Understanding & Controlling Aggression | Huberman Lab Essentials
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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
Stamford School of Medicine. Today we
are discussing aggression. I'm going to
explain to you that there are several
different types of aggression. For
instance, reactive aggression versus
proactive aggression. Meaning sometimes
people will be aggressive because they
feel threatened or they are protecting
those that they love who also feel
threatened. There's also proactive
aggression where people go out of their
way to deliberately try and harm others.
And there is indirect aggression which
is aggression not involving physical
violence. For instance, shaming people
and things of that sort. It turns out
that there are different biological
mechanisms underlying each of the
different types of aggression. And today
I will define those for you. I'll talk
about the neural circuits in the brain
and body that mediate each of the
different kinds of aggression. Talk
about some of the hormones and peptides
and neurotransmitters involved. I
promise to make it all accessible to
you. Even if you do not have any biology
or science background, I'm certain that
by the end of the episode, you will come
away with a much more thorough
understanding of what this thing that we
call aggression really is. And when you
see it in other people, I think it will
make more sense to you. And when you
observe it in yourself or the impulse to
engage in aggression, verbal or physical
or otherwise, I hope that you'll
understand it better as well. And of
course, the tools that I will describe
should allow you to modulate and control
aggressive tendencies or predispositions
to aggressiveness and just generally be
able to engage with people in a more
adaptive way. Overall, the context of
aggression really matters. So there are
instances where aggression is adaptive.
For instance, a mother protecting her
children. Of course, other forms of
aggression like unprovoked proactive
aggression, somebody simply being
violent to somebody else even when
unprovoked. Most of us cringe when we
see that kind of behavior. It can even
evoke aggression in people when they
observe that kind of behavior. Many of
you have probably heard the statement
that I believe arises from pop
psychology, not from formal academic
psychology, that aggression is just
sadness. It's a form of sadness that's
amplified and it shows up as aggression.
But when we look at the underlying
biology and the peer-reviewed literature
on this, nothing could be further from
the truth. We have distinct circuits in
the brain for aggression versus grief
and mourning. Those are non-over
overlapping. Now that doesn't mean that
you can't be sad and aggressive or in a
state of mourning and aggressive at the
same time. But the idea that sadness and
aggression are one in the same thing is
simply not true. And by understanding
that or perhaps by understanding that
irritability and aggression are not the
same thing, you'll be in a much better
position to apply some of the tools that
we will talk about in this episode in
order to be able to reduce or eliminate
or if it's adaptive to you to modulate
aggression. And yes, there are cases
where modulating your aggression, in
some cases even amplifying aggression
can be adaptive. One of the names that's
most associated with the formal study of
aggression is none other than Conrad
Loren. Conrad Loren
studied so-called imprinting behaviors
and fixed action pattern behaviors.
Patterns of behavior that could be
evoked by a single stimulus. The idea
that you can get a whole category of
behaviors like looking to somebody for
comfort and only them. The idea that
that you could get a huge category of
different behaviors in a bunch of
different contexts triggered by just the
presence of that person is remarkable
because what it suggested and what turns
out to be true is that there are neural
circuits, not just individual brain
areas, but collections of brain areas
that work together to engage a pattern
of behaviors. And that's the first
fundamental principle that we need to
define today. that when we talk about
aggression, we're talking about
activation of neural circuits, not
individual brain areas, but neural
circuits that get played out in sequence
like keys on a piano. But that playing
out in sequence means that aggression is
a verb. It has a beginning, a middle,
and an end. And it's a process. It's not
an event. And as you'll see, that turns
out to be very important in terms of
thinking about how one can halt
aggression, prevent it from happening
before it's initiated, or maybe even
prolonging aggression if that's what's
needed. Now, Conrad Loren had no real
knowledge of neural circuits. I mean,
obviously he knew there was this thing
that we call a brain and a nervous
system, and he knew that there were
chemicals in the brain and hormones and
things of that sort that were likely to
play a role, but he really didn't take
any measures to define what the neural
circuits were. But he did think about
what sorts of underlying processes could
drive something like aggression. And he
talked about one particular feature
that's especially important, and that's
this notion of a pressure. The idea that
yes, certain hormones will bias somebody
or an animal to be aggressive. Certain
neurotransmitter states, and you'll
learn what those are today, will bias
somebody to be more or less aggressive.
