Welcome to Huberman Lab Essentials,

where we revisit past episodes for the

most potent and actionable science-based

tools for mental health, physical

health, and performance.

I'm Andrew Huberman and I'm a professor

of neurobiology and opthalmology at

Stanford School of Medicine. And now for

my discussion with Dr. Rhonda Patrick.

Rhonda, welcome.

>> I am so excited to be here having a

conversation with you. So,

>> thank you. Well, I have so many

questions, but I want to start off with

a kind of a a new but old theme that

you're very familiar with. So,

temperature is a powerful stimulus as we

know for biology. And you've covered a

lot of material related to the utility

of cold, but also the utility of heat.

And as I learn more and more from your

content and from the various papers, it

seems that cold can stimulate a number

of things like increases in metabolism,

brown fat, etc., etc., but heat seems to

be able to do a lot of the same things.

And I wonder whether or not the

discomfort of cold, deliberate cold

exposure, and the discomfort of heat

might be anchoring to the same pathway.

So, would you mind sharing with us a

little bit about what happens when we

get into a cold environment on purpose

and what happens when we get into a hot

environment on purpose?

>> Let's take a step back and I think you

brought up a really important point

here. You know, we evolved to

intermittently challenge ourselves. And

before we had Instacart, where you could

basically just get your food delivered

to you, we were out hunting, gathering,

we were moving, and we had to be

physically fit. you couldn't, you know,

catch your prey if you were a sedentary

slob, right? Physical activity was a

part of everyday life. And caloric

restriction or intermittent fasting was

also a part of it. This is another type

of of of challenge. You know, we we

didn't always, you know, have a prey

that we caught or maybe temperatures

were such that, you know, there was

nothing for us to gather, right? So,

food scarcity was something common as

well as eating plants. So, getting these

compounds that I mentioned. So this is

these these are all types of stress

intermittent challenges that activate

genetic pathways in our bodies. These

are often referred to in science as

stress response pathways because they

respond to a little bit of stress. You

know physical activity is strenuous.

Fasting is a little bit stressful. Heat,

cold, these things are all types of

little intermittent challenges. There is

a lot of cross talk between these

stressors and the genetic pathways that

they activate. And these genetic

pathways that are activated help you

deal with stress and they do it in a way

that is not only beneficial to help you

deal with that little stressor exercise

or heat. It's it stays active and it

helps you deal with the stress of normal

metabolism, normal immune function

happening just life aging, right? So

this concept is referred to as hormesis,

right? This has a very profound

antioxidant, anti-inflammatory response

or you know or whatever the response is.

It could be the production of more stem

cells or something like autophagy. These

stress response pathways are activated

like by a a variety of stressors. So for

example, one pathway is called heat

shock proteins. And as their name would

apply, one would go, "Oh, they're

activated by heat." Well, correct. They

are activated very robustly by heat. But

you can eat a plant like broccoli

sprouts, which is high in something

called sulfurophane. And it activates

heat proteins among other things. It

also activates a very powerful

detoxification pathway called NRF2,

which helps you detoxify things like

carcinogens that you're exposed to. Cold

also activates heat shock proteins. Now,

you're going to more robustly activate

heat shock proteins from heat versus

cold, but there is some overlap.

>> You mentioned plants as a a route to

creating intermittent challenge.

There's a lot of debate, mostly online

about whether or not plants are our

friends or plants are trying to kill us.

Um, the extreme version from the

carnivore types, um, pure carnivore diet

types, is that plants are trying to kill

us.

>> These generalizations are kind of

they're just not useful. And I think

that a lot of people online um in the

blogosphere it it they gravitate towards

them because it's just easier and it's a

lot more sensational. But I do think

with respect to plants, there's just

evidence that sulfurophane is a very

powerful activator of the NRF2 pathway.

And this is a pathway that regulates a

lot of genes and a lot of genes that are

related to like glutathione production.

