Video summary
In this episode of Huberman Lab Essentials, Andrew Huberman explores the complex biology and psychology behind aggression, distinguishing between reactive forms driven by threat or protection and proactive aggression intended to harm others without provocation. He clarifies a common misconception that equates sadness with aggression, noting instead that distinct neural circuits govern these states; while one can experience both simultaneously, they are not biologically identical. Huberman introduces the concept of "hydraulic pressure," originally described by ethologist Konrad Lorenz, to explain how various biological and environmental factors accumulate over time until a threshold is reached for aggressive behavior. This model emphasizes that aggression is a process involving neural circuits rather than an instantaneous event triggered by a single brain area or hormone alone. The scientific investigation into the specific mechanisms of aggression centers on experiments conducted by Walter Hess using cats, which identified the ventromedial hypothalamus (VMH) as a critical region for generating aggressive behavior. Later research by David Anderson's lab and Dayu Lin at Caltech further refined this understanding, revealing that it is not testosterone itself but rather estrogen receptor-containing neurons within the VMH that drive aggression. Through optogenetics—a technique developed with tools from Karl Deisseroth—researchers demonstrated that stimulating these specific neurons could instantly switch a male mouse from mating behavior to lethal violence against another animal or even an inanimate object like a rubber glove, proving that this small cluster of approximately 3,000 neurons is both necessary and sufficient for aggressive output. A crucial biological nuance revealed by the transcript is the role of aromatase, an enzyme that converts testosterone into estrogen within the brain. This finding dispels the myth that high testosterone directly causes aggression; instead, it is the resulting increase in local estrogen levels binding to VMH neurons that triggers violent behavior. Consequently, individuals with genetic variants affecting estrogen receptor sensitivity or those lacking the aromatase enzyme show different aggressive profiles regardless of their circulating testosterone levels. Furthermore, this hormonal pathway is heavily modulated by environmental context, specifically day length and sunlight exposure. During short days (winter), higher melatonin and stress hormone levels combined with increased cortisol create a biological environment where elevated estrogen significantly heightens aggression, whereas long days suppress these effects through reduced melatonin and lower stress hormones. To manage or reduce aggressive tendencies, Huberman outlines actionable tools focused on regulating the internal "hydraulic pressure" of cortisol and serotonin. Strategies include maximizing sunlight exposure to eyes and skin early in the day to modulate circadian rhythms and prevent excessive aggression during winter months, as well as utilizing heat therapies like saunas (80–100°C for 20 minutes) or hot baths to lower cortisol levels naturally. For those seeking supplementation, ashwagandha is highlighted as a potent inhibitor of cortisol that should be used in cycles—approximately two weeks on followed by two weeks off—to avoid disrupting other hormonal pathways. Additionally, the efficacy of acetyl-L-carnitine is noted for reducing impulsivity and aggressive episodes in individuals with ADHD, suggesting that nutritional interventions can help shift behavioral tendencies when combined with broader lifestyle adjustments regarding stress management and environmental factors.
Read the full video transcript
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 ophthalmology at
Stanford 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-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 Konrad
Lorenz. Konrad Lorenz
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, Konrad Lorenz
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 would 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, pushed, 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 this
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 build-up of this
hydraulic pressure that Lorenz 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 say working on cats a
lot of people will 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
stimulating electrode into the 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 an
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
ventromedial 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, Karl Deisseroth. 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 Dayu
Lin, 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, Dayu, 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
Karl Deisseroth
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 cuz it's still eating
and mating and doing all the things that
mice like to do on 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, intromission, 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, uh he will dismount. But,
about halfway through the behavior, Di
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 the small set of
neurons within the ventromedial
hypothalamus. The shift in behavior is
almost instantaneous. Occurs within
seconds, if not milliseconds,
thousandths 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 to back to being
completely calm or at least not
attacking. Again, we don't know what the
mouse was feeling. Subsequent
experiments done by Dayu Lin 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 PAG, the periaqueductal 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
ventromedial 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 aggressive aggression and damage
on others is a particularly primitive
and troubling, or at least for the
observer or the person that experiences
a pretty disturbing event.
Dyu's lab has shown that activation of
the ventromedial hypothalamus triggers a
downstream circuit in the periaqueductal
gray, which then triggers a whole other
set of circuits of fixed action
patterns. Here we are back to Lorenz
again 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, gesticulating 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
levels, excuse me, of testosterone
endogenously 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 word that
ends in ASE, at least if it's in the
context of biology, it's almost always,
not always, but almost always an enzyme.
So, 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
ventromedial 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? I mean, most of us
don't think about a estrogen as the
hormone that stimulates aggression. But,
it 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, you know, 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's 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
neuromodulator 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 Lorenz talked about toward
aggression.
And
if
serotonin, the neuromodulator that's
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 stimuli, 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 seesaw 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
time-stamped, 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
a 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 health
care 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 day length,
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 adjust
their estrogen receptor sensitivity.
And that estrogen receptor sensitivity
can result in increased levels of
aggression.
Sometimes dramatic increases. However,
and also very interestingly,
photoperiod, meaning day length,
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 Trainor et al. The
title of the study is photoperiod
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 hyper-aggressive.
Almost always there's going to be an
interplay between genetics and
environment and as environment changes
such as day length 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 one-to-one 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. 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 I 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, 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 our 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 acetyl-L-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
symptomatology symptomatology, excuse
me, of ADHD. This was a randomized
double-blind placebo-controlled
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 the sake of today's
discussion, significant reductions in
aggressive behavior. They were able to
confirm the shifts in L-carnitine
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, but
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 milieu 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.