And yes, of course, there will be
historical features based on their
childhood, etc., etc. He understood that
there will be a constellation of things
that would drive people to be
aggressive. And he described a so-called
pressure, almost like a hydraulic
pressure. Just think about fluid
pressure in a small container being
pushed, push pushed until the can or the
container is ready to explode and how
multiple features, multiple variables
could impinge on that and create that
pressure. It turns out that's exactly
the way the system works. There is no
single brain area that flips the switch
for aggression. Although we'll soon talk
about a brain structure that generally
houses the propensity and the output of
aggression.
This notion of a hydraulic pressure that
can drive us toward aggressive behavior
or conversely can be very low pressure
and keep us in a state of
non-reactivity, maybe even passivity or
submissiveness is a very important
feature because it really captures the
essence of how neural circuits work when
we're talking about primitive behaviors
generally. And you can start to notice
this in yourself and in others. you can
start to notice when you are veering
toward aggression or when someone is
veering toward aggression, verbal or
physical. Now that veering is the
buildup of this hydraulic pressure that
Loren was referring to and it really
does have an underlying biological
basis. Now, it was some years later that
the first experiments came along which
really started to identify the brain
areas and the biological so-called
pressures that can induce aggressive
behavior. And the person that really
gets credit for this is a guy by the
name of Walter Hess who at that time was
working on cats. And I know that when
you say working on cats, a lot of people
would cringe. A lot of people have cats
as pets. And certainly cats can be
delightful. Some people like them more.
Some people like them less. Most people
cringe at the idea of doing experiments
on cats. In the time of Hess, very few
laboratories worked on mice. Most
laboratories worked on cats or rats. So
when I say he was working on cats, I
realize that probably evokes some
negative emotions in some of you, maybe
even aggression in some of you. What we
can do, however, is look at the data and
make use of the data in terms of our
understanding.
What Hess did was he had cats that were
awake and he was able to lower a
stimulating electrode into their brain.
Now keep in mind that the brain does not
have any pain sensors. So after a small
hole is made in the skull, electrodes
are lowered into the brain. This is
what's done commonly in human
neurosurgery. He was trying to identify
brain regions that could generate entire
categories of behavior. Eventually, his
electrode landed in a site and he
provided electrical stimulation to the
cat that caused this otherwise passive
purring relaxing cat to suddenly go into
an absolute rage when he stimulated this
particular brain area. And the fact that
when he turned off the stimulation of
this particular brain area, the cat very
quickly within seconds went back to
being passive calm kitty. And later
experiments done in mice but also in
humans confirmed that indeed stimulation
of this brain area evoked not just
behavioral aggression but also
subjective feelings of aggression and
anger. So what was this incredible brain
area? The so-called VMH or ventromedial
hypothalamus. The ventromedial
hypothalamus is a nucleus, meaning a
small collection of neurons, only about
1,500 neurons on one side of your brain
and a matching 1,500 neurons on the
other side of your brain. And that
combined 3,000 neurons or so is
sufficient to generate aggressive
behavior of the sort that Hess observed
in the cat. And believe it or not, when
you see somebody who's in a act of rage
or in an act of verbal aggression or in
an act of defensive aggression,
protecting their family or loved ones or
country, etc. Almost certainly those
neurons are engaged in that behavior.
Experiments done by David Anderson's lab
at Caltech were really the first to
parse the fine circuitry and to really
show that the ventromedial hypothalamus
is both necessary and sufficient for
aggressive behavior. What they did was
they identified where the ventromedial
hypothalamus was in the mouse. That was
pretty straightforward to do. It was
sort of known before they started these
experiments. And then they analyzed
which genes
meaning which DNA which of course
becomes RNA and RNA becomes protein.
