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Understanding & Controlling Aggression | Huberman Lab Essentials

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Understanding & Controlling Aggression | Huberman Lab Essentials

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910 segments

0:00

Welcome to Huberman Lab Essentials,

0:02

where we revisit past episodes for the

0:04

most potent and actionable science-based

0:06

tools for mental health, physical

0:08

health, and performance.

0:11

I'm Andrew Huberman, and I'm a professor

0:13

of neurobiology and opthalmology at

0:15

Stamford School of Medicine. Today we

0:18

are discussing aggression. I'm going to

0:20

explain to you that there are several

0:22

different types of aggression. For

0:23

instance, reactive aggression versus

0:25

proactive aggression. Meaning sometimes

0:27

people will be aggressive because they

0:29

feel threatened or they are protecting

0:31

those that they love who also feel

0:33

threatened. There's also proactive

0:35

aggression where people go out of their

0:37

way to deliberately try and harm others.

0:39

And there is indirect aggression which

0:42

is aggression not involving physical

0:44

violence. For instance, shaming people

0:46

and things of that sort. It turns out

0:49

that there are different biological

0:50

mechanisms underlying each of the

0:52

different types of aggression. And today

0:54

I will define those for you. I'll talk

0:56

about the neural circuits in the brain

0:57

and body that mediate each of the

0:59

different kinds of aggression. Talk

1:00

about some of the hormones and peptides

1:02

and neurotransmitters involved. I

1:04

promise to make it all accessible to

1:06

you. Even if you do not have any biology

1:08

or science background, I'm certain that

1:10

by the end of the episode, you will come

1:11

away with a much more thorough

1:12

understanding of what this thing that we

1:14

call aggression really is. And when you

1:17

see it in other people, I think it will

1:19

make more sense to you. And when you

1:21

observe it in yourself or the impulse to

1:24

engage in aggression, verbal or physical

1:26

or otherwise, I hope that you'll

1:28

understand it better as well. And of

1:30

course, the tools that I will describe

1:32

should allow you to modulate and control

1:35

aggressive tendencies or predispositions

1:37

to aggressiveness and just generally be

1:39

able to engage with people in a more

1:41

adaptive way. Overall, the context of

1:44

aggression really matters. So there are

1:45

instances where aggression is adaptive.

1:48

For instance, a mother protecting her

1:50

children. Of course, other forms of

1:52

aggression like unprovoked proactive

1:55

aggression, somebody simply being

1:57

violent to somebody else even when

1:59

unprovoked. Most of us cringe when we

2:01

see that kind of behavior. It can even

2:03

evoke aggression in people when they

2:05

observe that kind of behavior. Many of

2:07

you have probably heard the statement

2:09

that I believe arises from pop

2:11

psychology, not from formal academic

2:13

psychology, that aggression is just

2:17

sadness. It's a form of sadness that's

2:19

amplified and it shows up as aggression.

2:21

But when we look at the underlying

2:23

biology and the peer-reviewed literature

2:25

on this, nothing could be further from

2:27

the truth. We have distinct circuits in

2:29

the brain for aggression versus grief

2:33

and mourning. Those are non-over

2:35

overlapping. Now that doesn't mean that

2:36

you can't be sad and aggressive or in a

2:39

state of mourning and aggressive at the

2:40

same time. But the idea that sadness and

2:43

aggression are one in the same thing is

2:45

simply not true. And by understanding

2:48

that or perhaps by understanding that

2:50

irritability and aggression are not the

2:53

same thing, you'll be in a much better

2:54

position to apply some of the tools that

2:56

we will talk about in this episode in

2:58

order to be able to reduce or eliminate

3:01

or if it's adaptive to you to modulate

3:04

aggression. And yes, there are cases

3:05

where modulating your aggression, in

3:08

some cases even amplifying aggression

3:10

can be adaptive. One of the names that's

3:12

most associated with the formal study of

3:14

aggression is none other than Conrad

3:17

Loren. Conrad Loren

3:20

studied so-called imprinting behaviors

3:22

and fixed action pattern behaviors.

