#2420 - Chris Masterjohn

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Chris Masterjohn

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Chris Masterjohn, PhD, is a leading expert in nutritional science with a background in the biochemistry and molecular biology of nutrition. He is the host of the "Mastering Nutrition" podcast and founder of Mitomewww.chrismasterjohn-phd.com www.mito.me www.youtube.com/@chrismasterjohn

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0:09Thanksgiving food coma myth, mitochondria, and energy support (creatine, red light, macular health)
9:56Eye-support nutrients, vitamin A conversion, sunlight/vitamin D, and methylene blue for mitochondria
19:52Methylene blue, mitochondrial blockages, aging as mitochondrial decline, and creatine as a core support supplement

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Broda O. Barnes & Charlotte W. Barnes, Solved: The Riddle of Heart Attacks

Transcript

0:00

Joe Rogan Podcast, check it out.

0:03

The Joe Rogan Experience.

0:05

Train by day, Joe Rogan Podcast by night, all day.

0:09

Hi Chris, how are you?

0:13

Good, how are you doing?

0:13

Very nice to meet you.

0:15

Nice to meet you as well.

0:15

I have enjoyed your content online for a few years now, so it's really solid

0:20

stuff.

0:20

And I thought, what better day than to bring Chris in, right after everybody

0:24

fucked up their

0:24

diet.

0:24

Yeah, that's right.

0:27

Well, I just want to tell a public health message that you did not get sleepy

0:32

because

0:32

the turkey was high in tryptophan.

0:34

Yeah, that's weird.

0:36

Isn't that a weird one?

0:37

That's a weird myth that's persisted for a long time.

0:39

I mean, the weirdest thing is the origins of it.

0:42

Apparently, it came from researchers in the, I'm sorry, not researchers,

0:47

journalists in

0:48

the 80s who were trying to come up with a reason to explain why everyone was

0:53

tired after Thanksgiving

0:55

meal, and they just looked as far as, oh, turkey has tryptophan, which is an

1:00

amino acid that

1:01

is the precursor to melatonin, which is, you know, you could call it a sleeping

1:05

chemical.

1:06

So it makes you get tired at night.

1:08

That must be why.

1:09

But it turns out that A, turkey's not that high in tryptophan.

1:14

Like, even whey protein is higher in tryptophan than turkey is.

1:18

And then B, tryptophan doesn't make you tired.

1:20

Yeah, I dare anyone to go out and have, like, just a slice of turkey for

1:27

breakfast and see

1:28

if it knocks you out.

1:29

It's overeating.

1:31

It's, like, so obvious.

1:32

I mean, people are eating tons of stuffing, tons of sides.

1:36

They're eating so much food.

1:38

You're gorging.

1:39

It's a gorging day.

1:40

Yeah, for sure.

1:41

Yeah, I mean, it's not good.

1:43

And if, you know, if you look at, like, a lion in the wild, one thing that you'll

1:48

notice

1:48

is that they are on the prowl when they are hungry.

1:53

They're alert.

1:54

Their body's revved up.

1:56

And then they have a feast, and they just fall asleep.

1:59

And the reason is that we're, you know, our—you can even see this in

2:03

physiology.

2:04

They call the parasympathetic nervous system the rest and digest system.

2:09

And that's because we are biologically wired to be alert when we need to work

2:15

to get our

2:15

food.

2:16

And then we're wired to, you know, eat that food, feel like we've gotten our

2:20

fill, we've

2:21

done what we need to do, and now we can rest and take a sleep.

2:23

Yeah, it's normal.

2:25

I mean, there's a great video of these lionesses, these female lions, after

2:29

they've hunted and

2:31

killed and ate all this food.

2:32

And they're just lying there like this with these enormous bellies, just like,

2:36

uh, just

2:37

like your uncle on the couch watching football, just, uh.

2:41

Yeah.

2:44

I, you know, and I think one—so one thing that I think we should talk about

2:48

today is I've

2:49

been in nutrition research for 21 years, and I'm, you know, I think the crowning

2:56

thesis

2:56

of my work so far is that we really want to be thinking about mitochondrial

3:02

function at

3:03

the root of all health and disease.

3:04

And so I think an interesting way to see sleep is it's like, why do we have to

3:09

sleep eight

3:09

hours a night?

3:11

And I think with dreaming, there's obviously other things going on there, but

3:15

deep sleep,

3:16

the—one of the primary things that's happening is you need to give your

3:20

mitochondria a rest

3:21

because your mitochondria are what produce all the energy that you need for, uh,

3:26

for producing

3:27

everything in your body, for maintaining it, for repairing it, uh, and for

3:31

distributing it

3:32

properly and for keeping it going across the lifespan.

3:34

And so your mitochondria are going to essentially take a nap, take a rest.

3:38

They don't go off because you die, but they really turn down the volume of the

3:41

work they're

3:42

doing.

3:42

But then you take your metabolic rate way lower than that, and so you can build

3:47

up the

3:47

reserves of energy that you had used up the day before.

3:51

Um, and so it's, you know, that—that can explain a lot of recent findings

3:55

that are coming

3:56

out as well because there was that recent study where they looked at sleep

4:01

deprivation with

4:02

creatine supplementation.

4:04

And so they randomized people to either drink a placebo drink or drink 20 grams

4:09

of creatine

4:10

through the night, and they kept them awake all night, and they had them do

4:13

brain puzzle

4:14

quizzes.

4:14

And when the subjects were getting the 20 grams of creatine, they did way

4:19

better on the brain

4:20

puzzles, but they also complained about being tired a lot less.

4:25

And so the conclusion is creatine is somehow acutely preventing your brain from

4:32

suffering during

4:34

sleep deprivation.

4:35

And the rationale there is, you know, mitochondria are the powerhouse of the

4:39

cell or the power

4:40

plant that's producing the energy.

4:42

Creatine is like the power grid, and it distributes that energy throughout the

4:46

cell.

4:47

Um, and so if the purpose of sleep is to restore the energy that you used up,

4:51

but then you intervene

4:53

by putting creatine in there, now you can keep that energy going, and you can

4:58

go more hours

4:59

before you need to get rest and restore that energy because you've increased

5:02

your capacity

5:03

to distribute it.

5:04

That makes sense.

5:06

Um, that—that is an interesting thing because it's fairly recent that people

5:09

have talked about

5:10

this, right?

5:11

I mean, it used to be—people only thought of creatine as being a muscle thing,

5:15

uh, to—to

5:16

help you recover and help you build larger muscles.

5:18

But then over the last, uh, I would say year or two, I started hearing talking

5:23

about cognitive

5:24

function, and maybe even more than a couple of years, but about how it improves

5:28

cognitive

5:28

function.

5:29

The sleep thing, though, is very recent, right?

5:31

Yeah, the sleep thing was, uh, in the last year.

5:34

There is some literature on traumatic brain injury where 20 grams of creatine

5:39

for six

5:40

months doubles the rate of healing.

5:41

Whoa.

5:42

Um—

5:43

That's incredible.

5:44

But it's—yeah, the—the—the field is in its infancy, but I—I think that

5:47

I actually

5:48

almost a decade ago did a podcast on just creatine.

5:55

I called it more than a performance enhancer because there's—if you just look

5:59

at where

5:59

it's distributed in the body, almost every cell and every tissue has the creatine

6:03

system.

6:04

And so it really is this—and if you look at the literature, they'll say, well,

6:09

it's

6:09

more important in certain cells.

6:11

Like, it's really important in your muscles because your muscles have this very

6:15

polarized—sometimes

6:17

they're at rest, sometimes their energy demand is going through the roof.

6:20

Um, and it's really important in, uh, like, long cells.

6:24

So, for example, your retina is part of your central nervous system, and it's a

6:29

really long

6:30

cell that's, uh, coming from the brain into the eye.

6:33

And, uh, creatine helps move energy back and forth.

6:36

But if—if you just look at where—instead of where is it most important, you're

6:41

just

6:41

like, where is it?

6:42

It's like almost every cell in your body has creatine.

6:45

And it's helping distribute the energy that the mitochondria make throughout

6:48

your whole

6:49

body.

6:49

And that includes pumping stomach acid.

6:51

It includes, uh, sperm, uh, swimming up the vaginal canal.

6:56

And so if you—if you just look at where it is, you would think that creatine

7:01

would help

7:02

a lot more than muscles.

7:04

Um, and it just turns out that all you need to do is start studying it to start

7:07

seeing those

7:08

effects.

7:08

Is there any studies on creatine and the improvement of eyesight?

7:11

I'm not sure.

7:14

They're—not that I know of.

7:15

But—

7:15

Because that kind of makes sense, right?

7:16

I mean, it makes complete sense.

7:18

Like, you would—when it comes down to it, your—your ability to produce

7:24

energy is producing,

7:26

maintaining, and repairing everything in your body.

7:28

So you would expect to see anything that does improve your energy metabolism

7:33

improve literally

7:34

everything.

7:34

So it would be kind of shocking if you had no effect on that.

7:38

Um, but I'm not sure if—if there are good, uh, trials done on that.

7:42

I haven't seen them.

7:43

Um, speaking of improving eyesight, uh, I started doing red light about, I

7:49

guess, about a year

7:50

and a half, two years ago.

7:51

Got a red light bed.

7:52

And, uh, completely stopped whatever macular degeneration I was going through

7:57

and reversed

7:58

some of it.

7:59

So I don't have perfect vision, but my vision's better.

8:02

Like, it's—it's definitely better.

8:04

And it's not just through the red light.

8:05

It's also—it's got to be some of the supplements that I'm taking.

8:08

One of them, uh, I take, uh, a supplement from Pure Encapsulations.

8:13

No affiliations with them.

8:14

I just buy it.

8:15

It's, uh, called Macular Support.

8:17

And, uh, let's see what's got in there.

8:20

It's got lutein and a few other supplements that have been known to—

8:24

Yeah, that'll do it.

8:25

Is that it?

8:25

Well, yeah.

8:26

I mean, so with the red light, it is very interesting.

8:28

Whenever you think of red light, you want to think of your mitochondria because

8:31

the main thing

8:32

that we know about red, near-infrared, and far-infrared that they're doing is

8:37

they're

8:37

actually going straight into the mitochondrial engines that produce the energy

8:42

and helping

8:43

them produce more.

8:44

And they're also ordering the water structure inside the mitochondria to make

8:49

those engines

8:50

produce energy more easily.

8:52

And there was a study a few months ago that—it was just like a one-day study,

8:59

but it showed

8:59

that blasting people in the chest with red light improved their eyesight when

9:04

it was measured

9:05

the next day.

9:06

And they covered their eyes to make sure that the red light didn't go into the

9:09

eye.

9:11

And so the conclusion is, you know, it's not a clinical study, right?

9:16

And it's not like a one-year, how does it, you know, does it really improve

9:19

your eyesight

9:20

over one year?

9:20

We don't know.

9:21

But it shows proof of principle that red light is doing something systemically

9:27

that does not

9:28

have to go to your eye that does improve your vision.

9:31

And to me, that makes sense because your vision is going to be improved by

9:35

anything that acts

9:37

directly in your eye to improve energy production.

9:40

But you've got coordinated energy metabolism going on through your whole body.

9:43

Like your liver is doing tons of stuff to try to make your eyes healthy and

9:47

make your brain

9:48

healthy and so on.

9:49

So it makes a lot of sense.

9:51

But that—so I don't doubt at all that the bed is part of that.

9:56

But the lutein and zeaxanthin are well known to accumulate in the macula where

10:01

they have

10:02

a very specific role in protecting against macular degeneration.

10:07

And actually, the best source of those is egg yolks from chickens that are fed

10:15

anything that

10:16

has them.

10:16

But marigolds are super high in them.

10:18

So if they feed the chickens marigolds, they get super high levels.

10:22

And the egg yolk has fat that helps them get absorbed.

10:25

So in terms of—I mean, this is—you could take this with some eggs.

10:30

But I should feed my chickens marigolds.

10:33

Yeah.

10:34

If you have—

10:35

I have chickens.

10:36

If you have chickens and if you're spending your money on a lutein zeaxanthin

10:40

supplement,

10:41

you might be able to get a—maybe the marigolds are cheaper.

10:44

Maybe I'll just double it up.

10:45

Yeah.

10:46

So this is all the ingredients.

10:49

Does this stuff make sense as something that would help support eyesight?

10:52

It does.

10:54

I mean, the vitamin A is going to—that's going to depend on your genetics in

11:00

terms of

11:00

how good are you at converting beta carotene into the form of vitamin A that we

11:05

need, which

11:06

is most abundant in liver and egg yolks.

11:08

It's dependent on genetics.

11:13

It's—yeah.

11:13

So there's—you need—beta carotene is this big.

11:18

And if you chop it in half, you get vitamin A.

11:21

And so you have an enzyme in your digestive system that does that.

11:25

But that enzyme is dependent on a lot of things going right.

11:30

So you need to have good zinc status, good iron status, good thyroid status,

11:34

and all kinds

11:35

of stuff like that.

11:36

And actually, seed oils decrease the conversion.

11:40

So if you take that with canola oil, you're going to get less vitamin A out of

11:45

it than if

11:46

you take it with, you know, eggs and butter.

11:47

And then vitamin A activation is also dependent on mitochondrial function, too.

11:53

So I—you know, but it makes sense.

11:55

Vitamin A is great for your eye.

11:57

Vitamin C is a great antioxidant.

11:58

N-acetylcysteine, great antioxidant.

12:02

The glutathione—the Cetria stuff, I'm—I'm kind of—I think it's—I think

12:10

it's a little

12:10

bit of a over—over-hyped in terms of some—you know, another type of glutathione

12:16

I think

12:17

would have worked fine.

12:18

What's the best glutathione?

12:19

Well, the best—is it liposomal?

12:22

The best glutathione is the glutathione that you make yourself from protein

12:26

that you eat.

12:27

But if you're going to supplement with glutathione, there—I don't—if you're

12:34

talking about

12:35

bang for the buck, I just think straight-up glutathione is good.

12:38

And there are studies suggesting that there's marginal absorption benefits for

12:44

certain special

12:45

types, you know, but then they charge three times as much for that type.

12:49

And it's like, well, am I getting three times more glutathione out of it?

12:51

Not really.

12:52

So, you know, some people swear by liposomal glutathione, and if some—you

12:55

know, if you

12:55

swear by it, and if it does—it's saying for you, great.

12:58

Do you think it's, like, 10% better?

12:59

I think the jury is out on whether there might be 10, 20% better value for

13:07

those things.

13:09

So if I'm—if I'm going to take glutathione, I'm just going to take glutathione.

13:12

Got it.

13:13

Okay.

13:13

Is this—what you're saying about producing your own glutathione, that's the

13:17

same thing

13:18

as, like, vitamin D, right?

13:19

It's way better when your body produces it.

13:22

Um, if it does.

13:23

I mean, I—I don't think there's anything wrong with getting vitamin D from

13:28

food, but

13:30

you don't—the thing is, you do need sunlight, right?

13:34

So it's—you at least need to get 30 minutes of sunshine in the morning, which

13:42

is not going

13:42

to give you vitamin D, and then you need to get, like, 10 or 15 minutes of unprotected

13:46

sunshine in the afternoon, um, to get—you get vitamin D from that, but you

13:51

get other benefits

13:52

from it as well.

13:53

So I—I wouldn't say that there—that it's necessarily better to get the

13:58

vitamin D from

13:59

the sun than from a vitamin D supplement or from eating fish or from eating cod

14:03

liver oil,

14:04

but you don't want to—you don't want to say, well, I don't need to go out in

14:09

the sun.

14:10

I'm just going to take vitamin D.

14:11

Then you're not going to get the benefits of the sun because the sun gives you

14:13

other benefits.

14:14

Got it.

14:15

Yeah.

14:15

Is there anything that you can do—say if you live in Seattle and you're in

14:20

the winter,

14:20

it's just raining constantly.

14:22

Is there a tanning bed that gives you some of that?

14:27

Yeah, I—I do think that there is, um, there is some risk of tanning beds.

14:34

I'm not 100% comfortable—I—when I lived in New York, I would try to spend

14:40

40 minutes

14:41

in the afternoon sunshine for three quarters of the year, and during the winter,

14:45

the UV

14:47

index just wasn't high enough, and I—I get eczema in the winter because I'm

14:51

not getting

14:51

enough sun.

14:52

And so I would use a tanning bed not to get tanned, but I'd use, like, two,

14:56

three minutes

14:57

at a time just because it just had a systemic effect in, like, preventing the eczema

15:02

that

15:03

I would get in the winter.

15:03

I think you have to be careful with it because there—there is some concern

15:07

that it's—that

15:08

people are just—if they're tanning to tan, they're—they're going to wind up

15:11

with

15:11

too much damage to their skin.

15:14

But what I would do is, um, for morning sunlight, I think you can get, like, a

15:21

lux meter app

15:22

and just—some people are—some people, they think that it's—there's no sun

15:27

outside,

15:28

but actually it's, like, a hundred times or a thousand times brighter than

15:31

indoors and

15:31

their eyes are adjusting, and so it's, like, cloudy or overcast, but there's

15:35

still a lot

15:35

of value in going outside.

15:37

So I would say if you use a lux meter and it's, like, under 10,000, you could

15:41

get a,

15:41

um, like, a light therapy light at home to use to just, like, turn it on and

15:47

not look

15:48

straight into it, but kind of have it going into your eyes.

15:50

Um, and then for vitamin D, uh, you could—you could do, like, tanning bed,

15:58

but just try

15:59

to really keep it minimal, like, go in—go in for two or three minutes, not

16:03

like you're

16:03

trying to tan, you're just—

16:04

What I was getting at, is there a different kind of tanning bed?

