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Cognitive Decline Expert: The Disease That Starts in Your 30s but Kills You in Your 70s

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Cognitive Decline Expert: The Disease That Starts in Your 30s but Kills You in Your 70s

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3183 segments

0:00

And we have this white powder in front

0:02

of me. You got a big smile on your face.

0:04

>> I do because I don't care who you are,

0:05

you should definitely be having this.

0:08

Let's talk about creatine. Phenomenal

0:10

research shows you can creatine your way

0:12

out of sleep deprivation. It can protect

0:14

your brain against a concussion, stroke,

0:16

from stress. And there was a study done

0:18

on Alzheimer's disease patients. And

0:20

they found that patients not only

0:22

preserved their cognitive functions, but

0:24

they had more energy and they were able

0:27

to exercise more. And I know this

0:29

because I'm a clinician and over the

0:31

last decade I've been surrounded by the

0:33

greatest neurosurgeons in the world

0:35

studying the brain. And so I'm here to

0:37

tackle one disease and that is

0:39

Alzheimer's because it generally starts

0:42

in our 30s and 60 million people

0:45

worldwide have Alzheimer's. 70% being

0:47

women. And I get angry and I get

0:50

passionate because women have been lied

0:52

to. They've been underrepresented. They

0:54

downplay their symptoms or they're too

0:56

scared to ask their doctor for advice.

0:58

And what people don't really know is

0:59

that it is a preventable disease, but

1:01

it's like endstage cancer. Once you get

1:04

the diagnosis, there is no cure. And the

1:06

fact that so many people are at the

1:09

mercy of a disease that is preventable

1:11

is not okay with me. And I don't think

1:13

people understand these things. Like

1:15

people don't really know that we're

1:16

becoming more sedentary, which is a

1:18

disease. And there was a study that was

1:20

done on this that showed that if you do

1:22

10 air squats every hour, this can

1:24

compensate for your sedentary lifestyle.

1:26

And then we have several lifestyle

1:28

factors that can lower your risk of

1:30

getting Alzheimer's disease, as well as

1:32

showing you what 5 minutes a day can do

1:34

for your brain performance. Just using a

1:36

tennis ball and an eye patch.

1:42

Guys, I've got a quick favor to ask you.

1:44

We're approaching a significant

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subscriber milestone on this show, and

1:48

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the show haven't yet subscribed for

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ever done anything for you, giving you

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value in any way, it is simply hitting

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that subscribe button. And it means so

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much to myself, but also to my team

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go away as a team and celebrate. And

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

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So, that's a favor I would ask you. And

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won't let you down. And we'll continue

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to find small ways to make this whole

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production better. Thank you so much for

2:21

being part of this journey. Means the

2:22

world. And uh yeah, let's do this.

2:28

Louisa,

2:30

what is it you do in simple terms? And I

2:35

guess most importantly, why is it that

2:36

you do it? And why now?

2:38

>> Over the last decade, I've been studying

2:41

the brain. I'm both a clinician and an

2:44

academic. So, I get to see the brain and

2:47

I also get to research it. And I'm

2:50

really here to tackle one disease and

2:53

that is Alzheimer's disease.

2:54

>> Why is this so important now?

2:57

>> Right now because 60 million people

2:59

worldwide have Alzheimer's disease. That

3:03

number is going to triple by the year

3:05

2050. 110 million women will have

3:09

Alzheimer's disease by the year 2050.

3:12

This is a disease that robs you of who

3:16

you are, your complete identity. So,

3:19

we're going to get really into this

3:20

straight away cuz I brought Henry with

3:22

me, right?

3:23

>> And for anyone that can't see, Henry is

3:25

a model brain that she's holding in her

3:26

hands.

3:27

>> This is around 2 lb. And if you actually

3:30

feel it and you know, if you actually

3:32

feel a real human brain, it feels like

3:34

tofu, but this is everything you are.

3:36

And the fact that so many people are at

3:40

the mercy of a disease that is

3:43

preventable is not okay with me. It

3:45

doesn't sit well with me. We used to

3:47

think that women were disproportionately

3:50

affected by Alzheimer's disease because

3:52

we lived longer because age played a

3:55

role in it. But we now have substantial

3:57

evidence to show that it's not the fact

3:59

that women live longer or people in

4:02

general because dementia and Alzheimer's

4:03

disease are not part of the natural

4:05

brain aging process. For women, and they

4:08

differ from men, and we can separate the

4:10

sexes and talk about it, for women, it

4:12

is purely because being a woman is a

4:17

risk factor for getting this disease.

4:19

Now, if we go through and we have a look

4:20

at all of the people that currently have

4:22

Alzheimer's disease, 95% of them could

4:25

have been prevented because this is not

4:27

a disease of genetics. It's a disease of

4:30

lifestyle.

4:31

>> 95% of it could have been prevented.

4:33

>> Correct? We're we're born with our with

4:35

our genetic makeup. Meaning that, for

4:38

example, if you have a genetic mutation

4:40

on chromosome 4, you will get

4:43

Huntington's disease. There is nothing

4:46

we can do about that. That's how you

4:47

were born. But when it comes to

4:49

Alzheimer's disease, there's around 20

4:52

to 30 genes involved in the disease.

4:55

Only around 3%

4:58

of the disease cases right now were

4:59

driven through those genetic mutations.

5:03

The genetic mutations that you are born

5:05

with, you get them from mom and dad are

5:08

presinelin one, presinelin 2 and the

5:11

amaloid precursor protein. So you if you

5:15

have a genetic mutation in one of these

5:17

genes, you will get some form of

5:20

dementia.

5:21

>> What is the age range where people will

5:23

start to experience Alzheimer's?

5:25

>> Let's just actually take a broad

5:27

overview of what Alzheimer's disease is.

5:28

Okay. So you've probably heard of

5:30

dementia. Yeah.

5:31

>> So dementia is the umbrella term. So

5:34

Alzheimer's disease is sits under the

5:36

umbrella. It's a form of dementia.

5:38

There's fronttotemporal dementia which

5:40

is what Bruce Willis has. There's

5:42

dementia with Louis bodies. There's

5:44

Parkinson's dementia. There's vascular

5:46

dementia. This disease dementia or

5:49

Alzheimer's disease is a disease of

5:51

midlife. And so it generally starts in

5:55

our 30s. It starts in our 30s, but the

5:59

first symptoms show up in our late 60s,

6:03

70s and beyond.

6:04

>> When you say it starts,

6:06

>> yeah, our brain fully develops at around

6:08

25 years old. 25 to 30. And after that

6:12

that's when we if we don't take care of

6:14

our brain we start getting a decline in

6:17

these functions. Now let's go back to

6:19

the brain. The brain is 87 billion

6:22

neurons around 5 to 10,000 connections

6:24

per neuron. The my favorite area of the

6:27

brain is the cerebellum. And the piking

6:29

cells inside the cerebellum have upwards

6:31

of 50,000 connections per cell. So so

6:36

tightly dense and there is so much

6:38

happening. It takes 20% of the total

6:41

calories that you consume every day to

6:43

power this thing. And it's the most

6:46

vascular richch organ in the entire

6:48

body. Over time, through things such as

6:50

sleep deprivation,

6:52

poor diet, lack of physical activity,

6:55

environmental toxins, this slowly

6:58

erodess at the functioning of the brain.

7:00

And over time, this starts to compound

7:03

because that's what biology is.

7:05

Everything is compounding. One night of

7:07

sleep deprivation raises your risk of

7:09

amaloid beta, which is one of the

7:11

hallmarks of Alzheimer's disease

7:12

pathology, by 4%. That's just one night

7:15

of sleep deprivation. Imagine a new

7:18

mother or a shift worker or a physician

7:21

in their residency getting countless

7:23

nights of sleep deprivation day in and

7:26

day out. Imagine all of that

7:28

compounding. And what happens? Well, we

7:32

end up with either neuronal loss, which

7:34

is like the complete atrophy of certain

7:37

parts of the brain. And that's what is

7:40

mild cognitive impairment. Mild

7:41

cognitive impairment is a pre-dementure

7:43

state.

7:44

>> So, what is this that I have here? This

7:45

photo um of a brain.

7:48

>> You've got the sagittal view right now

7:49

of the brain. And we're looking at a

7:52

healthy brain on here. As you can see,

7:53

I'm going to show it up here on the left

7:56

hand side. You can see that the brain is

7:57

thick. We can see that the integrity of

7:59

the gray matter which sits out here is

8:02

thick. It's voluous. Okay. We can see

8:05

that the ventricles are smaller. We go

8:08

over here and we see thinning of the

8:10

cortex. You can see these big spaces

8:12

between the gy. These are thick because

8:15

the gray matter has atrophied. It's

8:18

shrunk. You can see that the space

8:20

between the cortex itself and the skull,

8:24

there's a bigger space. You can see

8:25

these ventricles here, these

8:26

butterflyshaped ventricles. This is

8:28

thicker. This is thinner. We can see

8:31

atrophy down here. So essentially, the

8:35

brain is getting smaller and smaller

8:38

>> at the age of 30. If I do everything

8:40

right, and we were to sort of plot this

8:43

on a graph of where I land at 70, what

8:47

is the variance of where I'll end up at

8:49

70? You know, my brain is quite

8:50

important to me. And I do worry. I think

8:52

like I think I worry in part

8:55

because I I I sit and interview a lot of

8:56

people at a lot of different ages and

8:59

one thing you notice as an interviewer

9:01

is some people at 60

9:04

have are razor sharp

9:06

>> and some people at 60 are not as razor

9:09

sharp.

9:10

>> Yeah.

9:10

>> Their ability to articulate their words,

9:12

their memory recall, their ability to

9:14

understand stats and stories, all of

9:15

this. And I sit here and go, I wonder

9:16

what the difference is.

9:17

>> Yeah. And that's actually beautiful

9:19

because it brings up this important

9:21

concept in neuroscience called cognitive

9:23

reserve. And that's your brain's ability

9:27

to withhold capacity to overcome

9:30

stresses. Okay. So you've probably heard

9:32

for example, let's use the analogy of

9:35

physical performance, your V2 max, which

9:37

is a measure of your peak respiratory

9:39

fitness. You know how well you can

9:42

utilize oxygen

9:43

>> when you are at a at a high intensity

9:46

state. How well does your body utilize

9:48

oxygen? The the fitter you are, the more

9:53

reserve you have to overcome stress.

9:56

Stress such as an infection, everyday

9:59

stresses, sleep deprivation, surgery,

10:04

the more reserve you have in your bank

10:05

to overcome that. The same is with your

10:07

brain. The more cognitive reserve that

10:10

you have, the more cognitive capacity

10:13

that you have been training year on and

10:16

year out will save you at 60 from

10:20

harmful insults such as you can get a

10:23

woman at the age of 80 with a head full

10:27

of amaloid beta.

10:28

>> Amaloid beta being

10:30

>> the one of the hallmarks of Alzheimer's

10:32

disease. You can get somebody with a

10:33

head full of amaloid

10:34

>> which is like a plaque on the brain.

10:36

>> Yeah. it it's a protein that's actually

10:39

it's a it's a protein that lives inside

10:41

the neuron itself and we can explain

10:44

what that is which I will in a second

10:46

but let me just tell you you can have a

10:48

head full of amaloid in this person and

10:50

they have retained their cognitive

10:52

functions then you can have somebody

10:54

else with hardly any amaloid but they've

10:57

lost their cognitive functions and this

10:59

all comes down to cognitive reserve

11:02

>> and cognitive reserve lives where in the

11:04

head

11:04

>> you've got around 5 to 10,000

11:06

connections per cell. Over time, those

11:09

connections fail. Now, those connections

11:11

are responsible for your thinking, your

11:13

processing speed. Every time you have a

11:15

thought, you build a new connection. The

11:17

more connections that you have, the more

11:19

things that you see, the more novelty

11:22

that you give your brain, the richer it

11:24

gets, the more stable it gets. So, the

11:26

ends of these of the neurons, we have

11:29

dendrites. And coming off the dendrites

11:32

are these little trees. Imagine a

11:33

branch. That's the dendrite. And all of

11:36

the leaves that come off it, all these

11:38

little dendritic trees, if you will, and

11:40

they connect to nearby cells, 10 10,000

11:43

cells over time, those are the

11:46

connections that fall. Those are the

11:48

connections that fail. They fail because

11:50

you don't utilize them.

11:52

>> So, the way that one would build reserve

11:54

at the age of 30 is to

11:57

>> is by exercising. We can build reserve

12:00

in a number of different ways. In fact,

12:01

there was a really wonderful study that

12:03

just came out that I just read about and

12:05

they found that those who preserved

12:06

cognitive capacity at 75 years old were

12:10

handwriting and reading. So, handwriting

12:14

and reading preserves cognitive

12:16

functions.

12:18

Exercise is one of the most potent

12:21

stimulus for brain health and

12:24

Alzheimer's disease prevention and

12:27

cognitive reserve. The more you

12:29

exercise, the bigger your brain.

12:32

>> What about scrolling on social media?

12:34

Does it improve my reserve if I'm

12:36

watching videos?

12:37

>> It's in the opposite.

12:38

>> Why would that be? Cuz I'm still

12:39

learning stuff.

12:40

>> Yeah.

12:41

>> When I'm on the internet.

12:42

>> Because what you're doing then is you

12:43

are relying on short dopamine hits.

12:46

Every time you scroll, you're sending

12:48

signals to your brain that you're

12:50

getting a dopamine hit. And your brain

12:52

gets used to it. Remember, your brain is

12:54

only there for two things, survival and

12:58

reproduction. So every time that you

13:01

stress your brain in the smallest amount

13:03

of times, you're giving it dopamine

13:04

hits, it doesn't allow us to do other

13:08

things for a sustained period of time

13:10

like focus, read, have a conversation.

13:14

>> So writing and reading are good for

13:16

building up my neurological reserves.

13:19

>> Yeah, neurological reserves. It doesn't

13:21

compare to what exercise can do for the

13:25

brain. And it's so sad because around

13:28

80% of the US population don't exercise

13:32

for at least 30 30 minutes a week, which

13:35

is actually quite scary. The physical

13:37

activity guidelines are 150 minutes to

13:40

300 minutes of moderate to rigorous

13:42

physical activity per week. What's the

13:44

most compelling study you've ever

13:46

encountered that proves that exercise is

13:48

central to Alzheimer's prevention and

13:50

brain health?

13:51

>> When we look at all of the data, we can

13:53

see that the biggest amount of return on

13:57

investment is from resistance training.

14:00

>> Resistance training being

14:01

>> strength training. One of the most

14:03

compelling studies was probably the um

14:05

the smart trial where they uh took a

14:07

group of people with mild cognitive

14:10

impairment and gave them two to three

14:12

times per week of resistance training

14:14

and they not only preserved their

14:16

cognitive functions. They enhanced their

14:18

processing speed. They enhanced their

14:20

fluid intelligence and they had slowing

14:23

of the gray matter.

14:25

>> The gray matter.

