Huberman Lab - Erasing Fears & Traumas Based on the Modern Neuroscience of Fear

Welcome to the Huberman Lab Podcast,

where we discuss science

and science-based tools for everyday life.

I’m Andrew Huberman,

and I’m a professor of neurobiology and ophthalmology

at Stanford School of Medicine.

Today, we’re going to talk about the neuroscience of fear.

We are also going to talk about trauma

and post-traumatic stress disorders.

The neuroscience of fear has a long history in biology

and in the field of psychology.

However, I think it’s fair to say that in the last 10 years

the field of neuroscience has shed light

on not just the neural circuits,

meaning the areas of the brain

that control the fear response and the ways that it does it,

but some important ways to extinguish fears

using behavioral therapies, drug therapies,

and what we call brain-machine interfaces.

Today, we are going to talk about all of those,

and you are going to come away

with both an understanding of the biology of fear

and trauma, as well as many practical tools

to confront fear and trauma.

In fact, we are going to discuss

one very recently published study

in which five minutes a day of deliberate exposure to stress

was shown to alleviate longstanding depressive

and fear-related symptoms.

We will get into the details of that study

and the protocol that emerges from that study

a little later in the podcast,

but it stands as a really important,

somewhat counterintuitive example

of how stress itself can be used to combat fear.

To give you a sense of where we are going,

I’ll just lay out the framework for today’s podcast.

First, I’m going to teach you

about the biology of fear and trauma,

literally the cells and circuits

and connections in the body and chemicals in the body

that give rise to the so-called fear response,

and why sometimes, but not always,

fear can turn into trauma.

I will also describe the biology of how fear is unlearned

or what we call extinguished.

And there too, you’re going to get some serious surprises.

You’re going to learn, for instance,

that we can’t just eliminate fears,

we actually have to replace fears with a new positive event.

And again, there are tools with which to do that,

and I will teach you those tools today.

Before we begin, I’d like to emphasize

that this podcast is separate from my teaching

and research roles at Stanford.

It is, however, part of my desire and effort

to bring zero cost to consumer information about science

and science-related tools to the general public.

In keeping with that theme,

I’d like to thank the sponsors of today’s podcast.

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So what is fear?

Well, fear falls into a category

of nervous system phenomenon

that we can reliably call an emotion,

and it is hotly debated nowadays,

and it’s been hotly debated really for centuries

what an emotion is and what an emotion isn’t.

Now, that’s not a debate that I want to get into today.

I think it’s fair to say that emotions include responses

within our body, quickening of heart rate,

changes in blood flow,

things that we experience as a warming

or a cooling of our skin,

but that there’s also a cognitive component.

There are thoughts, there are memories,

there’s all sorts of stuff that goes on in our mind

and in our body that together we call an emotion.

And there’s a vast amount of interest

and literature devoted to trying to understand

how many different emotions there are,

how different people experience emotions,

and that’s certainly a topic that we will embrace

in a future podcast episode.

But today, I just want to talk about fear as a response,

because when we talk about fear as a physiological response

and as a cognitive response,

then we can get down to some very concrete mechanisms

and some very concrete and practical tools

that can be used to deal with fear when fear is not wanted.

So let’s talk first about what fear isn’t.

Most people are familiar with stress,

both as a concept and as an experience.

Stress is a physiological response.

It involves quickening of the heart rate,

typically quickening of breathing,

blood flow getting shuttled to certain areas

of the brain and body and not to others.

It can create a hypervigilance or an awareness.

Typically that awareness is narrower,

literally narrower in space,

like a soda straw view of the world,

than when we are relaxed.

And it is fair to say that we cannot have fear

without having several,

if not all of the elements of the stress response.

However, we can have stress without having fear.

Likewise, people are familiar with the phrase

or the word rather, anxiety.

Anxiety tends to be stress about some future event,

although it can mean other things as well.

We can’t really have fear without seeing or observing

or experiencing some of the elements of anxiety,

but we can have anxiety without having fear.

So what you’re starting to realize is that fear is built up

from certain basic elements that include stress and anxiety.

And then there is trauma.

And trauma also requires a specific,

what we will call operational definition.

An operational definition is just a definition

that allows us to have a conversation

because we both agree on or mostly agree on

what the meaning of a given word is.

It makes conversations much easier.

In fact, I would argue,

if we all had operational definitions

for more things in the world,

that there would be fewer misunderstandings and arguments,

and we’d all move a lot further as a species.

But that’s another topic entirely.

The operational definition of trauma

is that some fear took place,

which of course includes stress and anxiety.

And that fear somehow gets embedded

or activated in our nervous system,

such that it shows up at times when it’s maladaptive,

meaning that fear doesn’t serve us well,

and it gets reactivated at various times.

Like when you first wake up in the morning,

if you’re not in the presence of something that scared you,

but you suddenly have what feels like a panic attack

and you’re in deep fear, well, that’s post-traumatic stress.

That’s post-traumatic fear.

So I don’t want to get bogged down

too much in the nomenclature,

but what I’m doing here is building up

a sort of a series of layers where stress and anxiety

form the foundation of what we’re calling fear and trauma.

And then there are other phrases out there

that we would be remiss if we didn’t mention

things like phobias and panic attacks.

Panic attacks are the experience of extreme fear,

but without any fear-inducing stimulus.

So it’s kind of like trauma.

And a phobia tends to be extreme fear

of something specific, fear of spiders, fear of heights,

fear of flying, fear of dying, these kinds of things, okay?

The reason for laying all that out there

is not to create a word soup to confuse us,

rather it is to simplify the issue.

Because now that we acknowledge

that there are many different phrases

to describe this thing that we call fear

and in related phenomenon,

we can start to just focus on two of these issues,

fear and trauma,

as it relates to specific biological processes,

specific cognitive processes,

and we can start to dissect how fears are formed,

how fears are unformed,

and how new memories can come to replace

previously fearful experiences.

So in this effort to establish a common language

around fear and trauma,

I want to point out autonomic arousal.

Autonomic arousal relates to this aspect

of our nervous system

that we call the autonomic nervous system.

Autonomic means automatic,

that’s somewhat of a misnomer

because there are aspects of your autonomic nervous system

that you can control,

but your autonomic nervous system controls things

like digestion, urination, sexual behavior,

stress, when you want to be awake,

when you want to be asleep.

It basically has two branches to it,

two branches meaning two different systems.

One is the so-called sympathetic autonomic nervous system,

has nothing to do with sympathy,

it has everything to do with increasing alertness.

Think of the sympathetic nervous system

as the alertness nervous system.

It’s what ramps up your levels of alertness,

ramps up your levels of vigilance.

Think about it as the accelerator

on your alertness and attention.

The other branch of the autonomic nervous system

is the so-called parasympathetic branch

of the autonomic nervous system.

I know that’s a mouthful.

The parasympathetic branch of the autonomic nervous system

are the cells and neurons and chemicals

and other aspects of your brain and body

that are involved in the calming nervous system.

So sympathetic is alerting, parasympathetic is calming,

and it acts as sort of a seesaw

to adjust your overall level of alertness.

So for instance, right now I’m alert,

but I feel pretty calm.

I’m not ready to go to sleep or anything like that.

I don’t feel like I need a nap.

I’m alert, but I’m calm.

I’m not in a state of stress or panic.

So that seesaw we could imagine is more or less level.

Maybe it’s tilted up a little bit

to the side of increased sympathetic or alertness

rather than parasympathetic because I feel wide awake.

If I were sleepy, the opposite would be true.

The parasympathetic side would be increased

relative to the sympathetic side.

There are many different aspects

to the autonomic nervous system,

but one of the main aspects is an aspect

that’s going to come up again and again and again today.

It’s very important that you understand what it is.

It’s called the HPA axis.

The HPA axis stands for hypothalamic pituitary adrenal axis.

The hypothalamus is a collection of neurons.

It’s an area of your brain real estate

that’s deep in the brain at the base of the brain

that contains many, many different areas

that control things like temperature

and desire to have sex, desire to eat, thirst.

It also controls the desire to not mate, have sex,

not eat, not drink more water or any other type of fluid.

So it has accelerators and brakes in there as well.

The hypothalamus connects to the so-called pituitary.

The pituitary lives close to the roof of your mouth.

It releases hormones into your bloodstream.

And so the hypothalamus has this ability

to trigger the release or prevent the release

of particular hormones like cortisol

or the hormones that go stimulate ovaries to produce estrogen

or testes to produce testosterone

or adrenals to produce adrenaline.

And speaking of the adrenals,

that A in the HPA are the adrenals.

You have two glands that sit above your kidneys

in your lower back.

They receive signals by way of nerve cells, neurons,

and by way of hormones and other things

released from the brain and elsewhere in the body.

And they release different hormones

and other types of chemicals into the body.

And the two main ones that you need to know about today

are adrenaline, also called epinephrine, and cortisol.

Both of those are so-called stress hormones,

but they’re not always involved in stress.

They’re also involved in waking up in the morning

when you arise, when you, excuse me,

when you rise from sleep.

And so this HPA axis should be thought of

in the following way.

The HPA axis includes a piece of the brain,

the hypothalamus, the pituitary, and the adrenal.

So it’s a beautiful three-part system

that can use your brain to alert or wake up your body

and prepare it for action.

And it can do that in the short term

by triggering the release of hormones and chemicals

that make you alert and ready to go right away.

And by triggering the release of neurotransmitters

and hormones and other chemicals

that give that alertness a very long tail,

a very long latency before it shuts off.

And that’s important because one of the hallmarks of fear

and one of the hallmarks of trauma

is that they involve fear responses that are long lasting,

even if those fearful events,

the events in the world that trigger the HPA axis

can be very brief,

like a car that almost hits you as you step off the curb

or something, a gunshot that goes off suddenly,

and it’s just a very quick,

like 500 millisecond or one second event.

The fear response can reverberate through your system

because the chemicals that are involved in this HPA axis

have a fast component and a longer lasting component.

And the longer lasting component can actually change

not just the connections of different areas of the brain

and the way that our organs work, like our heart

and the way that we breathe,

it actually can feed back to the brain

and literally control gene expression,

which can take many days and build out new circuits

and new chemicals that can embed fear in our brain and body.

And that might sound very depressing,

but there’s a reason and there’s an adaptive reason

why there’s the slow and fast phase of the HPA axis

and the fear response.

And fortunately, that gene expression

and the long arc of the fear response,

the way it kind of lives in our system,

kind of like a phantom in some ways,

can also be leveraged to undo the fear response,

to extinguish the fear response

and replace it with non-fearful associations.

So let’s dig a little deeper into the neural circuits

and biology of fear, because in doing that,

we can start to reveal the logic of how to attack fear

if that’s the goal.

We can’t really have a discussion about fear

without discussing the famous amygdala.

Famous because I think most people by now

have heard of the amygdala.

Amygdala means almond.

It’s an almond shaped structure on both sides of the brain.

So you have one on the right side of your brain

and one on the left side of your brain.

The amygdala is part of what we can call the threat reflex.

And this is very important to conceptualize fear

as including a reflex.

So much as you have reflexes

that cause you to lift your foot up

if you are to step on something sharp,

you literally have a reflex within your spinal cord

that causes you to lift up one foot

and extend the other one toward the ground.

Believe it or not, you always think

that you step on something sharp, you pull your foot up,

but you actually step on something sharp,

you pull your foot up and in pulling it up,

there’s another reflex that’s activated

that as you extend your other leg

so that you don’t fall over.

Similarly, in the process of experiencing fear,

you have a reflex for particular events

in your brain and body.

And that reflex involves things

like quickening of your heart rate, hypervigilance,

your attentional systems pop on,

increased ability to access energy stores

for movement and thought and so forth.

But just like that step on the tack reflex example,

all of the neural circuits that are associated

with being calm, with being able to go to sleep,

with being able to visualize the full picture

of your environment, literally,

to see your entire environment

or to hear other things around you,

all of those get shut down

when the so-called threat reflex gets activated.

And the amygdala is part of the threat reflex

so much so that we can really say

that it’s the final common pathway

through which the threat reflex flows.

In other words, the amygdala is essential

for the threat response.

But the threat reflex and the threat response

is kind of a dumb response.

It’s not a sophisticated thing.

It’s very generic.

And this is also a very important point.