Which DNA and therefore which proteins
are expressed in particular cells of the
ventromedial hypothalamus. And it turns
out that there's a particular category
of neurons in the vententral medial
hypothalamus that make an estrogen
receptor.
And it is those neurons in particular
that are responsible for generating
aggressive behavior. How did they know
this? Well, they used a tool that's
actually been described by a previous
guest of this podcast. We had an episode
with the psychiatrist and bioengineer
and my colleague at Stanford School of
Medicine, Carl Dyeroth. He and others
have developed tools that allow people
to control the activity of neurons
essentially by remote control by shining
light on those neurons. So in the
context of an experiment on a mouse,
which is what David's lab did, and these
were the beautiful experiments of Dulin,
who's now in her own laboratory at New
York University, put a little fiber
optic cable down into the hypothalamus
of the mouse. The mouse is able to move
around in its cage, freely moving, even
though it has a little tether. This
little wire, it's a very thin wire. And
that little thin wire is actually a
little what we call optrode. And the
experimentalist in this case Dou was
able to stimulate the turning on of a
little bit of blue light. And that blue
light activated only those estrogen
receptor neurons in only the
ventromedial hypothalamus. And the way
she was able to do that is she had
introduced a gene that had been
developed by our friend Carl Daiseroth
that allows light to trigger electrical
activity in those neurons. So if any of
that is confusing or if all of that is
confusing, here's the experiment.
There's a mouse in a cage has a little
wire coming out of its head. It doesn't
notice, believe it or not. We know this
because it's still eating and mating and
doing all the things that mice like to
do on a daily basis and sleeping, etc.
And the mere pressing of a button will
activate a little bit of light released
at the end of that wire. That light
activates particular neurons. In this
case, it's the estrogen receptor
containing neurons in only the
ventromedial hypothalamus. A large
number of experiments were done, but the
first experiment really was to put the
male mouse in with a female mouse who's
in the so-called receptive phase of
estrus. That is she will allow mating.
And he starts mating with her. and they
go through the standard repertoire of
mating behaviors that you observe in
mice, mounting, thrusting, intrammission
as it's called in the mouse sex world.
Um, well, I guess I don't know what the
mice call it, but that's what the
experimenters call it. And then
afterwards that he will dismount. But
about halfway through the behavior, Dau
turned on the light to stimulate these
estrogen receptor containing neurons
only in the male mouse. And what she
observed was incredibly dramatic. The
male mouse ceases from trying to mate
with the female mouse and immediately
tries to kill the female mouse. He
starts attacking her. Then she turns off
the light. The male stops and goes back
to trying to mate with the female mouse.
So I'm sure all of this was very
confusing and disturbing to the female
mouse. Nonetheless, that was the
repertoire. These are such dramatic
shifts in behavior triggered only by the
activation of only this small set of
neurons within the ventromedial
hypothalamus. The shift in behavior is
almost instantaneous. Occurs within
seconds if not milliseconds, thousands
of a second. The next experiment that
she did was to put a male mouse with
this stimulation with light capability
in its ventromedial hypothalamus into a
cage alone, but with a rubber glove
filled with air or water. Then she
stimulates the activation of these
ventromedial hypothalamus neurons and
the mouse immediately tries to kill the
glove. It goes into a rage attacking the
glove as if it were another mouse or
some other animate object. But of
course, it's an inanimate object. It's
just a rubber glove. She stops the
stimulation and the mouse immediately
goes back to being completely calm or at
least not attacking. Again, we don't
know what the mouse was feeling.
Subsequent experiments done by Dulin in
her own laboratory and other
laboratories have shown that the
ventromedial hypothalamus is connected
with a bunch of other brain areas. One
of them that I want to call out now is
the so-called P AG, the perryqueductal
gray nucleus. This is a large structure
in the back of the brain that houses
things like neurons that can create
opioids. We all know of the opioid
crisis, but these are neurons that can
produce endogenous means made by the
body chemicals that can cause pain
relief. You could understand why that
might occur in a circuit for aggression,
right? Even if one is the aggressor,
it's likely that they may incur some
physical damage and they'd want some
pain relief.