Um genes that are involved in

detoxifying compounds that we're exposed

to from our food like heteroscyclic

amines. In fact, there have been GIWA

studies. So, these are genetically um

these are studies that are um genomewide

associated studies. For people listening

uh that aren't familiar, people have a

variety of versions of genes. And um we

have a gene that's able to make um

heteroscyclic amines to basically de

detoxify it so it's not as harmful. Um

and and people that don't have a certain

version of that that's doing it well are

very prone to like colon cancer and

increased cancer risk. But if they eat a

lot of broccoli and cruciferous

vegetables, it negates that risk because

they're getting sulfurophane which

activates glutathione transferase and

synthes. So glutathione is a major

antioxidant in our brain and in our in

our vascular system in our body.

Basically, there's evidence eating

things like, you know, compounds that

are like sulfurophane or broccoli or

brocc broccoli sprouts which have like

100 up to 100 times more sulforophane

than broccoli are activating glutathione

in the brain. There's human evidence of

that.

>> Uh, can we cook the broccoli and still

get these nutrients or do we have to eat

raw? I confess eating raw broccoli is

really aversive to me.

>> So, you do somewhat lower the

sulurophane levels when you when you

cook the broccoli. However, um there was

a study a few years back that showed

adding 1 g of mustard seed powder ground

to your cooked broccoli increases the

sulfurophane by four-fold.

>> Are you eating this every day or most

days of the week?

>> Well, I had shifted to supplementation

with sulfurophane. There's another

compound and it's actually called

moringa. It's like a cousin and it

activates the NRF2 pathway similarly to

sulfurophane. And so I've been buying

this Koolie Moringa powder and I

add it to my smoothies.

>> So if you had to do your kind of top

three, your superstars of nutrients for

the brain and body, sounds like we've

got one set. What would you put in

alongside them?

>> Omega-3 uh the marine omega-3 fatty

acids. So these are found in marine

types of uh you know animals, fish, cold

water fish, fatty fish. Uh so so there's

a there's three fatty acids. There's

ALA, EPA, and DHA. If you get a high

quality one, it's in a triglyceride

form. Um, so you're you've got like a a

glycerol backbone with three fatty acids

and and that's attached and those are

either DHA or the EPA. And um or if you

have a lower quality fish oil

supplement, then you have what's called

e ethylester form. And it's not that

ethylester is bad. It just means take it

with food.

>> What's the dosage that you recommend

people get? I think two grams is um is a

good threshold. Now um the international

fish oil standards IFSO,

they have a website where they do

third-party testing of a ton of

different fish oil supplements from

around the world. And they measure the

concentration of the omega-3 fatty acids

in the actual supplement because nothing

is ever what it says on the bottle. And

then they also measure measure

contaminants. So, mercury, PCBs,

dioxins, things that you'd find

potentially in fish that were harmful to

humans. Uh, and they also measure

mercury and then oxidized fatty acids.

So, these omega-3 fatty acids are

polyunsaturated fatty acids which are

extremely prone to oxidation. So, please

keep your fish oil in the refrigerator.

They give you a total oxidation number.

It's called toto to no to ox to tottox

is what we call it for short. And um I

like it to be at least under 10, ideally

under six. It's really hard to find all

the right mixtures of things, but um

people can go to this website and they

can browse through the products.