14:26

>> Yeah. So your brain consists of both

14:28

gray and white matter. So gray matter

14:30

are the cell bodies that lives on the

14:31

outer side outer portions of your brain

14:34

and the white matter is deep within the

14:36

brain and that's where all of our

14:37

myelinated neurons live and over time we

14:41

see that we can have little lesions in

14:43

the white matter of the brain. So, a lot

14:47

of the times people will ask me,

14:49

"Stephen, I'm scared my mother had

14:52

Alzheimer's disease. I'm scared I'm

14:53

going to get it." And we were talking

14:55

about genetics before. And there's

14:58

another genetic risk factor that we

15:00

didn't talk about. The APOE E4 gene uh

15:03

is one of the the strongest risk factors

15:06

of getting Alzheimer's disease, but it

15:08

is not a foregone conclusion that you're

15:10

going to get it. So, Chris Hemsworth was

15:12

tested and he has two copies of this

15:14

gene. So you get two copies, one from

15:17

mom, one from dad. It's the apo

15:19

lipoprotein E gene and it comes in three

15:23

main variants. So you've got APOE E2,

15:26

ApoE3 and ApoE E4.

15:30

So I'm a 33 carrier. I've been tested

15:34

and that's the general population.

15:36

They're 33. So it doesn't raise my risk

15:38

of getting the disease, but it also

15:40

doesn't protect me. If you've got a copy

15:42

of the APOE E2 gene, it protects you

15:45

against the disease. But when you have a

15:47

copy of the APOE E4 gene, it raises your

15:50

risk by two to three times.

15:54

If you have two copies of the gene, it

15:56

raises your risk by 10 times. If you are

15:59

a male,

16:00

here's the devastating thing. If you are

16:03

a female with one copy of the gene, you

16:06

are at doubled the risk than your male

16:08

counterpart. So one copy of the gene of

16:12

ApoE4 gene for a female raises your risk

16:14

by about sixfold whereas two copies

16:17

raises your risk by 15fold.

16:21

>> And how would one go and get checked?

16:23

>> You can get the ApoE4 gene checked uh

16:26

with your doctor. It's a simple blood

16:27

test.

16:28

>> On this point of resistance training,

16:30

I've heard you talk about how the legs

16:33

>> Mhm.

16:34

>> are so important. Having strong legs,

16:37

>> having strong legs is by far the most

16:40

important tool in your toolbox for the

16:43

prevention of Alzheimer's disease. And

16:45

this was made certain to me when I read

16:49

a study done on identical twins, exact

16:52

same genetic profile,

16:54

>> and they tracked them. And they did

16:55

cognitive tests and MRIs, and they

16:58

tracked them over a 10-year period. And

17:00

what they found was that the twin who

17:03

possessed the greater strength and the

17:06

most leg power had a bigger brain,

17:11

larger gray matter volume. They

17:14

preserved their cognitive functions.

17:16

They uh did better on different

17:18

cognitive tests.

17:20

>> Why is resistance training increasing

17:23

the size of my brain?

17:24

>> Resistance training does so much for

17:26

your brain. The first thing is we have

17:28

to think about the journey that we're

17:30

going on, right? So when you look at all

17:33

of the studies, I want to make it really

17:35

clear, all of the studies show that in

17:38

order to produce the neural effects of

17:40

resistance training, you need to be

17:42

lifting at around 80% of your one

17:44

repetition max. So 80% of one RM. So

17:49

that's quite heavy. There is so much

17:52

controversy on social media right now.

17:54

Should I lift heavy? Should I lift

17:56

light? And when it comes to hypertrophy

17:58

alone, so increase in muscle, muscle

18:00

mass, muscle cell size, you can get

18:03

there, men can get there, women can get

18:06

there by lifting light, high reps, or

18:09

you can get there by lifting heavy and

18:11

low reps. It just depends on who you are

18:13

and how much time you have. But when it

18:15

comes to the brain specifically, you

18:17

want to be lifting heavy for several

18:19

reasons. The first one is when we lift

18:22

heavy, when we literally like when we

18:24

contract our muscle like this, we are

18:27

releasing a whole set of chemicals.

18:30

They're called myioines. And when

18:32

they're released from the muscle, they

18:34

go up to the brain and they do

18:36

beneficial things for our cognitive

18:37

performance, our cognition, and they

18:40

help with the growth and proliferation

18:42

of new neurons in the hippocampus.

18:45

And it's the first thing to go during

18:47

Alzheimer's disease. it actually

18:50

shrinks. This holds our memory. This is

18:52

where a lot of our memory consolidation

18:54

and learning takes place, which is why

18:57

short-term memory is the first thing to

18:58

go during this disease. Okay? And as we

19:01

get older and what we found is that you

19:05

can grow new neurons in the hippocampus

19:09

from structured exercise and consistent

19:11

exercise. the biggest growth is going to

19:14

occur because of BDNF, brain derived

19:18

neurotropic factor. So this is a growth

19:20

factor for the brain and it gets

19:22

released when we exercise. It gets

19:24

released abundantly when we are doing

19:26

aerobic training, when we're running,

19:28

when we're cycling for long distances,

19:31

but also gets released when we do

19:33

resistance training. Now, here's the

19:35

beautiful thing about it. When we do

19:36

resist resistance training and we're

19:39

releasing all of these myioines, these

19:41

myioines are signaling molecules. They

19:43

work together. So we've got one called

19:45

irri, okay? And that's a messenger

19:49

molecule. So what it does is it actually

19:51

helps BDNF express itself. So when we

19:55

release this myioin, it goes into the

19:57

brain, crosses the bloodb brain barrier

20:00

and it tells BDNF to express itself. So

20:03

then BDNF goes in and it helps grow new

20:06

neurons in the hippocampus. But then

20:08

we've got another mioine. Let's just

20:10

take isle 6. Interlucan 6 that comes

20:13

from the interlucan family.

20:14

>> What is that? Sorry.

20:15

>> The interlucan family is a a class of

20:19

pro-inflammatory cytoines. So these get

20:21

released when we are under stress or

20:23

you've got an infection or a virus for

20:25

example. But when we exercise, it

20:30

depends on where the site is. Interlucan

20:32

6 instead of acting as a

20:34

pro-inflammatory cytoine.

20:35

>> Mhm.

20:36

>> Instead of creating inflammation, it

20:38

acts as an anti-inflammatory cytoine.

20:40

So, it goes into the brain and it lowers

20:42

inflammation. In fact, this is uh one of

20:45

this was one of the uh first ever

20:48

myioines to be studied and they showed

20:51

that interlucan 6 is also responsible

20:54

for the down reggulation of tumor cell

20:56

growth. So exercise is a potent

21:00

anti-cancer intervention as well by way

21:04

of myioines. How much exercise does one

21:07

need to do to avoid the uh cancer

21:10

related um side effects but also the

21:12

Alzheimer's problem?

21:14

>> Well, just 30 minutes a day of aerobic

21:18

physical activity can downregulate 13

21:21

types of cancers and the most prominent

21:24

ones being breast cancer, colon cancer

21:28

and prostate cancer. So these three have

21:31

been studied most and you get your

21:33

anti-cancer effects from the myioine

21:36

release. So quite specifically when we

21:39

exercise we're getting a robust release

21:42

of something called natural killer

21:44

cells.

21:46

And when we get these natural killer

21:48

cells into the plasma and into the

21:50

bloodstream, they go into the tumor site

21:54

and they do what they were born to do.

21:57

They kill. So they go into the tumor

21:59

site and they start to kill the tumor

22:02

and this is where you get your

22:03

anti-cancer effects of it. But you can

22:05

also get it from the anti-inflammatory

22:08

effects of resistance training,

22:09

anti-inflammatory effects of aerobic

22:11

training. So these myioind

22:14

powerful in fact pharmaceuticals are

22:17

spending billions of dollars trying to

22:19

replicate these myioind.

22:23

I want both men and women lifting heavy

22:26

because you've got areas in your brain.

22:28

Right across here lives your motor

22:31

cortex.

22:33

Think of your brain as real estate.

22:35

There's real estate in your brain

22:36

reserved for lifting heavy. So every

22:38

time you lift a heavy weight as opposed

22:41

to a lightweight, it takes more neural

22:44

real estate to lift that heavy weight.

22:48

So the heavier you lift, the greater the

22:51

neural drive. The greater the neural

22:52

drive, the better it is for your brain.

22:55

>> If you had to do just one exercise for

22:57

the rest of your life to protect your

22:58

brain and you could only pick one,

23:00

>> what would it be?

23:02

>> Deadlift.

23:04

>> Why?

23:05

>> If done correctly, the deadlift can use

23:09

almost every muscle in your body. Erect

23:12

spine a you've got the glutes, you've

23:13

got the quads, you've even got seratus

23:15

anterior, you've got the you've got your

23:17

calf muscles. There is so much

23:19

compounding in that one lift would

23:23

probably be comparable to a barbell

23:25

squat as well.

23:26

>> According to the World Health

23:27

Organization, we're getting increasingly

23:28

more sedentary. I we're moving less and

23:31

less in part because of technology, but

23:33

also there was this really interesting

23:35

study done by the Cleveland Clinic where

23:37

they talk about people who are active

23:39

sedentary. And this

23:42

this felt a little bit personal if I'm

23:44

honest. It says a major finding in 2025

23:47

found a danger of being active

23:50

sedentary, which is people who exercise

23:51

for like 30 to 60 minutes but sit for

23:54

the remaining 10 hours a day. If you sit

23:57

for more than 10 hours a day, your risk

23:58

of cardiovascular disease increases even

24:01

if you meet weekly exercise goals

24:04

because prolonged sitting shuts down

24:06

lipoprotein lipes, an enzyme essential

24:08

for burning fat and cleaning glucose

24:11

from the blood.

24:13

That wasn't that's annoying to read

24:14

because I feel like that's me.

24:15

>> Yeah. And being sedentry is a disease.

24:20

You can change the trajectory of your

24:22

life by doing 10 air squats every hour

24:27

on the hour. And there was a study that

24:29

was done on this that showed that if you

24:31

do 10 air squats every hour, this can

24:35

compensate for your sedentary lifestyle.

24:36

Because unfortunately, this is the life

24:38

we're living in. We are becoming more

24:40

sedentary in our day-to-day lives. We're

24:42

sitting more. We're not going out as

24:44

much. There's younger kids uh on video

24:46

games. They're scrolling. There's so

24:48

much happening that is involving our

24:50

sedentary lifestyle, which is obviously,

24:51

like you said, increasing our risk of

24:53

type 2 diabetes, cardiovascular disease,

24:56

etc.

24:58

>> Yep. You can do it

24:59

>> like this.

25:01

>> There you go. 10 of those. If you do 10

25:03

of those, you can outweigh the benefits

25:06

of a 30 minute power walk

25:09

>> every hour.

25:10

>> Yeah. Yeah.

25:10

>> For how many hours?

25:11

>> 8.

25:13

>> Okay. So, I could set an alarm on my

25:14

phone.

25:15

>> Every hour. Just get up or every 45

25:17

minutes get up and do an air squat. And

25:20

this is primarily because have you heard

25:22

that when you eat you get a massive

25:24

spike of glucose. And the best way to

25:27

bring that glucose spike back down is by

25:30

doing any form of exercise. You can albe

25:32

it go out and go for a a fast run, do an

25:35

air squat, bring that uh bring that

25:37

glucose level back to baseline. And do

25:39

you think much about aerobic training as

25:42

a preventative measure for Alzheimer's?

25:45

>> I love aerobic training. Women are

25:47

facing a dilemma on social media because

25:49

they're being given so much information.

25:52

There is this huge uproar of should I do

25:58

zone 2 exercise or should I not do zone

26:01

2 exercise?

26:02

>> What is zone 2 exercise?

26:04

>> So we can think of uh physiology in

26:06

zones. Zone one is what you and I are in

26:09

right now,

26:10

>> right? Zone two is that next level up

26:13

and that's generally when we're looking

26:15

at exercising at around 60%

26:19

of our maximum heart rate and it's where

26:22

you can where you're jogging but you can

26:24

have a conversation but where you're

26:25

huffing and puffing. When we're

26:27

exercising we need to produce energy and

26:31

that energy firstly starts in the

26:33

mitochondria. So we need uh all of our

26:36

energy gets created. We create ATP and

26:39

that's how we are able to perform the

26:41

given task. As soon as we get out of

26:42

that zone and we go into zone 3, zone 4

26:45

and zone 5, we're producing energy

26:48

outside of the mitochondria in the

26:50

cytoplasm. And when we're doing that, in

26:54

order to do that, we're breaking down

26:55

glucose so fast via a pathway called

26:59

glycolysis. The byproduct of that is

27:02

lactate. And then we produce lactate and

27:06

that's actually a fuel source for the

27:08

brain. It's also a mioine, right? So

27:11

that's when we're in zone 3, zone 4,

27:14

zone 5. So a lot of women have been

27:18

doing zone 2. They've been going to the

27:20

gym. They've been doing zone 2. And I'm

27:22

trying to push women to get out of zone

27:25

2 for several reasons.

27:27

Not because it's not good for you. I

27:32

think all forms of exercise are good for

27:34

you. The more you move, the better,

27:36

right? But let's be really honest. A lot

27:40

of people in midlife are busy. They're

27:42

time poor. Men actually get a greater

27:45

return on investment by doing zone 2.

27:48

Women don't get the same return on

27:49

investment from doing zone 2. So, I'm

27:52

trying to push women to first work on

27:55

zone five, zone 3, zone 4, zone 5. If

27:59

they can, just do zone five.

28:01

Then do two to three sessions of

28:03

resistance training a week. And if you

28:04

have time left over, that's right there.

28:07

I've just described around 4 hours of

28:09

exercise. If you have time left over,

28:12

then you can work in zone 2. Now, zone 2

28:15

is great. If you're going to go out and

28:17

go for a long run, you're doing many

28:19

things. You are secretreting a lot of

28:21

BDNF, which we need. It's a growth

28:23

factor for the brain. You're getting a

28:26

massive uh amount of blood that's going

28:28

into the brain which is great as well.

28:30

It's sustained blood delivers oxygen and

28:33

nutrients to the brain. You're doing a

28:35

lot of things, right? But what you're

28:37

not doing is having a complete effect on

28:42

the chambers of your heart.

28:44

>> Is it better for me to do 5 km on a

28:47

treadmill or outside? I would say it's

28:50

better for you for the brain to do a

28:53

smaller amount of exercise and a higher

28:55

threshold

28:56

>> because I I was I think I read somewhere

28:58

one time that running outside is better

29:00

for the brain because it stimulates the

29:03

brain

29:03

>> of well you're outside so you've got so

29:05

many things around you. Imagine your

29:06

brain I told you it's got prime real

29:08

estate. Every part of the brain is

29:10

responsible for a different function

29:12

from what you see to what you hear. You

29:14

go outside and you can see so many

29:17

things. You've got forward ambulation.

29:19

So that's going to help you with drive,

29:21

motivation, dopamine, but then you're

29:24

also taking in the sounds, the senses.

29:26

It downregulates inflammation. So you

29:28

get so many other things from doing

29:30

that. Yes. But 5 km outside compared to

29:36

20 minutes of high aerobic physical

29:38

activity. What is better for the brain?

29:40

I would say that the zone 5 is better

29:43

for the brain. The zone 5 training does

29:45

a lot for the chambers of your heart as

29:47

well. Now, I'm going to grab this. We've

29:49

got a little model here, and we can see

29:51

that we have h a left chamber. We have a

29:55

right chamber, we have actually four

29:57

chambers of the heart, but we have

29:59

something in the heart called a

30:01

ventricle. We've got a left ventricle,

30:02

and we've got a right ventricle. Now,

30:04

the left ventricle delivers oxygenated

30:07

blood to the entire body. It's really

30:09

interesting because the chamber of the

30:11

left ventricle is like a is like a

30:14

muscle, right? It's responsible for

30:17

pumping blood to your entire body. It

30:20

first gives blood to the brain, which

30:22

means it's the most important part of

30:24

your body. After it's done giving blood

30:26

to the brain, it goes through to the

30:27

rest of the body. As we get older, we

30:31

get stiffening of these arteries. Okay?

