

we were talking about this with respect

103:40

to being in ketosis.

103:44

I don't feel that mid-afternoon crash

103:46

when I have the creatine. Not being on a

103:48

ketogenic diet, not being in ketosis.

103:51

It's very clear for me and I've done

103:53

this where sometimes I only do five

103:54

grams and then if I do that I'll notice

103:57

I'm like why am I tired right now? So

104:00

there's something interesting and maybe

104:01

it's placebo. I'm going to throw that

104:03

out there. Very possible. But I don't

104:05

know maybe the creatine is again it's

104:08

able to regenerate that energy quicker

104:10

and so that's also beneficial for the

104:12

brain. And now I I would say all these

104:14

creatine researchers a lot of them are

104:16

shifting to the brain. And it used to be

104:18

all muscle focused and now people are

104:20

super interested in what creatine is

104:23

doing to the brain, especially if you're

104:25

supplementing with more of it. And you

104:27

know, this is important for people that

104:29

are under a stressful situation, but

104:31

also for vegans because creatine is

104:34

found in food, mostly in animal products

104:36

like meat and poultry and fish, dairy. A

104:39

lot of vegans don't eat that. And I've

104:40

had so many of my vegan friends,

104:44

I've got them on the creatine, and it's

104:45

changed their lives. I mean, they're

104:47

like, "This is like incredible." You

104:49

know, can you imagine someone who's not

104:51

getting any creatine from their diet

104:52

because they eat no meat and all of a

104:55

sudden they start supplementing with 5,

104:56

10 grams of creatine and it's like they

104:58

have energy. Some people say they they

105:01

require less sleep, which is kind of

105:02

interesting. That's kind of a comment

105:04

I've heard many, many times from people

105:06

is that it's like their brain doesn't

105:08

need as much sleep. They have more

105:09

energy. So, um, I've been a big fan of

105:13

the creatine, um, not only for the

105:14

muscle, especially because, you know,

105:16

working out is something that's very

105:17

important, but for the brain as well.

105:21

I always thought of creatine as

105:22

something that you you took and you kind

105:24

of had to load up on, and then over a

105:26

couple of weeks or months, the effects

105:27

would kick in. But you're telling me

105:28

that if I had creatine in the morning,

105:30

that same day, I would experience

105:33

potentially improved cognition if I have

105:35

a big enough dose.

105:36

>> Yes. So, um, great question. A lot of

105:40

studies that have been done that you're

105:41

referring to have been done in the

105:44

context of exercise and muscular

105:46

performance. And the reason why people

105:50

have to load up on like they do a

105:52

loading phase, let's say 20 grams and

105:55

then they go down to this sort of

105:56

maintenance phase of five grams is

105:58

because it takes I don't know I think

106:01

it's about a month or so before you can

106:03

saturate your muscular stores of

106:06

creatine. And then

106:08

>> what does that mean? It means that um

106:09

the creatine which is actually stored in

106:11

your muscle as phosphocreatine is there

106:14

and ready to be used to make energy. So

106:17

so it takes again it takes about a month

106:21

or so to do that unless you are really

106:24

giving your muscles a high dose right.

106:26

So the five grams a day it only it can

106:28

only do it for so many days and then

106:30

finally you get saturated. When you do

106:32

this loading phase you kind of just

106:34

accelerate that whole process. And so

106:36

that's why when people are doing these

106:38

experiments where they want to test the

106:39

effects of creatine, they want they want

106:41

the participants to have really high

106:42

levels of creatine in their muscles

106:44

quick because they don't want to do a

106:45

month-long experiment, right? They want

106:47

the experiment to be like a couple of

106:48

weeks or a week. So that was kind of the

106:51

whole concept behind this loading phase.

106:53

If you're not someone who's going to

106:55

some kind of competition, you know, like

106:57

your CrossFit games or something, you

107:00

don't really need to do that loading

107:01

phase if you've already been

107:02

supplementing with five grams a day for

107:04

like a month. When it comes to the

107:06

brain, what's happening if you get above

107:08

that five grams, that's pretty much all

107:11

consumed by the muscle. You're having

107:13

some leftover in circulation and the

107:16

brain takes it up and it takes it up,

107:18

right? When it re what it really shines

107:21

is under that stressful condition, which

107:22

again for me, I feel like every day is

107:24

this is is like cognitively demanding

107:27

for me because I'm constantly, you know,

107:29

learning new material or learning new

107:31

information or working on things, right?

107:33

And so there's a lot of cognitive stress

107:35

on my brain. And so I feel like I'm

107:37

constantly under that stress. And that's

107:38

where getting the creatine in your brain

107:40

helps you make that energy quicker. And

107:42

so that's why like I've done I've had,

107:45

you know, been jetlagged and have have

107:46

to give a talk at you, you know, like

107:48

5:00 a.m. in the morning, my my

107:50

biological time after not getting sleep.

107:52

And I've done like 25 grams of creatine.

107:55

And it it's insane how much it helps me.

107:57

Again, it could be placebo because I'm

107:59

anticipating that effect, which is fine.

108:01

Placebo is a real thing. It's great. I'm

108:03

all about it. But there's some evidence

108:05

also that this works, right? That the

108:08

creatine is helping with under that

108:10

sleep deprivation and that stressful

108:12

condition.

108:12

>> I was reading about a study in 2025

108:15

where they

108:17

gave creatine to people that had

108:18

depressive symptoms alongside CBT

108:21

training. And the people that had

108:23

creatine and the cognitive behavioral

108:25

therapy training experienced a greater

108:27

improvement in their depression symptoms

108:29

than those who just received the

108:30

cognitive behavioral therapy, which is

108:33

which is incredible.

108:36

>> It's fascinating. I mean, depression is

108:38

a type of brain stress, right? I mean,

108:40

we know inflammation plays a role in in

108:42

depression. We know oxidative stress

108:44

plays a role in depression. And there

108:47

have now been some animal studies that

108:50

have shown creatine is somehow having an

108:51

anti-inflammatory effect. I that hasn't

108:54

all been worked out. So I don't know if

108:56

it's all just the energy component of

108:59

it. It could also be this other sort of

109:01

newly identified role that creatine's

109:03

playing in sort of having an

109:05

anti-inflammatory effect. And I don't

109:07

know much enough about that. I don't

109:09

know that there's enough even known

109:10

about that, but I do know that it

109:11

exists. And it's fascinating because

109:14

again I think where creatine really

109:16

shines in the brain and it's been shown

109:19

study after study is under some kind of

109:20

stressful condition depression or sleep

109:23

deprivation or there's a new study that

109:25

came out it was published I don't know a

109:28

month ago or so showing that it was a

109:30

very small pilot study and I want to

109:32

caveat this there was no placebo control

109:35

but it did show that giving people with

109:38

Alzheimer's disease creatine I believe

109:41

it was 20 grams a day did improve their

109:44

cognition. And so again, this is a whole

109:47

new field where now we're looking at

109:49

creatine in the brain, not just the gym

109:51

bros and not just the muscular effects,

109:54

but in the brain and how it's affecting

109:56

the brain and being beneficial for

109:58

cognition, for brain aging, for

110:02

depression.

110:03

>> Is there a link or an association with

110:05

cancer outcomes in creatine? Wondering

110:08

because I was there was there was a

110:09

study that I was looking at earlier.

110:11

Yeah, this one it says a a 2025 study of

110:14

25,000 people each found that for each

110:16

additional 0.09 grams of creatine over a

110:19

two-day average was linked to a 14%

110:22

reduction in cancer risk.

110:23

>> Right.

110:23

>> Which was in the Frontiers Journal and

110:25

reported by the BBC.

110:26

>> Yeah. That it's it's like a new

110:29

unexplored, you know, association here

110:31

where it's like I I don't know why

110:34

creatine is doing it. Is it the

110:35

anti-inflammatory effect? Is it who

110:38

knows? But again, I mean that I I was

110:40

aware of that study and it's like a

110:42

whole new area that needs to be explored

110:44

where you know some people were worried

110:46

about creatine actually causing cancer.

110:47

I've actually had people ask me that

110:49

question and it's actually the opposite

110:52

where it seems to be reducing cancer

110:53

risk.

110:54

>> The some of the other sort of

110:55

misconceptions around creatine are that

110:57

it's going to I mean there was this

110:59

stereotype that people take it they get

111:01

massive muscles and they become bloated.

111:02

So I think that put a lot of women off

111:04

in particular according to some research

111:05

that we actually did just to understand

111:07

perceptions of creatine in my investment

111:09

fund. But the other one was hair loss.

111:11

People think there's some sort of

111:13

association with hair loss. I.e. if you

111:15

take creatine you're more likely to lose

111:16

your hair.

111:17

>> Right. So there was this one study that

111:19

was published I don't even know how many

111:22

decades ago. Maybe you can pull it up

111:24

but it was in rugby players I believe

111:27

and these rugby players that were given

111:29

I I believe it was a high dose. Maybe it

111:30

was 20 grams. I can't remember the exact

111:32

dose but um they had increased levels of

111:36

dihydrotestosterone

111:37

DHT which is something that is linked to

111:42

androgenic alipcia. So this would be you

111:45

know basically your the the DHT can

111:47

affect the hair follicle and keep it in

111:50

this like stunted phase where it's not

111:51

growing and so that can cause hair loss.

111:54

And that one study didn't measure hair

111:57

loss. It just again looked at the the

111:59

DHT, the dihydrotestosterone levels.

112:02

It's never been replicated. There's

112:04

after so many decades, it's never had

112:07

any animal evidence showing that this

112:09

actually causes hair loss. Nothing has

112:11

really come up showing that this is

112:13

something to be concerned about. So, I

112:17

take it as, okay, it's like a one-off

112:19

thing. Who knows what was going on here?

112:21

But like, you would think if it was

112:23

real, it would be replicated after when

112:25

was it published? 2009

112:27

>> 2009.