>> What are some things that getting 2 to

four grams of EPA per day is going to

help with in our brain and the rest of

our body. I personally think it is one

of the most powerful

anti-inflammatory

dietary lifestyle things that we can we

can get easily that is going to

powerfully modulate the way you think,

the way you feel and the way you age. So

there's been lots of work by Dr. Bill

Harris and his collaborators looking at

what it's called the omega-3 index. So

this is actually the omega-3 level in

red blood cells. So red blood cells turn

over about every 120 days. So it's a

it's a long-term marker of omega-3

status. He's done a variety of studies

uh observational studies. So measuring

omega-3 index in people and then looking

at their mortality risk for example or

their cardiovascular disease risk. Uh

and what he has found is that most f

first of all um standard American diet

has omega-3 index of 5%. Japan, by

contrast, has an omega-3 index of around

10 to 11%. Big big difference there. And

they also have about a 5year increased

life expectancy compared to people in

the US. What he showed in his data was

that people that had a omega-3 index of

4% or lower, so close to what the

standard American is, but a little bit

lower, they had a 5-year decreased life

expectancy compared to people that had

an 8% omega-3 index. people that are in

the 4% omega-3 index range in order to

get to the 8% right the 5year increased

life expectancy if we're comparing the

two groups was to supplement with at

least 2 grams it was about 2 grams a day

uh and that and I think it was a little

bit less if it was triglyceride form but

I think 2 g is a good safe number so

most Americans that are not eating a lot

of fish and they're not supplementing

are probably around a 4 to 5% omega-3

index

>> where and how can somebody measure their

omega-3 index.

>> The omega-3 index is actually in the red

blood cells. And red blood cells take

120 days to turn over. So, if you're

going to do a baseline test, um, if you

want to know before supplementing what

your level is, you have to wait 120 days

before doing the second test after

supplementing to know how much you you

went up because the that's how long it

takes for your red blood cell to turn

over.

>> How is omega-3 and some of these other

related lipids, how are they having

these positive effects? What are some of

the purported, reported, and known

mechanisms?

>> Some of the the most well-known

mechanisms um do have to do with the the

omega-3 fatty acids being very powerful

regulators of the inflammatory process

in some way, shape, or form. Whether

that has to do with resolins that are

produced, so these from the metabolites

uh of like DHA for example, resolins

play a role in resolving inflammation.

like you want your inflammatory response

to be activated when it's supposed to

be, but you want to resolve that

inflammation in that inflammatory

response in a a timely manner, right?

And resolins help do that. And and so

resolins are one. And then there's these

specialized um promediating molecules,

the SPMs that also help resolve the

inflammation. Just so many different

ways and inputs. And so when we talk

about inflammation, honestly that that's

a big general term, but you're talking

about when you're talking about

serotonin release, um, you know, at the

level of neurons, you know, we know that

these inflammatory molecules cross the

bloodb brain barrier. It's known that

omega-3 actually specifically EPA is

able to help serotonin in inflammation

inhibits the release of serotonin. And

so EPA is actually able to blunt

inflammatory responses along with DHA as

well. DHA does that through resolins and

stuff and this then helps more serotonin

be released because you're you're not

having so much inflammation getting into

the brain and affecting serotonin

release right that's one mechanism and

then another would be well DHA itself

has been shown it's it's a very

important uh fatty acid that makes up

cell membranes many cell membranes

including in our neurons and as you very

well know Andrew the structure and

function of receptors of transporters

these membranebound proteins on the

surface of of our cells including

neurons are affected by the membrane

fluidity you know like how rigid and how

fluid the cell membrane is and DHA plays

a role in that and so for example in

animal studies if you make an animal

deficient in DHA their serotonin

receptors dopamine receptors they're

affected because the structure of them

is affected through the fluidity of the

membrane there's been some animal

studies and piglets and rodents as well

showing that consuming phospho lipid DHA

uh during fetal brain development like

gets way like 10 times more DHA in the

brain. Uh if you're supplementing with

your your 2 to four grams of fish oil, I

mean that you're going to get

phospholipid form anyway cuz your body's

going to make it.

>> So we have these plant-based compounds,

we have the omega-3s, so your PA, DHA,

and then you mentioned there's a third

category. What would you place in your

third category of foods or

supplement-based nutrients that brain

and/or body health can really benefit

from?

>> I mean, I think the most obvious would

be vitamin D. 70% of the US population

has inadequate vitamin D levels. 70 of

the wholeing US. So, this is everyone.

