Video summary
Andrew Huberman begins his discussion on working memory by distinguishing it from short-term and long-term memory, emphasizing its unique biological basis. Unlike long-term memories, which rely heavily on neuroplasticity mechanisms like Long-Term Potentiation (LTP) within the hippocampus to store facts or procedures, working memory functions as a transient neural circuit that runs algorithms repeatedly without storing information permanently. This system is critical for sequencing daily actions—such as making coffee before running and then immediately forgetting those steps once completed—and relies on specific dopamine availability in the prefrontal cortex. Huberman notes that while short-term memories are stored via network phenomena involving the hippocampus and neocortex, working memory does not involve significant neuroplasticity or new neuron formation (neurogenesis) but rather depends entirely on the immediate firing patterns of existing neural circuits to hold information briefly before discarding it. The core mechanism governing working memory is dopamine transmission within the mesocortical pathway, which follows an inverted U-shaped function regarding performance levels. Research indicates that individuals with low baseline dopamine availability in their prefrontal cortex have shorter working memory spans and struggle more with eliminating distractors or maintaining focus on a single task. Conversely, those with high dopamine levels can rule out distractions effectively but may face challenges with task switching if dopamine is increased too much beyond an optimal point. Studies using the drug bromocriptine demonstrate that increasing dopamine improves performance in individuals with low baseline levels but degrades it for those already operating at peak capacity or above, confirming that there is a precise "sweet spot" of dopamine required to balance attention and cognitive flexibility without causing confusion or reduced focus. To improve working memory, Huberman explores both behavioral interventions and pharmacological options, highlighting the importance of finding minimal effective doses rather than maximizing chemical input indiscriminately. He reviews studies on L-tyrosine supplementation, noting that while high dosages (15 grams) used in some research significantly improved multitasking performance, such amounts are impractical for general use; instead, he suggests starting with lower doses like 250 to 500 milligrams based on body weight. He also discusses Mucuna pruriens, a supplement containing L-dopa that acts similarly to Parkinson's medication but warns of its potency and the need for medical consultation before use. Additionally, Huberman mentions binaural beats at specific frequencies—40 Hz and 15 Hz—which have been shown in peer-reviewed studies to enhance visuospatial working memory by altering neural activity patterns without affecting emotional processing, offering a zero-cost tool for cognitive enhancement. Huberman concludes that managing focus and attention requires a synergistic approach combining behavioral tools, nutrition, supplements, and potentially prescription pharmacology like amphetamines or modafinil under medical supervision. He acknowledges the controversy surrounding ADHD medications but argues they have a legitimate place in treating subclinical challenges or clinical conditions when used correctly to increase neuroplasticity within relevant circuits. The overarching message is that working memory deficits are not necessarily indicative of global brain damage but often reflect dopamine availability issues that can be addressed through targeted interventions. Whether utilizing behavioral protocols like cold exposure, dietary adjustments with yerba mate for blood sugar regulation and antioxidant support, or specific supplements, the goal remains to optimize the delicate balance of neurotransmitters required for fluid thought processes, task switching, and sustained attention in everyday life without over-relying on any single method.
Read the full video transcript
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 are discussing working memory.
Working memory is a special category of
memory in which we are able to hold
small amounts of information in our mind
for short periods of time. Working
memory is also very closely related to
attention. So, for any of you that are
interested in how to develop better
focus and attention, understanding what
working memory is and some of the things
that you can do to improve your working
memory can be very beneficial. Today I'm
going to talk about what working memory
is, including some of the underlying
biology, although I promise
irrespective of whether or not you know
any biology or you are an expert in
biology, I'll make the conversation
accessible to you. In addition, I will
talk about tools to improve working
memory and I'll also compare working
memory to other forms of memory like
long-term memory and short-term memory.
And through that understanding, I'm
confident that you'll be able to develop
better focus as well as be able to
commit certain forms of information to
your short and long-term memory stores.
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 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. Our first sponsor is Mateina.
Mateina makes loose-leaf and
ready-to-drink yerba mate. I often
discuss yerba mate's benefits, such as
regulating blood sugar, its high
antioxidant content, the ways that it
can improve digestion, and possible
neuroprotective effects. I also drink
yerba mate because I love the taste.
While there are a lot of different
choices of yerba mate drinks out there,
I love Mateina because, again, they have
the no-sugar variety as well as the fact
that both their loose leaf and their
canned varieties are of the absolute
best quality. So much so that I decided
to become a partial owner in the
company. Although I must say, even if
they hadn't allowed me to do that, I
would be drinking Mateena is the
cleanest tasting and best yerba mate you
can find. I love the taste of brewed
loose leaf Mateena yerba mate and I
particularly love the taste of Mateena's
new canned cold brew zero sugar yerba
mate, which I personally helped them
develop. If you'd like to try Mateena,
go to drinkmateena.com/huberman.
Right now, Mateena is offering a free
1-lb bag of loose leaf yerba mate tea
and free shipping with the purchase of
two cases of their cold brew yerba mate.
Again, that's drinkmateena.com/huberman
to get the free bag of yerba mate loose
leaf tea and free shipping. Today's
episode is also brought to us by
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Okay, let's talk about working memory.
And let's start off this discussion by
comparing working memory to other forms
of memory that most people are more
familiar with, or at least when most
people hear the word memory, they
typically are thinking about long-term
memory, like one's ability to remember
the capitals of states or countries, the
different continents, directions from
one location to another, even one's
name. All of those things are examples
of long-term memory. I want to emphasize
that long-term memory really has two
components. There are what we call
declarative long-term memories. So,
these are the things that we can
declare, things like facts about
ourselves or the world or others. And
then there are procedural long-term
memories. Procedural long-term memories,
as the name suggests, are aspects of our
memory that allow us to perform certain
procedures. They're literally action
steps that we take to, for instance,
ride a bicycle or drive a car, which by
the way, we might not be conscious of
ourselves doing after we learn, that is,
after we pass information into our
procedural long-term memory. But, even
once those things become reflexive, they
are stored in our long-term memory. Now,
a discussion of long-term memory is not
the focus today, but
me being a neuroscientist, and I like to
think you all generally being interested
in the underlying biology, I'll just
mention that there's a key structure
within the brain that is part of a
larger neural network that is a
collection of structures, which is
absolutely essential for the formation
and storage of long-term memories. And
that's the hippocampus, which in Latin
means seahorse, and it does look a
little bit like a seahorse. But, we
actually have one on each side of your
brain, so we say hippocampi plural. And
so, what we know is that if people have
damage to their hippocampus of any kind,
that people have trouble accessing or
forming long-term memory, sometimes
both. And there's a lot more that we
could say about long-term memory.
Indeed, I did an entire episode of the
Huberman Lab Podcast about the formation
and storage of long-term memories,
including some tools to improve
long-term memory. We'll touch on a few
of those tools later today, but you can
access that episode if you go to
hubermanlab.com and just put memory into
the search function, and you'll find it
there.
In the meantime, if we want to
understand working memory, we not only
have to understand how it's different
from a long-term memory, but also how
it's different from short-term memories.
Short-term memory is a capacity that we
all have that, as the name suggests,
represents a short-term memory bank for
information that may or may not get
passed into long-term memory. So, for
instance, if you learned anything, and
of course you have, if you can
understand what I'm saying, you've
learned English language. If you can
write, you've learned how to write, et
cetera. Well, in order to learn those
things and to commit them to long-term
memory, the information required to do
those things and to have that knowledge
needed to be held in short-term memory.
And short-term memories are the sorts of
memories that we maintain for somewhere
between a few minutes and potentially a
few hours, maybe a little bit longer.
But only a certain percentage of that is
passed into our long-term memory. So,
for instance, if you listen to this
podcast or you go to a course lecture,
uh whether or not that lecture is about
cognitive material or whether or not
it's about learning a new physical
skill, regardless of what you learn,
you're only going to learn a certain
amount of that information.
But, were we to examine how much of the
information you just heard or that
you're hearing now you remember
immediately after this podcast episode
as compared to say a week later, we
know, based on gosh, probably millions
of scientific papers and studies, that
you're going to have more information in
your short-term memory stores shortly
after being exposed to new information
than you will later. In other words,
only a small percentage of what we
perceive, what we see, what we hear,
etc.,
gets passed into short-term memory and
then only a fraction of that gets passed
into long-term memory. Now, the neural
circuits for short-term memory and the
passage of short-term memories into
long-term memory
involve a lot of different brain
structures, but here again we can
implicate the hippocampus because the
actual passage of short-term memories
into long-term memories
occurs in part within the hippocampus
and then a lot of people don't know
this, some of the memories that we think
of as long-term memories are actually
distributed into the neocortex, which is
the outer portion of the brain. Now, the
point here is less to fill your mind
with different names of things and
nomenclature, but rather to get you
thinking about what's involved in
creating short and long-term memories,
and equally important, that even though
the hippocampus is critically involved
in the formation of short and long-term
memories, that the formation of short
and long-term memories is really a
network phenomenon. In fact, among the
more important themes that comes up
again and again on this podcast anytime
that we're talking about neuroscience or
actually biology in any case, is that
rarely if ever is there one location in
the brain where something happens.
Typically, it's a network phenomenon,
meaning it's the collaboration of a
bunch of different brain areas passing
information from one location to the
next and storing it in a kind of
distributed way. Now, another key thing
to understand about working memory and
how it is different from short- and
long-term memory is that the formation
of short- and long-term memories almost
always involves neuroplasticity.