112:29

>> Yeah. So, it was a group of rugby

112:31

players. They were given 25 grams a day

112:32

of of creatine. Um, but there was

112:34

actually a study, a randomized control

112:36

trial done in 2025, this year with 45

112:40

resistant trained men all given five

112:42

grams a day of creatine over 12 weeks.

112:44

And there was no significant difference

112:46

found in their hair outcomes or DHT

112:49

versus placebo.

112:50

>> There we go. When was that published?

112:52

>> 2025.

112:52

>> Oh, this year. randomized control

112:56

of

112:56

>> med. Well, I mean to get to get also to

112:58

your your other point about the water

113:01

weight gain. I know this is a real thing

113:03

because also several of my my

113:04

girlfriends were concerned about this as

113:06

well. And it's funny, you know, creatine

113:09

does bring water into the cell and but

113:13

that's actually a it's not a bad thing,

113:15

right? And it you're really not going to

113:17

get a big gain in weight. I mean, I

113:19

can't imagine. There's nothing more than

113:21

like two pounds,

113:22

>> you know, if if if anything at all. So,

113:26

I do think that is sort of uh something

113:29

that's I don't it's a it's a it's a fear

113:32

that's not justified in my opinion. I

113:34

mean, you lose you you gain, you know,

113:36

four pounds of water weight when you're

113:38

on your menstrual cycle.

113:39

>> Yeah. You mentioned fasting.

113:42

>> Yeah. There's been lots of conversation

113:43

around fasting, around whether it's

113:45

good, bad, how long to fast, or whether

113:48

just restricting your calories is the

113:50

same as fasting. A lot of people talk

113:52

about autophagy. My girlfriend talks

113:54

about water fasting. What is your

113:57

perspective on the role of fasting, how

113:59

we should do it, if we should do it,

114:00

when we should do it, who should do it?

114:02

>> I think it depends on what your goal is.

114:07

So you mentioned people talk about

114:09

calorie restriction and really you know

114:12

is the fasting just about the calorie

114:14

restriction and I think when it comes to

114:17

weight loss losing losing weight

114:21

predominantly hopefully fat not muscle

114:24

then calorie restriction is the main

114:27

thing to do here and intermittent

114:29

fasting is sort of a tool to get you

114:31

there. In other words, people that are

114:32

doing intermittent fasting tend to eat

114:34

fewer calories. And that's been shown in

114:36

several studies, even if they aren't

114:37

counting their calories because they are

114:40

limited in the amount of time they're

114:42

eating and then they're fasting for a

114:44

longer period of time. They end up just

114:46

consuming naturally fewer calories.

114:48

>> Being in a calorie deficit, is that

114:51

going to put you into the ketogenic

114:52

state that you get from not fasting?

114:56

>> No. Not if not necessarily. No, it's

114:59

not. So you can be in a calorie deficit,

115:02

but it it depends, right? So when you're

115:06

when you're in the fasted state, what's

115:08

important here is you're activating a

115:11

bunch of pathways that don't become

115:14

active when you're in a fed state. And

115:16

there's a lot of biochemical reactions

115:17

that sort of dictate all that. But you

115:20

mentioned autophagy, right? And and

115:22

that's the big one, and that's happening

115:24

only when you're really in a fasted

115:25

state.

115:26

>> What is it?

115:27

>> There's different types of it. So

115:29

generally speaking, it's the clearing

115:31

out of damaged stuff within your cell.

115:35

So what is damaged stuff? It can be

115:37

protein aggregates. For example, if we

115:39

think about in neurons, amaloid beta

115:42

protein aggregates. So autophagy could

115:44

play a role in clearing that out.

115:46

>> The plaques and stuff you get in your

115:47

brain.

115:47

>> Exactly. But you also get plaques in

115:49

your cardiovascular system. So autophagy

115:51

can play a role in clearing that out. Um

115:53

but it also can be fragments of DNA. It

115:56

can be, you know, all all sorts of gunk

115:59

and stuff that just can accumulate

116:00

inside of your cell. And so you're kind

116:02

of getting rid of that. Also, it can be

116:05

even on the level of, let's say,

116:09

it's the organal level. So you can

116:11

actually have your mitochondria. We

116:12

talked about mitochondria being the

116:13

major source of energy inside of our

116:15

cells. Mitochondria are very important

116:17

for the health of all of our cells, our

116:19

neurons, our muscle, because they

116:21

produce energy. But mitochondria also

116:24

accumulate a lot of damage quite easily

116:26

because they produce energy and they use

116:28

oxygen to do that. They make a lot of

116:29

what's called reactive oxygen species.

116:31

So these are things that can really

116:32

react with our DNA with proteins inside

116:36

of our our cells with with um lipids. So

116:39

the cell membranes. So your mitochondria

116:43

don't really have a repair system like

116:45

our DNA does. So we have DNA repair

116:47

enzymes that can repair damage to our

116:48

DNA, right? That's where magnesium comes

116:51

in. magnesium is required for these

116:53

enzymes to be activated to repair damage

116:55

to our DNA to prevent cancer. Our

116:57

mitochondria don't have that kind of

116:59

repair system. They have another repair

117:01

system and one of it is what's called

117:03

mphagy which is kind of a subp part of

117:06

autophagy and it's where the

117:08

mitochondria they accumulate damage. you

117:11

can essentially

117:14

take that mitochondria and get rid of

117:15

it, right? Or a piece of that

117:17

mitochondria that damage and get rid of

117:18

it through this sort of autoagy type of

117:21

thing, but it's called mopagy. And that

117:23

happens with other types of what are

117:25

called organels within our cells. So

117:28

this autophagy process, this autophagy

117:30

is sort of a general term, but it's

117:32

essentially the cleaning out of damage.

117:34

It's the repair process for damage. And

117:36

it's something that happens most the

117:38

time when we're in a fasted state, which

117:40

typically happens when we're sleeping.

117:42

>> How long do do I have to be in a fasted

117:43

state for?

117:44

>> I mean, it depends. I would say

117:47

that we haven't really worked that out

117:49

great in humans because people aren't

117:52

measure measuring biomarkers of

117:54

autophagy in humans. There have been

117:57

some studies that have looked at being

118:00

in a fasted state for like 16 hours. And

118:03

essentially once you get once you break

118:05

through that part of depleting all your

118:07

liver glycogen that's an important you

118:10

know precursor for activating autophagy.

118:12

So I mentioned earlier that happens

118:14

after about 12 hours right so as you get

118:16

to 12 13 14 15 16 hours then you're

118:20

probably getting to that state of

118:22

autophagy. Um however there's such

118:25

limited evidence evidence on that in

118:28

humans. A lot of it comes from animal

118:30

studies. With that caveat, I will say

118:33

that you can get a lot of benefits. So,

118:35

some of the metabolic benefits from

118:37

fasting include improved glucose levels,

118:40

improved um blood pressure regulation,

118:44

metabolic effects, improved for example,

118:46

weight loss. Right? Now, can you get all

118:49

of that from just doing caloric

118:51

restriction versus doing t like this

118:53

intermittent fasting? Right? You can get

118:56

a lot of it, but there have been studies

118:58

showing that doing doing this sort of

119:00

intermittent fasting is beneficial uh

119:03

for some of these metabolic parameters

119:05

outside of the caloric being in a

119:07

caloric deficit.

119:08

>> What does that mean? Metabolic

119:09

parameters

119:10

>> again glucose regulation, blood

119:12

pressure, your blood pressure control as

119:14

well. So these things have been shown in

119:16

in people that are doing timerestricted

119:18

eating. So they're basically doing a

119:20

type of intermittent fasting where

119:22

especially if they're doing a really

119:24

compressed window. So they're eating all

119:25

their food within six hours and then

119:27

fasting for like 18 hours.

119:30

That's really beneficial, right? Because

119:32

and even if they have the same amount of

119:33

calories as people that are calorically

119:36

restricted, they've compared those

119:37

head-to-head. people that are doing the

119:39

fasting have better improvements in

119:41

their glucose regulation, better

119:43

improvements in in um their blood

119:45

pressure than people that are even still

119:48

eating fewer calories but not doing the

119:50

fasting component.

119:51

>> So, what would you recommend for the

119:52

average person? I asked you earlier on

119:54

to give me a a sort of a perfect uh

119:57

a perfect prescription of what I should

119:59

do in terms of fasting

120:01

on a daily basis. Do you think I should

120:03

have eating uh sort of fasted windows

120:06

of, you know, 12 to 20 hours?

120:10

>> You know, I think it really depends on

120:12

what you're looking for. And personally,

120:14

if you are wanting to have this more

120:16

autophagy kind of potentially autophagy

120:19

activation where you're you're clearing

120:22

away stuff within your cells. Again, we

120:25

don't really know the hard number yet,

120:28

but I would say yeah, you probably want

120:30

to be around a 16

120:33

hour window of not eating.

120:35

>> What do you do?

120:36

>> I mean, it depends on the day, you know,

120:38

>> on an optimal day.

120:39

>> Most of the time, I'm I'm probably

120:41

eating all of my food within a 10-hour

120:43

window. And so, I'm fasted for 14 hours,

120:46

but optimally, like it all depends on my

120:49

family and like eating dinner with my

120:50

family and what's going on.

120:52

>> Do you ever do longer fasts? I don't do

120:54

I mean I would say a a day is like the

120:57

longest that I do but I do a lot of

121:00

exercise on top of that and so you can

121:02

kind of kick yourself into that

121:03

autophagy state a little bit more

121:06

because it's kind of like we talked

121:07

about this it's a way of sort of

121:08

supercharging your ketosis and so if

121:11

you're exercising and fasting um that

121:14

kind of supercharges that whole

121:17

autophagy system as well but um it I do

121:20

think it's a kind of an interesting idea

121:23

uh to do some longer fasts maybe once a

121:26

year, once a quarter depending

121:28

>> why

121:29

>> because you are activating that repair

121:31

process. Now you have to do resistance

121:33

training because you don't want to lose

121:35

muscle mass. Protein is important. It's

121:37

one of the signals for you know muscle

121:40

protein synthesis which is essential for

121:43

you know gaining muscle mass and

121:44

maintaining muscle mass. Right.