The Pag also is connected to a number of
neural circuits that eventually through
several processing stages stations,
excuse me, arrive at things like the
jaws. And in fact, stimulation of the
ventrome hypothalamus can evoke biting
and aggressive biting behavior. Now,
aggressive biting behavior is
particularly interesting because in
humans and especially in human children,
biting is something that while young
children might do as a form of
aggression, tends to disappear pretty
early in childhood. And if it doesn't,
it's often seen as a mark of pathology.
I think there is general agreement in
the psychology community and the
psychiatric community that past a
certain age the using of one's teeth to
impart aggress aggression and damage on
others is a particularly primitive and
troubling or at least for the observer
or the person experiences a pretty
disturbing event. Dou's lab has shown
that activation of the vententral medial
hypothalamus triggers a downstream
circuit in the perryqueductal gray which
then triggers a whole other set of
circuits of fixed action patterns. Here
we are back to Lorenzans with fixed
action patterns including swinging of
the limbs, right? Punching. This
wouldn't necessarily be controlled
punching, but also biting behavior. So,
it's remarkable to me at least that we
have circuits in our brain that can
evoke violent use of things like our
mouth or violent use of things like our
limbs that of course could be used for
things like singing or kissing or eating
or you know justiculating in any kind of
polite or impolite way. The point here
is that neural circuits not individual
brain areas evoke the constellation of
behaviors that we call aggression. Now,
many of you are probably puzzled or at
least should be because I've been
talking about this highly specialized
brain area, the ventromedial
hypothalamus, and this highly
specialized subcategory of neurons in
the ventromedial hypothalamus. These
neurons that make estrogen receptor and
yet the activation of those cells
triggers dramatic and immediate
aggression both in males and in females
and both against males and against
females. So, what's going on here? Most
of us think about estrogen and we don't
immediately think of aggression. Most of
us hear testosterone and we might think
about aggression. To make a long story
short and to dispel a still
unfortunately very common myth,
testosterone does not increase
aggressiveness.
Testosterone increases proactivity and
the willingness to lean into effort in
competitive scenarios. If people are
given testosterone or if you look at
people who have different le levels,
excuse me, of testosterone indogenously
that they naturally make, what you'll
find is that testosterone tends to
increase competitiveness, but not just
in aggressive scenarios. So, if somebody
is already aggressive, giving them
testosterone will have the tendency to
make them more aggressive. If somebody
however is very benevolent and
altruistic, giving them testosterone
will make them more benevolent and
altruistic at least up to a point. Turns
out there's evidence that in certain
context estrogen can make people more
aggressive. So what's going on here?
Well, what's going on is that
testosterone can be converted into
estrogen through a process called
aromatization. There's an enzyme called
aromatase. Anytime you have a word that
ends in asse at least if it's in the
context of biology it's almost always
not always but almost always an enzyme.
So arom the aromatase enzyme converts
testosterone into estrogen and it is
actually testosterone aromatized
converted into estrogen and then binding
to these estrogen containing neurons in
the ventromedial hypothalamus that
triggers aggression. I want to repeat
that it is not testosterone itself that
triggers aggression. It is testosterone
aromatized into estrogen within the
brain and binding to these estrogen
receptor containing neurons in the
vententral medial hypothalamus that
evokes aggression and dramatic
aggression at that. Now this effect of
estrogen causing aggression in the brain
is very robust. So much so that if you
take a mouse that lacks the aromatase
enzyme or a human that lacks the
aromatase enzyme and they do exist then
there is a reduction in overall
aggression despite high levels of
testosterone. It doesn't matter how much
you increase testosterone or any of its
other derivatives you do not observe
this aggression. This runs counter to
everything that we know and think about
the role of testosterone. So the next
time somebody says testosterone makes
people aggressive, you can say ah no
actually it's estrogen that makes people
aggressive and animals aggressive for
that matter. Now of course it is the
case that because males have relatively
less estrogen circulating in their brain
and body than females, right? because
they have testes, not ovaries. That
testosterone is required in the first
place in order to be converted into
estrogen to activate this aggressive
circuit involving these estrogen
receptor containing neurons in the
ventromedial hypothalamus. So, we've
established that it's not testosterone,
but testosterone converted into estrogen
that activates these circuits for
aggression. Nonetheless, it's still
surprising, right? Right? I mean, most
of us don't think about a estrogen as
the hormone that stimulates aggression,
but turns out it's all contextual. There
are beautiful data showing that whether
or not estrogen stimulates aggression
can be powerfully modulated by whether
or not days are short or days are long.