Neuroplasticity is the nervous system's
ability to change in response to
experience. Now, there are different
types of neuroplasticity. So, often when
we hear about neuroplasticity in the
popular sphere, people don't emphasize
that there are different types of
neuroplasticity and it's worth paying a
little bit of attention to what those
different types are.
There is, for instance, what we call
long-term potentiation. Long-term
potentiation or LTP, as the acronym
goes, is the strengthening of
connections between neurons as a
consequence of their repeated firing
very closely together in time. Okay,
there's a lot more to it, but if you've
ever heard the phrase fire together,
wire together, sometimes that is
misattributed to Donald Hebb, who did
talk about neuroplasticity. By the way,
Donald Hebb was a psychologist up in
Canada who talked about neuroplasticity
in the context of lots of different
forms of learning, but that fire
together, wire together phrase was not
actually stated by Donald Hebb. It was
stated by Carla Shatz, my colleague at
Stanford, and she was referring to LTP
but other forms of neuroplasticity that
occur mainly in development when neurons
fire very closely in time and thereby
strengthen those connections, which can
include LTP. Okay? So, for now, think of
LTP as anytime that some small group of
neurons, could be two neurons, could be
2,000 neurons are very active closely
together in time, and they have access
to one another physically, and the
consequence is often, not always, but is
often LTP. That is the strengthening of
those connections such that after that
barrage of activity subsides, those
neurons can speak to each other. They
can communicate through electrical
activity and chemical activity much more
easily. Their communication is more
robust. It's like removing a wall
between a conversation such that the
conversation can take place more
fluidly. Now, there are other forms of
neuroplasticity including LTD, long-term
depression, which, unfortunately, the
name often calls to mind ideas about
depression as a psychiatric or a
psychological symptom, but it has
nothing to do with that. Long-term
depression is simply the inverse of LTP.
It's actually the weakening or the
removal of connections that we call
synapses between neurons.
I want to emphasize that both LTP and
LTD are both critically involved in lots
of different kinds of learning, and both
of them tend to be involved in the
formation of both short-term memories
and long-term memories. And, this is
very important, in the removal of
short-term memories and long-term
memories, literally, forgetting of
certain things because,
as we all know,
there are many things that we will never
forget, and there are also things that
we almost always forget. Now, there's a
third form of neuroplasticity that's
involved in the formation of short and
long-term memories that's important for
us to discuss just briefly. But, I do
want to emphasize that there are not
just three forms of neuroplasticity.
There are many other forms, dozens, if
not more, things like
spike-timing-dependent plasticity,
paired pulse facilitation, and on and
on. But, the third type of
neuroplasticity that I'd like to mention
now is neurogenesis. Neurogenesis is the
formation of new neurons. Now,
neurogenesis is robust in the developing
nervous system. We know this. It's
robust in the developing nervous system
of animals and humans. However,
neurogenesis, the literal formation of
new neurons in the brain,
is a very exciting idea, and it does
occur, and it's very exciting in a way
that has motivated lots of popular press
outlets to talk about or to discuss
papers that have discovered neurogenesis
in the adult brain. Because
let's be honest, what's more exciting
than the idea that your brain can add
new brain cells later in life. And
indeed, that has been shown even in
people well into their 80s and 90s.
However, it's very important to note
that the total amount of neurogenesis
that occurs in the adult human brain is
infinitesimally small
as a mechanism for neuroplasticity and
learning as compared to the other forms
of neuroplasticity that we discuss, such
as long-term potentiation and long-term
depression. So, I don't want to, you
know, throw cold water on the topic of
neurogenesis. It's an incredibly
interesting and important topic, but all
too often they tend to eclipse the much
more common mechanism for the formation
of short- and long-term memories, which
are those other forms we just talked
about, LTP, LTD, etc. So, the point here
is that yes, indeed, there are new
neurons that can be added in the adult
brain, maybe even in the adult human
brain. And there is some evidence that
some of those new neurons are added to
the hippocampus. In fact, a particular
region of the hippocampus called the
dentate gyrus of the hippocampus. And
there's been a lot of controversy about
how much neurogenesis occurs or doesn't
occur, and whether or not it occurs
after puberty or not. There's a whole
field of people battling over this now
for several decades, but one thing is
very clear. Neurogenesis, while it's
very exciting and intriguing, is not the
main mechanism by which the formation of
short- and long-term memories occurs.
When you learn new information, as you
are right now, the storage of that
information in your short-term memory
networks, which is then passed on to
your long-term memory networks, and that
can be recalled, that allows you to
state certain facts about, for instance,
the existence of this thing called a
hippocampus. Hopefully, you will
remember that going forward. Or your
ability to perform any kind of motor
movement that you learned now or way
back in childhood.
Most of that is the consequence of the
strengthening of particular connections
and the weakening of other types of
connections. Those are the two major
forms of neuroplasticity. Okay, so I
don't want you to get the impression
that there's something wrong with my
memory and that I forgot that this
episode is not about short or long-term
memory, but that it's about working
memory. And indeed, I have not
forgotten. So, now is where I tell you
why I've been talking about short and
long-term memory and the mechanisms of
those. Because I want them to provide a
stark contrast for what we call working
memory. Working memory,
as far as we know, does not involve
neuroplasticity. Or at least, if it
does, it's not a particularly robust
aspect of working memory. Rather,
working memory is the reflection of a
particular neural circuit running an
algorithm over and over and over for
different types of information, but the
information isn't stored. It is actually
intentionally discarded. Now, what sorts
of daily activities and life activities
would require working memory?
The answer to that is basically
everything that you need to do but that
you don't want to remember. Now, what
types of things would those be? Well,
let's think about it. Most all of us
learned at some point in our life to tie
our own shoes. Presumably, you know how
to tie your own shoes. If you don't,
perhaps you should learn
or wear Velcro or slippers, I don't
know, but assuming you can tie your own
shoes, that's something that you know
how to do and you can do it as a
procedural long-term memory.
You can do that action. You don't have
to think about it too much. Working
memory would come into play when, say,
you wake up in the morning and you know
that you need to head out for a jog, but
you also need to make a cup of coffee
first and you need to remember where the
coffee is, where your shoes are, and
perhaps you're making a phone call or
you're having a conversation while you
need to tie your shoes and so on and so
forth. Working memory is basically the
taking in of information that's critical
for you to sequence your actions over a
short period of time and then forget
that sequence. For instance, I'm willing
to bet that you put your shoes on to go
running before you go running. That's
sort of a duh. And if you're like me,
you drink your water, your coffee, your
yerba mate before you go running. The
point here is that if you wake up in the
morning and you like caffeine before you
go for a run, there are certain series
of action steps that you need to carry
out to hydrate, make that cup of coffee
or tea, drink it, put on your shoes,
head out the door. You need to sequence
things properly, but you don't want to
commit your long-term or even your
short-term memory stores to carrying out
that sequence. You simply want to be
able to carry out that sequence and then
discard that information about the
sequence and focus your attention on,
for instance, what trajectory you're
going to run through the park or around
your neighborhood.
Then you want to discard that
information and you want to lean into
the next portion of your day and so on
and so on.
In fact, working memory is involved in
essentially every activity, both
cognitive and motor, from the point you
wake up in the morning until the time
you go to sleep at night for every
single day of your life. And we know
this because there are indeed people who
have diminished working memory or even
lack working memory entirely, although
the latter is somewhat rare, it has
happened. And as you can imagine, they
have a complete failure of ability to
sequence activities and their lives are
extremely difficult. They need a ton of
assistance from other people.
Even more assistance than do people who
have minimal or no long-term memory.
Okay, so this is really highlighting
just how important working memory is.
Working memory is basically the way that
you navigate any immediate environment.
And as I mentioned earlier, it's very
closely tied to attention because in
order to know what to do now and then
what to do subsequently and then
subsequent to that.
You need to be able to hold your
attention to the things you need to do.
So, working memory and attention
collaborate literally at a neural
circuit level and at a neurochemical
level in order to allow you to move
through your day in an adaptive
functional way. And people who have
challenges with attention or focus
or working memory, and sometimes it can
be hard to dissociate which one they're
having challenges with, really have a
hard time moving through life as
compared to people whose attention and
working memory is more robust. Now, the
good news is today we're going to talk
about working memory, some of the neural
circuits involved, and some of the
neurochemicals involved that can augment
or improve working memory, and we're
also going to talk about what one can do
to directly increase the amount of
neurotransmission of those particular
chemicals within the circuits that
control working memory. In other words,
to improve your working memory. Now, I
can talk about working memory and the
mechanisms, et cetera, all day long.
But, as is often the case, sometimes
it's better to not just learn about
concepts, but actually to experience
them in real time. So, what we're going
to do now is I'm actually going to give
you a working memory test. This is the
sort of working memory test that you
would take if you were to go into a
psychology laboratory or a neuroscience
laboratory and they were studying
working memory in humans. Now, there's
another advantage to us doing this in
real time right here as you're listening
or as you're listening and watching. And
that's because you're going to get data.
You're going to get information about
what your baseline working memory
capacity is, and you're going to want to
keep those data in your short-term
memory stores, maybe even your long-term
memory stores, but certainly your
short-term memory stores because shortly
later in this episode I'm going to talk
about different ways to improve your
working memory depending on where your
baseline working memory starts. Which,
by the way, turns out to be a pretty
good proxy for the levels of a
neuromodulator called dopamine within
the neural circuits that control working
memory. So, right now, let's take a
working memory task. We're going to do
this purely through audio form because I
realize some people are watching and
listening to this on YouTube and others
are just listening to this episode. So,
there are not going to be any visual
cues or slides that I present. And
that's perhaps what distinguishes what
we're about to do most from what would
happen in a laboratory. Typically in a
laboratory, there would be some visual
presentation of what I'm about to say,
but here because of the format that most
of you are consuming this information
by, we're going to do this purely by
audio.