121:46

>> So after a fast you want to break the

121:47

fast with something protein richch.

121:49

>> Absolutely. Definitely protein rich for

121:51

sure. Um, but I think also during a fast

121:54

if you can do some kind of you want to

121:57

you want to stimulate your muscles with

121:59

mechanical force because that's the

122:00

other signal to stimulate muscle protein

122:03

synthesis. And so I I think one of the

122:06

biggest concerns people had with fasting

122:08

and this was over the last 5 years or so

122:11

is that studies have shown people that

122:13

undergo intermittent fasting tend to

122:16

lose muscle mass because they're eating

122:19

fewer meals. they're not getting as much

122:22

protein and perhaps they're not doing

122:24

resistance training. Now, there have

122:25

been other studies that have looked at

122:26

people doing intermittent fasting and

122:29

resistance training and they don't lose

122:30

muscle mass because they are doing

122:32

they're getting that mechanical

122:34

stimulation of their of their muscles

122:36

which is preventing the loss of muscle

122:37

mass. And so, I think the take-home here

122:39

is if you are doing intermittent

122:41

fasting, you want to make sure you're

122:42

getting all your protein, 1.6 1.2 to 1.6

122:45

six grams of protein per kilogram body

122:48

weight per day depending on how much

122:51

you're resistance training. And you also

122:54

you want to make sure you're getting

122:55

your protein in that small window that

122:56

you're eating. And you want to make sure

122:57

that you're doing resistance training as

122:59

well. Those are two really important

123:01

things if you are going to do

123:02

intermittent fasting.

123:03

>> There was a study I read which is linked

123:04

to that which said linked to that but

123:06

sort of adjacent that says uh in in nine

123:09

human trials they found that 23% of

123:12

people enjoyed better sleep after

123:13

intermittent fasting. which I thought

123:15

was interesting.

123:16

>> Yeah, cause causation is obviously hard

123:18

to establish there, but

123:19

>> Right. I I think and that brings us to

123:22

this other sort of aspect of

123:23

intermittent fasting, which is

123:25

timerestricted eating. Essentially, what

123:29

what's the best thing to do is really

123:32

you want to you want to eat within an

123:34

earlier time window. And there's a lot

123:36

of reasons for that. One of them is that

123:40

when you eat later in the day, let's say

123:43

8 o'clock at night, nine o'clock at

123:45

night, your body is starting starting to

123:48

naturally make melatonin.

123:50

That's a hormone that's involved in

123:51

helping you get sleepy. Well, melatonin

123:55

also inhibits the production of insulin.

123:58

And so you basically

124:00

will have elevated blood glucose levels

124:02

when you're eating later in the day

124:04

because you're you're less you're you're

124:07

basically less gluc your your glucose

124:10

regulation is impaired somewhat, right?

124:13

So it's better to try to eat your food

124:15

earlier in the day, but then there's

124:17

also this this area of you want to

124:19

probably stop eating like 3 hours before

124:22

your natural bedtime. And that does

124:24

affect sleep. So, if you think about it,

124:26

when you're sleeping, you don't want to

124:27

be digesting. Like, there's all these

124:30

things that are activated during

124:31

digestion, and that's going to affect

124:33

the way you sleep. And so, there are

124:35

some interesting studies that have found

124:37

that people sleep better if they stop

124:40

eating at least three hours before bed.

124:42

That is something that I do try to do

124:44

almost daily. And um it's also something

124:48

that was very interesting. I think a

124:49

friend of mine, Dr. Dr. Sachin Panda at

124:50

the Sulkq Institute was one of the first

124:52

people to observe that. He's got this

124:55

this app that he um has called my

124:57

circadian clock and he used he's used

124:59

this app over the years for clinical

125:01

trials where people will take a picture

125:03

of their food and it timestamps the

125:06

foods that he knows what time they're

125:07

eating and when they stop eating.

125:09

>> And and people that are part of this

125:11

trial started to send him comments

125:12

going, "Oh, I stopped eating earlier and

125:15

all of a sudden my sleep is better." And

125:16

after you start to get about 10, 20, 30

125:20

people making the same comment, you

125:22

start to go, wait a minute, there's

125:23

something here, right? And so I think he

125:25

was one of the first people to actually

125:27

um observe that that correlation between

125:30

stop eating earlier and sleeping better.

125:34

>> Well, you talked about protein earlier

125:35

when we're talking about resistance

125:36

training and fasting.

125:39

When should I Someone told me that

125:41

you're supposed to take protein straight

125:42

after you did the a resistance training

125:44

workout. Straight after you lift the

125:45

weights like 30 minutes after. Does it

125:47

matter?

125:48

>> Well, we that's what was thought I think

125:50

previously for I don't know how many

125:52

years it was thought this was there was

125:53

an anabolic window, right? Where you

125:55

want to take in this protein within 30

125:58

minutes to an hour of doing your

126:00

resistance training. And that way the

126:03

amino acids that are anabolic like

126:06

leucine are going into the muscle and

126:08

building muscle essentially, right? We

126:11

now know that it's not really an

126:14

anabolic window. It's about your daily

126:17

protein intake because what exercise is

126:19

doing, what the resistance training is

126:20

doing is it's sensitizing all your

126:23

transporters and your muscle to amino

126:25

acids. And that's that's happening over

126:27

the course of 24 hours. So you can take

126:29

that protein in within that day and it

126:32

it really still do the same thing. So I

126:35

don't think you have to slam your

126:36

protein shake within 30 minutes to an

126:39

hour. Maybe maybe if you're like a

126:43

bodybuilder and you're really trying to

126:45

get that little tiny tiny tiny

126:47

percentage, maybe you'll have a little

126:48

bit of a benefit. But generally

126:51

speaking, most people what you want to

126:53

look at is your daily protein intake

126:55

because that's essentially um the most

126:58

important thing. And the exercise itself

127:00

is sensitizing all these, you know,

127:03

transporters on your muscle that are

127:04

allowing the amino acids to come in and

127:06

build protein, increase muscle protein

127:09

synthesis.

127:11

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129:13

There's a term that you've used a few

129:15

times which I'm I'm not super well

129:17

educated on, which is insulin

129:19

resistance.

129:22

What is insulin resistance? Is that

129:24

something associated with diabetes? And

129:26

therefore, does someone like me need to

129:27

care? I don't have diabetes.

129:29

>> Okay, let's take a step back. when you

129:31

are eating something that is going to

129:34

raise your blood glucose levels, right?

129:37

You

129:37

>> so like a piece of bread or some sugar

129:39

or whatever,

129:40

>> right? So essentially, if you're

129:42

increasing that glucose spike in your in

129:44

your bloodstream, you want to have that

129:47

glucose go somewhere. You want it to go

129:49

to your muscle and or sometimes it goes

129:51

to your atapost tissue. But in order to

129:52

do that, you have to activate insulin.

129:55

And insulin then causes these

129:58

transporters that usually aren't active

130:01

to kind of come up and take in the

130:03

glucose. So insulin resistance is when

130:06

you're basically constantly constantly

130:10

activating that pathway um such that

130:13

your cells don't respond to the insulin

130:17

like they used to. And so the insulin

130:18

isn't doing its job as well. And so

130:21

essentially your blood glucose levels

130:23

stay elevated and that causes all sorts

130:26

of damage the glycation and things like

130:28

that we've talked about.

130:29

>> So it's really insulin failure.

130:31

Insulin's failing to do its job.

130:33

>> Well, it depends because you're still

130:35

making the insulin but it's essentially

130:38

not the insulin receptor isn't

130:39

responding to that insulin and so it's

130:43

it's not doing its job. Yes, it's not

130:45

doing its job. But it's different from

130:47

type 1 diabetes in in the sense where

130:48

you're type 1 diabetes, you're actually

130:50

not even making the insulin, right? So

130:52

that's very different. So yeah, insulin

130:54

is not able to do its job. But insulin

130:57

resistance and I mean there's there's so

130:59

many different diseases that it's been

131:01

linked to. But everything I think

131:03

everything is so complicated. So I don't

131:05

know that everything's due to insulin

131:06

resistance, but it's like one component

131:08

of, you know, something that's

131:11

accelerating the way you age. I had a a

131:14

light doctor in here the other day, a

131:15

sunlight doctor the other day and we

131:16

spent a lot of time talking to talking

131:18

about light and sunlight and one of the

131:20

things that I've been really fascinated

131:22

by is red light therapy over the last

131:24

couple of months. Do you do have a sort

131:27

of red light therapy routine?

131:29

>> It's interesting that you ask. So red

131:30

light therapy in the scientific

131:32

literature called photobiomodulation.

131:34

Um, I know that's a complicated word,

131:37

but you know, there's essentially a

131:38

variety of different wavelengths that

131:41

can be used to stimulate physiological

131:45

processes like mitochondria inside of

131:47

your your cells to to do stuff, right? I

131:51

now am convinced that red light therapy

131:53

plays a role in helping with skin aging.

131:56

So, I do have a mask. It helps with with

131:59

skin aging and wrinkles. There have been

132:00

enough studies now that is pretty

132:03

convincing that it does seem to improve

132:05

the way skin ages. I do think the

132:07

important thing here is the parameters

132:10

that are done. It's not just wavelength,

132:12

but it's also like the energy, so

132:14

irradiance. And so you have to kind of

132:16

look at all those parameters and make

132:17

sure you can replicate that with

132:19

whatever product that you're using.

132:20

>> What about infrared saunas?

132:23

>> Infrared saunas or traditional saunas?

132:25

>> The infrared ones.