In other words, whether or not there's a
lot of sunshine or not. Day length is
converted into hormonal signals and
chemical signals. And the primary
hormonal and chemical signals involve
melatonin and dopamine and also the
stress hormones. So to make a very long
story short, in the long days where we
get a lot of sunlight both in our eyes
and on our skin, melatonin levels are
reduced. Melatonin is a hormone that
tends to produce states of sleepiness
and quiescence. It also tends to
activate pathways that tend to reduce uh
things like breeding and sexual
behavior. In long days, dopamine is
increased. Dopamine is a molecule
associated with feelings of well-being
and motivation and the desire to seek
out all sorts of things. And in long
days, provided we're getting enough
sunlight on our skin and to our eyes,
the stress hormones, especially cortisol
and some of the other stress hormones
are reduced in levels. If estrogen
levels are increased experimentally
under long day conditions, it does not
evoke aggression. However, in short
days, if estrogen is increased, there is
a heightened predisposition for
aggression. And that makes perfect
sense. If you think about what short
days do to the biology of your brain and
body, the melatonin signal goes up.
There's more melatonin circulating for
more of each 24-hour cycle. Stress
hormones are circulating more. Why?
Short days tend to be associated with
winter. In winter, we are bombarded with
more bacteria and viruses because
bacteria and viruses actually survive
better in cold than they do in heat. So,
shorter days are conducive to
aggression, not because days are short
per se, but because stress hormone
levels are higher, and because dopamine
levels are lower. Now, here's where all
of this starts to converge on a very
clear biological picture, a very clear
psychological picture, and indeed a very
clear set of tools that we can think
about and use. Under conditions where
cortisol is high, where the stress
hormone is elevated, and under
conditions where the neurom modulator
serotonin is reduced, there is a greater
propensity for estrogen to trigger
aggression. For males who make a lot of
testosterone relative to estrogen, you
have to swap in your mind this idea that
if testosterone is high, that means that
estrogen is low. Because if testosterone
is high, there is going to be some
aromatization, that conversion of
testosterone to estrogen. So anytime you
hear that testosterone is high, you
should think testosterone is high in the
body and perhaps estrogen is low in the
body, but that means that there's going
to be heightened levels of estrogen in
the brain and therefore increased
propensity for aggression. In females
who generally make less testosterone
relative to estrogen, there is
sufficient estrogen already present to
trigger aggression. So both males and
females are primed for aggression. But
that's riding on a context and that
context of whether or not you get a
tendency for aggression or not depends
on whether or not cortisol is high or
low. And I'm telling you that if
cortisol is relatively higher in any
individual, there's going to be a tilt,
an increase in that hydraulic pressure
that Loren talked about toward
aggression.