3:25

Patterns of behavior that could be

3:27

evoked by a single stimulus. The idea

3:29

that you can get a whole category of

3:31

behaviors like looking to somebody for

3:33

comfort and only them. The idea that

3:35

that you could get a huge category of

3:37

different behaviors in a bunch of

3:38

different contexts triggered by just the

3:40

presence of that person is remarkable

3:43

because what it suggested and what turns

3:45

out to be true is that there are neural

3:47

circuits, not just individual brain

3:49

areas, but collections of brain areas

3:50

that work together to engage a pattern

3:53

of behaviors. And that's the first

3:56

fundamental principle that we need to

3:57

define today. that when we talk about

4:00

aggression, we're talking about

4:02

activation of neural circuits, not

4:04

individual brain areas, but neural

4:06

circuits that get played out in sequence

4:08

like keys on a piano. But that playing

4:11

out in sequence means that aggression is

4:14

a verb. It has a beginning, a middle,

4:16

and an end. And it's a process. It's not

4:18

an event. And as you'll see, that turns

4:20

out to be very important in terms of

4:22

thinking about how one can halt

4:24

aggression, prevent it from happening

4:26

before it's initiated, or maybe even

4:30

prolonging aggression if that's what's

4:31

needed. Now, Conrad Loren had no real

4:34

knowledge of neural circuits. I mean,

4:36

obviously he knew there was this thing

4:37

that we call a brain and a nervous

4:39

system, and he knew that there were

4:41

chemicals in the brain and hormones and

4:43

things of that sort that were likely to

4:45

play a role, but he really didn't take

4:47

any measures to define what the neural

4:49

circuits were. But he did think about

4:51

what sorts of underlying processes could

4:54

drive something like aggression. And he

4:57

talked about one particular feature

4:59

that's especially important, and that's

5:01

this notion of a pressure. The idea that

5:04

yes, certain hormones will bias somebody

5:08

or an animal to be aggressive. Certain

5:10

neurotransmitter states, and you'll

5:12

learn what those are today, will bias

5:14

somebody to be more or less aggressive.

5:16

And yes, of course, there will be

5:18

historical features based on their

5:19

childhood, etc., etc. He understood that

5:22

there will be a constellation of things

5:24

that would drive people to be

5:26

aggressive. And he described a so-called

5:28

pressure, almost like a hydraulic

5:30

pressure. Just think about fluid

5:31

pressure in a small container being

5:33

pushed, push pushed until the can or the

5:35

container is ready to explode and how

5:38

multiple features, multiple variables

5:40

could impinge on that and create that

5:42

pressure. It turns out that's exactly

5:44

the way the system works. There is no

5:47

single brain area that flips the switch

5:49

for aggression. Although we'll soon talk

5:51

about a brain structure that generally

5:53

houses the propensity and the output of

5:56

aggression.

5:57

This notion of a hydraulic pressure that

6:00

can drive us toward aggressive behavior

6:02

or conversely can be very low pressure

6:06

and keep us in a state of

6:07

non-reactivity, maybe even passivity or

6:10

submissiveness is a very important

6:12

feature because it really captures the

6:14

essence of how neural circuits work when

6:17

we're talking about primitive behaviors

6:18

generally. And you can start to notice

6:21

this in yourself and in others. you can

6:23

start to notice when you are veering

6:25

toward aggression or when someone is

6:27

veering toward aggression, verbal or

6:30

physical. Now that veering is the

6:33

buildup of this hydraulic pressure that

6:36

Loren was referring to and it really

6:38

does have an underlying biological

6:39

basis. Now, it was some years later that

6:43

the first experiments came along which

6:46

really started to identify the brain

6:48

areas and the biological so-called

6:51

pressures that can induce aggressive

6:53

behavior. And the person that really

6:55

gets credit for this is a guy by the

6:57

name of Walter Hess who at that time was

7:01

working on cats. And I know that when

7:02

you say working on cats, a lot of people

7:04

would cringe. A lot of people have cats

7:06

as pets. And certainly cats can be

7:08

delightful. Some people like them more.

7:09

Some people like them less. Most people

7:11

cringe at the idea of doing experiments

7:13

on cats. In the time of Hess, very few

7:15

laboratories worked on mice. Most

7:17

laboratories worked on cats or rats. So

7:20

when I say he was working on cats, I

7:21

realize that probably evokes some

7:22

negative emotions in some of you, maybe

7:24

even aggression in some of you. What we

7:27

can do, however, is look at the data and

7:30

make use of the data in terms of our

7:32

understanding.

7:34

What Hess did was he had cats that were

7:37

awake and he was able to lower a

7:39

stimulating electrode into their brain.