One of the beauties of the fear system

is that it’s very generalizable.

It’s not designed for you to be afraid of any one thing.

Sure, there are some debates

and probably some good data out there

that support the fact that human babies are innately,

meaning it requires no learning,

innately afraid of certain things

like heights or snakes or spiders.

There’s debate about this

depends on the quality of the experiment, et cetera.

But the real capacity of the fear system

is that we can become afraid of anything

provided that this threat system is activated

in conjunction with some external experience.

So the way I’d like you to think about the amygdala

is not as a fear center,

but that it’s a critical component of the threat reflex.

I’d like you to also internalize the idea

that the threat reflex involves

this activation of certain systems

and suppression of all the systems for calming,

the parasympathetic system.

And now I’m going to describe the way

that information flows into and through this threat reflex.

And in doing that, it will reveal how specific things

like a spider, like a snake, like a physical trauma,

like a car accident, like a fear of public speaking,

whatever happens to scare you or scare somebody,

how that gets attached to this reflex.

Because this reflex is very generic.

It doesn’t really know what to be afraid of.

It only knows how to create the sensation,

this internal landscape that we think of as fear.

So while the amygdala might look like an almond,

it’s actually part of a much bigger complex

or collection of neurons called the amygdaloid complex.

That complex has anywhere from 12 to 14 areas,

depending on which neuroanatomist is naming things

and carving it up.

In neuroscience and in much of biology,

we like to joke that there are lumpers

and there are splitters.

So some people like to draw boundaries

between every little distinct difference and say,

oh, that’s a separate area and other people are lumpers.

And they say, well, listen, why complicate things?

Let’s lump those together.

I’m neither a lumper nor a splitter.

I’m somewhere in between.

I think the number 12 is a good number

in terms of the number of different areas of the amygdala.

Why is that important to us?

Well, it turns out that the amygdala

is not just a area for threat.

It’s an area for generating threat reflexes

that integrates lots of different types of information.

So for those of you that want to know,

I’m going to give you some names, some nomenclature.

For those of you that don’t, you can tune out for this,

but basically information from our memory systems

like the hippocampus and from our sensory systems,

our eyes, our ears, our nose, our mouth, et cetera.

So taste information, vision, auditory information,

touch, et cetera,

flow into the so-called lateral portion of the amygdala,

flows into, or the amygdaloid complex.

It flows into the lateral portion.

And then there are multiple outputs from the amygdala.

And this is where things get particularly interesting

because the outputs of the amygdala

have a lot of different areas,

but there are two main pathways.

One involves the hypothalamus,

which you heard about before,

this collection of neurons that control

a lot of our primitive drives for sex, for food,

for thirst, and for warmth, et cetera.

And it also feeds out to our adrenals,

those glands that you learned about a few minutes ago,

to create a sense of alertness and action.

It also feeds out, what I mean by feeds out, by the way,

is there are neurons that send wires,

we call those wires axons, connections,

where they can release chemicals

and trigger the activation of different brain areas.

So it feeds out to other brain areas, such as the PAG.

PAG is very interesting for our discussion today.

It’s the periaqueductal gray.

The periaqueductal gray contains neurons

that can trigger freezing, can trigger the,

some people talk about the fawning response,

which is kind of an appeasing response to traumatic events,

but some people outright freeze in response to fear, right?

We’ve heard of fight or flight,

and indeed the pathway that I’m describing

can create a sense of fight

and cause people to want to lean in in an aggressive way

to combat things that they’re afraid of,

or flight, to run away,

essentially to avoid, by mobilizing,

the thing that they feel they’re threatened by.

Now, even in the absence of some threat,

somebody that has, say, a fear of public speaking

might hesitate or move away from a podium,

or hesitate or move away from raising their hand,

if raising their hand meant that they might be called on

and would be public speaking.

So there’s fight and flight,

but there’s also the freeze response.

And the freeze response

is controlled by a number of brain centers,

but the periaqueductal grade, the PAG,

is central for this freeze response.

And neurons there also create

what are called endogenous opioids.

Many of you have heard of the opioid crisis,

which is a crisis of prescription medication

given out too broadly for people that don’t need it,

who become addicted to opioids.

Those are exogenous opioids.

But endogenous opioids are chemicals released from neurons

in the PAG and from elsewhere in the body

that give us a sense of numbing.

They actually numb us against pain.

And you can imagine why biology would be organized this way.

A threat occurs or something that we perceive as a threat,

we’re afraid of it,

and a natural analgesic is released into our body

because there’s likely to be an interaction

that’s very uncomfortable,

that’s physically uncomfortable.

So it’s like we have our own endogenous release

of these opioids, and that’s occurring in the PAG.

The other area, and again,

sorry to litter the conversation

with these names of structures,

but some people seem to enjoy knowing these structures.

You’re fine if you just understand what the structures do.

If you want to know the names, that’s fine.

But the other structure is the locus coeruleus.

The locus coeruleus creates a sense of arousal

by releasing adrenaline, epinephrine, and norepinephrine,

a related chemical into the brain.

So basically the activation of the amygdaloid complex

could be from any number of different things,

a memory of something fearful,

an actual sensory experience of something that’s fearful.

But then the fear response itself

is taking part because of the threat reflex gets activated.

And that’s threat reflex,

then sends a whole set of other functions into action,

freezing, activation of the adrenals,

activation of locus coeruleus for arousal and alertness,

activation of this endogenous pain system

or anti-pain system in the PAG.

That’s one pathway out of the amygdala.

The other pathway out of the amygdala

is to a very interesting area

that typically is associated with reward and even addiction.

So this might come as a surprise to many of you.

In fact, it came as a surprise to me.

I remember when these data were published,

but the amygdaloid complex actually projects

to areas of the dopamine system,

the so-called nucleus accumbens,

the mesolimbic reward pathway.

For those of you that want to look that up

or that remember from the dopamine episodes,

we have pathways in our brain

that are associated with pursuit, motivation, and reward.

And the neuromodulator dopamine is largely responsible

for that feeling of craving, pursuit, and reward.

And this threat center is actually able to communicate with

and activate the dopamine system.

And later you will realize why that is very important

and why you can leverage the dopamine system

in order to wire in new memories to replace fearful ones.

So I’ve been hitting you with a lot of names of things,

but for the moment,

even if you’re interested in all the neuroscience names

and structures and so forth,

I’d like you to just conceptualize

that you have a circuit in your brain,

meaning a set of cells and connections

that are arranged in the following way.

You have a threat reflex that can be activated

at any time very easily.

But what activates that threat reflex

can depend on two things.

One are prior memories coming from brain areas

that are involved in storage of memories,

or it can be immediate experiences,

things that are happening in the now, okay?

So were something fearful to happen right now,

your threat reflex could be activated.

Were you to remember something very scary

that happened to you in the past,

your threat reflex could be activated.

And that threat reflex circuit has two major outputs.

One of the major outputs is to areas that are involved

in the threat response, freezing, pain management,

and alertness.

And the other major output is to areas involved in reward,

motivation, and reinforcement, okay?

There’s a fourth component,

and I promise this is the last component

that we need to put into this picture

of the neural circuits for fear.

And this is a circuit that involves an area of the brain

called the prefrontal cortex and some of its subdivisions.

So literally in the front,

and it’s involved in what we call top-down processing.

Top-down processing is the way that your prefrontal cortex

and other areas of the brain can control

or suppress a reflex, okay?

A good example of this would be the step on the tack example

that I gave before.

So when you step on a tack,

you immediately pull up your foot

and you extend the other leg.

That’s the reflex that prevents you from injuring yourself

and from falling over.

However, if you wanted, not that you would want to,

but if you wanted, you could, for instance,

place your foot onto a tack

and decide not to pull your foot away.

It would be difficult.

And again, I don’t recommend that you do that,

but you could override that reflex, okay?

There are other examples of reflexes,

like for instance, getting into cold water.

Most people will start to, you know, huddle their body.

Most people won’t want to get into the cold water.

Many people will jump out, but all of that is reflexive.

And should you want to,

you could override that reflex through top-down processing.

You could tell yourself,

oh, I heard on a previous Huberman Lab podcast

or on an Instagram post that cold water exposure

can be beneficial for metabolism and resilience, et cetera.

And indeed it can.

And you can decide to get into the water

and to stretch out your body, not to huddle.

And you can fight those reflexes, okay?

The fighting of reflex is carried out

through top-down processing,

largely through the prefrontal cortex.

You provide a narrative, you tell yourself,

I want to do this, or I should do this,

or even though I don’t want to, I’m going to do it anyway.

So top-down processing is not just

for getting into cold water,

and it certainly isn’t for overriding reflexes

that can damage us, like a stepping on the tack example.

It is the way in which we can override

any number of internal reflexes,

including the threat reflex.

And the way that we do that is by giving a new story

or a new narrative to this experience that we call threat.

And you know the threat response.

The threat response is quickening of the heart rate,

quickening of the breathing.

We don’t generally like the feeling of adrenaline

in our system.

Some people are so-called adrenaline junkies,

and they get a mixture of dopamine and adrenaline

from certain high intensity events.

I confess in previous aspects of my life,

I’ve tended to like adrenaline.

I don’t think I was at the extreme of thrill-seeking,

but I’m somebody that, for instance,

I tend to like roller coasters.

I’ve done various things where I’m familiar with

and I enjoy the sensation of adrenaline in my body,

but I enjoy it because of the alertness that it brings

and the hyperacuity that it brings.

Many people don’t feel that way.

In fact, most people don’t like the sensation

of a lot of adrenaline in their system.

It makes them feel very uncomfortable and out of control.

We will do an entire episode about adrenaline

and adrenaline junkies and adrenaline aversives

in the future.

But the threat reflex inevitably involves the release

of adrenaline into the system.

And then it becomes a question of whether or not

you remain still, move forward or retreat

from that adrenaline experience.

And when I say the adrenaline experience,

I mean the threat reflex.

So this fourth component of fear is really our ability

to attach narrative, to attach meaning and to attach purpose

to what is by all accounts and purposes a generic response.

There’s no negotiating what fear feels like.

There’s only negotiating what it means.

There’s only negotiating whether or not you persist,

whether or not you pause or whether or not you retreat.

So this is usually the point in the podcast

where I think people start asking,

okay, well, there’s the biology, there’s the mechanism,

there’s the logic, how do I eliminate fear?

Well, it’s not quite that simple,

although by understanding the logic and the mechanisms

by which these circuits are built,

we can eventually get to that place.

I do want to plant a flag around a particular type of tool

or a logical framework around a particular set of tools

rather that we are going to build out through this episode.

And based on what you now know,

that the threat reflex gets input and it has outputs

and it’s subject to these top-down processing events,

these narratives, you should be asking yourself,

what sort of narrative should I apply to eliminate fear?

Well, first let’s take a step back

and just acknowledge the reality,

which is that fear is in some cases an adaptive response.

We don’t want people eliminating fears

that can get them injured or killed, right?

The reason that the fear threat response

and reflex exists at all is to help us from dying,

to help us from making really bad decisions.

It just so happens that a number of things happen to us

that are not lethal, that don’t harm us,

but that harm us from the inside.

And I think that, and here I’m borrowing language

from an excellent researcher

who’s done important work in this area at Harvard.

His name is Dr. Kerry Ressler.

He’s both a medical doctor and a PhD, so an MD-PhD.

He’s the chief scientific officer at McLean Hospital.

He’s a professor of psychiatry at Harvard Medical School,

and he’s done extensive and important work on fear.

I’m going to refer back to Dr. Ressler’s work

several times during this podcast,

including important and super interesting work

on transgenerational passage of trauma.

He’s a absolutely world-class biologist,

absolutely world-class clinician.

And Dr. Ressler has described fear before

as containing a historical component.

So it’s not just about a readiness for things

that might injure us or kill us in the immediate circumstance

but also protecting us for the future

because of our important need and ability to anticipate.

And what he describes are memories as protective

or memories as dangerous.

Some memories, even if they evoke a sense of fear in us,

are protective.

They protect us from making bad mistakes

that could get us injured or killed

or put us into really horrible circumstances.

Other memories are dangerous

because they create a sense in us of discomfort

and they tend to limit our behavior

in ways that are maladaptive,

that prevent us from having healthy relationships to others,

healthy job relationships,

healthy relationship to ourselves, frankly.

