0:00

Greetings listeners, in today's episode I'm

0:02

bringing you along to the American

0:04

Academy of Anti-Aging Medicine's Longevity Fest

0:06

Conference, where I had the honor

0:08

of presenting a keynote this last

0:10

December. We'll explore some

0:13

foundational yet effective tactics to enhance

0:15

longevity and prevent diseases. Additionally,

0:17

we'll delve into more intensive

0:20

lifestyle modifications that, despite their

0:22

demands, offer significant longevity benefits.

0:25

If you would like to view the slides

0:27

I presented along with this presentation, you

0:29

can find this episode on my YouTube channel

0:32

called Found My Fitness. In

0:34

this episode you will learn the

0:36

evidence that vitamin D deficiency increases

0:39

mortality and my thoughts on achieving

0:41

optimal levels partly through supplementation, why

0:43

magnesium deficiency reduces DNA damage repair,

0:46

and what this means for cancer

0:48

and aging. You'll learn

0:50

about the dangers of inadequate omega-3

0:52

intake and why you may want

0:55

to measure your omega-3 index to

0:57

make sure you are at least

0:59

in the 8% range. You'll learn

1:01

some practical take-homes for correcting vitamin

1:03

D, omega-3, and magnesium inadequacies, why

1:05

vigorous exercise is the best longevity

1:07

drug, and how increasing B.O.2 max

1:09

affects life expectancy. You'll learn some

1:12

of the most evidence-based protocols for

1:14

increasing B.O.2 max and how to

1:16

get a good estimate of B.O.2

1:18

max without directly measuring it in

1:20

a lab. You'll also learn what

1:22

science suggests it takes to reverse

1:25

20 years of age-associated structural changes

1:27

to the heart. The brain and

1:29

blood pressure benefits of vigorous exercise

1:32

and in particular why vigorous exercise

1:34

seems uniquely able to improve qualities

1:36

of cognition like focus, attention, and

1:39

generally reduces the aging of the

1:41

brain. You'll learn anti-cancer effects of

1:43

vigorous exercise and how exercise snacks

1:45

can be used to break up

1:48

sedentary time throughout the day and

1:50

why this is so beneficial. Before we

1:52

jump off to the presentation and in

1:55

the spirit of unwavering commitment to optimizing

1:57

health and longevity, I've put together a

1:59

guide that's stands at the intersection

2:01

of rigorous science and actionable strategies.

2:04

It's a blueprint that draws on

2:06

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2:08

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2:10

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2:12

You can access it now

2:14

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2:18

Within this guide, you'll find a

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2:22

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2:25

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2:27

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2:29

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2:31

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2:34

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2:36

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2:38

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2:40

terror. Central to

2:43

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2:45

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2:48

a key player in maintaining and

2:51

improving neural health. I

2:53

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2:55

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2:57

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3:00

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3:02

cutting-edge strategies I'm currently investigating. Each

3:05

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3:07

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3:09

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3:11

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3:16

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3:18

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3:20

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3:23

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3:26

Once again, you can

3:28

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3:30

at bdnfprotocols.com. And

3:33

now, I invite you to listen to

3:35

my presentation at the American Academy of

3:37

Anti-Agen Medicine's Longevity Fest. Good

3:40

morning. Nice

3:43

to be here today. I

3:46

was just mentioning that my son

3:48

eats about two cups of pomegranate

3:50

a day, so his urolithin A

3:52

levels must be off the charts, and

3:54

maybe he'll live to be 100, but probably gene

3:56

therapy is going to be involved in that. Today,

3:59

we're going to be talking about... about some of the. What?

4:01

I think are powerful lifestyle

4:03

habits that can affect the

4:05

way you age. So.

4:08

There's some what I call low hanging fruit,

4:10

so. These are things I think her. Really?

4:12

Easy as it can be. As simple as

4:14

a. You know, dietary

4:17

modifications? Or. A supplement you

4:19

tag. And. Then there's some things

4:21

that are. A little more effort for. Which.

4:24

Require effort. Arm. And so

4:26

that would course be exercising to what we're going

4:28

to get into that as well. I'm.

4:31

So. The first part of the

4:33

topic and is set about optimizing micro

4:35

nutrient deficiencies. And in the

4:37

second, Part we're going to be talking

4:39

about what kind of exercise and how.

4:42

It. Affects the way we age. I'm. On.

4:44

A molecular level as well. So.

4:48

First up, I think there's really

4:50

three. Main. Micro nutrient

4:52

deficiencies that I want to talk about for

4:54

a couple of reasons. One because there was.

4:57

Widespread prevalence in terms of

4:59

either it and deficiency or

5:02

inadequacy. And. To because I

5:04

think they. Played. A very important role in a

5:06

love. To. Geological processes,

5:08

And her body under. Affect the way we age,

5:11

So. First, we're going to talk about Vitamin

5:13

D. And most of you

5:15

guys probably have already heard enough.

5:17

About Vitamin D. But I'm. A

5:20

It's important to talk. About because it's is

5:22

more than a vitamin. So vitamin D

5:24

gets converted into a steroid hormone. And.

5:27

It. Goes into the nucleus

5:29

of cells. And. Interacts with

5:31

Dna so it recognizes a very specific

5:34

sequence of Dna called the Vitamin D

5:36

response Element. And in this

5:38

is encoded in our Dna. I'm

5:41

and. That interaction than

5:43

either turns jeans on and activates them.

5:45

Or it does. the. Opposite is sort of

5:47

turned them down and repress as them. So.

5:51

It's very important for orchestrating. I mean,

5:53

we're talking about. Over. Five.

5:55

Percent of the proteins encoding

5:57

human genome is regulated. By.

6:00

Vitamin D. Which. Is quite a lot.

6:02

On. And so you know you

6:05

can imagine if if you're running

6:07

a car and ear pistons are

6:09

are firing. I'm out of sync with

6:11

each other, I mean, that's kind of what's happening

6:13

when you when you don't have adequate levels of

6:15

vitamin. Your. Genes are being

6:17

regulated in the way. They're supposed to be of things

6:20

are being activated when they're supposed to be or repressed and

6:22

are supposed to be. Some things are kind of. In

6:24

Out and going going awry. I'm.

6:27

And as a mentioned about it is

6:29

is widespread problems In terms of inadequacies,

6:31

about seventy percent of the population has.

6:34

Inadequate levels of Vitamin D. Which.

6:36

Will talk about a minute. It's

6:38

about thirty nanograms per milliliter. Or life.

6:41

And. It's a very simple solution and that also

6:43

I like to talk about it because. It.

6:46

Is it's almost as the simplest, taking

6:49

a basically a supplement that cost a

6:51

penny upheld by to Monday supplements. Or

6:53

one the most affordable. Settlements out there and

6:55

and there's really just no reason other

6:57

than lack of. Education About.

7:00

Adam indeed for people to be

7:02

so discussion and insufficient. A

7:06

lot of reasons for the widespread

7:08

deficiency I'm We know we make

7:10

Vitamin D treanor skin so you

7:12

be be radiation is essential to

7:14

make Vitamin D three. Anything that

7:16

block that you've he be radiation

7:18

is going. To stop the production of

7:20

Vitamin D. So we're talking sunscreen. On

7:23

melanin, which is the dark skin pigmentation that

7:25

protects us from the burning raise of the

7:27

sun. I'm. Also is a

7:29

natural sunscreen. So that is also a

7:31

form of sunscreen. At also

7:33

when depending on where you live so

7:36

in northern latitude are you can be

7:38

radiation can even reached the atmosphere you

7:40

know several months out of the year.

