When I started studying how diet impacts
neurocognition and memory function, the
first model we were studying was a high
sugar model. The animals basically had
ad libitum access to a sugar solution
about the same percentage of calories as
a soft drink that we consume and
otherwise they had healthy food and
water. And with this model, the animals
show hypocample dependent memory
deficits when they're older. And these
seem to persist later into life even
though they're not consuming the sugar
anymore. There may be a role for the
microbiome. There's some changes in the
bacteria in the gut from the sugar model
that that may have a functional
connection to the memory impairments.
We've also looked at models where the
animals are consuming like a total junk
food diet. So we give them chocolate
peanut butter cups, ruffled potato
chips, rodent highfat, high sugar diet.
They show these memory impairments that
last even after you switch them to a
healthy diet.
>> 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 opthalmology at
Stanford School of Medicine. My guest
today is Dr. Scott Kenoski. Dr. Dr.
Scott Kenowski is a professor of human
and evolutionary biology and
neurobiology at the University of
Southern California. His lab studies how
hunger and memory interact and how the
mind and body impact appetite, body
weight regulation, food craving, and
choice. Dr. Kowsky's lab also studies
how different types of nutrients impact
brain development, and brain function
later in life. Today we discuss many
topics including GLP drugs, how they
work, how they impact hunger, and how
they impact things like longevity,
cognition, and drives in general. As
you'll soon see, Dr. Scott Kowski is an
encyclopedia of useful information about
how your brain and body control your
relationship to food. And today, he
shares that knowledge with you in a
clear, unbiased, and in many cases,
actionable way. It's a conversation
about the interactions that occur
between your brain and body involving
hormones, neurotransmitters, your
memory, and your experiences that I'm
confident will powerfully inform how you
think about food, your food choices, and
nutrition in general. Before we begin,
I'd like to emphasize that this podcast
is separate from my teaching and
research roles at Stanford. It is,
however, part of my desire and effort to
bring zero cost to consumer information
about science and science related tools
to the general public. In keeping with
that theme, today's episode does include
sponsors. And now for my conversation
with Dr. Scott Kenowski. Dr. Scott
Kenowski, welcome.
>> Thank you. Pleasure to be here. Thanks
for the invitation.
>> You work on a topic that people
experience every day, which is hunger,
feeding, and hopefully satiety. But we
also have this obesity epidemic, which
seems to be partially mitigated by the
GLP drugs. But there's a lot to this
whole thing that we call hunger and food
and appetite and weight and all of that.
And today you'll educate us about all of
it. But to start things off because it's
on everybody's mind, what are the GLPS?
What is this glucagon like peptide one
in its natural form in the body? And
then perhaps we can talk about the drugs
that increase their levels because
>> either everyone's taking one of these
now, coming off of one of these now,
thinking about taking one, hates the
idea that anyone's taking them, or is
has someone that they know is taking
one. So GLPS are here.
>> In its natural form, it's an increant
hormone. So it's secreted from the
distal intestines around food ingestion.
So there's a little bit of secretion
before the the meal actually starts.
Then there's additional secretion during
the meal and this gets into circulation.
There's also a source of GLP-1 that's
produced in the brain
>> in the brain stem uh nucleus tractus
solitarius. There's a population of
neurons that make GLP-1 and then
extensively send GLP-1 message
throughout the brain.
>> What do those do? Are they related to
hunger as well? the peripheral GLP-1 and
the central GP1 have very similar
effects. So they they're involved in
hunger suppression, but they seem to be
operating independently. So there
doesn't seem to be a strong connection
between the peripheral GLP-1
physiological system and and the neurons
that make GLP-1 in the brain. But they
they do both have appetite suppressing
effects,
>> but presumably they're doing other
things as well, right? Uh yeah, they're
they're helping to regulate blood
glucose levels to to stimulate insulin
secretion when when there's high levels
of glucose present in the blood. In
fact, the first application of of GLP-1
based drugs was for diabetes treatment,
not for obesity, but because they also
suppress appetite and food intake, which
leads to body weight loss. Um now
they're they're probably more widely
known for their for their weight loss
capacity present day, but they started
off as as diabetes treatment. My
understanding is that the GLP-1 drugs so
ompic wiggoi and on and on that they
increase levels of GLP-1
thousandfold more than we ever
experience naturally.
>> That's correct. Super physiological for
sure.
>> Is there anything known about the
potential downside to that um or upside?
>> Well, I mean most of what we know is is
an upside. I mean the people have been
taking GOP1 based drugs for for over a
decade now and and the clinical trials
support the efficacy of these drugs. The
there are side effects nausea and
emmesis emmesis being vomiting uh the
most common side effects and this can
lead to discontinuation in a lot of
people. They kind of tolerate it for a
certain period of time and then at some
point uh discontinue the treatment. Um,
so if there's any primary limitation of
these drugs, it's trying to to mitigate
those side effects and to to have more
long-term efficacy beyond the initial
weight loss.
>> I hear that some people nowadays are
taking far less than they are
prescribed. So go micro doing a term
borrowed obviously from the psychedelics
community in order to offset some of the
um side effects still get some appetite
suppression and perhaps also reduce
their cost because some of these are
quite expensive although many are moving
to generic forms. Are there any animal
andor human data that you're aware of on
micro doing or is this just a natural
experiment that people are doing?
>> I'm not aware of any any data on that.
Uh placeos are are very effective. So
there could be some of that involved.
I'm I'm old-fashioned and I like to see
the large clinical trials uh you know
randomized control clinical trials
before I I start to believe something's
actually working and we just don't have
those studies to date on on micro doing
>> seems like they probably won't be done.
I mean there's not really an incentive
for the the drug companies anyway to do
it. Like people taking less buying less
seems like not a good reason to start.
are so expensive to to conduct that it's
unlikely that anyone's doing that right
now or that they won't in the near
future.
>> So we're kind of left with anecdotal
reports in that zone.
>> I also hear about some nonweight loss
related benefits of the GLPS. In fact, I
know people who are of healthy body
weight who are taking quote unquote
micro doses or even full doses in order
to glean what they claim are some of the
benefits on cognition, on energy. A
friend who is diagnosed with chronic
fatigue syndrome has been micro doing it
and she loves the effects. She's working
with a physician obviously. She doesn't
like the appetite suppression because
she's already very lean and a little not
underweight but close to it. So, but it
speaks to the possibility that taking or
elevating levels of GLP-1 could be
beneficial for things unrelated to the
weight loss.
>> Absolutely. The the receptor for GLP-1
is not exclusively expressed in regions
of the brain that control appetite and
food intake and and glucose regulation.
They're pretty densely expressed
throughout the brain. And this is uh
including regions that are in the the
reward circuitry in the brain, the
misostryal pathway. Uh there's receptors
in the midbrain VTA, the the stridum
nucleus ccumbent. One of my favorite
brain regions is the hippocampus which
has a lot of GLP-1 receptors. So there's
definitely possibility of of
applications for these drugs or or
different GLP-1 receptor agonists for
substance abuse disorder and and
potentially even memory disorders and
and dementia.
>> Um and there's a lot of certainly
preclinical data to support that. Mhm.
>> Um the the clinical data are just
ongoing and and starting to come out
now. And part of the idea with the
applications of GLP-1 receptor agonist
to things other than appetite
suppression has to do with uh the the
capacity of these drugs to get into the
brain.
>> Um this is somewhat of a controversial
topic uh in our field of research. the
first generation of GLP-1 drugs. So 2005
to 2012, we collected some preclinical
evidence in rodents suggesting that uh a
large part of the mechanism of action
for food intake suppression was through
brain action. So the drugs would get
into the brain, activate receptors.
Whether these newer generation GLP-1
drugs like WGOI are getting into the
brain is less clear. Um really again
controversial. So some some studies will
mostly preclinical exclusively
preclinical will tag the the peptides
with the fluorescent molecule and try to
look at where it accumulates in the
brain and you see a lot of it clump into
the what's called the circumventricular
organs where there's no bloodb brain
barrier uh protecting the brain from
from the circulation. Um so there's a
school of thought that these drugs are
acting primarily in those
circumventricular organs but those
studies are tricky because fluorescent
molecules fade
>> and the brain has autofllororescent
signal. So we we could be missing
something with those fluorescent
studies. There's um better ways to do
this, but it's expensive and complicated
where you radio lababel the peptides
with like carbon 14 and you can actually
determine if it's getting into the brain
and where. Those studies, Elizabeth Ria,
Bill Banks and colleagues at University
of Washington are starting to do some of
those and it looks like some of the
early generation of GLP-1 drugs readily
get into the brain and some of the newer
ones less clear. Maybe it it takes a
little bit longer, but the jury is still
out. Um, where where they're getting
into the brain is not something we have
a clear understanding of at this point.
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to get up to 27% off. I'm sort of
veering us toward reward and
reinforcement and memory because even
though those are those are topics that
come up in the context of drug seeeking
of pleasure seeking and on and on in the
context of food you know what we
consider rewarding and what we crave are
very closely related and memory for what
we think is going to soothe us is also
um or satisfy us at the level of food is
also seems to be a strong component. I
know you've worked in these areas, but
as a way of of getting directly there, I
I'm very curious how the GLPs are
actually suppressing hunger. If let's
assume that it doesn't get into the
brain, that these drugs aren't getting
into the brain.
>> So, if I take a full dose or a micro
dose of of a GLP1 drug, what is the
sensation that people report? I' I've
never actually taken one, so I don't
know. Okay. So it but I hear like
presumably it's satiety but is that mean
fullness? Um people will talk about
reducing food noise in air quotes. What
is this at the level of biology?
>> So the GLP-1 normal physiological GLP1
that that we secrete in the body likely
has a paracrine mechanism of action.
>> Could you describe paracin?