16:07

That's maybe—

16:08

Oh, there are—yeah, so there are—there are, uh, different ratios of

16:12

wavelengths,

16:13

and the ones that have more UVB are the ones that are going to give you more

16:19

vitamin D.

16:20

So if you're—if you're just going to a tanning bed place, you, um, probably

16:27

the people—the

16:28

staff there tell them that you want, like, mixed wavelength that gives you a

16:32

mix of, like,

16:33

surface tan and deep tan.

16:35

Okay.

16:36

I think that's how they—because they don't know the vitamin D science, so, um,

16:40

I think

16:41

that's how you have to get the—the bed that gives you more vitamin D.

16:43

You have to tell them I want a mix of surface and deep.

16:45

That's funny.

16:46

Um, speaking of red light, and speaking of, um, uh, therapy in—that helps

16:52

your mitochondria,

16:53

what is your thoughts on methylene blue?

16:56

Methylene blue seems to be a very controversial supplement.

17:00

Some people think it's amazing, and it's a panacea for all that ails you, and

17:04

other people

17:05

are like, what are we doing here?

17:07

Why are you putting dye in your body?

17:09

Your piss is coming out blue.

17:10

This is weird.

17:11

What school are you in?

17:13

Methylene blue is something that could do wonders for your mitochondria if you

17:18

need it, and could

17:19

really hurt you if you don't.

17:20

And I think that there are—there are certainly a lot of people raving about

17:25

it on the internet,

17:27

and it's because there are—it's a mix of things.

17:29

So there are people that are treating themselves for a problem in their

17:33

mitochondria that they

17:34

don't know that they have, and then they get an outsized voice because they're

17:37

the ones

17:38

raving about how much it helped them, and so there's, like, selection.

17:41

You know, if some—you don't get—if people didn't get a benefit or if they

17:44

just felt a

17:45

little worse, they don't go raving about it on the internet as much.

17:48

Yeah.

17:48

So that's part of it.

17:49

There is also—part of it is that when you get up to a dose of around 10

17:54

milligrams or

17:56

so per day, for perspective, in clinical trials of Alzheimer's, they're using

18:02

200 milligrams,

18:03

but you can buy, like, a 0.5 milligram on Amazon.

18:07

So a lot of people are using, like, 0.5 milligrams.

18:10

But once you get up to 10 milligrams or so, you're getting some degree of

18:13

pharmacological

18:14

antidepressant effect because it's an MAO oxidase—monoimmune oxidase inhibitor.

18:19

And so I do think that there are some people who are—they're like, oh, I feel

18:23

so much

18:24

better, and it's like, yeah, bro, you're taking an antidepressant.

18:26

So that's part of it.

18:29

But if you look at what it actually does, it is a very nonspecific rewirer of

18:39

how your

18:40

mitochondria produce energy.

18:43

And if—you can think of it like, let's say there's a main road in the city,

18:47

and it's

18:47

the best road, and that's why everyone's on it, but it's blocked, and then they

18:52

set

18:52

up detours, people are—they're going to help the traffic because that road is

18:56

blocked.

18:56

There's—you actually can't get through there.

18:58

And so the side roads that would take you somewhere are actually better because

19:02

they're

19:02

not blocked, right?

19:03

So in the context where you need the detours, the detours help you.

19:08

But if the main road was not blocked and they start putting up detour signs and

19:12

people start

19:13

going out in the side roads, they're not going to get to their destination

19:15

faster.

19:16

They're just getting tricked by the mess, the chaos that was created by people

19:20

putting

19:21

up detour signs that they didn't need.

19:22

So methylene blue is something that goes into your mitochondria and sets up detour

19:26

signs

19:27

all over the place.

19:28

How does it do that?

19:30

So it—all right.

19:34

So what your mitochondria do to produce energy is they extract—they—you

19:39

know, you have

19:40

a molecule like carbohydrate or an amino acid from the protein that you ate or

19:45

fatty acid

19:46

from the butter you're eating.

19:47

You've got to break that apart.

19:48

You've got to take out the energy, and you've got to synthesize ATP with it.

19:52

The ATP is the general energy currency of the cell.

19:56

So mitochondria produce usable energy from food in the form of ATP.

20:01

When they do that, they have a bunch of different pathways through which

20:08

electrons flow.

20:09

And methylene blue is able to grab those electrons and put them somewhere else.

20:15

So it—they call it a redox cycler.

20:18

So it's taking an electron here, it's shuttling it over there, it's taking an

20:21

electron here,

20:21

it's shuttling over there.

20:22

And so if you have this very—let's say the normal way for your mitochondria

20:27

to produce

20:28

energy has a main road where the electrons just flow straight through, methylene

20:32

blue is

20:33

coming in and it's just, you know, taking that electron over here, it's

20:36

throwing it in

20:37

over there, and so on.

20:38

So if you've got a road that goes like this, and you've got a blockage right

20:41

here, and

20:42

methylene blue is just taking something out there and it's putting it over

20:45

there, you

20:46

actually wind up getting better energy with it.

20:48

But if you don't have a blockage, you're just creating random chaos in the

20:52

mitochondria.

20:54

And in animal experiments, what they've done is they've said, okay, let's give

20:58

these

20:59

animals inhibitors of their mitochondria at specific locations and see what

21:04

methylene blue

21:05

does.

21:05

And if you don't have any inhibitors, and if the animal is genetically healthy,

21:10

then you

21:11

add methylene blue, they get less ATP.

21:13

So the mitochondria is less effective at converting food to usable energy.

21:18

But if they do have an inhibitor, their ATP production goes down, you add methylene

21:22

blue, it

21:23

goes back up, right?

21:24

So if there's a blockage to get around, methylene blue helps.

21:28

So I think what's important if you really want to make sure that people are

21:34

using

21:34

methylene blue right is to actually do mitochondrial testing that will tell you

21:40

whether there was specific blockages are there.

21:42

I ran a biochemical optimization program a while back, and one of the clients

21:47

that I

21:48

had in there, he tried methylene blue, and he only got up to a half a milligram

21:52

or a

21:52

milligram, and his mood was worse, his fatigue was worse.

21:57

He had more anxiety, a bunch of problems that, you know, the dose was too low

22:02

to say it was

22:03

doing a pharmacological messing with his neurotransmitters.

22:06

And so I think it was just making his mitochondrial function worse.

22:10

And so the mitochondrial testing that we did on him showed that, you know, he

22:14

was not a candidate

22:15

for methylene blue.

22:16

And he actually had, you know, some really weird, like his mitochondria were

22:22

best at using a specific

22:23

amino acid cysteine and for energy, kind of weird and idiosyncratic.

22:30

And in his case, it was interesting because he had actually gravitated to a

22:34

steak-only carnivore diet, and he didn't feel like it fixed him, but he felt

22:39

like it, you know, took the edge off.

22:41

Like he was 50% better on the steak-only carnivore diet.

22:44

50% is a lot.

22:46

Well, yeah, it's a lot, right.

22:47

But he wanted the other 50%.

22:49

That's why he was coming to me.

22:50

So what was, you know, and figuring this out didn't get him to 100%, but it got

22:56

him to, you know, to get days with 75% because, you know, because he could use

23:03

strategic cysteine supplementation

23:04

to mimic the benefit he was getting from the steak, but he would be able to,

23:08

you know, be still in the fasting state because his workouts were better in the

23:12

fasting state and things like that.

23:14

So figuring that out allowed him to, you know, get from 50% to 75%.

23:20

But the methylene blue was putting him down at 5% instead of 50, you know.

23:25

Can I ask how old he was?

23:26

He wasn't that old.

23:29

He was in maybe 40.

23:31

I forget exactly, but 40, give or take five years.

23:35

And is that an age-dependent thing, like mitochondrial dysfunction?

23:37

Is it more common in older people?

23:39

For sure.

23:41

So what, I mean, I would argue that mitochondrial dysfunction and aging are the

23:45

same thing.

23:46

And, you know, there's a bunch of theories of aging, but if you take them all,

23:49

you can always ask the question, why?

23:51

There's like the information theory of aging.

23:54

Like, why is the information not being carried out correctly?

23:57

Or the oxidative stress theory of aging.

23:59

Well, why are you making more oxidative stress?

24:00

And I actually think it's way more simple than anyone is thinking about it.

24:06

It's mitochondrial energy production is producing everything in your body.

24:11

It's repairing it.

24:12

It's maintaining it.

24:13

And it's putting where it belongs.

24:14

That means that mitochondria produce the energy that they need to produce

24:18

everything in the mitochondria, right?

24:20

And so if you have a little gap in your energy production, like let's say you

24:24

get, I think one way to think of aging is, well, I've just, I've suffered

24:28

through so many cumulative insults.

24:31

Like, I got sick so many times.

24:33

I got injured so many times.

24:35

I had days where I didn't eat optimal nutrition so many times.

24:39

And I think what all those things are doing is like, well, you know, you, that

24:44

period of overtraining that you did, your mitochondria were, were forced to

24:49

help you give you the energy for, you know, that the extra set of squats that

24:54

you did.

24:55

And they had a little bit left over for themselves and they got, you know, a

24:59

half a percent worse at producing energy.

25:01

And so that sets up a vicious cycle because now, now that they could not repair

25:06

themselves as well, now they get a little bit worse and get a little bit worse.

25:11

And what you see, um, in the literature is that as people age starting around

25:17

age 18 through age 70 to 80, you're losing your mitochondrial function, average

25:24

rate of 1% per year.

25:26

So by the time you're 70, you have half the energy that you started out with

25:30

that baseline.

25:32

And that I, I, I think what explains that is, is just the vicious cycle of the

25:38

mitochondria got, they lost a quarter percent here or a quarter percent there.

25:43

And they just started repairing themselves less effectively because they're the

25:47

engines fueling everything, including that.

25:50

And so, but you know, the good news is that age only explains 25% of mitochondrial

25:55

function.

25:56

So it's the average that's going down at 1% per year.

25:58

The average person is half producing half the energy at age 70 than they were

26:04

at age 18.

26:05

But the spread around that is huge.

26:09

And with that, to me, the way that I spin that is that means that 75% of this

26:14

isn't under your control.

26:16

You're going to, you're going to go in a downward trend, but you're in control

26:20

of whether, you know, you're way undershooting that trend or you're way overshooting

26:24

it.

26:24

What you want to do is make your mitochondrial function as good as it can be at

26:29

any given age so that that downward trend will, you know, it'll be a lot slower.

26:35

And you can get to age 70 and you're not docked 50%.

26:39

You're just docked 10%.

26:41

And I think that's what's happening when you see some of these 70-year-olds who,

26:45

who, you know, are more fit than a lot of 25-year-olds, you know?

26:49

Yeah, interesting.

26:50

So what are the primary factors in regards to being able to maintain your

26:54

function?

26:55

Well, I think that everyone has idiosyncratic things.

27:00

And I think mitochondrial testing is, is very important.

27:03

But if I were to pick five things that just everyone should be doing for their

27:06

mitochondria, a lot of it does look like health advice you might get somewhere

27:11

else, but it actually is the best stuff, right?

27:15

So we mentioned creatine.

27:16

And I think creatine is really important because it's not in the mitochondria

27:20

so much as it carries forth the mitochondrial energy of the rest of the cell.

27:25

But that also feeds back in the repair functions for the mitochondria.

27:28

And so I think creatine, optimizing your creatine status is super important.

27:32

And I think that there, everyone who's not eating one or two pounds of meat per

27:38

day should be, should probably be taking creatine.

27:43

And you can think of it as, if you're eating red meat and you're eating it rare,

27:49

you can err on the side of one pound.

27:53

And if you're eating, and I would include as red meat salmon, which is like a

27:57

reddish fish and is actually quite high in creatine.

28:01

If you're eating white meat, white fish, and you're eating it well done, you

28:05

want to err on the side of two pounds because they don't have as much creatine.

28:09

Then you cook the creatine out of them and you wind up with much lower dose.

28:13

We should probably say salmon.

28:14

You're talking about wild salmon versus farm salmon, which has a dyed pink skin.

28:20

Well, it's not the red color.

28:22

I think it's coincidence that it's, that it's, I think the red color is

28:24

coincidence.

28:25

It's just a helpful way to think about it.

28:27

But it probably is the case at least, like every Atlantic farm salmon that I've

28:35

seen is, you can tell that it's, well, if you look up in a database, it's way

28:40

higher in fat.

28:42

But you can tell by looking at it that it just doesn't have that lean look that

28:47

wild salmon has.

28:48

So I think creatine is a function of the lean tissue mass.

28:51

And it might be the case that wild salmon are doing a lot more swimming.

28:58

Like maybe the wild environment is encouraging them to use their muscles in a

29:02

way that increases their creatine synthesis.

29:04

That wouldn't surprise me.

29:07

I have tried to steel man the case of, could there be a vegan diet that would

29:11

make you not need to supplement with creatine?

29:14

And the steel man that I've got for you is you'd have to be eating a half a

29:18

kilogram of tofu and a half a kilogram of quinoa per day.

29:22

And that's not typically what, and I might rip a hole in your digestive system,

29:27

but that's, but that's not typically.

29:31

Um, so I, I think that, um, I, most vegans should probably just supplement with

29:36

creatine and could call it a day there.

29:38

Um, so that's creatine.

29:40

I, we mentioned, uh, sunlight.

29:43

So sunlight is when you wake up in the morning.

29:47

I said before that your mitochondria have not gone to sleep literally, but they've

29:51

really slowed down there.

29:53

It's like they're on a nap and there's a transition when you wake up or the

29:57

mitochondria have to say, oh, you've woken up.

30:01

Now I need to, I need to wake up and I need to start producing more energy.

30:05

Um, and sunlight going into your eyes, being translated into your brain is the

30:13

signal that actually tells your brain to organize that.

30:17

And so what happens as a result of that is that signaling helps your mitochondria

30:22

adapt and start producing everything.

30:25

And it actually helps them adjust.

30:26

And if you don't have the morning sunlight, you are, you're going to have your

30:33

mornings full of suboptimal energy metabolism that is initiating that, that

30:38

vicious cycle of aging is that's what I believe.

30:42

Um, and then it's, and then it's also the case that the red and infrared light

30:48

from the sun is very beneficial to the mitochondria.

30:52

The best time to get that would be in the morning.

30:55

Um, when you go out in the afternoon, you've got to deal with like, can I get

30:59

two hours of this without getting burned?

31:01

But if you go out in the morning, you can stay out there for one or two hours

31:05

and you can get a lot of red and infrared light without worrying about burning,

31:09

uh, burning wavelengths.

31:10

And then the, I think the beds and other devices at home are great.

31:16

And where you want to start thinking about that is I'm getting benefit from red

31:21

and near infrared light, but I'm getting more.

31:24

I know that I could get more benefit if I got more of it than I'm able to get

31:28

through sunlight.

31:29

So start me, start getting those wavelengths with sunlight as your base and

31:33

then do whatever you want on top of that with whatever seems to be working well

31:37

for you.

31:39

So nutrition would be number three and every nutrient is needed for everything

31:45

in your body, but your mitochondria are using all kinds of nutrients and the,

31:50

there's this idea that floats around in society that nutritional deficiencies

31:55

are a thing of the past.

31:56

But if you just look at surveys, 93% of Americans are getting less than they

32:02

need of at least one nutrient.

32:04

30% have verifiable blood markers of at least one nutritional deficiency and 6%

32:11

have blood markers verifying more than one nutrient deficiency.

32:16

And I think those are all underestimates because when you're just looking at

32:20

the official stats on like how much of each nutrient should you eat, there are

32:23

way, there are a lot of people that have needs for way more, right?

32:27

So I think those stats are grossly underestimating how many people need to get

32:31

better nutrition.

32:33

So I think everybody should be getting better nutrition.

32:40

To kind of high level what that looks like, I think some good rules of, there's

32:45

lots of ways to skin a cat, but some good rules of thumb are different people

32:51

will do better with more plants or more animals.

32:54

But to, when you do eat animals, you should be eating them nose to tail.

32:57

So at least try to work in liver, at least try to work in bone broth or, you

33:01

know, something like that.

33:03

The closer to nose to tail you can eat your animals, the better.

33:06

Do try to diversify across proteins because there's just different vitamin and

33:11

mineral profiles in different types of protein.

33:15

Like if you can eat shellfish, eat some shellfish.

33:17

If you can eat fish, eat some fish.

33:18

You can eat dairy, eat some dairy.

33:20

And the more you diversify across those proteins, the better.

33:23

Most people don't eat enough protein.

33:25

Good rule of thumb would be at least a third of your plate should be protein.

33:29

But if it's, if you're talking like eggs and dairy products, you've got to

33:34

double that because they just, the amount of space they occupy per unit of

33:39

protein that they're giving you is, you know, a third of your plate is eggs is

33:44

not going to give you enough protein.

33:46

And then I think try to eat as broadly as you can from different types of

33:50

carbohydrates.

33:51

If you have to leave out something, leave out grains, try to eat whole, unprocessed

33:57

foods and try to eat most of your, try to eat 80% of your foods cooked at home

34:02

or prepped at home or whatever instead of eating out.

34:06

And make sure your digestion is in good order.

34:08

And those are kind of the, you know, the broad basis of nutrition.

34:12

Um, and, um, exercise is, is a very interesting one.

34:23

Um, so if you exercise is incredibly important to the signaling that produce

34:30

mitochondria, but why is that?

34:33

It's because you need mitochondria to produce energy for the exercise that you're

34:36

doing.

34:37

So I think a lot of people are too reductionist when they look at what type of

34:41

exercise should you do for your mitochondria.

34:43

If you try to do a study that says like, I'm trying to get more mitochondria in

34:47

my skeletal muscle, what's, what exercise is going to do it?

34:50

You're going to do, you're going to see endurance exercise outperforming other

34:53

things.