7:43

So. When you combine some of these factors of the say, take.

7:45

Someone with darker pigmentation. From let's

7:47

say East Asia and they move

7:49

somewhere like Chicago or they moved

7:51

to Sweden. Where. You know,

7:54

six months out of the year you're not even

7:56

getting that you've he be radiation. You're

7:58

talking about just a, you know, Compounding

8:00

effect on vitamin D

8:02

deficiency because. I'm you

8:04

know there's been studies out of the universe

8:07

is cargo that have shown. That.

8:09

For example, African Americans, Have

8:11

to stay in the sun anywhere between

8:13

six to ten times. Longer.

8:15

Than caucasians with fair skin to make

8:17

the same amount of Vitamin D three

8:20

in their skin. So. You're

8:22

talking. I mean it's it's a very. I mean, it's

8:24

a it's a compounding effect with respect to. To

8:26

the to the melon and nexen as well

8:28

And an age plays a role. for we

8:30

age you know everything is less efficient. On.

8:33

So you know a seventy year old makes

8:35

about. I think it's four times less. Vitamin

8:37

D three in her skin. Than. Their

8:40

former twenty year old self. So.

8:42

And then of course modern day societies that we

8:44

have. Were. Inside Indoors.

8:46

Where at our computers were in our cubicles? Where

8:49

technology in a we're Not out? Where? It

8:51

is. It's not an agricultural society. We're

8:53

not outside. You. Know as as

8:55

much as we used to be and

8:57

so I'm. Not I'm Mindy Is

8:59

this not being made in or stands? Like it was

9:01

a hundred years ago. So. There's a lot

9:03

of reasons why it's it's widespread. I'm

9:08

I like to show this the slide. It was

9:10

a study published several. Years ago. Two thousand and

9:13

nine. And and it's is

9:15

showing. I'm when you knock out

9:17

the Vitamin D receptor. In.

9:19

In mice. That. It

9:22

affects the way they age. So at

9:24

the top of the pally you can see

9:26

that both mice that wilde Heideman Vitamin C

9:28

receptor knockout. Sort. Of aging the same

9:30

and then four months later. The. Vitamin

9:32

D Receptor mouse is is is is.

9:35

It is an accelerated aging model and.

9:37

You know he i looked terrible but like

9:39

of the organs and and every level things

9:41

where. I'm a sort of accelerated in

9:44

the way they were aging. So.

9:46

I'm is is. Is kind of a nice visual

9:48

to see. But. Of course, we're

9:50

not mice, and I've always often wondered

9:52

why mice. Even need vitamin D because you know

9:55

they're nocturnal nam I'd aces one of those things where

9:57

it's like I don't know how much of that actually

9:59

translates to humans. Let's talk about the Human

10:01

Studies. I'm. You. We.

10:03

Know that there's a lot of the it

10:05

out there observational data that's. Correlated: Vitamin D

10:07

levels too low Vitamin D levels

10:10

to hire all cause mortality risk

10:12

hired a cancer mortality but there's

10:14

always that. Question of. Healthy.

10:16

User by us? Maybe. People with

10:18

sire vitamin D or outside. And more physically

10:21

active and of course you try to correct for

10:23

as many can be no confounding. Factors:

10:25

As possible it's you never really

10:28

can establish causation. That's. Where

10:30

I'm in Deeley and randomization comes into

10:32

play. Services. We, you know we. Have

10:34

a variety of genes that

10:36

are responsible for converting Vitamin

10:38

D three into twenty five.

10:40

Hydroxy vitamin D which is the. Most

10:43

it we know after circulating form of

10:45

vitamin d and then subsequently into the

10:47

steroid hormone which is when twenty five

10:49

hydroxy by to d. On. The

10:52

some of these gg that make enzymes. We

10:55

all are different and says some people have

10:57

ones that don't do it efficiently. I

10:59

miss him and dealing rent Physician takes. To

11:02

these teens this the single nucleotide

11:04

polymorphisms. In. These genes and says

11:06

okay, we're going to randomize them People

11:08

that have these genes that we know.

11:11

Make. Them basically have lower levels

11:13

of. Twenty Five Hydroxy Vitamin D.

11:16

And. See what? Their. You know, Corlett.

11:18

To Health. Outcomes like all cause mortality,

11:20

So. Front of a in a. Wave. Right away. Randomized and

11:23

people. And. People that have

11:25

genetically low Vitamin D levels independent

11:27

of what's your lifestyle is, they

11:29

have a much higher all cause

11:31

mortality. They. Have a higher cancer

11:33

related mortality and they have a higher.

11:35

Respiratory disease mortality on with

11:37

very little or no effect

11:39

on cardiovascular mortality. And

11:43

there's also been. Up

11:46

with randomized controlled trials. Obviously, you're not

11:48

going to have a lifelong randomized controlled

11:50

trial. Looking at. Mortality. But

11:52

there's. You know there's other biomarkers

11:54

that can be looked at. One is.

11:57

Epigenetic aging which I'm sure you grades

11:59

heard about yesterday. So

12:02

one study that took people that were vitamin

12:04

D deficient, and it's important to start out

12:06

with a cohort of participants that

12:08

are deficient, right? Because if you already

12:10

have someone that's sufficient, giving them a

12:12

vitamin D supplement really shouldn't do much because

12:14

they're already at a sufficient level.

12:17

So these were African-American individuals

12:19

that were also overweight, and

12:22

so they were very vitamin D deficient. They

12:24

were given a vitamin D supplement with 4,000

12:27

IU's of vitamin D a day, and

12:29

it decreased their epigenetic age by

12:31

almost two years. So

12:35

the question is, what is deficiency,

12:37

insufficiency, adequacy?

12:41

So technically, it's kind of, I

12:43

would say, depending on what institute

12:45

you're looking at, but the

12:47

Endocrinology Institute defines deficiency

12:50

as 25

12:53

hydroxyl vitamin D levels less than 20

12:55

nanograms per mil. Sufficiency is about

12:57

30, getting, you know, so

12:59

if you're insufficient, you're less than 30, but

13:02

if you're sufficient, you're more than 30. And

13:05

it seems as though the sweet spot for vitamin D

13:07

is between 40 to 60

13:09

nanograms per milliliter, and,

13:12

you know, there's all-cause mortality studies

13:14

also looking at vitamin D levels.

13:16

There's meta-analyses of these, you

13:19

know, ranging from 1960s all the

13:21

way to the, you know, mid,

13:23

like, 2015, and it's really, it

13:25

seems like 40 to 60 is a really good

13:27

sweet spot for the lowest all-cause mortality with vitamin

13:29

D. As I mentioned, 4,000, I

13:32

mentioned 4,000, I use a vitamin D a

13:34

day because that's the

13:36

tolerable upper intake for vitamin D,

13:38

so it's quite safe. And

13:42

in general, 1,000 I use

13:44

a vitamin D generally raises people's

13:46

blood levels by about 5 nanograms

13:48

per mil. So the key

13:50

is to just get a vitamin D blood test. Do

13:52

it, you know, after you're supplementing,

13:54

make sure your levels are adequate because, again,

13:56

a lot of these single

13:59

nucleotides... polymorphisms in genes that affect our

14:01

enzymes that are metabolizing vitamin D also

14:04

affect how we respond to supplemental

14:07

vitamin D and some people can require a

14:10

much higher dose than other

14:12

people. So really the key here is blood

14:14

test and measuring. You don't know

14:17

what you don't measure, right? So

14:21

the next micronutrient I want to kind of

14:23

shift gears and talk about is magnesium and

14:25

this again it's widespread inadequacy

14:28

here about half the US

14:30

population has inadequate levels of

14:32

magnesium. So magnesium is

14:34

found at the center of

14:36

a chlorophyll molecule. So plants,

14:39

you know, you know chlorophyll gives plants

14:41

their green color. So dark leafy

14:43

greens are a really good source of magnesium

14:46

and essentially people aren't eating enough

14:48

greens which is why half the

14:50

country doesn't have adequate levels of magnesium.