30:34

Stiffening of all of the arteries in the

30:36

heart. and we get we get something

30:38

called left ventricular hypertrophy. So

30:41

that's when the ventricle

30:44

the left ventricle it starts to get

30:46

thicker and when it gets thicker that

30:48

means that we can't it's not as strong

30:50

it can't pump a lot of blood as much as

30:53

it could when it was younger to the rest

30:54

of the body. Ben Lavine, Dr. Ben Lavine,

30:57

he's a sports cardiologist and he did

30:59

this landmark study which changed how I

31:02

thought about zone 5 training. He took a

31:06

group of sedentary males, average age, I

31:09

think it was around 47 to 55, so around

31:12

50 years old, and he scanned their

31:15

hearts. He did, you know, he looked at,

31:17

he did echo cardiograms, he took photos

31:19

of the heart. He did everything he could

31:21

to see when they was first starting the

31:23

protocol, what does their heart look

31:24

like? He then subjected them to around 4

31:29

hours of exercise per week. And that was

31:31

stratified against he did one resistance

31:34

training session a week. One was

31:36

highintensity physical activity at

31:38

around 90% of the maximum heart rate,

31:40

the V2 max heart rate. And then in

31:43

between he did some long sessions as

31:45

well, right? But it was all moderate to

31:48

rigorous exercise and that was done over

31:52

two years. At the end of those two

31:54

years, what he found was that he

31:56

remodeled the heart by 20 years. So he

32:00

reversed the age related effects and

32:02

defects of the heart by 20 years.

32:05

Essentially turning the 50-year-old

32:07

hearts into 30-year-old hearts just from

32:10

physical activity alone.

32:12

>> 4 hours a week for 2 years.

32:14

>> 4 hours a week for 2 years.

32:16

>> And what kind of exercise was it?

32:18

>> So he got them to do like let's say for

32:20

example one of the um one of the

32:22

protocols was exercising at 90% of your

32:25

maximum heart rate. So when we do this,

32:28

we're generally looking at increasing

32:30

our V2 max. So you've probably heard

32:33

that V2 max along with strength, but V2

32:37

max is the strongest predictor of all

32:39

cause mortality, right? So if you want

32:42

to improve your V2 max and if you want

32:45

to get the heart related changes that he

32:48

did, what you want to do is you want to

32:51

do 20 minutes of V2 max per week just to

32:54

keep your V2 max because it does decline

32:56

year on and year out. Starting at the

32:58

age of around 35, we start to see a

33:00

decline in V2 max. So, if we want to

33:03

work on our V2 max, we want to be doing

33:07

a what we call the Norwegian 4x4. It's

33:11

the gold standard of increasing your V2

33:13

max. So, you want to get your heart rate

33:15

elevated to 90 to 95% for 4 minutes on,

33:20

4 minutes off, repeat four times.

33:24

So, how do I do this? Well, I actually

33:26

do this twice a week because the more

33:29

you do, the better. I do this on a

33:32

stepper. I do this at the gym and I put

33:36

my stepper onto I think I'm at like a

33:38

level 14 and I'm working my way up and

33:42

I'm staying on there for 4 minutes and

33:44

then I'm having a complete stop and a

33:46

complete rest for 4 minutes and I'm

33:49

repeating that four times.

33:52

>> Mhm.

33:52

>> So what I'm doing in that moment, I'm

33:54

not just getting a massive shunting of

33:58

blood to the brain. Okay, which is good.

34:01

I'm not just getting a massive release

34:03

of myioines and exocines to the brain.

34:07

I'm also remodeling the heart. I'm

34:10

downregulating tumor cell growth. I'm

34:12

improving my cognitive performance. I'm

34:15

doing so much more than just exercising

34:17

alone.

34:19

>> So that's once once a week in Lavine's

34:22

study that reversed these guys hearts by

34:25

20 years. Y

34:26

>> um

34:26

>> that you do that once a week. you only

34:28

have to do that once a week, but he also

34:30

did um he did around 70% of maximum

34:33

heart rate for around 2 hours a week.

34:35

And he also threw in one resistance

34:37

training session.

34:39

So consistency is key.

34:41

>> I'm just looking at some of the findings

34:43

of that study and one of the surprising

34:44

things is it showed that there is a

34:48

biological exploration date per se for

34:52

the reversal of the heart. Yeah. And

34:54

then the heart retains its plasticity,

34:56

the ability to remodel itself until the

34:57

age of 65. If this intervention had

35:00

started after the age of 65, the heart

35:02

was too stiff to be physically remodeled

35:04

to get that 20 year reversal.

35:06

>> Yeah.

35:06

>> You have to start in late middle age.

35:09

>> Exactly. So midlife is the window of

35:12

opportunity for brain health and for

35:15

longevity.

35:16

>> I didn't realize you could sort of

35:18

remodel the heart yourself. That's

35:19

interesting.

35:20

>> Yeah, you can remodel the heart. And the

35:22

heart is amazing. Okay. Because what you

35:24

see with the aorta, right? So the aorta

35:27

goes up and we've got we've got two

35:29

we've got uh the main blood supply for

35:31

the brain exist in the vertebral

35:33

arteries. Okay? So there's branching off

35:35

of the aorta comes from the heart.

35:37

Vertebral arteries which supply the

35:39

posterior part of the brain and the

35:40

cerebellum with blood. And then you've

35:43

got the corroted arteries. So one on

35:45

each side branching off the aorta which

35:47

supply the uh frontal and middle part of

35:50

your brain with blood. The brain is the

35:52

most vascular rich organ in the entire

35:54

body. In times of stress such as

35:57

hypertension, okay, that is elevated

36:02

blood pressure. We see that we can

36:04

actually kill off the tiniest parts of

36:08

the blood vessels which are called the

36:10

capillaries. You can see the capillaries

36:11

up here. They supply even the bloodb

36:14

brain barrier. So they supply mainly the

36:16

outer cortex of the brain with blood.

36:19

When we have elevated blood pressure,

36:22

we are starting to kill off those tiny

36:25

little capillaries of the brain. Those

36:26

capillaries are feeding different

36:29

neurons in the brain and also feeding

36:32

the bloodb brain barrier. So when we get

36:35

breaking off of these, we lose the blood

36:37

supply, we lose the oxygenation, we get

36:40

um a breakdown of the bloodb brain

36:42

barrier itself, which is scary. And we

36:44

see that in patients who have got mild

36:47

cognitive impairment. You can call it,

36:49

you've heard of leaky gut, we can call

36:50

it leaky brain. If you have a leaky

36:53

brain, what happens eventually is so

36:55

your bloodb brain barrier sits like

36:58

this. Okay? And there are cells and we

37:00

call them parasites for example and

37:03

they're bound together by tight

37:05

junctions. That's what the bloodb brain

37:06

barrier is. It's like a you think of the

37:09

bloodb brain barrier as the bouncer of a

37:12

nightclub. They are all standing there

37:14

like this responsible for who can come

37:16

in and who can't. and they don't allow

37:18

some molecules to get in. But over time,

37:21

when this starts to degrade and become

37:23

leaky, they start to spread apart. And

37:26

when they do, you can have the passive

37:29

diffusion of all these molecules coming

37:31

in. And that's really bad for your

37:33

brain. So, we want to maintain the

37:35

integrity of the bloodb brain barrier by

37:37

maintaining the capillary health. We

37:40

don't want the capillaries to die.

37:42

They're one cell thick. Any type of

37:44

damage can damage them and kill them.

37:47

hypertension. There was a really great

37:48

study. It was called it was actually the

37:50

sprint trial and it was it's now the

37:52

gold standard for the recommendation of

37:55

120 over 80. What's

37:57

>> that?

37:58

>> So when you have your blood pressure

37:59

taken, we get the systolic over

38:02

diastolic. And you've probably I don't

38:03

know if you take your blood pressure,

38:05

but doing your blood pressure every day

38:07

is a really great inexpensive and

38:10

effective tool for maintaining good

38:13

brain health. So you measure your blood

38:16

pressure and if you are hypertensive

38:20

this is anywhere over

38:23

135

38:24

okay systolic over 135

38:28

that's when things start to break down

38:31

that's when we start to get the

38:32

breakdown of those small one cell thick

38:35

capillaries. So in this trial, in the

38:38

spring trial, what they found was that

38:40

when they aggressively manage these

38:43

patients and they bring their blood

38:45

pressure down, they did it

38:46

pharmacologically through something

38:48

called an ACE inhibitor. It's a

38:49

medication to drive down blood pressure.

38:51

When they bring it down

38:52

pharmacologically, these patients

38:55

preserved their brain gray matter and

38:58

their cognitive functions. So we now

39:00

have a gold standard. And this is what I

39:02

would recommend anybody on Amazon. And

39:04

it costs about $25 for a blood an

39:07

automatic blood pressure monitor. Do it

39:10

every single morning and watch your

39:12

blood pressure.

39:12

>> And then if it's high, what do I do

39:14

about it?

39:15

>> Well, outside of pharmarmacology, if we

39:17

don't want to take a medication, we want

39:19

to get stronger. And we want to do this

39:21

via exercise.

39:23

Stress is one of the biggest things

39:25

driving high blood pressure. manage

39:27

stress, manage cortisol, manage chronic

39:30

inflammation by way of exercise, sleep,

39:33

all of the things that mother nature

39:34

gave us.

39:36

>> I was just looking at the um the study

39:37

that reversed the heart by 20 years and

39:40

trying to figure out what exercises they

39:42

did. And as you said, the first one was

39:43

a highintensity workout, the 4x4.

39:46

>> Um then they did a long aerobic

39:48

exercise. Again, this is all once a

39:49

week. So 60 minutes once a week doing a

39:52

longer exercise like it could be hiking

39:55

or tennis or cycling. a moderate

39:56

intensity workout, 30 minutes where they

39:59

did the talk test, you should be able to

40:00

break a sweat but still be able to

40:02

speak. So that was once a week. And then

40:04

lastly, strength training once a week.

40:05

So it's really a variety

40:07

>> of exercises that caused such a profound

40:09

impact on the heart.

40:13

>> And I think cardiovascular diseases are

40:15

the single biggest killer.

40:17

>> Yeah. Cardiovascular disease,

40:20

dementia is the number one killer of

40:22

women in the UK. The number one

40:25

>> really. It's the number one cause of

40:26

death in Australia for both men and

40:29

women.

40:30

>> How does it kill you? Because we all

40:31

think about memory loss and stuff like

40:33

that, but

40:34

>> and so this is the actual devastating

40:36

part. We don't die of Alzheimer's

40:38

disease specifically. Over time, what

40:41

happens is in these patients, you have

40:43

to remember Alzheimer's disease is like

40:46

endstage cancer. Once you get the

40:49

diagnosis, there is no cure. There is no

40:51

going back. There is no reversal. you

40:54

have the disease and that's the scariest

40:57

part. Mild cognitive impairment, you can

41:00

slow the progression of that. Like I

41:02

said to you, it goes for 20 years. Mild

41:04

cognitive impairment, you can slow the

41:06

progression of mild cognitive

41:07

impairment, but as soon as you get

41:09

diagnosed on that awful day that your

41:12

mother or your friend gets diagnosed

41:14

with Alzheimer's disease, it's a sad

41:16

day. And what ends up happening with

41:18

these patients is you can die of

41:21

esphyxiation. You can die of you. Your

41:25

brain loses the signal to swallow. It

41:29

loses the signal to maybe you fall

41:32

because you've lost balance. It's really

41:35

it's a really scary moment, but it's not

41:37

like you die of Alzheimer's disease

41:40

specifically.

41:42

If you were diagnosed with Alzheimer's

41:44

disease,

41:48

it's an interesting reaction.

41:51

>> Because I would have no hope. I think a

41:54

a better question is

41:56

>> you'd have no hope.

41:57

>> If I was diagnosed with Alzheimer's

41:59

disease, there is nothing I could do.

42:03

>> How would that change

42:06

your life and the decisions you make? Or

42:08

would it at all? I would aggressively

42:12

aggressively exercise. I would monitor

42:15

my diet. I would aggressively monitor my

42:18

diet and I would potentially have a

42:20

ketogenic diet because what we've found

42:22

is that during this metabolic crisis

42:26

that happens in your brain, okay? Where

42:28

you lose the ability to use glucose as

42:31

your primary fuel source. So the brain

42:34

doesn't know how to use glucose as its

42:37

primary fuel source. So it's under

42:38

attack. during Alzheimer's

42:40

>> during Alzheimer's but also during this

42:43

window in of for women as well in the

42:45

pmenopause state. So the brain cell when

42:48

it's under attack and it can't utilize

42:49

glucose effectively and it doesn't have

42:51

any energy it starts to think about

42:54

survival. It starts to think what can I

42:56

do? I'm under attack. So it starts to

42:59

break down the myelin sheath. And in

43:02

that moment it's actually the

43:03

aststerittes they're the supporters of

43:05

the brain so of the brain cells. So they

43:08

start to think okay let's break down the

43:10

myelin sheath from that the astroytes

43:14

produce ketone bodies and then the

43:16

ketone bodies get shuttled into the

43:17

brain and that's how we use uh energy in

43:20

the brain. So in that state of metabolic

43:23

crisis I would make sure that I am

43:27

having a ketone rich diet or I may be

43:31

getting exogenous ketones. I would

43:33

aggressively exercise. I would

43:35

aggressively manage my my lipids. I'd

43:37

have a high intake of omega-3 fatty

43:40

acids and I would preserve if I could

43:42

any form of cognitive function by way of

43:46

talking to people by going outside,

43:49

socializing, having hard conversations

43:51

if I was intact and I could do so. I

43:54

would throw tennis balls to the wall.

43:58

So on that point of the ketogenic diet,

44:02

the reason is because ketones are an

44:03

alternative fuel source to glucose.

44:06

>> Y

44:07

>> and the brain likes ketones.

44:10

>> The brain loves ketones and it actually

44:12

utilizes them more effectively than

44:14

glucose. But glucose is the primary fuel

44:17

source for the brain. And here's what's

44:19

really interesting uh and devastating if

44:22

you will for females during the onset of

44:25

pmenopause, right? when we see a decline

44:28

in estrogen, right? We see a decline in

44:32

estrogen, what happens is a 30%

44:35

reduction in brain glucose metabolism.

44:38

So, when these receptors start to die

44:41

because we don't have uh we don't have a

44:43

lot of estrogen circulating in the

44:45

bloodstream anymore, what happens? Well,

44:48

we can't utilize glucose as effectively.

44:51

So during that state, that's when we

44:53

start to get the breakdown of the myelin

44:55

sheath to use that as uh as ketone

44:58

bodies as an alternative brain fuel

45:01

source.

45:02

>> So do you think women going through

45:03

menopause should be

45:06

considering a ketogenic diet? Yes, I do

45:08

think that I think that women who are

45:10

going through pmenopause and who are at

45:13

the mercy of this brain energetic crisis

45:17

should be adopting if they can a

45:19

ketogenic diet. It's one of the best

45:21

diets for the brain.