>> Yeah. So the the vagus nerve intervates
our our GI tract and there's receptors
for GLP-1 on the terminal. So right
where the nerve is contacting the
gastrointestinal tract, there's GLP-1
receptors and this paracrine mechanism
is where the GLP1 is released from these
L cells in the intestines and
immediately act on nearby receptors that
are expressed on on the vagus nerve. So
that's one mechanism through which GLP-1
both the GLP-1 drugs as well as our
physiological GLP-1 may be producing
this this feeling of satiation. Mhm.
>> So the vagus nerve communicates a lot of
within meal signals that contribute to
us stopping eating. Right? At some point
we get full. This process is called
satiation. GLP-1 is a big player in that
in that process.
>> Not exclusively through the vagus nerve
but probably largely through the vagus
nerve through this paracrine mode of
action. So this sends a signal to the
brain stem. That's the the first site in
the brain where the vagus nerve signals
to that the animals had enough food at
this point. The the stomach starting to
expand. There's nutrients entering the
intestines and there's uh sort of a
symphony of signals that that some act
through the vagus nerve, some don't, but
eventually lead to this feeling of
fullness and meal termination and and
GLP-1 is one instrument in that
symphony.
>> Does it turn off the desire for for food
as well? like people will talk about
less food noise and I know many people
who are taking these drugs some of whom
are really bullish about also exercising
some who aren't so we'll get to that a
little later but um they all talk about
reduced food noise which tells me that
before there was noise and I don't know
because I haven't asked them whether
they were aware of that noise. So I'm
trying to imagine having never taken one
of these what that noise is. I mean when
I see blueberries I want to eat them.
>> Mhm. But when I see bread or a steak or
something, I may or may not want to eat
them depending on when I ate last time
of day, this kind of thing. So, what is
food noise?
>> I am not someone who experiences food
noise either. So, it it's a bit of a a
strange idea to me.
>> Um, but I've certainly heard, same as
you, anecdotal evidence of people who
are taking GLP-1 based drugs and are
saying that, "Wow, it really really
canceled the food noise." Whether that's
based on receptor binding in the brain
in higher order brain regions that that
are involved in in memory and cognition
hippocampus prefrontal cortex we don't
know. Um again I think that's that's one
of the big gaps in this field is
understanding where the drugs are
acting. um are they getting to these
regions in the brain that that are
involved in higher order cognitive
processes that may mediate the food
noise or is this um basically just a a
gut vagus satiation mechanism? It's a
lot to uncover in that area still.
>> What's the evidence that the vagus nerve
is crucial for the action of GLPS and
suppressing hunger? If you do a
selective lesion to the the sensory
vagus nerve as it comes up from the GI
tract to the brain and then inject
GLP-1, it's not effective in in reducing
food intake.
>> Okay.
>> The native GLP1, not a long acting GLP-1
drug cuz that's a that's a different
story. They're in circulation longer can
get into the brain. But if you inject
the the short half-life native GLP-1 and
the animals have a sensory lesion of the
vagus nerve, they don't show the the
food intake reduction. This is work from
uh Wolf Gang Longhans in in Zurich and
his colleagues. They also knock down
using short hairpin RNA interference. So
you can dial down the expression of GLP1
on the Vegas nerve.
>> And those animals have a phenotype,
right? So they
>> they eat more. Yeah, they I believe as
larger meals.
>> Gotcha. So that's all consistent that
our body is telling our brain when we've
had enough because a fullness of the gut
and the presence of enough nutrients
have come in.
>> I was going to get to this later, but I
think now's a appropriate time given
what you just said.
>> Artificial sweeteners and low calorie
sweeteners are a really big topic
online.
There's some in my yearbook.
>> I believe I have some as well. stevia,
right? So, it would be a low calorie
quote unquote natural sweetener,
although there's some
>> manufacturing to take it from a plant to
like a a drink or a food, but different
than like sucralose, etc. Um, of course,
there seems to be three camps. One is
the camp that believes that these things
are terrible, that they alter blood
glucose, they mess up the microbiome,
and that they um maybe even cause brain
cancer. I mean, that people have made
that argument about aspartame. Um, I'm
not in that camp, but you you will see
people arguing this. The second group
seems to be the ones that just say,
"Look, this is not it's a non-issue that
these are inert in reasonable quantities
of consumption." And then there's the
third group, which I think is quite a
few people that kind of wonder like,
well, it's quote unquote humanmade and
like maybe this stuff isn't good. What
is the evidence the the research on
consumption of let's lump them for right
now lowc calorie artificial sweeteners
on development of appetite development
of the brain development of the system
that you work on and what does it tell
us
>> this is a very controversial topic
>> good and I don't think we have
definitive answers in any of to support
any of those three camps so when we
consume sweet taste
we have what's called there's a syphalic
phase response where we're releasing
insulin before the nutrients actually
get through the GI tract just from the
the simple taste of sugar in the mouth
and so this is part of our metabolism
right if you if this was a sugary drink
uh you take a sip you would have some
insulin being released to kind of
prepare the body prepare the physiology
for that pertabbation in blood glucose
levels and there is some
evidence in pre-clinical animal models
that if you disrupt the relationship
between sweet taste in the mouth and the
caloric consequences of consuming
something that you can have
pertabbations in in appetite uh in in
glucose regulation. Um kind of like
you're tricking the wisdom of the body,
right? So sweet taste means calories are
coming. Oh wait, but now now it doesn't.
And there's not a lot of definitive
evidence in in humans. There's been
randomized clinical trials generally uh
I won't I won't get into all that but
there's no definitive evidence from the
clinical trials in humans that it's good
for or or bad for weight loss. There's
some evidence in either direction. Um,
in the pre-clinical animal model world,
there's some evidence that if you give
animals habitual exposure to artificial
sweeteners that this will will disrupt
their capacity to metabolize sweet taste
later on and can potentially lead to
increased appetite and and weight gain.
>> Interesting. So, this is early life
daily exposure to artificial sweeteners.
>> Yeah. So, we we've done one study in my
lab and I can speak more confidently
about that. Um please
>> we had animals who were in the juvenile
adolescent stage of development. This is
um the period of life in which we we've
studied a lot in my laboratory in terms
of dietary factors on adult cognitive
processes. And we gave the animals a
little bit of art artificial sweeteners
to consume each day. And we kept it
within the FDA's acceptable daily intake
levels. So this wasn't necessarily a
sledgehammer. It might be something
equivalent of six of these a day,
something like that. and they consumed
it voluntarily. We didn't put it in the
drinking water. This was something they
liked. They would just get their daily
dose and carry on. And when the animals
were adults, we then tested
neurocognitive and metabolic effects of
having that exposure during development.
So, at this point, they're no longer
getting the the sweeteners. They're just
consuming healthy uh rodent chow and
water. And in this case, we we found
that the animals had some memory
impairments, which was an unexpected
finding. We don't really know the
mechanism for that. Um but they also had
some glucose regulatory um changes as
well. So if you infuse glucose and and
bypass the mouth, there's a insulin
spike and the animals that had this
exposure showed a larger insulin spike.
They also showed changes in the sweet
taste receptor expression on the tongue.
>> Um so we we found some changes. This is
not not like whopping sledgehammer
effects, but at least in that model with
with rodents consuming artificial
sweeteners daily during that
developmental stage, there is
potentially some impact on on
neurocognitive and metabolic processes
when they're adults.
>> Interesting.
>> The caveat is this is a rodent model.
>> Um, but we did use
>> three different sweeteners and it didn't
seem to matter which one we used.
>> Do you recall which of those?
>> Oh, yeah. We had stevia.
>> Mhm.
>> Uh Ace K.
>> Mhm.
>> And uh saccharine. Saccharine is not one
that's common in uh human beverages and
foods these days, but it's one that that
rodents like quite a bit. So a lot of
the rodent model artificial sweetener
literature is based on saccharine.
>> Okay. Thank thanks for clarifying why. I
always wondered when I was growing up,
saccharine was always on the table in
restaurants. Um sweet and low they think
it's one of them. Yeah. And uh nowadays
stevia, aspartame, and sucralose seem
far more common.
>> Uh I realize it's one study. Thank you
for clarifying that it's pre-clinical,
meaning animal study. You mentioned
before that you can find data that
support the use of low calorie and
artificial sweeteners for weight loss as
well as studies that contradict that. Is
there any work that you're aware of
that's going to try and reconcile this?
Because I feel like they are everywhere
now. And I don't demonize them.
Obviously not. I'm drinking one right
now. Uh but what's your thought on
these? I mean, do you actively avoid
them? I mean, you've had a few sips of
your drink. Um so apparently you don't
avoid them entirely, but do would you
given the state of the evidence uh
recommend people take a step back for
young kids consuming artificial
sweeteners or you you don't have to give
a recommendation, but
>> yeah, I don't think we have the evidence
for for recommendations at this point.
The literature's all over the place. Um
and and like you were alluding to a
minute ago, I don't think that this is
going to be solved anytime soon. There's
not going to be a randomized clinical
trial that's going to figure this out.
>> You know, there's some evidence that if
you replace habitual sweetened beverage
consumption with habitual artificial
sweetened beverage consumption, that
that could have some beneficial effects
on weight loss. But again, there's no
reliable uh trend line where you can say
this this is good or bad. So I don't
know which of the three camps that that
puts me in, but I consume Coke Zero
regularly.
>> Yeah. Yeah. Tastes great. It tastes
great. It tastes great. Yeah. So I guess
then the takeaway in my mind is if
people will have to decide whether they
want to be in the experimental or the
control group given what given what they
know, right? Uh which is kind of the
best scenario. People can know that the
state of evidence is mixed.
>> Yeah. and somewhat unclear and then they
can place them
>> and somewhat you know driven by
preclinical models. So that it's always
that that asterisk caveat.