7:40

Now keep in mind that the brain does not

7:42

have any pain sensors. So after a small

7:44

hole is made in the skull, electrodes

7:46

are lowered into the brain. This is

7:47

what's done commonly in human

7:49

neurosurgery. He was trying to identify

7:52

brain regions that could generate entire

7:56

categories of behavior. Eventually, his

7:58

electrode landed in a site and he

8:00

provided electrical stimulation to the

8:02

cat that caused this otherwise passive

8:07

purring relaxing cat to suddenly go into

8:10

an absolute rage when he stimulated this

8:13

particular brain area. And the fact that

8:14

when he turned off the stimulation of

8:17

this particular brain area, the cat very

8:19

quickly within seconds went back to

8:21

being passive calm kitty. And later

8:24

experiments done in mice but also in

8:26

humans confirmed that indeed stimulation

8:29

of this brain area evoked not just

8:31

behavioral aggression but also

8:34

subjective feelings of aggression and

8:36

anger. So what was this incredible brain

8:38

area? The so-called VMH or ventromedial

8:42

hypothalamus. The ventromedial

8:44

hypothalamus is a nucleus, meaning a

8:47

small collection of neurons, only about

8:50

1,500 neurons on one side of your brain

8:53

and a matching 1,500 neurons on the

8:55

other side of your brain. And that

8:57

combined 3,000 neurons or so is

9:00

sufficient to generate aggressive

9:03

behavior of the sort that Hess observed

9:07

in the cat. And believe it or not, when

9:10

you see somebody who's in a act of rage

9:12

or in an act of verbal aggression or in

9:16

an act of defensive aggression,

9:17

protecting their family or loved ones or

9:20

country, etc. Almost certainly those

9:23

neurons are engaged in that behavior.

9:25

Experiments done by David Anderson's lab

9:28

at Caltech were really the first to

9:30

parse the fine circuitry and to really

9:33

show that the ventromedial hypothalamus

9:35

is both necessary and sufficient for

9:37

aggressive behavior. What they did was

9:40

they identified where the ventromedial

9:42

hypothalamus was in the mouse. That was

9:44

pretty straightforward to do. It was

9:45

sort of known before they started these

9:47

experiments. And then they analyzed

9:49

which genes

9:52

meaning which DNA which of course

9:54

becomes RNA and RNA becomes protein.

9:57

Which DNA and therefore which proteins

9:59

are expressed in particular cells of the

10:03

ventromedial hypothalamus. And it turns

10:05

out that there's a particular category

10:07

of neurons in the vententral medial

10:09

hypothalamus that make an estrogen

10:12

receptor.

10:14

And it is those neurons in particular

10:17

that are responsible for generating

10:19

aggressive behavior. How did they know

10:21

this? Well, they used a tool that's

10:23

actually been described by a previous

10:25

guest of this podcast. We had an episode

10:27

with the psychiatrist and bioengineer

10:28

and my colleague at Stanford School of

10:30

Medicine, Carl Dyeroth. He and others

10:33

have developed tools that allow people

10:36

to control the activity of neurons

10:38

essentially by remote control by shining

10:40

light on those neurons. So in the

10:42

context of an experiment on a mouse,

10:44

which is what David's lab did, and these

10:45

were the beautiful experiments of Dulin,

10:47

who's now in her own laboratory at New

10:48

York University, put a little fiber

10:51

optic cable down into the hypothalamus

10:52

of the mouse. The mouse is able to move

10:54

around in its cage, freely moving, even

10:57

though it has a little tether. This

10:59

little wire, it's a very thin wire. And

11:00

that little thin wire is actually a

11:02

little what we call optrode. And the

11:03

experimentalist in this case Dou was

11:06

able to stimulate the turning on of a

11:10

little bit of blue light. And that blue

11:12

light activated only those estrogen

11:15

receptor neurons in only the

11:18

ventromedial hypothalamus. And the way

11:20

she was able to do that is she had

11:22

introduced a gene that had been

11:24

developed by our friend Carl Daiseroth

11:26

that allows light to trigger electrical

11:30

activity in those neurons. So if any of

11:31

that is confusing or if all of that is

11:33

confusing, here's the experiment.

11:34

There's a mouse in a cage has a little

11:36

wire coming out of its head. It doesn't

11:38

notice, believe it or not. We know this

11:40

because it's still eating and mating and

11:41

doing all the things that mice like to

11:43

do on a daily basis and sleeping, etc.

11:46

And the mere pressing of a button will

11:48

activate a little bit of light released

11:50

at the end of that wire. That light

11:53

activates particular neurons. In this

11:54

case, it's the estrogen receptor

11:56

containing neurons in only the

11:57

ventromedial hypothalamus. A large

12:00

number of experiments were done, but the

12:01

first experiment really was to put the

12:04

male mouse in with a female mouse who's

12:06

in the so-called receptive phase of

12:08

estrus. That is she will allow mating.

12:11

And he starts mating with her. and they

12:13

go through the standard repertoire of

12:16

mating behaviors that you observe in

12:17

mice, mounting, thrusting, intrammission

12:21

as it's called in the mouse sex world.