And so, I think that insufficient levels

defined as less than 30 nanogs per

milliliter. Um and and that's sort of

defined by the the endocrine society. Um

there's been a lot of different

metaanalyses of all cause mortality

studies where vitamin D levels are are

really seem to be ideal between 40 to 60

nanogs per milliliter. So basically the

point is that vitamin D is a steroid

hormone meaning it actually binds to a

receptor and um another receptor drizzes

with it vitamin the the retinoid

receptor and that complex goes into the

nucleus of a cell where your DNA is and

it rec recognizes little sequences of

DNA called vitamin D response elements.

They're called VDRES. There are specific

sequences of DNA that this complex

vitamin D re bound the vitamin D

receptor goes inside and recognizes and

turns on a whole host of genes, turns

off a whole host of genes. I mean, this

is this is important stuff.

>> What sorts of things is it stimulating?

>> Okay, so first of all, it's it's

regulating more than 5% of the protein

encoded human genome. One of the

important things that you'll find

interesting that I published on back in

2014 was that the VDRES in tryptophan

hydroxilase 2. So for people listening,

tryptophan hydroxilase

is an enzyme that converts tryptophan

into serotonin. So tryptophan is what we

uh an amino acid that we get from our

food. Um you convert serotonin, you

convert tryptophan into serotonin into

the gut in the gut, but you also do it

in the brain. However, serotonin does

not cross the bloodb brain barrier. So

tryptophan has to get into your brain

and then you have to convert it to

serotonin in your brain. Well, the

enzyme that does that in your brain is

called tryptophan hydroxilase 2 and it's

activated by vitamin D. But most people

I mean this is regulating our immune

immune cell immune system. It's

regulating uh our blood pressure you

know all that that's water retention you

know I mean bone of course homeostasis

5% more than 5%. I mean I can't tell you

like so much. where and what is a good

starting range for people to to think

about D3 supplementation and again foods

that can increase D3.

>> Um so vitamin D3 is a good way to

supplement with it. Um there vitamin D2

would be a plant source. You often find

it fortified in like foods like milk.

>> Yeah, vitamin D is naturally to some

degree in fatty fish, but you're not

going to correct a deficiency with

eating vitamin

D. you you're either going to correct it

with sun exposure, being in the right

area, having the right amount of sun,

and being the right age, um because as

you get old, you become very inefficient

at making vitamin D3 in your skin. There

have been uh a lot of these mandelian

randomization studies. So, these are

studies where scientists will look at

people that have these common variations

of a gene that's a little more than 1%

of the population. So, it's not a random

mutation. It's actually found in a in a

a sizable percent of the population. A

lot of times they'll look at genes that

are also involved in snips that

basically make the conversion of vitamin

either vitamin D precursor into D3 or in

D3 into 25 hydroxy vitamin D or into the

active steroid hormone which is 125

hydroxy vitamin D. So you're not looking

at vitamin D levels at all. You're

looking at just the snips and you know

if they have it they have low vitamin D.

People randomly have these genes and

it's not like there's no health status.

So um these these mandelium

randomization studies have found that

people that can't convert um into the

the precursor the 25 hydroxy vitamin D

which is usually what's measured. It's

the most stable form of vitamin D in the

body. Um they have a higher all-c cause

mortality if they can't do it. So people

with you know that don't have it have a

lower all-c cause mortality. They have a

higher respiratory related mortality.

They have a higher cancer related

mortality. They also are more likely to

get multiple scerosis. This has all been

done with mandelian randomization. And

so, um, it really does hammer home the

importance of measuring your vitamin D

levels and, uh, being being, uh, very

proactive about that. I mean, you can

you can get it done anyway. Your doctor

will do it. You ask them to do it, you

know. So, um, supplementation wise, um,

typically, if you don't have one of

those snips for for the most part,

taking 1,000 IUs of vitamin D will raise

blood levels by around 5 nanogs per

milliliter. So let's say you're

deficient, you're 20 nanogs per

milliliter and you want to get to 40.

You're going to need at least 4,000 IUs.