132:26

>> Infrared. So infrared saunas are a type

132:30

of sauna that is using

132:34

it's using you know essentially infrared

132:37

radiation right infr infrared

132:38

wavelengths to heat up the body. And so

132:42

they're not very hot. So if you look at

132:44

like the ambient temperature in an

132:45

infrared sauna it goes up to like 140

132:48

degrees Fahrenheit

132:50

which is very different from a

132:51

traditional sauna. So, infrared saunas

132:54

don't have all the same benefits as a

132:57

traditional hot sauna, something that

132:58

maybe goes up to 175, 180 degrees

133:01

Fahrenheit,

133:02

unless you are staying in that infrared

133:04

sauna for like a very long time, perhaps

133:07

even twice as long as you would or more

133:09

in a traditional sauna. The interesting

133:12

thing about infrared saunas, I would

133:14

say, um, so a colleague of mine, a

133:16

collaborator of mine, Dr. Ashley Mason,

133:17

she's at UCSF and she's been doing

133:20

what's called the heat bed study and

133:22

it's an infrared sauna that is

133:24

essentially a head out heat bed. So your

133:27

whole body is in this infrared sort of

133:31

bed, but your head is out of it. So your

133:33

head's not in it. And people um she's

133:36

done she's now done a couple of studies

133:38

and the most recent study has been done

133:41

in people with major depressive

133:42

disorder. So they have depression and

133:45

these people are are doing an infrared

133:47

sauna to a pretty extreme degree. So

133:50

she's elevating their core body

133:52

temperature by around 2°. So they're

133:56

essentially getting in a somewhat

133:58

feverish state. And in order to do that,

134:00

I mean, these people are in this

134:02

infrared sauna for well over an hour. So

134:05

not like most people that are doing

134:07

infrared saunas. You're probably staying

134:08

there for like 20, 30 minutes, right? So

134:11

people are getting very very hot to the

134:13

po to the point where their core body

134:14

temperature is going up to you know

134:16

increasing to um like one one and a half

134:19

to two degrees right and she's looking

134:23

at the effects on depression and so what

134:25

she has found is kind of amazing is that

134:30

people that are doing this infrared

134:31

sauna this heatbed

134:34

and doing cognitive behavioral therapy

134:36

CBT

134:37

they are experiencing massive

134:39

anti-depressant effect. So, there's

134:41

something called the Hamilton scale,

134:42

which is like a battery of tests that

134:44

are done to assess depression.

134:47

And just to give you like um some some

134:50

sort of basis of like if you if there's

134:53

something considered clinically

134:54

significant, then you have like a

134:56

three-point change on that scale. Well,

134:58

essentially this infrared sauna plus the

135:01

cognitive behavioral therapy improved

135:03

the Hamilton scale, you know, assessment

135:06

by 16 points. And these are people that

135:08

did four or eight rounds of it. So it

135:12

was over the course of either one month

135:13

or two months. Some people just couldn't

135:15

finish it because it is pretty intense.

135:17

Like you're you're heating your body up

135:19

quite a lot and you're sitting in this,

135:20

you know, infrared sauna for over an

135:22

hour and it's it's a it's a pretty

135:23

intense. But the magnitude of effect on

135:26

the antid-depressant effect was it's

135:28

it's stunning. And this kind of all

135:30

stems back from her mentor Dr. Dr.

135:34

Charles Raison his research that um was

135:38

essentially like an infrared sauna. So

135:40

he did something this was you know back

135:42

in 2016 he did this study where he put

135:45

people in this sort of infrared sauna

135:47

like thing and it it elevated their core

135:50

body temperature again by about two two

135:51

degrees. There are people with major

135:52

depressive disorder or he gave them a

135:54

sham control. So it was kind of hot and

135:57

people were thinking they were getting

135:59

the treatment but it was actually a

136:00

placebo. Okay. It was enough for them to

136:02

think they were getting the treatment,

136:03

but it wasn't ele elevating their core

136:04

body temperature enough. And they did

136:06

one treatment of this, okay? And he

136:08

showed that the people that did one

136:10

treatment of this had an anti-depressant

136:12

effect that lasted six weeks later after

136:15

one treatment. Sham control didn't get

136:17

this beautiful study. Um, you know,

136:20

Ashley kind of followed on that study

136:23

and showed multiple sessions of it

136:25

really had an even more robust effect.

136:28

But I say this because I don't want to

136:30

like I don't want to like say infrared

136:32

saunas aren't great. However, there's a

136:35

lot of benefits that have been related

136:38

to more hot traditional types of saunas,

136:41

finished saunas, for example,

136:42

traditional saunas that are that are

136:44

hotter, right? And so you're staying in

136:46

these 175 180°ree sauna for like 20

136:50

minutes. And it's associated with, you

136:53

know, lower cardiovascular rated

136:55

mortality. So if you you're doing it

136:56

four to seven times a week um that's

136:59

associated with a 60 sorry 50% lower

137:02

cardiovascular related mortality versus

137:04

doing it one time a week or all cause

137:07

mortality it's associated with 40% lower

137:09

all cause mortality versus doing it one

137:11

time a week. So

137:14

>> what's going on there?

137:15

>> Right. Exactly what's going on there?

137:16

And so the the the really fascinating

137:18

thing to me about this deliberate heat

137:22

exposure from a sauna is that it is sort

137:26

of mimicking moderate intensity aerobic

137:29

exercise. And this has actually been

137:31

shown, it's been compared head-to-head

137:33

to moderate intensity like cycling on a

137:35

stationary bike. A lot of the

137:37

physiological responses, so your core

137:39

body temperature goes up, your heart

137:40

rate goes up, right? When you're

137:41

exercising, your heart rate goes up.

137:43

Same thing happens when you're in a hot

137:45

sauna. your heart rate goes up, your

137:48

cardiac output is increased, right? Your

137:50

blood flow is increasing. All these

137:51

things are happening and they're very

137:52

similar. Exercise, heat stress, you're

137:55

sweating, right? To cool down your your

137:57

body. So, it's a way of sort of

137:59

mimicking this moderate intensity

138:02

exercise that doesn't really happen in

138:04

an infrared sauna if you do the same

138:05

amount of time as you're doing in a hot

138:07

sauna. Now perhaps if you increase that

138:09

time it would happen but there's all

138:11

these benefits that are happening with

138:14

just doing a deliberate heat exposure

138:16

from a sauna that

138:19

seem to not only sort of mimic

138:22

cardiovascular exercise but they add on

138:24

to it. So, we were talking about

138:26

cardiorespiratory fitness and how

138:28

important that is for longevity, right?

138:29

Where there have been studies that have

138:31

looked at people that exercise on a

138:34

stationary bike or they exercise on a

138:37

stationary bike and then follow that up

138:38

with a 15-minute sauna. And it's been

138:41

shown that those people that do the

138:42

15-minute sauna on top of the exercise

138:45

have a more a higher improvement in

138:47

their cardiorespiratory fitness. They

138:49

have more improved um levels of their

138:52

their cholesterol and lipids. their

138:53

blood pressure improvements were

138:55

greater. So there's this additive effect

138:57

of adding on the deliberate heat

138:58

exposure with the exercise that isn't

139:01

happening with exercise alone. So again,

139:04

that's sort of just more evidence of

139:07

why, you know, doing a deliberate heat

139:09

exposure like a sauna. In fact, hot

139:10

tubs, that's something that's also been

139:13

shown to improve blood pressure. In

139:14

fact, a study just came out a couple of

139:16

weeks ago showing that a hot tub is very

139:19

beneficial for improving blood pressure,

139:21

for doing all the same things that a

139:23

sauna does, which is kind of exciting

139:24

because not everyone has a sauna.

139:26

>> I heard that you sometimes rehearse

139:28

important talks and studies in saunas.

139:31

>> Yeah. I mean, this started back when I

139:34

was in graduate school. Um, I used to go

139:36

to this I lived across the street from a

139:38

YMCA and I used to go to this sauna and

139:40

use the sauna before I would go into my

139:42

lab and do experiments.

139:44

And there's a couple things I noticed.

139:47

One, I was able to handle stress better.

139:50

My stress of,

139:52

you know, failed experiments, mentors

139:55

putting all this pressure on me, all

139:56

that stuff, right? If I went to the

139:58

sauna beforehand, I was very much, it's

140:00

like I was more resilient to the stress.

140:03

And that was when I started to look into

140:06

the effects on the brain. And that's

140:07

where I also am very interested in

140:09

depression research as well, right?

140:10

Because you're you're causing like brain

140:12

resilience. But um once I started to

140:15

realize like this is affecting my mood,

140:17

this is affecting my ability to handle

140:19

stress. I was using the sauna like every

140:21

day. I mean I was like religious about

140:23

it. It was crazy. I mean it was like six

140:24

to seven days a week I was going in that

140:26

sauna.

140:27

And because it was like using it every

140:30

day, you have to multitask. you only

140:32

have so much time in the day, right? And

140:33

so I'd start rehearsing my

140:34

presentations, like going through them

140:36

in my mind while I'm sitting in the

140:37

sauna with these other people from the

140:39

YMCA who probably think I'm crazy

140:41

because I'm sitting here like saying

140:42

things, but I noticed that I was able to

140:46

remember things better if I had gone

140:49

through them in my head with the heat.

140:52

And it wasn't until many, many years

140:54

later, I mean, I kept doing that. Like

140:55

even sometimes when I travel and I'm

140:57

giving a presentation or a talk, I'll

140:59

get in the hot bath in my hotel room and

141:01

I'll just lay in the hot bath and I just

141:03

go through my talk in my head or I'll

141:05

like look at my notes and like if I

141:07

forget something I'll go through it in

141:08

my head. And it wasn't until several

141:10

years later that I started looking into

141:12

the science behind that. Like there's

141:13

something going on here. What is going

141:15

on? And I found that actually when you

141:19

go into the sauna, so there's a lot of

141:20

physiological changes that happen.

141:22

Growth hormone goes up. Um, in fact, it

141:24

depending on the the temperature and

141:25

duration, growth hormone can go up

141:27

anywhere between two-fold to like

141:30

16fold, like insane levels of of growth

141:32

hormone. But there's something else that

141:34

goes up called IGF-2,

141:37

and that is associated with improving

141:40

memory and learning. And so, there have

141:42

been animal studies that have done this.

141:44

And so, I've kind of connected the dots

141:46

here and go, maybe that's why. I don't

141:47

really know why. I mean, sometimes just

141:49

like a very strong emotional response

141:51

can sort of help you remember something

141:54

>> and you are at the end of the day

141:56

causing a very strong stress response

141:58

when you're getting in the heat.