12:23

Um, well, I guess I don't know what the

12:24

mice call it, but that's what the

12:25

experimenters call it. And then

12:28

afterwards that he will dismount. But

12:30

about halfway through the behavior, Dau

12:33

turned on the light to stimulate these

12:37

estrogen receptor containing neurons

12:39

only in the male mouse. And what she

12:40

observed was incredibly dramatic. The

12:43

male mouse ceases from trying to mate

12:45

with the female mouse and immediately

12:46

tries to kill the female mouse. He

12:48

starts attacking her. Then she turns off

12:50

the light. The male stops and goes back

12:53

to trying to mate with the female mouse.

12:54

So I'm sure all of this was very

12:56

confusing and disturbing to the female

12:58

mouse. Nonetheless, that was the

12:59

repertoire. These are such dramatic

13:02

shifts in behavior triggered only by the

13:04

activation of only this small set of

13:06

neurons within the ventromedial

13:07

hypothalamus. The shift in behavior is

13:09

almost instantaneous. Occurs within

13:12

seconds if not milliseconds, thousands

13:14

of a second. The next experiment that

13:17

she did was to put a male mouse with

13:20

this stimulation with light capability

13:23

in its ventromedial hypothalamus into a

13:25

cage alone, but with a rubber glove

13:27

filled with air or water. Then she

13:29

stimulates the activation of these

13:31

ventromedial hypothalamus neurons and

13:34

the mouse immediately tries to kill the

13:37

glove. It goes into a rage attacking the

13:39

glove as if it were another mouse or

13:41

some other animate object. But of

13:43

course, it's an inanimate object. It's

13:44

just a rubber glove. She stops the

13:46

stimulation and the mouse immediately

13:48

goes back to being completely calm or at

13:50

least not attacking. Again, we don't

13:51

know what the mouse was feeling.

13:53

Subsequent experiments done by Dulin in

13:55

her own laboratory and other

13:57

laboratories have shown that the

13:59

ventromedial hypothalamus is connected

14:00

with a bunch of other brain areas. One

14:02

of them that I want to call out now is

14:05

the so-called P AG, the perryqueductal

14:07

gray nucleus. This is a large structure

14:10

in the back of the brain that houses

14:12

things like neurons that can create

14:13

opioids. We all know of the opioid

14:16

crisis, but these are neurons that can

14:18

produce endogenous means made by the

14:21

body chemicals that can cause pain

14:24

relief. You could understand why that

14:26

might occur in a circuit for aggression,

14:28

right? Even if one is the aggressor,

14:31

it's likely that they may incur some

14:33

physical damage and they'd want some

14:34

pain relief.

14:37

The Pag also is connected to a number of

14:39

neural circuits that eventually through

14:42

several processing stages stations,

14:44

excuse me, arrive at things like the

14:47

jaws. And in fact, stimulation of the

14:48

ventrome hypothalamus can evoke biting

14:51

and aggressive biting behavior. Now,

14:53

aggressive biting behavior is

14:55

particularly interesting because in

14:57

humans and especially in human children,

14:59

biting is something that while young

15:02

children might do as a form of

15:04

aggression, tends to disappear pretty

15:06

early in childhood. And if it doesn't,

15:09

it's often seen as a mark of pathology.

15:12

I think there is general agreement in

15:13

the psychology community and the

15:15

psychiatric community that past a

15:16

certain age the using of one's teeth to

15:19

impart aggress aggression and damage on

15:21

others is a particularly primitive and

15:24

troubling or at least for the observer

15:26

or the person experiences a pretty

15:28

disturbing event. Dou's lab has shown

15:31

that activation of the vententral medial

15:33

hypothalamus triggers a downstream

15:34

circuit in the perryqueductal gray which

15:36

then triggers a whole other set of

15:38

circuits of fixed action patterns. Here

15:40

we are back to Lorenzans with fixed

15:42

action patterns including swinging of

15:45

the limbs, right? Punching. This

15:47

wouldn't necessarily be controlled

15:49

punching, but also biting behavior. So,

15:52

it's remarkable to me at least that we

15:54

have circuits in our brain that can

15:56

evoke violent use of things like our

15:59

mouth or violent use of things like our

16:01

limbs that of course could be used for

16:03

things like singing or kissing or eating

16:06

or you know justiculating in any kind of

16:09

polite or impolite way. The point here

16:12

is that neural circuits not individual

16:15

brain areas evoke the constellation of

16:17

behaviors that we call aggression. Now,

16:19

many of you are probably puzzled or at

16:20

least should be because I've been

16:23

talking about this highly specialized

16:24

brain area, the ventromedial

16:26

hypothalamus, and this highly

16:27

specialized subcategory of neurons in

16:30

the ventromedial hypothalamus. These

16:32

neurons that make estrogen receptor and

16:34

yet the activation of those cells

16:37

triggers dramatic and immediate

16:39

aggression both in males and in females

16:42

and both against males and against

16:44

females. So, what's going on here? Most

16:46

of us think about estrogen and we don't

16:49

immediately think of aggression. Most of

16:51

us hear testosterone and we might think

16:53

about aggression. To make a long story

16:54

short and to dispel a still

16:59

unfortunately very common myth,

17:01

testosterone does not increase

17:03

aggressiveness.

