Essentials: Micronutrients for Health & Longevity | Dr. Rhonda Patrick

Lab Es s, where we revisit past episodes for the most potent and actionable science-based tools for mental health, physical health, and performance.
, and I ofessor of neurobiology and ophthalmology at Stanford School of Medicine.
ussion . Rhonda Patrick.

be here a conversation with you.
o many ns, but I want to start off with a kind of a new but old theme that you’re very familiar with.
powerf ulus, as we know, for biology.
a lot o ial related to the utility of cold, but also the utility of heat.
and mo your content and from the various papers, it seems that cold can stimulate a number of things like increases in metabolism, brown fat, et cetera, et cetera.
e able lot of the same things.
r or no iscomfort of cold, deliberate cold exposure, and the discomfort of heat might be anchoring to the same pathway.
haring 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?
ack.
ught up ly important point here.
d to in ently challenge ourselves.
nstacar 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.
now, ca r prey if you were a sedentary slob, right?
as a pa veryday life.
tion or ittent fasting was also a part of it.
e of ch .
always now, have a prey that we caught or maybe temperatures were such that, you know, there was nothing for us to gather, right?
s somet mmon as well as eating plants.
mpounds mentioned.
re all f stress, intermittent challenges that activate genetic pathways in our bodies.
erred t ience as stress response pathways because they respond to a little bit of stress.
activit renuous.
bit st .

l types tle intermittent challenges.
rosstal en these stressors and the genetic pathways that they activate.
athways re activated help you deal with stress.
way th ot only beneficial to help you deal with that little stressor, exercise or heat.
it hel deal with the stress of normal metabolism, normal immune function happening, just life, aging, right?
referre hormesis, right?
found a ant, anti-inflammatory response or, you know, or whatever the response is.
duction e stem cells or something like autophagy.
se path e activated, like, by a variety of stressors.
e pathw alled heat shock proteins.
ould ap e would go, oh, they’re activated by heat.

very ro by heat.
lant li coli sprouts, which is high in something called sulforaphane.
at shoc ins, among other things.
very p detoxification pathway called NRF2, which helps you detoxify things like carcinogens that you’re exposed to.
heat s oteins.
o more y activate heat shock proteins from heat versus cold, but there is some overlap.
s as a o creating intermittent challenge.
bate, m nline, about whether or not plants are our friends or plants are trying to kill us.
from t ivore types, pure carnivore diet types, is that plants are trying to kill us.
ns are , they’re just not useful.
lot of online in the blogosphere, they gravitate towards them because it’s easier and it’s a lot more sensational.
respec ants, there’s just evidence that sulforaphane is a very powerful activator of the NRF2 pathway.
ay that tes a lot of genes and a lot of genes that are related to, like, glutathione production, genes that are involved in detoxifying compounds that we’re exposed to from our food, like heterocyclic amines.
been G dies.
cally, re studies that are genome-wide associated studies for people listening that aren’t familiar.
ty of v of genes.
that’s make heterocyclic amines to basically detoxify it so it’s not as harmful.
‘t have ain version of that that’s doing it well are very prone to, like, colon cancer and increased cancer risk.
ot of b and cruciferous vegetables, it negates that risk because they’re getting sulforaphane, which activates glutathione transferase and synthase genes.
major dant in our brain and in our vascular system and our body, basically.
ting th ke, you know, compounds that are, like, sulforaphane or broccoli or broccoli spouts, which have, like, up to 100 times more sulforaphane than broccoli, are activating glutathione in the brain.
nce of
ccoli a l get these nutrients or do we have to eat it raw?
w brocc really aversive to me.
lower t oraphane levels when you cook the broccoli.
a study years back that showed adding one gram of mustard seed powder ground to your cooked broccoli increases the sulforaphane by fourfold.
every most days of the week?
to sup ation with sulforaphane.
pound, s actually called moringa.
and it tes the NRF2 pathway similarly to sulforaphane.
ying th i Kooli moringa powder, and I add it to my smoothies.
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your k top three, your superstars of nutrients for the brain and body,
ot one
in alon hem?
omega- acids.
in mari s of, you know, animals, fish, cold water fish, fatty fish.
tty aci
nd DHA.
uality ‘s in a triglyceride form.
a glyce kbone with three fatty acids, and that’s attached.
r DHA o PA.
a lower y fish oil supplement, then you have what’s called ethyl ester form.
thyl es bad.
hat you end people get?
s a goo hold.
nal Fis tandards, IFSO, they have a website where they do third-party testing of a ton of different fish oil supplements from around the world.
e conce n of the omega-3 fatty acids in the actual supplement because nothing is ever what it says on the bottle.
measure inants, so mercury, PCBs, dioxins, things that you’d find potentially in fish that were harmful to humans.
re merc then oxidized fatty acids.
tty aci polyunsaturated fatty acids, which are extremely prone to oxidation.
fish o he refrigerator.
al oxid umber.