141:59

>> So, I like to use the sauna for a lot of

142:01

things. I do I do it depends on the day.

142:03

Sometimes I do it I like to do it before

142:05

bed. So, I'll do like the hot tub or the

142:06

sauna. It improves sleep. It improves my

142:09

sleep. And that has to do with the

142:11

growth hormone. It has to do with what

142:13

are called somnogenic cytoines. These

142:15

are inflam inflammatory molecules that

142:17

are made that are that cause sleepiness.

142:20

So if you think about when you're when

142:21

you're sick and you have, you know,

142:23

inflammation going on when you're when

142:24

you have an illness, you're very tired,

142:26

you're sleepy, you're producing a lot of

142:28

what are called somnogenic cytoines.

142:30

These are cytoines that are invol

142:31

inflammation molecules that are involved

142:33

in making you sleepy. Those are also

142:35

produced when you are undergoing

142:37

deliberate heat exposure like a hot tub

142:39

or and that's been shown uh as well as a

142:41

sauna. So sometimes I like to do the

142:42

sauna at night like to relax and help

142:44

help my sleep. Sometimes I like to do it

142:46

after a workout um to extend my, you

142:48

know, my workout like the study I talked

142:50

about where you're improving your

142:51

cardiory fitness as well.

142:53

>> Would you like some tea? My team can

142:55

make you some tea if you'd like some

142:56

tea.

142:56

>> I would love some loose leaf tea in a

142:59

metal cup.

142:59

>> Why Why don't you want this this tea?

143:01

what you're doing here is is tapping

143:03

into my sometimes my friends don't want

143:06

to talk to me because I'm like the

143:07

bearer of bad news, you know, where it's

143:10

like what am I what is Rhonda going to

143:12

tell me now that I shouldn't be doing

143:14

that I love doing, right? Another

143:16

obsession of mine of late has been

143:18

microlastic exposure. And I know you've

143:21

talked about this on the podcast before

143:22

and it's it's in it's in the news now. A

143:24

lot of people are sort of familiar with

143:25

microplastics, right? breakdown of

143:28

plastic particles that are tiny uh

143:32

depending on the size and getting into

143:34

our circulation. Right.

143:36

>> And when you think of microplastics, you

143:38

think of plastic. When you think of

143:39

plastic, you think, "Oh, that plastic

143:40

water bottle." Yeah. Well, I'll just

143:42

avoid that plastic water bottle, right?

143:45

What you don't realize is that

143:48

everything everything has plastic. So,

143:52

you have here this to-go coffee cup,

143:54

which I don't know how many coffees I

143:57

and teas I've had in a to-go coffee cup,

144:00

but it's hundreds. Hundreds and

144:02

hundreds. And the thing that's so

144:04

disturbing is I learned that, you know,

144:08

these many most all of these plastic I

144:10

mean, sorry, these um paper looking

144:12

coffee cups are actually lined with

144:14

plastic. They're lined with a plastic

144:17

liner to prevent like the liquid to, you

144:20

know, leeching into the paper, right?

144:22

And that plastic lining when you add

144:24

heat to it, i.e. boiling water for tea

144:28

or hot coffee, it accelerates the

144:30

breakdown of the plastic lining. So,

144:32

you're drinking microlastic beverages

144:36

and also the chemicals associated with

144:38

them. So there was this plastic study

144:39

that was done that showed heating up

144:42

plastic essentially causes these these

144:46

toxic you know plastic associated

144:48

chemicals like BPA bisphenol A which is

144:51

an endocrine disruptor. It disrupts

144:53

hormones. It sort of mimic mimics

144:55

estrogen. So you know it's it's

144:59

sometimes like called an estrogen

145:00

mimemetic. It causes that to leech into

145:02

your beverage 55 times more.

145:05

>> 55 times

145:06

>> 55fold. Yes.

145:08

>> Which is 5,500%.

145:10

>> A whole lot. Yes. And so you're talking

145:12

about drinking, you know, plastic

145:15

chemicals and microplastics.

145:17

So that was like, okay, well, fine. I'm

145:20

going to bring my mug in anytime I'm

145:22

traveling and ask them to put my coffee

145:24

in that. So I I see so many people with

145:27

these to- go, you know, paper cups and

145:29

and and they're drinking coffee in it.

145:30

And it's like it's so hard for me

145:32

because I realize it's like this plastic

145:34

soup that you're drinking. Now you have

145:36

a tea bag on top of that and that is

145:39

something that there have been over the

145:41

course of the last seven or eight years

145:44

there have been studies that have come

145:45

out that these these tea bags are

145:49

composed of made of you know there's

145:51

plastic polymers in them and so there's

145:54

thousands of microplastics that are

145:56

released in every milliliter of tea from

145:59

these tea bags and there's a variety of

146:01

different tea bags essentially all of

146:03

them release microplastics the ones

146:05

that's that that look like they won't

146:07

release them. So now, while I used to

146:10

drink a lot of tea when I'm on the go, I

146:12

I bring my own with me. I bring my own

146:14

looseleaf tea with a little, you know,

146:16

one of those little steepers that can

146:18

steep the tea. And I use that because

146:22

mostly because the heat, you know, it's

146:23

just it's accelerating that breakdown.

146:26

Yes, I'll drink plast I mean, I'll drink

146:28

water out of a plastic bottle sometimes

146:30

when I'm traveling because there's no

146:31

other options. And actually, there was a

146:33

study that just came out. I'm sure you

146:35

saw it. Did you see the study that

146:36

showed glass had higher levels? So,

146:40

water that was in glass had higher

146:42

levels of microlastic than water that

146:44

was in plastic containers. This was a

146:45

study that came out of France.

146:47

>> Oh, come on.

146:47

>> You didn't see this study?

146:49

>> No.

146:49

>> Oh my gosh. This is like everywhere.

146:51

Everywhere. I mean, it came out, I don't

146:53

know, in the last two weeks or so. Um,

146:56

the study came out of France and it was

146:58

essentially showing that glass bottles

147:01

had more microplastics in the liquid

147:04

that they contained than plastic bottles

147:07

which contain liquid. And you might go,

147:10

"What? That makes no sense, right? I

147:12

mean, why would the glass have plastic

147:15

particles at a higher level than a

147:16

plastic bottle?"

147:18

Well, it turns out that the paint on top

147:20

of the lid of the glass bottle

147:24

has is it has plastic polymers in it.

147:26

And so the paint is flaking off and

147:30

getting into the water that is contained

147:33

in the glass bottle. There is I think a

147:35

silver lining here and that is well okay

147:38

there might be more microplastics in the

147:41

beverages that are in the glass bottle

147:42

compared to the plastic bottle but the

147:44

size matters. So it was shown that the

147:46

size is larger in the glass bottles

147:50

compared to the plastic bottles and

147:51

>> the size of the plastic

147:52

>> the the size of the microplastic. And

147:55

there's a reason why this is important

147:56

because microlastics and nanoplastics as

148:00

you get smaller in size they get

148:02

smaller. They're called nanoplastics.

148:04

Those are the most dangerous because it

148:06

can be more easily absorbed in the gut

148:09

and get into the circulation. If it gets

148:11

into circulation, it can more easily

148:13

bypass the bloodb brain barrier and get

148:15

into the brain. Size matters and so the

148:18

larger size flaking off from the paint

148:22

is less likely to be absorbed by the gut

148:25

and to get into circulation. Now, this

148:26

has to be shown. I'm sure that's going

148:29

to this study is going to be done next.

148:30

Like, this is going to be the next

148:31

study. It hasn't been shown yet.

148:33

>> I've heard you talk about fiber as well

148:35

playing a role in getting microplastics

148:37

out of our body.

148:38

>> Okay. So, yes. So, fiber is interesting.

148:40

This all comes from animal studies. And

148:42

fiber seems to play a role in the

148:44

absorption of microplastics and

148:46

nanoplastics in your gut cells. And

148:48

that's really important because if you

148:50

don't absorb them, it's excreted through

148:52

feces, right? And it's been shown we

148:54

only absorb about 1 to 2% of these

148:56

microplastics that we're ingesting.

148:59

Fiber, what it does is two things. One,

149:03

it moves the microplastics through the

149:05

intestines quicker, right? Which is what

149:07

fiber does. But I think the more

149:09

important thing is the type of fiber. So

149:11

you want this fermentable type of fiber,

149:14

soluble fiber. That's the kind of fiber

149:16

that's really good for your gut

149:17

microbiome. And what that does is it's

149:20

essentially creating this viscous

149:22

gel-like sort of gel-like, you know,

149:25

mucousy stuff inside of your gut that

149:28

encapsulates the microplastic so that it

149:30

can't be absorbed by the gut, you know,

149:33

what are called the gut epithelial

149:34

cells. And so if you're essentially not

149:37

able to absorb those microplastics, then

149:40

they're not getting into circulation.

149:41

And that's like the biggest thing that

149:43

you can do, right? Is is not get them

149:45

into circulation. Now, this is all based

149:47

on animal evidence. I did speak with

149:49

with a microplastics researcher at a

149:52

Harvard, Dr. um Carrie Nadal, and she

149:55

wasn't even aware of this, and now she's

149:57

like on it. So, I'm hoping that there'll

150:00

be some human human evidence coming soon

150:02

looking at whether or not microplastics,

150:04

if you're eating fiber, if that can

150:06

basically blunt the absorption of the

150:09

microplastics into the system. I think

150:11

people that are eating more fiber in

150:13

their diet probably are getting less of

150:16

that microplastics into their into their

150:17

system, but that hasn't been shown in

150:19

humans. It's only been shown in animals.

150:21

>> I'm guessing you don't eat canned soup

150:22

either.

150:25

>> Yes. Yeah. So the canned soup is

150:27

interesting. You know, again,

150:30

aluminum cans are lined with this

150:32

plastic, you know, lining and that

150:35

prevents the the sort of breakdown of

150:37

the of the the aluminum, right, the

150:40

metal.