So this language of memories as protective

or memories as dangerous in the context of fear

is not something that I said.

It’s really something that I lifted from Dr. Ressler

in one of his many impressive lectures.

And it’s an important aspect of fear

because much of the fear system is a memory system.

It’s designed to embed a memory

of certain previous experiences in us

such that the threat reflex is activated

in anticipation of what might happen, okay?

So let’s talk for a second about how certain memories

get attached to this fear system.

And this brings us to a beautiful

and indeed Nobel prize winning aspect

of biology and physiology, which is Pavlovian conditioning.

Many of you are probably familiar with Pavlov’s dogs

and the famous Pavlovian conditioning experiments.

They go something like this.

You know, if you and Pavlov did these experiments

and ring a bell, a dog doesn’t do much

in response to a bell.

It might attend to it,

but it doesn’t salivate typically in response to the bell.

However, if you pair the ringing of a bell

with a presentation of food enough times,

the dog will salivate in response to the food.

Eventually you take away the food,

you just ring the bell

and the dog will salivate in response to the bell, okay?

So in the context of so-called Pavlovian conditioning,

these things have names like condition stimulus

and unconditional stimulus and responses.

People often get these mixed up

and it can be a little confusing,

but I’m just going to make it really simple for you.

The unconditioned stimulus is the thing

that evokes a response unconditionally.

So food is the unconditioned stimulus

in the example I just gave.

A foot shock or a loud bang would be

the unconditioned stimulus in, for instance,

an experiment geared toward exploring fear.

That unconditioned stimulus is unconditional.

It unconditionally evokes a startle

or in the case of food, salivating.

The bell in the previous example

is what we call the conditioned stimulus

or the conditioning stimulus.

Sometimes people mix these up.

The conditioned stimulus is paired with the thing

that naturally creates a response.

And then eventually the conditioned stimulus

creates the response itself.

You might think, well, that just seems, you know,

endlessly boring and simple,

but this is actually the way that our fear systems work.

Except unlike Pavlov’s dogs,

you don’t need many, many pairings of a bell

with some unconditioned stimulus in order to get a response.

You can get what’s called one trial learning.

And in this circuit that involves the amygdala,

the threat reflex, and all this other, you know,

stuff that I was talking about earlier,

the system is set up for learning.

It’s set up to create memories and to anticipate problems.

It’s a very good system

because it was designed to keep us safe.

And so the way to think about this is that for many people,

one intense experience, one burn, one bad breakup,

one bad experience, public speaking,

one bad experience with somebody’s pet snake

or whatever it happens to be

can cause intense fear in the moment,

a long reverberatory experience of fear,

like trouble sleeping that night and the following night,

memories of the experience that are troubling,

physiological responses that are troubling.

Essentially, it gets wired in as a fear with one trial,

which is quite different

than the other forms of neuroplasticity.

Neuroplasticity, of course,

just being the nervous system’s ability to change

in response to experience.

Other forms of neuroplasticity like learning a language,

learning music, learning math, those take a while.

We don’t generally get one trial learning

to positive or neutral experiences.

We get one trial learning to negative experiences.

So there’s this asymmetry in how we’re wired.

So now you should understand how classical conditioning

as it’s called occurs.

You go to give a piano recital as a kid,

you sit down and you freeze up and it’s horribly embarrassing

and even if you just freeze up for a few seconds,

the heart rate increase and the perspiring,

the sweating, and the shame that you feel

leads you to want to avoid playing instruments

or public displays of performances

for a long period of time

unless you do something to overcome it.

That’s one trial learning.

Some people, it tends to be more

an accumulation of experiences.

They have a bad relationship that lasts an entire summer,

an entire year, or God forbid, a decade.

And then they have what they feel

of a general sense of fear

about closeness to others and attachment.

These are common fears that people experience.

Fears can be in the short-term,

fears can be in the long-term,

they can be in the medium-term.

Again, the fear system is very generic.

It’s wired to include memories that are very acute,

that happen within a moment,

or that include many, many events in long periods of time

that kind of funnel into a general sense of,

you know, relationships are bad

or this particular city or location is bad.

So there’s a key, what we call temporal component.

There’s a component of the fear system

being able to batch many events in time

and create one specific fear,

or take one very specific isolated incident

that happened very briefly

and create one very large general sense of fears.

And I’ll give an example of the latter

just to kind of flesh this out a little bit.

I had a friend come visit me in San Francisco

some years ago and their car got broken into,

unfortunately, a frequent occurrence in San Francisco

in the middle of the day.

Never leave anything in your car in San Francisco.

They’ll break in in the middle of the day, doesn’t matter.

Police can be having coffee right there

in front of them, they’ll still do it.

For reasons we could discuss, this is a problem.

They got their belongings taken

and they decided they were never coming back

to San Francisco.

This was an isolated incident

that forever colored their view of the city,

which I, frankly, understanding the fear system,

I can understand.

We can have isolated incidents

that wick out to broad decisions about entire places,

or we can have many experiences

that funnel into very specific isolated fears

about particular circumstances, places, and things.

So I like to think that by now

you have a pretty good understanding

of the circuits that underlie the threat reflex,

the fear response, and how we have top-down control,

meaning we can attach a narrative to the fear response,

and that the fear response can be learned

in association with particular events, okay?

I haven’t really talked about how the learning occurs.

And so I just want to take a moment and describe that

because it leads right into our discussion

about how to eliminate fears,

and indeed how to replace fears

with more positive experiences.

There’s a process in our nervous system

that we call neuroplasticity.

Neuroplasticity broadly defined

is the nervous system’s ability

to change in response to experience.

But at a cellular level,

that occurs through a couple of different mechanisms.

One of the main mechanisms

is something called long-term potentiation.

Long-term potentiation involves the strengthening

of particular connections between neurons,

the connection sites between neurons we call synapses.

Actually, technically, synapses are the gaps

between those connections,

but nonetheless,

synapses are the point of communication between neurons,

and those can be strengthened

so that certain neurons can talk to other neurons

more robustly than they happened to before.

And anytime we talk about a particular event,

the car, the snake, the public speaking,

the trauma, the horrible experience,

wiring into the fear system,

what we’re talking about is a change in synaptic strengths.

We’re talking about neurons

that previously did not communicate well,

communicating very well.

It’s like going from a old school dial-up connection,

or even an old school telephone connection,

or Morse code connection of communication

to high-speed ethernet, to a 5G connection.

It gets faster, it gets more robust,

and it’s very, very clear.

That’s what happens when you get long-term potentiation.

And long-term potentiation

involves a couple of cellular mechanisms

that are going to be relevant to our discussion

about treatments to undo fear.

And I’ll just throw out a couple of the names

of some of those cellular elements right now.

The main one is the so-called NMDA receptor,

N-methyl-D-aspartate receptor.

And what this is, is this is a little docking site,

like a little parking slot on a neuron.

And when a neuron gets activated very strongly,

like from an intense event,

in the example of my friend, the intense event,

almost certainly activated NMDA receptors

related to their concept of protecting their property

in their cars, the break-in to their car

caused the NMDA receptor to be activated.

Normally, that NMDA receptor is not easily activated.

When it is activated, it sets off a cascade,

a series of signals within those neurons

that change those neurons.

It changes the genes they express.

It shuttles more parking spots

to the surface of those cells

so that the communication to those cells becomes easier.

It becomes faster.

And so the way to think about the NMDA receptor

is it’s used sometimes for normal things

that we do every day,

making cups of coffee and things like that,

but it’s often used for learning.

It’s used for creating new associations

in our nervous system.

And so the activation of the NMDA receptor and LTP,

and it involves some other things

that you may have heard of,

like brain-derived nootropic factors and calcium entry,

things that we can leave for a discussion for a future time.

But basically a whole cascade of events happen within cells

that then make just even the mere thought of something

or somebody or some event that happened

able to activate that threat reflex, okay?

So long-term potentiation is one of the main mechanisms

by which we take formerly innocuous or irrelevant events

and we make them scary.

We make them traumatic.

Our neurons have mechanisms to do this.

Now, fortunately, the NMDA receptor

and long-term potentiation

can also run the whole system in reverse.

You can get what’s called long-term depression,

and that doesn’t have anything to do

with the depression associated with low mood.

What we’re talking about is a weakening of connections.

You can go from having a very high-speed ethernet connection

between neurons, so to speak,

to a connection that’s more like Morse code

or is like a poor dial-up connection, a really weak signal.

And that’s what’s happening when you extinguish a fear,

when you unlearn a fear.

So now I’d like to talk about therapies

that are carried out in humans that allow fears to be undone,

that allow traumas to be reversed

such that people no longer feel bad

about a particular person, place, or thing,

either real interactions with that person, place, or thing,

or imagined interactions with that person, place, or thing.

That process, as I just mentioned,

also involves things like the NMDA receptor,

but rather than strengthening the connections,

the first thing that has to happen

is there needs to be a weakening of connections

that associate the person, place, or thing

with that threat reflex.

Subsequent to that, we will see

there needs to be a strengthening of some new experience

that’s positive, okay?

This is a key element of where we are headed.

Contrary to popular belief,

it is not going to work to simply extinguish a fear.

One needs to extinguish a fear and or trauma

and replace that fearful or traumatic memory

or idea or response with a positive response.

And this is something that’s rarely discussed

both in the scientific literature,

but certainly in the general discussion

around fear and trauma.

There’s this idea that we can extinguish fears,

we can rewire ourselves,

we can eliminate our traumas, and indeed we can,

but that process has to involve

not just becoming comfortable

with a particular fearful event or trauma,

but also attaching a new positive experience

to that previously fearful or traumatic event.

There are a lot of different approaches out there

that are in clinical use

to try and alleviate fear and trauma,

and indeed PTSD, post-traumatic stress disorder.

It might be surprising to learn

that many of those treatments, such as SSRIs,

the selective serotonin reuptake inhibitors,

things like Prozac and Zoloft and similar,

and other antidepressants,

or things like benzodiazepines,

which are essentially like painkillers.

They create elevation in certain transmitters in the brain

like GABA, among others.

They can have a pain-relieving effect.

They are generally, however, considered anxiolytics.

They reduce anxiety.

And even antipsychotic drugs or beta blockers,

sometimes called adrenergic blockers,

drugs that are designed to prevent the heart

from beating too fast or to reduce blood pressure,

to reduce some elements

of that hypothalamic pituitary axis response

that we talked about earlier.

Many people experience some degree of relief

from the symptoms of anxiety and fear and PTSD.

In taking these various compounds.

Indeed, that’s why they’re prescribed so broadly.

But you may find it interesting to note

that none of those current treatments

are based on the neurobiology of fear,

at least not directly, right?

People that take SSRIs oftentimes

will experience a reduction in anxiety.

It depends on the dosage and the individual, of course,


And you have to work with a doctor, a psychiatrist

to determine whether or not they’re right for you

and the correct dosage, if they are right for you.

But that modulation of anxiety can indirectly

reduce the likelihood that one will have a panic attack

or experience of fear or an intense experience of fear

or reliving of a trauma.

But the SSRIs themselves are not plugging

into some specific mechanism related

to how fear comes about in the system.

It’s an indirect support.

That’s important because if the goal of modern psychiatry

and the goal of modern biology is to provide

mechanistic understanding that leads to treatments,

we need to think about what are the sorts of treatments

that tap into the very fear circuits

that we described before.

The fact that there are memories attached

to a generic threat reflex and response,

and the threat reflex response can be linked up

with the dopamine system and can be linked up

with other systems that are involved in pain relief

and anxiety and so forth.

And so that brings us to which treatments

are directly related to the fear circuitry

and the circuitry related to trauma.

And the primary one to begin with

is the so-called behavioral therapies.

Now, oftentimes we all wish, I think, from time to time,

that there’s some specific pill that we can take,

or there’s some machine or device

that we can plug our finger into,

or that we can put on a headset and all of a sudden

we just rewire our nervous system,

fear is gone, trauma is gone, but it doesn’t work that way.

And when we think of language and narrative

as a tool to rewire our nervous system,

in comparison to those kinds of ideas

about pills and machines and potions,

it starts to seem a little bit weak, right?

If we just think, oh, well, how could talking

actually change the way that we respond to something?

But actually there are three forms of therapy

that purely through the use of language

have been shown to have very strong positive impact,

meaning reduce fears and traumas.