14:53

Magnesium is a co-factor for

14:55

over 300 different enzymes in

14:57

the body, a lot of metabolic processes

15:00

so it's important for the

15:02

production of energy in the form of ATP. It's

15:04

important for the utilization of energy in the

15:06

form of ATP but it's

15:08

also important for repairing DNA

15:11

damage. So DNA repair enzymes

15:13

require magnesium to function and

15:16

this is where I think the

15:19

aging, its role in aging

15:21

comes into play because DNA damage

15:24

is something that's happening every day. It's happening

15:26

right now and all of us as you

15:28

know are we're metabolizing food

15:30

was we're breathing in oxygen,

15:32

immune system slightly activated whatever.

15:35

It's constantly happening and our bodies are repairing

15:37

that damage but it's an

15:39

insidious type of damage, right? It's not something that

15:41

you can just wake up and look in

15:43

the mirror and see, right? You're not, you're

15:46

not, scurvy is like okay my gums

15:48

are bleeding and something's wrong you can see

15:50

that right? DNA damage isn't something that you

15:52

really think about on a daily basis but

15:54

it's happening and it accumulates with age.

15:57

So you want to be able to repair that Damage.

16:00

Effectively right. On for many

16:02

reasons, so Dna damage can lead

16:04

eventually. Over. The course the several. Decades

16:06

to oncogen equitation second lead

16:08

to cancer. And. So they're

16:10

ben Actually a variety of studies

16:12

in a beloved and correlated magnesium

16:14

level of magnesium intake. With cancer

16:17

mortality. So there was one study that

16:19

found for every. One hundred milligrams

16:21

of magnesium intake. There.

16:23

Was a twenty four percent decrease

16:25

in pancreatic cancer. Risk

16:28

and also another study that found

16:30

that people that had the highest

16:32

levels of magnesium there in the

16:34

top quintile. Had. A forty

16:36

percent lower all cause mortality compared to

16:39

people in the lowest. And then they

16:41

had us fifty percent decrease in cancer

16:43

mortality compared to people in the lowest.

16:45

So. Magnesium. Is

16:47

one of those. I'm. Again,

16:49

I think it's best to try. To get from dietary

16:51

sources dark leafy greens are a great source.

16:53

But also supplemental. Forms of Magnesium I

16:56

think is a great sort of insurance

16:58

so to speak. So I'm. Magnesium.

17:00

Glycine aids. Magnesium malaise me like

17:02

magnesium citrate, these are all pretty

17:04

bio available forms of magnesium. The.

17:07

Requirements for: magnesium. The plan

17:09

on age, gender, So you know men

17:12

require a little bit more than women. It's somewhere

17:14

like four hundred milligrams a day for man, In

17:16

somewhere like three hundred a three fifty or something

17:18

like that for women. I. Miss your

17:20

athletic. If you're sweating, if you're.

17:23

In a physically I still I use

17:25

a sauna. I'm you actually

17:27

can require anywhere between ten to

17:29

twenty percent above the arts. Yeah,

17:31

because you do lose magnesium. Three

17:34

sweat. So. If passed,

17:36

the Us population isn't meeting even

17:38

that our dna. Then. You can

17:40

imagine the physically active people are probably

17:42

you know fairing even worse because. They're.

17:44

Already that their requirements are even higher. So.

17:47

It's a simple solution. Simple,

17:49

died sept dirt dietary modifications.

17:51

Supplement. You can take. i'm to help

17:53

sort of get your magnesium levels

17:55

hair So

18:02

Omega-3 is the

18:04

last micronutrient that I want to cover

18:06

before getting into the next part of my talk.

18:10

And Omega-3, there's three forms of it.

18:12

So there's ALA, which is found

18:14

in plant forms like Black

18:16

Seed, Walnuts. There's

18:19

EPA and DHA, which are marine

18:21

sources. So they're found in seafood.

18:24

And there's a study out of Harvard that was published, gosh,

18:26

it was like 2009. This

18:30

study identified the top six preventable

18:32

causes of death. So these

18:34

are things that are lifestyle related. So

18:39

hypertension, for example, smoking,

18:42

avoiding hypertension, avoiding smoking,

18:44

those were some

18:46

of the top six preventable causes of

18:49

death. Well Omega-3, not getting enough Omega-3

18:51

from seafood, so this was a marine

18:53

source of Omega-3, EPA and DHA, was

18:55

in that top six. And

18:58

researchers from Harvard had identified

19:01

that not getting enough Omega-3 from

19:03

seafood was responsible for about 84,000 deaths a year.

19:09

And that was compared to trans

19:11

fats. So trans fats were also,

19:13

consuming trans fats were one of

19:16

the top preventable causes of death.

19:19

Well, eating trans fats were responsible for 82,000

19:21

deaths per year, pretty much the same as

19:24

not getting enough Omega-3 from seafood.

19:27

And what's funny is that everybody knows about

19:29

trans fats. You walk into any supermarket, any

19:31

grocery store, everything's marketed, oh, zero

19:33

trans fats, zero trans fats. But

19:36

nobody's thinking about they're not getting enough

19:38

Omega-3. They're not eating

19:40

enough seafood or fish or taking microalgae

19:43

or fish oil supplement

19:45

to get Omega-3. And

19:48

so I just kind of like to highlight

19:50

that because it's, again, I think

19:53

that the way thinking about food

19:55

in that, you know, what do we

19:57

need to feed our body, our materials?

20:00

metabolism, we need co-factors, magnesium, vitamin

20:02

D, omega-3. These

20:05

are things if we focus on what we need to

20:07

consume, we don't end up eating all the

20:09

other stuff. And so people sort of

20:11

get fixated on what to avoid and don't think about

20:13

what they're actually supposed to be taking in, what they're supposed to

20:16

be eating. So

20:18

the omega-3 index is one of the best

20:21

measures of omega-3. So this was pioneered

20:23

by Dr. Bill Harris

20:25

and his colleague Von Schacke many

20:27

years ago back in

20:30

2004 and it's measuring

20:32

omega-3 levels in red blood cell

20:34

membranes as opposed to plasma phospholipids.

20:37

And the reason for that is because it is

20:40

a long-term biomarker of omega-3. So

20:42

your red blood cells take about 120 days

20:44

to turn over, whereas

20:46

your plasma phospholipids, it's more like if

20:49

you get your omega-3 levels measured and it's

20:51

plasma phospholipids, it's more like what did I

20:53

eat the past week or something

20:56

like that. So it's

20:58

kind of a comparison is

21:00

fasting blood glucose would be the

21:02

immediate biomarker and then the

21:05

HBA1c is your long-term blood glucose level.