So, the first test of your working
memory is very simple.
I'm going to read off a series of
letters. And your task is to remember as
many of those letters as you can.
The first string of letters is J K Z P I
Okay, just to make this really easy, I'm
going to say it twice. Although
typically in a working memory task, it
would just be said once, but I'm going
to make this extra easy.
J K Z P I
Okay?
Now, you in your own head can try and
recite back those letters if you like.
Okay. Second string of letters.
R O M K L E
Right, I'm going to make this extra
simple and do it again. Not typical for
a working memory task, but there are
some working memory tasks where that
happens.
R O M K L E
Okay?
Now, a third string of letters. This
one's going to be a little bit longer.
So, queue up that working memory and
attention.
W A C Q V D N
I'll repeat that again. W A C Q V D N
How many of the letters I just read can
you remember? Okay, so depending on how
many letters you can remember,
perhaps you have a low, moderate, or
high degree of working memory.
Keep in mind that some of you are
perhaps doing other things. You're
attending to driving or other tasks
within your home or your office.
And so perhaps you weren't able to pay
full attention. So there'll be some
variation there. But nonetheless, after
reading each of those strings of
letters, you were asked to recall those
letters in your mind. And if you wrote
them down and you're rereading them,
yes, that's cheating.
But how about this? What if I were to
ask you now about the simplest first
string of letters, the one that
consisted of only five letters?
How many of you can remember any of
those five letters now?
Okay, I can't hear you and if you're
shouting them out, I can't see you if
you're raising your hand. But chances
are most of you have forgotten the first
series of letters. Even though it was
quite short and you could remember it
early on. That ability to remember that
string of letters when you first heard
them,
and indeed I read them twice. So I'd be
very surprised if any of you couldn't
remember that string of letters after
hearing them twice. But I also read you
some other letters in the interim, okay?
So that now, just a couple minutes
later, I'm asking you to remember that
first string of five letters. And
assuming that you didn't write it down
and you're not cheating, chances are you
remember anywhere from two to zero of
those letters in that first word. Which
is a perfect example of your working
memory. Nothing got committed to
short-term, much less long-term memory.
Rather, your working memory was able to
work with that information, hold it in
mind for just as long as you thought you
needed to know that information. But
then,
thank goodness,
that information was discarded.
You didn't know that I was going to ask
you for that first string of letters
again after reading you the longer
string of letters, but I did that
deliberately to show you how your
working memory works. So, in some sense,
the working memory task is a bit unusual
in that it's a test of yes, memory in
the very, very short-term, but also a
test of your ability to forget, to
discard information that's not critical.
And that gets us back to the original
definition of working memory, which is
our ability to attend to specific small
batches of information, remember it for
just as long as we think we need to, and
then to discard that information. And by
the way, if you want to know what those
first five letters were,
they were J K Z P I.
I'd like to take a brief moment and
thank one of our sponsors, and that's
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So, now's where we talk a little bit
about the neural circuitry and the
neurochemistry of working memory. Now,
it's important that we do this because
in a few minutes you're also going to
learn that people generally fall into
two broad bins of having a high or low
baseline of a certain neurochemical in
the brain that affords them either high
or low working memory capacity. Now, in
reality it's a distribution. In fact,
it's what we call a normal distribution.
So, it really isn't two bins, but during
today's discussion and in fact in a lot
of laboratory studies, we can actually
bin people into these two groups. The
neural circuitry underlying working
memory involves a lot of different brain
locations, that is a lot of different
neural networks collaborating to create
this thing we call working memory.
However, there are a couple of key hubs,
that is locations within the brain that
are especially important for working
memory.
The ones that I'd like to focus on today
involve the prefrontal cortex. So, this
is neural real estate that resides just
behind the forehead and
the neurons in the brain stem, so
further back in the brain, that
manufacture dopamine and that send their
little wires that we call axons up to
the prefrontal cortex to release
dopamine. Dopamine is a neuromodulator.
Many people are familiar with dopamine
and familiar with it in the context of
motivation and drive. Sometimes people
mistakenly think it's only involved in
pleasure, but dopamine is involved in
motivation and drive.
When dopamine systems go awry, that is
if their levels get too high, that can
create manic states, it can create
addictive states.
When dopamine levels are too low, you
can get movement challenges such as in
Parkinson's, which is a deficit or a
literal destruction of the neurons that
manufacture dopamine. There are a bunch
of different areas of the brain that
those dopamine neurons in the brainstem
project to, but for right now, we're
going to focus almost entirely on the
dopamine projections from the brainstem
to the prefrontal cortex, which is
called the mesocortical
circuitry. I'm not going to get into the
origins or the meaning of the
mesocortical versus other dopamine
projection systems. I did that in a
couple of episodes about ADHD and
attention and dopamine in particular,
and you can find those at
hubermanlab.com. Just put dopamine and
circuits into the search function and it
will take you to those particular
timestamps where I described that. But,
since we want to keep things fairly top
contour at the level of neural circuitry
here, just know that there are a bunch
of neurons that manufacture dopamine
back in the brainstem that send their
axons, those little wires, up to the
prefrontal cortex, and that the amount
of dopamine released
per unit time, so in a certain amount of
time, strongly dictates the extent to
which working memory capacity is going
to be high, medium, or low. Now, I want
to be very clear because I'm going to
come back to this a little bit later
again and again.
It is the case that when dopamine levels
are lower,
that is, either there are fewer neurons
that have the potential to release
dopamine in the frontal cortex, or for
whatever reason less is being released
in the frontal cortex, that working
memory performance tends to be lower as
compared to conditions where dopamine
release or the availability of dopamine
is higher. However, it is not the case
that more dopamine is always going to
equate to improved working memory. This
is so important that I'm going to say it
again. It is not always the case that
increasing the amount of dopamine
transmission in the frontal cortex leads
to improvements in working memory. There
is a specific criteria that allows us to
predict whether or not it will improve,
or maintain, or actually degrade working
memory performance. So, before you head
to the end of the podcast to try and
figure out ways to increase dopamine to
improve working memory, please keep that
fact in mind. Don't just commit it to
your working memory, commit it to your
short- and long-term memory because
that's very important if your goal is to
improve your working memory. With that
said, I do want to describe just a
little bit of research showing the
relationship between having a low
working memory span as it's called, the
ability to only remember a few letters
or numbers or short batches of
information as compared to a high
working memory span, meaning longer
strings of letters, longer strings of
numbers, which of course in the real
world translates to being able to carry
out shorter versus longer action
sequences
as described earlier in the scenario
where you're getting up in the morning
and you're making coffee and you're
heading out for a run, etc., etc. People
do differ in terms of their working
memory capacity and there's a classic
study done by Cools and D'Esposito and
colleagues. This was published in 2008
where they had a way to label the amount
of dopamine that is available for
release in the frontal cortex in human
subjects.
They did this by the injection of a
specific dye. That dye gets taken up
specifically by the neurons in the brain
that manufacture dopamine. Then they
were able to image the brains of those
people while those people were wide
awake using something called positron
emission tomography. Again, the specific
tool isn't necessarily important but
since some of you like to know and what
they found is that for people that had a
high working memory span, that is could
remember long strings of numbers or
letters or other information,
they tended to be the people that had
more dopamine available for release in
the frontal cortex either because they
had more of the dopamine neurons
themselves or similar number of neurons
but those neurons had more dopamine to
release, okay?
And they also found the converse.
Individuals that had a low working
memory span and ability had less
dopamine available for release. So, that
establishes a correlation but it's not
causal. A different study, which is also
a classic,
was carried out by
Brazos Brown, Ross Wald, and Goldman.
And this is a really important study
because in this study they were able to
introduce small amounts of dopamine
directly into the cortex
and evaluate working memory capacity.
Now, anytime a working memory test is
done, the same pattern always emerges.
This is regardless of any dopamine being
infused into the brain, which is
people and animals, for that matter, are
very good at remembering short spans of
numbers, letters, or other types of
information. So, if you tell them one
thing, like the letter A, and then you
ask them, "Do you remember the letter?"
almost everybody remembers that. But if
you give them a string of 10 letters,
they remember fewer of those 10 letters.
That's sort of obvious, but it's an
important point to emphasize
nonetheless.
And so, there's a kind of a dropping-off
curve of performance as one progresses
from fewer to greater number of items to
be remembered.
In this study, when dopamine was
introduced to the frontal cortex,
the number of things that individuals
could remember simply increased. It was
a very straightforward result. More
dopamine introduced allowed longer
letter, number, and information strings
to be remembered. And of course,
forgotten, because that's what working
memory involves, remembering and then
discarding of information shortly
thereafter. Now, the findings that I
just described complement what I said
before, which is the naturally occurring
experiment. Bring people into the lab,
measure their working memory span, look
at how much dopamine they make. Higher
dopamine, better working memory. Lower
dopamine, lower working memory.
The experiment I just described was one
in which dopamine is introduced, showing
that dopamine is very likely the
rate-limiting, or the capacity-limiting,
it's probably the better way to put it,
the capacity-limiting
neuromodulator for improving working
memory.