And those three are prolonged exposure therapy,

cognitive processing, or CPT,

and cognitive behavioral therapy.

And I’m not going to go into the entire literature

around prolonged exposure, cognitive processing,

and cognitive behavioral therapy,

but I will just illustrate the central theme

that allows them to work.

Now, remember that the circuit for fear,

the circuit for trauma involves this generic reflex,

and then there are those top-down elements

coming from the forebrain.

It’s very clear, because it’s been measured,

that if you look at the amount of anxiety,

the pure physiological anxiety response

of quickening of heart rate, flushing of the skin,

sometimes quaking of the hands, the experience of fear,

over time, when people recount or retell their trauma,

that the first time they do that,

especially when it’s recounted in a lot of detail,

there’s a tremendous anxiety response,

sometimes even as great or greater

than the actual exposure to the fearful event or trauma.

And obviously, this is something that is done

with a clinician present,

because it is very traumatic to the person.

They’re literally reliving the trauma in full, rich detail,

and they are encouraged to provide full, rich detail.

They’re often encouraged to speak in complete sentences,

to flesh out details about how they felt inside,

to flesh out details about their memories

going into this traumatic or fearful event,

going through it, and after, really digging in

to all the nuance and contours of these horrible experiences.

But what’s remarkable is that in the second and the third

and the fourth retelling of these traumatic

or fearful events, that anxiety response

and the amount of the physiological response,

I should say that the amplitude

of the physiological response,

becomes progressively diminished with each retelling.

Now, some of you might be saying,

well, duh, you tell a story enough times

that eventually it wears off,

just like if you watch a movie enough times

and you hear the same joke enough times,

eventually it doesn’t have the same impact,

but that needn’t be the case, right?

You could imagine that this high amplitude anxiety response,

this high amplitude activation

of the sympathetic nervous system in retelling

would actually create a even deeper routed fear response

and trauma, but that’s not what happens.

And every clinician I spoke to

in anticipation of this episode,

which include clinical psychologists, psychiatrists,

and people who actually work on the fear system

at a biological level said the exact same thing,

which is that a detailed recounting

of the traumatic and fearful events is absolutely essential

in order to get the positive effects

of prolonged exposure, cognitive processing

and cognitive behavioral therapy.

Again, this has to be done with the appropriate support.

This isn’t something that should be taken lightly

because as we’ve mentioned before,

the fear response can have a very long lasting

contour to it.

People can sometimes have trouble sleeping

for days and days.

And afterwards we’ll talk about sleeping a little bit,

but the point is that the retelling is important.

And the idea here is to take what was a terrible

and extremely troubling, meaning physiologically troubling,

psychologically troubling story,

and turn it into what is essentially a boring bad story.

Okay, it never really becomes a good story

at this point in the treatment process

that we’re describing.

So a terrible event is a terrible event, period.

But there’s a way in which the retelling of that event

starts to uncouple the threat reflex from the narrative.

And with each successive retelling in detail

of these traumatic events, of these fearful events,

the threat reflex is activated

at a progressively lower and lower amplitude

such that eventually it just becomes a really bad,

really boring story.

Now that’s one part of the process of getting over a fear.

It’s what we call fear extinction.

And we can bring ourselves back to our earlier example

of Pavlovian conditioning,

because many studies have been done

both in animals and in humans showing that, for instance,

if you pair a tone, you know, a bell or a buzzer

with a foot shock that an animal or a person

will brace themselves for the foot shock.

Eventually you can just give the bell or tone

and the person will experience that same freezing up

or the same fight or flight or freeze response.

So they do condition that.

But if you give the tone or the bell over and over

and there’s no foot shock, there’s no pain.

And in humans, this is sometimes done with foot shock.

Sometimes, believe it or not, with mild burn.

There are even some studies, there’s older studies,

you couldn’t do those now, nor would you want to.

But eventually what happens is the tone,

the bell no longer evokes that response, okay?

So you see this as a reversal of the classical conditioning

and we call that reversal extinction.

So the retelling of this traumatic or fearful narrative,

excuse me, fearful narrative,

is essentially an extinction process.

Now, how is this done?

One can do this in a therapist’s office face-to-face,

that’s sometimes done.

It’s sometimes done in group type settings

where people actually stand up

or sit in front of a group, small or large,

and recount in detail their traumatic experience.

It’s sometimes done by people

writing out the experience in detail.

And which one of these is most effective

isn’t really clear.

The literature points to the fact that

a feeling of trust, obviously,

between the patient and the clinician

or the person and the group is essential.

Some people don’t have access to

because of finances or other limitations

to therapy of that sort.

In that case, journaling in detail

has been shown to be effective.

Although again, I want to caution people

about reactivating traumas without consideration

for the kinds of social support they might need

around that reactivation.

And we will talk a little bit later

about some of the chemicals involved in social support

and why those help extinguish fears.

So the thing to embed in your mind

is that recognition of the early traumatic

or fearful event in detail over and over

is key to forming a new non-traumatic association

with that event or person.

So that’s part one.

You need to diminish the old experience.

And when I say diminish,

I mean reduce the amplitude of the physiological response.

Now, this is just but one approach.

I’m going to talk about other approaches

to eliminating fear and trauma as we go forward.

But I want to emphasize that diminishing the amplitude

of the physiological response is the first step.

So it’s like a clearing away of the association

between the person, place or thing and that threat reflex.

But even after that’s occurred,

there’s an essential need to relearn a new narrative.

Why is there essential need to relearn a new narrative

or create a new association?

Well, that has to do with that fear reflex circuitry.

As you recall, there are outputs to areas of the brain

that are associated with dopamine release and reinforcement.

And that we now know offers the capacity

for these fear circuits and these circuits

that underlie trauma to be mapped onto new experiences

that are of positive association.

So I’m going to give a kind of basic example.

It’s a kind of a silly example,

but I’m giving it as a template

for what could be any number of other different examples.

Example I’ll give is let’s say a kid is biking

to play soccer, soccer practice,

and they get into a bad car accident, okay?

Terrible thing to happen, but they survive, they recover.

And somehow, and we really don’t know why

certain fear memories get wired in more broadly

or more narrowly.

Somehow this kid just doesn’t even want to bicycle anymore.

And they actually don’t even want to play sports.

And they actually just don’t want to go anywhere.

They’re kind of isolating

and not interacting with friends very much at all.

It’s a pretty broad response.

It didn’t have to be that way.

Some kids would just decide they don’t want to cycle anymore

down that particular street.

Well, the process of retelling the narrative to a clinician

would allow an extinction of the fear response, right?

So a reduction in the heart rate,

a reduction in the narrowing of focus,

a reduction in all the things that we consider fear.

But a really good cognitive behavioral therapist

or somebody that understands the neuroscience

of fear and trauma would understand

that that’s not sufficient.

That’s what’s really important is that this child,

this hypothetical child, relearn a new narrative

that they don’t just manage to bike to soccer practice

or manage to spend time with friends,

but that they actually start wiring in

new positive associations with biking to practice,

with playing soccer, with social events.

And, and this is the somewhat surprising feature of this,

and that they link that back

to that early traumatic experience.

That it’s not just that they’re replacing

a bad experience and memory with a good experience

and memory, but they’re actually holding in mind

in these top-down narrative circuits, if you will,

they’re holding in mind,

ah, I’m not just biking to soccer practice.

I’m actually biking to soccer practice

and I’m enjoying it despite the fact

that I was in a bad car accident,

despite the fact that two months ago or two years ago,

or maybe even 10 years ago,

I couldn’t even leave my room

or I didn’t want to associate with anybody.

So the building up of the positive associations are key.

And the linking of those positive associations

with the earlier traumatic event is key

for the following reason.

The top-down circuitry from the prefrontal cortex

to this threat reflex circuit

is not like the other connections in that circuit.

The other connections in that circuit

are what we call glutamatergic and excitatory.

They are all about activating other neurons,

like a chain reaction.

One neuron activates, the next activates,

the next like dominoes falling.

These top-down circuits that feed into the threat reflex

and all its parts is what we call inhibitory.

It tends to prevent activation of those given circuitries.

It tends to prevent activation of the threat reflex.

So it’s acting as a break.

And so when we think of positive experiences

being associated with what was previously

a negative experience,

we’re not talking about forgetting

that the car accident was horrible

or forgetting that the assault was absolutely dreadful.

We’re talking about attaching a new positive memory

to the circuitry so that the previous fear response

is far less likely to occur

and that it remains extinguished.

So just to make sure this is absolutely clear,

there’s a first step which involves retelling and reliving

in order to extinguish the fear and the trauma,

to reduce the amplitude of the response.

Then there’s a need to replace

or attach positive experiences

to the earlier what would be traumatic response.

The extinction has to go first.

This is key.

You can’t simply say,

oh, you know, the car accident was actually a good thing

because I stayed home a lot that year and I got to study.

You can tell yourself that, and that could also be true,

but that won’t necessarily and probably won’t eliminate

the fear or the traumatic association of the car accident.

And again, I’m using car accidents

as a general example or a generic example here.

Okay, so there’s a three-part process.

One, diminish the old experience

through repetitive narrative.

Almost inevitably, the initial repetition of that

is going to be very high amplitude and quite troubling,

but over time it will reduce, right?

You’re turning the terrible, really upsetting story

into a terrible, boring story.

That’s the extinction process.

Then there’s a relearning of a new narrative

that includes some sort of sense of reward,

and that sense of reward has to be tacked back

onto the traumatic event

or what was previously a traumatic event.

And that is all through narrative.

It’s all through cognition.

And I think this is a very important point.

Oftentimes, I think we tend to undervalue

the importance of rationalization

and of story and of narrative.

But the prefrontal cortex is this amazing capacity

of our brain real estate to create meaning,

to attach meaning and purpose

to things that otherwise are just reflexive.

And in the example of an ice bath,

it might be a little trivial.

In the example of the kid with the car accident,

it becomes a little more relevant.

And in the example of things like people surviving

genocide or attaching stories of great victory

to what were previously thought of as stories of great loss,

of time, of people, of any number of things,

that process of narrative is one of the major ways

that the human brain rewires itself.

Narrative should not be undervalued

as a tool for relieving fear and trauma.

In fact, narrative is one of the best and most potent ways

that we can rewire our fear circuitry,

and that indeed we can form completely new relationships

to things over time.

So basically, narrative should not be undervalued

as a tool to rewire our nervous system,

but it has to be engaged in the correct sequence.

And that correct sequence is first extinction,

then relearning a new narrative with positive associations

and attaching those positive associations

to the formerly traumatic or fearful event.

Now, I mentioned prolonged exposure therapy,

cognitive processing, and cognitive behavioral therapy.

For those of you that are seeking relief

from fear and traumatic events,

you can look up licensed clinicians that can carry out

those one or several of those types of therapies.

I get a lot of questions about other forms of therapy.

One of the ones that comes up a lot is so-called EMDR,

eye movement desensitization reprocessing,

developed by Francine Shapiro in the 80s.

Eye movement desensitization reprocessing

involves moving the eyes side to side

while recounting a traumatic or fearful narrative,

typically with a clinician present.

Why would that work?

Well, basically, when I first heard about EMDR

from my stance as a vision scientist,

I thought the whole thing was kind of crazy

and half-baked, frankly.

I heard these theories that, oh,

it recreates the eye movements in rapid eye movement sleep

or REM sleep, and that’s completely false.

It does not.

I heard the argument EMDR activates both sides of the brain,

which I guess hypothetically

was thought to be important somehow.

And frankly, there’s no evidence whatsoever

that EMDR activates both sides of the brain

in a way that’s beneficial.

I mean, by looking from side to side,

just because of the way that binocular visual circuits

are organized, it will do that.

But it never made any sense to me why EMDR would work

until several years ago when I saw,

because I reviewed no fewer than five papers,

some in animal models, others in humans,

looking at lateral eye movements,

meaning eye movements from side to side with eyes open,

not eyes up or down.

And what was observed in these experiments,

in all of them actually, all five of those papers,

was a dramatic reduction in the activation

and actually an inhibition, a suppression of the fear

or threat reflex circuitry, which was a jaw dropper for me.

I thought, wow, actually it was a jaw dropper eye widener

for me, I thought, oh my goodness,

maybe this EMDR stuff works according to some mechanism

and maybe this is the mechanism.