And if serotonin, the neurom modulator
that is associated with feelings of
well-being and sometimes even of slight
passivity, but certainly of well-being,
if serotonin is low, there's also going
to be a further shift towards an
aggressive tendency. So if we return to
Lorenz's hydraulic pressure model of
aggression and other internal states, we
realize that external stimula, things
that we hear, things that we see, for
instance, someone saying something
upsetting or us seeing somebody do
something that we don't like to others
or to us, as well as our internal state,
our subjective feelings of well-being,
but also our stress level, our feelings
of whether or not we have enough
resources and are content. with what we
have all of that is converging on this
thing that we call internal state and
creating this pressure of either to be
more aggressive or less aggressive. Now
we have some major players feeding into
that final pathway that question of
whether or not will we hit the other
person. Will we say the thing that is
considered aggressive? Will we not say
it? Again, there are many things
funneling into that question and
dictating whether or not the answer is
absolutely I'll fight back or I'm going
to attack them even unprovoked. we
really can boil them down to just a few
common elements. And I'm telling you
that those elements are whether or not
cortisol levels are relatively lower or
relatively higher. Again, relatively
higher is going to tend to make people
more reactive. Why? Because
reactivity is really a function of the
autonomic nervous system, which is sort
of like a seessaw that oscillates
between the so-called sympathetic
arm of the autonomic nervous system,
which tends to put us into a state of
readiness through the release of
adrenaline. Cortisol and adrenaline when
they're circulating in the brain and
body make us more likely to move and to
react and to speak. It's actually what
will induce a kind of low-level tremor,
which is an anticipatory tremor to be
able to move more quickly. Right? a body
in motion is more easily set into
further motion. That is, and in terms of
keeping cortisol in a range that's
healthy and doesn't bias someone toward
high levels of aggression and
irritability, that's again going to be
set by a number of larger modulators or
contextual cues. And I've talked about
some of those on the podcast, but I'll
just briefly recap them now. Obviously,
getting sunlight in your eyes early in
the day and as much sunlight as you
safely can in your eyes throughout the
day is going to be important. Again,
because of this effect of estrogen in
long days, not increasing aggression.
However, in shorter days, estrogen
increases aggression because of the
increase in cortisol observed in short
days. Another way to reduce cortisol was
discussed in our episode on heat and the
use of sauna and heat, but also hot
baths. It turns out that hot baths and
sauna can be very beneficial for
reducing cortisol. All the details on
that are included in the episode on heat
and it's timestamped. So you can go
directly to that if you want to learn
about the temperatures and the various
durations. But to just give a uh
synopsis of that a 20 minute sauna at
anywhere from 80 to 100° C is going to
be beneficial for reducing cortisol. If
you don't have access to a sauna, you
could do a hot bath. And of course, some
of you may be interested in exploring
the supplementation route. And for
reductions in cortisol, really the uh
chief player there is ashwagandha, which
is known to decrease cortisol fairly
potently. I should just warn you that if
you're going to use ashwagandha in order
to reduce cortisol, first of all, check
with your doctor or healthcare provider
before adding or subtracting anything
from your supplementation or health
regimen. Of course, I don't just say
that to protect us. I say that to
protect you. You are responsible for
your health, what you take and what you
don't take. Chronic supplementation with
ashwagandha can have some not so great
effects of disruption of other hormone
pathways and neurotransmitter pathways.
So the limit seems to be about 2 weeks
of of regular use before you'd want to
take a break of about 2 weeks. So
ashwagandha again a very potent
inhibitor of cortisol but with some
other effects as well. Don't use it
chronically for longer than 2 weeks. But
if your goal is to reduce cortisol,
let's say you're going through a period
of increased irritability and aggressive
tendency, maybe you're also not getting
as much light as you would like. And
perhaps also if there are other um
circumstantial things leading you
towards more aggressiveness and your
goal is to reduce aggressiveness, that
can be potentially helpful. And in light
of all this stuff about cortisol and
estrogen and daylength,
I should mention that there are in fact
some people who have a genetic
predisposition to be more irritable and
aggressive. There is a genetic variant
present in certain people that adjusts
their estrogen receptor sensitivity
and that estrogen receptor sensitivity
can result in increased levels of
aggression. sometimes dramatic
increases. However, and also very
interestingly, photo period, meaning
daylength is a strong modulator of
whether or not that aggressiveness turns
up or not. Whether or not that person
with the particular gene variant is more
aggressive or not depends on how long
the day is and how long the night is.
One particular study that I like that
references this is trainer at all. The
title of the study is photo period
reverses the effects of estrogens on
male aggression via genomic and
non-genomic pathways. This was a paper
published in the proceedings of the
National Academy of Sciences. It really
points to the fact that rarely is it the
case that just one gene will cause
somebody to be hyperaggressive.
Almost always there's going to be an
interplay between genetics and
environment. And as environment changes,
such as daylength changes and the length
of night changes, so too will the
tendency for people with a given genetic
variant to be more aggressive or not.