>> So the memory system yeah
>> in the context of food. I'm fascinated
by this because I I happen to love what
most people consider healthy foods maybe
to an unhealthy level. But I realize
that some people have this relationship
to certain foods where they just accept
that it that food, however unhealthy,
just needs to be a part of their life in
some way. It's kind of interesting. It's
kind of how I feel about caffeine. And I
wonder if that's memory based. You know,
if if there's some association early in
life or later in life and the food
provides something beyond just comfort,
what is the evidence that our memory of
a food experience can play an important
role in how we frame that food in our
behavior?
>> Our memory of eating occasions can have
a powerful effect on how much we eat
subsequently. Um, let me just give you a
couple examples. So, in one study from
Suzanne Higs and colleagues, they would
have people consume a pizza lunch and
then they would have them come in a few
hours later and then they would prime
them to really think about the memory of
that pizza lunch in one group. Uh,
another group was primed to think about
something else. I don't remember exactly
what the other experimental condition
was, but not that lunch. And there might
have been a third control group that
would had no priming. And they were
given, they call them uh biscuits in the
UK, but we we call them cookies. They
were given a biscuit cookie taste test.
And they would look at whether that
memory priming had an effect on how much
they ate at the at the cookie taste
test. And if they were primed to
remember the lunch they had just
consumed, they consumed fewer of these
biscuits or cookies. So in in general
the the memory of recent eating will
contribute to eating less at the
subsequent eating occasion. There's
another interesting study by Jeff
Brunstrom and colleagues where they had
um I think it was tomato soup. So it was
a bowl that had a parasaltic pump that
was either putting
more soup into the bowl or pulling it
out.
>> But the uh the participants were not
aware that that was happening. So, they
saw a certain volume of of soup and they
consumed the whole bowl, but that could
have been a mismatch. It could be that
they're seeing 300 and they're consuming
500 mls or they're seeing 500, but
they're actually pulling the soup out,
so they're consuming 300. So, this is a
way to manipulate the memory of the
meal. How much did you think that you
you consumed?
>> So, sort of a magic bowl of soup where
I'm continuing to to eat soup, but the
levels are not going down.
>> Yeah. that or that or they're going down
more than they would just by consuming
it.
>> And if you asked them to rate their
hunger right after consuming the soup,
>> it didn't matter what they saw. It was
based on how much they actually
consumed, right? So that that's sort of
the the wisdom of the body. Uh but then
a couple hours later that that flipped
and their hunger ratings were more
driven by what they saw, what they think
they consumed versus what they actually
consumed.
>> Interesting.
>> Yeah. In fact, re to me really
interesting because you said like the
wisdom of the body piece is great. Like
you've eaten till you're full, till
you're satiated. But then you said the
memory of how much one thought they
consumed impacts what you eat your next
meal.
>> I don't think the study actually had
them eating after that. This was a
self-reported hunger rating.
>> Got it.
>> But, you know, presumably it could
extend to how much you would eat at a
subsequent meal.
>> So much of it seems psychological.
>> Yeah. Yeah, they, you know, I think
we've all experienced like when we're
really, really busy. I know there are
some people who just seem to eat a lot
more during stress and some people like
their appetite just shuts off. They
forget to eat is what we say, you know,
or they're too busy to eat. Um, is there
any indication that people been into one
or the other category like people that
forget to eat or people who eat when
stressed?
>> So, we we study how eating impacts
memory systems. Mhm.
>> Um, we mammals when we evolved, we
didn't have food readily available,
right? You had to compete for for food
resources in a very complicated
environment. And a lot of the systems
that are traditionally studied for their
role in metabolism and appetite and
satiation control actually have uh
beneficial effects on promoting
memories. And our view is that that
makes sense because when an animal
encountered nutrients, this is a very
important event for that animal. It it
would be advantageous to remember what
was consumed, what were the consequences
of that consumption. Um can I find this
food uh down the road in the future and
trying to remember where where the food
was located. So we think that these
systems that are responding to nutrients
when we eat are actually promoting
memory function. Um potentially this is
a system that evolved because of how
important it would have been to remember
these
>> these eating occasions these days maybe
less so in modern human environments.
You can find a cafe and you don't need
to remember exactly where everything is.
It's relatively easy to get food. But we
think that these these satiation
systems are very much tuned in into the
memory systems in the brain and and our
focus has been on the hippocampus.
>> I'm guessing that your students probably
ask you this from time to time, which
is, you know, when and what and how much
should they eat in order to optimize
brain function? That dreadful word
optimize. Not one I particularly like,
but I feel like it's highly individual.
I'm most focused when I haven't eaten in
a while up to a point and I'm thinking
about food all the time. I guess that's
food noise. And if I eat something
>> and I don't eat too much, I'm good. But
if I eat just a bit too much, then I'm
sleepy. Like it seems like energy and
focus and memory and learning. I mean,
there's a it's kind of a narrow bridge
to walk.
>> Yeah. And as you pointed out, I think
there's a lot of individual differences
in this. I always ask my undergraduate
class, how do you guys eat? You know,
I'm I'm traditionally eat three meals a
day, but some of them graze all day,
never eat a proper meal. Some of them
eat one meal a day. And I'd like to
assume that many of these individuals
sort of fall into what's a sort of a
natural eating pattern
>> for them as opposed to being um
something that's forced on them by their
schedule and course demand. But yeah, I
don't think there's one recipe for when
should you eat, how many times a day,
how much uh in what's the distance
between eating and some kind of mental
activity or cognitive demand. Yeah, it
seems like it's
>> worth doing some selfexperimentation for
people to, you know, I mean, the my read
of the the data on intermittent fasting
is that
>> it's one effective way to lose weight,
but people can also lose weight by
>> just eating fewer than maintenance
calories across three or even more
meals. Like I think for so many years,
we got excited that like there was going
to be this magic solution to eating and
weight maintenance. But
>> one of the godfathers of obesity
research is uh George Bray and he was
asked and it was a chapter in a book but
he was talking about what's the right
diet. I mean this was when this was
written it was Atkins diet and all
Mediterranean diet and all these
different diets and his perspective and
one that I for the most part share is
that the best diet is one that you can
stick to and that's going to be a
different approach for for different
people.
>> Let's talk more about the memory system
because I'm I'm intrigued by this. You
study not how memory impacts food
intake, but how food intake impacts
memory.
>> I would say we're on both sides of that.
>> Okay. So, let's talk about how food
impacts memory. If I want my memory
system to be as robust as possible, what
should I avoid,
>> right? We can talk about what to do, but
what what what clearly should one avoid
besides alcohol, head injuries, you
know, uh opiates and methamphetamine. I
think we all agree on that those are bad
for memory. When I started studying how
diet impacts neurocognition and memory
function, we were working with adult
animals and we were using what we refer
to as a western diet. So this is a diet
that maybe 35% of calories from fat uh
15% coming from sugar and and a lot of
that simple sugar. So you know simple
sugar carbohydrates not not complex
starch carbohydrates and that in animal
models can lead to hippocample dependent
memory impairments if the animals are on
this diet for even even like a week but
generally these studies take a a few
months and the hippocample dependent
memory processes seem to be more
susceptible to the negative impacts of
these diet than other kinds of memories
that don't rely on the hippocampus. So
the hippocampus is somewhat of a canary
in the coal mine. And when I started my
lab at here in Los Angeles, um we were
looking at um development. So shifting
away from adult models and looking at if
you give animals individual components
of a diet during the juvenile adolescent
phase of development, is there a longer
term impact on their memory systems? And
the first model we were studying was a
high sugar model. Um, so the animals
basically had ad libitum access to a
sugar solution about the same percentage
of calories as a as a soft drink that we
consume and otherwise they had healthy
food and water. And with this model, the
animals show hypocample dependent memory
deficits when they're older. And these
seem to persist later into life even
though they're not consuming the sugar
anymore. So we we had a few studies with
that model. um there may be a role for
the microbiome. There's some changes in
in the bacteria in the gut from the
sugar model that that may have a
functional connection to the memory
impairments. We've also looked at models
where the animals are consuming like a
total junk food diet to try to look at
at mechanisms. Um but again, it's the
same kind of thing. So if the animals
consume a junk food diet, so we give
them chocolate peanut butter cups, uh
ruffled potato chips, uh rodent highfat,
high sugar diet, they show these memory
impairments that last even after you
switch them to a healthy diet.
>> That's not to say that we couldn't
reverse these
>> memory impairments with some kind of
other intervention other than just
putting them back on a healthy diet. Um
but at least in rodents and during this
developmental window, these kinds of
foods have a long-term impact on
neurocognition. We have a pre-print
which is um not a peer-reviewed
publication yet. It's sort of in in the
process of becoming that hopefully
someday where we were trying to look at
food processing from a mechanistic
individual variable perspective. So in
food processing is a term we all hear
alter processed foods. The way this is
studied in humans is there's this NOVA
classification system where you have
four different categories of food
processing where the alter processed
food is basically just you know shitty
food and then uh the the other end of
the extreme is you know perfect raw
vegetables and completely unprocessed
food.
And that's not really mechanistic in
terms of what types of processing
matter because food food processing
there's a lot of processes that happen
to to food in modernized food industry.
So we wanted to try to take it one
variable at a time and we ended up heat
treating the food. So this is an
otherwise healthy food and we baked it
for an hour at at a high degree high
temperature. And the idea behind this is
that it induces something called the
mayard reaction. The mayard is used in
cooking because it enhances the flavor
of food. So this is something that we do
for a reason. Um this is a chemical
reaction that happens depending upon the
the nutrient composition, the pH, a lot
of factors, but when you heat treat
food, you can get this this mayard
reaction. Do
>> you want to just describe the the
subjective experience of it? Like if I
took a carrot Yeah.