ll it f t.
at the under 10, ideally under 6.
find a right mixtures of things, but people can go to this website and they can browse through the products.
s that two to four grams of EPA per day is going to help with in our brain and the rest of our body?
it is o he most powerful anti-inflammatory dietary lifestyle things that we can get easily that is going to powerfully modulate the way you think, the way you feel, and the way you age.
s of wo r. Bill Harris and his collaborators looking at what is called the omega-3 index.
the om evel in red blood cells.
turn ov t every 120 days.
marker ga-3 status.
of stu bservational studies, measuring the omega-3 index in people and then looking at their mortality risk, for example, or their cardiovascular disease risk.
nd is t t, first of all, standard American diet has omega-3 index of 5%.
has an 3 index of around 10% to 11%.
there.
about a ear increased life expectancy compared to people in the U.S.
is data at people that had a omega-3 index of 4% or lower, so close to what the standard American is, but a little bit lower.
r decre fe expectancy compared to people that had an 8% omega-3 index.
the 4% index range, in order to get to the 8%, right, the five-year increased life expectancy, if we’re comparing the two groups, was to supplement with at least two grams.
ams a d
a littl ess if it was triglyceride form, but I think two grams is a good, safe number.
hat are ting a lot of fish and they’re not supplementing are probably around a 4% to 5% omega-3 index.
omebody e their omega-3 index?
s actua the red blood cells.
take 1 to turn over.
to do a ne test, 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 went up because that’s how long it takes for your red blood cell to turn over.
some of other related lipids, how are they having these positive effects?
e purpo eported, and known mechanisms?
ll-know nisms do have to do with the omega-3 fatty acids being very powerful regulators of the inflammatory process in some way, shape, or form.
do wit vins that are produced, so from the metabolites of like DHA, for example, resolvins play a role in resolving inflammation.
inflamm esponse to be activated when it’s supposed to be, but you want to resolve that inflammation and inflammatory response in a timely manner, right?
do that
e one.
ese spe d promediating molecules, the SPMs, that also help resolve the inflammation.
ent way nputs.
about ation, honestly, that’s a big general term, but you’re talking about when you’re talking about serotonin release, you know, at the level of neurons, you know, we know that these inflammatory molecules cross the blood brain barrier.
ga-3, a specifically EPA, is able to help serotonin, inflammation inhibits the release of serotonin.
lly abl unt inflammatory responses along with DHA as well.
gh reso nd stuff.
more s n be released because you’re not having so much inflammation getting into the brain and affecting serotonin release, right?
m.
uld be, DHA itself has been shown, it’s a very important fatty acid that makes up cell membranes, many cell membranes, including in our neurons.
l know, , the structure and function of receptors, of transporters, these membrane-bound proteins on the surface of our cells, including neurons, are affected by the membrane fluidity, you know, like how rigid and how fluid the cell membrane is.
e in th
animal s, 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.
nimal s in piglets and rodents as well showing that consuming phospholipid DHA during fetal brain development gets like 10 times more DHA in the brain.
ting wi 2 to 4 grams of fish oil, I mean, you’re going to get phospholipid form anyway because your body’s going to make it.
ong tim there are things that we can do to improve our sleep, and that includes things that we can take, things like magnesium threonate, theanine, chamomile extract, and glycine, along with lesser known things like saffron and valerian root.
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ant-bas ounds.
s, so y a DHA.
ned the third category.
e in yo d category of foods or supplement-based nutrients
ody hea really benefit from?
most o would be vitamin D.
ulation adequate vitamin D levels.
.
.
insuff levels defined as less than 30 nanograms per milliliter.
defined endocrine society.
of diff eta-analyses of all cause mortality studies where vitamin D levels
deal be 0 to 60 nanograms per milliliter.
oint is itamin D is a steroid hormone, meaning it actually binds to a receptor
r dimer th it, the retinoid receptor.
es into cleus of a cell where your DNA is.
ittle s s of DNA called vitamin D response elements.
s.
sequenc NA that this complex vitamin D bound to the vitamin D receptor
ognizes rns on a whole host of genes, turns off a whole host of genes.
ortant
s is it ating?
ll, it’ ating more than 5% of the protein-encoded human genome.
t thing you’ll find interesting that I published on back in 2014
and try hydroxylase 2, so for people listening,
ase is me that converts tryptophan into serotonin.
amino at we get from our food.
han int onin in the gut, but you also do it in the brain.
does no the blood-brain barrier.
o get i r brain, and then you have to convert it to serotonin in your brain.
at does n your brain is called tryptophan hydroxylase 2,
by vita
mean, t regulating our immune cell, immune system.
blood e, you know, all that water retention, you know.
urse, h sis, 5%, more than 5%.
l you, o much.
good s range for people to think about D3 supplementation?
at can e D3.
good wa pplement with it.
uld be source.
ortifie ike, foods like milk.
natural some degree, in fatty fish.
g to co deficiency with eating fish for your vitamin D.
going ect it with sun exposure, being in the right area,
ount of nd being the right age.
old, yo e very inefficient at making vitamin D3 in your skin.
ot of t ndelian randomization studies.
s where ists will look at people that have these common variations of a gene
e than he population.
m mutat
in a s percent of the population.
y’ll lo enes that are also involved in SNPs
the co n of either vitamin D precursor into D3
xyvitam
steroid e, which is 125-hydroxyvitamin D.
ng at v D levels at all.
ust the
y have y have low vitamin D.
e these
here’s th status.
randomi studies have found that people that can’t convert
the 25 yvitamin D, which is usually what’s measured.
e form min D in the body.
all-cau ality if they can’t do it.
t have a lower all-cause mortality.
respira lated mortality.
cancer- mortality.
likely multiple sclerosis.
one wit lian randomization.
es hamm the importance of measuring your vitamin D levels and being very
t.
it don ere.
it.
it.
wise, t y, if you don’t have one of those SNPs, for the most part,
vitami l raise blood levels by around 5 nanograms per milliliter.
defici
per mi r.
to 40.
d at le 00 IUs.
re goin stubborn and not get their D levels tested and simply
take so is that reasonable?
for mos e will be reasonably safe.
iteratu scientific literature, it is extremely hard to get like
h would major concern with really high levels of vitamin D3 supplementation.
ng like ds of thousands of IU a day for a long time.
re have tudies looking at people that are deficient in vitamin D.
s Afric icans that were given a 4,000 IU a day vitamin D supplement
to suff levels.
ler stu I would like, but it reversed their epigenetic aging by like
again, hormone.
e than our protein encoding human genome.
tamin D ill need to get out into the sun, correct?