45:24

>> I didn't really understand this idea

45:25

that during menopause there was a

45:29

glucose

45:30

deficiency or metabolism problem in the

45:32

brain.

45:32

>> 30% reduction in brain glucose

45:34

metabolism. Is this why women report to

45:36

having brain fog and all these kinds of

45:39

things?

45:39

>> Yeah, absolutely. Because when the brain

45:41

can't utilize its fuel source

45:43

effectively, what happens? Well,

45:46

metabolites start to shift. We don't

45:49

sleep properly. Around 60 to 65% of

45:53

women in menopause report having a hot

45:56

flash or night sweats. It wakes them up

45:58

at night. That's also causing cognitive

46:01

decline and brain fog. So, I mean, this

46:05

graph is pretty shocking.

46:06

>> Um, can you explain what it shows?

46:09

>> Oh, this is showing the um estrogen

46:12

levels at birth going through all of the

46:14

life cycles that a woman will go

46:16

through, puberty, pmenopause, and then

46:18

eventually menopause. There is one thing

46:21

that is certain.

46:24

After age, I mentioned earlier being a

46:27

woman is the next strongest risk factor

46:29

for getting this disease,

46:31

>> forgetting Alzheimer's. forgetting

46:32

Alzheimer's and that largely lies in our

46:37

par in our menopausal shift that occurs

46:40

the downsizing of estrogen. However, we

46:44

do have forms of estrogen that we can

46:47

you know supplement with.

46:48

>> So I just need to keep the estrogen up.

46:50

>> Yeah.

46:50

>> Because then the brain health is going

46:52

to be up and normal.

46:54

>> This is where the controversy lies. Yes

46:56

and no. So I want everyone to understand

46:58

I am sitting right now. So my entire

47:00

doctoral thesis is focused on women and

47:03

Alzheimer's disease and I'm Switzerland

47:06

right now when it comes to hormone

47:08

replacement therapy. That is replacing

47:11

your hormones.

47:12

>> You're Switzerland.

47:12

>> I'm Switzerland. Meaning that there is

47:15

no evidence to suggest right now we

47:18

don't have largecale randomized control

47:20

trials to show that hormone replacement

47:22

therapy prevents dementia. So what I

47:25

will tell you is this. It is a signal.

47:27

It is a supporter. It will help you do

47:31

the things that can lower your risk of

47:34

dementia. We've seen multiple times that

47:39

having hormone replacement therapy can

47:41

reduce your risk of getting Alzheimer's

47:43

disease by up to 30%. We know that. But

47:46

it's not because estrogen alone is

47:50

minimizing your risk. It's because when

47:53

you have estrogen, it helps get rid of

47:56

the hot flashes. It helps with the night

47:58

sweats because during menopause when we

48:01

actually have a disregulation of the of

48:04

estrogen in our brain, what happens in

48:06

the hypothalamus which is an area in the

48:09

brain that controls our temperature

48:11

regulation when we lose the ability to

48:14

monitor our temperature for a woman.

48:17

What will happen is when she feels the

48:20

slightest bit hot, her temperature, you

48:24

know, is rising a little bit. The

48:26

hypothalamus doesn't know what to do.

48:27

So, it signals, I'm super hot. So, it'll

48:29

raise your temperature right up, and

48:31

that's a hot flash. And then it'll bring

48:32

it right down. And as a result, this is

48:35

keeping women up at night. And we know

48:37

that sleep deprivation is a risk factor

48:39

for Alzheimer's disease. Of course, it

48:40

is. compounding sleep deprivation will

48:45

accumulate amaloid beta in your brain.

48:48

So if we can replace if we can use

48:51

hormone replacement therapy as a signal

48:53

and as a support to help us sleep at

48:56

night then that's a good thing. Another

48:59

thing estrogen is anabolic to muscle.

49:03

>> What does that mean?

49:04

>> It means that it helps with muscle

49:06

protein synthesis.

49:07

>> Oh it helps me make muscle.

49:09

>> Yeah. We've got estrogen receptors on

49:10

our bone. We've got estrogen receptors

49:12

on our muscle. So if estrogen is

49:15

anabolic to muscle, if estrogen helps

49:19

with muscle protein synthesis, if

49:23

estrogen helps with bone mineral

49:24

density, then replacing estrogen during

49:27

that menopause state is going to help us

49:30

with all of the risk factors of

49:31

Alzheimer's disease.

49:33

>> So when does estrogen I mean it really

49:36

in this image drops off a cliff

49:37

>> and Yeah. And it varies. So it tends to

49:40

generally happen at around 45 years old

49:42

as an average and that that pmenopause

49:45

stage lasts around 10 years

49:48

>> but it starts going down on this graph

49:50

at about 30.

49:51

>> It starts to go down and everyone's

49:53

different. Okay, you can have a woman in

49:55

her late 30s go into pmenopause or the

49:58

general age is around 42 to 45. Most

50:01

OBGYNS that I've spoken to say that you

50:04

need to start checking in with your

50:07

doctor at around 40 years old to check

50:09

for this.

50:10

>> So, do you thinking about my fiance now,

50:12

do you think that

50:14

someone like her should go on hormone

50:17

replacement therapy at like 40?

50:18

>> Well, so that's the that's the big

50:20

question. That's the elephant in the

50:21

room. Should you go on hormone

50:22

replacement therapy or should you not?

50:24

And that's definitely a conversation

50:25

between you and your physician. However,

50:28

we've got largecale studies right now to

50:31

show that we don't have to be afraid of

50:34

hormone replacement therapy. And without

50:36

going too deep into the weeds, there was

50:38

a massive study that was done, the women

50:40

women's health initiative, that scared

50:42

women out of taking hormone replacement

50:45

therapy in fear

50:47

>> of getting breast cancer. Correct. We

50:49

went from having 40% of women on hormone

50:53

replacement therapy to just 4% of women

50:56

on hormone replacement therapy. We know

50:58

that even at the onset of menopause, a

51:02

woman's risk of having a heart related

51:05

event triples. A woman's risk of getting

51:10

Alzheimer's

51:11

disease increases. So there is something

51:15

to posit here about the benefits of

51:17

hormone replacement therapy that we

51:20

still haven't yet studied.

51:22

>> Will you do hormone replacement therapy?

51:24

>> I definitely will.

51:25

>> And what kind of hormone?

51:26

>> And look, so this is really interesting.

51:28

So um this was given to me by a friend

51:30

and there's this is the um this is the

51:32

capsule. So this is estradile and

51:35

progesterone. Okay, so progesterone is

51:38

that one that's going to help you sleep

51:39

at night. This one here is vaginal

51:42

estrogen. So, this is a cream that

51:45

actually gets uh you know, depending on

51:47

how it is, it can get inserted and the

51:50

vaginal estrogen apparently if you put

51:52

it on your face is probably the best

51:55

form of skin care that you could ever

51:57

have. Yeah, we have estrogen receptors

52:00

all over our tissues, including our

52:02

skin. These are estradiol inserts. So,

52:05

that's not the cream itself, but if you

52:07

get vaginal estrogen in the form of a

52:08

cream, you can put it on your face and

52:10

it can help with skin elasticity,

52:13

collagen, uh dermal thickness. This is

52:15

why I'm actually most excited about it.

52:18

>> So, I mean, is this are these the only

52:19

ways that one can do hormone?

52:22

>> No, there's also um a patch, and that's

52:24

what most women are opting in for. The

52:26

transmal patch

52:27

>> when the time comes.

52:28

>> Uh I will probably do the the the patch.

52:32

>> Why? because it's the the easiest.

52:34

That's the one that um I've researched

52:36

the most. Uh I'm not afraid of hormone

52:38

replacement therapy in the slightest.

52:40

You do have to, you know, everyone has

52:41

to check with their doctor, but I

52:44

definitely think that this is going to

52:46

be one thing that is going to help with

52:48

the Alzheimer's disease crisis that is

52:51

occurring.

52:53

>> Go ahead.

52:54

>> I mentioned earlier plaques, right? So a

52:58

lot of people ask well what

53:00

distinguishes Alzheimer's disease from

53:03

the rest of the dementias and it comes

53:06

down to two proteins amaloid beta and

53:09

tow protein and here's where it gets

53:11

really interesting and actually dates

53:13

back to 1901 the first ever Alzheimer's

53:16

disease patient Augusta she was 52 years

53:20

old and she went to the hospital her and

53:22

her husband went complaining of

53:25

difficulties of word finding

53:28

word fluency and she couldn't remember

53:30

where she put her keys and her husband

53:34

said she is delirious and Augusta told

53:38

the doctor on board he was a

53:41

psychiatrist his name was Eloise

53:43

Alzheimer she said to him and I quote I

53:47

don't know who I am anymore

53:50

as I mentioned this disease robs you of

53:52

who you are in 1906 066 August busted

53:57

died and that was the first ever patient

54:02

to be recorded of having Alzheimer's

54:05

disease and so postmortem they cut her

54:09

brain open and they found that she had

54:11

these plaques in her brain and they

54:13

didn't really know they didn't really

54:14

understand what it was but that was the

54:16

first ever induction of this disease in

54:19

society and ever since then ever since

54:22

then we are still trying to tackle this

54:24

disease in the 2000s We had this notion

54:28

that Alzheimer's disease was the amaloid

54:30

cascade hypothesis. Meaning that great

54:33

Alzheimer's disease means when you get a

54:35

head full of amaloid, this toxic protein

54:37

that builds up. So we were demonizing

54:39

this protein. We were demonizing this

54:42

peptide protein that builds up in the

54:44

head. And so then came the medications,

54:48

okay? In the form of IV drugs. So you go

54:52

to the hospital, you get an IV in the

54:54

promise that it will clear out amaloid.

54:57

Great, we've got a cure. But what they

54:59

found was that when they were taking out

55:01

the amaloid in these brains, they were

55:03

taking with them brain tissue and

55:06

causing microhemorrhages.

55:08

And in some patients, it was resulting

55:11

in death.

55:13

So we now know that the problem here

55:18

isn't amaloid. In fact, amalloid is a

55:23

antimicrobial peptide. So, amaloid is

55:27

actually a good thing. Amalloid beta is

55:31

a good thing because it protects the

55:33

brain cells. Now, here's what happens.

55:36

We have this beautiful process during

55:38

sleep that occurs when we get into deep

55:41

sleep. We activate the glimpmphatic

55:44

system. Okay? So, the glimpmphatic

55:47

system comes from the word gals. Gal

55:50

cells. We have gleal cells in the brain.

55:52

They sit outside of the neurons and this

55:55

is what uh is responsible for immunity.

55:59

They're our chief um immune response

56:01

cell. During deep sleep they shrink and

56:04

when they shrink all of this amaloid

56:06

beta that's floating around in the

56:08

cerebral spinal fluid gets washed out.

56:11

So it's like a washing machine that

56:13

occurs in your brain. Right? But what

56:16

tends to happen in Alzheimer's patients

56:18

is they don't get a chance to wash out

56:21

the amaloid. What happens in pmenopause

56:25

and menopause due to the hot flashes,

56:27

you don't get to get into deep sleep

56:29

because you're having a fragmented sleep

56:30

because you're waking up due to hot

56:32

flashes and night sweats. So that is

56:34

what's do that is what's causing the

56:36

buildup of amaloid. Now stick with me.

56:39

We've got another protein that is a

56:43

hallmark of Alzheimer's disease. It's

56:45

towel protein and towel lives in the

56:48

axon of the cell. The one that I said is

56:51

covered in the myelin sheath and what

56:54

happens under times of stress. What

56:57

happens is this tow protein

57:00

phosphorolates.

57:01

So it breaks off and basically tow

57:05

protein stabilizes the microtubules.

57:08

Okay, imagine these railro road tracks

57:11

in the axon, okay? Just going up and

57:13

down the axon.

57:14

>> The axon's in the in the cell or in the

57:16

brain.

57:16

>> And so the the the brain cell itself,

57:18

the neuron is the neuron cell body and

57:21

the axon is like the trunk of the tree.

57:24

>> Okay.

57:25

>> Right. So holding up the tree are

57:28

microtubules and those microtubules are

57:31

bound by tow proteins. The the tow

57:33

proteins keep the microtubules intact.

57:35

So the trunk of the tree is stabilized

57:38

and it sits there. Why does it need to

57:40

be stabilized? Because that's how speed

57:42

of thought travels. Information

57:44

processing speed travels up there. When

57:48

the tow protein phosphorolates,

57:50

it starts to form tangles. They're

57:53

called neuroiary tangles. So that

57:56

happens in the axon. And when all these

57:58

tangles clump together, we get the

58:01

collapse of this axon, the collapse of

58:05

these microtubules.

58:06

So we're not just having a cascade of

58:10

environmental disaster inside the

58:12

cerebral spinal fluid of the brain and

58:14

inside the brain, outside the cells.

58:16

We've also got this cascade happening

58:18

inside the cell body itself. So the

58:21

brain is under attack inside the cell

58:23

and outside the cell.

58:25

>> Why? Why exactly? Why? Why does this

58:28

happen? Because of how we treat our

58:30

brains.

58:32

>> Because of how we treat our brains.

58:33

>> Yes. The reason why your brain is

58:36

hyperphosphorilated and the reason why

58:38

these tower proteins are

58:40

hyperphosphorilated is because of many

58:42

things. One is we have seen time and

58:45

time again that we have estrogen

58:48

receptors

58:50

that are on in the brain cell themselves

58:53

in the axon. So when we don't have

58:55

adequate estrogen, estrogen actually is

58:59

so smart what it is doing, it's blocking

59:02

an enzyme that is responsible for

59:06

phosphorolating

59:08

the towel. So if we don't have the

59:10

estrogen there,

59:13

then the towel, the enzyme is there to

59:15

phosphorolate the towel and break it

59:18

down and cause these neuropiary tangles.

59:20

But let's just say you're a man and you

59:22

don't have you don't need the testo you

59:24

don't need the estrogen there. Although

59:26

testosterone is neuroprotective.

59:28

Testosterone actually aromatizes into

59:31

estrogen which is why you actually have

59:34

an extra added protection in your life.

59:37

Um

59:39

what else causes this? Well stress.

59:41

>> You're talking about sleep there.

59:42

>> Yeah. So sleep is, I think, by far the

59:45

most underrated

59:47

Alzheimer's disease prevention tool that

59:50

we have. It's underrated because

59:53

we have been doing it all our lives and

59:55

we think that we can just go to sleep

59:57

and the magic happens. But I think now

59:59

in 2026, we actually need to train for

60:03

sleep. So during deep sleep we activate

60:07

the glimpmphatic system and sadly a

60:10

large proportion of us aren't getting

60:12

into deep sleep. So sleep is uh one of

60:15

the reasons.

60:16

>> How do you sleep?

60:18

>> Yeah, I sleep I make sure I sleep 7 and

60:20

1/2 hours a night.

60:22

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61:53

A lot of people struggle with sleep and

61:56

um they've just kind of gotten used to

61:58

it. I hear this from friends of mine

62:00

that will say, you know, I'm a bad

62:01

sleeper. I'll sleep for 5 hours. And

62:02

they kind of have just gotten used to

62:04

it. Do you think that's okay?

62:07

>> No.

62:09

And they will pay for this in their 60s

62:12

and 70s.

62:13

>> How do you know?

62:14

>> Because I know that just one night of

62:16

sleep deprivation is raising your risk

62:18

of amaloid beta by at least 4 to 5%.