>> and I just ate it. Most people know what
that tastes like. But m if I took of
that carrot and I um sliced it and
basted it with some uh butter, maybe a
little bit of olive oil, some salt and I
stuck it in the oven and um cooked it
until it was soft. It come out it has
almost like a meat like quality to it
taste. Um that um it's a little tangy
but savory. Um is that that's what
you're referring to, right?
>> Yeah. Yeah. I mean the the actual flavor
components that are result of the mayard
reaction are not not well understood. So
we we can't point to certain flavonoids
and say that oh this is it's making it
taste like this. But in general,
>> you know, if you if you bake a
casserole, it's going to taste better
than before you baked it, right?
>> Yeah. Lord knows.
>> So we were trying to to create this
chemical reaction in otherwise healthy
food. And what happens when you heat
this food up is there's
>> chemical byproducts of this process.
They're called advanced glycation
endroducts. The acronym is AGES.
And these chemicals are actually in our
normal physiology. So we have AES
circulating. We have receptors for AES.
It's the rage receptor, which is pretty
cool name for receptor. And this system
is it's generally associated with
diabetes and aging and things that we
don't think are uh great great things.
And when you heat food, depending upon
the chemical composition of the food,
the temperature, etc., you get these AES
that are introduced into the food
itself. So we're basically looking at if
animals consume this ageenriched diet is
what we were calling it during
development or is there an impact on on
cognitive processes when they're adults
and it it turns out again just the
caveat is this is unpublished work but
preprint is that we we see memory
impairments with this ageenriched diet.
Uh we think that there may be a role for
the microbiome. there was a population
of bacteria that was eliminated through
the heat treatment process and when we
reintroduced it to the animals uh we
were able to reverse these memory
impairments.
>> When you say memory impairments, could
you describe the type of of memory
impairment and and um I'm not trying to
review your paper, but the are these big
effects? I mean, they're obviously
statistically significant or you
wouldn't be describing them the way you
are, but just to frame in our minds, uh,
are I mean, are these animals can they
remember where something was placed and
come back to it later? Uh, or is it that
sort of like getting into challenges
with higher order memory?
>> We we use a a variety of memory
procedures in our lab. Some of the more
common ones is we have a a maze actually
about the size of this table where
there's holes on on the edge of the maze
and the animals are using visual spatial
cues surrounding the maze to remember
where things are located. This is a
hippocample dependent type of spatial
learning and memory and we've done
different versions of this but generally
they're trying to remember where food
was consumed.
>> So they crawl into a little tunnel they
eat a meal and then the next day we ask
them do they remember where that tunnel
is? We also do memory tasks that do not
involve food where the animals are
placed in an arena and they have to
remember which objects they've seen in
which locations before. It's kind of
like a okay, I've seen this object
before, but if I haven't seen it in this
new location, the animal will
preferentially investigate that object.
>> Um, these are just some of the examples
of hippocample dependent memory tests
that we use. Um, in terms of effect
size, it that's that's a little bit
tricky. I mean, it I'm not saying that
it's the equivalent of having a lesion
to that brain region,
>> but in some of these memory tests, you
you have above chance performance and
then you have not that. And generally,
we see the the control treatments will
have above chance performance, giving us
some indication that the animals
remember above chance where that food
was located or which object they've seen
in which location. And with some of
these diet manipulations, the animals
are performing basically a chance. So,
they're not showing us any evidence that
they remember where they got the food
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subscription. I don't want to um make
too much of the findings, nor do I want
to place you in the position of feeling
like you have to, but I'm I'm intrigued
by this result because for the last 5
years or so, there's been this
unofficial naming of Alzheimer's like
dementia as um type 3 diabetes, which I
know drives certain physicians and
neurologists absolutely bonkers because
that's not an official diagnosis term.
But I think we do on the other hand now
well appreciate that diet impacts the
brain and that really disrupted
metabolic function like chronically
elevated insulin due to elevated blood
glucose from either food intake or
otherwise is problematic for the brain.
And as a consequence, a lot of people in
the spheres that I find myself in these
days are trying to offset their
potential memory loss in the future or
even treat the memory loss of their
parents or spouse by saying, "Hey, look,
at a minimum, we can control food
intake. Might not be a cure, but you
know, some are trying ketogenic diets,
for instance. Some are trying to manage
blood glucose using metformin or
bourberine, neither of which I do. I
should be clear. Um, uh, some are taking
even more aggressive measures and now
there's this the discussion about the
GLPS is like maybe these will improve
longevity of brain function or improve
memory. So, I don't think it's too much
of a leap to just chop it up around this
topic. Uh, and just with the caveat that
you're not talking about specific data,
what are your thoughts on this this
notion that maybe some major component
of age related dementia, maybe even
Alzheimer's, is earlier in life or
current food intake related?
>> Yeah, I there's pretty strong evidence
from perspective studies. I mean they're
correlations but from perspective
studies showing that midlife dietary
patterns and met metabolic status can be
associated with an increased risk of
dementia
>> uh later in life including
visceratoposity.
So the the connections appear to be
there. Um, in animal models, we have
transgenic models of of Alzheimer's
where animals have gene mutations that
lead them to at a later point in their
life develop symptoms that are analogous
to to human Alzheimer's. And in the
pre-clinical world, there's evidence
that consuming a western diet, so again,
a high percentage of calories from fat
and simple sugars can exacerbate that
pathology, can essentially lead the
animals to develop the the symptoms of
that Alzheimer's and this transgenic
model earlier than they would if they
were consuming a healthy diet. So, the
the connections are are there. I think
it's more prospective than something you
can deal with once symptoms arise. I I
don't think that I think it's it's more
important to have a healthy dietary
pattern throughout life
>> as opposed to once there's a problem,
you know, switching
>> switching at that point.
>> Yeah. So, it's sort of the and here I am
heavily uh joking stereotyping sort of
like were you raised in West Los Angeles
where everyone's talking about eating
healthy all the time? It's like a major
topic of focus. Are you from an area
like um an area of the country where
nutrition isn't prioritized
or are you sort of like most people
where grew up eating some healthy foods
with a mix of some ice cream and pizza
and
>> and uh a little bit of alcohol for most
you know like I mean most people are in
this kind of mish mash and yet we see
people with Alzheimer's who are dealing
with metabolic dysfunction and we see
people who get Alzheimer's who otherwise
look healthy might I don't see how we
can draw a one to one correlation
between food. Yeah.
>> Yeah.
>> Yeah. There there's correlations but
it's it's not a direct line.
>> Mhm.
>> It seems these days that people just
feel really good talking about the fact
that exercise is one of the few things
we can do to maintain or improve brain
function. I'm not aware of any studies
showing that exercise actually makes
people smarter. I think it places the
body and brain in a position to go learn
and get smarter or to hold on to what
they've got. But the the question I
can't seem to find an answer to is are
the positive effects of exercise on
cognition and memory are they the
consequence of improved metabolic
function. End of story. Or is there
something else there?
>> I think the answer is probably both.
Mhm.
>> Um, getting back to this this diet model
in rodents where we have a western diet,
there is some evidence that exercise can
reverse those those memory deficits and
in part that's happening through changes
in the brain.
>> Interesting. So, for the animals that
were fed an an unhealthy diet, let's
just call it, and then later are put on
a healthy diet and exhibit these um
long-standing memory deficits, if they
exercise, they can rescue those
deficits.
>> That's been shown in in rats. Yeah.
>> Interesting. And I recall, I never
worked in this area, but that one could
um do a memory test where you actually
have the animals swim to find a platform
>> water.
>> So, does the exercise have to be related
to the memory task itself or can they
just run on a wheel and that rescues
their memory?
>> Well, there's treadmill models and
there's wheelr running models of
exercise in rodents. One of the reasons
that we don't use the the procedure you
were talking about is it's it's
stressful for the animal. Mhm.
>> They don't like being thrown into water
and and there's a physical demand, you
know, to swim. And so we we try to avoid
that particular task where the the
exercise capacity of the animal has any
>> any input at all into their performance.
We're talking about here sits right at
the edge of like where modern brain
health and longevity care is at. It's
like on the one hand we're talking about
like what one eats, whether one
exercises and brain function, but to my
knowledge there's nothing else known
about Alzheimer's that tells us to do
something specific
>> besides also trying being a lifelong
learner and social connection. Okay,
those are critical too obviously, but
there's tons of stuff it seems that can
impair the system. But we actually have
in hand very few things besides
exercise, quality nutrition, social
connection, and ongoing curiosity to try
and maintain brain function. I realize
this isn't your specific area of focus,
but when you look out on the landscape
of dementia and Alzheimer's research,
>> preclinical or in humans, what like
you've spent some time in the
hippocampus as a researcher, like do you
think we're going to get to the place
where what we call Alzheimer's is is a
reflection of a bunch of bad choices
plus some genetic preloading of the
system, um some susceptibility that
might be heightened in some people, or
do you think there's really a a disease
that that is independent of all that.
>> We haven't come very far in terms of
finding effective treatments for
Alzheimer's as I'm sure you know and one
thing that that we've been doing in my
lab is to try to think outside of the
box and try to think about how the gut
might be connecting to this pathology as
opposed to just looking at what chemical
processes are are changing in the brain.
>> One example of that is we've done some
work with
>> with the Vegas nerve. I think I
mentioned earlier and if you leion the
vagus nerve the as it's coming out of
the gut the gastrointestinal intervating
components of the nerve animals show
hippocample dependent uh memory
impairments. So there's a connection
between the the vagus nerve and the
hippocampus and we're interested in
trying to understand is that connection
relevant to Alzheimer's and dementia
pathology.
>> We don't know yet. There was one study
in a a population in Taiwan that in the
1980s, maybe a little bit into the '9s,
people would get vegottomies. So they
would get a trunkal vagus nerve lesion
for stomach ulcers. That was a somewhat
common treatment at the time.