34:54

And that's because endurance activity requires more mitochondrial function in

34:59

the muscle.

35:00

Um, if you're doing like hypertrophy or strength training and you're doing

35:04

short sets, your muscles burning a lot of glycogen, it's less dependent on its

35:09

mitochondria.

35:10

So you're not going to see the mitochondrial function there, but that doesn't

35:13

mean you're not improving mitochondrial function because now all that really

35:16

means is the liver is stepping up to assist the muscle.

35:18

Like if, if you're doing sprinting, your muscles burning through tons of

35:23

carbohydrates, making a lot of lactate.

35:25

If that lactate's not being metabolized in the skeletal muscle, it's going to

35:29

the liver to get converted back to glucose.

35:31

So your liver, now you're training your liver's mitochondria when you're doing

35:34

strength training, you're doing hypertrophy.

35:36

Um, so I think the right way to look at it is just, you should be exercising

35:41

all the things that are functions that you need to keep.

35:45

And that means endurance, it means strength, it means mobility, it means

35:48

agility, it means balance, it means proprioception, it means being able to

35:52

respond to your environment.

35:54

I think, you know, to some degree, like just playing a sport that has other

35:57

people in it is important because if someone's throwing a Frisbee and you need

36:00

to react to that, you're training mitochondria in your brain that are able to

36:04

energize the systems that provide your reaction time.

36:07

And I think cognitive, um, you know, exercise for your brain is things like

36:12

working on your memory and on your, uh, creative synthesis and all, all those

36:18

different aspects.

36:19

And I, I do think that a lot of people are thinking about this when they're 25,

36:23

they're like, well, I don't care if I can memorize a string of 25 numbers, but

36:27

you're going to care if you can't remember anything when you're 75, you know?

36:32

So I, I think that we, we need, really need a broad, um, thought about this,

36:37

but, but by the way, do you know what athletes live the longest from the, from

36:42

the pros?

36:43

Hmm.

36:45

Let me guess.

36:46

Baseball.

36:49

It's, it's, it's, it's, it's actually gymnasts and pole vaulters have, have

36:54

eight years on the general population.

36:57

Um, and if you, if you look at, there was a study that came out earlier this

37:03

year and it tallied up all of the pro sports players from all of the countries

37:08

who had the dates of their death published and who were, who were notable

37:13

enough to have been, had an article published about them.

37:18

And so they had many hundreds, I forgot, I forgot the exact sample size, but

37:23

they were able to, um, uh, statistically adjust the, the mortality rate to the

37:29

general population from which the athlete came.

37:32

So if, you know, if it was a Greek athlete, they were adjusted to the mortality

37:37

rate of Greece when they, when they died, um, like how, what you would expect

37:41

after adjusting for location and age and so on.

37:45

And in the male athletes, you had gymnasts and pole vaulters with eight years

37:50

on the population and you've got cyclists who've, and of course you've got sumos,

37:56

sumo wrestlers are 10 years below.

37:59

And you have a lot of sports like that have high injury rates that are

38:03

especially a lot of stuff that has impacts to the hands, martial arts and

38:08

things like that.

38:09

We're probably the sport itself and its impact on training your body's energy

38:14

systems is positive, but just the injury rate is, is taking you out.

38:20

So you're, you're kind of like not, you're kind of in the middle, you're very

38:23

close to the general population.

38:25

Um, cyclists only have two years on the general population.

38:29

And so what, what I thought was interesting, I think a few things are

38:32

interesting about that.

38:33

So first of all, there's a lot of people in the longevity space are taking most

38:37

of their information about how they should train for longevity from people who

38:42

specialize in cycling.

38:43

Really?

38:44

Well, I, yeah, I'm not going to name names, but there's, you know, a lot of

38:47

just the people out there who are, you know, that's where it's coming from.

38:51

And I, you know, it makes a lot of sense that cycling is, you know, it's good

38:55

for cardiorespiratory fitness.

38:57

There's a lot of data that having good cardiorespiratory fitness is a key

39:01

factor for longevity.

39:02

But when you look at a study where gymnasts and pole vaulters have six extra

39:06

years on the cyclists and the cyclists only have two extra years on the general

39:10

population, I'm like, huh, what, you know, it's not all about the cardiorespiratory

39:15

fitness.

39:16

And so when I think about there's, it's, you know, it's an observational study.

39:20

You can't prove cause and effect, but it just does make you think.

39:23

And the way that I think about that is a few things.

39:26

So first of all, the commonalities between gymnasts and pole vaulters, they're,

39:31

it's definitely not height because gymnasts tend to be short and pole vaulters

39:36

are tall.

39:37

And so the height cancels out.

39:38

Definitely they're fit.

39:42

They do both have, it is interesting that they have, you know, cyclists have a

39:46

good lower body and gymnasts and pole vaulters have a good upper body.

39:51

So I do think that's interesting that it does make you, it does make you wonder

39:56

if you could skip leg day, but I don't advocate skipping leg day, but, um, but

40:01

to me, like what I think is actually going on here is, um, I, I think that

40:07

functionality of movement throughout the whole body to facilitate.

40:14

Um, very, uh, to facilitate the kind of skills that they have, um, is, is

40:23

training, it's training in things that are getting left out when you just make

40:29

sure that your heart and lungs are able to support your running or your cycling.

40:33

And I think that some of those involve, are probably related.

40:40

I don't know what they're not dying of.

40:42

So presumably they're getting less heart disease or like getting less cancer

40:45

and they're getting less neurological disease because that's what people are

40:48

dying of.

40:48

Right?

40:49

Like the, in the average, if you get a far enough for someone to analyze why

40:52

you died, um, you know, they're like diabetes and hip fractures and things like

40:56

that are, are hitting younger people.

40:58

But in general, if people are dying cause they got old, they're dying of heart

41:02

disease first, cancer second, and neurologic, like they outlive those two

41:06

things.

41:06

You get this diverse spread of things that people die of in neurologic, diverse

41:10

neurological diseases becomes pretty heavy.

41:12

So I think cardiorespiratory fitness is probably the biggest thing in

41:16

preventing heart disease, but cancer becomes very interesting because.

41:21

There was a, there was a, there was a study in rodents that showed that

41:27

stretching prevents tumor growth.

41:30

And I thought this was wild.

41:33

I first heard about this on one of Huberman's shows.

41:37

And so I looked up the study and I was like, this is wild because I happen to

41:42

know some other things about immune function.

41:45

So one, uh, thing is that when, when in T cells, which are important both to

41:51

prevent infections and are also important because they attack you during autoimmunity.

41:58

And they're also important because they kill cancer for T cells to be activated.

42:03

What they do is they don't have enough energy themselves.

42:08

So they push off the local environment and that pushing off creates, um, motor

42:14

proteins inside that generate the energy to activate the T cell.

42:20

And what cancers do is they modify their extracellular environment to

42:25

compromise that because it's harder for the T cell to push off of it.

42:30

Now I know another thing from Crohn's research, which is that the best way to

42:36

cure Crohn's disease besides some of the drugs that they're on is a liquid diet.

42:42

And the recent research on how the liquid diet works is that it removes the

42:46

pressure in the intestine that is pushing out and is causing inflammation to

42:51

activate and attack the body.

42:53

Right.

42:54

So I'm synthesizing these three things.

42:56

And I'm like, this makes a lot of sense that the relative proportions and how

43:01

stretched out and like, what is the quality of your joint tissue and things

43:07

like that probably has a lot of severely underappreciated, uh, causation in

43:13

terms of cancer and autoimmune disease.

43:18

So I think it would be very interesting to see if actual like functional

43:22

mechanical activity, like if you optimize for functional mechanical activity,

43:28

such that you can swing around from acrobat, uh, from a trapeze and flip around

43:34

in the air and swing on rings and push yourself up and stuff like that.

43:40

Does that pay forward into better immune function because your body is more

43:44

properly structured?

43:46

I can't prove that, but I think it's very interesting to think about for, for,

43:50

for those two exercises.

43:51

Um, and then it is very interesting to me that gymnasts and pole vaulters both

43:58

spend a lot of time upside down and they don't stay upside down for very long,

44:04

but they just, they repeatedly are upside down quite a bit.

44:07

Right.

44:08

Right.

44:08

And so this is just, again, this is all just hypothesizing interesting ideas,

44:13

right?

44:14

So one interesting idea is that a vibration plate is the sedentary man's

44:21

gymnastics and that, you know, flipping upside down, um, is better at

44:29

circulating body fluids than walking.

44:34

And like a vibration plate is better than walking, but actually spending time

44:37

upside in the upside down state and flipping around is actually very good for

44:41

circulating the fluids in your body.

44:43

I don't, I, you know, I can't prove any of this, but it's all very interesting

44:46

to think about.

44:47

But what I can't, what I kind of conclude from this is you don't want to get

44:52

sucked into just optimizing VO2 max or something like that.

45:00

You really want to, the lesson from the gymnast is like, what are all the

45:04

things that a gymnast can do that I can't do?

45:07

And I should be able to approximate them in the best way that I can.

45:10

And I take that a little bit more, more literally.

45:14

So I, I actually do like, uh, I am trying to convert all my workouts into like,

45:19

what's the gymnastic version of this?

45:21

Um.

45:22

And you think it's because of flipping?

45:24

You don't think it's just, I'm just, I think they're both involving

45:28

coordination, explosive movement.

45:30

Right.

45:31

And I, I think that, I think that, I think that, yes.

45:34

So I think this, the skill training is, is big for spill off into neurological

45:39

disease because, but I'm just trying to connect them to the three things.

45:45

So I, like, like, I, I, I, I'm not sure exactly what they have lower rates of

45:48

death from.

45:49

We, we need more studies to, to see that.

45:51

But the, um, but the body mechanics, I think is a very interesting possible

45:56

explanation of why they'd have lower rates of cancer.

46:01

And the, what you just said, I think is a great explanation of why they would

46:04

have lower rates of neurological disease.

46:07

And I think it's kind of like, you know, if you look at, I think another thing

46:11

that people mistake in the longevity space is they spend too much time thinking

46:16

about.

46:17

Revert, like reverse engineering, uh, a hundred backwards.

46:21

What do I want to not have lost by that time and not enough time just being in

46:26

peak function?

46:28

Because if you look at bone mass, for example, bone mass goes, uh, up until you're

46:34

in your mid twenties, maybe 25 to 30.

46:38

There's a little bit difference with men and women, but then it just goes down

46:41

after that.

46:42

And if you want to have good bone mass, when you're 75, the, like the most

46:47

important asset you could possibly have is to have really good peak bone mass.

46:52

So I really think that like, it's just like I said before, you might not think

46:57

memorizing a string of 25 numbers is important at any age, but you know, if, if

47:03

you're going to have really awesome peak memory, that gives you a lot of room

47:08

to decline later on.

47:10

Whereas if you're trying to reverse engineer, like what you don't want to be

47:14

able to not remember when you're 75, I think you're just setting the bar way

47:18

too low.

47:19

Right. So if you're, if you're 20, you should be thinking about like, what are

47:23

all the sports I can't do and not, you know, I'm not saying there's anything

47:27

wrong with picking a sport, but, but I do think it's, it would be good for

47:32

everyone.

47:34

When they're young enough to do so to just try a different sport once a year

47:37

and maybe they don't love it and they don't fall in love with it, but maybe

47:40

they learn something like, Oh, I didn't realize I couldn't do that.

47:43

So for example, I did a last year, I did a little bit of BJJ and I did a little

47:49

bit of boxing and I was like, God damn, like my feet don't move like they used

47:55

to, um, in boxing.

47:57

And in BJJ I was, I was getting a little dizzy doing forward and backward rolls

48:00

and I was like, I don't spend enough, this is before I started thinking about

48:03

the gymnast being upside down.

48:05

I was like, I don't spend enough time being upside down.

48:07

So I was like, so I bought some mats and then now I just, you know, I do, I do

48:11

one forward and backward roll every day, no matter, I don't do BJJ right now,

48:15

but I just do one forward and backward roll every day as part of my morning

48:18

routine.

48:20

Um, but I've also switched, like, I was like, why would I overhead press when I

48:24

could try to do, um, I can do wall pushups now.

48:26

I, my hope is by next year I'll be able to do handstand pushups, but I've, I'm

48:30

working on a handstand right now.

48:32

So we'll see how that goes.

48:33

But, um, I think just cause you can focus on one thing.

48:39

You can really miss out that like, Oh, my favorite workout activities don't, I

48:44

mean, this is how many people are doing all their favorite workout routine

48:48

activities.

48:49

And forgetting that they don't have any rotation, they don't have any side

48:53

bending, you know, like, like if, if you would just, you just like try a

48:56

different sport and be like, Oh, what am, what did I not realize I wasn't able

49:00

to do at all?

49:01

And, and then pick that and put it in your workout.

49:03

Um, you know, cause if you've got a great programmer, then maybe your workout

49:07

is perfect, but I think most of us are, can like be gravitate towards some of

49:11

the exercises that we think are good.

49:14

And even if you, even if you think you're mixing it up, like CrossFit, CrossFit

49:18

managed to eliminate rotation from everything.

49:21

Like that, like every sport that involves throwing a ball involves rotation,

49:25

right?

49:25

They do sometimes they throw the ball sideways against a wall.

49:29

There's, there's some rotation.

49:30

Maybe they worked it in when I did CrossFit, the ball throwing we did was wall

49:34

balls.

49:35

And it was, so it was like, depends on, I think it depends entirely on who's

49:38

teaching it, but if you're doing windmills, windmills are kind of a form of

49:43

rotation.

49:44

There's a lot of ab exercises they do that are rotational.

49:47

Yeah.

49:47

All right.

49:48

So I, that maybe that wasn't fair, but, um, but my point is that like a lot, a

49:52

lot, a lot of, a lot of people are not doing any rotation.

49:55

Um, and, and so I, I just, I just, you just want to tap into that, that

50:01

diversity of like, what functions am I not exercising when I exercise them?

50:07

When we're talking about skills, we're talking about the neurological system

50:13

and the cognitive system synergistically in a dance.

50:17

Um, when you talk about old people and one of the things that happens when

50:21

cognitive function declines is you, you lose your ability to do puzzles.

50:27

And one of the ways to stave that off, they believe is like do crosswords, do a

50:31

bunch of different things, your concept chess, do something that's actively

50:36

making your mind fire and work.

50:38

Wouldn't it just make sense that a skill versus just a workout, just bench

50:43

pressing and squats and stuff like that, but it's an actual skill where you do

50:47

like Muay Thai hitting pads or even light sparring that you're, you're thinking

50:53

as well as exercising, which is very different.

50:57

Because you're, you're, you're, you're consciously aware of your opponent's

51:01

movement, you're calculating it, you're, you're, you're trying to time things.

51:06

There's a whole dance going on between your body and your mind that doesn't

51:10

really exist in straight workouts.

51:13

Yeah.

51:14

That alone, I would think would fight off a lot of the age related decline in

51:19

physical activity or physical function.

51:22

Yeah.

51:23

I think there are, you mentioned a couple of things in there.

51:26

So I think it's a separate thing to have a skill and have strategy and to have

51:31

reaction time.

51:32

But I, but I think you definitely want to be hitting all those bases.

51:35

So I think it's, it's good to have a general checklist of what should you be

51:40

exercising and see that it like takes strength and, and break it down into the

51:45

different planes.

51:46

And then also take skill, you know, it's hard to work everything at once, but

51:55

you got to find a way to, um, maybe, maybe you cycle through switching your

52:04

focus, but you find like, what is, if I, if I worked on really being able to

52:11

jump rope without tripping my feet up.

52:15

So, um, if I, if I worked on this last quarter, um, how am I going to take that

52:20

skill and not lose it?

52:21

For me, for me, for example, like I really focused on jump roping when I

52:25

realized how horrible I was at it when I was forced to do in boxing.

52:28

Um, and so I, I very intensively tried to get good at jump roping and now I don't

52:33

want to work on it anymore, but I've just taken in like, okay, every morning I

52:38

have to do 50 uninterrupted jump ropes just in the course of my warm warmup.

52:44

Just to kind of keep whatever skills that you've developed.

52:45

Yeah, just to, just to make sure that like, I'm not losing the basic capacity

52:50

to do that, that coordination.

52:52

Yeah.

52:52

And if I start to, then I realize I have to work on it more.

52:56

Mm, yeah.

52:57

Um, new things I think would enhance that even more maybe than things that you're

53:01

very comfortable with and things you're very efficient at.

53:05

Like, say if you're an athlete in whatever sport and you say, you know, I'm

53:10

going to try jujitsu or I'm going to try martial arts.

53:13

Like, something completely new like that where you're working out but you're

53:18

really thinking because you've got to like really concentrate.

53:22

It's not like a natural movement to throw a sidekick.

53:25

You have to really concentrate on picking your knee up, twisting your body and

53:28

all that jazz.

53:29

Like, I think stuff like that would, you know, just keep everything firing, no?

53:35

I think you, yeah, I mean, I think you should do a mix.

53:38

Like, you always want to be pushing yourself to a new, um, to new achievements

53:44

but then you also, I think you want to structure things so that you don't lose

53:48

the ones that you, that you did.

53:49

Right.

53:50

Like, I, I think a lot of us go through life just making achievement and losing

53:54

it.

53:54

Oh, yeah.

53:55

And we're like treading water and going nowhere.

53:56

I, when I really got into jujitsu, I stopped doing any kickboxing for a long

54:01

time.

54:02

And every now and then I would just hit the bag and just like, oh, I still can

54:05

do it.

54:06

But then, um, I started training Muay Thai again and it was kind of shocking

54:11

how long it took me to get, like, the flow back.

54:15

Like, where it really, like, comes off smooth.

54:19

Everything seemed like a little labored and it was just disheartening.