21:07

So it's sort of similar here. So

21:09

omega-3 index is a really important

21:12

way to measure omega-3 and it's

21:14

now being increasingly used in many

21:16

scientific studies. Of course, many, I

21:18

think a lot of conflicting data out there also

21:20

has to do with the fact that plasma phospholipids

21:23

were measured. And again, it

21:25

goes down to this, well, was it just

21:27

that they didn't eat omega-3 in the last

21:29

week or they did? And so we're saying

21:31

they have high omega-3 because of that just

21:34

recent dietary choice, right? So

21:37

omega-3 index was, this is again from Bill

21:40

Harris's group. He found, him and his colleagues

21:42

found that people with a high omega-3

21:44

index, which is defined as 8%, at

21:47

least 8%, had a 90% reduced

21:50

risk of sudden cardiac death compared to people with

21:52

a low omega-3 index of 4%. The

21:56

standard, in the US, the

21:58

omega-3 index, most people, it's about 10%. It's less than

22:00

5%, so it's about 4%. So most

22:02

people in the United States are at

22:04

a very low omega-3 index. They don't eat enough

22:07

seafood and fish. So

22:09

sudden cardiac death is reduced by 90% if you're

22:12

in that high omega-3 index group. Cardiovascular

22:14

disease is the number one killer in the

22:16

United States and actually in most

22:19

all developed countries. Every 33

22:21

seconds, someone dies of a heart

22:23

attack. So anything you

22:25

can do to improve cardiovascular health is

22:28

really, really on your side in terms of

22:30

improving health span, improving your lifespan. The

22:35

high omega-3 index also from Bill Harris's

22:37

group found that people again with an

22:40

8% omega-3 index had

22:42

a five year increased life expectancy

22:45

compared to people with a 4% omega-3 index. So

22:48

that was the low end. And it's

22:51

interesting because in Japan, their

22:54

life expectancy on average is

22:56

about five years longer than in the

22:59

United States or average life expectancy is five

23:01

years less here than in Japan.

23:04

And they happen to have an omega-3 index in

23:06

general above 8% whereas again, I mentioned

23:09

we're below 5%. So

23:11

sort of an interesting sort of observation

23:14

that also correlates with the increased average

23:16

life expectancy in a country that eats

23:18

a lot of seafood. But

23:20

this is what really I think is

23:23

almost, it's eye opening. It's

23:26

part of the same study from Bill Harris's group where

23:28

they stratified these participants and looked at

23:31

their omega-3 index and then also look

23:33

at their smoking. So the

23:35

very, very top curve, the green curve, people lived

23:37

the longest if they had the 8% omega-3

23:39

index and

23:42

they were non-smokers. And

23:44

the very, very bottom curve, the red

23:46

one was people that were smokers and

23:49

had a low omega-3 index, 4%. So

23:52

they had the lowest life expectancy.

23:54

But this is what blows my mind. If

23:57

you look at the orange and blue curves,

23:59

they're completely, completely overlaid on top of

24:01

each other. So people that

24:03

had a high omega-3 index but

24:05

smoked had the same life

24:08

expectancy as people that didn't smoke

24:10

but had a low omega-3 index. So

24:12

essentially, if you just look at this data alone, smoking

24:15

was like having a low omega-3 index. And then

24:18

just, again, it's one of those things where, of

24:20

course, it's observational data and you can never really

24:22

establish causation. But I just feel

24:24

like that's really eye-opening because,

24:27

again, everyone knows smoking is bad for

24:29

you, but nobody's thinking about how

24:31

we're not getting enough omega-3. And

24:34

how easy is it to take

24:36

a fish oil supplement, for example,

24:38

or increase your salmon

24:40

intake? So

24:43

to summarize this part of my talk with

24:45

respect to micronutrients, we talked about vitamin D,

24:48

low-hanging fruit, as simple as a

24:51

supplement, 4,000 IUs a day is

24:53

a pretty good start to get

24:55

most people who are deficient to a sufficient

24:57

level. That's been shown in several studies. Getting

25:00

people from a deficient level up to a

25:02

sufficient level can be done with 4,000 IUs of vitamin

25:04

D a day. Omega-3 fatty

25:07

acids, getting the omega-3 index

25:09

test, you

25:11

want your levels to be in the 8%. You

25:14

want to be high. And then

25:16

there's been studies showing that it takes

25:19

around 2 grams of supplemental

25:21

omega-3 to get from a 4% omega-3

25:23

index to an 8%. It's

25:26

really not that hard. And

25:28

then, again, omega-3

25:31

is found in prescription form. I

25:33

didn't go into all the randomized controlled trials today, because

25:35

that would take the remainder of my

25:38

time here. But you

25:40

can get omega-3 in

25:42

purified apoelester form, either in

25:44

the form of EPA only, Vesipa,

25:46

or DHA plus EPA, Lovesa. And

25:49

those are prescribed in 4 grams a day

25:51

per dose. And so what I said

25:53

was sort of conservative. It takes about 2 grams

25:55

a day just to get from a 4% on average, 4% omega-3 index to an 8%. And

26:00

again, it's as simple as getting the test done and

26:04

supplementing and then testing again and seeing if you're

26:06

getting your index up to 8%. And

26:09

then magnesium, we talked about getting

26:12

that RGA, hitting it with

26:15

either increasing or a combination,

26:17

ideally, of increasing leafy greens

26:19

and also taking a supplement.

26:21

Magnesium, bisonate, citrate, malate are

26:23

all pretty bioavailable sources of

26:25

magnesium. Okay,

26:29

so we're going to shift gears and we're going

26:31

to get into the effortful part of

26:34

this presentation, this talk. This

26:37

requires putting in the work, right? This

26:39

isn't as simple as taking a pill. But

26:42

at the very least, I think that taking

26:45

the pill is easier for a lot of

26:48

people. But then there's, of course,

26:50

the people that want to go this step further and they're willing

26:52

to put in the effort. So let's talk about that. We're

26:54

going to talk about why I'm convinced

26:58

that vigorous exercise is the

27:00

most powerful longevity drug that

27:02

you're going to get more than

27:04

metformin, more than rapamycin, more

27:06

than any of those things. If you could pill

27:08

up what you could do with vigorous

27:10

exercise, then I think that is like

27:12

right now the best longevity drug we

27:15

have for delaying the aging process

27:17

and improving health span and improving

27:19

lifespan. So when I say

27:21

vigorous exercise, what do I mean? Generally

27:25

speaking, of course, there's

27:27

a sliding scale here because you can take someone

27:29

who's completely sedentary and never really done any

27:31

aerobic exercise. Vigorous exercise for

27:33

them is going to be probably more

27:36

what light to moderate exercise is

27:38

for people that are physically active. But

27:40

generally speaking, once you kind

27:42

of adapt and get

27:44

used to being physically active, vigorous

27:46

exercise is about getting to 80

27:49

percent your max heart rate or

27:51

estimated max heart rate. That's

27:54

really what I'm talking about, 75 to 80 percent

27:56

of your maximum heart rate. So,

28:00

cardiorespiratory fitness, this

28:02

is one of the best biomarkers for

28:05

longevity, in my opinion. So,

28:08

cardiorespiratory fitness is measured

28:11

empirically by VO2max. So, that's

28:13

the maximal amount of oxygen that you can take

28:15

up during maximal exercise.

28:20

So, when I use VO2max, sometimes

28:22

these are interchangeable, cardiorespiratory fitness, VO2max,

28:24

I kind of use them interchangeably in this

28:27

talk, but VO2max is just directly measuring

28:30

cardiorespiratory fitness. So, cardiorespiratory

28:32

fitness is associated with

28:34

improved longevity. It does improve longevity.