62:23

just one night.

62:25

>> So you can imagine the accumulation of

62:27

this. Not only that, we know that you're

62:30

interrupting with the hormones that are

62:32

responsible for hunger and society. We

62:34

know for hunger and satiety. We know

62:37

that you're increasing your risk of type

62:40

2 diabetes with um sleep deprivation.

62:43

But not just that, we also see that this

62:47

compound effect can't be reversed.

62:50

Meaning that a lot of people think, I'll

62:53

just sleep for 6 hours a night and then

62:55

just bank on it on the weekend. But

62:57

sadly, that's not how our brain works.

62:59

It's not like debt that we can repay to

63:01

the bank.

63:02

>> I heard from Matthew Walker the other

63:04

day though that we can save it up. He

63:06

said um he said you can't make up for

63:08

lost sleep.

63:08

>> Exactly.

63:09

>> But if on Monday I've got something

63:11

where I know I'm going to be deprived.

63:13

He says on the weekends like Saturday

63:15

and Sunday, if I got a huge amount of

63:17

sleep, it's kind of like

63:18

>> I can use that. Yeah, it's kind of like

63:21

Yeah, it's kind of like the reserve.

63:22

Yeah, actually I do this. I do long haul

63:25

flights. I'll be it like 6 hours between

63:28

LA and New York, but also to Australia.

63:30

And so if I know I'm going on a long

63:32

haul flight, I'll bank on my sleep for

63:35

about a week leading up to that cuz I

63:37

know I'm going to be sleepd deprived on

63:38

the plane. So, if you were one of those

63:40

people that struggles with sleep, that's

63:41

listening right now and they're slightly

63:43

concerned that, you know, you talked

63:45

about this um glimpmphatic system which

63:47

sort of comes out at night and cleans up

63:49

the brain

63:50

>> and they're hearing, you know, my

63:51

glimpy system isn't going to be optimal

63:53

if I'm not sleeping.

63:54

>> If that was you, and for whatever

63:56

reason, you start sleeping poorly.

63:58

>> Mhm.

63:59

>> What would you do about it?

64:01

>> I would get really serious about

64:03

examining my lifestyle the day before.

64:07

So, this generally involves two things.

64:09

You have to ask yourself, are you having

64:10

trouble falling asleep or are you having

64:12

trouble staying asleep? A lot of

64:16

women report trouble falling asleep,

64:20

meaning they've got a racing mind. Men,

64:22

too, they've got this racing mind. They

64:24

can't, you know, just stop that default

64:27

mode network and the the racing thoughts

64:29

that happen. That's one thing.

64:32

And then there's the I can't stay asleep

64:35

meaning that uh I'm waking up due to

64:38

heat. I'm waking up because uh I'm

64:40

stressed and I'm having bad dreams.

64:42

There's all different reasons as to why

64:43

you wake up. So for the person who is

64:46

having trouble falling asleep at night,

64:48

I would strongly recommend

64:51

introducing a supplement called GABA,

64:55

which is gamma aminoic acid. It's our

64:59

chief inhibitory neurotransmitter.

65:02

And when you have this, it really helps

65:05

stabilize all those thoughts. It helps

65:06

with erasing mind and it can help calm

65:09

you down at night. The next thing I'll

65:12

do is I will think about what I'm

65:15

eating. Actually, it turns out that um

65:18

eating starchy vegetables, something

65:20

that's going to make you like, you know,

65:22

sweet potatoes for example, it's going

65:24

to have a better benefit uh backloading

65:27

uh your carbs at night for helping you

65:29

sleep. If you start training for sleep

65:33

as if sleep is your marathon and start

65:35

preparing for that at 8:00 p.m. at

65:37

night, getting off, you know, don't

65:40

email, don't have any hard

65:41

conversations, don't watch anything

65:43

crazy at night, you'll settle your mind

65:46

down, you'll settle your nervous system

65:48

down,

65:50

but where I think uh most of the

65:52

optimization occurs is when you're

65:55

actually in sleep. I would also work on

65:59

um sleep regulation. So, what we know is

66:02

that in order to fall asleep and stay

66:03

asleep, our core body temperature needs

66:05

to drop at least 2°. And I'm doing this

66:09

with a temperature controlled mattress

66:11

cuz it's working on thermal regulation.

66:13

A lot of people who don't have that can

66:16

do uh several things like sleeping with

66:18

their feet outside of the sheets or turn

66:21

turning the the air conditioning on, the

66:23

thermostat on to cooling the room, to

66:24

cooling down your body temperature, core

66:26

body temperature. One thing that um you

66:28

can supplement with is glycine, which I

66:32

think is amazing because it helps with

66:33

sleep by way of temperature regulation.

66:37

It can bring down your core body

66:38

temperature. And in fact, and I don't

66:40

know too much about the mechanism behind

66:41

this, glycine itself has one of the

66:46

greatest longevity benefits for

66:49

improving lifespan. So, taking glycine

66:52

can also help with that. Now, in terms

66:54

of the person who is having trouble

66:57

staying asleep,

66:58

>> what about this one? You don't talk

67:00

about the um the old ashwagandha.

67:03

>> Oh, yeah. Ashwagandha is great. Okay.

67:05

Ashwagandha is going to help you with

67:09

stress. And you've got here Ashwagandha

67:12

rodeiola. So, what they both are, they

67:15

are adaptogens.

67:17

And basically an adaptogen is great

67:19

because it it goes in and it adapts to

67:22

what is happening in your body. So let's

67:24

just say you have elevated cortisol. And

67:27

this tends to happen you know during

67:29

different cycles during the day mainly

67:31

during the uh daytime when we wake up

67:33

where cortisol levels are at its peak

67:35

but it can also happen at night. Having

67:37

this can actually stabilize that

67:40

cortisol because it can go in and

67:41

combine to cortisol and bring it down.

67:44

likely if something is not elevated and

67:47

it's low, it can bring it up. So, it's

67:49

really good. It's an adaptogen and

67:52

studies show that you can actually take

67:54

this three times a day and you won't

67:56

feel fatigued. It doesn't disrupt

67:58

anything and it pairs really well with

68:01

caffeine, for example. So does

68:02

theineine. So, this is actually a really

68:04

great um adjunct to your supplement

68:07

stack. And you really talk about how you

68:10

need to sort of warm up to warm down or

68:13

warm up to go to sleep.

68:14

>> Oh, yeah.

68:15

>> Starting at like 7:00 p.m.

68:16

>> Yeah. Starting at like 8:00 p.m. And

68:18

that's in line with circadian rhythm and

68:20

circadian biology. You want to try and

68:22

when it comes to sleep and your

68:25

circadian rhythm, you kind of want to

68:27

mimic the sun and mother nature. And

68:30

when does the sun start to go down? It

68:32

starts to go down at around 8:00 p.m.

68:34

depending on where you are in the world.

68:36

And

68:38

when this happens, we also get the

68:40

natural release of I love that you're

68:43

taking that, by the way. You must be

68:44

stressed right now. You get the natural

68:47

release of melatonin. So melatonin is

68:50

that sleepy hormone that gets released

68:52

in response to darkness. This may also

68:54

be another reason why somebody somebody

68:56

is having trouble falling asleep and

68:58

staying asleep. So we want to get the

69:00

natural release of that. So, these bio

69:03

hacks that occur right now, sleeping

69:05

with our red light mask on, dimming the

69:07

lights. Look, dimming the lights is

69:09

great. Um, I've actually replaced all of

69:11

my light bulbs um at home with in my

69:15

bedroom as well with red light bulbs.

69:17

So, I'm getting um I'm getting rid of

69:20

the blue light, the junk light. I'm

69:21

replacing it with red light to help down

69:23

regulate the nervous system. Yes, I do

69:26

wear blue light blocking goggles or

69:28

glasses, I should say. Do I think that

69:30

they're providing an immediate and huge

69:34

benefit? I don't know. But they could

69:36

have a minor benefit there. So warming

69:40

down involves doing these things that

69:41

are going to help you downregulate your

69:44

nervous system so you can fall asleep

69:46

faster.

69:48

>> Sticking on supplements for a second.

69:52

Omega-3.

69:53

>> Yes.

69:53

>> Um I've got some omega-3 here. I've got

69:55

two of them here. Mhm.

69:57

>> But when I brought both of them out, you

69:59

said that I've got to be quite careful

70:00

about what brand I buy, but also

70:02

something about temperature.

70:04

>> So, by far out of all of the

70:06

supplements, omega3 is probably the only

70:10

one that you have to make sure that you

70:14

look at the supplement label for there.

70:17

There was this study that was done that

70:19

showed that around 95%

70:23

of the most popular omega-3 supplements

70:26

in the US, and there was about 85 of

70:28

them that were tested, exceeded the

70:31

normal oxidation level, meaning that

70:35

these pills, because they're omega-3

70:38

fatty acids, they come from fish oil,

70:39

they are oil, they can become rancid and

70:43

oxidized. And they usually do this when

70:46

they're in a heated environment. Here

70:48

are the here are the rules of thumbs.

70:50

One, you want to look for a manufacturer

70:52

that is highly credible and that is

70:55

certified.

70:57

>> Certified.

70:58

>> Yeah. So NSF certified. So it's an

71:01

external governing uh board that

71:03

certifies them on, you know, everything

71:06

heavy metals. They make sure that the um

71:08

oxidation levels are met and they make

71:10

sure that, you know, what's in the

71:11

capsule is actually in the capsule.

71:13

That's another thing that is scary. The

71:15

supplement industry is highly

71:17

unregulated. And I treat my omega-3s the

71:20

same way I treat my olive oil. You want

71:23

to get oil that is sourced in the area

71:26

that you are. We're in California right

71:28

now. So, you might want to find an

71:30

omega-3 that is sourced in California.

71:33

>> Do I want to put it in the fridge?

71:34

>> You want to put it in the fridge the

71:35

moment that you get it.

71:36

>> Really? Yeah.

71:37

>> Why does nobody talk about that?

71:38

>> I'm not sure. But, um, it's just the

71:41

same as olive oil. You don't want the

71:43

olive oil to become rancid, so you don't

71:44

leave it near the near the stove. You

71:47

want to put it in a cupboard away from

71:49

the stove.

71:50

>> And these are good for the brain.

71:52

>> Oh, omega-3 is by far uh one of the most

71:55

potent stimulus that you could have for

71:56

the brain. They help with cell membrane

71:59

fluidity. So, where your cells meet

72:02

neuron to neuron, they create something

72:03

called a syninnapse. And in order for

72:05

that to occur, we have a massive influx

72:08

of all of these neurotransmitters,

72:11

dopamine, serotonin. We've also got

72:13

calcium and potassium. And these help

72:16

our brain cells communicate. Okay? We

72:19

want to make sure that our membranes,

72:21

the cell membranes are fluid and they

72:24

glide in order to help with that

72:26

synaptic transmission. Another thing

72:28

that they do is

72:31

they are comparable to an NSAID, an

72:36

anti-inflammatory

72:38

medication.

72:39

These have massive anti-inflammatory

72:42

effects. In fact, I think that these

72:45

have the safety profile of an FDA

72:49

approved drug and there's only benefits

72:52

from it. There's no side effects from

72:53

it. Uh not just that 60% of our brain is

72:58

made of fat.

73:01

70% of that is made of DHA. And DHA

73:07

comes from omega-3 fatty acids. So why

73:10

do I not want to replace my brain or the

73:14

fat in my brain with what it's made of?

73:17

And that's what you do when you have

73:18

omega-3 fatty acids. In fact, there's

73:21

been several trials um to show that

73:24

omega-3 fatty acids are most beneficial

73:27

and most effective for mild cognitive

73:31

impairment patients,

73:33

people who have the APOE4 gene and

73:36

people who have got Alzheimer's disease

73:39

because when I told you that our we get

73:42

the breakdown of the bloodb brain

73:44

barrier, those parasites on the bloodb

73:47

brain barrier require DHA. In fact,

73:50

there's a transporter on the outside of

73:54

our brain that allows the um that allows

73:57

the DHA to come in and get into the

73:59

brain.

74:01

>> And I know you're a big fan of vitamin D

74:03

as well because there's been some very

74:04

encouraging studies done there.

74:05

>> Vitamin D is phenomenal. We have vitamin

74:08

D receptors all over our brain brain

74:11

stem and and they're abundantly

74:14

found in the hippocampus and the memory

74:16

centers of our brain. And there was this

74:19

act there was actually a study done on

74:22

centinarians in China.

74:24

>> Centinarians?

74:25

>> Yeah. Those who lived to 100, but it was

74:27

done in women. And they showed that the

74:30

women who preserved their cognitive

74:32

functions and who didn't get Alzheimer's

74:34

disease had high levels of vitamin D. So

74:38

they weren't vitamin D deficient. In

74:41

fact, being vitamin D deficient can

74:43

increase your risk of all cause dementia

74:45

by 40%.

74:47

likely being having a high level of

74:50

vitamin D which is around 60 nanogs per

74:53

deciliter can lower your risk of getting

74:57

Alzheimer's disease by around 80%.

75:00

>> And then we have this white powder in

75:03

front of me.

75:05

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

75:07

I do because there is just so much

75:11

benefit to this. Depending on which

75:13

brand you've bought, of course, but I

75:16

can't say enough about creatine. I have

75:20

my parents on creatine. They're 71 years

75:23

old. I've got my dad on highdose

75:24

creatine. I've got my mother on lowdose

75:26

creatine. It's the most widely studied

75:29

supplement on the market.

75:31

>> I've never seen you this excited. I'm so

75:33

excited because I think that this is a

75:36

really cheap and effective way to get

75:39

everything you want from both your

75:41

physiology, an upgrade on your

75:43

physiology and your neurohysiology.

75:46

So, let's actually talk about creatine

75:48

because I know it gets a lot of air

75:50

time, but women and men are still scared

75:53

of it. And they're scared of it for two

75:55

reasons. One, they're scared it's going

75:57

to cause kidney damage. And two, it's

76:00

they're scared their hair is going to

76:01

fall out. And I'm going to address both

76:04

of those fears. But first, let's talk

76:06

about what it is. So, creatine is a

76:09

naturally occurring molecule. We it's we

76:12

get we produce around 2 to three grams

76:14

of creatine per day. Gets secreted from

76:16

a bit from the brain, but a lot from the

76:18

liver. And 2 to three grams a day is

76:22

great, but it's not enough. So, we have

76:23

to supplement with it. And all through

76:26

the 90s and all through the 2000s,

76:28

people were supplementing with five

76:30

grams a day. That is this scoop here. 5

76:32

g of creatine per day. Now that we're

76:35

getting more uh rigorous with our brain

76:38

health studies, we have found that

76:40

creatine has enormous benefits for the

76:43

brain. But here's the problem. When you

76:46

have 5 g of creatine, you're saturating

76:48

the muscles. Okay, remember the muscles

76:51

are so hungry, so they get first dibs

76:53

and they take up all of that creatine.

76:56

So then there's none left for the brain.