And indeed many laboratories, not mine,

but many laboratories are now pursuing that idea

and it’s looking very likely.

Why would that happen?

Well, just very briefly, lateralized eye movements

of the sort that I’m describing

and I’m moving my hand like this,

but I’ll just do it with my eyes,

even though it’s a little embarrassing to do that

because I know it looks strange, I don’t mind,

because I’m doing EMDR and EMDR reduces activation

of the amygdala and related circuitries,

which reduces anxiety and reduces the amplitude

of the threat reflex,

reduces sympathetic autonomic arousal.

In other words, we feel calmer or we feel less alert,

less stressed when moving our eyes from side to side.

And the just so story about this is that

these are the sorts of eye movements that we do

when we are ambulating, moving through space,

through some sort of self-generated motion.

And one can make up a pretty reasonable story

in the evolutionary context or ethological context

that forward movement and fear

are generally incompatible with one another,

that generally a fear response

involves a freezing or retreating.

Some people will advance,

but that’s usually a trained advance in response to fear,

so first responders and so forth.

Most people freeze or retreat when they’re afraid.

Forward movement generates these eye movements.

It does seem to suppress activation of this threat reflex

and the amygdala in particular.

So for the many EMDR practitioners out there,

these papers I think are a great celebration.

And I think there is now increasing excitement about EMDR

in the psychiatric and psychological community

for its utility for treating fear, trauma, and PTSD.

However, I should point out that in discussing EMDR

with various colleagues of mine at Stanford and elsewhere,

I was told that EMDR has been shown

to be beneficial in particular

for single event type traumas or fearful experiences,

not so much for relieving the trauma

or feelings of fear associated, for instance,

with an entire bad marriage or an entire childhood,

but more for single, more acute events

that can be described within a very kind of brief narrative,

brief, not necessarily in time,

but that the car accident,

the bad interaction with another individual,

the assault, God forbid, these sorts of things.

And I realized we’re down in the weeds of topics

that are unpleasant.

And so I have great sensitivity to that,

but I think it’s also important that we be realistic

about the kinds of things that traumatize people.

So is EMDR useful?

Well, it seems like it works for these single event

or kind of constrained event type traumas

that people can describe while moving their eyes

from side to side,

generally in the presence of a clinician.

However, if we think back to the model

of how you extinguish and then replace a trauma or fear,

remember, you have to diminish the old experience,

the amplitude of that, you need to,

that’s the extinguish portion.

Then you need to relearn a new narrative

and attach reward to the old traumatic event.

EMDR only really taps into the extinction

of the physiological response to the old experience.

I’m sure that there are EMDR practitioners out there

that are thinking about the attaching

of the new narrative and reward,

but there I’ve heard less

and I’ve seen fewer peer reviewed papers on that.

So let’s think about this logically.

Let’s say, and indeed it’s the case

that sitting down in a chair,

moving eyes side to side deliberately

for some period of time reduces activation

of the threat reflex.

I, or the patient in this case,

recites or repeats over and over the traumatic event

or the fearful event.

I’m doing that in the presence

of a lower amplitude response.

Remember back to where we talked

about how the retelling works best.

If the first time it’s done,

there’s a huge amplitude response.

And then with each successive repeat,

that response, the threat response gets lower and lower.

With EMDR, you’re sort of short circuiting,

you’re kind of sneaking around the corner

of that high amplitude response.

And so you’re, it’s taking a somewhat different approach

of trying to extinguish the bad feelings in body and mind

associated with an experience

by reducing the physiological response.

So it’s somewhat different.

And at least to my knowledge,

and EMDR practitioners, please correct me,

but at least to my knowledge,

there isn’t an active component to EMDR

of relearning a new narrative and attaching reward.

Now, reward and attaching reward

requires a somewhat high amplitude sympathetic arousal.

It requires a feeling of a victory, which is arousal, okay?

It’s positive arousal, not negative arousal,

but it is arousal.

So I’m not focusing on this

to try and diminish the potential impact of EMDR.

I know many people have achieved great relief from EMDR,

but it doesn’t tap into all the aspects

of the extinction and relearning

that we talked about previously.

And therefore I think on its own,

at least in many cases,

is unlikely to be a complete therapy for fear and trauma.

If there are people out there

who’ve had terrific results with EMDR,

please let us know in the comment section.

On YouTube would be the ideal place.

If you’ve had bad experiences with EMDR

or it didn’t work for you, also let us know.

I think that EMDR practitioners,

like most practitioners in the psychiatric

and psychological space,

are eager to expand their practices

in order to make them more effective,

rather than clinging ardently to something

that perhaps is incomplete

or that doesn’t work for certain individuals.

So I think they would appreciate that feedback, as would I.

So, as I mentioned before,

most of these therapies are done in conjunction

with a skilled, often one would hope, credentialed clinician.

There are many people, however,

that don’t have access to that

or who are working through stuff.

They have things in their past

that are very uncomfortable to them.

And I’m aware that many people are working

through those things, through journaling,

through talking to a friend,

through any number of different

sort of non-traditional approaches.

One thing that really pertains to everybody

who’s working through fear and trauma of any kind

is the importance of social connection

as it relates to the chemical systems

and the neural circuits associated with fear and trauma.

And this is a emerging literature in neuroscience

that is really a beautiful one

because it’s a very conserved biology.

We see it, believe it or not, in flies, in fruit flies,

a commonly used model system, in mice,

and indeed in humans as well.

And this is the work of David Anderson’s group at Caltech,

of, again, of Dr. Ressler’s group at Harvard Medical,

and elsewhere, of course.

And this is the work as it relates to tachykinin.

Tachykinin is a very interesting molecule in our brain.

And it turns out that tachykinin is activated in neurons

of what’s called the central amygdala

and some nearby structures.

So really smack dab within the middle of this threat reflex

very soon after some traumatic

or fear-inducing event occurs.

And it actually sets in motion a number of other things,

including changes in gene expression and potentiation,

meaning long-term potentiation,

activation of NMDA receptors, and so on,

in the circuits that reinforce

that fearful or traumatic experience.

Now, what’s interesting about tachykinin

is also that it’s been shown to lead

to low to moderate levels of anxiety

and even kind of aggression, irritability.

Tachykinin levels are further increased

by social isolation.

And that social isolation is oftentimes

what can exacerbate preexisting traumas or fearful events.

And in a kind of beautiful symmetry

to that kind of dark and depressing story,

social connection with people that we trust,

and it doesn’t have to be direct physical contact,

but just social connection,

conversing with, sharing a meal with,

it could be physical touch if that’s appropriate,

those sorts of connections actually serve

to reduce the effectiveness

or even the levels of tachykinin.

So the important point here is that trauma

is traumatic in and of itself.

Fearful events are hard in and of themselves.

And if people are working through them,

either through clinical work or through individual work,

it is important.

And ideally, one would still be trying

to access social connection outside

of that specific work related to the trauma.

Now, it doesn’t necessarily have to be outside of that.

For instance, if you have a good relationship

with a clinician or therapist

to the point where there’s real trust

and you feel a social connection with them, wonderful.

But for many people,

they have a more transactional relationship

to the EMDR practitioner or to their therapist,

or they’re working through things on their own.

And it’s really important to understand

that regular social connection,

trusting social connection of any kind

is going to be very beneficial for that process.

And so this is not kind of just hand wavy, new agey stuff

like, oh, you need social connection.

There’s a actual neurochemical basis for social isolation

that has an amplifying effect on fear and trauma.

And there is a neurochemical basis for the relief

from fear and trauma and isolation.

And in the ideal circumstance,

one is working through these traumas and fears

very intensely in a very dedicated way,

but then is also engaging

in the sorts of social interactions

that are going to diminish the amount of tachykinin

and going to suppress those very circuits

that would otherwise be amplified.

So next I’d like to talk about some really interesting

and almost kind of eerie scientific findings,

and that’s the transgenerational passage of trauma

or predisposition to fear and trauma.

This is a scientific literature

that’s been debated many times

over the last really 50 plus years,

but in more recent studies have really proven

that we as humans have the capacity

to inherit a predisposition to trauma or fear.

Now that doesn’t necessarily mean

that we will become traumatized or experience extreme fear

just because our parents or grandparents experienced that.

It’s a predisposition.

It’s a bias.

Let me explain the papers that focus on this

for a little bit,

and then we’ll talk about what this means for each of us.

One of the most important papers in this area

comes to us from someone I mentioned earlier,

Dr. Kerry Ressler at Harvard.

And the title of the paper is

Association of FKB5 Polymorphisms and Childhood Abuse

with Risk of Post-Traumatic Stress Disorder

Symptoms in Adults.

And there are other papers as well.

Another one from the Ressler Lab,

first author, Brian Diaz, D-I-A-S.

Parental Olfactory Experience Influences Behavior

and Neural Structure in Subsequent Generations.

I’m going to summarize these papers

and their general contour and papers related to them,

although feel free to look up the papers I just described.

We will provide a link to them in the caption

if you’d like to go further.

But basically these explorations involve

looking at the histories of human individuals

who had trauma or abuse of some kind in their childhood,

and then looking at the likelihood of fear

and PTSD type symptomology in their offspring.

And essentially what they identified is that indeed,

if you had a parent,

and there does seem to be a kind of a bias

toward an effect where if the father had abuse,

and it’s severe abuse or moderate abuse,

that abuse causes a change in his genetics,

in his sperm, that can be passed on to offspring

such that the offspring have a lower threshold

to develop trauma or extreme fear

to certain types of events.

Now, what’s important to point out

is that predisposition or bias

is not necessarily to the same sorts of events.

It’s not that the abuse itself gets passed

from one generation to the next.

It’s a predisposition.

And the title of that paper mentioned FKB5,

excuse me, FKBP5 polymorphisms.

And the FKBP5 polymorphism maps

to a location in the genome that’s associated

with the so-called glucocorticoid system

with cortisol release.

So the predisposition that one might inherit

from having a parent, father or mother,

but stronger tendency to inherit it from the father

who experienced abuse is one in which

the glucocorticoid system, the cortisol system,

and that HPA axis that we talked about before,

the hypothalamic pituitary adrenal axis

is sensitized or reactive in a way

that sets a lower threshold to become traumatized

or very afraid of certain types of events.

But it’s not unique to the specific type of abuse

that the parent experienced.

Now, this is really, really important

because a lot of times out there,

I will hear that there’s passage

or transgenerational passage of actual trauma,

the specific trauma.

Now that could be through narrative telling.

You know, if somebody is exposed to a lot of narrative

about their parents’ trauma in one form or another,

it may be that they start to internalize

some of that trauma.

And there could be,

because we obviously can’t rule it out,

there could be some other signatures

of prior specific traumas they get passed on to offspring.

But more likely, and certainly what these data

about these polymorphisms point to,

is that what gets passed on is a propensity

for the threat reflex to get activated

and attached to a wider variety

or to less intense types of inputs and experiences.

And the important point to take away from this

is that it’s not some magical, mysterious,

and mystical thing that’s being transplanted

from parent to child.

It’s a gene or it’s a modification in a set of genes

that gives a heightened level of responsivity

to fearful type events

or even a heightened level of responsivity

such that things that wouldn’t be fear-inducing

or trauma-inducing to certain individuals

can trigger fear and trauma in these children

that inherit this particular gene.

Now, that doesn’t necessarily mean that they are fated

to forever be traumatized or live in fear.

That’s simply not the case.

It’s just a genetic predisposition.

Regardless of whether or not you had a parent

or parents that were traumatized or not,

there’s no evidence, at least as far as I’m aware,

that the treatments for trauma should be any different.

As far as I know, there aren’t gene therapies

currently aimed at these particular variants

like FKBP5 and so forth

that could reverse those particular genetic underpinnings

of the trauma predisposition.

So this transgenerational passage of trauma,

I think is extremely interesting in large part

because it brings us back to this idea

that the threat reflex is part of a larger sensory system.

Normally we think of seeing as a sensory system

or hearing as a sensory system,

but the threat detection and threat learning system,

the fear learning system, is in many ways a sensory system.

It’s just a sensory system

that is very generic in its response.

That generic response, again, is good

because it allows for flexibility,

but it’s bad because it reduces specificity.