28:37

And the biggest improvements you're going to get is if

28:40

you're going from low normal,

28:42

so for your age group, for your gender,

28:44

if you're low normal, and going anywhere above

28:47

that is where you get the biggest bang

28:49

for your buck. So, people that

28:51

have a low normal VO2max, if

28:53

they just go up to 8th,

28:55

if they're below, sorry, if they're

28:58

below normal, and they go up

29:00

to just low normal, they get about a 2.1 increased

29:04

life expectancy. If they're

29:06

below normal, and they go up to

29:08

high normal, they get almost a three-year

29:10

increased life expectancy. And then if they

29:12

go from below normal to the upper amount

29:14

of normal, so this is the top 5%

29:17

of the population, this is more like you're getting

29:19

into the elite athlete level, that's

29:21

associated with almost a five-year increase in

29:24

life expectancy. So,

29:26

just to give you some perspective here, about half

29:29

of the U.S. population is they

29:32

have a low normal cardiorespiratory fitness, and

29:34

the other half has about a high

29:36

normal cardiorespiratory fitness.

29:38

So, again, just mostly

29:41

having to do with being physically active or

29:43

not being physically active. And

29:45

on average, for every unit

29:47

increase in VO2max, it's

29:50

associated with a 45-day increase

29:52

in life expectancy. And

29:54

there was a really important study published in JAMA back in

29:56

2018 that I just like to mention

30:00

because it kind

30:02

of established that there was no

30:04

upper limit to the mortality reduction

30:07

of having a high cardiorespiratory fitness.

30:09

I mean, obviously within normal human

30:11

life expectancy ranges, right? So

30:15

people that were in the bottom 25% of

30:19

cardiorespiratory fitness or their VO2 max.

30:22

And also I like these studies because they're

30:24

measuring something empirically. I'm talking about

30:26

VO2 max, right? This is a

30:28

fitness test that's done, it's measured, it's

30:31

empirical versus a

30:33

lot of studies and conflicting data out there

30:35

where you have these questionnaires. How

30:37

physically active are you? And

30:39

you think about your last week or month

30:42

and then that's like you extrapolate it out and you

30:44

go, okay, well, based on this last week, this is

30:46

how physically active we think this person is over

30:48

their lifetime or whatever. And

30:52

I just, it's not a very, it's

30:54

all we have in some respects, but

30:57

if you can measure something empirically,

31:00

it's gonna really help clear up

31:02

a lot of the confounding and a

31:04

lot of the conflicting data that

31:06

you see out there. So I really

31:08

like studies that measure VO2 max because

31:10

it's something that's actual, it's actually empirical

31:12

rather than going off the questionnaire, right?

31:15

Those have all sorts of problems. Now going

31:18

from the low bottom 25% of

31:20

VO2 max up to the elite level, so

31:22

you're talking about the top 2.3%, I mean,

31:24

these are the elite athletes, that's

31:27

associated with an 80% reduction

31:29

in all cause mortality. So

31:31

comparing those two groups, people in the low 25% group

31:34

versus the like the elite level. But

31:38

even going from the high cardio

31:40

respiratory fitness, so this is the top

31:42

25% of the population, they're

31:46

good. I mean, these are people that are, they're

31:48

committed exercisers, they're really, they're physically active. If

31:51

they go up to the elite level, they

31:53

get a, you know, even 20% more reduction in

31:55

all cause mortality. So

31:57

if you compare the elite to

32:00

the high cardio respiratory fitness, they're

32:02

good. fitness, you're still getting a 20% lower

32:05

all-cause mortality by just moving up to that

32:07

elite level. What

32:09

was really interesting about this study was that

32:11

being in that low 25% group, they're in

32:16

the bottom 25% for VO2 max, that

32:19

was comparable to either

32:22

same risk or greater risk than

32:25

for mortality, early mortality as

32:27

type 2 diabetes, as smoking,

32:29

and as having heart disease.

32:32

So again, putting that into perspective,

32:35

we all think about these diseases and how they're increasing

32:40

our early mortality risk, but just not

32:43

having a good cardio respiratory fitness can do

32:45

the same thing. So

32:48

how do you improve your VO2 max? How do

32:50

you improve your cardio respiratory fitness? Well, any

32:53

aerobic exercise is obviously

32:55

going to be good for small

32:57

changes in cardio respiratory fitness. But

33:00

in particular, there have been meta-analysis

33:02

that have found that vigorous intensity

33:05

exercise, as I mentioned, and particularly

33:07

high intensity interval training, which

33:09

we're going to talk about. So this is

33:11

where you're doing short bursts

33:13

of very vigorous exercise. You're at least

33:16

at 80% max heart rate, sometimes going

33:18

even above that, and then having

33:20

rest periods and doing those intervals. And

33:23

why that's important is because there have been

33:25

some studies that have found that even people

33:27

that are meeting the guidelines

33:30

for moderate aerobic

33:32

exercise, so they're doing two

33:34

and a half hours of

33:36

moderate intensity aerobic exercise per

33:38

week, about 40% of those people

33:41

do not respond. In other words, they do not

33:43

get VO2 max improvements. They are

33:46

not improving their cardio respiratory fitness

33:48

by doing two and a half hours of moderate intensity

33:51

exercise every week. And

33:53

it's not really known why exactly

33:55

there's this non-responder effect, but that's

33:57

large for some of the population. However,

34:01

when those people do more

34:03

of a high intensity interval

34:05

training workout, they do more vigorous exercise and

34:07

they start to respond and improve their VO2

34:09

max. And it's thought because

34:12

VO2 max, cardiorespiratory fitness, to

34:14

get those changes, to get those improvements you

34:16

really have to increase cardiac output. So

34:19

the stronger the signal, the more

34:21

intense the signal, the adaptations are

34:23

greater. So your body responds by

34:25

improving the delivery of oxygen to your

34:28

tissues, right? So that's essentially what you're

34:31

wanting to improve your cardiorespiratory fitness. And

34:33

so that's, it's kind of thought why vigorous

34:36

intensity and particularly high intensity interval

34:38

training is so important for improving cardiorespiratory

34:40

fitness. And one

34:42

of the, there's been

34:44

several studies looking at this and

34:46

for example, Dr. Martin Gabbala, out

34:48

of McMaster University over in Ontario,

34:51

Canada, has done a lot of

34:53

studies looking at different high

34:55

intensity interval training protocols. And

34:57

it really seems if you're really wanting to improve

35:00

that cardiorespiratory fitness, that you

35:02

have to do longer intervals. So three to five

35:04

minute intervals of just the

35:07

maximum intensity that you can maintain

35:09

for that three to five minutes. And

35:11

so a really good and well studied, a

35:13

lot of evidence on the Norwegian four by

35:15

four protocol. So this is four minutes

35:18

of the highest intensity that you can do. And

35:21

then it's three minutes of recovery. So you're really

35:23

going down to like light,

35:25

light exercise. You want your heart rate to go down.

35:27

You want to sort of really give yourself some rest

35:29

so that you can do it again. So you repeat

35:31

this four times. That's why it's called four by four.