76:58

We also lose a bit of the

77:00

bioavailability when the creatine goes

77:02

into the brain. It crosses the bloodb

77:03

brain barrier, but when it goes into the

77:05

brain, we lose some of it. So, we have

77:08

to supplement with more than 5 g. And

77:12

one of the studies that changed my

77:14

thinking came out last year. It was the

77:16

first ever pilot study done on

77:18

Alzheimer's disease patients. You're

77:20

talking about patients whose brains are

77:23

under attack. They're in an energetic

77:25

crisis. They cannot produce energy

77:28

effectively. ATP is all skewed. Brain

77:32

glucose metabolism is skewed. They don't

77:34

remember left from right. Cognitive

77:36

functions are declined. They put them on

77:38

at 20 g of creatine per day,

77:41

>> which is how much? I mean

77:43

>> that well actually that is four of this.

77:47

So you want to go one and I don't know

77:50

if they did this all at once. That's

77:52

two. Or if they did it like me over four

77:56

separate intervals throughout the day.

77:58

There we go.

77:58

>> That's a lot of

77:59

>> That's a lot. Which is why you probably

78:01

want to have this skewed throughout the

78:03

day, which is what I did. I had 20 grams

78:06

today. I had five grams in the morning,

78:08

five midm morning, and then I think I

78:10

had 10 all at once before I got here. So

78:13

that is a lot for all at once. And what

78:16

they found was that these patients not

78:19

only preserved their cognitive

78:22

functions, but they had more energy and

78:26

they were able to exercise more. And it

78:30

blew my mind that it does not matter how

78:34

old you are. It doesn't discriminate

78:37

based on gender. Creatine doesn't

78:39

discriminate based on age. It doesn't

78:41

discriminate based on weight. It doesn't

78:44

discriminate based on pathology or

78:47

disease states or ethnicity.

78:51

It is just there. It is there to support

78:53

you. It's the most widely studied

78:54

supplement on the market.

78:56

>> And it's all risk.

78:58

>> It's all reward. There is no risk. It's

79:00

helping with cell energy metabolism. So

79:02

basically, it's helping ATP

79:06

create energy.

79:09

>> So if you're someone that is low energy,

79:11

you should definitely be having

79:12

creatine. I don't care who you are, you

79:13

should definitely be having creatine.

79:15

>> People with brain fog and

79:16

>> yeah, people with brain fog, you know, I

79:19

think one of the greatest benefits are

79:22

men who are in football, football

79:25

players, you can actually, it's actually

79:28

a protective molecule. So, what studies

79:31

has shown is that at high doses of

79:34

creatine, around 30 grams a day, it can

79:38

protect you against insults. insults

79:41

meaning you take a hit to the head like

79:43

a concussion.

79:45

>> H

79:45

>> it can protect your brain against a

79:47

concussion. It can protect your g brain

79:49

against a stroke. It can protect your

79:51

brain from stress. The best thing about

79:53

creatine is that it works in the

79:55

background of stress. I think that's

79:57

where most that's where you'll get most

79:59

of the benefits from.

80:02

>> After hearing so much about creatine on

80:03

this podcast, I started recommending it

80:04

to all of the people in my life. There's

80:06

one particular person actually that's

80:07

probably out out there in my house at

80:09

the moment who had gone through uh

80:13

cancer treatments.

80:14

>> Yeah.

80:14

>> And had survived cancer treatments and

80:17

in their words wasn't the same on the

80:19

other side of the cancer treatments. And

80:21

I talked to her about um creatine and

80:23

she said to me the other day she I think

80:25

the exact quote was

80:28

>> I feel like I've got my life back

80:30

>> because it's she's been taking creatine

80:31

every single day for the last I'd say 5

80:34

months or so.

80:36

>> It's funny you said that because just

80:38

recently in the last two weeks uh this

80:41

study was done to show the anti-cancer

80:44

effects of creatine. And if my memory

80:48

serves clear, they uh they dosed it at

80:52

uh they dosed it at 0.36 g per kilogram

80:57

of body weight. So if you are a 70 kilo

81:00

person, if my mathematics is correct,

81:02

you're looking at around 25 g of

81:04

creatine per day that can have the

81:07

effects, the anti-cancer effects.

81:09

>> So the the study you're referring to,

81:10

I'll put up on the screen as well for

81:11

anyone that wants to see it. It's um the

81:13

NANS 2025 study, which is a major study

81:15

involving over 25,000 adults, found a

81:18

linear negative association between

81:20

dietary creatine and cancer prevalence.

81:22

For every standard deviation increase in

81:24

dietary creatine intake, the risk of

81:27

having cancer decreased by roughly 5% to

81:29

18% depending on the demographic.

81:32

>> That is wild.

81:35

This protective association was

81:36

strongest in adults over the age of 50,

81:39

suggesting that as we age, maintaining

81:41

higher creatine levels might be more

81:43

critical for cellular health and immune

81:45

surveillance.

81:47

>> Well, if you think about life and think

81:49

about energy, um we need energy to

81:53

survive. We need energy to fight off

81:56

infections. We need energy to fight off

81:59

stress, preserve our normal normal

82:02

bodily functions. So when we are at the

82:05

mercy of a low energy crisis, we can't

82:08

fight off tumor cells, we we can't fight

82:11

off these uh debilitating diseases. So

82:14

it actually makes sense that with more

82:16

energy and with more functional energy,

82:18

meaning like if our cells can function

82:20

better, it makes sense that you can see

82:22

a reduction in cancer incidents likely

82:24

you can see a reduction in Alzheimer's

82:26

disease incidents. when I said that

82:29

creatine works in the background of

82:31

stress. Also, there was uh there's been

82:35

phenomenal research to show that you can

82:40

basically creatine your way out of sleep

82:42

deprivation. If you've had a uh if

82:45

you've had a a long night and you you're

82:47

sleep deprived, maybe you slept four,

82:49

five, 6 hours, you're sleepd deprived,

82:51

you can take uh you can take highdose

82:54

creatine in the form of around 15 to 20

82:56

grams a day and you can reverse the

82:59

negative effects associated with that

83:01

sleep deprivation.

83:03

>> Does it matter what time you take the

83:04

creatine?

83:05

>> It doesn't matter what time you take the

83:07

creatine. It doesn't degrade in hot

83:09

water. it uh you can take it any time

83:13

throughout the day and it doesn't matter

83:16

whether you're taking it right before

83:17

exercise, during exercise, after

83:19

exercise, it works phenomenally. Some

83:22

people uh researchers are now uh

83:24

wondering if taking it at night before

83:26

bed helps with sleep performance and I

83:29

think that that's a really exciting

83:30

area. But the one thing that I want to

83:33

tell everybody because a lot of people

83:35

are scared of this biioarker called

83:38

creatinine meaning that

83:41

>> oh my doctor said that to me.

83:42

>> Yeah. So meaning that you've got a a

83:45

high creatinine level. And this is a

83:48

marker of it's one marker of kidney

83:50

function. But this is where I find it uh

83:54

really invaluable. And this is where a

83:55

lot of the nonsense comes around on

83:57

Instagram and social media. A lot of

84:00

people say, "Well, I had so much

84:02

creatine that my doctor told me to get

84:03

off it because my creatinine levels were

84:05

high." But creatinine levels are high

84:06

during times of stress, during times of

84:09

intense physical activity. Uh, and also

84:12

people who have a lot of muscle mass,

84:15

>> higher muscle mass, that's you have

84:17

higher creatinine levels. What you want

84:19

to test a greater marker of kidney

84:22

function and GFR

84:25

is cyatin C. So all you have to ask,

84:28

it's really easy. Ask your doctor, could

84:31

I please get cyatin C in my blood work?

84:35

And if that is elevated and without not

84:39

within normal range, then maybe get off

84:42

creatine. But right now, I cannot see

84:46

any reason as to not have creatine every

84:50

single day. I think every single person,

84:52

no matter what age you are, everybody

84:54

should be supplementing with creatine.

84:57

Now, there was this uh recent study that

85:00

came out on menopausal women and it was

85:04

a really small study. It was a

85:06

randomized control trial and they split

85:10

women into four groups and these were

85:13

permenopausal women. They split them

85:16

into lowd dose creatine where I think

85:18

they were having 750 mg a day, medium

85:22

dose which was around 1.5 g a day. Then

85:27

they had them supplement with a range of

85:30

both creatine monohydrate and creatine

85:34

hydrochloride. This was a hydrochloride

85:36

creatine study. And then there was a

85:38

placebo group. What they found was a

85:41

very small study, very small group. What

85:43

they found was that those in the medium

85:46

range having the 1.5 had substantial

85:50

increases in their mood and their

85:52

cognitive functions. So creatine is now

85:56

being explored in females across the

85:59

lifespan as it relates to permenopause,

86:02

pregnancy, menopause, and dementia. So

86:06

there's just there it's it's it's

86:08

phenomenal.

86:10

The only thing I want to point out, what

86:12

you want to look for when it comes to

86:13

creatine are two things when it comes to

86:16

manufacturing standards. You want to

86:18

look A, has it been NSF certified? And

86:22

B,

86:24

you want to look for is it Creapure? And

86:27

that's the gold standard of creatine and

86:29

it comes from Germany and a lot. So the

86:33

one that you've got there, I can tell

86:34

it's not Creapure.

86:36

>> Excuse me.

86:36

>> I know my creatine. How can you tell

86:38

what it is by looking at it?

86:39

>> I can just tell. I can I I I bet you a

86:42

million dollars that it is the brand

86:44

that I think it is because it's got this

86:47

powdered icing sugar substance. If it

86:50

was pure gold standard Creapure, it

86:53

would be gritty. The reason why it's

86:56

like this is because a lot of

86:58

manufacturers want to add these

87:00

different agents in there in order for

87:02

it to mix well. This probably mixes

87:05

really well. A lot of uh people also

87:08

complain of feeling uh GI distress when

87:11

they take it. And all I have to say is

87:14

that's not a reason to stop taking it.

87:16

Maybe take two grams at a time, maybe

87:19

take three grams at a time, but don't

87:21

stop taking it.

87:23

>> What do you test for with your own

87:24

health and how frequently do you test?

87:27

>> I test every 3 to four months.

87:29

>> What do you test?

87:30

>> Oh, I do everything. Um Oh, I've I I

87:33

just did um lab work. uh December 15th,

87:39

the day before my birthday. I do it, you

87:40

know, around that age. But every year,

87:42

funnily enough, I test my biological

87:44

age.

87:44

>> What is your biological age?

87:45

>> It came back as 22.

87:47

>> Okay. What's the most important test

87:49

they don't typically do that you think

87:50

everybody should be doing?

87:52

>> Lipoprotein little a raises your risk of

87:55

having a heart related event or raises

87:58

your risk of getting cardiovascular

88:00

disease, but it's hereditary. And then

88:03

for for dementia,

88:04

>> this is a really exciting part at least

88:06

in the US. We now have a predictable way

88:09

of picking up on mild cognitive

88:11

impairment and picking up on these

88:13

Alzheimer's hallmarks. Tao protein, PTA

88:16

217, it's called on blood work and

88:19

amaloid beta. So we can now pick up on

88:21

this with 90% accuracy of a PET scan.

88:26

>> What are those cards over there?

88:29

These are here to test your processing

88:31

speed.

88:32

>> Pink.

88:34

>> So,

88:34

>> it says pink on it.

88:35

>> Yeah. So, this is actually a great

88:36

measure of brain function. Your brain

88:38

processes visual information 15 times

88:41

faster than written words. And so, this

88:43

is going to test your uh brain function.

88:46

Okay.

88:46

>> So, what I want you to do is you're

88:48

going to see the color.

88:49

>> Yeah.

88:49

>> I want you to actually say the color of

88:51

the card, not the word.

88:52

>> Okay. Let me just program my brain. Say

88:55

the color, not the word. Okay. Are you

88:57

ready?

88:58

>> Green,

89:00

orange,

89:01

yellow, green,

89:04

orange,

89:06

green,

89:08

orange, yellow,

89:11

pink, orange, green.

89:15

>> Now, let's do the reverse. I want you to

89:16

say the words.

89:17

>> Wait, let me just

89:20

Okay. Yellow, blue, green, black,

89:26

purple.

89:27

brown.

89:28

>> Okay, so you're good.

89:29

>> Thank you. Let's do it to Jack. Jack,

89:30

you come sit in the J.

89:33

>> You caught him off guard and he hasn't

89:35

got creepy. And that's behind

89:37

>> there. Grabs a creep.

89:38

>> He It's an unfair advantage.

89:42

>> Okay, you ready?

89:43

>> Wait. So, what am I doing?

89:44

>> Just say the color of the card.

89:46

>> Okay, just the color of the card. Yeah.

89:48

Okay. Ready?

89:49

>> Green. Uh, orange, pink, yellow,

89:54

yellow.

89:56

Yeah. Orange,

89:58

pink.

89:59

>> Now, let's rolls reverse. I want you to

90:01

say what's on the card itself. So, just

90:03

read it.

90:03

>> Okay. Brown, purple, pink,

90:08

green,

90:09

black, yellow.

90:11

>> Okay. So, now we're going to test it

90:13

even more. That was the starting one.

90:15

Not good.

90:15

>> Not too bad.

90:16

>> That was not too bad. So, I want you

90:19

This actually involves us standing up

90:21

and using a tennis ball. So, we're going

90:22

to train your visual cortex, which sits

90:25

at the back here in the occipital lobe.

90:26

We're going to train your um processing

90:29

speed, your reaction time, your hand eye

90:30

coordinations. One of the best exercises

90:32

that you can do, physical exercises, is

90:34

actually hand eye coordination drills.

90:36

Tennis, racket sports. But I'm going to

90:39

show you what 5 minutes a day can do for

90:42

your cognitive reserve and your brain

90:44

performance just using a tennis ball and

90:46

an eye patch.

90:48

>> Okay. So,

90:52

>> first things first,

90:54

>> I'm going to give you this tennis ball.

90:56

Yeah.

90:56

>> And for the whole time, I want you to

90:58

throw the ball with an overhand grip.

91:01

>> Oh, like this?

91:02

>> Yep.

91:02

>> Okay.

91:03

>> So, I want you to just throw it with the

91:04

right arm and catch with the right arm.

91:07

>> Over. I mean, what's this one?

91:08

>> Underarm.

91:09

>> I'm just checking the wall. Okay. Okay.

91:12

So, like this.

91:13

>> So, you might want to move back where

91:14

the chair is. Okay. No, you would

91:16

>> cut that. Cut that out.

91:22

Good. So now throw with the right and

91:25

catch with the left and alternate.

91:27

>> Yep.

91:28

>> Okay.

91:33

>> You've got it. So what we're doing,

91:35

we're engaging almost all the executive

91:38

functions. Now you've got hand. You

91:40

should be able to do this for a minute.

91:42

Okay. Okay.

91:42

>> Now we're going to make it even harder.

91:44

It's like placing weight as well. Well,

91:46

I I'm not going to do the one with the

91:47

eye patch. I'll do the next one. Okay.

91:49

So, basically what you want to do, and

91:52

if you do it with a black ball, it's

91:54

actually Oh, even better.

91:58

So, now we're going to make it a bit

91:59

hard and a bit neurally demanding. We're

92:02

going to put an eye patch on you, which

92:03

is really going to block out like 50% of

92:05

the vision.

92:06

>> Okay. Which eye?

92:08

>> Any eye.

92:09

>> Let's do the left one.

92:11

>> Now, let's see how many you can do. I

92:13

think you we counted around eight

92:14

before. a pirate.

92:15

>> I just need you to look at

92:18

>> what? Wait, this is not flattering.

92:23

>> Okay,

92:23

>> let's go.

92:24

>> Oh, that's so different.

92:25

>> Yeah.