>> So for people who are going to be

stubborn and not get their D levels

tested and simply say, "Oh, I'll just

take some D3." Is that reasonable? 1,000

to 5,000 IUs for most people will be

reasonably safe. If we look at the the

the literature, the scientific

literature, it is extremely hard to get

like hypercalcemia, which would be the

major concern with really high levels of

vitamin D3 supplementation. I mean,

we're talking like hundreds of thousands

of IU a day for a long time. And by the

way, there have been studies looking at

uh people that are deficient in vitamin

D. Um, in this case it was uh

African-Americans that were given a

4,000 IU a day vitamin D supplement to

bring them back to sufficient levels.

And um this was a this was a smaller

smaller study than um I would like but

it reversed their epigenetic aging by

like 3 years because

again it's a hormone. It's regulating

more than 5% of your protein encoding

human genome. So, if I'm taking vitamin

D3,

I still need to get out into the sun.

Correct. Absolutely.

>> Okay. Okay. So, we've we talked about

these plant-based compounds, the

omega-3s and D3. Is there anything that

um that to supplement based or food

based compounds that you, you know, you

think are especially useful for brain

and or body health?

>> I do think magnesium is important in

there as well. I mean, I think, you

know, again, about 40% of the US

population doesn't get enough magnesium.

It's an essential mineral we're supposed

to be getting from our diet. Magnesium

is also involved in making ATP, the the

energetic currency of our cells.

They're, you know, basically all of our

cells need ATP to do anything. And um

they're al it's also involved in

utilizing ATP as well as DNA repair

enzymes. These are enzymes that are

involved in repairing damage to our DNA.

I personally think that magnesium

insufficiency causes an insidious type

of damage daily that you can't look in

the mirror and see like when you're

deficient in vitamin C you're like my my

gums are falling apart I have scurvy

right but like you can't see DNA damage

you can't see it but it's happening it's

happening right now in my body and it's

happening in your body it's happening

normal metabolism it's happening you

know every day um but we repair that

damage we have repair enzymes in our

body called DNA repair enzymes they

require higher magnesium. Magnesium is a

co-actor for them. Well, magnesium is at

the center of a chlorophyll molecule.

Chlorophyll is what gives plants their

green color. So, dark leafy greens are

high in magnesium. Basically, what is

the 40% insuffic insufficiency in the US

tell us people aren't eating their

greens. They're eating their packaged

food. They're eating their processed

food. The standard American diet isn't

really high in dark leafy greens.

>> So, kale, what are some other examples?

>> Kale, spinach, chard, like Swiss chard,

rainbow chard, um romaine lettuce. So

supplementation with magnesium, it can

cause GI distress at like high doses. I

personally like to take around 130 or

135 milligrams. Um that way it's not

like um a huge bolus to my gut. You can

take like magnesium 3 and8 for example

and it doesn't affect the gut as much. I

would say malite would be the best. That

has to do with the short chain fatty

acids being good for the gut. I think

mal malate's awesome and I always try to

eat green apples. They're really high in

malic acid. and um tart cherries. Tart

cherries are really high in it as well.

>> You've talked a lot about the use of

deliberate cold exposure. What sort of

activity or stimulus do you do you think

is a reasonable and particularly potent

one uh to use in terms of cold?

>> So today I did 3 minutes at 49° F. I

have a cold tub. I definitely do cold

when I'm going to do a podcast, when I'm

going to give a talk or when I'm

anxious. I feel good. I feel more

focused which is why I usually do it

before any type of public speaking.

>> So the mooden enhancing effects that you

report those are almost certainly a the

consequence of having slowly elevating

but significantly elevated dop do

dopamine that goes on for hours. That's

almost a dreamlike profile for dopamine

because most everything else like an

aderall, a rolin, a cup of coffee and a

um and a workout drink or pre-workout

drink or something is going to give you

a big spike in adrenaline and dopamine

and a big crash. But the advantage of

not doing it too often is that you're

not cold adapted. Now, it's very hard

for anyone to get truly cold adapted. I

some people start to look forward to the

cold and what I think they're looking

forward to is the feeling afterward,

that dopamine rush. Uh but if you get

cold adapted, then it certainly blunts

the some of the effect.