>> Medicine loves to start with a
sledgehammer.
>> Start with a sledgehammer.
>> You had ulcers. Let's give you a vag
let's cut let's cut the major connection
between the brain and body. Oh goodness.
>> And it was effective for that.
>> Yeah. Um but what's what's interesting
is we have in other countries not so
much the US they they have impeccable
medical records that are kept for
decades and you can look at okay if an
individual had a trunkal veonottomy for
stomach ulcer what's the probability of
developing uh dementia later on and
there there does seem to be in one small
study a positive correlation so there
may be some risk factor for for
vegottomy in humans and developing
Alzheimer's of some kind of some kind of
pathology later on.
>> We're interested in looking at that in
in a different cohort in the Swedish
National Registry,
>> looking at whether we can kind of dig in
a little bit deeper and
>> and find out whether there's um any risk
in humans of having Vegas nerve
disruption and Alzheimer's pathology. In
animals, we can study this a little bit
more directly. Mhm.
>> So we have a transgenic uh Alzheimer's
model in a rat. So they basically
develop the the amaloid and talpathology
in the hippocampus in an age dependent
fashion. So when they're older, pretty
pretty decent model as far as these
things go. And we have devices that are
called veagal nerve stimulation devices
>> and we can implant them. Um there's
different kinds of VNS devices. the one
that we're working with, it relies on
mechanical distension and contraction of
the stomach.
>> So, it's basically sutured to the
stomach and it only sends a stimulation,
electrical stimulation to the nerve when
the animals are eating because that's
when you get the natural expansion and
contraction of the stomach.
>> And we're interested in knowing whether
these devices can I don't want to say uh
eliminate the Alzheimer's pathology, but
potentially improve the outcome in these
animals. That's something that that's
ongoing
>> right now. We have shown that these
devices can rescue the memory
impairments from an unhealthy diet.
>> So we we think there's some kind of
functional benefit potentially of veagal
nerve stimulation in in models of memory
impairment. Um but still in the baby
stages of of trying to figure that out.
I can make up a simplistic story in my
mind that I'm sure is only partially
true if at all but uh it goes something
like this that the memory systems of the
brain which clearly involve the
hippocampus that's un not debated
evolved first to keep us alive as
opposed to make us remember you know
sweet memories from
>> first junior high school dance cuz that
was really awesome. Just kidding. the uh
um and that nothing is more fundamental
to survival than our ability to keep
ourselves nourished and hydrated from
day to day. So that a huge component of
our hippocample function is
>> is nested in our gut's ability to
communicate with our brain. Hey, these
nutrients came in at this timing, in
this amount in the context of a bunch of
other things. Like I feel like most
neuroscientists would agree and you work
on this system. So I think am I on solid
ground there?
>> Yeah. And not just the Vegas nerve
either. We start the Vegas nerve, but
also if you look at at hormones that are
involved in appetite and metabolism that
that get into the brain like insulin and
>> ghrein,
>> there's a lot of receptors for these
hormones in the hippocampus. So that
seems to be an alternative pathway
through which
>> the hippocampus is getting insight into
the the metabolic state of the animal
through these circulating humoral
signals like leptin is another one that
that gets into the brain from
circulation. It's really receiving the
the the neural connection from the vagus
nerve, but also the humoral sort of
longerterm energy status connection from
these hormones. Um, it it's
>> similar in many ways to the hypothalamus
in terms of the receptors that are
expressed there. And of course, the
hypothalamus is the classic feeding
center in the brain. That's where these
AGRP palm C neurons are that I know
you've discussed previously. That's the
traditional feeding center. But um we've
been for a number of years now been
making a case that hey the hippocampus
is really important for this too.
>> And feeding eating appetite is not a
reflexive response. It's very
complicated. It's it's a very complex
decision that has to be made when an
animal decides whether to forage, where
to forage, you know, what to eat. Um
these are not not simple behaviors. So
it it to me it makes a lot of sense that
these complex behaviors are not
exclusively being mediated by these
brain substrates that are thought to to
control more basic homeostatic
regulatory processes like the brain stem
and the hypothalamus. But you also have
these higher order inputs that are um
very much tuned into this behavior as
well. Mhm. So here's the model I'm sort
of simplistic model I'm coming up with
in my head that the the hypothalamus has
these switches
>> find food, eat,
>> yeah,
>> stop eating, etc. And we pretty much
know what those switches are, the
location of the neurons and so on
because of the work of
>> you and excellent colleagues in the
field. And then there's this other
system that we've been talking about
that's a major topic of focus. this body
to brain vegas to hippocampus kind of uh
memory system and it's so interesting
that you know when an animal or a human
doesn't eat well meaning enough
macronutrient sure most people are
getting enough macronutrients at least
in this country I realize there are
exceptions but but not enough
micronutrients not enough of the
essential fatty acids the vitamins and
minerals the protein relative to the
calories they're taking in when that
ratio is skewed in the wrong ction then
the memory system suffers and so if we
adhere to the adage use it or lose it
right I I kind of getting this picture
after all these years in neuroscience
that like our brain develops and our
parents and we do as well as we can we
don't control everything at the
beginning and then we do the as well as
we can then we sort of land in this
early stage of adulthood of like 20 mid
20s 30s and then our goal is to hold on
to what we have and improve on it if we
can right I mean that's there's
you know, new about the statement I just
made, but that the gut is constantly
updating. Like the body is getting what
it needs. Therefore, if you're a neuron
in the hippocampus, you can basically
stay functional and alive. Otherwise, it
sounds like neurons start cashing out.
They might not die entirely. But, I
mean, this it's a different picture of
nutrition that I think is so important.
And I think it fits well with what we're
learning about dementia and Alzheimer's
that there is this blood sugar but also
nutrient related aspect to it. So if
this system from the body to the brain
is is really a core feature of keeping
memory online and maybe even making it
better without feeling the need to make
specific recommendations. How do you
personally think about this in the
context of your own food intake? Is it
like okay eat well but not too much. We
know that. But what what do you think
about doing that could keep this system
robust? Because presumably you want to
do that. I realize and I want to be very
clear. I'm not asking you to make
recommendations but you're you're more
versed in this perhaps than anyone I've
ever spoken to about this body brain
connection as it relates to memory and
food intake.
>> So I'm just curious where your mind is
at and bracket it as many times as many
caveats as you need to feel comfortable.
But I'm curious and I'm certain many
other people are curious. I don't make
specific recommendations about what
people should or shouldn't eat, but I do
share our results with with people who
have kids who may be thinking about, you
know, what what do I feed my kid? And I
always make the very important caveat
that we're studying rodents. We think
are a good model for for memory systems,
for for energy, metabolism. They are a
good model for humans, but it's a very
important caveat. That said, there is
evidence in humans that support some of
what we are doing in rodents. So, for
example, um Dick Stevenson and
colleagues did some studies in healthy
adults. So, this is undergrad students
age approximate and looked at their
habitual dietary patterns and then how
well they did on hippocample dependent
memory tasks. So, these otherwise
healthy adults, they're not diabetic
really just normal healthy young adults.
there was connections between habitual
sugar consumption and saturated fatty
acid consumption and how well they did
on these memory tests. That's not to say
that these can't easily be reversed by
consuming a healthier diet.
>> But I do think it it's worth looking
into what we know in humans, which is
very little because humans um
unfortunately aren't that good at
reporting what they actually eat.
>> This is a major limitation in doing
these kinds of studies with rodents. We
control what they eat. We measure it. We
have 100% near 100% accuracy of of what
they're eating and how much.
>> Even with phones nowadays where all they
have to do is take a picture.
>> It's improved it. Yeah.
>> Is it that they lie or they just too
lazy or they
>> I don't I don't want to say it's that,
but I it it's just not an accurate
process to date. I I think having the
the apps involved are going to make it a
little bit better. Mhm.
>> There's caveats with both the animal
model research because the rats and and
the human research because we don't have
a lot of control about what they're
eating and how accurate their reporting
is. But that said, there there does seem
to be um evidence in humans to support
what we're doing in in rats. So I I
guess it not making
precise dietary recommendations, but
excess sugar not good. Um excess
saturated fatty acids not good. I wonder
why um we've gotten so good at process
creating quote unquote highly processed
or even partially processed food that's
designed to taste really really good so
people consume more of it independent of
its micronutrient and and other value.
Why can't we engineer foods that have
robust amounts of micronutrients? Like I
just think this would be a great thing
and parents want their kids to be
healthy and adults want to be healthy. I
don't think anyone wants to feel sick.
So, provided um it was safe, I would
love to eat a bowl of blueberries that
had like 10 times as many polyphenols.
I I would pay more for those
blueberries. I don't know how much more.
I guess it would kind of depend, but it
seems that the engineering can be used
to push the quality of food in
either direction. And I don't understand
why this isn't happening. And people
will say, "Oh, because they just want
you to buy more and more." Okay, that's
true. But you can still keep food
tasting good. Very good in fact. So why
aren't people engineering better, more
nutritious food?
>> As as you're alluding to, I think the
the technology is there. I I think it's
just the the sea change hasn't happened
in terms of where the demand is, where
the production is. I'd like to think
that a sea change is possible. I mean
the
>> the food industry is over 60% of
calories that not maybe not you or I but
like many people consume come from alter
processed foods in in the US.
>> So that that's a lot over 60%.
>> And that's a direct product of largely
that the food industry producing these
kinds of foods. what you're saying
sounds great. Like if there's a sea
change in demand or or some other top-
down regulatory change in the food
industry. Yeah, I think I think that's
certainly a
>> optimistic because even if people aren't
eating enough fruits and vegetables, if
if you can spike it otherwise unhealthy
diet with like two pieces of fruit a day
and one vegetable, which is not what you
know sufficient, but if you overload
those with more micronutrients, it just
seems so straightforward to do. Yeah, I
mean clearly the ultrarocessed food
industry has hacked the get people to
desire more piece as well as the
marketing piece to drive it through like
cartoons and clever marketing and
celebrity marketing and this kind of
thing. It just seems obvious to me now.