We can essentially become fearful or traumatized by anything

if the circuit gets activated,

and these particular children inherit a predisposition

for more things and less intense things to traumatize them.

In a few minutes, we are going to discuss

some of the behavioral treatments,

including some really new exciting protocols

for dealing with fear and trauma.

But for a few minutes,

I’d like to discuss some of the drug treatments

that are starting to emerge as potential therapeutics,

in particular for PTSD.

The two drug treatments I’d like to focus on

are ketamine-assisted psychotherapy

and MDMA-assisted psychotherapy.

Currently, ketamine-assisted psychotherapy is legal.

It is approved, provided it is prescribed

by a board-certified physician in the United States.

I’m not certain about other areas of the world.

MDMA, also sometimes called ecstasy therapy,

is in clinical trials in the US.

It is still an illegal drug to possess or to sell,

so I want to be very clear about that.

However, MDMA is being explored as a potential therapeutic

for PTSD and other forms of trauma.

And of course, ketamine and MDMA

are also both being explored for chronic depression,

eating disorders, and a number of other

psychiatric disorders.

But for the moment, I would just like to touch on

ketamine and MDMA as they relate to the fear circuitry

and trauma circuitry that we’ve described

in the early part of the episode and throughout the episode,

because I think that in viewing them through that lens,

we can gain some additional insight

into how they might be providing the sorts of relief

that some of the early clinical studies

are starting to point to.

Ketamine is a dissociative anesthetic.

That’s right, it’s a dissociative anesthetic.

Its main function is to create a state of dissociation.

And I’ve never taken ketamine personally,

so I can’t describe the experience of it,

but a colleague of mine in psychiatry

shared their experience with a patient’s experience of it

as making that patient feel as if, quote,

they were getting out of the cockpit of a plane,

but that they were observing themselves doing it.

And this was, of course, during a approved

therapeutic session that they were doing this,

and they were in some sort of intense visualization

about a traumatic experience.

They were describing some of their depressive symptoms

as well as the trauma.

And the narrative that they basically created

or took away from this, and that was relayed to me,

was one in which the patient felt like

they were in their own body,

but they were also viewing their own body from the outside.

So dissociative, in other words.

Again, I’ve never had this experience.

Some of you may have with ketamine or through other means,

but we might want to just take a moment

and think about what ketamine actually does

and what dissociation actually does

at the level of neural circuits.

And for that, we can look to this really beautiful paper

that was published by my colleagues,

Karl Deisseroth in psychiatry,

Robert Malenka also in psychiatry,

Legion Low also at Stanford.

They paired up or teamed up rather

to explore how systemic ketamine

adjusts circuitries in the brain.

And what they discovered was that

it changes the rhythm of cortical activity

in certain layers of the cortex.

The cortex is like a layered sandwich.

The cortex, of course, being the outside of the brain.

And there was a particular rhythm,

a one to three Hertz rhythm.

One to three Hertz just means a particular frequency

of electrical activity.

In this case, in these layer five neurons

of retrosplenial cortex.

So you don’t need to know much about retrosplenial cortex

or a one to three Hertz rhythms.

I think the important thing to just take away from this

is that there is now starting to be an understanding

of how drugs like ketamine work

to create this subjective experience

that this patient and other patients

describe as dissociation.

You know, dissociation in its essence

is really about not feeling what’s happening.

It’s about viewing what’s happening

from a different perspective

than what normally one would view that experience from.

And so if we kind of plug that general notion

of dissociation and ketamine induced dissociation

into the circuit that we talked about before

where we have this threat reflex involved in the amygdala,

these outputs for freezing or for reward in the accumbens.

And we’ve got this prefrontal narrative coming down

as top-down processing.

It brings us right to that prefrontal cortical input

to the threat system and that narrative.

What seems to be the case in my review

of the paper I just described,

plus a review on how ketamine assisted trauma relief

might work is that it somehow allows the patient,

the individual to recount their trauma

while feeling either none or a very different set

of emotional experiences that they experienced

in the actual trauma or fearful experience.

So it’s a remapping of new onto old,

new meaning new feelings onto old feelings

while staying in the exact same narrative.

So it’s a little bit like EMDR

of suppressing the threat reflex,

but it seems to bring in a replacement

of previous emotional experiences and sensations

in the body with new ones.

And so in that way, we can sort of view,

or we can try and view ketamine assisted psychotherapy

for the treatment of trauma as bringing together

the three elements that we talked about before.

You want to diminish the intensity,

the potency of the old original trauma experience

or fear experience.

So that seems to be accomplished through this dissociation

and maybe through the kind of anesthetic component.

So it’s a reduction in pain in the body,

a dissociation, a kind of observing of the self

that leads to the extinction of the trauma and the fear.

But then there also seems to be an automatic

or kind of built in a relearning of a new narrative

and new set of experiences,

which is the next step that we described earlier.

So it’s an intriguing therapy.

It’s one that’s really catching on

and there are many, many clinics around the US

that are now doing it.

Whether or not it turns out to be the ultimate treatment

for trauma and for fear, isn’t clear.

My colleagues in psychiatry tell me that that’s unlikely,

although it does seem to be beneficial

for a number of people,

especially people that are experiencing trauma

or have existing traumas and fear

that are coupled with depressive symptoms

because the data on ketamine and depression

seems to be quite strong.

So now let’s talk about MDMA.

MDMA also sometimes called ecstasy or molly

in its recreational form is a powerful synthetic drug

that at least as far as we know,

creates a state in the brain and body

that is unlike any other chemical state

in the brain and body that’s normally experienced.

What do I mean by that?

Well, we have several neuromodulator systems in our body.

Neuromodulators are chemicals that change the likelihood

that certain neural circuits will be active,

meaning they can make it very likely

that certain circuits will be active

and make it very unlikely

that other neural circuits will be active.

Good examples of neuromodulators are dopamine,

serotonin, acetylcholine, norepinephrine.

These tend to work on different systems

in the brain and body,

but they tend to be activated more or less in parallel.

You can have dopamine released in your brain

and also norepinephrine.

You can have serotonin released in your brain

and also acetylcholine.

So it’s not an all or none kind of thing,

but the degrees to which these things are activated

tends to vary.

And there is a little bit of a seesaw type phenomenon

with dopamine and serotonin.

Dopamine most commonly associated

with activating neural circuits

related to motivation, craving, and reward.

And serotonin more typically activated

in response to situations or conditions

in which we are very happy and content with what we have.

So dopamine is more about pursuing and seeking.

Serotonin is more about kind of pleasure and satisfaction

with resources that we have in our immediate sphere.

They don’t tend to,

serotonin doesn’t tend to place the brain and body

into a mode of action quite as much as dopamine does,

more or less.

MDMA is a unique compound

in that it leads to very large increases

in the amount of both dopamine and serotonin

in the brain and body simultaneously.

And that’s a unique circumstance

that is just simply not seen under normal conditions.

From a subjective standpoint,

people under the influence of MDMA

in the therapeutic setting

tend to report immense feelings of connection

or resonance with people or even things,

with music, with objects.

Certainly if it’s being done in conjunction

with a family member or a partner or with a therapist,

they will feel extremely connected to that person.

They’ll feel a very close understanding and association,

oftentimes that goes beyond words.

There is a chemical reason for that.

It turns out that MDMA causes massive release of oxytocin,

this neuropeptide that’s associated with pair bonding

and with bonding generally.

The oxytocin system and the serotonin system

are closely linked to one another in the brain and body,

and they tend to be co-released often at the same times

and by the same sorts of events.

So MDMA is one mechanism

by which oxytocin is released in these massive amounts.

And I should just relay some of the levels of oxytocin

because they’re really quite striking,

gives a kind of a more vivid picture

of why it is that MDMA would make people feel

so associated in a positive way

with the various things that are happening to them

while they’re under the influence of the drug.

So the paper related to this that I’d like to highlight

is in the journal Psychoneuroendocrinology.

The title of the paper is

Plasma Oxytocin Concentrations Following MDMA

or Intranasal Oxytocin in Humans.

And just remarkably MDMA increased plasma oxytocin levels

to 83.7, this is an average,

83.7 picograms per milliliter,

about 90 to 120 minutes into the MDMA session

compared to a typical level of 18.6.

So this is a massive increase in oxytocin.

And I think that massive increase in oxytocin

is part of the reason why people have these feelings

of close resonance and association.

Now, the dopamine increases are generally what lead

to the feelings of euphoria inside of the MDMA session.

And then the serotonin increases it is thought

are what lead to the feelings of safety and comfort.

So again, a very unusual chemical cocktail

that would never be seen,

at least not at this amplitude under any normal conditions

outside of an MDMA clinical psychotherapeutic session.

Why would this state of mind and body be potentially useful

for the treatment of trauma?

Well, indeed it is revealing itself to be useful

for the treatment of trauma.

Again, these are legal clinical trials

where people are doing this and discovering this.

What it seems to allow is a very fast relearning

or new associations to be tacked on

to the previously traumatic experience.

So again, it brings us back to the same model

of how people extinguish fears and traumas

and replace them with new experiences

when there is no drug treatment involved.

There needs to be a diminishing of the old experience,

meaning an extinction,

and then a relearning of a new narrative.

What the chemical milieu of MDMA seems to be doing

is creating an opportunity for all that to happen very fast

without the need for many repetitions of the original trauma

and reliving of the original trauma,

probably because the reliving of it

inside of one of these MDMA sessions

is very acute, very intense.

Plus, it seems to be offering the opportunity

to extinguish and rewrite in

or write in a new narrative associated with that trauma

very quickly as well.

So what this means is that treatments like MDMA

that are under investigation in these clinical trials

are unlikely to be magic potions, if you will,

that allow access to a particular process

that would otherwise not be accessible.

It’s more that the typical process

of trauma and fear reduction

that’s carried out in things like prolonged exposure,

cognitive processing, cognitive behavioral therapy

seems to be compacted into a much shorter session

and that session is performed at a much higher intensity,

higher intensity because the chemical milieu of the brain

is completely different.

I mean, the experience of MDMA

is one in which people have a very heightened

sense of euphoria, a very heightened sense of connection.

So those positive experiences are essentially primed

to be written in and over the traumatic experience.

And because of the high levels of serotonin in the system

and probably oxytocin as well,

there’s a safety that’s written into the situation

that allows people to lean into perhaps narratives

or components of narratives

that they would otherwise be holding back from.

So these are powerful compounds.

And I think the future of MDMA-assisted psychotherapy

for trauma in particular is holding great promise as of now,

meaning at the time of the recording of this podcast.

Again, I want to reiterate that these are clinical trials

that are being done legally.

These drugs are still illegal to possess

or sell outside of clinical trials.

Doing this sort of thing is punishable,

but it does seem that the FDA

and some of the related bodies

that control these sorts of things

are eyes open to this stuff.

And I think it’s very likely in the next few years,

things like MDMA and certainly ketamine

is already in widespread use

within the psychiatric community.

And I think we’re going to be seeing a lot more of that.

One thing we have not touched on yet

is how do you know if you’re traumatized?

How do you know if you have chronic fear

or a debilitating fear?

Much of the psychiatric community focuses

on how many other problems people might have,

trouble sleeping, trouble eating,

trouble maintaining quality work or schoolwork and so forth.

And all of those are certainly very valid criteria

and necessary criteria for determining

whether or not somebody meets clinical diagnosis or not.

But there’s a biological component

that I think we can all assess for ourselves.

And that’s one of interoceptive versus exteroceptive balance

and that sounds confusing,

but it’s actually really easy to understand.

We can focus our perception on the external world,

events going on around us beyond the confines of our skin

or within the confines of our skin.

A focus and a perception on the external world

is what’s called exteroception.

And a focus on what’s happening inside us is interoception.

And we have the capacity

to build mental appraisal into that, right?

I can, for instance, stop for a moment

and assess how my stomach feels, how hungry I feel,

how quick my heart is beating.

Some people, by the way, are much better at sensing

whether or not their heart is beating at a particular rate

and others, not so much.

Some people can actually count their heartbeats

without having to take their pulse

by placing pressure on their wrist or their neck.

Some people can’t.

In other words, some people have

very high interoceptive awareness and other people less so.

This whole business of fear and trauma

relates to taking external experiences

and funneling those experiences into this thing

that I’m calling a threat reflex or the fear circuitry.