150:42

Uh unfortunately it also causes these

150:46

chemicals like BPA that are in the

150:47

plastic lining to leech into the in this

150:51

case the soup or the beverage or the

150:54

liquid that they're contained in. Right?

150:56

There was this study that showed I think

150:59

it was was it a th00and% increase of BPA

151:02

after drinking a soup out of a can

151:05

versus a soup out of a glass. A

151:07

thousand% increase in bisphenol A

151:10

levels. I mean that is

151:11

>> bisphenol A levels being

151:13

>> BPA

151:14

>> which is the bad thing in microplastics.

151:16

>> It's the it's one of the bad chemicals

151:18

in plastics that is an endocrine

151:21

disruptor. So it's disrupting hormones

151:25

and you know that can play a role in a

151:28

lot of different things um depending on

151:32

what we're looking at. So it's hugely

151:35

important for obviously like

151:37

neurodedevelopment in children. So like

151:39

pregnant women but even like you know

151:42

disrupting disrupting hormones in

151:44

general like mimicking estrogen I mean

151:46

that's not something that guys want to

151:48

do either right so it does it is

151:51

something to be aware of but the thing

151:53

is is that you know BPA it was this

151:55

beautiful marketing strategy that came

151:58

out I don't know how many years ago but

152:00

all this BPA was replaced with something

152:03

else that wasn't BPA it was BPS and so

152:06

now everything is marketed as BPA free

152:08

And people think that is like, oh, oh,

152:11

it's not dangerous. It's BPA free.

152:13

However, what it's replaced with is

152:16

doing the same thing as BPA, if not

152:17

worse. And that's been now shown in

152:19

multiple studies. So, it's also an

152:20

endocrine disruptor. It's doing the same

152:22

thing. And yet, people think, you know,

152:24

that it's it's safe because it's BPA

152:27

free.

152:28

>> Did you hear about this study of people

152:30

that live close to a golf course?

152:32

>> Yes.

152:34

Yeah. There's a study that came out, I

152:36

don't know how, it was very recent,

152:37

maybe a month

152:37

>> 2025.

152:38

>> Yeah. So maybe I think it was a couple

152:40

months ago, and the study showed that

152:42

people that lived near within a mile or

152:45

so of golf courses had a much higher

152:48

incidence of Parkinson's disease. Right.

152:50

>> It says 126% higher risk,

152:54

>> right? Okay. So then why is that? Right.

152:56

Okay. And this is where I want to get

152:57

into the the pesticides issue because

153:02

it's it's known like any scientist

153:04

that's done research in neurogenerative

153:07

disease. It's one of the ways that you

153:10

induce Parkinson's disease in animals is

153:13

you give them insect. You give them

153:16

essentially a pesticide. So rotinone

153:19

being one, paraquat. And what that does

153:21

is a mitochondrial toxin. So it's it's

153:24

basically causing the mitochondria to

153:27

die and then essentially when the

153:29

mitochondrias are are dying or

153:32

apoptosing you know the cell under goes

153:33

apoptosis and dying. So you're

153:35

essentially you can induce Parkinson's

153:38

disease in mice by giving them these

153:40

types of essentially you know these

153:42

types of insecttoides and herbicides. So

153:46

it's well known that that can cause you

153:48

know Parkinson's disease. It's important

153:50

to know that it's mostly the ingestion

153:53

of it and not the inhalation of it. And

153:55

that was a big concern because it gets

153:57

into the water source and that's what's

154:00

thought to be the underlying cause.

154:02

People that are living close to a golf

154:04

course, it's getting into it's

154:05

contaminating the water source

154:07

essentially. And so people are are

154:10

drinking these these you know this

154:13

basically these pesticides, insecticides

154:16

and herbicides, right? So, um, a water

154:19

filter like a reverse osmosis, you know,

154:21

water filter, something like that that

154:23

can filter out some of these molecules,

154:25

hugely important. And I think that's the

154:27

solution to people that are living near

154:28

a golf course or people that are living

154:30

near any to sort of agricultural place

154:33

where they're using a high volume of

154:35

these types of, you know, herbicides.

154:37

>> What is the most important thing we

154:39

haven't talked about that we should have

154:40

talked about? run.

154:42

>> I think we talked a little bit about

154:44

magnesium, but I don't know that we

154:46

talked enough about magnesium and it is

154:50

important because it's something that is

154:53

required for

154:56

gosh over 300 different enzymes in your

154:59

body need it to function properly. So,

155:01

it's what's called a co-actor and I

155:04

mentioned DNA repair enzymes. So,

155:06

there's it's also used to make energy.

155:09

So, you need magnesium to make energy

155:11

and to use energy. You need magnesium to

155:14

repair damage that's happening all the

155:16

time. And close to 50% of the population

155:19

in the United States does not have

155:21

adequate levels of magnesium because

155:24

they're not eating the foods that they

155:25

need to to get the magnesium. Dark leafy

155:28

greens. I mentioned it's at the center

155:30

of a chlorophyll molecule. There have

155:32

been studies that have shown that for

155:34

every 100 millgram decrease in magnesium

155:40

intake, there's a 24% increase in

155:42

pancreatic cancer incidents and that's

155:45

in a dose dependent manner. So you keep

155:46

going up and up. I think that people

155:50

don't realize that they're not getting

155:51

enough magnesium. Magnesium is required

155:53

to make to turn vitamin D3 into the

155:56

steroid hormone. So some people have a

155:58

magnesium, you know, insufficient amount

156:00

of magnesium they're taking in and

156:02

they're actually not able to make enough

156:03

vitamin D into that steroid hormone.

156:05

Again, magnesium is controlling 300

156:08

enzymes. Some of those enzymes are

156:10

actually the ones that are converting

156:12

vitamin D3 into the steroid hormone. So

156:15

magnesium is hugely important. It's

156:17

something that can be easily corrected.

156:21

The deficiency can be easily corrected

156:23

by taking a supplement but also eating

156:25

more leafy greens which is the best

156:27

source of magnesium. The question is

156:30

what do supplements do? What kind of

156:32

supplement do you take? How much should

156:33

you take? All these things are I think

156:35

questions that people are interested in.

156:37

>> So I've got some magnesium here. Is um

156:40

is taking magnesium going to have a

156:42

positive role then on my my speed of

156:45

aging?

156:46

>> I do think so. I think so. Yes. We

156:48

talked about cancer incidents, right?

156:51

Magnesium. So, I think magnesium is one

156:53

of those sort of minerals that is c when

156:58

you when you don't have enough of it,

156:59

it's causing that insidious damage over

157:02

time that accumulates and then rears its

157:05

ugly head, you know, in the fifth,

157:06

sixth, seventh decade of life. And that

157:08

ugly head happens to be cancer. So I do

157:11

think that if you are able to avoid

157:14

magnesium deficiency and insufficiency,

157:17

then you are going to be able to

157:19

basically make sure there's enough

157:21

magnesium around for everything in your

157:23

body to use it with with what it needs

157:25

it for. So um

157:27

>> and I've heard you say that 50% of

157:29

people are deficient in the United

157:30

States in magnesium,

157:31

>> right? Close to 50%. And not to mention,

157:33

you just talked about, you know,

157:34

electrolytes. athletes, they actually

157:37

require between 10 to 20% more magnesium

157:40

than the general population because of

157:42

their magnes their magnesium losses are

157:44

so great and so they can be even more

157:46

deficient. Magnesium is needed for red

157:48

blood cells and so you know people can

157:50

have lower energy as well. So,

157:52

magnesium, magnesium is so important for

157:54

so many different things. And you know,

157:56

like I said, I think there I do think

157:57

there's a trade-off here where whatever

158:00

magnesium you are getting from your

158:02

diet, if you're not getting enough of

158:03

it, it's probably going to make energy

158:05

instead of being used to repair damage

158:07

because you need to make energy every

158:10

day, right? That's the most important

158:12

thing. If you don't make energy, you

158:14

die. Like, you can't survive. So

158:16

whatever magnesium your body is getting,

158:19

it's not going to that process of

158:22

repairing DNA, which doesn't really

158:24

matter until you're in your, you know,

158:27

fifth, sixth, seventh decade of life and

158:28

cancer, you know, risk increases, right?

158:31

And so there's this idea, this put out

158:34

by my mentor Dr. Bruce Ames, called

158:36

triage theory. And he's shown some

158:38

evidence of it. Magnesium is one of them

158:40

where magnesium seems to be triaged to

158:43

energy production at the expense of

158:45

repairing your DNA.

158:47

>> What does that mean? It means that if

158:49

you're not getting enough magnesium

158:51

through your dietary intake and you're

158:53

not supplementing with it, whatever

158:54

magnesium that you're getting, there's

158:56

300 different enzymes that need it to do

158:59

their function that your body is finding

159:02

a way to triage it to the most essential

159:05

functions that are going to basically

159:07

help with short-term survival.

159:09

>> Triage means it's basically allocating

159:11

>> Yes. It's allocating it to the the

159:14

processes inside your body that are

159:16

essential for short-term survival right

159:18

now.

159:19

>> Long-term health, diseases of aging,

159:22

like cancer, that doesn't matter as

159:25

much, right?

159:26

>> If you're deficient,

159:27

>> yeah, your body your body basically

159:29

says, "No, I don't I'm not going to give

159:30

whatever precious magnesium I have right

159:33

now to prevent cancer because I need to

159:35

live long enough to reproduce and pass

159:37

on my genes." And cancer doesn't happen

159:39

until I'm well well past that. Right? So

159:42

this idea, it's called the triage theory

159:44

and he's he it's been shown for um

159:46

several different micronutrients.

159:47

Another one is vitamin K. So vitamin K

159:49

is really high in dark leafy greens.

159:52

Well, what Bruce Bruce um has shown is

159:56

that vitamin K is important for a couple

159:58

of things. One, it's important for blood

160:00

coagulation, blood clotting, and that

160:03

all happens in the liver. You activate

160:05

proteins in the liver for blood

160:07

clotting. If you don't have vitamin K,

160:09

you can't do that, right? It's it's one

160:11

of the reasons why when a baby's first

160:13

born, they give it a vitamin K shot so

160:15

that they have blood coagulation.