That's a fancy nerd-speak way of saying
more dopamine allows for better working
memory. But a critical feature of this
experiment is that they did a number of
experiments where they didn't introduce
dopamine, but instead they introduced
other neuromodulators to the prefrontal
cortex, such as norepinephrine
or serotonin. And the interesting
finding is that the addition of
norepinephrine or serotonin, which of
course are other neuromodulators that
can change the firing patterns of
neurons in the prefrontal cortex, but
elsewhere as well.
It's just that in this case they were
added to the prefrontal cortex had no
effect on working memory. It neither
improved nor degraded working memory
when those neuromodulators were
introduced. In other words, dopamine and
perhaps only dopamine seems to be the
dominant neuromodulator for regulating
the degree
that is, whether or not you have
small, medium, or large amounts of
working memory capacity in the
prefrontal cortex. And of course, there
have been a bunch of other experiments
that are worth mentioning briefly in
this context, such as taking people that
have a high working memory capacity and
then indeed have their brains imaged and
one sees that they have high levels of
baseline dopamine, especially the
dopamine projecting to the prefrontal
cortex, and then they're given a drug
that depletes dopamine within the
prefrontal cortex and their performance
drops. And so what's so nice about the
literature around working memory is that
while I'm not covering all of that
literature exhaustively,
it all tends to jive. It all points in a
direction whereby the levels of dopamine
being released in the prefrontal cortex
during working memory tasks correlates
very strongly with capacity to perform
working memory task. Lower dopamine,
lower working memory span, as it's
called. Higher dopamine, higher working
memory span. Okay, so next we're going
to do another working memory task,
different than the one we did earlier.
And we're going to do that with a
specific purpose in mind, which is for
you to be able to determine what your
working memory capacity is,
and by extension, your baseline levels
of dopamine or at least the levels of
dopamine that are likely being released
into your prefrontal cortex while you do
these working memory tasks. In other
words, we're going to try and figure out
whether or not you are of the low,
medium, or high working memory capacity.
And of course, we're doing that in part
to try and establish whether or not you
likely have low, medium, or high amounts
of dopamine available for release in the
prefrontal cortex. Of course, we're not
putting you into a positron emission
tomography scanning device. We aren't
able to do that for obvious reasons.
But, keep in mind that what we're about
to do is very similar and in some cases
identical to laboratory studies where
the researchers were trying to determine
what people's levels of dopamine within
these particular neural networks we've
been discussing, the mesocortical
pathway, are likely to be. In other
words, performance on the working memory
task that we are about to do is a decent
indication of what the dopamine levels
that are available for release in your
prefrontal cortex perhaps might be. Now,
I say perhaps might be because I don't
want to cause any unnecessary alarm if
for instance, you fall into the low
working memory span group. In fact, if
you fall into the low working memory
span group, there are actually some
terrific tools that you can use to
improve dopamine transmission in those
pathways and improve your working
memory. I also don't want people to get
the impression that somehow performance
on this working memory task is
reflective of some larger dopamine issue
in the brain and certainly it is not, I
repeat, it is not diagnostic of
Parkinson's or any kind of
neurodegenerative condition. Although, I
will say that deficits in working memory
are common in patients with Parkinson's
for obvious reasons. Those patients have
deficits in dopamine neurons, not only
production, but the number of dopamine
neurons.
It's one of the hallmark features of
Parkinson's, but also in things like
traumatic brain injury, et cetera. But,
the working memory task that you're
about to take, when given to a general
population or a group of undergraduates
or, you know, so-called normals or
typical control subjects, which all of
you are. Okay? So, unless you're dealing
with a traumatic brain injury or you
know you have Parkinson's,
we know that the data that you're going
to get back right now is very similar to
the data that people get back when they
do these sorts of studies in a
laboratory. That is, it's typical for
some people to have a short working
memory span, some people to have a
medium working memory span, and some
people to have a high working memory
span. And today we're actually just
going to divide into two bins, short
working memory span and high working
memory span. And we can have some degree
of confidence that correlates with the
amount of dopamine available for release
in the frontal cortex.
But, and this is a very important point,
as we progress along this discussion of
working memory, the neural circuits,
dopamine, etc., I want to make clear
something that I said earlier, which is
that it is not the case that increasing
the amount of dopamine that's available
always increases working memory span. In
fact, there's a common circumstance
whereby people with a relatively high
degree of working memory capacity
increase their dopamine levels even
further using pharmacology or other
methods that we'll discuss, and their
performance actually can degrade. Okay?
So, if any of that is confusing now,
we'll make it all very simple going
forward, so that if you decide to
implement any of the protocols discussed
in this episode, that you are aware of
what you can expect and whether or not
you are in the category of people that
should or perhaps should not incorporate
those protocols. Okay, let's test your
working memory again. This time the
working memory task is going to be a
little bit different than the one you
did previously. This working memory task
involves me reading six different
sentences to you, and your job is to pay
attention to these six sentences,
because you're going to be asked some
information about these sentences in a
few moments. The first sentence is
real estate costs are going up.
The second sentence is
the Atlantic Ocean is warm in summer.
The third sentence is there's a lot of
interest now in electric cars.
The fourth sentence is some reptiles eat
only once a year.
The fifth sentence is
kids nowadays look at screens more than
60% of their waking life.
And the sixth and final sentence is
football can mean different sports
depending on the country.
Okay, so I read you six sentences.
They were moderately long, I confess.
Your job for the working memory task is
now to recall as many of the final words
of each of those sentences as you can.
I'll give you a few moments to do that.
Now before I tell you what the final
word of each of those sentences actually
is,
I want to remind everybody that working
memory capacity
follows a normal distribution. So some
of you will be able to remember the
final word of perhaps five or even six
of those sentences, although I must say
that is exceedingly rare.
Some of you are going to be able to
remember three to four of the final
words of those sentences, and that's
more typical. That actually represents
the average or the mean, as we call it.
And then fewer people, although still
many of you, will only be able to
remember one or two of the final words
of those sentences.
Okay, so now I'm assuming that most of
you have tried to call to memory the
final word of as many of those six
sentences as you can. And maybe you've
written them down or you've typed them
into your phone or you have some record
of what you recall those six final words
of those sentences are.
Now I'm going to tell you the actual
final word of each of those sentences.
The final word of the first sentence was
up, because as you may recall, the
sentence was real estate costs are going
up.
The final word of the second sentence
was summer,
because the sentence was the Atlantic
Ocean is warm in summer.
The final word of the third sentence was
cars. Because the sentence was there is
a lot of interest in electric cars.
The final word of the fourth sentence
was year. Because the sentence was some
reptiles eat only once a year.
The final word of the fifth sentence was
life. Because the sentence was kids
nowadays look at screens more than 60%
of their waking life.
And the final word of the sixth sentence
was country. Because the sentence was
football can mean different sports
depending on the country. Okay, so be
honest with yourself and tell yourself
and you don't have to tell anyone else
if you don't want to,
how many of the final words of those six
sentences you could remember correctly.
It's important that you remember them
correctly.
Again, the number of words that you can
recall, that is your working memory
span, is going to vary from person to
person. But we can take the normal
distribution of those scores and sort of
draw a line down in the middle and say
that if you could remember three to six
of the final words of those sentences
correctly, you're going to fall into the
high working memory span group.
Whereas if you could only remember one
or two or maybe zero of the final words
of those six sentences, then you're
going to be in the low working memory
span group. Again, I don't want to alarm
anybody. This doesn't mean that you have
any global memory deficits or dopamine
deficits, but it is important,
especially if you plan to apply any of
the protocols to improve working memory,
that you faithfully, that is you
accurately report your working memory
performance at least to yourself. Now,
as you recall, whether or not you have
low or high, and here we are just
binning into low and high. There's no
medium. We've divided it right at that
line. We're saying if you can remember
three to six, we're calling that high
working memory span, at least for this
discussion. And if you can remember
fewer than three, even down to zero,
of the final words of those sentences,
that's low working memory span. We're
dividing it in two. We've divided you
into two groups. and we do know
when this has been done in large numbers
of human subjects
and some in some cases all of those
subjects have their brains imaged for
the amount of dopamine available for
release in their prefrontal cortex that
short working memory span correlates
with lower amounts of dopamine whereas
higher working memory span or longer
working memory span whatever you want to
call it correlates with more dopamine
available for release in the prefrontal
cortex.
Now this is where things get really
interesting and frankly really exciting
for everybody especially the folks in
the low working memory span group. Work
from Marcus Bizzito and colleagues at UC
Berkeley as well as other laboratories
have explored the consequences of
increasing dopamine levels in the brain
of
typical populations of individuals. So
these are not people with Parkinson's or
TBI but undergraduate students which we
do realize is not completely
representative of the quote unquote
normal population outside the university
but also people from the community so
people who are not university students
and so on.
And the ways that they've increased
dopamine in those individuals had tended
to rely on pharmacology. So these are
prescription drugs that most often have
been developed for the treatment of
Parkinson's in order to increase
dopamine levels but for some other
purposes as well drugs like
bromocriptine which we know are
so-called dopamine agonist. An agonist
is a drug that has the consequence of
increasing the amount of a given
neurochemical in this case dopamine
whereas an antagonist is a drug that
either blocks or prevents or somehow
lowers the total available amount of a
certain chemical such as dopamine or
serotonin etc. So bromocriptine
is a drug that increases dopamine. So
when human subjects came into a
laboratory didn't take any drug no
bromocriptine yet and of course they
were being evaluated for whether or not
they were taking any meds for ADHD,
their caffeine consumption, etc. There
were certain rule-ins and rule-outs for
that study.