>> But I want to be cold adapted because

that means I have more mitochondria in

my atapost tissue and and perhaps even

muscle like that's been shown. Shivering

is a very inefficient way to produce

heat, which is what your body is trying

to do when it's exposed to cold. And

your muscles are basically contracting

and and and um and producing heat from

that, but that's just not very

efficient. So, uh the the more eloquent

way to do it or elegant, I guess, uh way

to do it is, you know, to basically have

your mitochondria produce tons and tons

of heat. So, mitochondria are these

little organels inside of your cells

that are responsible for producing

energy. Usually that's in the form of

adenosine triphosphate ATP and that's

what lets everything function inside

your body from your neurotransmitter

production to your heart beating etc.

Basically your mitochondria um they're

like a little battery. So they have a

they have well they have a double

membrane first of all their structure

but they have a negative charge on the

inside and they have a positive charge

on the inner membrane. Basically you can

uncouple that that charge and so that

positive charge protons start leaking

out of the mitochondria and your

mitochondria freak out. So this is

called uncoupling it. And they start to

it's maximum respiration as we call it.

They try to make as much energy. They're

like I got to get those that that that

proton back that gradient the

electrochemical gradient. And so they

just go insane and they um in this case

it's uncoupled energy. So the energy

they're making is actually heat not ATP.

Uh but heat is but you're essentially

burning substrate. So who cares? You're

burning you're burning glucose. You're

burning your lipids. you know, you're

you're basically burning things and

making heat. And so, um, that's what

uncoupling does. And that is a much more

efficient way of producing heat than

shivering. And so, as you become more

adapted, um, maybe the the the longer

duration that you've you've stayed in

the cold or the more times you've done

it, you'll no longer shiver anymore. You

will start to then just do this

uncoupling type of thermogenesis as it's

called. And um another type of

adaptation that occurs is you actually

produce more mitochondria in your

atapost tissue. And um and that actually

happens also regulated by norepinephrine

or noradrenaline through a protein

called PGC1 alpha. And what that protein

does is it makes more mitochondria in

your atapost cell. So per atapost cell

you're getting more mitochondria. It's a

beautiful way to basically make more

heat when you're it's it's one of those

things where it's like it's your body's

going, "Okay, I'm going to be exposed to

this cold next time. How can I make sure

I don't die? Oh, I can have more

mitochondria and I'm going to make more

heat." And so you're making more

mitochondria in your atapost tissue. And

and this is often referred to as like

the browning of fat. And the reason for

that is because if you look under a

microscope at a lipid droplet, you know,

basically um a fat cell, uh not a lipid

droplet, atyposite, um you'll find that

it looks darker because there's more

mitochondria in there. So, it's referred

to as browning fat. That's awesome. You

want more mitochondria in your muscle.

It's associated with um improved muscle

mass, improved endurance. I mean,

mitochondria are essentially they're the

making energy in your cell. And we, you

know, we don't make more mitochondria

normally like you have certain inputs.

Extra high-intensity interval training,

exercise can do it. Your cells are

turning over, you make new cells, you

replace old ones where your

mitochondria, um, you don't really do

that for the most part. You can,

mitochondrial biogenesis does happen,

but you have to stimulate it to happen.

And, um, the way your mito like what

happens with your mitochondria is they

essentially are bobbing around inside of

your cells and then they they fuse with

other mitochondria, exchange all their

content, mitochondrial DNA, and then

fizz back apart. And that's how they

kind of stay youngish. But like as you

age, you you keep doing that with the

same pool of mitochondria and you're

going to get a bunch of old mitochondria

mixing old stuff together, right? So why

wouldn't you want to like bring up new

healthy young mitochondria into that

pool, right? So in my mind when I hear

mitochondrial biogenesis, I'm like

aging. Like that's the first thing I

think of.

>> Uh so anyways, cold exposure does that.