17:04

Testosterone increases proactivity and

17:07

the willingness to lean into effort in

17:10

competitive scenarios. If people are

17:12

given testosterone or if you look at

17:15

people who have different le levels,

17:18

excuse me, of testosterone indogenously

17:20

that they naturally make, what you'll

17:22

find is that testosterone tends to

17:24

increase competitiveness, but not just

17:27

in aggressive scenarios. So, if somebody

17:29

is already aggressive, giving them

17:31

testosterone will have the tendency to

17:34

make them more aggressive. If somebody

17:36

however is very benevolent and

17:38

altruistic, giving them testosterone

17:39

will make them more benevolent and

17:41

altruistic at least up to a point. Turns

17:43

out there's evidence that in certain

17:45

context estrogen can make people more

17:47

aggressive. So what's going on here?

17:50

Well, what's going on is that

17:52

testosterone can be converted into

17:55

estrogen through a process called

17:57

aromatization. There's an enzyme called

17:59

aromatase. Anytime you have a word that

18:01

ends in asse at least if it's in the

18:04

context of biology it's almost always

18:06

not always but almost always an enzyme.

18:08

So arom the aromatase enzyme converts

18:11

testosterone into estrogen and it is

18:13

actually testosterone aromatized

18:16

converted into estrogen and then binding

18:20

to these estrogen containing neurons in

18:22

the ventromedial hypothalamus that

18:25

triggers aggression. I want to repeat

18:27

that it is not testosterone itself that

18:29

triggers aggression. It is testosterone

18:31

aromatized into estrogen within the

18:34

brain and binding to these estrogen

18:36

receptor containing neurons in the

18:37

vententral medial hypothalamus that

18:39

evokes aggression and dramatic

18:41

aggression at that. Now this effect of

18:43

estrogen causing aggression in the brain

18:46

is very robust. So much so that if you

18:49

take a mouse that lacks the aromatase

18:52

enzyme or a human that lacks the

18:53

aromatase enzyme and they do exist then

18:57

there is a reduction in overall

18:59

aggression despite high levels of

19:01

testosterone. It doesn't matter how much

19:03

you increase testosterone or any of its

19:06

other derivatives you do not observe

19:08

this aggression. This runs counter to

19:11

everything that we know and think about

19:12

the role of testosterone. So the next

19:14

time somebody says testosterone makes

19:16

people aggressive, you can say ah no

19:18

actually it's estrogen that makes people

19:21

aggressive and animals aggressive for

19:23

that matter. Now of course it is the

19:25

case that because males have relatively

19:29

less estrogen circulating in their brain

19:31

and body than females, right? because

19:33

they have testes, not ovaries. That

19:36

testosterone is required in the first

19:38

place in order to be converted into

19:40

estrogen to activate this aggressive

19:42

circuit involving these estrogen

19:44

receptor containing neurons in the

19:45

ventromedial hypothalamus. So, we've

19:47

established that it's not testosterone,

19:50

but testosterone converted into estrogen

19:52

that activates these circuits for

19:54

aggression. Nonetheless, it's still

19:56

surprising, right? Right? I mean, most

19:57

of us don't think about a estrogen as

19:59

the hormone that stimulates aggression,

20:02

but turns out it's all contextual. There

20:04

are beautiful data showing that whether

20:06

or not estrogen stimulates aggression

20:08

can be powerfully modulated by whether

20:12

or not days are short or days are long.

20:14

In other words, whether or not there's a

20:16

lot of sunshine or not. Day length is

20:19

converted into hormonal signals and

20:21

chemical signals. And the primary

20:22

hormonal and chemical signals involve

20:25

melatonin and dopamine and also the

20:28

stress hormones. So to make a very long

20:29

story short, in the long days where we

20:31

get a lot of sunlight both in our eyes

20:33

and on our skin, melatonin levels are

20:35

reduced. Melatonin is a hormone that

20:37

tends to produce states of sleepiness

20:39

and quiescence. It also tends to

20:41

activate pathways that tend to reduce uh

20:43

things like breeding and sexual

20:45

behavior. In long days, dopamine is

20:48

increased. Dopamine is a molecule

20:50

associated with feelings of well-being

20:52

and motivation and the desire to seek

20:55

out all sorts of things. And in long

20:57

days, provided we're getting enough

21:00

sunlight on our skin and to our eyes,

21:03

the stress hormones, especially cortisol

21:05

and some of the other stress hormones

21:07

are reduced in levels. If estrogen

21:09

levels are increased experimentally

21:11

under long day conditions, it does not

21:14

evoke aggression. However, in short

21:16

days, if estrogen is increased, there is

21:19

a heightened predisposition for

21:21

aggression. And that makes perfect

21:24

sense. If you think about what short

21:26

days do to the biology of your brain and

21:28

body, the melatonin signal goes up.