But, certainly people that were taking
any kind of prescription medication for
ADHD were not included in the study
or were eliminated from the study
because
those drugs can indeed increase dopamine
as well as some other neuromodulators
such as norepinephrine and epinephrine.
I covered all that in the two ADHD
episodes that I did, which again you can
find at hubermanlab.com. Just go to the
search function, put in ADHD. In any
event, in these studies they took people
that had not taken any drugs to increase
dopamine,
had their working memory measured very
similarly to the way that you measured
your working memory a few minutes ago
with the six-sentence
business that we did.
And then they took bromocriptine, and
they either took a low, a moderate, or a
high dose of bromocriptine.
And
90 minutes later, they took a working
memory task. And what was observed was
very interesting. You can probably
predict what it is based on everything
I've said up until now. Individuals that
initially had low baseline levels of
dopamine and therefore shorter working
memory span,
so they only remembered zero to about
three of the final words of that
six-sentence series,
their performance significantly
improved. They were able to remember
four and in some cases up to six of the
final words of those sentences.
Now, that is in complete agreement with
everything we said up until now.
Simply says that dopamine is important
for working memory. If you start off
with lower
dopamine stores or dopamine availability
for release in the prefrontal cortex,
lower working memory performance,
increased dopamine through ingestion of
bromocriptine,
which is a dopamine agonist,
all of the circuit changes that we want
and would expect to improve working
memory occur, and indeed working memory
improves. Okay? Very straightforward.
That's interesting, but the even more
interesting part of the study is that
individuals that already had high
working memory span, when they took
bromocriptine at a low or a moderate
dose,
their working memory did not increase
further. Now, if somebody was already
getting six of the final words of those
six sentences, well then of course they
couldn't improve their performance
anymore. But many of the people in the
high
working memory span group of course only
remembered four, in some cases three.
Typically it would be four, five, or six
of the final words of those sentences.
When they took bromocriptine at low or
moderate doses,
their working memory did not improve
significantly. There was either no
change or a very modest change. And
here's where things get really
interesting. When individuals who
already had a high working memory span
took the highest dose of bromocriptine,
and by the way, studies verified that
the amount of dopamine available indeed
increased, so that was important to do
and they did that,
well, their working memory performance
actually decreased,
such that now they had a short or a low
working memory span. So, what this tells
us is that the relationship between
dopamine and working memory follows an
inverted U-shaped function. So, imagine
a U and then just flip it over, meaning
if you have low dopamine availability in
the prefrontal cortex, working memory
span is short. As you increase that
amount, working memory becomes greater,
but if you increase the amount of
dopamine in the prefrontal cortex too
much, working memory span actually drops
significantly below the baseline that
you started with. Now, this is important
for a number of reasons, not the least
of which is the known relationship
between
working memory and attention. Now, this
is very important to understand in the
context of ADHD, but also for people who
don't have ADHD and are struggling to
maintain focus and attention and carry
out working memory tasks throughout
their normal everyday life, not in the
laboratory, but just moving through
life. Because these days we hear a lot,
a lot, a lot about people struggling
with focus and attention. Perhaps, we
don't know, perhaps in part due to
overuse of smartphone, social media,
etc. Although there's not yet a direct
causal relationship that's been
established.
The data that are emerging suggests that
indeed overuse of those things can cause
problems, but
regardless of the source, there does
seem to be more ADHD both in kids and in
adults and subclinical
challenges in focus and attention. And
here's where things get really
interesting as it relates to the neural
circuitry. Work from Desposito and
colleagues and other laboratories as
well have shown using the similar
paradigm that I described before, giving
people drugs to increase their baseline
levels of dopamine above their initial
starting point of short or long-term
memory span capacity.
And then had people perform different
types of working memory tasks that tap
into two different aspects of attention
and working memory. Up until now we've
been talking about working memory as
kind of just one thing. But working
memory actually involves two things or
at least two things. The first is that
in order to carry out a working memory
task and to attend to something, to
really focus, we need the ability to
rule out distractors. We need to be able
to not pay attention to things that
would otherwise distract us.
In addition to that, we need to be able
to switch from one context to the next,
right? Making the cup of coffee to
putting on one shoes and heading out the
door. And in some cases layering
different contexts together, talking on
the phone while tying one shoes and so
on and so forth.
What this work shows us is that the
ability to task switch and context
switch, that is to shift around what it
is that we're paying attention to and
interleave different things that we're
paying attention to, something that's so
critical for moving through our daily
lives, is largely dependent on the
dopamine projections to a structure in
the brain called the basal ganglia,
which is a structure I've talked about
before on this podcast, but if you
didn't hear about it, we can just
broadly define the structure as being
involved in movement generation and
stopping movement generation. In fact,
it's often discussed as the neural
circuitry that generates go as in do
commands and no go, don't do commands.
So, the basal ganglia are involved in
task switching and they're involved in
task switching in part by sending
certain commands to go do certain things
and no go to not do other things, all
right? Task switching. Stop doing this,
start doing that. Start doing that, stop
doing this.
And sometimes to varying extents, right?
I mean, we can take any real-world
scenario of tying one's shoes while
talking on the phone and we could
microanalyze it in the context of this,
but I think if you think about it just a
little bit, you'll understand that in
order to perform daily tasks, we need to
be able to task switch and that's not
always a start one task and start a new
task and oftentimes we're interleaving
different tasks to varying degrees. Now,
the other aspect of working memory and
attention is to eliminate distractions,
to not pay attention to the irrelevant
stuff in one's environment or even the
irrelevant stuff on your own body, like
you can't get distracted by, you know, a
button that, you know, might not be only
partially buttoned or maybe some little
something on your sleeve if you're
trying to do something else at that
moment, okay? And people with ADHD and
people who have subclinical challenges
in focus really have a hard time with
this, right? You know, the sort of
stereotype is, you know, the oh look, a
squirrel, that whole thing. But really
this typically exists as a more subtle
and challenging phenomenon for people
where they either can't remember what
they were doing or they're simply drawn
down different trajectories, different
thought trajectories or action
trajectories and then they have a hard
time making it back to the original
thing that they were trying to focus on.
And we know based on these studies of
dopamine and neuroimaging that
eliminating distractors is largely the
consequence of dopamine neurons
projecting to the prefrontal cortex.
Okay, now why am I telling you all this
neural circuitry stuff? Well,
yes, there are a bunch of studies
showing that if you selectively activate
the neurons that send dopamine into the
basal ganglia, you improve task
switching ability without an improved
ability to rule out distractors. Or if
you selectively increase the amount of
dopamine from neurons projecting to the
prefrontal cortex, that you're able to
selectively improve the elimination of
distractors without improving
task switching ability. For practical
purposes in this discussion, we want to
pay careful attention to whether or not
the data tell us that those particular
protocols, those particular approaches
are globally increasing dopamine, that
is increasing the activity of dopamine
neurons projecting to the basal ganglia
and the prefrontal cortex, or
selectively to the basal ganglia, or
selectively to the prefrontal cortex.
And what I can tell you now is that
fortunately there are several protocols,
some of which are behavioral, some of
which involve specific over-the-counter
supplements, and some of which involve
prescription pharmacology that can tap
into each of these systems independently
as well as globally increase dopamine to
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Okay, so let's talk about protocols to
improve working memory, specifically by
way of changing levels of dopamine in
the brain. Now, I've discussed dopamine
many times before on this podcast. In
fact, we have entire episodes devoted to
optimizing and regulating dopamine, and
of course dopamine comes up within the
context of the ADHD episodes and other
episodes as well. And again, if you have
specific questions about dopamine or any
other topic for that matter, if you go
to hubermanlab.com, that website has
been engineered so that you can put one
word, such as dopamine, but also
multiple keywords, so perhaps dopamine
exercise or dopamine cold plunge, etc.
into the search function and it will
take you to the specific timestamps of
multiple episodes where those topics
were discussed, as well as newsletters
where some of that information has been
condensed into short PDF form, etc. So,
we certainly are going to cover some
material about improving dopamine for
sake of improving working memory now,
but if you're generally interested in
the science and pharmacology of dopamine
and protocols to modulate dopamine
levels, all of that can be found at
hubermanlab.com. Okay, so let's say you
have a short working memory span or a
moderate working memory span and you
want to experiment with increasing
levels of dopamine for sake of improving
working memory. Now, there are a lot of
different ways that one could imagine
doing that. Let's start with the
behavioral tools known to increase
dopamine stores. That is, shown in
peer-reviewed studies to increase
dopamine stores within certain circuits
of the brain that are relevant for
working memory performance. And the
protocol that immediately leaps to mind
is the use of certain non-sleep deep
rest protocols. Now, non-sleep deep rest
or NSDR is actually a term that I coined
because there is a practice that's been
established for many hundreds of years
called yoga nidra, which actually means
yoga sleep, whereby individuals,
potentially you, if you decide to do
them,
lie down, listen to a script, that is,
listen to an audio script, which
generally instructs you to do long
exhale breathing, to deliberately relax
your musculature of your face and of
your body. And yoga nidra typically also
involves doing certain intentions. And
the instruction always given at the
beginning of yoga nidra is that you
should try to not fall asleep. Now, some
people sometimes fall asleep, some
people don't fall asleep, but the idea,
and there are data to support that yoga
nidra puts people into kind of a shallow
pattern of sleep. Um certainly not deep
sleep and not rapid eye movement sleep,
but it's a very interesting and unusual
brain state for which we're starting to
understand more. And actually, uh I have
some plans in the not-too-distant future
to collaborate with Matthew Walker, the
author of the book Why We Sleep, and
some other colleagues to try and figure
out what exact patterns of neural
activity are taking place in the brain
and rest of nervous system during yoga
nidra and this similar protocol, which I
call non-sleep deep rest. The difference
between yoga nidra and non-sleep deep
rest is that non-sleep deep rest doesn't
include any of the intentions and
removes a lot of the kind of opaque or
sometimes called mystical language from
the protocol. Now, a great thing is that
yoga nidra scripts or protocols, as well
as NSDR scripts or protocols, are
available totally zero cost. You can
find them certainly on apps like Waking
Up, but also on YouTube. For instance,
if you put NSDR and my last name,
there's a 10-minute NSDR script there.