A recent paper published in the journal Science,

so absolutely spectacular journal,

Science, Nature, and Cell

being the apex journals of scientific publishing,

gets at this issue of where in our mind

and how do we assess whether or not

what we are feeling internally is reasonable

given what’s going on externally.

And it’s a really fascinating study.

I’m just going to highlight a little bit of it for you

and then I’ll touch on some of the relevant aspects

and how that can be adopted into a practice

to assess and reduce fear and anxiety.

The title of this paper,

published just a few weeks ago in Science,

is Fear Balance is Maintained by Bodily Feedback

to the Insular Cortex in Mice.

We’ve not talked too much about the insula,

also called the insular cortex.

This is a brain area that my lab has worked on

and other labs have worked on.

It’s a brain area that has within it a map

of our internal interoceptive landscape.

It’s a map of our internal bodily sensations.

It’s a really interesting structure.

So the way this study was carried out

is that subjects were taught or conditioned

to a particular danger signal

through repeated presentation of a sound with a foot shock.

So there’s a sound and there’s a foot shock.

And as you know from our earlier discussion

about Pavlovian learning,

conditioned stimuli and unconditioned stimuli,

eventually the sound alone comes to evoke the fear response.

And that’s just classical conditioning.

The insula is this brain area that’s associated

with determining whether or not one’s internal sensations,

gut, heart, lungs, et cetera,

are reasonable or not given the external circumstances.

It can even measure or is associated

with our understanding

of what are called atrial baroreceptors.

These are blood pressure sensors.

So believe it or not, when your pulse rate increases

or you feel like you’re stressed out,

your atrial baroreceptors are sending a signal

to your insular cortex and your insular cortex is saying,

wow, I’m really stressed out, my blood pressure is up.

You don’t actually have to measure your blood pressure

with a cuff, your insula is doing it for you.

It’s not getting a quantitative readout,

but it’s getting a qualitative readout.

The main effect of inhibiting

or reducing the activity of the insula

was that the intensity of an outside world experience

led to a range of different internal effects.

In other words, for most people,

a mild shock would induce a mild increase in heart rate,

a mild increase in blood pressure,

whereas an intense shock to the skin

would lead to a big increase in heart rate

and a big increase in blood pressure.

Turns out the insula is important

for establishing that match of intensity.

And when the insula is inhibited,

what ends up happening is that a mild shock

can create a big increase in blood pressure

and that can be maintained such that

anything that’s paired with that shock,

like a bell or a tone

would lead to a big increase in blood pressure.

You’ve probably seen examples of this in the real world.

Maybe this is even you.

Some people are very jumpy in response

to just even small changes in their environment.

So if somebody’s working and you walk in

and you say, hello, and they’ll go,

and they’re kind of, they’re jumpy.

They have a low threshold to a big anxiety or fear response.

Other people are really calm.

I recall my bulldog, unfortunately he passed away,

but before he passed away,

if you walked in the room and you said,

hey Costello, he might turn his eyes in your direction.

He had a very high threshold to respond.

He was pretty low anxiety animal.

A lot of people are like that.

You come up behind someone, you say, hello,

and they just turn around real slow

or they might just turn around at normal speed

and say, hello.

Whereas other people would jump out of their seat.

The insula seems to be involved in calibrating

how big or how high amplitude

a given physiological response is.

So it’s pairing the internal landscape

with the external world.

And this might seem like just a mechanistic

but non-actionable point.

But what you’ll see from the next study

that I’m going to describe is that recalibrating

the relationship between outside events

and internal responses, which is the job of the insula

is actually something that’s under our control.

And through a very simple, very short protocol,

we can actually recalibrate that system so much so

that we can potentially reduce the amount of fear and trauma

that we experience in response to a memory

or to a real event.

And the entire process can occur very quickly.

So I’m really excited to tell you about this next study

for a number of reasons.

First of all, it’s extremely recent.

Second of all, it’s very well grounded

in our current understanding of the mechanisms

of stress, trauma, and PTSD

and unlearning of stress, trauma, and PTSD.

And third, it points to a actionable protocol

that while certainly is not the only approach

that I think people could or should take

for fear, trauma, and PTSD,

is one that I think we are going to see implemented

into the clinical setting very soon

if it’s not happening already.

Now, there’s a fourth reason I’m very interested in it,

which is that my lab works on stress, stress relief,

and tools for managing sleep and improving focus, et cetera.

And one of the hallmarks of the studies

we’ve been doing lately

is very brief five-minute-a-day interventions

of the sort that was used in this particular study,

although I should emphasize I had nothing to do

with this particular study.

Now, this particular study was carried out

in an animal model, in mice.

The work in my laboratory focuses on human subjects,

but the similarities of the stress system,

at least at the level that it was explored in this study,

I think have great relevance,

maybe even direct relevance to humans.

So the title of this study is

Repeated Exposure with Short-Term Behavioral Stress

Resolves Pre-Existing Stress-Induced

Depressive-Like Behavior in Mice.

Again, this study was in mice.

And basically what they did is they stressed out mice,

got them depressed,

and you actually can do that in a mouse,

using a restraint protocol,

and that’s a long-lasting restraint protocol

of 15 minutes or more.

Mice don’t like it.

You do it often enough.

They stop working so hard in their life,

in their mouse life, to gain food, to gain mates.

They show depressive symptoms at a number of levels.

They show elevated glucocorticoids.

You see the same thing in humans, okay?

Chronic stress in humans lasting weeks or more

does the same exact thing.

So again, a very close match here

in terms of mechanism overall.

And then what they did was a very counterintuitive thing.

Rather than give these animals stress relief

at the level of reducing their anxiety with benzodiazepines

or giving them a nice little mouse vacation

or enhanced or enriched environment,

things that have been done in a lot of previous studies,

what they did is they subjected them

to five minutes a day of intense stress,

but only five minutes a day.

And what they found was miraculously,

but also very convincingly,

daily short bouts of intense stress actually undid,

reversed the effects of chronic stress.

And it did this at the level of glucocorticoids,

of hormones, of neurotransmitters,

and a number of other different mechanisms.

Now, I find this very exciting for a number of reasons,

but in particular, because my laboratory,

in collaboration with David Spiegel’s laboratory,

our associate chair of psychiatry at Stanford,

been exploring how five minute a day respiration protocols

can alleviate stress.

And while those data are not yet published,

they are at the stage

where I’m comfortable talking about them.

And we are seeing some very impressive

and significant effects on stress reduction,

not just from respiration protocols

that allow people to calm themselves,

but also respiration protocols that bring people

into a heightened state of autonomic sympathetic arousal,

AKA stress.

As my colleague, Dr. David Spiegel,

he’s an MD, psychiatrist, and PhD,

likes to say, when it comes to trauma, anxiety, and PTSD,

and the treatment of trauma, anxiety, and PTSD,

it’s not just the state that you are in

or that you go into, it’s how you got there

and whether or not you had anything to do with it.

And this brings us right back to those top-down mechanisms

and the narrative around

what we are experiencing internally.

So let’s zoom out and I’ll explain how this works

and what to do about it.

We have this brain structure called the insula.

We talked about the insula a few minutes ago.

The insula is calibrating how we feel internally

versus what’s going on externally.

It’s involved in setting whether or not

what we are feeling is appropriate given what’s happening.

We have a system that can generate threat responses.

And in the case of trauma, PTSD, and extreme stress,

chronic stress, that system gets ramped up

so that it takes very little, maybe even just a memory

or maybe even an association that we’re not even aware of,

you know, a location triggers something

we’re not even aware of it,

and we start experiencing that symptomology.

How do we recalibrate the system?

Well, most of the approaches that are out there

involving drug treatments,

typical drug treatments would involve

suppressing the level of internal arousal,

just trying to bring that down.

Now, some of those drug treatments work,

but oftentimes they don’t.

And if you think about it,

it’s probably not surprising that they don’t

because by taking a drug that just lowers your anxiety,

overall, you’re creating a different

sort of miscalibration of the system.

So what we’ve been doing in human subjects

is having them do either breathing protocols that calm them,

and I’ll explain what that is in a moment,

or doing breathing protocols that increase their level

of autonomic arousal and seeing how that impacts

their response to stress overall,

not just during that particular breathing protocol.

So the calming protocol that we use

involves these physiological sighs.

I’ve talked about these previously

on the podcast and elsewhere,

but if you just need a reminder,

if you haven’t heard about it,

there’s a pattern of breathing that we all do in sleep

when our carbon dioxide levels in our bloodstream

get too high, and we do this when we get claustrophobic,

meaning we do it reflexively,

and that’s a double inhale through the nose

followed by a long exhale.

So it’s,

and yes, the inhales should be through the nose,

and yes, the exhales should be done

through the mouth ideally.

So it’s a big filling of the lungs

through two breaths back-to-back inhales,

even if you can only sneak in a little air

on that second one,

no talking if you’re going to do it right,

and then a long exhale,

which allows you to offload a lot of carbon dioxide

in the exhale.

And we have people doing that in real time,

anytime they experience stress,

but the particular breathing protocol

that we’ve been giving human subjects

is for them to do the repeated,

what we call cyclic sighing.

So double inhale, exhale, double inhale, exhale,

double inhale, exhale, repeatedly for five minutes,

which is actually a pretty long time to repeat that,

but you can do it pretty slowly.

And people report,

and the data point to the fact that it’s very calming.

People feel more relaxed afterwards,

and that relaxation wicks out

into other aspects of their life.

Now, we did not look at stress and trauma

in that condition.

We also have another condition

where people do what’s called cyclic hyperventilation,

which is very different

and creates a very different internal state

and is somewhat stressful.

It’s five minutes a day of stress,

much like the study that I just described.

And it involves basically doing this,

what I’ll do in a moment,

for five minutes, which is hyperventilating,

which is,

ah, ah, ah, ah, ah,

but not continuously for the five minutes

because many people would pass out

or feel extremely uncomfortable.

It involves inhale, exhale, inhale, exhale, very deep,

inhale through the nose, exhale through the mouth.

And then every 25 or 30 breaths or so,

doing a full exhale and holding one’s breath,

lungs empty for about 25, maybe 30, maybe even 60 seconds,

and then continuing until five minutes is up.

Subjects report and our data indicate

that people feel a heightened level of autonomic arousal.

In fact, I can feel it right now,

even from that very brief cyclic hyperventilation bout

I just did.

You feel a heating up.

You feel a, some people will perspire.

Some people get wide-eyed.

Some people feel agitated.

That’s adrenaline being released into your system.

Now I’m not suggesting everyone run out and do this.

And if you have a predisposition to panic attack

or anxiety attacks, please don’t do this

because it is very stimulating

and can trigger those sorts of attacks.

But this five minute a day protocol

of cyclic hyperventilation does lead to big increases

in autonomic arousal.

So it’s stressful in air quotes,

but to bring us back to the,

my colleague, David Spiegel’s quote,

it really was him that said it, not me.

It’s not just about the state that you’re in.

It’s about the state that you’re in plus how you got there

and whether or not you directed entry into that state.

And that point of that one directs their own entry

into a state deliberately is really key.

And I think it has an important implications

for whether or not there’s stress relief and fear relief

and trauma relief from bringing oneself

into a state of increased autonomic arousal.


Because of the way that that fear

and trauma circuitry is organized.

If you recall, it’s got these components

of how external events can trigger

an internal stress response and fear response

and trauma response,

but there’s that top-down prefrontal component

that can inhibit certain aspects

of that fear and threat circuitry.

Now, earlier we were talking about that prefrontal circuit

being engaged through narrative,

through self-directed deliberate narrative.

It’s the person deliberately retelling the story.

Here, we’re talking about a deliberate reactivation

of the sensations in the body.

So where I think this is all going,

meaning where my laboratory and the Spiegel Laboratory

and other laboratories out there are taking this,

is you can imagine a very brief five minutes a day,

two weeks was the time that they did this

for five minutes a day for two weeks,

intervention in which people

with the support of a clinician, we would hope,

would deliberately induce a physiological state

that’s very stressful, right?

Not shying away from the stress response,

but increasing their own stress response deliberately

and maybe in conjunction with recounting

the traumatic or fearful circumstance.

This is far and away different

than the kind of state of mind and body

that would come about in a ketamine-assisted

trauma-induced psychotherapy session

or a MDMA-assisted trauma psychotherapy session,

or in a purely narrative-based psychotherapy session

aimed at alleviating fear or trauma.