Now, of course, in the absence of
detailed genetic testing for this
particular estrogen receptor variant,
most people, I'm guessing you are
probably not walking around knowing that
you have this gene or not.
Regardless, I think it's important to
pay attention to how you feel at
different times of year depending on
whether or not summer, whether or not
it's winter, whether or not you're
getting sufficient sunlight, meaning
viewing sufficient sunlight or not,
whether or not you're getting sufficient
sunlight exposure to your skin or not,
whether or not you're indoors all the
time. Generally, those things correlate
with season, but not always. You can go
through long bouts of you know hard work
in the summer months when days are long
but you're indoors a lot and getting a
lot of fluorescent light exposure late
in the evening and perhaps that's when
you're feeling more aggressive. So we
have to be careful about drawing a
onetoone relationship between any
biological feature and certainly
psychological or behavioral feature like
aggressiveness. But it's I believe
helpful to know that these genetic
biases exist. How they play out again
they shift our biology in in a general
thematic direction. They don't change
one thing. They change a variety of
things that bias us toward or away from
certain psychological and behavioral
outcomes and the various things that we
can do in order to offset them. And we
described those earlier in terms of
trying to keep cortisol low by getting
sufficient sunlight regardless of time
of year and regardless of whether or not
you happen to have this particular
genetic variant. I want to share with
you a study that's focused on kids, but
that has important ramifications for
adults as well. There are many kids out
there that suffer from so-called
attention deficit hyperactivity disorder
or ADHD. There are also many adults we
are finding that are suffering from
ADHD. In any event, the study I'm about
to share with you explored how a
particular pattern of supplementation in
kids with ADHD was able to reduce
aggressive episodes and impulsivity and
increase self-regulation.
And the title of the study is efficacy
of carnitine in the treatment of
children with attention deficit
hyperactivity disorder. even though they
put carnitine in the title that what
they focused on was whether or not a
cetal LC carnitine supplementation could
somehow adjust the behavioral tendency
of these kids with ADHD. And to make a
long story short, indeed it did. There
was a very significant effect of acetyl
carnitine supplementation on improving
some of the symptomology symptomology,
excuse me, of ADHD. This was a
randomized double blind placeboc control
double crossover study. They showed
significant reductions in their
so-called total problem score. The total
problem score is a well-established
measure of behavioral problems in kids
with ADHD and I should say adults with
ADHD. Reductions in attentional problems
overall reductions in delinquency and
most important for sake of today's
discussion significant reductions in
aggressive behavior. They were able to
confirm the shifts in alcarnitine
within the bloodstream of these kids.
that is they were able to correlate the
physiology with the psychological
changes. So studies such as this I think
are useful because they point to the
fact that
very seldom if ever will there be one
supplement or one nutritional change or
even one behavioral change that's going
to completely shift an individual from
being aggressive and impulsive. rather
that by combining different behavioral
regimens, by paying attention to things
like time of year and work conditions
and school conditions and overall levels
of stress and likely therefore levels of
cortisol, etc. that you can use
behaviors, diet, and supplementation as
a way to shift that overall internal
millu from one of providing a lot of
internal hydraulic pressure, as it's
been called throughout the episode,
toward aggressive impulsivity and relax
some of that hydraulic pressure and
reduce aggressive tendencies. Thank you
for joining me for our discussion about
the biology, psychology, and actionable
tools around aggression. And as always,
thank you for your interest in science.
Ask follow-up questions or revisit key timestamps.
This episode explores the biological and psychological underpinnings of aggression, debunking myths about its causes and defining the neural circuits involved. Huberman explains that aggression is not a single brain event but a process driven by specific neural circuits, notably involving the ventromedial hypothalamus. He clarifies that estrogen, rather than testosterone, is primarily responsible for triggering aggression through aromatization. Furthermore, he provides science-based strategies to modulate aggressive tendencies, including managing cortisol levels through sunlight exposure, heat therapy, and specific supplements like ashwagandha and acetyl-l-carnitine.
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