54:22

Like, oh, I don't really have these skills.

54:24

Like, I have to, like, re-acquire them.

54:26

You know, I know how to do it.

54:28

I've done it.

54:29

But it's just like, right now, everything's a little, the pathways are filled

54:33

with mud.

54:34

You know what I mean?

54:35

It's not clean.

54:36

It's not nice and sharp.

54:37

Everything is a little funky.

54:39

And, you know, but if you want to get good at jujitsu, you don't have time for

54:42

two hours of Muay Thai a day.

54:44

You just don't.

54:44

You know, so it's like you got to pick your poison.

54:47

You got to pick what you like and what you don't like.

54:49

Yeah, well, I think you have to decide what your goal is and what your metric

54:55

is.

54:56

Like, there's no way that anyone is going to be good at, like, seven, you know,

55:00

going to be elite level at any two sports or, like, great at any seven, right?

55:05

So, I think you have to say, like, okay, do I want to be really good at Muay

55:09

Thai?

55:10

And that's, you don't have to do that to have healthy aging.

55:15

Right, right, right.

55:16

There are things that you do at Muay Thai that you do have to be able to do to

55:20

have healthy aging.

55:21

So, if you're just thinking about it from the perspective of how do I know that

55:25

I'm engaging in healthy aging, I think you don't want to say, like, oh, I need

55:30

to be as good as I ever was at Muay Thai.

55:33

You just have to say, okay, like, why am I bad at some of that?

55:37

And is that something that I need in general?

55:39

And I think oftentimes by doing something like that, you can think about it and

55:44

you can realize, oh, what I really can't do is I'm not agile anymore.

55:48

I really can't, like, shift my weight quickly anymore.

55:51

Or I really can't, like, my reaction time is slow.

55:54

Like, I just keep getting hit in the head because I don't move it.

55:58

You know, if you're realizing those things, then I think you've got to you have

56:01

to find some way to train those because you need those for everything.

56:04

And it's just it's easy to not challenge yourself in life and don't realize

56:08

what you're losing.

56:10

So you do have to challenge yourself with something you're not able to do to

56:13

figure out what you're weak in.

56:14

One of the things I want to bring up you brought up earlier, you were talking

56:20

about martial artists and perhaps, like, injuries accumulating over time and

56:26

you lose some of your function because of that.

56:29

Like, you mentioned hands, hand injuries.

56:33

Is that something that people need to take into consideration that maybe they

56:37

don't, that maybe just physical damage, like, in terms of getting hit and

56:42

physical damage perhaps from overtraining, physical damage certainly from

56:47

cutting weight.

56:49

You know, a lot of these guys cut weight and they're basically on death's door

56:52

24 hours before a fight, which is, I think, completely insane.

56:56

And the most avoidable damaging thing about martial arts competition.

57:01

And yet it's ubiquitous.

57:02

It's like almost everyone does it.

57:04

Yeah, I mean, I think there is a degree of subjectivity to it.

57:10

If you're, you know, if your idea of what a life well lived is, is to win an

57:16

event that might have you die in the next three years, then, you know, how are

57:22

you going to argue with that, that value that someone has adopted?

57:26

But if, if you are thinking about it from the perspective of how do I stay

57:31

healthy through, how do I live a long, healthy life, then injury prevention has

57:36

to be your number one consideration, not your number two.

57:41

I think even if you're trying to say, like, how, how can I be the strongest I

57:46

could be, you would still need injury prevention to be number one.

57:51

Because, you know, how many people take three months off from a lift that they're

57:57

working on and wind up six months behind where they had been when they start

58:02

again as a result of that injury?

58:05

And where would they have been if they spent that six months getting stronger?

58:08

And if you're going to do that every two or three years, like that's taking a

58:13

lot, like a huge toll off even the skill that you could develop and your

58:17

maximal capacity at that.

58:19

But like I was saying at the beginning, I, I do, I really think that the

58:23

simplest explanation for why mitochondrial function declines 1% per year and

58:28

gets cut in half by age 70 is just this, like, when I was injured, my mitochondria

58:34

were completely obsessed with healing from that injury.

58:37

And a little bit came out of the account used to repair the home base.

58:42

That's what I was getting at.

58:42

Yeah.

58:43

Yeah.

58:43

So for someone who's had, like, say, a martial artist who's had broken hands,

58:47

broken ribs, knee surgery, shoulder surgery, a lot of these guys have gone

58:51

through a bunch of stuff like that.

58:53

Like, so each one of those things is taking a small toll.

58:56

Yeah.

58:57

Yeah.

58:58

That's not something that people consider.

59:00

You think, oh, you recovered from that injury.

59:03

Now you're 100%.

59:04

But you're 100% with the tax of having recovered from that injury.

59:09

Yeah.

59:10

And a lot of people aren't necessarily fully recovered from the injury either.

59:14

Oh, many, many aren't.

59:15

Yeah.

59:15

Many, many aren't.

59:16

I, you know, I, I talked to, to, to a guy once who was, you know, he got

59:23

injured in marathon running and he, he thought he was recovered.

59:29

I thought he wasn't recovered.

59:30

And he was, thought he was, there was some kind of metabolic stuff wrong with

59:33

him because he's getting sick all the time.

59:35

I'm like, bro, you didn't recover yet.

59:36

Like, what are you doing going out and doing all that running?

59:39

Like.

59:39

What was the injury?

59:40

I don't remember the, I forgot the specific injury, but, uh, one of, one of the

59:45

common running injuries.

59:48

Yeah.

59:48

One of the things that's really common in MMA, um, is someone getting knocked

59:53

out and then getting knocked out again because they come back too quickly.

59:57

Uh, it happened recently in a big fight.

1:00:00

Um, uh, and it's just, there's, there's a thing that happens with these guys

1:00:05

where they just want to get back in there and get a win.

1:00:09

And a lot of times they're like, I'll be ready.

1:00:12

I won't get hit again.

1:00:13

I know what I did wrong.

1:00:14

I'll, I'll be better this time.

1:00:15

But they're more vulnerable now.

1:00:17

Like they can get knocked out.

1:00:19

It, is this just neurological damage?

1:00:24

Is this, this just a function of the concussion?

1:00:27

Or do you think it's a function of the concussion, the recovery from it and the

1:00:30

diminishing capacity of the body because it had to recover from that traumatic

1:00:34

injury?

1:00:35

I think it's all of those.

1:00:36

It's the, but that too, right?

1:00:38

So it's not just the fact that you got knocked out and your brain is more

1:00:41

vulnerable now.

1:00:42

It's like, no, no, no.

1:00:42

Your body's more vulnerable.

1:00:44

You're probably not as strong as you were.

1:00:45

You're probably not recovering as quickly.

1:00:47

Yeah.

1:00:48

I mean, the, the brain is, it's a small part of the body, but it's massively

1:00:52

outsized in terms of the energy that it consumes.

1:00:54

And so think about if, think about if you're, you know, if you're actually

1:00:59

healing the ability for it to, like, if it's just sucking even more

1:01:02

disproportionate energy from the body and just think about how much the rest of

1:01:07

the body works to support the brain.

1:01:09

Like the liver is working all day long to make the brain get enough energy.

1:01:12

So, yeah, there's, there's no way that healing from a brain injury is not

1:01:17

taking a toll systemically.

1:01:19

That's impossible.

1:01:20

But to accelerate or enhance that, creatine, you think would be a very good

1:01:25

option?

1:01:26

I mean, creatine is one of the ones that's been demonstrated to do that.

1:01:30

And it, and it's been studied 20 grams a day.

1:01:33

I don't think anyone really knows, like, do you need 20?

1:01:35

Is 30 better?

1:01:36

Could have been done with five.

1:01:38

But the, most of the brain research is being done with doses around 20 grams.

1:01:44

And there's, the thought is that the, you know, the muscles are going to take

1:01:48

first dibs and you need to have a high dose to get it to the brain.

1:01:51

We don't, there's a lot we don't know about that.

1:01:55

But, you know, as a default, like if I was healing from a traumatic brain

1:01:59

injury, I would, I would take the creatine.

1:02:01

And then I, you know, I think when, if you have something that's this serious,

1:02:05

you do want to, like, know what your limiting bottlenecks are.

1:02:09

So I think actually doing mitochondrial testing is, that's, like, one of the

1:02:13

applications would be, like, oh, now it's really important that I have a six-month

1:02:18

window where I need to maximize everything I can.

1:02:21

And so, you know, testing to understand your unique needs, I think, would be,

1:02:26

it would be a way to supercharge that process when it's needed.

1:02:31

And I think that there are, and, you know, so to take this back to, like, what

1:02:36

can people do in general, I think methylene blue, you mentioned, is one of

1:02:40

those ones where, like, I wouldn't even, I personally wouldn't even take it

1:02:44

without testing showing that I need it.

1:02:47

But CoQ10 is an interesting one because CoQ10 is actually made in the body and

1:02:52

it is found in food.

1:02:53

And so there, you know, methylene blue was, a lot of people emphasized that it

1:03:00

was the first, it was the first drug.

1:03:03

So it was, like, the first, you know, example of pharma, basically.

1:03:09

But before that, it was actually patented as something that would turn your

1:03:13

clothes blue but wouldn't come out in the wash.

1:03:17

That was the patent on methylene blue.

1:03:20

And, you know, whereas CoQ10, you eat food, it's there.

1:03:24

Your body makes it itself.

1:03:26

What kind of food is it in?

1:03:28

Heart is the best.

1:03:30

And so I was saying before, you should be eating nose to tail.

1:03:33

Like, if you're going to eat meat, you should be eating heart.

1:03:34

I personally, most of my meat is actually a blend of, it's like 60% ground beef

1:03:45

and the rest of it is a blend of liver, heart, kidney.

1:03:49

And there are some other, mine is just liver, heart, and kidney.

1:03:52

There are some other companies that I've seen recently come out with ones that

1:03:56

include spleen and adrenals and very small percentages.

1:03:59

But that's, I do strongly believe in a food first, pharma last approach.

1:04:07

And that doesn't mean, like, I'm against pharma, but it means that even with

1:04:11

supplements, like, if you can meet a need with food, you should meet the need

1:04:16

with food.

1:04:17

You should use supplements in a strategic sense, not as a replacement for a bad

1:04:21

diet.

1:04:22

And those supplements should, you know, what you would do next is say, like,

1:04:26

okay, I'm really having trouble getting enough whatever nutrient.

1:04:30

Maybe I'll supplement to compensate for that.

1:04:33

But I think you should go down the line with, you know, other things that are,

1:04:38

like, supplements of things that occur naturally in your body that are, of

1:04:42

course, safe to be in your body because they're always going to be there.

1:04:47

Maybe you can supplement with that to help break a vicious cycle of aging or to

1:04:54

stimulate a virtuous cycle of healing that, you know, I would – once you're

1:05:01

getting all your nutrients and you're trying to do that from food, I think that

1:05:04

you could start playing around with that stuff.

1:05:06

But even then – so CoQ10 is a great example.

1:05:10

I would try eating more heart before I would try supplementing with 400

1:05:14

milligrams a day of CoQ10, for example.

1:05:17

Can I ask you this?

1:05:17

Does it matter if it's chicken heart, beef heart?

1:05:19

Is there a superior?

1:05:21

I don't think we have enough data to say that.

1:05:26

So CoQ10 is one of those things where the nutritional databases are not that

1:05:30

– I mean, you're not even going to find it in USDA database, but there's

1:05:33

published literature.

1:05:35

But I have not seen all the different hearts compared.

1:05:38

So how do we know that CoQ10 is in heart?

1:05:40

Well, wherever it's been measured in heart, it's there.

1:05:43

So like the representative examples of heart that were used were like an order

1:05:47

of magnitude higher in CoQ10 than anything else.

1:05:50

And is it dependent upon – I'm sorry.

1:05:53

Oh, we just haven't seen all of the different hearts compared to each other.

1:05:57

Is it dependent upon how it's cooked?

1:05:59

Like whether it's rare, well done?

1:06:02

I think you lose some during cooking, but it's – I forget how much and I don't

1:06:08

think it's all of it.

1:06:10

So it's – I think it's – you're always – I mean, you're always – the

1:06:13

more gently you cook your food, the better off you are in every conceivable

1:06:17

case.

1:06:18

It might not always taste the best.

1:06:20

Except for parasites, of course.

1:06:23

I mean, you don't need to make a steak well done to avoid parasites.

1:06:26

Well, not steak, but pork.

1:06:27

Right, right, yeah.

1:06:28

Or other things, especially some wild game.

1:06:31

Yeah, I mean, right.

1:06:33

So taking that into account, the nutrient value of the food is always going to

1:06:37

be highest when the food has been cooked relatively gently.

1:06:42

But anyway, so CoQ10 is interesting because it's hard to argue against taking

1:06:48

it from the literature because there's dozens of clinical trials.

1:06:53

Quite a bit of it is in heart disease.

1:06:55

It looks pretty promising in various forms of heart disease.

1:07:00

But if you look at that literature, what you see is a dose response where at 1

1:07:05

to 200 milligrams per day of CoQ10, the average person's glucose, insulin, and

1:07:12

blood pressure looks better than not taking it.

1:07:15

But the average person at 400 milligrams of CoQ10 is actually having worse

1:07:21

blood pressure, glucose, and insulin than they were without taking it.

1:07:27

And the variability around that is huge.

1:07:31

So one person is probably going to be worse at 100 milligrams, whereas another

1:07:35

person might get their best at 400 milligrams.

1:07:37

But it's like if you looked at the literature and you would say, where is the

1:07:41

sweet spot where the average person is going to be doing really good?

1:07:45

It would be 100 to 200 milligrams a day.

1:07:47

But I think there are – I've seen a lot of edge cases on either side where

1:07:53

some people get miracles and some people get – I wouldn't say catastrophe,

1:07:59

but they just get worse off.

1:08:01

So a lot of people complain about insomnia.

1:08:05

They complain about their heart racing or heart palpitations, various things

1:08:09

like that, overstimulation, feeling like the lights are too bright or the

1:08:14

sounds are too strong or whatever, just hypersensory awareness.

1:08:18

From CoQ10?

1:08:18

It's not common, but it's –

1:08:21

Is it higher?

1:08:21

I mean, all the people do uncommon stuff always ask me about it.

1:08:23

Right.

1:08:24

At higher levels?

1:08:25

No, at just like 100 milligrams.

1:08:29

Normal level.

1:08:29

There are just hypersensitive people out there.

1:08:31

Okay.

1:08:31

And then –

1:08:32

And is this rare?

1:08:33

Is this like –

1:08:34

I don't know how common it is.

1:08:36

So, I mean, what I can tell you is that across the trials, you see some people

1:08:42

reporting GI side effects, which is super common.

1:08:47

You don't see a lot of this mentioned, but you never know if they were looking

1:08:52

for it.

1:08:52

Like, a lot of times the side effect list is dependent on what side effects

1:08:56

they asked about.

1:08:57

Is this something you take with food or without food?

1:09:00

It would be better to take it with food.

1:09:04

And is the side effects – is it dependent upon when they take it?

1:09:07

Like, whether it's morning or evening?

1:09:10

I think for some people that have complained about insomnia, they have thought

1:09:16

that it was worse when they took it in the evening.

1:09:20

Makes sense, right?

1:09:22

Yeah.

1:09:22

Yeah.

1:09:22

So, maybe increase function if you took it early or maybe increase energy

1:09:27

levels?

1:09:28

Well, you know – okay.

1:09:30

So, I think – let me set the stage for this with just kind of like – I

1:09:34

think this really helps explain, like, what should you actually be thinking

1:09:38

about to know that you're healthy?

1:09:42

And I think we struggle a lot with – like, I think the medicine just thinks

1:09:46

that being healthy is just not having any disease.

1:09:50

And I think we, as kind of the wellness community or whatever, like, like, a

1:09:56

really good definition of health for me is you should – you should be abundantly

1:10:02

supplied with all the energy that you need to fulfill the goals that you're

1:10:07

trying to fulfill.

1:10:09

You should be adaptable and you should be adaptable enough to be able to handle

1:10:14

things changing that were out of your control or your own purposeful changing.

1:10:19

And I think the North Star for you to see when – to know that you are healthy

1:10:26

is that your energy to anxiety ratio is very high and your libido is very

1:10:33

strong.

1:10:34

And so, I – when you start losing – you use energy not only to produce,

1:10:40

maintain, repair everything, but you also use it to distribute everything.

1:10:47

And so, one of the things that you do with, like, the last 10% of energy you

1:10:51

make is help determine where all the energy goes.

1:10:54

And so, a lot of people think that, like, if their mitochondrial function is

1:10:57

declining, they should feel tired all the time.

1:11:00

But that's not necessarily the case.

1:11:02

It might be that you're just losing the energy that you need to actually help

1:11:07

– you know, the mitochondrial chemical energy to help control how you use

1:11:11

energy.

1:11:12

And so, you are wasting it as anxiety and that's coming out of productivity.

1:11:19

So, it's like you look at – you look at how much energy did I have yesterday

1:11:25

and what did I get done?

1:11:27

If the answer is, well, I felt wired all day, but I wasted most of it thinking

1:11:33

about why my wife insulted me and then worrying about how I was going to pay

1:11:38

the bills.

1:11:39

And so, I didn't actually get any work done.

1:11:41

Like, that's a good sign that you're – you are losing control over where your

1:11:47

energy is going.

1:11:48

So, you're not – you're just – that's not good.

1:11:50

That's not healthy.

1:11:52

Healthy is you have abundant energy to put towards productive things.

1:11:57

And so, you should see from that that you feel energized when you need to be

1:12:03

alert, that your anxiety levels are very low, that your libido is very high.