21:30

There's more melatonin circulating for

21:32

more of each 24-hour cycle. Stress

21:34

hormones are circulating more. Why?

21:37

Short days tend to be associated with

21:38

winter. In winter, we are bombarded with

21:41

more bacteria and viruses because

21:43

bacteria and viruses actually survive

21:46

better in cold than they do in heat. So,

21:48

shorter days are conducive to

21:50

aggression, not because days are short

21:53

per se, but because stress hormone

21:55

levels are higher, and because dopamine

21:59

levels are lower. Now, here's where all

22:00

of this starts to converge on a very

22:02

clear biological picture, a very clear

22:04

psychological picture, and indeed a very

22:06

clear set of tools that we can think

22:09

about and use. Under conditions where

22:11

cortisol is high, where the stress

22:13

hormone is elevated, and under

22:16

conditions where the neurom modulator

22:17

serotonin is reduced, there is a greater

22:21

propensity for estrogen to trigger

22:23

aggression. For males who make a lot of

22:25

testosterone relative to estrogen, you

22:28

have to swap in your mind this idea that

22:30

if testosterone is high, that means that

22:32

estrogen is low. Because if testosterone

22:34

is high, there is going to be some

22:36

aromatization, that conversion of

22:38

testosterone to estrogen. So anytime you

22:40

hear that testosterone is high, you

22:42

should think testosterone is high in the

22:44

body and perhaps estrogen is low in the

22:46

body, but that means that there's going

22:47

to be heightened levels of estrogen in

22:48

the brain and therefore increased

22:51

propensity for aggression. In females

22:53

who generally make less testosterone

22:56

relative to estrogen, there is

22:57

sufficient estrogen already present to

22:59

trigger aggression. So both males and

23:02

females are primed for aggression. But

23:06

that's riding on a context and that

23:08

context of whether or not you get a

23:10

tendency for aggression or not depends

23:13

on whether or not cortisol is high or

23:15

low. And I'm telling you that if

23:16

cortisol is relatively higher in any

23:19

individual, there's going to be a tilt,

23:21

an increase in that hydraulic pressure

23:24

that Loren talked about toward

23:26

aggression.