35:34

And this is one of the best protocols for improving

35:36

VO2 max. If you

35:38

don't want to go into a lab to

35:40

get your VO2 max measured or you don't

35:42

have access to it for whatever reason, one

35:45

of the best evidence based ways

35:47

of measuring VO2 max at

35:51

home, so to speak, not necessarily home

35:53

is what's called the 12 minute run

35:55

test or walk test depending on your

35:57

fitness level. Essentially,

35:59

you need some sort of wearable

36:01

device that can track your distance, so

36:05

Apple Watch, your Fitbit, whatever, and

36:08

you need to have a flat surface that

36:10

you can run on, so like a track

36:12

field, and you wanna run for 12 minutes

36:15

or walk, depending on your fitness level, the

36:17

maximum intensity that you can maintain for that

36:19

12 minutes. And basically your

36:21

distance is gonna be covered, and then

36:23

you look up this equation, and it

36:25

converts your VO2 max based on that distance.

36:27

And the reason you don't want hills and

36:29

stuff is because that'll make you run, the

36:33

distance will be less. So you wanna make sure you're

36:35

giving yourself a flat surface so that

36:37

you actually are more accurate in determining what

36:40

your distance is during that 12 minute run test. This

36:47

study out of UT Southwest

36:50

in Dallas by

36:52

Dr. Ben Levine is

36:54

really what has convinced me that

36:57

vigorous exercise is extremely important

37:00

for the heart and the way the heart ages. So

37:03

I mentioned cardiovascular disease, I mean that's the number one

37:05

killer in developed countries, right? So

37:09

as we age, our heart undergoes certain in

37:11

and out of all changes. It gets

37:14

smaller, it shrinks, it gets stiffer,

37:16

less flexible, and this affects a

37:18

lot of things. It affects our

37:21

cardiovascular disease risk. It affects

37:23

our cardiovascular fitness, the ability for

37:25

us to do aerobic exercise. And

37:29

so what Ben did in

37:31

this study, Dr. Levine did in this study was

37:33

really remarkable. He took a cohort of

37:36

participants that were 50 years old on

37:38

average, and these were sedentary

37:40

individuals that were otherwise

37:42

healthy. So they didn't have any

37:44

type two diabetes, hypertension,

37:47

et cetera. They were quote unquote

37:49

healthy, but they were sedentary. And

37:53

he separated them into two groups. So the first

37:55

group was the control group who did sort of

37:57

stretching and yoga for two years.

38:01

And then the second group was the exercise intervention

38:03

group. So these are the people that were going

38:05

to be doing the exercise. And

38:07

it ended up being a vigorous exercise protocol,

38:09

but because they were sedentary, it started out

38:11

sort of lower to moderate intensity.

38:14

And by the time it was six months, these

38:16

individuals are doing five to six hours a week

38:19

of aerobic exercise with

38:21

a large percentage of that time being

38:24

in what's called the maximal steady

38:26

state. And that's what I'm talking

38:29

about when you're going as hard as you can and

38:31

you maintain that for about 20 or 30 minutes. So

38:34

it's usually around 75, 80% max heart rate. And

38:37

you're doing that for about 20 to 30 minutes. They

38:40

also did the Norwegian four by four

38:42

protocol once a week. And

38:45

after two years, they

38:47

essentially reversed these structural changes in

38:50

their aging heart by

38:52

like 20 years. So their

38:54

hearts were essentially looking more like a 30 year

38:56

old heart after that two years

38:58

of vigorous intensity exercise. Now, like I

39:00

mentioned, they were doing five to six

39:03

hours a week of vigorous, a large portion

39:05

of it in vigorous exercise. But

39:07

it's simply astonishing, you know, the structural

39:10

changes that they found. So there

39:12

was more than 25% improvement in the

39:14

elasticity of the heart after those

39:16

two years, particularly in the left ventricular

39:18

muscle of the heart. Of

39:21

course, they did increase their their their VO two max by

39:23

about 20, 20% as well. So

39:27

it's just quite astounding that you can take a

39:29

50 year old, put them on a pretty intense

39:31

exercise program for two years, and

39:33

essentially reverse a lot of the structural changes

39:36

that happen, you know, in with

39:38

the heart with the aging process. Blood

39:43

pressure improvements are also, you

39:45

know, for people that are willing to put in the

39:48

effort most of the time, and there's always non

39:50

responders, but they can have drug

39:52

sized effects. In other words, they can be

39:54

comparable to some drugs that

39:56

are given to reduce hypertension. So

39:58

there's been an analysis of 24

40:01

different randomized controlled trials found that six

40:03

weeks of a pretty You

40:05

know moderate to vigorous intensity Exercise

40:08

20 to 60 minutes of that three to

40:10

four days a week Like

40:13

had almost drug-sized effects in reducing

40:15

blood pressure. So, you know, high

40:17

hypertension is not only a risk

40:20

factor for cardiovascular disease It's

40:23

also a very very important risk

40:26

factor for dementia and

40:28

Alzheimer's disease So there's every reason

40:30

to want to not have hypertension and

40:32

20% of young people aged, you

40:35

know 18 to 39 have hypertension

40:37

and then half the you

40:39

know about half the US population You

40:41

know older adults have have hypertension. So it's

40:44

a very common you

40:46

know thing that again

40:48

can be modified

40:50

to it to quite a bit of an

40:52

extent with aerobic exercise

40:55

particularly vigorous intensity exercise Let's

41:00

talk a little bit about on the molecular level

41:03

Why I why I'm talking about vigorous exercise

41:05

and really that 80% max heart rate It

41:08

has to do with the fact that you are pushing

41:11

when you push your muscles to work

41:13

harder Then the oxygen can

41:15

get to them to make energy

41:17

they shift to from

41:19

using mitochondria and using oxygen

41:22

for energy to using glucose

41:24

through glycolysis and It's

41:27

a quick process that doesn't require oxygen. It makes

41:30

lactate as a byproduct. Only

41:32

it's not a byproduct. We Often

41:35

thought about it as a metabolic byproduct, but it's

41:37

so much more than that. So

41:39

lactate generated from muscles is

41:43

Is what it's an extra kind it's

41:45

a myokine and it's a signaling

41:48

molecule it gets into circulation and it

41:50

is Consumed by the

41:52

brain. It's consumed by the heart

41:55

by the liver Also, by the

41:57

muscle. it's consumed as a. Very

42:00

easily utilize the bill source of energy

42:02

but also as a single molecule as

42:04

will talk about in this is called

42:06

the lactase shuttle. it was pioneered. By doctor

42:08

towards props out on out of U. C. Berkeley.

42:11

And when I say sibling molecule, it's

42:13

a way for your muscles to directly

42:15

communicate with other. Parts of the body like the

42:17

brain. Arm and so lactate

42:20

itself has been. shown. To be

42:22

responsible for increasing brain drive

42:24

Neuro Tropic Factor both. In the

42:26

plasma, As As and Human studies on. Humans.

42:29

Exercise. Lactate. Correlates

42:31

with the Bdnf activation. Plasma Bdnf

42:33

can cross over the blood brain

42:35

barrier. But. Also, animal studies showing

42:37

that it directly increases. Ranger Abner Trophy

42:40

Accept factor. In the brain. So.

42:42

Bdnf his arm. A very

42:44

important nurture of exact or it's response

42:46

of responsible for on neural. Plasticity.