There's also an issue and I'd love your
thoughts on this in the in the science
field itself. I mean years ago I used to
occasionally come across an article in
my journal neuroscience which you know
back then I think still now is a
respectable journal. Um, it would be
like blueberry intake correlated with
improved cognition in rats. You'd
occasionally see that, but I noticed
that that kind of work got pushed aside.
There seems to be more of an emphasis on
finding relationships between the bad
stuff and deficits. And I which I think
is essential, but I
>> guilt I'm very very much guilty of that
too. Well, and and no, I think it's
important work, but I feel like loss of
function and sort of well, gain of
function is kind of a loaded term now,
but it just means like things that push
things in the it potentially.
>> I think part of the problem with what
you're getting at in the pre-clinical
world is a standard rodent diet is very
healthy, right? This is like 10 to 15%
of calories from fat. The the
carbohydrate source is complex
carbohydrates. So, we're kind of
starting with incredibly healthy
baseline. That's not to say there's not
more room for looking at certain
extracts, supplementation, and whether
they can have beneficial effects, but
with the standard rodent diet, the
animals are
>> they're not showing memory impairments
on that. Does that make sense? Is it
sort of easier to make something go
wrong
>> than to take an already healthy baseline
and and improve upon it?
>> Yeah. I mean, I think it's I'm not going
to blame science for this, but I feel
like in some ways that's what led to
this proliferation of like diet books
and this is the way to, you know, make
your brain healthy. This is the way
because there was just there was a lot
of empty space for people to step in and
there didn't need to be any kind of
formal structure that they had to obey.
So, in some sense, it's like
>> the landscape was perfect for that.
>> Absolutely. Lacking a strong scientific
literature in this area, anything goes.
Right.
>> Right. Right. Because I think by now we
all know what we shouldn't do.
>> Yeah.
>> And we and most many people try not to.
I there's also I've been reading about
this that with the the advent of the
GLPS we we are entering perhaps the
first time in nearly 75 years where we
might start to see thamin deficiencies
and nut micronutrient deficiencies in a
like fully modernized culture because
people aren't eating enough and when
they are eating they're saying oh you
know I'll just have like a little bit of
this donut have a little bit of this
salad and um you know salad in most
places doesn't actually provide that
nutrient probably the salads that you
make or that you can buy at a really
good market. Um, you know, but if you
look at like most salads is a couple
people pieces of iceberg lettuce, like
slices of cucumber, tomato, like that's
not that's not what we're talking about
when we're talking about getting
sufficient fiber and vitamins and
minerals, right? So it could be that we
end up with a a large
population of people who are um kind of
skinny fat because of the loss of muscle
with the GLPS if they're not exercising
plus micronutrient deficient. And in
terms of hippocample function, it seems
like that would be maybe as bad as as
obesity. That's not a concern that I
have. But part of the reason for that is
that people don't take in general, they
don't take these GLP-1 drugs for a long
period of time. A a majority uh will
discontinue treatment within two years
of starting
>> because of side effects or cost
>> because of the side effects. Another
reason for discontinuation in in elderly
populations, um there's lean mass loss,
which is um I'm not saying that the GOP1
drugs preferentially uh reduce lean
mass. I'm not saying that at all. But
there's when you lose weight, you lose
both fat and lean mass. So that's
another common use for discontinuation.
But people just aren't staying on these
drugs long enough to
>> really have I mean to my knowledge
there's never been micronutrient
deficiency issues in any of the clinical
trials which that's most of what we know
is from those clinical trials.
>> Those are about a year or two as I
recall.
>> Yeah. Typically um but those trials are
done in individuals. Everything's
controlled. Mhm.
>> the diabetic and or obese.
>> Now, it's it's a whole new world out
there where where people can get their
hands on these that
>> that don't need them. Um, so I think
there are a lot of potential issues with
GLP-1 based drug use in lean individuals
that we just don't have any grasp on
because we haven't we haven't done those
clinical trials and probably won't.
>> It's almost like a perfect storm like in
in a country the United States where
healthy eating has never been a theme if
I'm honest.
>> Yeah. you know, it's just not as a
somebody as a a parent from South
America, it's like like the foods they
champion are healthy foods.
Overabundance of meat admittedly in
Argentina, but like the idea is like
people from Eastern Europe will talk
about like their their comfort foods are
often very healthy. They have a lot of
nutrients in them like south of France
and Scandinavia and Americans will roll
their eyes. They'll be like, "Ah, you
know, this, you know, but it it's a
reality that, you know, fried chicken,
pizza, cotton candy, hot dogs, apple
pie, these are like the American corn,
these are the these are the American
foods."
>> And so, in the absence of a complete
revision of how we think about food and
health, I feel like
>> what's needed more than ever is people
need to be educated on what to eat to
keep their brain healthy. Like it's the
one of the most common questions I get
and I end up having to revert to like
all the other like exercise, sleep, and
all the other stuff like you can give
answers protein, fruits, vegetables, but
my observation is that some people will
do that and many many people are just
they're looking for a pill or a solution
and the GLP seem to have provided a
solution at least to the weight piece.
>> Yeah.
>> But I'm it doesn't seem that they've
provided a solution to the nutrient
piece and that has me concerned frankly.
Any weight loss program it should have
some nutrient and physical activity
components embedded in that program.
Right? Simply taking a pill is not the
optimal way to to lose weight
>> and the clinical trials where we have
data from there is nutritional
guidelines and and physical activity
guidelines embedded within those trials.
>> They are having them exercise
>> uh typ most of them. Yeah. I can't I
can't say every single one but yeah
>> I mean this is one of the most common
sets of questions that I get around the
the issues we're talking about today
just incidentally like uh should I be
taking JLPs like what about you know
what should I eat when I'm taking a GLP
you know can I micro dose it uh can I go
off it uh what about the muscle loss
like you know it's like I think this is
the going to be a major theme for the
next 5 to 10 years and that's in adults
so to say nothing of the the questions
about kids and GLP I don't know that
there are any data on GLP's drugs in
younger populations. I'm sure there are,
but I'm not aware of them.
>> I'm not deeply familiar with them, but I
I believe that uh semlutide may be FDA
approved in some populations of
teenagers, but I don't remember the
specific parameters for that.
>> I'd like to take a quick break and
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to claim a free sample pack. Let's say
that uh you had a enormous vault of
funds to do research on anything in this
system or any other system for that
matter. Have you ever played that
experiment? It's just too painful to
think about given today.
>> It's it's a little painful.
>> All right. Well,
>> unless you're unless you're offering the
vault.
>> No, but if you could do any experiment
here, like didn't have to write a grant
to do it and you felt like what would
that experiment be? like what what do
you think is really needed in this field
to start to really connect the dots or
or just that you think would be a fun
entertaining experiment cuz let's face
it scientists like to do experiments
also for fun.
>> In many ways I'm lucky that we are doing
some of those experiments now like the
example I gave earlier with the the
Vegas nerve stimulation device in this
transgenic Alzheimer's model. it. That's
what I want to be doing is try to think
about how how the gut might be
>> not just connected to the pathology but
potentially understanding that
connection can lead to novel treatments
that haven't really been considered or
applied before. We are working on what I
would like to be working on which is in
some ways it's a a benefit of the the
NIH funding model that you have
flexibility in what you study. Of
course, you you put a proposal in and
it's reviewed and if you're lucky enough
to get the funding, you're you're doing
a lot of what you intended to do, but
you're you're able to have a little bit
of flexibility and oh, we found this
unexpected uh result, so we're going to
go with this this direction with it. Um,
so yeah, I'm very fortunate to be doing
what I want to be doing in in the lab
these days.
>> I'd like to know more about the nature
of the signal from the Vegas to the
hippocampus. I mean these days most
people who've heard of Vegas think about
it as a calming pathway. They've heard
about humming or long exhale breathing
which is a different branch of the
Vegas. That's that's all still true
about calming the body. But my
understanding is that the ascending the
from the body up to brain veagal
connections are mostly
um excitatory. They are mostly about
creating more arousal in the brain not
more calm. And I think that confuses a
lot of people. But my friends who do
neurosurgery tell me that if a patient
is, you know, maybe drifting under a
bit, you can do veagal stimulation to
make them more alert again. So clearly
there's something there. So I'm curious
what the nature of the signal from the
gut to the brain is. Is it like we have
food, we have nutrients, and that's sort
of a bunch of gates. Like if you have
enough fatty acids, enough protein,
enough um glucose, then three gates have
to be open and then boom, there's a
signal because the the gut
>> I think even for neuroscientists, we
tend to forget that the gut doesn't go,
"Hey, we just ate this amazing lentil
soup." It's just the lentil soup has an
effect and then electrical currents get
sent up and the signals in my mind are
kind of crude. And so is it that then a
bunch of excitation is released in the
hippocampus and now you can keep the
neurons alive because excitation is good
for neurons.
>> So the excitation
>> is that like kind of the picture?
>> It's not one common signal, right? So
there's there's mechano receptors in the
stomach and they're picking up on
distension of the stomach when when food
is in the stomach and that that's a
veagal signal but that's distinct from
chemoceptors in in the intestines. So
you get this um sort of different timing
of different signals as the meal is
being it's not as if there's just this
unified electrical signal that's coming
to the brain and and these um the
neurons of the vagus nerve and the noto
ganglia they express different
receptors. They're very heterogeneous.
They're not all the same kind of neuron
responding to the same thing. Mhm.
>> We don't know a lot about, you know,
what the signal is when it gets to the
brain stem, but we do know that there's
there's many different things that are
contributing to that that signaling
pathway.
