This discussion explores how intermittent physiological stressors, such as heat, cold, fasting, and certain nutrients, activate hormetic stress response pathways in the body, leading to enhanced resilience, health, and performance.
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Welcome to Huberman Lab Essentials,
[music] 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.
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.
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
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
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.
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?
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?
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 [snorts] 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.
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,
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 [snorts] 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,
mitochondria, >> [snorts]
>> [snorts]
>> 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 [snorts] 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.
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
[clears throat] 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
>> 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 [snorts] 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.
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. [clears throat] 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.
>> Totally.
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