1:12:08

And, you know, you can adapt that on an age-dependent manner but – and that

1:12:14

you are able to sleep very deeply.

1:12:16

And if all your energy is keeping you up at night and then the next day you're

1:12:21

sleep-deprived, like, your biggest problem is you're just not putting the

1:12:24

energy to where it's supposed to go.

1:12:26

So, I think when you're looking at something like that, you could say, well,

1:12:29

maybe CoQ10 is just increasing their energy.

1:12:31

But to me, that – they lost a little bit of energy and they lost the energy

1:12:35

that they needed.

1:12:36

Like, they lost the top 10 percent of their energy and then they – that made

1:12:40

them not be able to control where the next 20 percent went.

1:12:43

And so, it spilled over into their heart was racing or it spilled over into

1:12:47

they couldn't fall asleep at night.

1:12:50

But I've also – you know, I've also seen other edge cases where people get

1:12:53

miracles from CoQ10 that you also are not going to find in the literature.

1:12:58

So, I had this –

1:13:00

What kind of miracles?

1:13:00

I'll give you one example.

1:13:02

So, in the program that I had, I had a client named Jacqueline and she lost her

1:13:09

period at 28.

1:13:11

So, she – you call that amenorrhea but she described it as I hit menopause

1:13:16

way too early.

1:13:17

She didn't have her period for 10 years.

1:13:20

So, we did mitochondrial function testing on her that showed that, like, you

1:13:24

have a specific need for a lot of CoQ10.

1:13:26

And what was crazy was she had gone to functional medicine practitioners, did

1:13:32

homeopathy, all kinds of – you know, just went to whatever she could find.

1:13:36

And nothing ever changed that.

1:13:39

But what's crazy is that, like, functional medicine practitioners often give

1:13:42

bagfuls of supplements to their patients.

1:13:45

And, you know, so she had gotten, like, normal doses of CoQ10 in the past, like,

1:13:48

100, 200 milligrams.

1:13:50

But based on the testing that we did, we said, like, you should probably

1:13:53

experiment with 700, 800 milligrams.

1:13:56

Whoa.

1:13:57

So, which, you know, by the way, is above where the average person's glucose

1:14:01

and insulin gets worse.

1:14:04

But two weeks into taking the CoQ10, she got her period back.

1:14:08

Wow.

1:14:09

After 10 years.

1:14:09

That's crazy.

1:14:11

After 10 years, yeah.

1:14:12

That's nuts.

1:14:12

That's crazy.

1:14:12

So, I think the – I think CoQ10 is a – it's methylene blue.

1:14:17

I'm a little bit more hardcore.

1:14:18

Like, you really got to do the testing.

1:14:20

Whereas CoQ10, I'm kind of like, you know, you should play around with it.

1:14:24

Like, you very well may benefit from 100 to 200 milligrams a day.

1:14:27

But my food-first, farm-to-last approach says, are you eating heart?

1:14:31

Right.

1:14:32

Did you eat heart today?

1:14:32

Right, right, right.

1:14:33

Yeah.

1:14:33

Well, that completely makes sense.

1:14:35

And it also completely makes sense that it would be more bioavailable in food.

1:14:39

You'd absorb more of it.

1:14:40

I think that's – you know, that could be part of it.

1:14:44

But then it's just –

1:14:44

Comes in a natural form.

1:14:45

It's just also there's so much other stuff in the food, you know?

1:14:47

Right.

1:14:48

So, it's like people get obsessed with whether they should be taking this thing

1:14:52

or that thing.

1:14:52

But that thing, if you got it from that food, give you 36 other things.

1:14:55

Right, right, right.

1:14:56

And it's just –

1:14:57

And they work together.

1:14:58

Yeah.

1:14:58

And they work together and they can also become imbalanced.

1:15:01

So, I think a lot of – mitochondrial energy metabolism is – the bottlenecks

1:15:08

that people can have is kind of like jammed up traffic.

1:15:11

And a lot of times you can megadose something.

1:15:14

And the main problem of megadosing that for anyone would be it would be imbalanced

1:15:19

with something else.

1:15:20

But if you've got a blockage and that's something else, now you've just got

1:15:24

like a train wreck happening in your mitochondria because you're activating one

1:15:28

pathway that has to flow through the next one where you had your blockage and

1:15:31

it's just like that.

1:15:33

So, you can go online, for example, and find communities where people are raving

1:15:36

about high-dose thiamine.

1:15:38

And the RDA, the government-recommended amount of thiamine to get is around

1:15:42

like 1.3 milligrams.

1:15:44

There's people out there who are like, oh, everyone should be taking 2,000

1:15:47

milligrams per day.

1:15:49

But I saw one case where this happened before I knew the person, but they had

1:15:55

fatigue so bad that they couldn't get off the couch.

1:15:59

And so, she was self-rating her energy at zero.

1:16:02

And a practitioner said, oh, you should really try this high-dose thiamine.

1:16:07

So, she went on 1,100 milligrams a day.

1:16:09

So, not 2,000, but big, right?

1:16:11

And a lot of people get miracles out of this and they are vocal.

1:16:15

They make communities on Facebook and so people get the idea that everyone who

1:16:19

tries it is benefiting from it.

1:16:21

But she – her energy did improve a little bit, but she developed a new,

1:16:27

completely new motor dysfunction problem, unsteady gait.

1:16:32

It just kept getting worse the whole time she was taking the thiamine.

1:16:36

She had an existing problem with dizziness that got a lot worse.

1:16:42

And a major issue for her was that she had to clear out the thiamine.

1:16:45

But the mitochondrial testing that we did on her basically showed that, like,

1:16:50

it explained it because it's – because she, you know, had a block in the

1:16:54

pathways that would be most sensitive to megadosing that supplement.

1:16:57

And so, you know, winding that back and re-nourishing those other pathways

1:17:01

helped her.

1:17:02

I do think that a lot of people, if they're going to go into the wild, wild

1:17:07

west of megadosing random supplements, should do their own testing of glucose,

1:17:13

ketones, and lactate at home.

1:17:16

A lot of people test their glucose.

1:17:17

Not a lot of people test their lactate.

1:17:19

But I'm 100% confident that that woman, had she – had the practitioner said,

1:17:25

try the thiamine and see what it does to your lactate.

1:17:29

And if it goes down, it's good.

1:17:31

And if it goes up, it's bad.

1:17:32

I think she would have stopped it after the first few days.

1:17:36

And the new onset motor dysfunction never would have happened.

1:17:39

And so maybe she wouldn't have done mitochondrial testing with me until months

1:17:43

after that, but it wouldn't have been a big deal because she had this real-time

1:17:47

indicator of mitochondrial dysfunction that she tested herself at home that

1:17:51

showed her, oh, I'm trying this, you know, out-of-left-field thing.

1:17:55

Let's see, am I getting a stress signal out of it or am I getting the signal

1:17:58

that my mitochondria are calming down and are more happy with their function,

1:18:02

which is really what lactate is telling you.

1:18:05

And, you know, most people who do lactate testing do it in exercise.

1:18:08

And what you see in exercise is when your body is under an incredible amount of

1:18:12

stress, you see lactate levels go up in the blood.

1:18:15

You know, halfway through a pro basketball game, lactate is through the roof,

1:18:20

right?

1:18:20

Well, you know, if I took – if I take thiamine and the next day it looks like

1:18:24

I'm halfway through the basketball game when I wake up, that's a sign that

1:18:27

something is out of whack in my body, right?

1:18:31

So, but, you know, to go back to, like, if they – if the perspective was you

1:18:36

might need more thiamine, so you should try adding some nutritional yeast to

1:18:42

the dishes that you want to impart a cheesy flavor to, which is what

1:18:46

nutritional yeast tastes like, because nutritional yeast is really high in thiamine.

1:18:50

Then that probably wouldn't have happened because the dose would have been a

1:18:53

lot lower.

1:18:54

She would have gradually gone into it much more gradually.

1:18:56

But also, whatever those blockages were would have the other nutrients

1:19:00

assisting them, so the thiamine wouldn't be so out of balance.

1:19:04

So it's not just that you absorb it better or whatever.

1:19:07

It's also just the food – going food first really helps correct for errors

1:19:13

that are a problem with your expertise.

1:19:17

Warren Buffett once said that a diversified portfolio is great protection

1:19:22

against ignorance.

1:19:24

He said it doesn't really make sense if you know what you're doing.

1:19:27

But if you don't know what you're doing, you really should diversify.

1:19:30

Yeah, and so that's what food – food is a diversified portfolio.

1:19:34

And if you don't have the expertise to run around taking different things that

1:19:39

you don't – if you don't understand the biochemical pathway of the thing you're

1:19:43

megadosing, you are not a candidate – that's like buying an ETF and you don't

1:19:48

even know what an ETF is.

1:19:50

You know, like it's like – give that to your financial advisor.

1:19:53

And so, yeah, I think that food first, pharma last is the food first part of

1:20:00

that is really just a protection against – but like I do have the expertise

1:20:06

and I still do food first because I know that my expertise in my own body is

1:20:11

incomplete.

1:20:13

And so, you know, I might know a thousand times more than the average person

1:20:17

about what thiamine does in the body, but thiamine is doing things in my body

1:20:20

and I don't know what they are.

1:20:22

So I'm not going to – I'm not going to assume I know everything just because

1:20:26

I have like, you know, top-notch expertise in the field.

1:20:30

Right.

1:20:31

When you're talking about methylene blue and CoQ10 and the benefits on

1:20:36

mitochondria, is – what are the – what's the mechanism?

1:20:40

And are they similar?

1:20:41

Is it – are they interchangeable?

1:20:44

They are not similar and they're not interchangeable.

1:20:49

So CoQ10 is – and, you know, ask me if you want me to go into even more

1:20:54

detail, but if you extract energy from food and then you need to carry that

1:20:59

energy through a pathway, CoQ10 is about two-thirds through that pathway.

1:21:04

And it's just – it's like if you were going down a road and you had to take a

1:21:07

shuttle across the river to get to your next destination and then you go get on

1:21:11

the next train or something like that.

1:21:14

But so CoQ10 is just part of the transport pathway as the electrons come

1:21:18

through that are taken out of food to ultimately convert to ATP.

1:21:22

Methylene blue is – you know, if CoQ10 is like the main ferry, methylene blue

1:21:28

is this guy running around waving his hands in the air.

1:21:32

Oh, you know what methylene blue is like?

1:21:34

It's like those fake taxis at the airport where like you're trying to go to the

1:21:38

taxi line and they come right up to you and they're like, excuse me, sir, do

1:21:42

you need a taxi?

1:21:43

But it's like the shady taxi where – so methylene blue is like the – it's

1:21:47

like an army of the shady taxis.

1:21:49

And they're like, oh, don't take the ferry.

1:21:51

Come over here, right?

1:21:52

And so if the ferry is blocked, methylene blue would be great because, you know,

1:21:56

if there's no taxis left, you want the – you'll take the shady way because

1:22:00

you've got to get somewhere.

1:22:01

So methylene blue is – it's operating on the outer edges of the main pathway

1:22:07

and it's giving you alternatives.

1:22:10

But the mitochondrial pathway that you were born with is the one that is best.

1:22:15

It's the most efficient one.

1:22:17

So like I was saying before, methylene blue is great if you have a blockage

1:22:21

there and you need a detour.

1:22:23

It makes you worse off if you don't.

1:22:25

CoQ10 is – it's the reason you can overdose on it is because it's like, okay,

1:22:30

there's a river and you've got to get a ferry going across it.

1:22:34

Well, what happens if there's 10 ferries or there's 50 ferries or there's 150

1:22:37

ferries?

1:22:38

At some point, they're going to be running into each other and you're just

1:22:41

going to clog up that – at some point, putting more vehicles into any pathway

1:22:45

just makes things worse with the traffic that results.

1:22:49

And if you have too much traffic, you get accidents.

1:22:50

And, you know, train wrecks and car crashes and your mitochondria aren't good

1:22:54

for you.

1:22:56

Do CoQ10 have a similar benefit in terms of like red light therapy, increasing

1:23:01

mitochondrial function?

1:23:02

I think they could be synergistic.

1:23:05

CoQ10, by the way, it also helps you make more mitochondria and that's called

1:23:11

mitochondrial biogenesis.

1:23:14

Exercise also helps you make more mitochondria and I do think that you – like

1:23:18

– so you should never take CoQ10 as an excuse to not exercise because

1:23:21

exercise is very specifically putting the mitochondria where they belong to

1:23:27

meet the adaptation that you are stressing.

1:23:30

So that's – you know, that's mitochondrial biogenesis number one.

1:23:35

But CoQ10 will help with that.

1:23:37

You don't always want mitochondrial biogenesis.

1:23:41

I do think like testing is another case where – that might be a case where

1:23:44

like you could use a high-dose CoQ10 to try to stimulate more mitochondria if

1:23:48

testing shows that you're – you don't have enough and that's your like

1:23:51

limiting bottleneck.

1:23:56

So like the average person whose CoQ10 levels are just a little lower where

1:24:00

they should be, it really is just acting as that kind of like you open up the

1:24:05

biochemistry textbook, you see the place of CoQ10 in the mitochondrial energy

1:24:09

production pathways and it's just doing the basic textbook thing of helping you

1:24:14

move those electrons along on the path to convert food to ATP.

1:24:19

One of the things you brought up earlier was seed oils impeding the absorption

1:24:25

of certain nutrients.

1:24:26

Seed oils are a weird thing because, you know, so many people pushed against

1:24:32

them and said, hey, these are essentially industrial lubricants that have been

1:24:37

converted to food oil for profit and it's not really the best stuff that we

1:24:42

should be consuming.

1:24:44

And then you have a bunch of online contrarians that say, oh, there's nothing

1:24:47

wrong with seed oils.

1:24:49

This is all nonsense.

1:24:50

There's no data.

1:24:51

There's no studies.

1:24:52

And I don't understand that thought process.

1:24:56

And when you know what they're made with, with hexane and all the whole fucking

1:25:02

disgusting process of making them versus pressing olive oil.

1:25:07

Look, to me, it just seems so obvious that one of them you should probably

1:25:12

avoid.

1:25:13

And then when it's connected to all sorts of inflammation and all sorts of

1:25:17

various issues and what you were talking about earlier, impeding the absorption

1:25:22

of certain nutrients.

1:25:23

What do you think is going on?

1:25:27

First of all, why are people defending seed oils?

1:25:31

And what is the real problem with seed oils in a human diet?

1:25:36

Seed oils make your tissues more vulnerable to damage and they don't damage

1:25:45

your tissues.

1:25:47

And so one of the problems that has caused a lot of controversy, and I think

1:25:51

the reason there's so much back and forth over this, is that it takes the right

1:25:56

type of study to see seed oils making your tissues more vulnerable to damage.

1:26:04

Because you need enough time for the damage to play out, and you need people

1:26:09

who are more vulnerable to the damage.

1:26:12

And we've been talking a lot today about how aging is increasing that tissue

1:26:20

damage.

1:26:21

Like everything is, your repair capacity goes down as you grow older because

1:26:26

your mitochondrial energy production is going down.

1:26:29

And one of the things you want to look at is what do seed oils do to you by the

1:26:35

time you're 75, and you don't just want to look at what do seed oils do to you

1:26:40

when you're 25, because you might not be seeing the capacity for the increased

1:26:45

vulnerability of tissue damage.

1:26:48

Another thing is the trials have to be long enough, both because it takes time

1:26:53

to see the process of tissue damage play out, and also because we know from

1:26:59

long trials of seed oils that short trials are useless.

1:27:06

And there are a lot of the people who are talking the loudest in defense of

1:27:10

seed oils are looking at trials that last seven weeks long or 12 weeks long,

1:27:15

and they're ignoring trials that were done in the 50s, 60s, and 70s that were

1:27:21

five to eight years long.

1:27:24

And I'm just like, you know, by all means, analyze the shorter trials, but do

1:27:29

it in the light of what we know from the longer trials.

1:27:32

And the most important of the longer trials was the LA Veterans Administration

1:27:37

Hospital study.

1:27:38

And this was the primary paper on it was published in 1969.

1:27:42

So it takes us back in history.

1:27:44

But there was a period between World War II and 1970s where there was a lot of

1:27:51

motivation in the research community to do these grand randomized control

1:27:57

trials of nutrition.

1:28:00

We don't have that anymore, and I think it's because scientists love to, in

1:28:05

their collective imagination, to say that what they're doing is they're just

1:28:11

carrying forth a linear path of addressing knowledge gaps left from the

1:28:16

previous literature and just making a linear progress in science.

1:28:21

But they're really not because the incentive structure is to publish a large

1:28:27

number of papers in high-impact journals on a yearly basis as your university

1:28:32

reviews get done.

1:28:34

And so if you're going to – and then there's other incentives too because you

1:28:38

have to get grants with preliminary data.

1:28:41

So you have shorter studies that you then say, well, I'm going to do a longer

1:28:44

study now, and it keeps the grant cycle going.

1:28:47

And then the people who write the grants want to see things getting published

1:28:50

out of those papers.

1:28:51

So for you to be like, I'm going to do a 12-year randomized controlled trial of

1:28:56

seed oils is – it's going to be hard to get the people – get all this box

1:29:00

checked.

1:29:01

Like you might not be publishing a paper for a while.

1:29:03

So what the LA Veterans Administration Hospital study showed was that they

1:29:08

randomized people to seed oils or traditional fats.

1:29:14

So the – in the first two years, you had a little bit of a heart disease

1:29:18

benefit, but then it wore off over time.

1:29:21

And so the heart disease mortality basically by the end of the trial was just

1:29:25

kind of flat.

1:29:26

But the cancer was the same for the first two years.

1:29:31

But then at the two- to five-year mark, it started diverging, and you see, oh,

1:29:33

it looks like there's something there.