42:49

Said. That the ability of your. Your. Brain

42:51

your neurons in your brain to

42:53

adapt to changing environment. It's very

42:56

important during the aging process in

42:58

as things are. You know, changing

43:00

and stuff. At your you want your your

43:02

your brain to adapt. To the changes. It's

43:04

also important for depression on people with

43:06

depression. Don't often adapt to changing

43:09

environment and it is. Partly responsible

43:11

for some the depressive symptoms. But

43:13

be brave Radner topic that are also

43:15

is important for neurogenesis the increase of

43:18

new neurons perfectly and some brain reasons

43:20

like the hippocampus. Which. Is involved

43:22

in learning and memory. I'm it's

43:24

an it's in it. It helps in

43:27

an existing neuron survive their been animal

43:29

studies that have shown. That when

43:31

you cook, when you induce and to do

43:33

exercise and they get those learning and memory

43:35

improvements that have also been found in human

43:37

studies. That. If you give them a

43:39

drug and block brain. Derived our topic factor:

43:42

they don't get those learning and memory benefits.

43:44

Are really seems as though brained Ragnar

43:46

traffic factor is important to get those

43:48

learning and memory benefits. From. Exercise

43:51

and again lactate. Is.

43:53

a key single molecule that increases

43:55

brainer abner a terrific factor lactate

43:57

is generated from you're exercising muscles

43:59

when forcing them to work hard. This

44:02

isn't just going on a brisk walk, this

44:04

is really getting your heart rate up, sweating,

44:06

getting flush in the face. Lactate

44:09

is also a signaling molecule to

44:11

increase neurotransmitters in the brain. This

44:13

has been shown in both human studies and animal studies,

44:16

so it's important for the production

44:18

of serotonin. So studies have found that

44:21

people that exercise produce a lot of

44:23

lactate, this correlates with an increase in

44:25

serotonin, which also correlated

44:28

with improved impulse control.

44:30

Serotonin plays an important role in many neurological

44:33

processes, including impulse control. So they're

44:35

being able to have

44:37

this inhibitory effect, which also plays a

44:40

role in focus and attention. Norepinephrine

44:43

is another one that's been shown. So as

44:46

we're exercising really hard, our muscles are working harder,

44:48

our heart is working harder, but our brain is

44:50

also working harder. And there have been

44:52

human studies out of, I believe

44:54

it's Norway, that I found that the

44:56

lactate produced during vigorous intensity

44:59

exercise crosses the blood

45:01

brain barrier, it's consumed by the brain, and

45:03

this correlates with a burst of

45:06

norepinephrine production, which fuels

45:08

the brain to work harder during exercise.

45:10

It's also important for focus and

45:12

attention and some of those effects that you get after,

45:15

you know, after you do like a vigorous intensity

45:18

workout. So

45:21

there's some protocols that have been shown

45:23

to maximize brain drive neurotrophic factor in

45:25

humans, and some of these have also

45:27

correlated with lactate levels. It

45:29

seems as though like the the

45:31

best is getting getting the best of both

45:33

the world. So you want vigorous intensity, about

45:36

80% max heart rate, but you

45:38

also want duration. So you want to get like 30

45:41

to 40 minutes of that is the

45:43

most robust at increasing brain drive

45:45

neurotrophic factor as measured in

45:47

plasma on people, but 20 minutes will also

45:50

increase it as well. Just 30 to

45:52

40 minutes does it even more. There's

45:55

also some protocols that are more high intensity interval

45:57

training. So Doing six rounds

45:59

of. Forty second intervals. We're going

46:01

as hard as you can for

46:03

forty second, followed by recovery period.

46:06

I'm. Also really increases brain. Drive

46:08

Narrow topic factor. In fact, It increases

46:10

at forty five times more. People.

46:13

And compared to to individuals that are

46:15

during about an hour and a half

46:17

of more lower. And tensile intensity cycling.

46:19

On about twenty five percent their their B

46:21

O two max peak. I

46:26

want to just shift gears for a minute

46:28

and talk about some of the anti cancer

46:30

effects of. Vigorous. Intensity Exercise

46:32

I'm you know, the independent of

46:34

their immune system. So the immune

46:36

system. Exercise. Activates immune system

46:38

is a robust effect. On a variety

46:40

of on. You. Know. Anti

46:43

Anti Many static affects their

46:45

but I'm just a mechanical

46:48

force. Of blood flow

46:50

Blood flow. Actually affects what are

46:52

called circulating to herself. Circulating.

46:54

To resolves escape from the primary side

46:56

of the to earth, get into circulation,

46:58

eventually travel the distant. Sites. In

47:00

the name, take residents and establish a new

47:02

tumor elsewhere So this is metastasis. I'm.

47:06

So. Circulating to resolve you. Obviously

47:08

I do not want to have them. Are

47:11

in circulation because they can. Apply

47:13

role and classicist. While. The searing

47:15

forces of blood flow itself can

47:18

tell they circulate circulating to resolve.

47:20

Because. On every cell surface we have

47:22

a mechanical. Arm were we

47:24

have these mechanics mccann over sectors.

47:27

That. Respond to movement. And

47:30

cancer cells are all wonky and disrupted,

47:32

messed up and so they just can't

47:34

handle that movement. And they die. So. The

47:36

them the more intense to exercise, the more

47:38

the great of the blood flow. The.

47:40

The higher proportion of circulating to resolve

47:43

that are that are actually I'm on

47:45

undergo a hostess and and die. The.

47:48

Rents and Studies Looking at people that undergo.

47:50

About six months of a robot exercise and

47:52

were between fifty. To seventy percent max heart rate for

47:54

a one hundred and fifty minutes a week. That.

47:57

Significantly reduces the circulating. To

47:59

resolve. in people with anywhere

48:02

between stage one to stage three, colon cancer.

48:04

Other studies have found and correlated

48:06

that circulating tumor cells are

48:09

linked to a three times higher risk of

48:11

cancer recurrence and a four times

48:13

higher risk of cancer mortality in people with

48:15

cancer. Also stage three

48:17

colon cancer patients that engage in aerobic exercise

48:20

have a 40% reduction in

48:22

cancer recurrence and a 63% reduction

48:25

in cancer mortality. So

48:27

exercise is also a very

48:29

important, plays a very important role in

48:32

cancer metastasis and also

48:34

in helping as an

48:36

adjunct therapy to treating cancer as well. But

48:41

you don't have to do the 40 minutes

48:44

of vigorous intensity exercise

48:46

every day to get

48:48

benefits. So there's something called exercise

48:50

snacks. These are very short

48:53

and anywhere between one to three minute bursts

48:55

of intense exercise. You're getting your heart rate

48:57

up 75, 80, 90% max heart rate. You

49:01

can be doing anything from jumping

49:04

jacks to sprinting

49:06

stairs to high knees to air

49:08

squats. There's a lot of ways

49:10

to do it and you do it just in

49:12

a short burst. So it's a

49:14

really great way to break up the work

49:17

day. It's also a really great

49:19

way to improve metabolic health, particularly

49:21

when you time it around meals, which

49:23

we'll talk about in a minute. And the way it does

49:25

that partly, well, there's a lot of mechanisms that

49:27

play, but one of them again comes back

49:30

to lactate being generated, you

49:32

know, very acutely from

49:34

exercising muscle, which then causes

49:36

glucose transporters on the muscle

49:38

surface to translocate to the

49:40

muscle surface. So these are

49:42

glute four transporters. These then allow glucose

49:44

circulating in circulation to then being taken

49:46

up into muscle, therefore improving your

49:49

blood glucose levels. And it also improves

49:51

insulin sensitivity as well. When

49:53

they're timed around mealtime,

49:56

anywhere between 30 minutes to an hour.