>> What sort of um cardiovascular other

types of training do you do? Uh do you

do hit? Imagine you are doing

high-intensity interval training.

>> I do a lot of highintensity interval

Tabatas on a stationary cycle three

times a week and I do a 10-minute just

10 uh because it's efficient and I push

my ass. I push myself really hard.

>> That's the Tabata.

>> It's a 20 seconds on 10 seconds off and

it's 10 minutes

>> and on means you're pedaling like your

life depending on

>> you're maxing it. And then um I always

have my sauna on preheating up. I get it

to about 189° F. I hop right in the

sauna after my Pelaton. I literally like

down a bunch of water and then I get in

and and then I like either um read a

science paper, prepare for a

presentation or a podcast or I um hash

over things in my mind. And it's

interesting because I would use the uh

sauna to memorize things. I don't know

if it has to do with the like the stress

response like when you when you have an

emotional trigger like you remember

things better, right? Absolutely. The

idea that being in this semi-stressful

environment would aid in the learning

and and retention of information is is

really well substantiated by this

beautiful work by a guy named James

McGaw. He was at UC Irvine for a while

and then I think at uh University of

Arizona as well. They have a great

memory group at both places. Very strong

in learning and memory both places. and

he was the one that really defined this

um kind of uh inverted U-shaped function

for the relationship between adrenaline

and memory. Basically, if you're too

relaxed and not stressed enough, you're

not going to remember any information.

At peak levels of stress, you actually

are a memory machine, at least within

the context of whatever it is you're

trying to learn. So, it very well what

you're describing is very well matches

with that. And then of course it tapers

off as you really increase adrenaline to

the point where people are starting to

lose autonomic function where they're

just they're panicking basically. The

other thing that that I would like to

ask you about is in the sauna of course

there's vasoddilation and profusion of

blood to the brain is a wonderful way to

enhance cognition.

>> The vasoddilation does occur. So there's

a lot of overlap between moderate

intensity aerobic exercise and heat

stress. And as you can imagine when

you're exercising you're elev elevating

your core body temperature. you're

you're sweating and um when you're

actually in the sauna, blood does get

redistributed to the skin to facilitate

sweating. But much like exercise, blood

flow in general is improved to the

brain, to the muscles, everywhere. So um

you know I think generally speaking that

I and this you know there's studies

showing that sauna use is associated

with a much lower risk of dementia and

Alzheimer's disease like people you know

people that use it four to seven times a

week have greater than 60% reduction in

dementia risk and Alzheimer's disease

risk compared to people that use it only

one time a week. Um people that use it

two to three times a week have something

like a 20 a little greater than 20%

reduction in risk. is a dose dependent

effect on dementia risk and Alzheimer's

disease risk. Uh it also has a profound

like there's a there's a big link

between the cardiovascular system and

the brain obviously blood flow a big one

right you know like you you need to get

blood to your brain. Um but

cardiovascular mortality so mortality

from cardiovascular disease if people

use or actually this was men if men use

the sauna four to seven times a week

it's a 50% reduction in cardiovascular

related mortality compared to one time a

week. Uh again dose dependent manner two

to three times a week is something like

24% lower um death from cardiovascular

disease. There's also lower, you know,

sudden cardiac death like a heart attack

that's like 60 something greater than

60% lower if if men use it four to seven

times a week versus once. Again, a dose

dependent thing. And this is all work

from Dr. Yari Linen. He's in um the

University of Eastern Finland and just

one of the the the world's experts on

sauna use. The more you do the sauna or

any sort of heat stress, whether it's a

hot tub or jacuzzi, um you you become

adapted. you're you're basically start

to sweat at a lower core body

temperature to cool yourself down. All

these sort of physiological changes

start to happen earlier. Uh and and so

um I stay in for like 30 minutes like I

mean so I stay a long time. That's a

lot. You have to listen to your body. Um

most of the studies uh that I just

talked about were from um the the

duration the time spent in the sauna

when I said 50% reduction in

cardiovascular disease related death.