There are a lot of yoga nidra scripts.
If you prefer a female voice, there are
a lot of different excellent female
voices out there. One in particular that
I like very much is Kelly Boys. First
name Kelly, last name b o y s. She has
both Yoga Nidra and NSDR scripts of
various durations of anywhere from 8
minutes all the way out to I believe 45
minutes.
Why am I telling you all this? Well,
there've been several studies, but in
particular one, and I do realize we're
talking about only one study, but the
results are really intriguing
as it relates to what we're talking
about today.
In this study, they had individuals do
effectively an NSDR protocol. They call
it Yoga Nidra, and the protocol call
they used was essentially a Yoga Nidra
script. They had people lie down and
listen to a Yoga Nidra script and to
perform Yoga Nidra, and they
evaluated the amount of dopamine
available within the brain both prior to
and after performing this Yoga Nidra
script. And what they discovered was
that
after performing a Yoga Nidra protocol,
the baseline levels of dopamine, that is
the amount of dopamine available in the
basal ganglia and a few other structures
of the human brain, of course
was increased by
as much as 60%
as compared to individuals that did a
different protocol, not Yoga Nidra, not
NSDR. Now, did that study evaluate lots
of different durations of Yoga Nidra,
aka NSDR? No. They looked at fairly long
hour plus Yoga Nidra sessions. However,
there's some other data that have
explored Yoga Nidra, aka NSDR,
in the context of cognitive performance
and a few other circumstances, all of
which point to the fact that cognitive
performance and in particular cognitive
performance tasks that have a working
memory element to them. So, they weren't
the exact working memory tasks that you
did earlier, but they have a working
memory element to them. That is,
subjects had to keep certain small
batches of information in mind and then
discard that information in order to be
able to perform the task well.
All of those show significant
improvements in task performance. So,
while something like NSDR or Yoga Nidra
might sound kind of mystical or kind of,
you know, wishy-washy or I guess as the
kids say, weak sauce, to some of you, it
is anything but weak sauce. It is really
powerful stuff. And it's powerful stuff
as it relates to the very neurochemicals
and neural circuits that are involved in
working memory. So, if I were to take a
step back and just say, "Okay, what are
some zero cost, very low, if any risk
protocols that one could perform in
order to improve dopamine levels without
having to ingest anything, take
anything, really do much of anything at
all, except lie there, do this
progressive muscle relaxation, there are
a few other things involved in NSDR as
well, which you'll learn if you decide
to try them, and improve or increase the
levels of dopamine availability in the
brain significantly, well, then NSDR and
Yoga Nidra really are the first-line
tools if one wants to do that. I think
it's reasonable to say that. And as I
mentioned before, there's no reason to
think that there's any risk of doing
NSDR or Yoga Nidra, you know, provided
that you're lying down in a safe place
as opposed to like in the middle of the
road or something. But assuming you do
it in a safe location, I would encourage
you to try it for really for 20 to 30
minutes when you first explore it.
Perhaps you do longer, although I
personally have a hard time doing long
Yoga Nidra scripts regularly. A full
hour is a big commitment. I don't
generally have that much time. I often
will do a 10-minute NSDR. Have there
been brain imaging experiments done for
each and all of these Yoga Nidra scripts
to determine the amount or if there's
any dopamine increase within the brain?
No. But I think that we can safely
extrapolate from that wonderful study
out of Scandinavia that showed that when
human subjects do this Yoga Nidra
protocol, that there's a significant
increase in baseline dopamine levels
within key neural structures that relate
to working memory. Now, many of you have
perhaps heard that getting in a cold
plunge or taking a cold shower, or
provided you can do it safely, getting
into a cold ocean or a cold lake can
significantly, maybe even double or even
triple your circulating dopamine levels.
And indeed, that is true.
It has been shown that when people get
into cold water, typically up to their
neck, and that cold water, by the way,
can range in temperature anywhere from
low 40s to low 60s, depending on how
long you stay in, that there is a
significant increase in the so-called
circulating catecholamines. What are the
catecholamines? The catecholamines are
dopamine, norepinephrine, and
epinephrine. Now, the evidence for the
catecholamine increase in response to
cold water mainly stems from two
studies, and in particular one, and in
that particular study, they had people
get into
I wouldn't say super cold water, it was
in the low 60° and by the way, I'm
speaking in Fahrenheit here.
And they had those human subjects
submerge in water up to their neck. I
think they actually had them sitting in
lawn chairs on the bottom of a pool, uh
but again, their heads were above water,
so they could breathe. And they stayed
in for quite a long while, you know, 45
minutes or longer. And it was observed
that there was a big, big, statistically
significant increase in epinephrine,
norepinephrine, and dopamine that lasted
several hours or more. This is one of
the reasons why, if you've ever done
deliberate cold exposure, as it's
called,
it often is uncomfortable when you get
in, but then when you get out, you feel
different. You feel really good in most
cases, provided, if you're me, you take
a warm shower afterwards. Yes, I like to
do that. I realize if you want to
increase your metabolism, perhaps it's
better to not warm up afterwards. I like
a nice warm shower or to get in the
sauna afterwards. That's just me. But
nonetheless,
deliberate cold exposure clearly induces
a state shift of mind and body that most
people, provided they do it correctly
and they don't go into water that's
far too cold for them for too long,
they report as pleasant. And I think
it's reasonable to assume that some of
that is the consequence of these
increases in catecholamines, which is
why many people opt for a cold shower,
which if you're me, cold shower followed
by a warm or hot shower, or a cold
plunge in the morning, or maybe even
just once or twice a week. Many people
like them. Typically, people like
getting out of them and the feeling that
they have after they do them, although
some of you sickos really like the
feeling of getting in and being in it,
but not me.
The point here is that if we were to
take a look at the landscape of
zero-cost behavioral tools, in fact,
behavioral tools that could potentially
save you money, meaning reduce your
heating bill,
that are known to increase the very
neurochemicals,
aka dopamine, that are involved in
improving working memory. I think it's
reasonable to assume that a cold shower
about 30 to 60 minutes prior to doing
any kind of working memory task or any
kind of activity that would require
increased focus,
could be, okay, we don't know this,
specific studies have not been done, but
could be in theory,
it makes sense mechanistically, it's
logically sound,
could be done after deliberate cold
exposure. And indeed, many people report
not just feeling a bit of, you know,
mild euphoria or feeling good after
deliberate cold exposure, but also an
increased capacity to focus. In fact, so
much so that a lot of people who do
deliberate cold exposure say that they
don't require as much caffeine in order
to maintain their alertness and energy,
which shouldn't be surprising to us at
all, right? I mean, it's increasing
catecholamines, we know this. So, that's
another protocol that you could explore
as well. Is there an important
difference or not between deliberate
cold exposure done by cold shower or
deliberate cold exposure in a cold
plunge or the ocean?
Frankly, there haven't been a lot of
studies comparing those, but
I think it stands to reason that if you
have access to a a cold plunge or a cold
body of water that you can safely get
into up to your neck for 30 seconds to a
minute, if it's 50° or less, right? If
you get in colder water, we know, for
instance, if you get into, say, 45°
water and you only get in for 30
seconds, you're going to get a big
increase in the catecholamines, perhaps
as big as the catecholamine increase
that you would get from being in 60°
water for 45 minutes. Most people don't
have 45 minutes to sit around in water
up to their neck, so most people opt for
30 seconds to
as much as 3 minutes deliberate cold
exposure in a shower or cold plunge or
other body of water.
Again, only do this if you can do it
safely. Never, ever, please
for the love of God, please never, ever
do any kind of hyperventilation
breathing or breath holding while doing
deliberate cold exposure because you can
pass out, you can die. Don't combine
breath work and deliberate cold
exposure. Just don't. Separate those two
things completely, okay? But deliberate
cold exposure, we know is a very
reliable way to increase the
catecholamines, which includes dopamine.
So, if you want to explore deliberate
cold exposure protocols, get into the
nuance of temperature and duration, et
cetera, you can find that completely
zero cost. Go to hubermanlab.com, go to
the menu tab, scroll down a newsletter,
and go to the cold exposure newsletter,
where it details all of that in short
PDF form. Now, some of you are probably
asking, "Hey, what if I was in the high
or long working memory span group? I
ought to have high baseline levels of
dopamine. Should I not do Yoga Nidra
or NSDR? Should I not
do deliberate cold exposure?" Well,
there you're just going to have to
experiment. Again, there's essentially
zero risk to doing Yoga Nidra NSDR, as I
mentioned before. Deliberate cold
exposure, there's always some risk
getting into water, cold water. People
always want to know how cold. Well, the
newsletter gets to this, but I'll just
tell you right now as well.
The ideal temperature is the temperature
that you can safely get into and stay in
for a duration of 30 seconds to 3
minutes before getting out. Some people
opt to go longer, but I think 30 seconds
to 3 minutes is a good duration to work
with for most people, especially if
you're going to do it frequently.