50:00

It dramatically has an effect on blood

50:02

glucose levels and insulin sensitivity, particularly in

50:04

people with metabolic syndrome, type 2 diabetes.

50:06

So it's a great way also, you

50:08

just get out, do some high needs

50:10

for a minute or jumping

50:12

jacks or do something that you can do quickly

50:14

to get that exercise

50:16

snack in. And another

50:19

way to proving metabolic health, I'll just mention briefly

50:21

because we're running out of time, is

50:24

through improving mitochondrial biogenesis, the

50:26

generation of new healthy young

50:28

mitochondria. It's been trying to do

50:30

this in muscle cells and this is also happening

50:32

through lactate. Lactate is a

50:35

signaling molecule yet again increasing the

50:37

expression of a very important

50:39

protein involved in mitochondrial biogenesis called

50:42

PGC1 alpha. And

50:44

so it plays an important role in increasing

50:46

new mitochondria in muscle. This has

50:48

been shown in human studies, but also animal studies

50:50

have found that exercise increases

50:53

lactate, which crosses the blood-brain barrier and

50:56

gets into the brain and increases mitochondrial

50:58

biogenesis in the hippocampus and

51:00

neurons in the hippocampus. So

51:02

mitochondria in neurons and the hippocampus are being increased.

51:05

I don't know why that mechanism wouldn't be

51:07

conserved in humans. So the

51:09

fact that it's happening in animals is

51:12

also encouraging. But

51:15

exercise snacks are also associated with

51:17

improved longevity. So I

51:19

was talking about this sort of deliberate form of

51:21

exercise snacks where you're doing high knees or jumping

51:23

jacks. Well, there's large

51:26

studies that have been underway

51:28

and have been published and there's ongoing

51:30

studies looking at vigorous intermittent lifestyle

51:32

activity. So it's a type of exercise snack

51:34

where you use everyday life situations to get

51:37

your heart rate up high for a minute

51:39

or two minutes or three minutes. For example,

51:42

you have to take the stairs every day to get to work.

51:44

Once you're walking up the stairs, you sprint. So

51:48

people are wearing these

51:50

accelerometers and so their heart

51:52

rate is being measured and you know, scientists have been

51:54

able to gather all this data and they found that

51:56

people that have engaged in one to two minutes of

51:59

vigorous intermittent lifestyle activity activity three

52:02

times a day have a

52:04

40% reduction in all cause

52:06

and in cancer mortality and a

52:08

50% reduction in cardiovascular related mortality.

52:10

This is compared to non-exercisers.

52:13

Now also people that even identify themselves

52:15

as non-exercisers, so you know they're doing

52:18

this vigorous stair climbing and stuff but

52:20

they don't actually go to the gym

52:22

or do any leisure time activity, they

52:24

still get these improvements. So it's

52:27

a really great way to break up sedentary time. Being

52:30

sedentary itself is an independent risk factor

52:32

for all cause mortality, cancer mortality, so

52:34

in other words just periods of when

52:36

we're sitting like now is a

52:38

risk factor even if you you're gonna go to

52:40

the gym you know later today. So

52:43

breaking up sedentary time is really important,

52:45

there's a lot of ways to break

52:48

up your sedentary time and I think that these exercise

52:50

snacks are a great way to do it. You just

52:52

get up and you do high

52:54

knees for one minute, two minutes, three

52:56

minutes and I really kind of wanted to just have

52:58

everyone do it for 30 seconds if we could do that

53:00

real quick I'm gonna ending my talk. So if you guys

53:03

could just get up and we're gonna do high knees right

53:05

now so that is where you do the you try to

53:07

get your leg as high as you can and you do

53:09

the opposite hand up and then we're gonna just do it

53:11

or just do it for 30 seconds but really try to

53:13

do it as hard as you can if you're wearing heels

53:15

take them off. You ready? Set, go, alright.

53:21

Get your heart rate up you really want to get your heart rate up

53:23

so go fast. Now remember

53:28

we're doing 30 seconds and

53:31

I said one, two minutes you

53:33

do this you're actually gonna be tired you're

53:35

probably like oh my gosh is it's not up

53:37

yet. Alright

53:44

we're only gonna do 30 seconds because of

53:46

time alright time but

53:49

as you can see it works

53:52

right so maybe

53:56

maybe we get a little more brain dry neurotropic faster.

54:00

a little more attentive for the next talk. And

54:05

I just want to close by saying, yeah,

54:07

we've talked a lot about vigorous intensity exercise,

54:10

but the reality is that any

54:13

exercise you can do to form

54:15

a habit, that you can do on

54:19

a daily basis, if it's not vigorous

54:21

intensity, any kind of

54:23

exercise is beneficial. So keep

54:25

that in mind. I was kind of

54:28

going for the top here, like you want to

54:30

reach for the stars, but really what you

54:32

want to do is to form a habit. So that's

54:34

the most important thing. With

54:36

that said, we talked about a lot today. I

54:39

think I've covered a lot of the summaries,

54:42

avoiding micronutrient insufficiencies, addressing

54:44

the lack of, you know, vigorous intensity

54:46

exercise. But again, forming that habit, do what

54:48

you can do. I think I've given you guys

54:51

a lot of tools here to measure things,

54:53

try to implement some reason four

54:55

by four, which is brutal. Or

54:58

just do exercise next. You guys tell the next speaker,

55:00

you know, in a couple of hours, we got to get up and get our

55:02

blood flow higher, heart rate

55:04

up. And with that, thank

55:07

you so much for listening today. Hope you

55:09

guys learned something. As

55:11

we conclude today's exploration into the realms

55:13

of cognitive enhancement and the science of

55:15

longevity, I hope you've gained valuable

55:17

insights that not only pique your interest, but

55:20

also motivate you towards actionable steps.

55:23

In line with today's discussions, as mentioned

55:25

at the start of this episode, I

55:27

have worked with my team to meticulously

55:29

develop a guide that serves as a

55:31

practical extension of our conversation. This resource

55:33

is centered around the critical role

55:36

of brain derived neurotrophic factor,

55:38

or BDNF, a key

55:40

player in your brain's ability to

55:42

adapt, learn, and even regenerate. It's

55:45

about turning the science of neuroplasticity

55:47

into tangible practices that can significantly

55:49

impact your cognitive function and decelerate

55:51

the aging process of your brain.

55:54

This guide takes a deep dive

55:56

into specific lifestyle adjustments, focusing

55:58

on exercise. nutrition, and

56:00

beyond that have been shown to boost

56:02

BDNF levels and in turn, cognitive

56:05

health. It also includes a

56:07

special segment, Rhonda's Protocols, where I

56:09

share both my personal experimentation

56:11

and science-backed strategies aimed

56:13

at enhancing cognitive performance

56:15

and longevity. These

56:18

are not just guidelines, but a

56:20

framework for integrating these practices

56:22

into your life tailored to

56:24

foster significant cognitive improvements. For

56:26

those ready to translate today's

56:29

insights into action, I invite

56:31

you to download this guide

56:33

at bdnfprotocols.com. It's

56:35

crafted for anyone passionate about leveraging

56:37

science to enhance cognition and to

56:40

use a handful of key lifestyle

56:42

tactics to meaningfully impact brain aging

56:44

and improve the quality of cognition

56:47

today. Once again,

56:49

you can find this

56:52

protocols guide at bdnfprotocols.com.

56:55

Thank you so much for listening and I'll talk to you

56:57

guys soon.