160:16

>> On your YouTube channel, you made a

160:18

video about magnesium, which I recommend

160:20

everybody goes and watches if you are

160:21

interested in going deeper on this

160:23

subject. And um on your YouTube, I found

160:25

a stat that said for every 100 milligram

160:28

drop in magnesium intake is linked to a

160:31

24% higher risk of pancreatic cancer.

160:36

>> Yes.

160:36

>> Which is shocking. It is. And again, it

160:39

comes down to the DNA repair enzymes

160:43

that are that require magnesium to be

160:46

activated. And if over a lifetime,

160:48

you're part of that 50% of the

160:50

population in the United States that

160:51

doesn't get enough magnesium, then

160:54

you're talking about not being able to

160:55

repair damage to your DNA over decades.

160:58

And essentially what that means is, you

161:00

know, at some point damage happens to

161:02

your DNA in the right part of a gene

161:04

that is what's called encogenic. it's

161:06

cancer-causing and so eventually it's

161:08

going to cause cancer if you're not able

161:11

to repair that damage, right? And so

161:14

getting enough magnesium is important to

161:16

make sure you're repairing that damage.

161:18

And um it's not only important for

161:20

cancer, but also all cause mortality. So

161:22

there's also studies showing that people

161:24

with the highest magnesium levels have a

161:28

40% lower all-c cause mortality than

161:30

people with the lowest magnesium levels.

161:33

and they have a 50% lower cancer related

161:36

mortality compared to people with the

161:37

lowest levels. So again, cancer is still

161:39

in there and we're seeing that magnesium

161:42

intake is very important with respect to

161:45

cancer. And that is something that, you

161:47

know, people don't realize when they're

161:49

not getting enough of magnesium in their

161:51

diet, they're not eating their leafy

161:52

greens or they're not taking a

161:54

supplement that they're sort of

161:56

affecting their long-term risk of

161:57

cancer. So people with high magnesium

162:00

levels have a 50% lower risk of cancer

162:03

death than those with low levels,

162:06

>> right?

162:08

>> H and is that you you obviously can't do

162:12

like a double blind placebo control test

162:15

on that. So they're they're really

162:16

establishing causation. So it could be

162:18

other things like it could be the other

162:20

dietary factors that go into go into

162:23

that. Maybe if we think about causation,

162:25

people that eat a lot of hamburgers

162:27

don't have a lot of like leafy greens.

162:30

>> Exactly. You nailed it. Um, essentially,

162:33

magnesium is packaged in these foods

162:35

that are beneficial like dark leafy

162:37

greens. And there's so many other

162:39

benefits along with them that you can't

162:41

establish causation and say, "Aha, it's

162:43

just the magnesium." I would argue it's

162:45

probably not just the magnesium, but

162:47

magnesium does play an important role.

162:50

It's just you can't of course pinpoint

162:52

it to just magnesium because you're

162:54

right there are many other important

162:57

healthy things in these micronutri in

162:59

these plants that are beneficial for

163:01

health as well.

163:02

>> There was a really random thing that I

163:04

think parents might appreciate us

163:05

talking about which was when I was

163:07

looking at your work you mentioned this

163:09

chemical that if parents take while

163:11

their baby is inside them mothers take

163:15

the baby is smarter.

163:17

>> Yes. Choline.

163:18

>> Choline.

163:19

>> Choline. Yeah, choline is an essential

163:22

nutrient that is it's really

163:25

concentrated in egg yolk. That's a

163:28

really good source of choline, but it's

163:31

important for

163:33

it's a precursor for the

163:34

neurotransmitter acetylcholine.

163:37

It's also important for producing all

163:39

these epigenetic changes called

163:42

methylation that regulates the way our

163:43

genes are expressed. And it's also um

163:47

very important for our cells like the

163:51

membranes of our cells and it it makes

163:53

something called phosphotidyl choline.

163:55

It's doing so many things is the point

163:56

I'm getting to. I don't want to get into

163:57

all this nitty-gritty because people can

163:59

get lost in that. But the point is that

164:02

peg women that were given like the RDA

164:04

close to the RDA it was like 500.

164:06

>> What's the RDA? the recommended daily

164:09

allowance. Actually, I think in this

164:11

case it was the DRRI, the the dietary

164:14

recommended intake. So, pregnant women

164:16

were were given close to what is the

164:18

dietary recommended intake. So, they

164:19

were given 480 milligrams a day of

164:22

choline or they were given almost double

164:24

that. So, they were given 930

164:27

milligrams a day. And I don't remember

164:31

what trimester uh they started in but

164:34

they were given this you know throughout

164:36

a certain time frame and during

164:38

pregnancy and then a variety of

164:40

cognitive tests were done after the

164:42

child was born. And the children that

164:44

were given the mothers that had children

164:46

that were given the really high choline

164:48

intake the 930 milligrams scored better

164:50

on all these IQ tests. And so

164:52

essentially their children were smarter

164:55

if they if they if their mother had

164:57

taken choline throughout pregnancy. And

164:59

I think this is really interesting

165:00

because it's the one easy thing that

165:02

people can do. They can supplement with

165:04

choline andor they can eat a lot of eggs

165:07

with egg yolk which is something I I did

165:09

both during pregnancy. I was eating

165:11

probably like six eggs a day and

165:14

supplementing with choline. So I was

165:16

doing both. And um every mo every mother

165:19

wants to think or every parent wants to

165:21

think that their child is smart. But

165:22

>> I bet your child is smart.

165:24

>> He's a smart cookie. Yeah.

165:25

>> How old is he now? Almost 10.

165:26

>> Seven.

165:27

>> Seven. Okay. We have a closing tradition

165:29

on this podcast where the last guest

165:30

leaves a question for the next guest not

165:32

knowing who they're leaving it for. And

165:33

the question left for you.

165:37

Interesting.

165:39

If you could go back and change one

165:42

thing about your life, what would it be?

165:46

And you cannot say nothing. That's what

165:48

it says.

165:50

>> I would say the one thing that I would

165:53

change, I'm 47 years old, just turned 47

165:58

last month. I have one child.

166:02

And I think if I could go back in time,

166:05

I would change my decision to only have

166:08

one child and I would have another

166:10

child.

166:13

>> Why?

166:16

Because

166:19

I love being a mother. I love the joy

166:23

that children bring

166:26

to your life is it's unexplainable until

166:29

you experience it. Everything about it,

166:32

helping shape them, learning with them,

166:36

going through hard times and

166:39

experiences, but also experiencing the

166:40

joys.

166:43

I regret sort of you know I had children

166:47

later in life because I was really

166:49

pursuing my career and

166:52

it is definitely challenging being an

166:55

entrepreneur that's a mother. I made a

166:59

decision that I was going to have one

167:00

child because I wouldn't be able to do

167:04

as much of what I love doing outside of

167:06

being a mother if I had more than one

167:08

child. And now I realize that say that

167:11

when I'm older and closer to dying,

167:15

I know now that

167:18

I'm not going to think about doing one

167:20

more podcast when I'm on my deathbed.

167:22

I'm going to think about all the

167:24

experiences I've had with my family. And

167:26

I do I do have a pretty balanced I would

167:29

say balanced personal life and family

167:32

life with my career.

167:34

I don't know that it was the easiest

167:36

decision to make where I had to sort of

167:39

give up some of my intellectual pursuit,

167:42

some of my entrepreneurial my

167:44

productivity essentially.

167:47

I had to give some of that up to to to

167:49

be the best mother that I wanted to be

167:51

to be present with my husband and my my

167:54

son and enjoy everything that I enjoy

167:56

because that takes time. and that time

167:57

that I'm with them, I am not doing my

168:01

podcasting or my research or any of

168:03

that, right? And I'm happy with that

168:06

decision. And in fact, I would even give

168:08

up more of it for another child. Um, and

168:13

that's a very personal thing that I'm

168:14

discussing. So hopefully

168:17

I'll be okay with it.

168:20

>> It's not the first time I've heard this.

168:23

>> Really?

168:23

>> Yeah. No. Yeah, it's not the first time.

168:24

I I hear this a lot which is fascinating

168:27

to me from from high performance women.

168:31

>> It is it's you know

168:34

I say that it's very hard to be a very

168:39

high performing female and mother at the

168:43

same time. Uh you either have to

168:45

sacrifice being present with your family

168:48

or your health because you don't sleep

168:51

as much. uate, you know, you're you're

168:53

basically

168:54

not going to be getting as much sleep

168:56

because you're going to be working

168:57

rather than sleeping during some of the

168:58

those hours, right? So, I do I do think

169:02

that it is very challenging and I'm not

169:05

saying that um there aren't really high

169:07

performing mothers out there, but it is

169:10

it is a very difficult thing to do.

169:14

>> When you say you you made the choice to

169:15

have one, was that an intentional

169:17

choice? I you and your partner did

169:19

family planning and said we want one or

169:21

was it because you said your child is

169:23

seven you said you're 47 so at 40

169:25

obviously it's it's becomes a little bit

169:27

more tricky than it than it does when

169:28

your 30s to conceive

169:30

>> right so I think what in in my case um I

169:34

I got pregnant when I was 38 for the

169:36

first time and I gave birth when I was

169:39

39

169:40

>> so I was pretty late already

169:43

>> and at that point

169:46

I didn't you know as I It was I was so

169:48

overwhelmed and my productivity had gone

169:50

down so much just from that event

169:54

>> that I was worried that I wouldn't be

169:57

able to keep it up if I did another one

169:59

right away, which I had to do because I

170:01

had waited so long. Now, why did I wait

170:03

so long? I was pursuing my career, you

170:05

know? I mean, and I would argue now that

170:08

I could have had a kid in graduate

170:10

school. I could have had a child as a

170:13

post-doal fellow, but again, it's one of

170:16

those things where you just you keep you

170:17

want to like get through this milestone

170:19

and then this milestone and then you

170:20

want everything to be perfect and you

170:21

start to like this perfectionism can

170:23

sometimes be a double-edged sword,

170:25

right? Yeah.