23:28

And if serotonin, the neurom modulator

23:32

that is associated with feelings of

23:34

well-being and sometimes even of slight

23:36

passivity, but certainly of well-being,

23:39

if serotonin is low, there's also going

23:41

to be a further shift towards an

23:43

aggressive tendency. So if we return to

23:46

Lorenz's hydraulic pressure model of

23:49

aggression and other internal states, we

23:52

realize that external stimula, things

23:55

that we hear, things that we see, for

23:57

instance, someone saying something

23:58

upsetting or us seeing somebody do

24:01

something that we don't like to others

24:03

or to us, as well as our internal state,

24:08

our subjective feelings of well-being,

24:10

but also our stress level, our feelings

24:12

of whether or not we have enough

24:13

resources and are content. with what we

24:15

have all of that is converging on this

24:17

thing that we call internal state and

24:19

creating this pressure of either to be

24:21

more aggressive or less aggressive. Now

24:22

we have some major players feeding into

24:25

that final pathway that question of

24:28

whether or not will we hit the other

24:29

person. Will we say the thing that is

24:32

considered aggressive? Will we not say

24:34

it? Again, there are many things

24:36

funneling into that question and

24:38

dictating whether or not the answer is

24:39

absolutely I'll fight back or I'm going

24:41

to attack them even unprovoked. we

24:43

really can boil them down to just a few

24:45

common elements. And I'm telling you

24:46

that those elements are whether or not

24:48

cortisol levels are relatively lower or

24:52

relatively higher. Again, relatively

24:53

higher is going to tend to make people

24:55

more reactive. Why? Because

24:58

reactivity is really a function of the

25:00

autonomic nervous system, which is sort

25:02

of like a seessaw that oscillates

25:04

between the so-called sympathetic

25:07

arm of the autonomic nervous system,

25:08

which tends to put us into a state of

25:10

readiness through the release of

25:11

adrenaline. Cortisol and adrenaline when

25:13

they're circulating in the brain and

25:14

body make us more likely to move and to

25:17

react and to speak. It's actually what

25:18

will induce a kind of low-level tremor,

25:20

which is an anticipatory tremor to be

25:22

able to move more quickly. Right? a body

25:24

in motion is more easily set into

25:26

further motion. That is, and in terms of

25:28

keeping cortisol in a range that's

25:31

healthy and doesn't bias someone toward

25:33

high levels of aggression and

25:35

irritability, that's again going to be

25:37

set by a number of larger modulators or

25:40

contextual cues. And I've talked about

25:41

some of those on the podcast, but I'll

25:43

just briefly recap them now. Obviously,

25:45

getting sunlight in your eyes early in

25:47

the day and as much sunlight as you

25:50

safely can in your eyes throughout the

25:51

day is going to be important. Again,

25:54

because of this effect of estrogen in

25:56

long days, not increasing aggression.

25:59

However, in shorter days, estrogen

26:01

increases aggression because of the

26:04

increase in cortisol observed in short

26:06

days. Another way to reduce cortisol was

26:09

discussed in our episode on heat and the

26:11

use of sauna and heat, but also hot

26:13

baths. It turns out that hot baths and

26:15

sauna can be very beneficial for

26:17

reducing cortisol. All the details on

26:19

that are included in the episode on heat

26:20

and it's timestamped. So you can go

26:22

directly to that if you want to learn

26:23

about the temperatures and the various

26:25

durations. But to just give a uh

26:27

synopsis of that a 20 minute sauna at

26:31

anywhere from 80 to 100° C is going to

26:35

be beneficial for reducing cortisol. If

26:37

you don't have access to a sauna, you

26:39

could do a hot bath. And of course, some

26:41

of you may be interested in exploring

26:42

the supplementation route. And for

26:44

reductions in cortisol, really the uh

26:46

chief player there is ashwagandha, which

26:49

is known to decrease cortisol fairly

26:52

potently. I should just warn you that if

26:53

you're going to use ashwagandha in order

26:55

to reduce cortisol, first of all, check

26:57

with your doctor or healthcare provider

26:59

before adding or subtracting anything

27:01

from your supplementation or health

27:02

regimen. Of course, I don't just say

27:03

that to protect us. I say that to

27:05

protect you. You are responsible for

27:07

your health, what you take and what you

27:08

don't take. Chronic supplementation with

27:10

ashwagandha can have some not so great

27:13

effects of disruption of other hormone

27:15

pathways and neurotransmitter pathways.

27:17

So the limit seems to be about 2 weeks

27:19

of of regular use before you'd want to

27:21

take a break of about 2 weeks. So

27:24

ashwagandha again a very potent

27:25

inhibitor of cortisol but with some

27:27

other effects as well. Don't use it

27:29

chronically for longer than 2 weeks. But

27:31

if your goal is to reduce cortisol,

27:33

let's say you're going through a period

27:34

of increased irritability and aggressive

27:36

tendency, maybe you're also not getting

27:38

as much light as you would like. And

27:40

perhaps also if there are other um

27:43

circumstantial things leading you

27:44

towards more aggressiveness and your

27:45

goal is to reduce aggressiveness, that

27:47

can be potentially helpful. And in light

27:49

of all this stuff about cortisol and

27:52

estrogen and daylength,

27:54

I should mention that there are in fact

27:57

some people who have a genetic

27:58

predisposition to be more irritable and

28:02

aggressive. There is a genetic variant

28:06

present in certain people that adjusts

28:09

their estrogen receptor sensitivity

28:12

and that estrogen receptor sensitivity

28:15

can result in increased levels of

28:17

aggression. sometimes dramatic

28:19

increases. However, and also very

28:22

interestingly, photo period, meaning

28:24

daylength is a strong modulator of

28:28

whether or not that aggressiveness turns

28:30

up or not. Whether or not that person

28:33

with the particular gene variant is more

28:36

aggressive or not depends on how long

28:38

the day is and how long the night is.

28:40

One particular study that I like that

28:42

references this is trainer at all. The

28:45

title of the study is photo period

28:46

reverses the effects of estrogens on

28:48

male aggression via genomic and

28:50

non-genomic pathways. This was a paper

28:52

published in the proceedings of the

28:54

National Academy of Sciences. It really

28:55

points to the fact that rarely is it the

28:58

case that just one gene will cause

29:01

somebody to be hyperaggressive.

29:03

Almost always there's going to be an

29:05

interplay between genetics and

29:06

environment. And as environment changes,

29:09

such as daylength changes and the length

29:11

of night changes, so too will the

29:12

tendency for people with a given genetic

29:15

variant to be more aggressive or not.