1:29:35

The five- to seven-year mark, it's, you know, traditional fats down here, and

1:29:39

this gap starts widening where seed oils are up here.

1:29:42

And then by the end of the study, total mortality was kind of flat the whole

1:29:47

time, but it just started to diverge at the end of the study to favor seed oils

1:29:51

causing more death.

1:29:53

And this study was the longest, and it was also the one where the only trial

1:29:58

ever done with seed oils where the people – the mean age was 65.

1:30:03

So the people were older than in every other trial.

1:30:05

And one of the important things about being old is that that's what makes you

1:30:09

able to get cancer.

1:30:11

There are some childhood cancers, but in general, people start getting cancer

1:30:15

when they live long enough to not die of heart disease first.

1:30:20

So doing the trial in older people for longer is what allowed you to see that

1:30:25

the seed oils seem to be able to cause cancer.

1:30:29

And what the author's conclusion was, was that because the total mortality was

1:30:33

just starting to diverge at the eight-year mark, and because they had a

1:30:37

plausible reason for it, that the cancer was exploding,

1:30:40

they said, we have ultimately left the question of whether these oils are toxic,

1:30:46

unresolved, and the one thing that we need is instead of the previous goal of

1:30:51

the trials being five years long, that the trials be done well in excess of

1:30:56

eight years.

1:30:57

So scientists think that they're just, like, looking at the older children,

1:31:00

they're saying, oh, what was the gap in the knowledge that we need to solve

1:31:03

next?

1:31:04

Well, I'm telling you, they concluded in 1969 that the gap in the knowledge was

1:31:08

we need a trial that's a lot longer than eight years, and what did we get?

1:31:12

Seven to 12-week trials.

1:31:14

It's kind of like that, who was it, Peter Thiel, or someone had a tweet that

1:31:18

was like we, they promised us flying cars and all we got was 180 characters or

1:31:23

something like that, whatever that quote is.

1:31:26

You know, they promised us well in excess of eight-year trials was the next

1:31:30

thing we needed to study, and, like, you know, 50, 60 years go by, and all we've

1:31:35

got is these seven-week trials and 12-week trials.

1:31:39

Now, we also know why seed oils would take a while to have such negative

1:31:43

effects, because it actually takes you four years just for your tissues to

1:31:48

start looking like the seed oil you're eating.

1:31:51

Like, if you switch from butter and olive oil today and you go on corn oil, it's

1:31:57

going to take four years for your tissues to fully look like the corn oil.

1:32:02

And then once that happens, you've got secondary effects, so you start getting

1:32:07

your vitamin E levels depleted much faster.

1:32:10

But it takes a while for the vitamin E levels to go down in order for other

1:32:15

effects, other results of that, like the increased vulnerability to the tissues

1:32:21

being destroyed.

1:32:22

All that stuff is like you're not even starting to see it until five, six years

1:32:27

go by.

1:32:29

And so I think that's the big reason that there's so much controversy is that

1:32:33

for whatever reason, there's some people who just don't want to look at the

1:32:38

older trials that were very long, and they're spending all their time looking

1:32:42

at these very short-term trials.

1:32:44

And, you know, is there a motivation behind that, or is it just laziness? I'm

1:32:48

not sure.

1:32:48

I think it's attention.

1:32:50

I think part of it is attention.

1:32:51

Yeah, it's a big part of it.

1:32:53

Part of it is justifying the contrarian position with these short-term trials,

1:32:58

because then you could dunk on people and get attention.

1:33:02

Yeah, I mean, that makes a lot of sense.

1:33:04

Like, everyone has to get attention somehow if they want to make it in this

1:33:09

world.

1:33:10

Well, that's the side effect of this influencer culture, you know, and it's one

1:33:13

of the things I really appreciate about your work.

1:33:15

You are very evidence-based, and you, you know, I've been paying attention to

1:33:20

your stuff for a long time.

1:33:22

It's, you're, you're never hyperbolic, it's always very rational, it's very

1:33:26

balanced, and I think that is really important, because there's a lot of people

1:33:32

that they make these videos, or they have social media posts, and it's

1:33:39

insulting, inflammatory, and they're doing it for attention.

1:33:43

And they're doing that, you know, that kind of behavior for attention, along

1:33:47

with science.

1:33:48

They're, they're adding the science into it.

1:33:49

But it seems like the science is just a vehicle for them to get attention.

1:33:53

Yeah, well, I mean, that's, that's unfortunate, because there, there is health

1:33:58

hanging in the...

1:34:00

I know, I know, it is unfortunate, but it's also common, you know, it's really

1:34:04

common.

1:34:04

You know, you, you see it in all sorts of different disciplines, you know, you

1:34:08

see it in our archaeology, you see it in everything.

1:34:11

There's people that want to dunk on their opposition, and that's part of how

1:34:15

they're getting attention, is by insulting people, and you see it, but when you

1:34:20

see it in nutrition, it's just, it's really weird, you know, because it's not

1:34:25

necessary.

1:34:26

And the people that are getting attention, whether it's Andrew Huberman, or

1:34:30

yourself, a lot of people that are just doing evidence-based stuff, and being

1:34:34

really rational about it, and that's how they're getting attention.

1:34:38

And other people are seeing them and going, I need to dunk on that guy in order

1:34:41

to elevate my social profile.

1:34:43

And the seed oil thing is a weird thing to defend.

1:34:48

It's just, just on the way that it's manufactured.

1:34:53

If you just watch the process and go, do you want to eat that?

1:34:56

Do you want that?

1:34:57

Or do you want butter?

1:34:58

Butter seems way better.

1:35:00

It seems way more normal.

1:35:01

It seems like your body would accept butter a lot easier than it would accept

1:35:05

this fucking insane process where you're dumping a bunch of chemicals into this

1:35:11

goop,

1:35:11

this nasty shit that you're pushing out of rapeseed oil, and you're calling it

1:35:17

canola oil.

1:35:18

And you know how many people think canola oil is corn oil, because corn is canola?

1:35:22

You know, you think of corn, oh, corn oil, it must be good for you, it's

1:35:25

vegetable oil.

1:35:26

Well, it is funny that they named it after a con.

1:35:28

It's fucking weird.

1:35:29

A con?

1:35:30

Yeah, there's an article, not by me, but by someone else, called The Great Canola,

1:35:35

and it's about how canola oil is a con.

1:35:39

Yeah.

1:35:40

It's a big name, but anyway.

1:35:42

That's a good way to put it, because canola oil is a con.

1:35:45

Yeah.

1:35:46

Because many people, I've seen canola oil where they have a fucking image of a

1:35:52

corn, of an ear of corn.

1:35:54

Have you ever seen that on the label?

1:35:56

I don't look at canola oil labels, but this was-

1:36:00

It's been a while since I bought a bottle of canola oil.

1:36:01

If there's something you can find that shows that, because I hope I'm not

1:36:05

having a false memory,

1:36:06

but I'm pretty sure there used to be a canola oil that had like an ear of corn

1:36:10

on it.

1:36:10

It's rapeseed, and it's an industrial lubricant, and that's what they used to

1:36:16

use it for, and it's a byproduct.

1:36:19

It's a weird, funky thing that they have to pour a bunch of shit into just to

1:36:23

take the smell out of it, just to take the rancid smell out of this weird oil

1:36:28

that you're cooking with.

1:36:30

Yeah.

1:36:31

You can buy cold-pressed seed oils.

1:36:34

It's not what most people are eating food with, but I still think that the

1:36:41

fundamental problem with-

1:36:44

It's not just the processing.

1:36:45

It's also, if you look at ancestral human diets, no one ate fatty acid

1:36:50

compositions that looked like that,

1:36:52

because the reason that they usually use hexane to extract it is because it's

1:36:57

actually difficult to extract using purely mechanical methods.

1:37:01

So olives can be pressed into oil-

1:37:04

Right, and that is a type of seed oil, right, if you thought about it.

1:37:07

Well, no, an olive is a fruit oil.

1:37:08

A fruit, but avocado, is that a fruit as well?

1:37:10

Avocado oil?

1:37:13

Yeah, avocado oil is pressed out of the avocado.

1:37:16

Right, and that's specific-

1:37:18

Because the flesh is super high in fat.

1:37:19

Right, so it's just the pit inside of it is the seed.

1:37:22

Yeah, I don't think they make-

1:37:24

You're not getting anything from that.

1:37:24

Yeah, I don't think they make oil out of that.

1:37:26

So it's a fruit oil.

1:37:28

So whether it's olive oil, the high heat ones are avocado oil.

1:37:34

That's one that people like to cook with, right?

1:37:36

Yeah, well, okay, so-

1:37:38

Are there any issues with that?

1:37:42

So cooking with an oil, one issue is the smoke point, because the oil is

1:37:48

burning at its smoke

1:37:49

point, and that probably is more of an indication of flavor than it is of

1:37:56

health, but it is generally

1:37:59

going to correlate.

1:37:59

Like if the oil is burning, you're more likely to have damage to the oils, and

1:38:04

consuming damaged

1:38:05

oils is bad for you.

1:38:10

So there's the smoke point, there's the fatty acid composition, and there's the

1:38:16

solvents

1:38:16

and other chemicals left over from the processing, and I think all of those are

1:38:20

an issue.

1:38:21

But the fatty acid composition is like, seed oils has become the common thing

1:38:26

to use as

1:38:27

a nickname, but what you're really thinking about is that they're high in polyunsaturated

1:38:35

fatty

1:38:36

acids, or PUFAs, and those polyunsaturated fatty acids are just like, it

1:38:40

happens to be most

1:38:42

things, most oils that are currently on the market for food consumption that

1:38:49

are very high

1:38:50

in polyunsaturated fatty acids, are what we call seed oils.

1:38:53

So that's, you know, that's why we call it that way.

1:38:56

But the actual fatty acid composition, like if you go back to any oil that was

1:39:04

easy for humans

1:39:05

to produce before, say 100 years ago, then you don't see those, like there, you

1:39:15

don't see a strong

1:39:17

tradition of large consumption of rapeseed oil going back because, or cottonseed

1:39:24

oil, or corn oil,

1:39:26

because it's, I mean, try squeezing a corn kernel, it's not that squeezable.

1:39:31

And so when you have

1:39:33

these very small, hard things, that's why you wind up getting solvent

1:39:39

extraction, but you had to do the

1:39:42

solvent extraction because it was not easy otherwise to get oil out of those

1:39:47

things. The solvent is a whole

1:39:51

other thing. I was in a lab once where someone had us analyze residual hexane

1:39:58

in foods, and they just

1:40:02

bought a bunch of grocery store foods. And I was, I was kind of managing the

1:40:07

data analysis while someone

1:40:09

I worked with was doing the hexane measurements. But let me just say that if it's

1:40:14

extracted with

1:40:15

hexane, it's got hexane left over. And we saw something that was not hexane. We

1:40:19

didn't know what it

1:40:20

was, but it was some chemical solvent that was massive in the pump spray oils.

1:40:27

And I, after I

1:40:29

saw that, I was like, I'm never using a pump spray oil. Cause they, cause they,

1:40:33

like you could put

1:40:34

olive oil in like a mechanical spray bottle and that's fine. But like Pam and

1:40:37

those other ones,

1:40:38

they, they're using chemicals to, to make the, the spraying work. And it's,

1:40:44

there's something that's

1:40:46

some chemical solvent that's just like way, like massive proportions in it. So

1:40:50

after I saw that,

1:40:51

I just stopped, stopped using that. I won't go near those.

1:40:54

Yeah. I don't go near those anyway. But what about a grapeseed? I know grapeseed

1:40:59

is one that people

1:40:59

like to cook with cause it has a high smoke point.

1:41:01

Yeah. I, I would put grapeseed oil in the category of a seed oil that I wouldn't

1:41:09

consume in high

1:41:10

quantities.

1:41:10

And is hexane an issue with that as well?

1:41:12

Not, I mean, not if it's cold pressed. I mean, you can get like organic cold

1:41:18

pressed

1:41:18

grapeseed oil that is not solvent extracted. It's not RBD. It's, it's, you know,

1:41:25

not heated.

1:41:26

But you still have to deal with the polyunsaturated fatty acids.

1:41:29

Yeah. I mean, it's, it's very, you're, you're paying a lot to get a high

1:41:31

quality product,

1:41:32

but it's still like, you know, there might be studies out there about some

1:41:37

therapeutic benefits

1:41:38

of some of the components of the grapeseed oil, but I don't, I wouldn't want to

1:41:42

make those fats be

1:41:43

the major oil in my diet because I think you're just overload. Like it's high

1:41:48

in antioxidants.

1:41:49

And so you're going to get benefit. There's going to be beneficial things in it,

1:41:52

but I don't think

1:41:54

that those fats are what you want to be your main fatty acid consumption.

1:41:59

What about if you were searing a steak in grapeseed oil? Would that be an issue?

1:42:04

I mean, the less of the oil that's there, the less of an issue it is. You know,

1:42:10

if you're just

1:42:10

coating the pan with it and it's convenient because it doesn't have a high

1:42:13

smoke point,

1:42:14

I wouldn't worry too much about it. But I wouldn't, I wouldn't be one healthy

1:42:18

fats.

1:42:18

I wouldn't want to be consuming like a tablespoon or upwards of grapeseed oil a

1:42:21

day.

1:42:22

So I think we would agree that the issue with saturated fatty acid, saturated

1:42:30

fats and just

1:42:31

in the zeitgeist, saturated fats, we have demonized since whatever that study

1:42:38

was with the,

1:42:39

where the sugar company bribed those scientists. Was it the fifties, the sixties,

1:42:44

wherever it was,

1:42:45

where they spent, uh, it started, uh, it started back then. The, the kind of

1:42:49

the, the crowning

1:42:50

turning point was 1984 when time magazine had, uh, a picture of a frowning face

1:42:58

made out of eggs and

1:42:59

bacon. And, and the cover said, hold the eggs in butter. Uh, cholesterol has

1:43:04

been proved deadly

1:43:05

in our diets. We'll never be the same.

1:43:07

And we got to pull that photo up. That's so crazy. They really did that.

1:43:11

Yeah. They, they actually, they, they reversed it a few years ago where they,

1:43:16

they took the same

1:43:17

image, but they made it a smiley face and they were like, now we know eggs are

1:43:20

good for you.

1:43:21

But meanwhile, how many lives did you ruin with your shitty advice? Um, it's so

1:43:26

stunning.

1:43:28

Yeah. You can do it. You can see the two right there. Yeah. You can see both

1:43:31

side by side.

1:43:32

Crazy. Um, yeah. So the one on the right is the upper left hand corner. Yeah.

1:43:37

That the upper

1:43:37

left hand corner is the new one. And the one on the right is the 1984 one.

1:43:41

Scientists labeled fat,

1:43:43

the enemy. They were wrong. Yeah. You didn't print the whole thing. They got

1:43:47

fucking bribed

1:43:48

and not a lot of money. That's, what's really crazy. It ruined society, ruined

1:43:53

diets for what?

1:43:55

$50,000. So for $50,000, people started eating margarine and eating seed oil

1:44:02

and not eating

1:44:02

butter and not, not consuming cholesterol, which is, you know, the building

1:44:07

blocks for hormones.

1:44:08

It's such an important aspect of the human diet. And when you tell people that,

1:44:14

like I tell

1:44:14

people I eat mostly meat, they go, what about your cholesterol? I just take a,

1:44:18

I don't know

1:44:20

what to tell you. Go, go read. I just can't, you know, I can't sit there and

1:44:25

tell you

1:44:25

that higher LDL cholesterol is actually associated with longer lifespans. It's

1:44:30

like, there's,

1:44:31

there's a lot to this whole cholesterol thing. And I think it's kind of been

1:44:35

fucked around

1:44:35

with by the mainstream media reporting on these sort of ancient narratives,

1:44:41

these narratives

1:44:42

that, not ancient, but you know, these narratives that were set up in the fifties

1:44:45

and sixties,

1:44:46

whenever it was in the eighties, the time magazine thing that people just

1:44:49

repeat, they don't look

1:44:51

into it. They just repeat it over and over again. And they're really worried.

1:44:54

Like I'm

1:44:54

trying to eat less, less red meat. Like why, why are you trying to eat less

1:44:57

meat? Well, it's,

1:44:58

you know, cholesterol. Like, Oh boy.

1:45:02

Yeah. I, well, I do think that you don't, you don't want to see your blood

1:45:06

cholesterol

1:45:07

going crazy high because that can be a sign that you're not using it well,

1:45:11

right? Like

1:45:12

if your cholesterol is turning over and it's being used to make bile acids to

1:45:18

support your

1:45:19

digestion, it's being used to make adrenal hormones and sex hormones. It's

1:45:23

being used to

1:45:24

make testosterone. It's being used to make brain synapses to support your

1:45:28

memory. Like all those

1:45:30

things, uh, that cholesterol does are incredibly important, but I think a lot

1:45:35

of people, their

1:45:36

cholesterol going up can be a sign that they're not using it properly. And so I

1:45:41

think that's

1:45:42

why you do see, uh, you know, there, it like the, it, it is true that if you

1:45:48

take people at a certain

1:45:49

age, um, you can see inverse correlations between cholesterol levels and

1:45:55

mortality. But if you take

1:45:56

people who are younger and you look at who's going to get heart attacks later,

1:46:01

you do see that higher

1:46:03

cholesterol when you're younger prospectively predicts a higher risk of heart

1:46:06

disease later.