170:25

>> Where your perfectionism then is like,

170:28

okay, well, you're you're going to have

170:29

a trade-off here. Yeah.

170:30

>> And that trade-off for me was my

170:31

reproductive lifespan. You know, I'm I

170:34

was older when I started having

170:35

children. know there's a lot of

170:37

technologies out there now that can help

170:38

with that but at you know 47 it's I

170:41

would say not looking good.

170:43

>> Uh I think I ask about this and I'm

170:45

curious about this because me and my

170:47

partner I'm 32. She's turned 33 last

170:49

week. We don't have any kids. We've been

170:51

together for almost seven years now I

170:53

think. And so you can imagine in my life

170:56

how easy it would be to make excuses

170:59

that I need to get through this year

171:01

because this big thing's happening or

171:03

I'm moving to LA so now's not the right

171:05

time. And then she's got her business

171:06

going on so now is not the right time

171:07

for her and she's traveling and doing

171:09

these retreats around the world so

171:10

that's not perfect timing. And then

171:12

because of this podcast, I've played the

171:14

scenario forward because I get to meet

171:16

people who are a little bit further down

171:17

the line than me. And I get to ask them

171:19

about their regrets and the decisions

171:20

they wish they'd made and were they

171:22

intentional about fat family planning,

171:23

did they wish they'd done it earlier?

171:25

And the thing it's changed in me is it's

171:27

made me realize that to start the

171:29

process, if it's something I want to do

171:32

well before I'm ready because there is a

171:35

there whether we like it or not, there

171:37

is a biological clock. And the thing

171:40

that I've observed in the guests,

171:41

specifically high performance women,

171:43

whether you Ronda Rousey, the UFC

171:46

champion, who I sat and interviewed and

171:48

who was in tears talking about her

171:49

failed IVF for the I don't know the

171:52

fifth, sixth, seventh time, or other

171:54

women that have sat here and interviewed

171:55

and looked in their faces is the regret

171:58

of having that decision taken taken away

172:01

from you is going to be much much worse

172:04

than

172:05

the inconvenience

172:08

of the choosing an imperfect time to

172:11

have the kid. So, funnily enough, I w I

172:13

don't people don't really know this cuz

172:14

I don't talk about this, but I walked

172:15

away from this podcast a couple just

172:17

after hearing this story over and over

172:18

again and I went to the women in my

172:20

lives and I was like, it's like super

172:22

annoying being that guy cuz especially

172:23

as a guy saying it, I'm like, by the

172:25

way, family planning as early as

172:28

possible is probably a good idea. and

172:30

whether that means freezing your eggs or

172:32

freezing your embryos or just giving

172:34

yourself the option in the future um is

172:37

probably a good idea. And it was so

172:39

interesting to actually see the reaction

172:40

to me saying that to some of the women

172:42

in my life that I care about like my,

172:43

you know, my siblings or my partner

172:47

because upon saying it, it wasn't

172:51

incredibly wellreceived because

172:54

I think it's a confronting thing to say

172:56

to somebody

172:58

because there's a bit of a stigma

172:59

associated with like freezing your eggs

173:01

and IVF and freezing your MBOS's. And

173:03

even with my partner, the first time I

173:05

said it to her, it was it was almost as

173:08

if I was like insulting a little bit,

173:11

insulting her. That's almost the the how

173:13

I thought she took it for the first

173:14

three or four minutes. But then when I

173:16

explained what I was saying by like give

173:19

let's give ourselves the option when

173:21

we're older, you know, if you know,

173:23

let's just give ourselves the option.

173:24

And also, if you go through these

173:25

procedures when you're younger, you have

173:27

higher quality yield from the eggs you

173:29

freeze or the embryos you freeze. Let's

173:30

just give ourselves the option. And then

173:32

she kind of turned 5 minutes into the

173:33

conversation and then she got super

173:35

excited about it like 15 minutes in and

173:37

now we're like super excited. So like

173:39

we're we're trying to conceive but also

173:41

we're going to be freezing our eggs and

173:43

freezing embryos in this year in

173:45

September because and I've just tried to

173:48

be a really big influence to the women

173:49

in my life to like give yourself the

173:51

option. And I say this because I've seen

173:53

the regret on this podcast and that's

173:55

what I'm saying. And I think all I think

173:56

all people that can and I know it's

173:57

expensive as early as you can should

174:00

consider the fact that we live in a

174:02

world that is driving productivity that

174:05

is making us work later and later in

174:06

life that is making us more obsessed

174:08

with our careers and without us really

174:10

knowing it there is a clock and it's

174:12

robbing us of the option to make family

174:15

planning decisions.

174:16

>> 100% agree. I I can't I can't agree

174:20

more. Exclamation exclamation everything

174:23

you just said. I mean, if I had frozen

174:25

my eggs or we had done, you know, IVF

174:27

and frozen embryos that were viable and

174:29

healthy, then we'd have the option,

174:31

right? I mean, it's it's it's it's so

174:34

true. And I don't know. I think I think

174:38

I was just really blinded by and

174:41

overwhelmed by, you know, how much work

174:43

I have to do and thinking, "Oh, there's

174:45

no way I could do more than one."

174:47

Because, again, I when I'm a mother, I

174:50

go all in.

174:51

>> Yeah.

174:51

>> When I'm a podcaster, I go all in.

174:53

That's exactly,

174:54

>> you know, it's not just, you know, when

174:56

I have a guest on, like I really like I

174:58

need to like be really interested in

174:59

them and, you know, so there's it's all

175:01

in, but not giving myself that option is

175:04

a big regret, you know, where at least

175:06

if I had frozen my eggs down, then I

175:08

would be at a point now this if I had

175:10

done this, you know, when I was 39 or 40

175:13

or even if I had done it the first time,

175:15

you know, when I was earlier in my 30s,

175:17

I should have done that, you know, but

175:19

um I just didn't have the foresight

175:22

enough to to do that and I and I do

175:24

regret it. So, it's great. It's great

175:26

that you talk about it to the the women

175:28

you that are in your life and even on

175:30

the podcast.

175:31

>> We're really bad at forecasting the fact

175:34

that we will change

175:37

this. And I think this is like really at

175:38

the heart of it. Like we're really bad

175:40

at forecasting the fact that our current

175:42

state of mind might not be our future

175:43

state of mind. But you've only got to

175:44

look backwards in your life and realize

175:46

how different you are and how you think

175:47

and what your priorities were. I was in

175:48

nightclubs at 18 and 19. I there's

175:51

nothing for me going to a nightclub now

175:53

be like a form of like it'd be like

175:54

waterboarding me. It'd be like torture.

175:56

I changed and so at like 35 at 40 45

176:00

there's a high probability that I'm

176:02

going to have a different perspective

176:03

than the one I have now. So give myself

176:04

the option at 45 to like you

176:07

know so that's kind of how I think about

176:09

it and I say this out publicly because I

176:11

just think I don't like I don't like

176:13

seeing that regret in people.

176:15

>> It's hard. Yeah, it it's definitely

176:17

hard. Thankfully, I do have this joy in

176:19

my life and I'm so glad I have that.

176:22

But,

176:23

>> and I have to acknowledge the fact that

176:25

many people even if they did want the

176:27

option for fertility reasons can't have

176:29

children. So, um it's not still not an

176:32

option for everybody because there are,

176:33

you know, people have certain health

176:35

complications and um other issues which

176:38

prevent them from having kids even if

176:39

they wanted to and even if they're young

176:40

and I've got friends in my life that

176:42

unfortunately are in that situation. But

176:45

yeah, thank you so much for the work

176:48

that you do. It's um it's really really

176:49

important work in part because you're so

176:51

unbelievably engaging, but you're so

176:53

because of your obsession, you're so

176:55

unbelievably rigorous and in the detail

176:57

of the things you talk about. And as you

176:59

said, there's so many people around the

177:00

world, and I know because we we meet

177:01

them wherever we go in the world that

177:03

don't have access to this information

177:05

like they're not going to be on PubMed

177:06

reading through the journals and trying

177:08

to distill these big words. And I think

177:09

you do a brilliant job of educating many

177:12

many millions of people in every corner

177:13

of the world through your YouTube

177:14

channel and your Instagram etc. and um

177:17

making these like complicated things

177:18

accessible and if if if you're

177:20

successful in that which you very much

177:21

are you're you're tilting the trajectory

177:23

of their life but also therefore their

177:25

future and their kids' lives and their

177:27

kids' kids' lives and um and that's a

177:29

really wonderful thing and we need more

177:30

public educators like you that have the

177:32

talent of articulation and engagement

177:34

that you do. There's they're very very

177:36

rare and hard to come by. I do a podcast

177:38

where I look at all these people and

177:39

you're like the very very best at it and

177:41

you've done it for so unbelievably long

177:42

and that's why. So, thank you so much

177:43

for educating us and allowing us to live

177:45

the future that uh that'll be most

177:47

conducive with our health and happiness.

177:49

>> Well, thank you so much Stephen for the

177:51

really engaging conversation and for

177:52

asking the hard questions.

177:54

>> Thank you.

177:56

This has always blown my mind a little

177:58

bit. 53% of you that listen to the show

178:01

regularly haven't yet subscribed to the

178:03

show. So, could I ask you for a favor?

178:05

If you like the show and you like what

178:06

we do here and you want to support us,

178:07

the free simple way that you can do just

178:09

that is by hitting the subscribe button.

178:11

And my commitment to you is if you do

178:12

that, then I'll do everything in my

178:14

power, me and my team, to make sure that

178:16

this show is better for you every single

178:18

week. We'll listen to your feedback.

178:19

We'll find the guests that you want me

178:21

to speak to, and we'll continue to do

178:22

what we do. Thank you so much.

178:27

[Music]

178:29

Heat. Heat. N.

178:31

[Music]

178:44

[Music]

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