92:26

>> Wow. This feels significantly harder.

92:28

>> I know. Let's go.

92:30

>> This feels No, this feels like really

92:31

hard. Let me just double check.

92:32

hell.

92:34

>> That's That's really That's so hard.

92:38

This is

92:40

>> There you go. You've got it.

92:42

>> Joking.

92:44

Okay, let's alternate now. Left hand,

92:46

right hand,

92:48

>> left hand, right around like this.

92:49

>> Yeah,

92:52

>> you're training your visual system to

92:55

work under load and under stress. So,

92:58

when you do this,

93:00

>> I'm interrupting you.

93:01

>> No, it's okay.

93:03

>> You got it. You got it. You got it.

93:05

Good. Good. Good. And then to even make

93:07

it even harder. Okay.

93:10

>> Stand on your right foot.

93:11

>> Yeah.

93:12

>> And put your other foot. There you go.

93:13

>> Or on one leg. Yep. Standing on one leg

93:15

is now engaging the cerebellum.

93:18

>> Okay,

93:19

>> we're getting spatial awareness. Let's

93:21

go. Posture.

93:22

>> Left, right, left, right.

93:22

>> Yep.

93:24

>> Oh my gosh.

93:30

>> You got it.

93:32

>> I want to see you do it

93:34

>> with the eye patch on.

93:35

>> Yeah.

93:35

>> Wow.

93:39

I mean, I can be great. My eyelashes

93:42

have gone now. It's okay. We can AI that

93:44

out.

93:45

>> This actually looks great.

93:46

>> Mhm.

93:47

>> Okay, we're ready.

93:50

Well, I blame my nails. I blame my

93:53

nails. Let's do it.

93:57

>> Okay.

93:58

>> It's hard.

93:59

>> It's so hard.

94:00

>> And so, what is this doing? It's

94:02

>> This is engaging executive functions,

94:05

processing speed, hand eye coordination.

94:08

>> And you did this with NBA players. I did

94:10

this with NBA players to improve uh

94:12

their executive functions, decrease

94:15

their reaction time,

94:17

>> and this will this will change my brain

94:18

if I do this frequently.

94:20

>> Not just that, but you're also improving

94:22

cognitive reserve. You're building new

94:24

connections between the brain cells.

94:26

You're strengthening neural networks and

94:29

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94:32

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94:33

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94:36

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94:50

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94:53

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94:54

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95:00

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95:12

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96:24

>> So doing hard things is what is going to

96:29

improve brain function over the

96:31

lifespan. Doing hard things tells your

96:34

brain that you can do hard things.

96:37

Meaning have you ever heard of this um

96:40

brain area a little area in the brain

96:42

called the anterior mid singular

96:45

>> cortex? Yes, I have.

96:47

>> What do you know about it?

96:49

>> I'll let you say it.

96:50

>> Well, it's shown that it's larger in

96:52

what we call super ages and people who

96:55

age really well and who can uh withhold

96:59

a lot of uh cognitive capacity and it's

97:03

really profound in people who can diet

97:05

well. It gets bigger when we do hard

97:08

things. So, when we do really hard

97:10

things, this area in the brain gets

97:12

bigger. And basically

97:14

what that is, it's reserve for when life

97:18

gets hard. It means it basically tells

97:20

your brain that no matter what happens,

97:23

no matter what event comes my way, I

97:25

have the ability to go in, welcome it,

97:29

and push through it no matter how hard

97:31

it's going to be. When you give up or

97:35

when you don't do hard things, this

97:37

little area doesn't grow. It doesn't get

97:40

bigger. So doing these neural activating

97:45

uh drills that we just did, going to the

97:47

gym and pushing well above your

97:50

threshold and pushing really hard is

97:52

going to help uh grow this little area

97:54

of the brain.

97:55

>> And they call this the willpower muscle.

97:57

>> The willpower. This is why I think that

98:00

um when people go out to set their goals

98:03

during the year and they say, "I'm going

98:04

to lose 20 pounds. I'm going to do this.

98:06

I'm just going to increase my

98:07

willpower." I think it's not willpower,

98:11

it's neurobiology.

98:13

>> I think it's really important to just

98:15

spend a little bit of moment talking

98:16

about this part of the brain because

98:17

when I discovered it, I found it

98:19

absolutely fascinating. And I think it

98:20

was Andrew Huberman who said

98:22

>> either to me or he said publicly that he

98:25

thinks it's one of the most fascinating

98:26

or important discoveries of the last

98:28

century.

98:29

>> Of course, well, you think about um how

98:31

we're living our lives. We're we're

98:33

punishing ourselves for not being able

98:36

to read a book, for not being able to

98:39

pay attention. How many, you know,

98:40

people are now diagnosing, self

98:42

diagnosing themselves with ADHD, low

98:44

attention spans, and they're blaming it

98:47

on environment? They're blaming it on

98:49

circumstances when they should be

98:51

blaming it on neurobiology and they

98:53

should be blaming it on their brain

98:55

state. this area of the brain if you can

98:58

push it and this is why these super

99:01

aagers seem to have

99:02

>> what's a superager

99:03

>> a superager is somebody who is aging

99:06

well so they're going through life uh

99:08

low uh cardiovascular disease state

99:11

they've maintained their cognitive

99:13

functions they're at the age of 80 90

99:16

with a a V2 max profile of maybe a 50 or

99:20

60 year old so they're aging quite well

99:23

biologically

99:25

So these you know super ages have many

99:28

many different facets to them and one of

99:30

them is a larger mid singular cortex.

99:35

Conversely the AMCC anterior midsular

99:38

cortex shrinks in people who live

99:40

sedentary lives or avoid challenges. It

99:44

literally atrophies if you play it safe

99:46

in life too often. Growth only occurs

99:49

during resistance. If you love taking

99:51

ice baths and you take one, your AMCC

99:53

doesn't change. If you hate the cold but

99:56

force yourself to do it anyway, the AMCC

99:59

grows.

100:00

>> Scientists now view the AMCC as the seat

100:03

of the will to live. Its size and

100:05

activity level are strong predictors of

100:07

how long an individual will survive

100:09

after a major setback in their life,

100:10

whether it's a health setback or a

100:12

surgery.

100:15

>> There's something really philosophical

100:17

about that as well. You know, if you I

100:19

don't know if you read um stoicism or

100:21

anything, but it it it really dates back

100:24

to how the Stoics lived their life,

100:28

especially Marcus Aurelius, with being

100:30

able to push through hard times. Little

100:33

did they know that it was this little

100:34

area in the brain.

100:36

>> Yeah. Yeah, I think I was telling the

100:38

story the other day of Roosevelt and

100:40

what happened in his life as a young man

100:41

when he came home one day on Valentine's

100:43

Day and found that his mother and his

100:45

wife of who had just had his newborn

100:47

baby had both died, one upstairs, one

100:49

downstairs, and he went off to the bad

100:51

lands for two I think it was 2 to four

100:53

years. The Badlands in America were just

100:55

this like horrific um natural place

100:58

where he'd get up at 4:00 a.m. ride

100:59

these like horses in the freezing cold

101:02

where like the horses would literally

101:03

die standing still because it was so

101:05

horrific. He did that to two years to

101:06

like deal with the grief. But when he

101:08

came back to New York City after this

101:10

two years in the Badlands, all of his

101:11

friends said he was just a completely

101:13

different man. He had and what they now

101:15

know from a neuroscience perspective is

101:17

that he didn't just build his muscles.

101:19

He literally like rewired his his brain.

101:21

He went on to become the youngest US

101:22

president of all time. He got shot um

101:25

during a speech and carried on doing the

101:26

speech. He led the charge in various

101:28

wars. He's just this unbelievable. I

101:30

think he won the Nobel Prize. and they

101:32

point at those two years in the bad

101:33

lands and say actually that that forged

101:35

not just the man but his his brain his

101:37

AMCC. The studies also show that

101:40

athletes consider consistently show much

101:42

larger AMCC volume and studies show that

101:46

individuals struggling with obesity

101:47

often have smaller AMCC's but but it

101:50

begins to grow the moment they start a

101:53

successful challenging dietary or

101:55

exercise intervention. that it's that

101:57

word challenging because when you place

102:00

stimulus upon a system, it adapts and

102:04

grows and that is neurobiology at its

102:08

most infinite source. And this is why we

102:12

get the breakdown of these synapses.

102:15

This is why we get into a place of going

102:18

from 5,000 to 10,000 connections to

102:21

2,000 or no connections. these dendritic

102:24

spines end up breaking down because we

102:27

don't do the hard thing. And I also

102:29

think being deep rooted in neurobiology,

102:32

you can see that everything is cause and

102:33

effect and it's a cycle. Uh if you don't

102:37

do the hard thing, you don't grow the

102:39

AMCC. You don't grow the AMCC, you don't

102:42

do the hard thing again. And it's just

102:44

this loop and it's this cycle which is

102:47

why so many resolutions, New Year's

102:49

resolutions end by February 1st. It's

102:53

why we have the obesity epidemic. It's

102:57

largely why I think we've got a a crisis

103:00

of people not being able to uh meet

103:02

their goals.

103:04

I'm just fascinated from an evolutionary

103:06

perspective as to why we needed one and

103:08

like why it wasn't just always big

103:10

>> in the pursuit uh you know

103:11

evolutionarily uh in the pursuit of

103:14

hunting and going out and and hunting

103:17

for food sources and being motivated to

103:20

do that in a near starvation state when

103:23

times were tough

103:25

>> and so when times got easier we didn't

103:27

need it as much so we could conserve I

103:31

guess our energy so we could like scale

103:32

down our willpower when times were good.

103:34

>> Well, it's interesting that you say that

103:36

because this brings up the whole brain

103:38

rot and AI era just like with, you know,

103:41

in uh 2024, Oxford dictionary, I think,

103:44

named brain rot the word of the year.

103:47

And it's interesting because it plays

103:49

into evolution and what's happening with

103:52

this AMCC, meaning like we're just there

103:55

scrolling at mindless information every

103:58

day, training our brain to get these

104:00

small dopamine hits, these small rewards

104:03

from doing absolutely nothing.

104:07

>> What do you think of these uh chat bots

104:10

that everybody's using at the moment to

104:11

write for them and think for them, etc.?

104:13

>> Oh my god. I think it's uh on the

104:16

spectrum of being so incredible but

104:19

being so detrimentally harmful. I know

104:23

this with myself. So I was a

104:24

mathematician. I did my masters of

104:26

mathematics and I was able Steven to the

104:30

trigonometry and pure calculus that I

104:33

could do back then with just my head and

104:35

a pen was fascinating. Now I'm going to

104:39

I'm going out and I'm calculating on

104:41

chat GPT the bill the the the 20% tip on

104:45

top of this bill. How much does it cost?

104:46

And I think how dumb am I actually

104:49

getting? So I think it's both good and

104:52

bad. I think the rate of decline we're

104:55

seeing in people reading books and

104:56

exercising their brain is declining. Um,

104:59

and our ability to

105:02

think

105:04

and and use our our cognition is

105:07

declining.

105:09

>> Louis, I've I've um waited uh a long

105:12

time to ask you one particular question,

105:15

which is I think is very important,

105:17

which is you're clearly very passionate

105:19

about this stuff.

105:21

One might say you're pretty obsessed

105:22

with it. You come across as pretty

105:24

obsessed.

105:25

>> Do I?

105:26

>> You do. Yeah. Why?

105:29

>> We are living in a society

105:33

that doesn't allow women to ask for what

105:37

they want. We're living in a society

105:39

that doesn't allow women to ask for what

105:42

they need. And when this happens, it

105:45

results in 70% of all Alzheimer's

105:48

disease cases being women. It results in

105:51

80% of all autoimmune diseases being

105:55

female. And these are largely

105:58

preventable diseases. And when I ask why

106:01

and I hear that women are wildly

106:04

misrepresented in academic literature,

106:07

when I when I see women who downplay

106:10

their symptoms or they're too scared to

106:12

ask their doctor for advice or they're

106:14

too scared to ask somebody else for

106:16

advice because of what they're going

106:18

through or they're ashamed of some of

106:20

their symptoms, I get angry and I get

106:22

passionate. And it reminds me of my

106:26

grandmother who uh she was my best

106:28

friend. Her name was Louisa. And

106:31

>> you're named after her.

106:32

>> I was named after her. Yes. And we spent

106:35

every day together. And And I'm getting

106:37

emotional now cuz I remember her. And

106:40

she sadly died of pancreatic cancer. It

106:43

was ovarian cancer that went to

106:44

pancreatic cancer. And

106:48

she never asked for what she wanted. And

106:50

she never asked for what she needed,

106:52

which was help. She didn't understand

106:55

her symptoms. She didn't go to the

106:58

doctor when she needed to because she

107:01

was just more

107:04

inclined to look after the family and

107:07

look after the household. And when the

107:10

time came that she was given her

107:12

diagnosis, I was sitting there with her.

107:14

It was um it was at home and the doctor

107:17

came. She did a house call and my

107:20

grandmother looked at her. She hardly

107:22

spoke that much English and she said,

107:24

"Please, is there something I can do? I

107:26

don't want to die." And the doctor said,

107:29

"There's I'm sorry, there's nothing you

107:31

can do." And I spent every day with her

107:34

in the hospital. And I think about that,

107:36

it's been almost 20 years now, but I

107:39

think about that moment and I kick

107:41

myself thinking, why didn't we why

107:44

didn't we get her a scan? She told us

107:47

several times that her stomach was

107:49

hurting. She told her several times that

107:51

she felt pain. She never she hid her

107:55

symptoms. She hardly ever ate at one

107:57

point and we never stopped to think

108:00

about why and she never stopped to think

108:02

about why. So I think about her every

108:04

day. And then I think about my mother

108:06

too and these women, you know, first

108:11

generation, they came uh we migrated to

108:14

Australia from a country called Cyprus

108:16

and they've just been so they put

108:21

themselves second and they they just

108:24

look after the family and I can't stand

108:26

that. And when I see women coming in as

108:29

patients

108:30

or caregivers, I think to myself, do you

108:34

not know that there is something for you

108:36

to do? And most women don't. And I I

108:40

can't believe the amount of money that

108:41

we are spending that is going towards

108:46

putting us on rockets to go to Mars, but

108:48

we haven't yet found a cure for this

108:52

disease that is largely preventable.

108:54

It's just not okay with me. And I would

108:57

hate to see women go through this.

109:00

>> The emotion is still very present in

109:02

your face even though it was so long

109:04

ago.

109:05

>> It was so long ago. I mean, I was very

109:07

close to her. I'm very close with my

109:09

mother. I I check in with her twice,

109:12

three times a day. And I just don't

109:14

think it's fair. I think women deserve

109:17

the truth. They've been lied to. They've

109:20

been underrepresented.

109:22

And

109:23

we need to change that. with Louisa,

109:25

your grandmother, what are those range

109:29

of emotions that have turned into this

109:32

incredible fire? You have

109:33

>> anger.

109:35

>> Anger is one of the emotions. Anger at

109:39

society that places women to be

109:43

everything. To be a a mother, a

109:47

caregiver, to go to work, to represent

109:52

the family. women represent 51% of the

109:56

total population

109:58

and then it becomes I feel political if

110:01

that's an emotion because you think

110:03

about health care you think health care

110:06

should be accessible to everybody but it

110:08

seems as though especially in this

110:10

country that health care is only really

110:12

accessible by those with a high

110:14

socioeconomic status and that I'm not

110:17

okay with so it does become political

110:20

even though healthcare I Yes, healthcare

110:23

is political because policies have been

110:25

set, but a woman in need is apolitical.