ked abo e plant-based compounds, the omega-3s and D3.
hat fit plement-based or food-based compounds that you, you know,
ially u or brain and or body health?
m is im in there as well.
u know, about 40% of the U.S. population doesn’t get enough magnesium.
ineral upposed to be getting from our diet.
nvolved ing ATP, the energetic currency of our cells.
basical of our cells need ATP to do anything.
t’s als ved in utilizing ATP as well as DNA repair enzymes.
hat are ed in repairing damage to our DNA.
that ma insufficiency causes an insidious type of damage daily that
he mirr see.
ficient amin C, you’re like, my, my gums are falling apart.
t?
see DN e.
ut it’s ing.
t now i dy and it’s happening in your body.

s happe ou know, every day.
damage.
mes in y called DNA repair enzymes.
ium.
ctor fo
at the of a chlorophyll molecule.
gives their green color.
s are h magnesium.
the 40% iciency in the U.S. tell us?
g their .
r packa d.
r proce od.
an diet really high in dark leafy greens.
ome oth ples?
d, like chard, rainbow chard, romaine lettuce.
with ma , it can cause GI distress at like high doses.
o take 130 or 135 milligrams.
ike a h us to my gut.
agnesiu 8, for example, and it doesn’t affect the gut as much.
would b est.
the sh in out fatty acids being good for the gut.
esome.
eat gr les.
in mal .


eally h it as well.
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ot of t le also making an effort to eat more leafy greens and supplementing
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about of deliberate cold exposure.
ty or s do you think is a reasonable and particularly potent one
cold?
e minut 9 degrees Fahrenheit.

d when ng to do a podcast, when I’m going to give a talk,
.