The reason I like these sorts of interventions

is that A, they are very low cost or even zero cost, right?

One could, you could imagine doing this while journaling

or while recounting a particular experience.

Again, they’re very compact.

Five minutes a day for two weeks

is what was done in this particular mouse study.

We don’t know if that translates directly

to the human study or not.

What was interesting is that if they used

longer daily bouts of stress, like 15 minutes a day,

that actually exacerbated the trauma

and exacerbated the fear.

So one has to be very careful.

Stress and deliberate entry into stress

and self-stressing are very potent tools.

They’re very sharp blades that it does appear,

or it’s likely can help alleviate trauma and fear.

But how long to do this,

exactly what the protocol should be

is still something that needs to be cultivated.

I know there are going to be people out there

that nonetheless are going to want to experiment

with some of this.

I will say that I do not think it matters

how one gets into that stressed state,

provided it is self-directed.

And that therefore could be called shower.

It could be ice bath.

It could be anything that induces an acute,

meaning a sudden onset of adrenaline and is self-directed.

That’s really the key feature here.

So I’m very excited about these data,

both the five-minute intervention data

from the animal study,

the work that’s ongoing in my laboratory

and Dr. Spiegel’s laboratory,

and the work that’s being done on the insula.

Because I think what we’re starting to see now

is a picture of fear and trauma and PTSD

that has this sensory component,

what’s happening in the world around us,

this internal and terraceptive component,

how appropriate are the signals

that are occurring in my body?

I mean, let’s face it,

if you almost get hit by a car

and your heart rate is 140 beats per second,

and that lasts for a little while

and you’re kind of stressed out

and you don’t get the best night’s sleep,

that’s pretty normal.

That means you have a healthy fear system.

If that persists and you’re dealing with a lot of issues

a week later, six weeks later, two years later,

then it’s moved into the realm of trauma and PTSD.

So we need to always be taking into account

the different components of the circuitry.

I do think that deliberate self-directed entry

into these short bouts of stress

is a very promising approach.

And it’s one that if people are going to experiment,

I just, again, want to caution people

with anxiety or panic disorders,

be very cautious, probably don’t do it.

Ideally, you would do this in conjunction

with support from a clinician.

But I’m also aware that there are a lot of people out there

that are dealing with trauma

and dealing with post-traumatic stress of various kinds,

and that they’re desperate

for various self-directed intervention approaches.

So just very briefly,

I want to touch on some of the lifestyle

and supplementation factors that can impact things

like fear and trauma and getting over fear and trauma.

To make a long story short,

there are many things that we all can and should do

to support our overall mental and physical health.

And these are the foundational elements

of quality nutrition, what that means to you,

quality sleep on a regular basis,

ample sleep on a regular basis.

We have an episode on how to master sleep.

In fact, we have four episodes

that you can go to or elsewhere

and scroll down, and you can find those episodes

in order to get your sleep really dialed in, as they say.

If you’re sleeping regularly and for sufficient duration,

all of the systems of your fear circuitry

are going to function better,

mainly because the autonomic nervous system

becomes very dysregulated

when we are not getting good sleep on a regular basis.

Dysregulated means that out of nowhere,

we can have a higher propensity

to have sympathetic activation,

or we can feel really tired and wired.

You know, that seesaw that I described earlier

of alertness and calmness,

of sympathetic and parasympathetic,

in that analogy, we can imagine that seesaw has a hinge

and that hinge can neither be too tight nor too loose.

If it’s too tight,

you can get locked into chronic activation of alertness

or chronic fatigue.

If it’s too loose, you’re bouncing all over the place

and you might be real tired and wired one moment,

and then, you know, really hyper alert.

Sleep resets that balance and resets that hinge

to the appropriate tightness, if you will,

so that all these circuits,

and not just the circuits related to fear,

but also the circuits related to cognition,

clear thinking, to be able to spell out

very clear, detailed narratives,

to feel like you are in control.

You are deliberately bringing yourself into these protocols,

if that’s what you intend to use.

All of that functions much better

when you’re sleeping well and eating well.

We talked about social connection.

Those are all indirect supports of trauma relief

and of getting over fear, but they are essential, okay?

I think of them sort of like the tide.

When the tide is high enough, a boat can leave harbor,

and if the tide is not high enough,

then that boat is going to be stranded on shore,

and in this analogy, the boat stranded on shore

is your attempt or anybody’s attempt

to try and work through something.

Very hard to do when we’re sleep deprived.

Very hard to do when we’re not fed enough

or fed the proper foods for you,

and that’s a highly individual thing,

and social connection, as we talked about earlier,

creates a general sense of support

for the ability to move through things,

but also chemical support

at the level of suppressing tachychinin, okay?

So those foundational elements are absolutely key,

but they are indirect.

I just want to briefly mention a few of the things

that some people find great benefit from

in the supplementation realm

as it relates to anxiety, stress, fear, and PTSD,

but I want to point out that, again,

these are somewhat indirect in their support,

and most of them focus on reducing anxiety overall.

The two that I want to focus on

are two that I’ve never talked about on this podcast before

because I’ve done podcasts before on stress

and managing stress in the kind of shorter term,

so we’ve talked about ashwagandha in a previous podcast.

Check out the podcast on stress

if you’re interested in how that might be relevant

as well as other tools,

but the two are interesting ones.

The first one is saffron, of all things,

but there are 12 studies, believe it or not,

that orally ingested saffron at 30 milligrams

seems to be a reliable dose for reducing anxiety

on the standard inventories,

the Hamilton Anxiety Rating Scale,

for those of you that want to know,

and these are significant effects,

and these were carried out in both male and female subjects.

Here, I’m only referring to human studies.

Several of these were double-blind studies.

There’s a meta-analysis of the positive effects,

meaning anxiolytic effects,

anxiety-reducing effects, that is, of things like saffron.

Definitely have to check with your doctor,

make sure it’s right for you,

but they’re fairly impressive effects

when you really think about it,

given that these are legal over-the-counter substances.

Again, check with a doctor.

The other one is inositol.

Inositol has been shown to create

a very notable decrease in anxiety symptoms.

It’s a fairly high dose that’s used,

but believe it or not,

the potency of this effect is on par

with many of the prescription antidepressants.

That’s pretty impressive.

These studies, again, are double-blind studies

that all showed decreases in anxiety.

These were done in males and females.

The age range is very broad, which is great,

18 all the way up to 64 across the studies that I looked at.

One of the more important things

is that the dosages are quite high,

18 grams of inositol taken for a full month,

and it does take some time

for these symptoms of anxiety to be improved.

The low dose range was about 12 grams of inositol,

so as high as 18, as low as 12 grams.

But then again, pretty impressive results

considering that these are

over-the-counter supplement compounds.

There’s even some evidence, I should just mention,

that the inositol is also used

for things like obsessive compulsive disorder.

We will do a full episode on OCD in the future.

You can count on that.

But in the meantime, inositol does seem

to have some positive effects on anxiety,

and therefore, it might provide

a kind of supportive indirect effect

for people that are trying to work through trauma and PTSD.

Now, the question is, when would you take it?

Well, by the logic of what we spelled out today,

you probably would not want to take it during a session

or prior to a session where you were trying

to amplify the intensity of an experience

and the recounting of an experience

in efforts to eventually extinguish that experience, right?

Because if you put a drug or a compound of any kind,

prescription drug or supplement of any kind,

into your system, you are essentially short-circuiting

the extinguishing effect, right?

So you could imagine doing this outside of that session

as a way to kind of bring your system

back to baseline, perhaps.

So if you’re going to use these sorts of things,

you want to think about them logically.

And this also really points to the fact

that many of the things that people are doing out there

to self-medicate over use of alcohol or other substances

to try and calm themselves

because they have fear, anxiety, and PTSD

are actually driving that fear, anxiety, and PTSD

deeper into their system,

or at least is not allowing it to relieve itself

through any attempts to recount or replay

and using these top-down narrative circuits

or other approaches.

And the last compound I want to mention

is a particularly interesting one

because it’s neither an anxiolytic,

nor is it something that increases overall levels

of stress and alertness,

but it has some kind of MDMA-ish-like contour to it.

It does not produce, as far as we know,

the same mental effects or physical effects as MDMA

by any stretch,

but that’s the substance that I’m referring to rather

is kava.

Kava has been shown in eight studies

to have a very potent effect on reducing anxiety,

but what’s interesting about kava

is that kava functions by increasing GABA,

this inhibitory neurotransmitter in the brain.

Remember, GABA is the inhibitory neurotransmitter

that is used, that’s employed by the very neurons

in the prefrontal cortex

that serve to inhibit the threat reflex.

So it seems to increase GABA, but it also increases dopamine

and that’s a somewhat unusual compound.

I’m not aware of many compounds

that simultaneously increase GABA and increase dopamine.

And as you recall, that threat reflex has outputs

that tap into the dopamine system.

Now that’s a big leap to go from a compound

that increases GABA and dopamine

and look at a circuit spelled out on paper in front of us

and say, oh, well, there’s GABA and dopamine in this circuit

and therefore this is a good compound to take.

But the effects of kava in human studies

are pretty interesting as it relates to anxiety,

stress, PTSD, and fear.

I’m not going to summarize all of these

because there are eight studies that I’m aware of,

but I’ll just mention again, these are double-blind studies.

So the trial design is solid.

The age ranges are anywhere from 18 to 64,

which is a nice broad age range.

The number of subjects is quite high, both men and women,

no signs of hepatotoxic signals,

so meaning a liver toxicity,

although of course, check with your doctor.

But what was interesting is that

after a period of about three weeks of treatment

with anywhere from 150 milligrams

of what are called active kava lactones,

okay, so there are dosages that relate to that kava.

So 100 milligrams of extract of kava

is a kind of a reasonable typical dose in these studies,

but that spells out to a certain amount of kava lactones.

So you have to kind of boil down

to what is the appropriate dosage.

And it turns out it’s extremely broad.

You’ll see evidence of 50 milligrams,

you’ll see evidence of 300 milligrams,

it’s kind of all over the place.

But each of these studies alone and together

point to the fact that kava does seem to produce

a very potent anxiolytic and general kind of improvement

in depressive symptoms

and reduction in generalized anxiety across the board.

So it’s an interesting compound.

I’ve never actually tried

any of the compounds I just mentioned.

Kava, saffron, or anisotol.

So I can’t report on them personally.

I just know that a number of listeners of this podcast

are interested in supplements

and legal over-the-counter approaches

to their biology and psychology.

And so that’s why I mentioned them.

Those were the three for which I found

the most convincing evidence

and the largest bulk of evidence.

So if you’re interested in exploring those,

proceed with caution, but they do seem quite interesting.

So today we’ve reviewed a large amount of information

about the biology of pathways in the brain and body

that underlie the fear response

and that give rise to chronic fear

and in some cases to trauma and PTSD.

We also touched on a large variety of approaches

to dealing with fear, trauma, and PTSD

that currently exist in the clinical landscape out there.

I also touched on some of the emerging themes.

For instance, this short five minute a day

deliberate self-directed stress of any kind

through respiration or other approaches

of increasing adrenaline as an approach

that might be viable.

I should emphasize might be viable

for enhancing the speed or the potency of treatments

to reduce fear or eliminate trauma.

Most important I believe is to understand

and really think about the logical structure

of the circuits that underlie fear and PTSD.

Because in doing that, each of us,

all of us can think about what sorts of treatments

and approaches make the most sense for them.

I also hope that it will help people lean

into certain practices involving re-exposure

provided that’s done in a supportive environment,

re-exposure to a given traumatic event

in an attempt to extinguish that.

Obviously you want to do that safely,

meaning psychologically safely and physically safely.

There are great practitioners out there

that can help you with that work.

There are also a number of people out there,

I am certain that are carrying certain traumas

or certain fears that they would like to alleviate

that are not in the extreme clinical realm.

And that’s the reason why I touched on a number of things,

including some self-directed practices

that might be useful and reasonable for them to explore.

I realize we covered a lot of information today.

If you’re enjoying and or learning from this podcast

and you’re not traumatized

by the amount of information covered,

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If you go to slash Huberman,

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And last but not least,

thank you for your interest in science.

Thank you.

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