1:46:07

And I don't think that's because cholesterol causes heart disease, but I think

1:46:13

it's because

1:46:14

it's a reflection of your overall metabolism being more slow in terms of

1:46:20

actually using up the

1:46:22

cholesterol. And that's, and that also, but it's interesting though, that if

1:46:27

you look at the

1:46:28

mechanisms of how does cholesterol, like how does cholesterol cause atherosclerosis,

1:46:35

the cholesterol

1:46:36

is inside a lipoprotein, which is like a spherical container for the

1:46:41

cholesterol. It's got a bunch of

1:46:44

fat soluble vitamins and other things in it. But the outside is, uh, fatty

1:46:49

acids, uh, specifically

1:46:51

in the form called phospholipids. But the, what happens that drives the atherosclerotic

1:46:57

plaque is

1:46:57

that the fats you get from seed oils that are carry that are on the outside of

1:47:01

it get damaged.

1:47:02

And when they get damaged, the immune system recognizes it as a toxin that

1:47:06

could hurt the

1:47:07

blood vessel. And so the immune system gobbles it up and sequesters it. And

1:47:11

that, that

1:47:11

sequestering is like a quarantine. Um, and that's, that's what the plaque

1:47:15

develops from.

1:47:16

And so that's why, like, even though you see prospectively that if your

1:47:23

cholesterol is higher,

1:47:24

that that predicts that you're more likely to get heart disease later in the

1:47:28

randomized controlled

1:47:29

trials, you saw something quite different when they used seed oils to lower the

1:47:34

cholesterol. So

1:47:36

the Minnesota coronary survey was another, uh, it was, I mentioned the LA

1:47:42

veterans administration

1:47:43

hospital study. That was, these were the two double blind randomized controlled

1:47:47

trials that were done

1:47:48

of seed oils. The Minnesota coronary survey was very big. It was the only one

1:47:52

that included women

1:47:53

and it wasn't as long, but, um, but it was way larger.

1:48:01

And back when they published the results, it looked like there was an 8%

1:48:06

increase in the risk of heart

1:48:08

disease with the seed oils, but they mentioned that they measured actual atherosclerosis

1:48:14

and they

1:48:15

didn't report it. So decades later, like, I think it was about 10 years ago,

1:48:22

researchers noticed this

1:48:24

and they said that, well, these guys that did the study are dead, but I wonder

1:48:28

if the atherosclerosis

1:48:29

results are around. So they did some digging and it turned out that in the

1:48:33

basement of the house

1:48:35

that the lead investigator lived in, who had died a long time ago, uh, there

1:48:40

were boxes of data that had

1:48:43

not been published from that study. And they included all the atherosclerosis

1:48:46

measurements. And what they

1:48:47

found was that the seed oil group had double the atherosclerosis. Not only that,

1:48:53

but every 35

1:48:55

milligram per deciliter drop in cholesterol was associated with something like

1:49:00

30% more heart

1:49:02

disease. And so the original results didn't look very, they didn't look good

1:49:06

for seed oils. They

1:49:07

looked bad, but they didn't look that bad. And they, you know, they weren't

1:49:10

statistically significant,

1:49:11

but it was because there was a lot of, uh, you know, people were coming in and

1:49:17

out of the, of the trial

1:49:18

and kind of weakened the results. But this, you know, the, the atherosclerosis

1:49:22

results and the correlations

1:49:23

that were buried in those boxes show that when you look at the data from that

1:49:27

angle, like the seed oils

1:49:28

look a lot worse. And I think what you're seeing there, this is one of the

1:49:32

reasons why there's so

1:49:33

much, um, material to work with to, to make controversy out of this is that you

1:49:40

see that people with

1:49:41

higher cholesterol when they're younger are more likely to go on to have a

1:49:44

heart attack.

1:49:45

But when you use seed oils, which lower the cholesterol in the blood, but

1:49:50

increase the

1:49:51

amount of these easily damaged fatty acids that carry the cholesterol and they

1:49:56

get damaged and

1:49:57

they drive the atherosclerotic plaque. That's why you see this, this divergence,

1:50:02

like that correlation

1:50:04

exists there, but not everything that you do with your diet to change it, to

1:50:09

try to make the

1:50:10

correlation work in your favor. Does you good?

1:50:12

Right. Yeah.

1:50:13

Right. I read that. Um, I'd read something about that and also something about

1:50:17

there is, uh, there's

1:50:19

a profound difference between someone who consumes their cholesterol. Like say,

1:50:23

if you're on

1:50:24

you just a seed oil free, um, just vegetables and meat with healthy fats, like

1:50:33

those kinds of

1:50:35

carbohydrates or those kinds of proteins and fats without complex carbohydrates,

1:50:41

without consumption

1:50:42

of a lot of grains, without that, there's a difference in the, the results that

1:50:46

they were

1:50:47

having in terms of the impact of cholesterol.

1:50:50

In general, you are going to have higher cholesterol if you're eating less

1:50:56

fiber.

1:50:59

Right. And is it in, in, in at all dependent upon the activity level of the

1:51:04

person? Like

1:51:06

you're talking about using the cholesterol.

1:51:08

Well, I, yeah, I think, I mean, this, this is a great tie back to the things

1:51:12

you were talking

1:51:13

about before, because the clearance of cholesterol from your blood is driven by

1:51:19

the mitochondrial

1:51:21

energy production that gives your brain the signal that you are in a state of

1:51:26

abundance and

1:51:27

should put that cholesterol toward good things. And you have a bunch of

1:51:31

hormones that communicate

1:51:32

that leptin, insulin, thyroid hormone are all involved. But what is ultimately

1:51:38

driving

1:51:39

this is your brain, especially in the hypothalamus is taking information in

1:51:43

that says, are you getting

1:51:45

enough food for me to consider this a state of abundance where I ramp up your

1:51:51

digestion? I ramp

1:51:53

up your libido, I ramp up all these things. Um, and we tend in nutrition

1:52:00

science to think that this is

1:52:02

about calories or it's about carbs and it is about those things. But if you are

1:52:09

half as good at

1:52:12

mitochondrial conversion of food to ATP as the next guy over, um, you know, is

1:52:21

your hypothalamus going

1:52:23

to, going to give you full credit for the food you ate in terms of calculating

1:52:26

your state of

1:52:27

abundance? It's not, it's going to dock you by half. And this is because the

1:52:31

hypothalamus takes all

1:52:32

these signals. And then it looks at inside the hypothalamic cells. It looks at,

1:52:36

okay, how well do I

1:52:37

convert that those food molecules into ATP using my mitochondria? And if it's

1:52:43

50% dropped, it's going to

1:52:44

dock you in your state of abundance. And it's going to say, you know, actually

1:52:47

you ate all the food, but you

1:52:49

didn't get all the energy. And so we're just going to let things stagnate. And

1:52:53

the cholesterol is going

1:52:55

to go up in the blood, your sex hormones are going to go down. And, you know,

1:52:59

you can get, you can look at

1:53:02

that and say, well, there's an age, you're going through andropause, there's an

1:53:05

age dependent decline

1:53:07

in testosterone and adrenal hormones and stuff like that. And then you can do

1:53:11

hormone supplementation

1:53:12

therapy, but what you're not actually fixing in that, but that can also be kind

1:53:16

of a negative feedback

1:53:17

loop. Like if you're supplementing everything that your cholesterol would turn,

1:53:21

that your body would

1:53:22

turn cholesterol into, that also is going to slow cholesterol turnover because

1:53:27

your body's like,

1:53:29

oh, I don't, I don't need, like, I don't need to turn that into testosterone if

1:53:31

I'm supplementing

1:53:32

with it. So I think that we, what we're missing in the whole discussion is

1:53:38

thinking about how do we,

1:53:40

how do we ramp up mitochondrial energy production? How do we prevent it from

1:53:43

declining and aging

1:53:44

so that the body, so that the brain can rightly perceive that I am in a state

1:53:50

of abundance and it is

1:53:51

rational to turn, to ramp up this metabolic rate. I think there are, it's, when

1:53:58

you have a marker like

1:53:59

this, it's not like every single case of high cholesterol represents a failure

1:54:04

to convert it

1:54:04

into anything good. Some people just produce more cholesterol or they absorb

1:54:08

more cholesterol.

1:54:09

And I don't think those are all equal in terms of their heart disease risk or

1:54:13

their health

1:54:13

implications, but sluggish metabolism, like high cholesterol is in general a

1:54:18

sign of sluggish

1:54:19

metabolism under the average, the average set of circumstances. And a really

1:54:24

interesting thread that

1:54:25

got left behind in 1976 is Brota Barnes wrote this book called Solved the Riddle

1:54:33

of Heart Attacks in

1:54:34

1976. And his perspective was all about thyroid hormone. And he argued that

1:54:40

people who died of infectious

1:54:42

diseases were hypothyroid, um, we allowed them to live longer. Now all the hypothyroid

1:54:47

people are

1:54:48

getting heart disease. The reason he thought that is because thyroid hormone

1:54:52

communicates to your whole

1:54:53

body that you are in a state of abundance. And so if your brain thinks that you're

1:54:57

not, and you add

1:54:59

thyroid hormone in now, your whole body is receiving the false signal that you

1:55:03

are in a state of

1:55:04

abundance and you feel better and many things improve. And you can argue about

1:55:07

whether that's good or bad,

1:55:08

but you're intervening at the point of the communication instead of at the

1:55:12

point of actually

1:55:13

creating the abundance. But thyroid hormone does signal, uh, take up

1:55:17

cholesterol from the cell,

1:55:19

move it along, do things with it. And so no matter whether you're hypothyroid

1:55:23

or not,

1:55:23

people were up through the night up until the 1970s, they were lowering

1:55:28

cholesterol and they were

1:55:29

lowering heart disease risk by just putting everyone who had high cholesterol

1:55:31

and thyroid hormone.

1:55:33

And the reason they stopped doing it is because, uh, some practitioners got

1:55:37

overzealous and they

1:55:38

killed a few people because they overdosed them. Um, but Broda Barnes argued

1:55:42

that you will, we don't

1:55:44

have to be overzealous and overdose. Then we can just be rationally dosing

1:55:47

thyroid hormone. I,

1:55:49

my perspective is different from Broda Barnes. I, you know, I take what he said.

1:55:52

I think there's a lot

1:55:53

of value to it, but I say like, why is thyroid communicating the state of

1:55:57

abundance? It's because

1:55:58

your mitochondria are doing a great job producing, converting your food to ATP.

1:56:02

Now you don't have

1:56:04

to have a mitochondrial dysfunction to have low thyroid hormone because you're

1:56:07

not in a state

1:56:08

of abundance. You can just not eat any food. So, you know, if you look at the

1:56:10

metabolic consequences

1:56:12

of starvation, you just don't eat any food, your thyroid hormone go in the gutter.

1:56:15

Um, so there are

1:56:17

people out there who just aren't eating enough. Like that is a thing, but it's

1:56:21

also just natural in the

1:56:22

process of aging that we're all getting progressively dysfunctional mitochondria

1:56:26

and that we can

1:56:27

intervene at any point to have at least 75% of control over that. And so we

1:56:31

want to step up the

1:56:32

game and, you know, work. So I, if there's two things that people take away

1:56:37

from this, from me

1:56:39

today, I would want it to be always think about your mitochondria first. And

1:56:43

when you're thinking

1:56:45

about them, always go with a food first, pharma last approach. So naturally

1:56:50

create a state of

1:56:51

abundance in the best way that you can, and then move on to other things after

1:56:55

you've done that.

1:56:56

That way, if you're going to intervene with testosterone replacement or thyroid

1:57:01

hormone or

1:57:01

statins or whatever else, I mean, statins are mitochondrial toxins. They're

1:57:04

kind of kind of productive

1:57:05

from a mitochondrial energy production standpoint. Um, and on that note, you

1:57:11

know, so statins for the

1:57:13

debates of statin associated myopathy are, are, are the rates of them are

1:57:19

debated. The rates at which

1:57:21

statins cause diabetes is debated, but it's there. And it's because statins

1:57:26

actually inhibit your CoQ10

1:57:27

synthesis, but they also inhibit other things in the mitochondrial energy

1:57:31

production engines that you

1:57:33

can't take a supplement for. So there's just no way around that statins will

1:57:37

decrease your

1:57:37

mitochondrial function. So I think by not thinking about mitochondria first, it's

1:57:42

like,

1:57:42

instead you take these people with mediocre mitochondrial function, um, their

1:57:48

LDL in their

1:57:50

blood would get taken into their cells. You would do valuable things with it.

1:57:53

If the state of abundance

1:57:55

was present, because not only does this, all the signaling say, do something

1:57:59

with the cholesterol,

1:58:00

but the way you can actually get cholesterol into the cell is to burn through a

1:58:04

bunch of ATP with

1:58:05

motor proteins that actually move it from outside the cell to inside the cell

1:58:09

in order to facilitate

1:58:10

that turnover. So we've got a situation where we know that everyone could

1:58:13

improve their mitochondrial

1:58:15

function, but instead of doing that and then saying, okay, do we really need a

1:58:18

statin? We just say,

1:58:20

oh, go straight for the statin. And now you're hurting the mitochondrial

1:58:23

function even more. And you're

1:58:24

saying, well, it's a, it's the ROI is good enough because I'm lowering their

1:58:28

cholesterol and they won't get

1:58:29

heart disease. And yeah, their mitochondria aren't doing as great, but that's

1:58:32

okay. Cause we lowered

1:58:33

the cholesterol. I think that's totally backwards. You should, you should

1:58:37

always be trying to optimize

1:58:38

mitochondrial function first. You should always be doing that with natural

1:58:42

foods before you try

1:58:43

anything else. And then, and then move on, like just set the foundation, set a

1:58:49

good foundation and

1:58:50

then build your house on top of it. However you want. I'm not saying never do,

1:58:54

never use any

1:58:55

pharmaceuticals. I'm just saying, you know, if you're going to put, if you're

1:58:58

going to build your

1:58:59

house out of pharmaceuticals, do it on a good foundation.

1:59:01

Right. Do make an educated decision. What, what can be done to increase thyroid

1:59:05

function?

1:59:06

The first thing is you actually want enough food and you want good mitochondrial

1:59:13

conversion of the

1:59:14

food to ATP, but there's other things that could be important to having good

1:59:18

thyroid function as well.

1:59:19

Like having, if you just look at what is thyroid hormone. So thyroid hormone is

1:59:25

made from the amino acid

1:59:26

tyrosine, which you get from the protein in the food that you eat, and then you

1:59:30

add iodine to it. So if you

1:59:32

don't have enough protein, you're not going to have good thyroid function. If

1:59:34

you don't have enough

1:59:35

iodine, you're not going to have good thyroid function. So those are the, those

1:59:38

are the, you know, step one

1:59:41

basics of the one-on-one of the nutrition that I need to have good thyroid

1:59:44

hormone.

1:59:45

And is iodine from supplementation or from food?

1:59:48

You can supplement with it, but I, again, I always believe in food first.

1:59:52

And what's rich in iodine?

1:59:53

There are many things that can be rich in iodine, but it's highly dependent on

1:59:59

the soil. So a potato,

2:00:01

for example, from one part of the United States could be a hundred times richer

2:00:07

than a potato from

2:00:08

another part of the country. So that's a problem. Seafood is reliably high in

2:00:14

iodine because the

2:00:16

rainfall just facilitates the minerals just falling into the ocean. So it's,

2:00:20

you know, a lot of the places

2:00:21

that are low in iodine, it's because the pattern of the evaporation causes the

2:00:25

iodine to evaporate

2:00:26

into the clouds. But then like the cloud pattern goes around some mountain and

2:00:29

it never drops back

2:00:30

down on you. And so you get these areas of the country where they're just on

2:00:34

the wrong side of

2:00:35

the mountain and they just get, you know, progressive decline in the iodine. So

2:00:39

I do think that it's good

2:00:40

for people to eat just some seafood because like if you eat one or two pieces

2:00:45

of fish per week,

2:00:46

for example, or you eat a little bit of seaweed every day, that's going to

2:00:50

cover your bases.

2:00:51

Whereas like if your food comes from one area, you might be able to get enough

2:00:55

iodine just eating

2:00:56

whatever you want. And in another area you won't. I personally add in a quarter

2:01:02

teaspoon of kelp

2:01:03

powder to my food prepped meals per day. It's just always in there. It's got a

2:01:09

little bit of flavor,

2:01:10

but I just mix it into everything so you don't even taste it. It's like, it's

2:01:13

just like I fortify my

2:01:15

own. I fortify my food myself instead of letting the government do it. But, you

2:01:19

know, so that's one

2:01:21

way to do that. And then there are some things that increase your iodine

2:01:26

requirement. So women

2:01:28

with big breasts, for example, can need much more iodine because iodine, the

2:01:33

breasts are a sink for

2:01:35

iodine. Part of that is just the nature of the tissue. And part of it is very

2:01:39

logical because if you do have

2:01:41

a baby, you are going to start feeding the baby the iodine. And so that might

2:01:44

be part of why that's

2:01:45

prepped. But there's some evidence that a lot of breast problems are solved by

2:01:51

extra iodine. So

2:01:52

fibrocystic breast disease, for example, there's some support for getting 10,

2:01:57

15 times the normal

2:01:59

amount, or even 50 times the normal amount of iodine. And I think that's

2:02:03

because some women with very

2:02:05

large breasts just, they just, you know, 98% of it goes there. And then there

2:02:11

are also like the less,

2:02:13

the more toxic your living environment is, the more iodine you're going to need,

2:02:18

because there's a lot

2:02:19

of bromine that's in synthetic materials for couches. It's flame retardants. So

2:02:26

all kinds of paint and

2:02:28

materials that are used in household living can be a source of environmental

2:02:33

bromine. And then fluoride,

2:02:35

if you drink fluoridated water and you brush your teeth with fluoridated

2:02:38

toothpaste, it's going to

2:02:39

increase your need for iodine as well. So there are, there's a bunch of reasons

2:02:43

that people might

2:02:45

want to, well, I'll say this. I think it's crazy that every time I've seen a

2:02:49

woman who's on thyroid

2:02:50

hormone and I've seen, and I've, you know, had them get iodine data, their iodine

2:02:56

is low and they've

2:02:58

never gotten it tested before. And I just, you know, there's these, medicine

2:03:02

has these myths about

2:03:03

nutrition that like we solved all the nutritional deficiencies a hundred years

2:03:06

ago. So we don't

2:03:07

need to think about it, but they did these dumb ass things that made that like

2:03:11

nullified that. So

2:03:13

for example, the reason that we didn't have iodine deficiency anymore is

2:03:17

because they fortified salt

2:03:19

with it. They said, everyone eats salt. So let's just put the iodine in the

2:03:22

salt. And so everyone

2:03:23

got, had fortified salt, but then what did they do? They came along and they

2:03:27

said, don't eat the salts.