So, that temperature should be safe for
you to stay in for that duration, but
uncomfortable enough that there's some
impulse to want to get out, that you
have to work to stay in there, that you
have to kind of overcome that adrenaline
release and the impulse to get out.
Okay, so, for some people that's going
to be 45°, for some people be 40°.
Depends on how cold adapted you are,
depends on how rested you are. There is
no specific temperature. You have to
really gauge for yourself and so err on
the side of caution and you can
experiment provided you experiment
within the margins of safety. So, if you
found during the working memory task
that you took today that you have a very
good working memory,
I don't think there's any reason to
avoid Yoga Nidra NSDR and deliberate
cold exposure. In fact, there may be
reasons to increase your dopamine and
other catecholamines by way of NSDR Yoga
Nidra deliberate cold exposure
perhaps for working memory performance.
Maybe it could increase further.
Perhaps it would decrease performance in
which case there you got your answer.
You don't have to do those protocols
again and you certainly wouldn't want to
do them before anything that involves a
lot of working memory and attention. But
of course, those protocols have other
benefits as well. So, there's no reason
to avoid them entirely just perhaps
avoid them within the context of trying
to improve working memory. However, if
you're somebody that has challenges with
working memory, challenges with
attention, challenges with focus, well
then I think that the protocols I've
been talking about up until now would be
an excellent first foray into the sorts
of things that you could do to increase
dopamine and of course those other
catecholamines as a way to see whether
or not it augments your focus and
attention and working memory capacity.
Now, some of you are probably shouting
shouting shouting. What about exercise?
Doesn't exercise increase dopamine? It
does. Yes, there are other things that
increase dopamine. It's not just
exercise. There are activities that
increase dopamine. Some people are
probably saying, "Wait, doesn't playing
video games increase dopamine? Sex
increases dopamine. Chocolate increases
dopamine." Yes. Yes, indeed those things
can increase dopamine. What's
interesting and important about the
protocols I've been talking about
however, NSDR Yoga Nidra deliberate cold
exposure, is not just that they increase
dopamine but the duration over which
they increase dopamine. Okay, this is
very important. If you want to
understand more about the relationship
between dopamine
spikes as they're called and dopamine
baseline and why I'm emphasizing these
tools that cause large long-lasting
increases in baseline dopamine, check
out the episodes I did on optimizing
dopamine. We've got a link to them in
the show note captions. Now, before I
talk about other ways to increase
dopamine for the sake of improving
working memory,
things like over-the-counter supplements
like L-tyrosine,
Mucuna pruriens, things like that. I do
briefly want to mention, and I promise,
briefly. I know sometimes I say briefly
and then I spend 20 minutes telling you
about something, but very briefly, I
just want to spend 2 minutes telling you
about protocols that we do not yet know
whether or not they increase dopamine
levels, but we do know that they improve
working memory. Because after all, this
episode is about working memory, not
just about dopamine and working memory.
It has been shown that the use of
binaural beats, okay? Binaural beats
being the presentation or the listening
to sounds of different frequencies in
the two ears, typically by headphones. I
think that's been shown to work best.
And there's a subtraction between the
two frequencies such that the brain
tends to entrain or start to follow a
particular frequency within, not the
entire brain, but certain neural
circuits. So, if you've heard of, say,
15 Hz binaural beats or 40 Hz binaural
beats,
that doesn't mean that you listen to a
15 Hz sound or a 40 Hz sound. You listen
to two different frequencies of sound,
right? Hertz is just a measurement of
sound frequency,
in each of the two ears, and then the
difference between them is 40 Hz or 15
Hz. And there are several studies that
show, not enormous, okay? I want to be
clear, small to moderate improvements in
working memory performance, but in some
cases, significant improvement. And I'll
provide a link to these two papers in
the show note captions, but I'll just
briefly describe them by way of their
title and their major conclusions. The
first is a study entitled The Effects of
Binaural and Monaural Beat Stimulation
on Cognitive Functioning in Subjects
with Different Levels of Emotionality. A
really interesting study published in
2019. It was a relatively small number
of subjects, only 24 participants, 16
males, eight males, between 19 and 31
years old, listen to these 40 Hz
binaural beats, and by the way, it's
very easy to find apps and other sources
of 40-Hz binaural beats at zero cost or
nominal cost out there. Um you simply
look for 40-Hz binaural beats.
And looked at performance on working
memory tasks, as well as some other
cognitive tasks, and found in some cases
a small to moderate
but significant improvement in cognitive
performance on working memory tasks.
The aspect of the study looking at
emotionality did not find a significant
effect. So, it doesn't seem that
emotionality uh impacts things there,
but nonetheless, that study plus the
other one entitled "The Effect of
Binaural Beats on Visuospatial Working
Memory and Cortical Connectivity".
This was a study published in 2016.
Found generally something similar.
In this case, they were using 15-Hz
binaural beats, and here I'm I'm
paraphrasing.
Produced
network activity characteristic of high
information transfer with consistent
connection strength. What they're really
talking about is changes in neural
activity patterns within the brain that
led to or at least were correlated with
improvements on visuospatial working
memory. Visuospatial working memory
tasks are different than the working
memory tasks that you performed earlier.
Visuospatial working memory tasks
involve the cognitive generation that is
within your head of the so-called
visuospatial sketchpad. So, it's this
idea that you see something, and then
you kind of sketch it out in your mind.
You have to know the relationships
between things in space, pay attention
to what they are, keep those in mind
again cuz it's working memory just as
long as is necessary to perform a task.
That's what visuospatial working memory
is. As you can imagine, it translates to
an enormous number of everyday
activities required for focus and
attention and learning and performance.
And indeed,
15-Hz binaural beats was able to produce
a small but significant improvement in
that sort of working memory task. So,
I want to emphasize again, we don't know
the relationship between binaural beats
and dopamine, at least not from these
studies, but I felt I'd be remiss if I
didn't mention these two studies that
show that 40 Hz binaural beats, 15 Hz
binaural beats can indeed improve
working memory performance. And in these
sorts of scenarios, individuals are
listening to the binaural beats while
they are doing the working memory task,
and in some cases before they are doing
the working memory task. Either seems to
work, it depends on the study. There are
a bunch of other studies, but I thought
I'd mention binaural beats because I
know a number of people are interested
in them. Again, non-pharmacologic
zero cost because you can find tools for
binaural beat generation zero cost out
there approaches to improving working
memory. Okay, what about
over-the-counter compounds that are
known to increase circulating dopamine
that can potentially improve working
memory, and that indeed have been shown
in peer-reviewed studies to improve
working memory by way of increasing
circulating
presumably brain levels of dopamine.
Well, I can think of two specific
categories of supplements, that is,
over-the-counter compounds that at least
at this point in time are legal in the
United States that can increase dopamine
levels. Those two are L-tyrosine, which
is an amino acid precursor to dopamine,
and Mucuna pruriens, which is a, believe
it or not, it's the uh a velvety bean or
the outer component of this velvety bean
that contains or is equivalent to 99%
L-dopa. L-dopa is a key component in the
biochemical cascade leading to the
production of dopamine. In fact, L-dopa
is often prescribed for Parkinson's
patients as a means to increase their
dopamine levels. There are at least
three studies that I am aware of of the
use of Mucuna pruriens to increase
dopamine for the treatment of
Parkinson's. In other words, Mucuna
pruriens increases dopamine levels, and
yes, it has been shown to improve some
of those symptoms of Parkinson's
patients. We're not talking about
treatment of Parkinson's today. I want
to caution people uh against any sort of
use of supplements to treat Parkinson's
or other conditions without consulting
your doctor. All right, that's very,
very critical to point out. If we're
talking about ways to increase dopamine
for sake of improving working memory by
way of supplementation, I think we
should start with L-tyrosine because
L-tyrosine, unlike Mucuna pruriens, is a
bit further up. Actually, it's way
further up the biochemical cascade
leading to dopamine production. However,
it has been shown in several studies
that L-tyrosine supplementation can
indeed increase dopamine. And, moreover,
and here I'm quoting in the title of a
study published in 1999, which I realize
is a few years back, but of course
there's some excellent studies from a
few years back or more,
"Tyrosine improves working memory in a
multitasking environment." Now, this
particular study from Thomas et al. has
some interesting aspects and some
aspects that made me go a little bit
wide-eyed, but not necessarily wide-eyed
because the results are so dramatic. In
fact, when one looks at all of the data
in this paper, what you find is that
supplementing with L-tyrosine, as they
did in this study, did indeed lead to
improvements in working memory under
multitask conditions, as the title
suggests.
Those improvements were significant, but
they weren't enormous, okay? They were
statistically significant, but they were
not enormous increases. Now, what was
enormous, and the reason I got wide-eyed
and still get wide-eyed, is that the
dosages of of L-tyrosine used in the
study are really big. They had subjects
take 150 mg per kilogram of
L-crystalline tyrosine.
They had them take it in applesauce for
whatever reason or placebo. And they did
a number of different control conditions
to make sure that whatever effects of
L-tyrosine they observed were in fact
due to L-tyrosine supplementation. Why
am I going wide-eyed when I see this 150
mg per kilogram of
tyrosine? Well,
I weigh 220 lb, so that's about 100 kg.
So, if I weigh 100 kg, and it's 150 mg
for every kilogram, that means that if I
were a subject in the study that they
would give me 15,000
milligrams. That is 15 grams of
L-tyrosine prior to doing these
cognitive tasks. Now, 15 grams of
tyrosine to me
seems like a very, very high dose and I
frankly can't in good conscience
recommend that. Why? Well, maybe I'm
just hypersensitive to L-tyrosine, but
I've taken
1,000 or 1,500 milligrams of L-tyrosine
and I've definitely experienced an
increase in alertness from taking 1.5
grams, not 15, 1.5 grams of L-tyrosine.