>> So, I don't think about it as just one
unified, hey, we've eaten. It's it's
very nuanced.
>> So, it's a song, not a gong.
>> Yeah. Exactly. We've identified how this
information gets to the hippocampus. So
from the brain stem there's an input to
the medial septum and then there's a
acetylcholine producing neurons in the
medial septum are then intervating the
hippocampus. So it's kind of a a three
tier uh pathway through which the gut at
least from the Vegas this information is
getting to the hippocampus. So
acetylcholine is the currency that we've
been studying most recently in this gut
brain hippocampus axis.
>> Interesting. Maybe we could drill into
that a little bit because we had Michael
Kilgard on the podcast who if people
haven't seen that he trained with the
Mike Merson kind of like one of the
granddaddy modern granddaddies of of
adult neuroplasticity and the the data
on increasing acetylcholine and the
effects on adult plasticity to me still
after all these years having spent so
much time in that literature are still
kind of jaw-dropping. Like if you get
acetyloline levels in the brain acutely
elevated, you ungate
incredible plasticity, which is not to
say people should go do use nicotine.
And by the way, if you're thinking about
using nicotine, folks, if you use
nicotine every day, you actually blunt
the system. You reset the threshold.
This is why it's technically only a
cognitive enhancer if used every once in
a while. So like I just want to put that
out there because otherwise people will
be looking up how to spike the system.
But I'm really interested. So what is
the acetylcholine doing for the
hippocampus when the gut sends this song
of hey we've got these nutrients it like
what is the nature of that signal? So
using uh fiber photometry
>> recording we can look at the activity of
neurom modulators like acetyloline when
the animals are awake and doing
something like eating a meal.
>> Cool.
>> And what we found is if you if you track
the acetyloline release into the
hippocampus when the animals are
actively eating so they're holding food,
they're chewing it, they're swallowing,
the acetyloline levels are ramping up
when that's happening. And then when
they stop, take a break, look around a
little bit, starts to ramp down
>> and it kind of jigsaws like this
throughout the meal. But one important
finding is at the end of the meal, the
the baseline levels are higher than they
were at the beginning.
>> So it's it's like a a staircase in some
ways. It's kind of like up down up down,
but then eventually it's it's higher. We
think that that elevated postprandial
level of acetyloline hippocampus is to
allow the animals to remember what what
the hell's going on, you know, like just
ate this meal. Where am I? Can I get
back here and do this again?
>> That's definitely how I felt when I went
to Portland some years ago and I had the
best croissant I've ever had in my
entire life, including in comparison to
France. Yeah.
>> And I have a memory map of how to find
that place, assuming it's still there.
Um,
>> probably is. It's It's
>> If it was that good, it's probably
>> It was that good. And um I don't consume
that many croissants, especially not
these days, but like yeah, there's
really something to it like when you get
awesome taste, awesome hopefully
nutrients. Also,
>> it's like you collect your prior
experiences leading to that. And I can
see why that would be important for
survival reasons, but I could also see
why if this system was hijacked by
highly processed foods that um why we're
so in trouble nowadays
>> and we we see the the same the animals
are eating a healthy food versus like a
highfat, high sugar diet, we see the
same acetyloline profile.
>> So this really does have an analog to
like Tik Tok scrolling versus reading a
a chapter in a challenging book or
interesting story.
>> Yeah. One one thing you said that made
me think of something. You mentioned the
taste and the nutrient. We don't see
this with with taste alone. So if the
animals consume uh stevia a
non-nutritive sweetener, we don't see
that the acetyloline release patterns in
the hippocampus. So it is we haven't
done it the other way around where we
infuse the nutrients without taste.
That's something that's in our queue to
do in the near future. But I my guess is
what is that you need the combination of
of taste and postoral nutrient sensing
to drive this this veagal acetylcholine
signaling the hypocampus. How much is
being done to really parse the the
character of the signal from the body to
the brain? You know, the bodyb brain
connection some years ago was considered
really hippie- dippy and now everyone
talks about it and the Vegas is the
superighway champion of this body brain
thing. We talk about in the context of
breathing, meditation, trauma therapy,
psychedelic therapies, learning, food,
now food intake. And I get really
excited when there's a repeating theme
coming through on this podcast when I
sit down with experts like yourself. And
I I'm wondering especially as a person
coming from the visual system where we
can describe like okay when a human sees
a bar of light at this orientation of
this intensity we can trace the whole
cascade. Now that's a sensory system.
This is a sensory system. Do we know
what the nature of the signals are?
>> Unlike the visual system that
introsceptive awareness is a very messy
process. You know it's it's not a
precise process. We we can discriminate
between I'm extremely hungry or I'm
extremely full.
>> But in between that, this is very much
unlike the visual system. The these
sensory inputs coming in are there's
some neural, there's some endocrine.
It's like a a a symphony of chaos in
some ways. I don't think we're ever
going to get to the precise level of at
least maybe I shouldn't say ever but in
the near future of really understanding
the nature of that signal the gestalt of
that signal
>> one thing I I since I've been talking
about the hippocampus a lot it seems to
be where this interceptive awareness is
being processed in the brain
>> so give you an example if you take a
human who's densely amnesic who has
damage to bilateral al damage to the
medial temporal lobe including the
hippocampus and these individuals have
episodic memory impairments. So their
their memory span is you know between 10
30 40 seconds depending upon the
individual and you have them eating food
they'll consume a meal uh experimentter
goes away comes back with another meal
they'll eat the next meal and this will
happen even a third time they don't
remember eating the meal but what's
always fascinated me about this study
and studies like this uh I think Paul
Rosen did the first one is that if you
ask them to rate their hunger and
satiety level like on a scale of 0 to
10, they will be a seven out of 10 after
eating three meals in a row. So, of
course, they're getting this gut
feedback to the brain. They're probably
even feeling full, but they don't know
how to interpret that signal. The
hippocampus is needed to understand what
that that signal means. And there's
analogous studies in rodents. Like if
you do a lesion to the hippocampus, a
normal animal can learn that a high
level of energy restriction is different
from not being food restricted. Like
they can use that as a cue to predict
something's about to happen, like a foot
shock or a food pellet's coming. If you
leion in the hypocampus, they they can't
do that. So it's um intraceptive
agnosia. to seem to be unaware of what
this intraceptive signaling means. Even
if they're detecting it at the sensory
level, it doesn't doesn't mean what it's
supposed to mean. Doesn't allow them to
appropriately guide their behavior based
on that that signal or sympathy of
signals to do the appropriate action.
>> It seems that some people have so much
interceptive awareness and other people
do not. And I I wonder how that relates
to uh food intake. You know, we've
hosted
>> world-class choreographers on here and
athletes and I always think of the
people who move for a living
>> as being really in tune with their body
and obviously they are. But then there's
the rest of the population where we're
not really trained to think about how
our body feels in the context of daily
living. We just kind of like live. when
it comes to intraceptive awareness of
hunger versus fullness
>> that can be impaired with with a highfat
high sugar diet as well. So that's
that's a a process that is plastic and
susceptible to what we eat. I'm
mandatorializing here again, but I feel
like so much of the challenge in being a
or the task rather of um being healthy
um these days, especially in the United
States, is trying to figure out like
what the fundamental healthy baseline
was or is. And trying to get to that
because clearly
processed foods, but also just the
nature of life. Like you even said it
earlier, like three meals a day for you.
Some people it's one meal a day. Like
they all can work and that's great.
That's also part of the challenge is
people figuring out what works for them.
>> Yeah.
>> And we don't really have like one system
that our our brain body connection is
optimized for. We're built for. And I'm
guessing that's because we went through
periods of feast and famine as we
evolved. We need this system to be
dynamic.
>> Yeah. feast and famine and also physical
activity as it relates to our our daily
lives. So you and I are physically
active, but here we are sitting down.
>> Yeah, we sit and talk for a living.
>> We sit and talk a lot. Stare at screens.
>> To me, I chuckle sometimes that a lot of
what we're doing for health nowadays is
about moving the outdoors inside. So
it's like people have their like red
light and their gyms and their we bring
plants inside and we you know hydrate.
What's that?
>> Are these real?
>> They are real. We have we have someone
come by. Yeah, they do a really good job
taking care of them despite the black
walls. They get their light. There's
this idea that like there's a proper way
that we're trying to get back to. But I
like to think about human evolution sort
of from where we are now and kind of
like it's the front edge leading
forward. And it seems again that like
we're really focused nowadays as a
culture, as a health culture on trying
to figure out like what's the bad stuff
that we didn't know was bad and what's
the bad stuff that hijacked us that we
didn't realize hijacked us. Whether it's
highly processed food or whether it's uh
very short form content or like and we
we have always like process of error
correction like we sort of stumble
forward and then we kind of get pulled
back error correction keep going. I mean
these are the issues that people really
wonder about like what should I eat to
keep my memory? I guess the question
what shouldn't I eat? what shouldn't I
do is far easier to answer. But the
omega-3 fatty acids seem to have a
pretty decent literature. There's a
woman, forgive me, I'm forgetting the
name, we'll put in the show not caption,
who a laboratory up at UC Santa Barbara,
who's looked at um supplementation with
omega-3s during pregnancy and brain size
and function in human offspring. Um it
seems like the omega-3s, the
polyphenols, enough protein, it seems
like those are critical. Yeah, there's a
few players that are established. You've
hit on on the main ones. Yeah.
>> What is your read of the omega-3
literature in terms of uh like if you
have you done experiments where you give
it animals enhanced levels of omega-3?
>> We have not done that.
>> No. The in my lab, we're focused more on
what's what's bad, you know, what's not
>> optimal for brain development. And the
only interventions that we've done is
either replace a bacterial population in
the gut
>> or to just simply switch to a healthy
diet. So we we I'm aware of of those
studies, but we haven't modeled that in
in our lab.