2:03:29

It's going to give you a heart attack. And so what they didn't realize was when

2:03:33

they told people to

2:03:34

not eat the salt, now they're not getting their iodine. And now, you know, so

2:03:37

there's some places

2:03:37

where there's like, I talked to one cardiologist who works out in the Midwest.

2:03:41

He says, I see people

2:03:43

walking in with a, look, you can see the lump in their throat now. And, um, and

2:03:48

they have a goiter,

2:03:49

which is just like the, a goiter is a very hungry thyroid gland where it's like,

2:03:54

I don't have any

2:03:54

iodine. Where's the iodine just starts growing to try to find it. And you wind

2:03:57

up with, you can feel

2:03:59

a lump in your throat, not see anything, but if it gets really, really bad, you

2:04:02

can see a bump in

2:04:03

the neck. And if it gets insanely bad, you can have like a grapefruit hanging

2:04:07

from the neck that

2:04:09

doesn't happen anymore. But, but, you know, this cardiologist told me like, I

2:04:12

actually see people

2:04:13

with goiter now, but no one's looking for it because they don't think people

2:04:16

get goiter anymore.

2:04:17

And so most, they just, most of them just walk around with a lump in their neck

2:04:21

until they find

2:04:22

me, he said. That's wild. Yeah. No salt in the diet is so wild. Yeah. That,

2:04:27

that one is so crazy.

2:04:28

And then there are, there are other things too, like you, you, the supplement

2:04:32

that you're taking

2:04:33

has glutathione in it. Well, selenium is a mineral that helps you use glutathione

2:04:39

to protect

2:04:41

your thyroid gland from damage. And there are a number of trials that show that

2:04:48

selenium lowers

2:04:49

the, the autoimmune antibodies that occur in Hashimoto's thyroiditis, which is

2:04:55

a type of

2:04:55

autoimmune thyroid problem. And the reason it does that is because it's helping

2:05:00

glutathione protect

2:05:01

the thyroid from damage because producing thyroid is a very messy process. But

2:05:05

that also, you know,

2:05:07

if you look at what that would imply, it would also imply that all the other

2:05:12

antioxidant nutrients are

2:05:14

very important in the thyroid as well, because vitamin C and zinc and copper,

2:05:19

manganese, and a whole

2:05:21

suite of iron, even, you know, too much iron is bad for you, but you need iron

2:05:25

to protect yourself from

2:05:27

oxidative stress. So all of these things are helping prevent tissue damage in

2:05:31

the thyroid gland, which

2:05:33

helps prevent the immune system from going haywire, trying to deal with that

2:05:37

damage. And so all of

2:05:40

those things are, are important for thyroid hormone.

2:05:42

One more thing I want to talk to you about is you brought up our arterial, I

2:05:46

don't know how to say

2:05:47

that word right, arterial sclerosis. What is the supplement natto kinase?

2:05:53

Yeah, natto kinase is an enzyme that helps break down blood clots. And atherosclerosis

2:06:02

is what it

2:06:04

really is, is the immune system quarantining damaged particles. Those particles

2:06:10

are damaged because you

2:06:12

loaded them with seed oils, and then your mitochondrial function declined, and

2:06:16

you lost your defense against

2:06:17

the damage. And then you got, you know, progressively more seed oil damage that

2:06:22

in the immune system is

2:06:23

trying to protect the blood vessel from it. That's what the plaque is. But that

2:06:27

plaque is highly

2:06:28

inflammatory.

2:06:29

This is a crazy statement. So plaque that people have always considered to be

2:06:34

from the most people

2:06:35

will tell you it's from cholesterol. If you ask the average person, you believe

2:06:39

it's really from

2:06:40

seed oils.

2:06:40

I'm not alone in this. So if you...

2:06:47

No, I don't think you are.

2:06:48

If you go back, so if you go back to 1984, when we saw that Time Magazine

2:06:51

picture, the other thing

2:06:52

that was going on politically and scientifically in 1984 was the NIH consensus

2:06:58

conference that said that

2:07:00

they had proven, like Time Magazine cover was a reaction to the NIH consensus

2:07:05

conference,

2:07:06

where they said, we as the scientific community now certify that we are in

2:07:11

consensus that cholesterol

2:07:13

is the cause of heart disease. And that's why Time Magazine ran with that cover.

2:07:17

Was Fauci running the NIH back then?

2:07:21

Ha ha ha ha ha. Fauci...

2:07:24

Because that's when did the age crisis start?

2:07:26

That was... So Fauci was not running this, but that was, I think, possibly also

2:07:32

the year that

2:07:32

Fauci took over at NIAID.

2:07:35

Oh, okay.

2:07:36

Yeah. It's, you know, it's a sidebar, but there's a very interesting study that

2:07:41

looked at

2:07:43

the average age of principal investigators of studies. Principal investigator

2:07:49

means like the guy who ran

2:07:50

the lab. And so since 1984, the average age of an NIH funded principal

2:07:57

investigator has gone up by

2:07:59

one year per year. And so that looks like the one group took over the money in

2:08:08

1984, and then they've

2:08:11

just been giving themselves grants ever since. And now they're really old. That's

2:08:15

what that looks like.

2:08:18

But anyway, so yes, I think, I believe, you can fact check me on this, but I

2:08:22

believe Fauci took over

2:08:23

NIAID, where he got, where he became very in control of a lot of NIH money in

2:08:29

that same year.

2:08:30

So it's really weird the way these years work out. Like, you know, like 1913,

2:08:36

you've got

2:08:37

Federal Reserve, you've got World War I, you've got all these changes to the

2:08:41

structure of the government.

2:08:42

Like, they picked this year out of history, and there's always these big,

2:08:46

massive big things all

2:08:48

happening in different areas. But anyway, so there was something in there in

2:08:51

1984. Maybe it was

2:08:54

self-fulfilling prophecy from Orwell. But anyway, so the chair of the NIH Consensus

2:09:03

Conference in 1984

2:09:04

was Daniel Steinberg. Daniel Steinberg passed away a few years ago. But he was

2:09:09

kind of, there were three

2:09:11

big names that came out of that conference. And Steinberg was one of them. And

2:09:16

the others were

2:09:17

Brown and Goldstein, who won the Nobel Prize in 1985, the next year, for, you

2:09:22

know, you can see how they

2:09:24

hooked up their Nobel Prize. So they, 1985, they got the Nobel Prize for

2:09:28

discovering the LDL receptor,

2:09:30

which is the thing that brings cholesterol from your blood into your cells. And

2:09:35

all the drugs that

2:09:36

work on this are targeting that receptor. So that became the springboard for

2:09:41

all the drugs that

2:09:42

people are on for cardiovascular disease now. So this is kind of funny that the

2:09:45

Nobel Prize was,

2:09:46

it was probably in the fix in 1984. You know, that was the other thing they

2:09:50

were working on.

2:09:51

But because there's no way that would have happened if the 1984 Consensus

2:09:55

Conference didn't happen.

2:09:55

But the point I want to make is that Daniel Steinberg agrees with me. I didn't

2:10:00

come up

2:10:01

with this idea myself. I mean, he's dead now. But, you know, for decades, he

2:10:07

was one of the people

2:10:08

who believed that because it was his lab that discovered that the PUFAs, which

2:10:15

are seed oil

2:10:16

fats, have to become damaged on the outer membrane of the LDL particle for it

2:10:20

to get taken up by the

2:10:22

immune system. That was his discovery. And he's the guy that chaired the

2:10:26

conference that led to

2:10:27

the Time Magazine cover. So I'm not pulling this out of my ass. I'm pulling

2:10:31

this out of my having

2:10:33

read Daniel Steinberg's papers. And so he was, this is how olive oil became the

2:10:41

darling

2:10:41

of the Mediterranean diet, which is, you know, the Mediterranean diet is kind

2:10:46

of funny because it's

2:10:48

not that big. It's very loosely based on what they eat in the Mediterranean.

2:10:51

And it's really just kind

2:10:54

of like a branding thing where they said like, okay, well, this diet is good

2:10:57

enough for us to say,

2:10:58

eat this, this, this, and this, and we're going to call it Mediterranean. But

2:11:00

anyway,

2:11:02

so what happened was after the LA Veterans Administration Hospital study showed

2:11:09

in 1960,

2:11:11

well, actually they published it a few years later. So somewhere in the early

2:11:14

seventies,

2:11:15

it's kind of looking like seed oils cause cancer. And so they're looking at

2:11:19

that and they're like,

2:11:20

well, maybe corn oil is not the best. And they're like, well, we already told

2:11:25

people to eat the corn

2:11:26

oil because they can't eat the saturated fat. So we can't tell them, go back to

2:11:28

the butter.

2:11:29

So what are we going to tell them to eat? And they were like, well, olive oil

2:11:32

is a nice balance.

2:11:33

It's kind of in between the two. It's not saturated fat, but it's probably not

2:11:37

going to cause cancer

2:11:38

like we're worried about this. And so olive oil was kind of born out of that.

2:11:43

And Steinberg's

2:11:44

perspective on promoting olive oil as being good for heart disease was, you

2:11:50

know, Steinberg is saying,

2:11:52

I'm worried that the real problem with these lipoproteins in the blood causing

2:11:57

the plaque

2:11:58

is actually the seed oils that we're telling people to eat. And so, yeah, we

2:12:03

can use cholesterol as a

2:12:04

marker for that, but I don't know that I want to be telling people to eat corn

2:12:07

oil. So what am I

2:12:08

going to tell them to eat? Cause I'm going to have egg on my face, pun intended.

2:12:12

If I, you know,

2:12:13

if I tell them to go back to eating eggs and butter. So olive oil is this happy

2:12:17

middle ground where

2:12:18

maybe we can consume a lot of, we can consume olive oil to our heart's content

2:12:22

and it's not going to

2:12:25

create the tissue damage that drives the plaque, but it's also not going to

2:12:28

ramp up the cholesterol.

2:12:29

And so we can just navigate the middle that way. And I, you know, I, the reason

2:12:36

that no one

2:12:37

appreciates this is because medicine thinks in binaries. So I, I have this

2:12:45

saying, all medical

2:12:48

diagnoses are false, but some are useful. And I, I take this from a staying in

2:12:53

statistics,

2:12:54

which is all models are false, but some are useful. And what that is, is an

2:12:59

appreciation that

2:13:00

once you impose a model on the data, you're now biasing it towards the way you

2:13:05

think about it.

2:13:07

And, you know, the, and so it's like, it's a reality distortion filter to make

2:13:12

the data more

2:13:12

usable. So if I can use the model to try to predict something and I see it's

2:13:16

true, I might leave details

2:13:17

behind, but I'm focusing on the things that helped me make those decisions. So

2:13:22

a medical diagnosis is a

2:13:24

hypothesis that the patient will respond to the treatment that they're given.

2:13:28

And you test that

2:13:29

hypothesis by giving the patient that treatment, and then you see if they get

2:13:33

better. And if they don't

2:13:34

get better, you take them off the treatment. That's why, you know, some things

2:13:38

they just,

2:13:39

people just stay on the drug they're put on, but look at how they, they treat

2:13:42

depression or

2:13:43

epilepsy. They, you know, the epilepsy, they just put them on one benzo and it

2:13:46

doesn't work. They

2:13:47

put them on the next one. They keep rotating until they find one that, that

2:13:50

stops the seizures

2:13:51

depression. They put people on one antidepressant. Oh, it doesn't, didn't work.

2:13:54

We'll put them on the

2:13:55

next one. They just rotate through it because they're, they're just looking at

2:13:58

it. Like they have a

2:13:59

model that's predicts their hypothesis that they'll respond. They didn't. So

2:14:02

they switched them

2:14:03

onto the, onto the next approach. So because medicine cares about triaging

2:14:10

decisions about

2:14:12

what to do for, for treatment, they say, I only need a model that helps me do

2:14:18

that. And I can ignore

2:14:19

all the other details. But what happens is you leave these historical threads

2:14:23

behind. Like the fact that

2:14:26

the chair of the conference that proved to put in your magazine that everyone

2:14:32

had to change their diet

2:14:34

because of the concept that they said was proven, that is now the basis for the

2:14:40

drugs that I'm going

2:14:41

to prescribe you. The fact that he had these, you know, that he also showed

2:14:45

that it was seed oils in

2:14:47

the membrane of the LDL particle that drive the plaque doesn't matter because

2:14:50

that doesn't change

2:14:51

whether I'm going to give you a statin, you know? And so, and so if it doesn't

2:14:57

change how I'm going to

2:14:58

treat you, it doesn't matter, which means that I could ignore it. If someone

2:15:02

asked me what you should

2:15:03

eat, you know, but, but, but the problem was when they did the randomized

2:15:07

controlled trials with the

2:15:08

seed oils, they were like, Oh, it doubled the atherosclerotic plaque. What do

2:15:12

we do? Put it in the box in the

2:15:14

basement? Um, you know, and so there's all this, this like, well, yes, those

2:15:18

details are true, but

2:15:20

master John, get out of my hair. I don't want to, but I don't, I can't handle

2:15:23

the truth, you know?

2:15:24

Right, right, right. And so how does natokinase? Oh yeah, right. Cause I

2:15:29

brought you way off track.

2:15:30

I did it. I, I did it. Uh, okay. So the problem, when you get out, when you get

2:15:38

a heart attack or a

2:15:39

stroke from atherosclerosis, it is not because in all, in like 98% of cases, it

2:15:47

is not because

2:15:48

the plaque occluded the blood vessel and stopped the blood flow. In fact,

2:15:54

usually when a plaque

2:15:56

develops, it, it develops backwards. Like it, it just, um, so you're like, let's

2:16:01

say this is your

2:16:02

blood vessel. The plaque's going to bulge out this way instead of this way,

2:16:06

because your body tries not

2:16:08

to narrow the blood vessel because you do need the blood flow, right? So it's

2:16:12

almost never the case

2:16:13

that the plaque is just squeezing the blood vessel shut. What happens is the

2:16:16

inflammatory process

2:16:18

inside the plaque, which is especially driven by the seed oils oxidizing in

2:16:22

there and going rancid.

2:16:24

That's not the only factor, but it's one of them. That process degrades the

2:16:30

collagen that covers the

2:16:33

plaque and it makes micro tears and the micro tears and the collagen get healed

2:16:41

by scar tissue that gets

2:16:43

laid on top of it. And so when you get narrowing into the blood vessel, it's

2:16:47

because you're building

2:16:49

up scar tissue on top of like, it keeps breaking and you keep building scar

2:16:52

tissue on it. But if it

2:16:54

breaks and you get a blood clot that is big enough in the acute moment to block

2:16:59

the whole artery, that's,

2:17:02

that's what usually causes most heart attacks. Natokinase is an enzyme derived

2:17:08

from natto, which is a

2:17:10

Japanese fermented soybean paste. That is also incidentally very high in

2:17:16

vitamin K2, which helps you protect

2:17:19

against calcium deposits that weaken the plaque and make it more likely to rupture.

2:17:24

So actually just

2:17:25

eating natto would be better. This is food, why food first works, right? If you

2:17:30

had K2 and natokinase,

2:17:33

you'd be even better off, but the natokinase helps break apart blood clots. So

2:17:36

if in some people you

2:17:39

might just have a predisposition because you've got systemic inflammation where

2:17:43

like you just clot more

2:17:45

easily, or you might have someone who's got a genetic defect and the ability to

2:17:48

degrade clots.

2:17:49

And so their baseline clotting is higher than normal. If that's the case, then

2:17:54

they're even more

2:17:55

likely to get a heart attack or a stroke when the plaque ruptures because their

2:17:59

baseline predisposition

2:18:01

to clot is higher. And then on top of that, if you've got someone with really

2:18:06

bad atherosclerosis,

2:18:08

they might be clotting all the time. Like any, every day might be a new day

2:18:11

where they can have a heart

2:18:12

attack. And so in both of those cases, natokinase is going to degrade the clots

2:18:17

as soon as they occur

2:18:18

and it's going to lower the total clotting. And the downside risk of that is,

2:18:23

you know,

2:18:24

maybe you bleed too easily if you get cut, but the upside potential of that is

2:18:28

if you're one of the

2:18:29

people who are a candidate for any one of these days now, you're going to get a

2:18:32

heart attack or

2:18:33

stroke, having taken nine, 2000 IU of natokinase that day may have prevented

2:18:40

you from getting a

2:18:41

heart attack or stroke because the clot formed and you degraded it more quickly.

2:18:45

Fascinating. Listen, this is a lot to take in, but let's do this again.

2:18:51

Yeah, please. And tell everybody where they can find you and where you are on

2:18:55

social media and your

2:18:57

website and all that. I write a newsletter at chrismasterjohnphd.substack.com

2:19:02

and you can

2:19:03

look into my mitochondrial testing at mito.me. All right. Thank you very much.

2:19:08

This is really

2:19:08

fun. I really appreciate it. I'm glad we did it. All right. Bye everybody.