29:18

Now, of course, in the absence of

29:19

detailed genetic testing for this

29:21

particular estrogen receptor variant,

29:23

most people, I'm guessing you are

29:24

probably not walking around knowing that

29:26

you have this gene or not.

29:29

Regardless, I think it's important to

29:31

pay attention to how you feel at

29:33

different times of year depending on

29:35

whether or not summer, whether or not

29:36

it's winter, whether or not you're

29:37

getting sufficient sunlight, meaning

29:40

viewing sufficient sunlight or not,

29:41

whether or not you're getting sufficient

29:42

sunlight exposure to your skin or not,

29:44

whether or not you're indoors all the

29:46

time. Generally, those things correlate

29:48

with season, but not always. You can go

29:51

through long bouts of you know hard work

29:53

in the summer months when days are long

29:55

but you're indoors a lot and getting a

29:56

lot of fluorescent light exposure late

29:58

in the evening and perhaps that's when

29:59

you're feeling more aggressive. So we

30:01

have to be careful about drawing a

30:02

onetoone relationship between any

30:04

biological feature and certainly

30:06

psychological or behavioral feature like

30:08

aggressiveness. But it's I believe

30:10

helpful to know that these genetic

30:12

biases exist. How they play out again

30:15

they shift our biology in in a general

30:18

thematic direction. They don't change

30:20

one thing. They change a variety of

30:22

things that bias us toward or away from

30:24

certain psychological and behavioral

30:25

outcomes and the various things that we

30:28

can do in order to offset them. And we

30:30

described those earlier in terms of

30:32

trying to keep cortisol low by getting

30:33

sufficient sunlight regardless of time

30:35

of year and regardless of whether or not

30:37

you happen to have this particular

30:39

genetic variant. I want to share with

30:40

you a study that's focused on kids, but

30:43

that has important ramifications for

30:46

adults as well. There are many kids out

30:48

there that suffer from so-called

30:49

attention deficit hyperactivity disorder

30:51

or ADHD. There are also many adults we

30:54

are finding that are suffering from

30:55

ADHD. In any event, the study I'm about

30:58

to share with you explored how a

30:59

particular pattern of supplementation in

31:02

kids with ADHD was able to reduce

31:05

aggressive episodes and impulsivity and

31:08

increase self-regulation.

31:10

And the title of the study is efficacy

31:12

of carnitine in the treatment of

31:13

children with attention deficit

31:15

hyperactivity disorder. even though they

31:17

put carnitine in the title that what

31:18

they focused on was whether or not a

31:21

cetal LC carnitine supplementation could

31:24

somehow adjust the behavioral tendency

31:26

of these kids with ADHD. And to make a

31:28

long story short, indeed it did. There

31:31

was a very significant effect of acetyl

31:33

carnitine supplementation on improving

31:35

some of the symptomology symptomology,

31:37

excuse me, of ADHD. This was a

31:40

randomized double blind placeboc control

31:41

double crossover study. They showed

31:43

significant reductions in their

31:45

so-called total problem score. The total

31:47

problem score is a well-established

31:49

measure of behavioral problems in kids

31:51

with ADHD and I should say adults with

31:54

ADHD. Reductions in attentional problems

31:56

overall reductions in delinquency and

31:59

most important for sake of today's

32:00

discussion significant reductions in

32:03

aggressive behavior. They were able to

32:05

confirm the shifts in alcarnitine

32:08

within the bloodstream of these kids.

32:09

that is they were able to correlate the

32:11

physiology with the psychological

32:13

changes. So studies such as this I think

32:15

are useful because they point to the

32:17

fact that

32:19

very seldom if ever will there be one

32:21

supplement or one nutritional change or

32:24

even one behavioral change that's going

32:26

to completely shift an individual from

32:28

being aggressive and impulsive. rather

32:31

that by combining different behavioral

32:34

regimens, by paying attention to things

32:36

like time of year and work conditions

32:38

and school conditions and overall levels

32:40

of stress and likely therefore levels of

32:43

cortisol, etc. that you can use

32:45

behaviors, diet, and supplementation as

32:48

a way to shift that overall internal

32:50

millu from one of providing a lot of

32:53

internal hydraulic pressure, as it's

32:55

been called throughout the episode,

32:57

toward aggressive impulsivity and relax

33:00

some of that hydraulic pressure and

33:02

reduce aggressive tendencies. Thank you

33:04

for joining me for our discussion about

33:06

the biology, psychology, and actionable

33:09

tools around aggression. And as always,

33:12

thank you for your interest in science.

Interactive Summary

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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