110:30

And my grandmother was a-political and

110:33

her needs

110:35

just were not met.

110:39

anger,

110:40

>> frustration at the system, frustration

110:43

at the fact that we still have only 4%

110:47

of women taking hormone replacement

110:50

therapy in fear that they're going to

110:52

get this disease, uh that they're going

110:53

to get breast cancer, utterly frustrated

110:57

at the cycles of administration who

111:01

vouched to help you. you look to your,

111:04

you know, your government and your

111:06

administration

111:07

to look up to, to guide you when you

111:10

have Secretary Kennedy in 2014 go on

111:15

national television and say, "Vaccines

111:18

are totally safe. I had all my kids

111:20

vaccinated. They've eradicated some of

111:22

the most deadliest diseases that have

111:25

plagued this world. Vaccines are so

111:27

safe." to fast forward to 2025

111:30

saying vaccines are so unsafe. Do not

111:33

trust your medical doctor. You need to

111:36

take your health into your own hands.

111:39

You start to lose trust.

111:42

And it's not that we're uninformed.

111:45

It's the fact that we are confused

111:48

because we hear vaccines are bad. Oh,

111:51

vaccines are good. Vaccines are are

111:54

really good. Take them. Don't get your

111:56

kid vaccine. You've got women here who

111:59

don't even know their they they don't

112:02

even know how to get on the internet or

112:05

order a blood testing. You're expecting

112:07

them to take their health into their own

112:08

hands. So, it upsets me that you see

112:11

women who are so vulnerable

112:13

being sold a a a vaccine lie which could

112:17

potentially save them from a disease

112:20

which could potentially save them or

112:22

their child from getting the flu,

112:27

hepatitis B,

112:29

menitis, which was just eradicated from

112:32

the vaccine schedule. Um, I'm not, this

112:35

is not meant to be political. I am I am

112:37

a scientist. I am not. This is not

112:39

propaganda. This is not ideology. This

112:42

is just women who deserve to be treated

112:47

better.

112:49

>> You're 36.

112:53

Louisa passed away when you were how

112:55

old?

112:55

>> Oh, I was uh probably 18 at the time.

112:59

>> You were 18 when you

113:00

>> Around that 18, 19

113:01

>> when she got the diagnosis.

113:03

>> Yeah, it was very fast. It was within a

113:06

two month time frame. Not even.

113:08

>> And had she not got that diagnosis and

113:10

had you not sat there and watched her

113:12

ask that doctor if there's something

113:13

that she could do,

113:16

>> do you think your career would have

113:18

taken this course?

113:19

>> I became utterly obsessed with disease

113:22

management. But when I first saw a human

113:26

brain, I was 21. I was in a lab and we

113:30

had to go into a cadaavver lab and I saw

113:32

a brain being harvested from a a body

113:35

that was donated and I stayed back that

113:37

day. I remember and I helped in the

113:41

pathology lab and when I saw that brain

113:44

I knew that I wanted to dedicate my life

113:46

to it. So ever since then I've been in

113:48

OS and it's where I feel most alive.

113:51

>> Why why did you want to dedicate your

113:53

life to it? Because when you know what

113:56

the brain is that it is responsible for

113:58

the life that we have and you can use it

114:00

for your advantage to overcome any

114:02

obstacle that comes your way you become

114:05

obsessed with understanding it.

114:07

Metacognition is thinking about your

114:11

thoughts and every day if you can think

114:13

about why you think about the things you

114:16

think about you can challenge yourself

114:20

to overcome any adversity. Is there a

114:23

cost to your obsession and your passion?

114:25

>> Yes.

114:26

>> What's the cost?

114:27

>> I moved away from my family to be

114:28

surrounded by the greatest neurosurgeons

114:31

in the world, which I am, and I'm very

114:33

thankful for that. I moved away from a

114:35

population of 22 million to come to the

114:38

hardest city in the world,

114:40

>> New York.

114:40

>> New York City.

114:41

>> Are you still paying a cost?

114:43

>> I'm still paying a cost. My health pays

114:45

a cost.

114:46

I've missed family events, traveling for

114:50

my career.

114:53

But I wouldn't have it any other way

114:56

because the people that I've met have

114:58

forged the way for me to live the life

115:00

that I want. I'm surrounded by

115:02

incredible thought leaders in health and

115:04

medicine. And

115:07

>> so what is success to you then at the

115:10

deepest possible level? What is success?

115:12

We meet again in 10 years time. You say

115:14

my life has been a success or I feel

115:16

successful. I'm a Louisa says I am a

115:20

successful woman. What does that mean?

115:21

What happened?

115:23

>> Being able to control my brain states.

115:27

>> Being able to control your brain states.

115:30

>> I think that the ultimate form of

115:33

success and high performance or being

115:36

able to perform at your peak is being

115:40

able to go from brain state to brain

115:42

state and then be able to recover.

115:45

>> What do you mean by brain state? meaning

115:47

like being able to get switched on when

115:50

you need to be switched on and invite

115:52

the neurotransmitters involved in that.

115:53

Norepinephrine, adrenaline, dopamine,

115:56

but not having that in constant

115:58

overdrive and being able to know when to

116:01

switch off. And I think that that is

116:02

what high performance is. The book that

116:04

changed my mind on that was flow by Mihi

116:07

Chicksimni, which actually speaks about

116:09

the flow state. So being able to know

116:12

how to uh separate yourself in these

116:16

states.

116:17

>> Any goals outside of your professional

116:21

>> kids, family, life? Love kids, family.

116:24

>> Yeah, definitely.

116:26

>> It's tough, isn't it?

116:28

>> It's tough. I was saying earlier to my

116:30

friend that, you know, I kind of just

116:31

thought the minute I wanted to have

116:33

kids, they would just appear. But it's

116:35

not so strange.

116:35

>> That's what I thought, too, until I

116:36

realized, oh, but I'm the woman.

116:41

I actually have to bear the the children

116:43

as well,

116:45

>> which is a big sacrifice and an

116:46

>> honor. It's an honor and a privilege and

116:48

a sacrifice that I think everybody Yeah,

116:51

I I mean I think I I definitely want.

116:55

>> Are you hopeful for all of your

116:57

professional endeavors?

116:59

>> Yes,

117:00

>> you are hopeful.

117:01

>> I'm in control.

117:04

you think we're going to move in a good

117:06

direction as a society as it relates to

117:10

>> Alzheimer's and

117:13

>> Yes, I I am hopeful for that. I'm

117:16

hopeful for the message that I'm getting

117:18

across. I think uh social media is

117:21

providing the platform for free

117:22

education and for people to understand

117:25

that they have agency over their brains.

117:28

Uh, I'm not hopeful for um anybody

117:32

saving us or coming in and giving us a

117:35

easy way forward.

117:36

>> Do you ever have days where you wish you

117:38

were less obsessed with your craft?

117:41

>> Has there ever been a day where you're

117:42

like, you know, I wish I was just a

117:43

little bit less captivated by this?

117:45

>> Sometimes I do. Yeah, I think if I

117:47

didn't, well, I'd be probably back home

117:50

in Australia living an average person's

117:53

life. I'm not saying that that's it. I'm

117:55

just saying, you know, maybe I would

117:56

have done it done my life differently.

117:58

>> I have days like that where I think if

118:02

obviously cuz the obsessed brain is the

118:04

one making this decision. So, it's quite

118:06

difficult to detach. But like if you put

118:08

a knob in front of me and I could just

118:10

turn it down just a little bit, would I?

118:12

Now, my obsessed brain is is the one

118:14

making this decision. So, my obsessed

118:16

brain is like, "Fuck it, turn it up."

118:17

>> But I think I do wonder sometimes. I am

118:20

the way that I am, right? Um, but I do

118:22

wonder sometimes if I would be

118:26

happier overall if I could just turn it

118:29

down a little bit.

118:30

>> But isn't the whole point of life to

118:33

know thyself and in pursuit of something

118:36

bigger and better?

118:37

>> Yeah, it is. But I just sometimes worry

118:39

about what I'm sacrificing and whether

118:41

at some point, I don't know, when I'm on

118:42

my deathbed at 80 years old, I'm going

118:43

to look back and say, "Actually,

118:46

I made a bad trade."

118:48

>> Well, exactly. And but we're never going

118:50

to know that. I I think about that

118:52

often. I know you think about that often

118:54

and you think, well, if the world came

118:55

to a a collapse tomorrow, what would you

118:58

regret today not having done?

119:02

>> I think it would be like making more

119:04

memories with people I love. I think

119:05

that's one of the big ones. I think

119:07

>> did you hear what you just said? Making

119:09

more memories

119:10

>> and imagine losing those. Imagine a life

119:13

full of like

119:15

>> you know creating these experiences and

119:17

these memories to have them being taken

119:20

away from you.

119:22

>> Yeah.

119:23

>> To not being able to recognize your

119:24

wife, your kids, and looking in the

119:28

mirror and not being able to recognize

119:29

yourself.

119:31

>> That's why Alzheimer's is just such a

119:33

disgusting, sinister, like horrific

119:36

thing cuz

119:38

Yeah. It's just

119:40

>> the most heartbreaking thing to to lose

119:43

someone while they're still alive.

119:45

>> Yeah. And to lose yourself. We've got

119:46

this one woman who looks in the mirror

119:49

and she says, "Who's that?"

119:52

>> Really?

119:52

>> Yeah. And you know, it's it's sad

119:54

because two years ago she knew who I was

119:56

and now she asks, "Are you my daughter?"

119:59

And when you're confronted with that

120:01

every single day, it gets you thinking.

120:04

You don't live a normal life. You don't

120:06

live an average life because you do

120:08

think about every facet of medicine. You

120:11

think about history. You think about

120:13

diseases. And then you think about life

120:15

and the people that you spend the most

120:16

time with.

120:18

>> We have a closing tradition where the

120:20

last guest leaves the question for the

120:21

next not knowing who they're leaving it

120:22

for. And the question left for you is,

120:25

what is God to you?

120:27

God is

120:30

that power that you feel and have faith

120:33

in that you cannot see. The power that

120:38

um

120:41

basically makes you feel like there is

120:43

somebody there that has you and that is

120:46

guiding you

120:49

that

120:51

always has a a path for you knowing

120:54

>> you you believe in God. Yes, I'm I'm I'm

120:56

a I'm I'm Christian. I'm Greek Orthodox.

120:59

>> When you see the brain deteriorating in

121:02

such a way and you think about this

121:04

concept of prayer, like asking God to

121:06

help me with something, doesn't it feel

121:08

pretty I mean, it's the definition of

121:10

like hopelessness is watching your brain

121:12

deteriorate. And I think some part of my

121:15

struggles with religion since I was an

121:17

18-year-old and I came from a very

121:19

religious family was seeing injustice in

121:21

the world. And there's doesn't seem to

121:23

be much greater injustice than watching

121:24

someone's brain just deteriorate in

121:26

front of their family.

121:28

>> Yeah. Or somebody going through losing

121:30

their child and you start to think about

121:33

God.

121:34

>> People pray for I can't find my keys. I

121:36

want my football team to win. And I go

121:38

there's no point. If people praying for

121:40

an Alzheimer's cure are having no luck,

121:42

then maybe I should stop praying for

121:44

Manchester United to win.

121:45

>> Yeah. If you understood the intricacies

121:50

of how we were actually brought into

121:52

this world from the point of conception,

121:56

from the point of conception to the

122:00

point of neural development, how a baby

122:02

is formed and how precise everything has

122:06

to be for you to come out the way you

122:09

did.

122:11

It is so beautiful and so miraculous and

122:14

so rare. even though there are billions

122:16

of people in this world that you cannot

122:21

just turn to biology anymore, you have

122:23

to turn to something bigger. And I used

122:27

to, trust me, even as a as a Greek, as a

122:30

Christian who's read the Bible, I even

122:34

in my early 20s when I was getting into

122:36

medicine and science, I I was so gung-ho

122:38

about

122:40

we we're born in a body, we die in a

122:43

body. But then when you get so deep into

122:47

the literature of science and medicine

122:49

and biology,

122:51

it's hard to ignore God. And it's hard

122:54

to ignore that there is a higher power

122:56

out there. And why is it that there are

122:58

chapels in hospitals?

123:03

>> Because people want to go to heaven.

123:05

Because people want an alter an

123:09

alternative method of getting through

123:12

whatever it is that they can get

123:14

through. Something that science and

123:16

medicine cannot offer and believing in

123:20

something that is not there or something

123:22

that hasn't occurred yet is having

123:23

faith.

123:28

I work in neurosurgery and some of the

123:30

cases you think this person's not coming

123:32

out of here alive and the fact that they

123:34

do and they preserve their cognitive

123:36

functions and they look next to normal

123:38

after they've had a massive tumor

123:40

resected which is a true story from here

123:43

the tumor was going all along this one

123:45

woman's face who was 78 years old who

123:48

traveled here from France to have the

123:51

tumor reected how is it that she's

123:53

walking and she's cognitively normal and

123:55

she's not even on any medication the

123:57

next day. How is that possible? Is it

123:59

God? Is it just miraculous

124:01

neurosurgeons? There's just some things

124:03

that medicine can't answer.

124:07

>> I agree with that. I am I don't think

124:10

I'm arrogant enough to say that I know

124:13

and I'm curious

124:15

and I think I'll never know.

124:17

>> Yeah.

124:17

>> So, I guess that's where we need to have

124:18

faith.

124:19

>> Yep.

124:20

>> Louisa, thank you so much. Um it's very

124:21

important that you do the work that you

124:23

do because uh it's people like yourself

124:25

that are so passionate, so obsessed and

124:26

so good at communicating that um help

124:29

average people who aren't who don't have

124:31

access to the wisdom and the research

124:32

and studies and information that you

124:34

have understand all of these things. And

124:36

it's through this understanding that we

124:37

can make better choices and preserve our

124:38

life, preserve our brains and if we

124:40

preserve our brains, we preserve

124:41

everything that matters.

124:42

>> Correct. Thank you.

124:43

>> So thank you for doing what you do and I

124:44

appreciate your passion and dedication

124:46

to it because it's very very important.

124:47

I know it comes at a cost. So, I feel

124:50

obliged to tell you that as a normal

124:52

person who isn't involved in your field,

124:53

we're grateful.

124:54

>> Thank you so much, Stephen.

124:55

>> Thank you. YouTube have this new crazy

124:57

algorithm where they know exactly what

124:59

video you would like to watch next based

125:01

on AI and all of your viewing behavior.

125:04

And the algorithm says that this video

125:06

is the perfect video for you. It's

125:08

different for everybody looking right

125:10

now. Check this video out and I bet you

125:12

you might love it.

Interactive Summary

Louisa, a clinician and brain researcher, explains that Alzheimer's is a largely preventable lifestyle disease that often begins decades before symptoms appear. She emphasizes the importance of building 'cognitive reserve' through heavy resistance training, high-intensity aerobic exercise (Zone 5), and deep sleep. The discussion covers the critical role of sleep in cleaning the brain via the glymphatic system, the specific neurobiological challenges women face during menopause, and the profound benefits of supplements like high-dose creatine, omega-3, and vitamin D to protect the brain and improve cognitive performance.

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