, which I usually do it before any type of public speaking.
ng effe t you report, those are almost certainly a consequence of
ting bu ficantly elevated dopamine that goes on for hours.
amlike for dopamine because most everything else, like an Adderall,
coffee pre-workout drink or something is going to give you a big
and do and a big crash.
f not d too often is that you’re not cold adapted.
for an get truly cold adapted.
o look to the cold.
ey’re l forward to is the feeling afterward, that dopamine rush.
adapte it certainly blunts some of the effect.
ld adap ause that means I have more mitochondria in my adipose tissue
scle, l t’s been shown.
ineffi ay to produce heat, which is what your body is trying to do
o cold.
e basic ntracting and producing heat from that.
very e t.
t way t , or elegant, I guess, way to do it,
e your ndria produce tons and tons of heat.
these organelles inside of your cells that are responsible for

he form nosine triphosphate, ATP.
s every unction inside your body, from your neurotransmitter production
ng, et
ochondr y’re like a little battery.
they h ouble membrane, first of all, their structure.
ative c n the inside.
itive c n the inner membrane.
uncoupl charge.
e charg ons start leaking out of the mitochondria.
ia frea
ncoupli
it’s ma espiration, as we call it.
much e
to get roton back, that gradient, the electrochemical gradient.
insane
t’s unc energy.
re maki ctually heat, not ATP.
u’re es ly burning substrate.

‘re bur ucose, you’re burning lipids, you know, you’re basically burning
eat.
uncoupl does.
more ef way of producing heat than shivering.
re adap ybe the longer duration that you’ve stayed in the cold or
ve done u’ll no longer shiver anymore.
hen jus is uncoupling type of thermogenesis, as it’s called.
adapta at occurs is you actually produce more mitochondria in your

appens gulated by norepinephrine or noreadrenaline through a
-alpha.
in does makes more mitochondria in your adipose cells.
, you’r ng more mitochondria.
y to ba make more heat when you’re, it’s one of those things where
‘s, you s going, okay, I’m going to be exposed to this cold next

I don’
mitoch and I’m going to make more heat.
g more ndria in your adipose tissue.
ten ref o as like the browning of fat.
that is e if you look under a microscope at a lipid drop, you know,
l, not drop, it adipocyte, you’ll find that it looks darker
e mitoc in there.
as bro at.

hondria r muscle.
h impro cle mass, improved endurance.
a are e lly either the making energy in your cell.
e don’t ore mitochondria normally.
in inpu h intensity interval training exercise can do it.
ing ove make new cells, you replace old ones.
ria, yo really do that for the most part.

nesis d pen, but you have to stimulate it to happen.
tochond ke what happens with your mitochondria is they essentially
inside cells.
with ot ochondria, exchange all their content, mitochondrial DNA, and then

kind o young-ish.
, you k ng that with the same pool of mitochondria, and you’re going
ld mito a mixing old stuff together, right?
want t bring up new, healthy, young mitochondria into that pool,

I hear ondrial biogenesis, I’m like aging.
st thin nk of.
posure at.
vascula her types of training do you do?

oing hi nsity interval training.
intensi rval Tabatas on a stationary cycle three times a week.
e, just cause it’s efficient and I push my ass.
y hard.

10 sec f, and it’s 10 minutes.
pedali your life depended on it.

ave my n preheating up.
89 degr renheit.
sauna a Peloton.
wn a bu water and then I get in and then I like either read a
are for entation or a podcast, or I hash over things in my mind.
g becau uld use the sauna to memorize things.
has to the, like the stress response.
you ha motional trigger, like you remember things better, right?