And in fact, at a subjective level, I
can feel a meaningful increase in
alertness and focus from 500 milligrams
of L-tyrosine. So, I can't in good
conscience suggest that people replicate
the exact dose protocols within the
study. Nonetheless, the study, as the
title suggests, shows that supplementing
with L-tyrosine can indeed increase
working memory capacity, especially in a
multitasking environment, which in many
ways carries over to the sorts of
requirements for working memory and
attention capacity to get through life
in a very
focused, for lack of a better word, way.
In a very regimented, do this, do that,
task switch, multiple things,
interleave. That's what moving through
one's day, or at least work day, or
anything that requires cognition and
focus entails. So, first of all, I'll
just say what I always say when
discussing any kind of compound or
prescription drug, never add or remove
any supplement from your supplement
regimen, if you have one, without
consulting with your health provider
first to make sure that you are safe to
take that particular supplement. Now,
many physicians, MDs, are not familiar
with most supplements, so you'll
probably need to bring some literature
um to the phone call or to the visit.
But, of course, there are many health
care providers, including some MDs, that
are open to supplementation,
especially these days um as supplements
have become
uh I would say generally more accepted.
I mean, there are certain ones like
vitamin D3 that and fish oils and things
like that that are more common than
L-tyrosine, but there are many
physicians who are open to discussions
about supplements such as L-tyrosine. If
you know that you can supplement with
L-tyrosine safely and you opt to do so,
what dosages would you potentially take?
Well,
here we have to
look at the dosages used in these
studies. I think it's only fair, it's
only safe that we acknowledge that these
dosages are really, really high. And I
think the logical, the safe thing to do
would be to start with the minimal
effective dose. So, if you weigh 50 kg,
rather than start right off with, you
know, the equivalent dosage to this
study, maybe you start with 250 mg of
L-tyrosine. If you weigh a bit more like
me, you're 100 kg or 75 kg, maybe you
take 500 mg of L-tyrosine and see
whether or not you experience a
significant effect on working memory,
attention, and performance. So, the idea
here is to establish the minimal
effective dose. I should also point out
that some people, not all, but some
people experience a bit of a crash after
L-tyrosine supplementation such that
they feel more alert, more focused,
better ability to perform working memory
tasks, move about their day, but then
three or four hours later experience
kind of a drop. So, you need to be
mindful of that. In fact, you need to be
mindful of any kind of pharmacology
where you're increasing dopamine. This
is one of the reasons why I like the
behavioral protocols that we talked
about earlier because they're known to
create big but long-lasting and slowly
tapering off increases in dopamine and
other catecholamines. Now, for those who
are curious about and perhaps even want
to try Mucuna pruriens, please
absolutely talk to your doctor first.
Mucuna pruriens is essentially the
equivalent of L-dopa. L-dopa is a
prescription drug, as I mentioned
before. And Mucuna pruriens
potently increases dopamine.
What dosages of Mucuna pruriens can
increase dopamine? Well, typically in
studies of Parkinson's patients, but
also studies exploring typical people
who don't have Parkinson's in cognitive
tasks or in sports performance have
explored anywhere from 1 to 5 g of
Mucuna pruriens. Mucuna pruriens again
is a very potent way to increase
dopamine and here if your health care
provider approves it and you decide to
try it, I would suggest starting with a
very very low dose. Again, to find the
minimal effective dose. So, maybe even
just 500 mg, not even going to the 1 g
dose. Maybe even 250 mg and really
evaluating how much Mucuna pruriens can
produce a meaningful of impact on
working memory and attention for you.
So, Mucuna pruriens is kind of a bridge
between over-the-counter supplements and
prescription drugs. I say it's a bridge
because it is oh so similar to that
prescription drug L-Dopa. And of course,
there is a long list of prescription
drugs that are known to be dopamine
agonists. Several of which, many of
which in fact have been shown to improve
working memory. You already learned
about one of those before, which is
bromocriptine. Now, you need a
prescription from a physician to get
bromocriptine. But, bromocriptine we
know based on the work from Desposito
and colleagues that I talked about
earlier,
increases dopamine. It does so in about
90 minutes. It achieves peak levels of
dopamine in about 90 minutes and
improves working memory in individuals
that start off with a low working memory
span and we know from neuroimaging,
those are the individuals with lower
baseline levels of dopamine. So, should
you run out and ask your doctor for
bromocriptine? Maybe. Most doctors won't
prescribe bromocriptine for that reason.
I should mention that work from
Desposito lab and other laboratories
have shown that
one of the hallmark features of
traumatic brain injury, especially
frontal lobe injury,
as well as certain neurodegenerative
conditions like Parkinson's but other
forms of dementia, as well as ADHD,
involve deficits in working memory and
attention, which makes sense given what
we know about the symptoms of those
conditions.
And that bromocriptine
has been prescribed off-label for the
treatment of those conditions to some
degree of success. However, those are
off-label circumstances. Right now,
as far as I know, bromocriptine is not
prescribed specifically for those
conditions at a kind of whole population
level. It's not one of the drugs on the
lookup table for ADHD or TBI, but
certain well-informed neurologists and
physicians do prescribe it for that
reason. There are other dopamine
agonists that are relevant in this
context. The ones that I think most of
you will be familiar with are the drugs
that increase dopamine and
norepinephrine
for the treatment of ADHD. And I did an
entire episode of the Huberman Lab
Podcast about those compounds, things
like Adderall, things like Ritalin,
which by the way is quite different than
Adderall in terms of how much dopamine
relative to norepinephrine it causes the
increase of. I cover all that in those
episodes. Again, you can simply go to
hubermanlab.com, put ADHD Adderall or
ADHD Ritalin, and I talk about other
things as well. I also talk a little bit
about modafinil, which is a
entirely different category of drug
known to improve cognitive performance
in some cases in ADHD, but in everybody.
So, there are a lot of different drugs
that can improve working memory.
Most of those do so by increasing
transmission of dopamine or availability
of dopamine, somehow changing dopamine
levels in the brain by increasing them.
So, if you're somebody that has
challenges with working memory, focus,
and attention, please see those
episodes, and please talk to your doctor
about potentially using pharmacology to
increase dopamine. However, and this is
very important, many people who have
challenges with focus, attention, and
working memory,
and fall under the category of
subclinical levels of ADHD, and even
some individuals with ADHD, young and
old, manage their symptoms, and in some
cases improve their focus through the
use of behavioral tools, nutritional
tools, supplement-based tools in ways
that either allow them to reduce their
total prescription drug dosages, and in
some cases come off them entirely. Now,
I am definitely not saying that people
should come off those drugs entirely.
And in fact, I want to take a really
firm stand here, cuz I know this is a
bit controversial, but I'm just going to
tell you, having evaluated
the whole literature several times over
now, I do think I personally believe
that there is a strong case for certain
children and adults to take these
compounds that increase
dopamine and epinephrine. Yes, those
compounds are different forms of
amphetamine, but those compounds we know
can increase neuroplasticity, the
rewiring, LTP, LTD, etc. within the
neural circuits that control focus,
attention, and working memory. And so,
they do have their place for certain
individuals. We don't want to rule those
out. Are they over-prescribed?
My feeling is that yes, they are
probably over-prescribed. However, there
are a number of individuals that
strongly benefit from them as well. So,
if you are going to explore the use of
those compounds for sake of improving
working memory, certainly if you're
going to explore them for sake of
improving working memory and focus in
young kids,
please, please, please talk to your
physician. Because they're prescription
drugs, you would need to talk to a
physician anyway, but regardless of
whether or not you're trying to improve
focus and working memory in a child, in
an adult, someone with TBI, someone with
Parkinson's,
I think it stands to reason that you
would arrive to that conversation with
some knowledge of not just the
prescription drugs that are potentially
available, but also some of the
supplement-based tools, some of the
behavioral tools,
because as we know, and as a good friend
of mine, who's an excellent physician,
says, "Better living through chemistry
still requires better living." Meaning,
yes, prescription drugs can have a
positive impact on these aspects of
brain function in a way that can really
improve lives, but that behavioral tools
also work. In fact, they can collaborate
in a very synergistic way to increase
the amount of neuroplasticity in the
relevant circuit. So, I'm of the mind,
and I think more and more people out
there, I like to think are of the mind
that behaviors,
nutrition, supplement-based tools, and
prescription drugs all can have their
place to varying degrees, depending on
the circumstances and the individual.
Okay, so today we talked about working
memory, this incredible capacity of our
brain. In fact, a specific set of brain
circuits designed for us to
absorb information, that is perceive it
in our environment, use the relevant
parts, and then chuck it. Just get rid
of it. Forget it.
So very different than short- and
long-term memory, which we also
discussed and we talked about a few of
the mechanisms as well.
I think you'll agree that working memory
is one of the more incredible aspects to
brain function. I mean, if you think
about this is a set of neural circuits
that engage the same algorithm over and
over in different contexts in order for
us to be able to navigate new
environments, familiar environments, to
interleave different activities,
different strategies, to task switch, to
rule out distractors. It's oh so
critical to every aspect of our waking
life. And fortunately, there are also
zero-cost and low-cost behavioral,
supplement-based, and prescription-drug
approaches to improving this incredible
thing we call working memory. So it was
a pleasure to share some of those with
you today as well. If you're learning
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