What was shown was that men that were in

the sauna for only 11 minutes, even if

they used it four to seven times a week,

that reduction was only like 8%. Instead

of 50, it had to be greater than 19

minutes. So like 20 minutes is the sweet

spot at about 174° F. To me that's a

very strong data that this is more

causal than some you know corlary thing

because that's always the problem with

observational studies including these

which they corrected for a whole host of

factors like cholesterol you know

exercise just everything everything

under the sun I mean they corrected for

those and on top of that you have the

dose dependent nature of the duration

the time spent in the sauna and the

frequency so to me it's like something's

going on here plus there's been studies

intervention studies where it's you

know, comparing directly head-to-head

moderate intensity aerobic exercise on a

stationary cycle to 20 minutes in a

sauna, they're they're physiologically

the same things happen. So,

heart rate elevates while you're doing

the activity, blood pressure increases

while you're doing the activity, but

then after heart rate decreases, resting

heart rate decreases below baseline,

blood pressure is improved. So, it

decreases below baseline. This is

happening the same in moderate intensity

cycling versus sauna. So again, the

sauna like this heat stress, there's

something about it that really mimics

this moderate intensity aerobic

exercise, which is really great for

people that can't go for a run, that

can't even get on a bike. Um, so you

know, disabled people, granted there are

some safety concerns, they're they're

pretty mild. Um, but they do exist. uh

you know so people that had a recent

heart attack or have some rare kind of

heart disease or problem drinking

alcohol never do that elderly people low

uh prone to low blood blood pressure

always talk to a physician before doing

the sauna it is it is stressful um

>> pregnant

>> pregnant women oh yeah I definitely um

avoided saunas when I was pregnant so

for those healthy fit people out there

already exercising there's a synergistic

effect by also adding a sauna into that

routine and to me that's great and um

there's So many beneficial things

happening uh with the with the heat

stress. In addition to like mimicking

aerobic exercise, there's the heat shock

proteins that we talked about earlier.

Many animal studies have been done

looking at Alzheimer's disease uh you

know like

a human like Alzheimer's disease in a

rodent and heat shock proteins

protecting from it you know. So um heat

shock proteins are robustly activated in

humans. And this has been shown to uh

even o you know 50% higher over baseline

levels after just 30 minutes at 163

degrees Fahrenheit in the sauna. So um

and they stay activated at least in

rodents for you know 48 hours at least.

Um, so you know, having these heat shock

proteins around, making sure they're

they're properly taking care of our our

proteins so they're not aggregating in

our brains and in our in our plaques

could be another potential way that

sauna is protecting from Alzheimer's

disease and um other, you know,

cardiovascular health as well as

longevity.

>> I know people are probably desperate to

know what if they don't have a sauna. I

could imagine that a hot bath would work

almost as well. Is that right?

>> Yeah. So there's been some studies

looking at for example activation of

heat shock proteins also brain drive

neurotrophic factor increases with heat

stress. Um and so uh the the hot bath at

around 104 degrees Fahrenheit which is

typically what studies will use for

temperature and um it's at 20 minutes

from the shoulders down and and that is

like a very robust activation in heat

shock proteins and in uh brain drive

neurotic factor

>> and then heat shock proteins are also

protecting against muscle atrophy. So

that's also having to do with the

protein structure and the muscle tissue

as well. This has been studies in animal

you know animal data um as well as some

recent human data as well. It was local

hypothermia or local heat treatment but

um essentially it showed that it

protected I mean it was like there was a

study where um they were looking at

muscle disuse and it was it was

something like the local heat treatment

prevented like almost 40% of the muscle

atrophy from disuse.

>> We covered a lot of of territory but I

just want to thank you again. It was

extremely thorough and extremely

informative. On behalf of the listeners

and uh just directly from me, thank you

so much for your time. I learned a ton.

My pleasure. Thanks for having me on. It

was really awesome conversation. So, I

enjoyed it a lot.

>> Let's do it again.

>> Totally.

>> Great.