in thi stressful environment would aid in the learning and retention
is real substantiated by this beautiful work by a guy named James

for a
a univ of Arizona as well.
emory g both places, very strong in learning and memory, both places.
that re fined this kind of inverted U shaped function for the relationship
and mem
e too r and not stressed enough, you’re not going to remember any information
tress.
memory , at least within the context of whatever it is you’re trying

you’re ing is very well matches with that.
it tape as you really increase adrenaline to the point where people
e auton nction, where they’re just, they’re, they’re panicking basically.
t I wou to ask you about is in the sauna, of course, there’s vasodilation
ood to in is a wonderful way to enhance cognition.
es occu
overla en moderate intensity, aerobic exercise and heat stress.
ine, wh re exercising, you’re elevating your core body temperature,
ting.
ually i auna, blood does get redistributed to the skin to facilitate
like ex blood flow in general is improved to the brain, to the

nk gene peaking that, and this, you know, there’s studies showing
ssociat a much lower risk of dementia and Alzheimer’s disease.
ow, peo t use it four to seven times a week have greater than 60%
ia risk zheimer’s disease risk compared to people that use it
k.
two to imes a week have something like a 20, a little greater than
sk.
ndent e n dementia risk and Alzheimer’s disease risk.
und, li e’s a, there’s a big link between the cardiovascular system
ously b ow, a big one, right?
need to ood to your brain.
mortali mortality from cardiovascular disease, if people use, or
en, if the sauna four to seven times a week, it’s a 50% reduction
elated ty compared to one time a week.
nt mann to three times a week is something like 24% lower death from
ase.
you kn den cardiac death.
ttack.
thing, than 60% lower if, if men use it four to seven times a

dent th
k from i Laukunen.
ity of Finland and just one of the, the, the world experts on sauna

sauna sort of heat stress, whether it’s a hot tub or jacuzzi,
pted.
cally s sweat at a lower core body temperature to cool.

hysiolo hanges start to happen earlier.
r like tes.
stayed ng time.

to your
that I alked about were from the, the duration, the time spent

uction iovascular disease related death, what was shown was that
e sauna ly 11 minutes, even if they used it four to seven times a
n was o e 8% instead of 50.
r than tes.
is the pot at about 174 degrees Fahrenheit.
y stron that this is more causal than some, you know, corollary
‘s alwa problem with observational studies, including these, which
a whole f factors like cholesterol, you know, exercise, just everything,
e sun.
ted for
you ha dose dependent nature of the duration, the time spent in the
ency.
someth oing on here.
tudies, ention studies where it’s like, you know, comparing directly
ate int aerobic exercise on a stationary cycle to 20 minutes in a sauna.
ysiolog the same things happen.
tes whi re doing the activity, blood pressure increases while you’re

t rate es, resting heart rate decreases below baseline, blood pressure

ow base
he same erate intensity cycling versus sauna.
, like at stress, there’s something about it that really mimics this moderate
xercise is really great for people that can’t go for a run, that
bike.
led peo anted, there are some safety concerns, they’re, they’re pretty
xist.
that h cent heart attack or have some rare kind of heart disease
g alcoh er do that.
, prone blood pressure.
ysician doing the sauna.
ful.


ly avoi nas when I was pregnant.
y fit p ut there already exercising, there’s a synergistic effect by
into t tine.
reat.
benefi ings happening with the, with the heat stress.
mimick obic exercise, there’s the heat shock proteins that we talked

have b e looking at Alzheimer’s disease, you know, like a human
sease i ent and heat shock proteins protecting from it, you know.
ins are ly activated in humans.
hown to or, you know, 50% higher over baseline levels after just 30
ees Fah in the sauna.
ctivate ast in rodents for, you know, 48 hours at least.
g these hock proteins around, making sure they’re, they’re properly
our pr
egating brains and in our, in our plaques could be another potential
rotecti Alzheimer’s disease and other, you know, cardiovascular health,
y.
robably ate to know what if they don’t have a sauna.
t a hot ould work almost as well.

e studi ing at, for example, activation of heat shock proteins,
urotrop tor increases with heat stress.
e hot b around 104 degrees Fahrenheit, which is typically what
r tempe
from t lders down.
ke a ve st activation in heat shock proteins and in brain drive neurotrophic

protei also protecting against muscle atrophy.
ng to d the protein structure and the muscle tissue as well.
tudies al, you know, animal data as well as some recent human data as
hyperth r local heat treatment, but essentially it showed that it

, there study where they were looking at muscle disuse and it was,
ke the eat treatment prevented like almost 40% of the muscle atrophy

, of te , but I just want to thank you again.
orough remely informative on behalf of the listeners and just directly

or your


e on.
me conv n.
ot.