>> Tell me about the microbiome studies.
>> Sure. Um, so we we basically had I'm not
a microbiologist, so I just want to
leave with that. My my background is
psychology. So I got into the microbiome
um largely by accident and and curiosity
about 10 years ago. And we found that in
this early life excessive sugar model
that we were using in rats years ago,
the microbiome was completely different.
So if you do like a principal cord
analysis and you kind of see the the
overall pattern of the bacterial
population, the animals getting the
sugar were just extremely different. And
that could be for a lot of things. It
could be from the sugar or it could be
these animals are consuming a lot of
their calories from the sugar. So,
they're getting less fiber and and and
less um nutrients that are in the chow.
That aside, there's definitely a a
change that's happening. And we looked
at individual populations, can we
correlate the abundance of this
population with the animals memory
performance in one of these memory tests
that I described earlier? And in one
case we had a population
parabacterioides
that was elevated in the sugar group. I
think maybe twofold enough that it was
significant and noticeable and it was
negatively correlated with uh memory
performance. So then we in a separate
study we did an an antibiotic treatment
to kind of wipe out the bacterial
population a little bit not completely
eliminate and then in that state we
enriched this population into the gut
and the animals showed memory
impairments even though they had never
consumed sugar. So we were able to kind
of replicate and and it in many cases
the memory impairments were more severe
when we enriched this population
>> but it was enriched maybe eightfold and
>> more than what you were getting from the
sugar. So that's an example where we
found a population that seemed to be uh
negatively impacting the performance.
>> In the preprint paper that I mentioned
earlier where we have this heat treated
ageenriched diet model we found another
population. And this one's lacticous.
It's a lactic acid producing bacteria
that was completely eliminated when we
heat treated the diet. And in this case,
its performance was positively
correlated with memory performance. And
we were able to rescue the memory
impairments by enriching that
population. So these are the kinds of
things that we can do with with
microbiome studies. There's of course
fecal transplant. Um we haven't done
much of this but a lot of people have in
the field where you you just transplant
the fecal and seal content from one
group of animals to another and in that
case you can kind of replicate um some
of the behavior simply by doing that.
But in that case you're changing
everything. It's not just a single
bacterial
>> population. So we we've looked more at
can we identify a bacteria that seems to
be changed by the diet and correlated
with what we're looking at and then can
we replicate or reverse something by by
putting it in.
>> Very cool. I I'm excited to read the
preprint and see the paper uh come to
publication full fruition because for a
long time when I talk to my colleagues
about microbi who work on the microbiome
like okay which bacteria are beneficial
and they go diversity. I go I get it.
which ones are most beneficial and I
realize in this case you did a rescue.
So you had a diet just to summarize in
case people miss any like although you
described it beautifully a diet that
leads to some memory impairments. This
is the diet associated with these mayard
high heat reactions you can rescue some
or all of the deficit by replacing a
single bacteria. That doesn't mean that
increasing that bacteria to super
physiological levels will increase
memory linearly but um so this is
offsetting damage uh what we call rescue
or used to be called gain of function
but now people run ran with that term
and different not a popular term
>> and I've been just kind of obsessed with
like okay I get it like gut microbiome
diversity but which bacteria are the
ones that we want and it's very very
difficult for anyone experts in that
field to give me a clean answer and I
think it's because they just don't know.
>> I think yeah I think that's it. I don't
think there is a clean answer and and
part of the reason for that is
in 2012 that's when the approximately
when the human microbiome project ended
and before that point we didn't really
have an idea about the genetic makeup of
the bacterial population in the human
gut.
>> So if you go pre20 this was not really a
field of research. In fact, if you did a
a PubMed hit, so PubMed is the database
for biomedical publications. 10 years
ago, you might have pulled up 7,000
hits.
>> Mhm.
>> Today, 250,000.
>> It's just such a new field of biomedical
research that we don't we don't have
these answers. And
>> yeah, you can find some bacterial
populations that, as I've just described
a few, that seem to be bad in one
context or or good in a different
context, but then it it can be
completely flipped in a different study
with a different treatment.
>> And the abundance of one population is
going to affect the abundance of, you
know, hundreds if not thousands of other
population. It's just such a complicated
thing
>> and it's such a new field of research
that
>> um I don't think you can say with
>> clarity like here are the good bacteria
and here are the bad bacteria. We're not
even close to that.
>> Yeah. The throwaway answer right now is
diversity. It reminds me of uh the '9s.
Uh I'm old enough to remember it was
like exercise and I was like well what
kind of exercise? And people said well
weight training isn't good because
muscles will turn to fat after you stop.
So cardiovascular exercise you say what
form and now it's very nuanced. It's
like some combination of highintensity
interval training longer slower training
resistant like now we have answers
because there's been 20 plus years or 30
plus years of really good studies and
people attacking it seriously. I I've
got a family member who right now is
taking a very high dose um spectrum of
antibiotics because they unfortunately
had a a sepsis type situation and they
they are very sharp in the mind
ordinarily and they were saying um
they're really struggling to think
>> like really struggling to think and so
they're trying to repopulate their gut
bacteria with uh you know the I'm a big
proponent based on Sonnenberg's work of
low sugar fermented foods so sauerkraut
kimchi kefir you all these incredible
foods that we know really support the
gut microbiome. And so they're doing
that and feeling better, but of course
they're destroying their gut microbiome
intentionally every day at the same
time. And I said, if you can just get
through this period, defeat the
infection, you're going to experience
such a robust return, but it's a slow
system. Like this isn't the kind of
thing where you take a pill and you feel
better. That the gut microacteria take,
as my understanding is, it can take
weeks or months to really build up a
quote unquote healthy gut microbiome.
It's not something you just do overnight
or with one meal.
>> No, it's not. And it's very plastic
dynamic system like it with with some
exceptions. There's um Have you heard of
C diff?
>> No.
>> So, this is a uh like a intestinal issue
where generally from people in a
hospital were taking antibiotics.
Antibiotics deplete bacteria and they'll
deplete good and bad bad bacteria. And
with CIFF, there's bacteria that
normally keep this CIFF in check. And
with CIFF, there's um a lot of this
bacteria which leads to um sort of
violent GI distress and can even lead to
death. And there's an FDA approved fecal
transplant procedure for this specific
syndrome. So um and I believe it's it's
typically with a single transplant
>> amazing
>> is enough to correct this in in a high
percentage of individuals. Um so there
there you know there's a bright future
for this. Mhm.
>> I don't think we're there yet. I mean,
to my knowledge, that's the only FDA
approved.
>> There could be others, but that's the
only one I'm aware of feal transplant or
targeted bacterial treatment. Um, but I
think it's just such a new field of
research. We're we're definitely in the
baby stages of understanding this
complex relationship.
>> I was a little bit dismayed when I heard
early on that your ideal gut microbiome
is really established
in the first three years of life. And I
thought there's no way my parents got
this exactly right. But then we learned
that it's a little bit like the way
learning and neuroplasticity was
discussed. It used to be considered that
okay up until your teens, early 20s,
that was the opportunity for wiring the
brain a particular way and then it's
locked in. And we know that's not true
at all. And so there's great plasticity,
if you will, to the system, which I find
immensely reassuring.
>> Yeah. And diet is a hu and probiotics.
These are are
>> This is how you change the
>> that plasticity.
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Yeah, I I now think about the gut so
differently than I did even a couple
years ago based on conversations like
this. Like there's the veagal pathways
which we don't know the time scales they
work on but they can be relatively fast.
And then there's the gut microbiome. I I
think about the gut like gut health as
and its relationship to general health
including brain health as I need to give
my gut microbacteria the things they
need so that they can create the things
that my brain and body need. So it's
just like raw materials, short- chain
fatty acids leading to neurotransmitter
neuro neurom modulator production like
serotonin. I just need to give them what
they need. And no, this isn't a a a you
know a product endorsement because my
observation is that it comes mainly from
these low sugar fermented foods getting
enough fiber um and not stressing too
much because stress can also impair the
gut microbiome and then getting enough
sleep. And so maybe at the end of the
day it really is all about supporting
the gut microbiome. Guessing there are
other things too. It seems that
important. And I think I'm it's only
really sinking in for me just how
important it is. And as a child of the
born in 75 like the '9s were just
terrible for this. It was like lowfat. I
guess there was some emphasis on that
period as well. Yeah.
>> Yeah. It was it was the advent of
margarine and processed foods really
came in.
>> Alstra the fortunately I never never had
an ostra chip. I wasn't interested in
the the uh the leakage. Yeah, that's it.
That was enough of a barrier. Um
we'll move to reinforcement in a moment,
but you reminded me of the '9s when the
the Fenfen uh drugs were released. Uh
fenflloramine.
These were supposed to be blockbuster
drugs, kind of like the GLPs, but they
were basically stimulants, right? And
then people started having heart
attacks. Is that is that medics? Yeah,
there's some cardiovascular outcomes
that uh were unwanted and
>> led to the discontinuation of that. And
then the the obesity drug market was
dormant for many many years until around
2010 and beyond when we um it wasn't
just GLP-1 drugs. There was a few other
ones that have kind of fallen out of
favor because the GLP1 drugs are the
most effective. But yeah, there was a
period of time and probably largely due
to the fenfen
>> issue where pharmaceutical companies
were not interested in developing
obesity drugs, but
>> at this point 40 over 40% of US adults
are obese. It's hard to over 40%
>> over 40%.
>> That's unbelievable.
>> So it's it's uh it's not something that
can be ignored now. In the '9s wasn't
40%.
>> Yeah.
>> Might have been 20 then.
>> Yeah. I mean it's hard for people to
remember and I'm not being disparaging
of anyone. Uh, but just by recollection,
like in junior high school or high
school, there were probably a few kids
in my class that were, you know, visibly
quite overweight. Maybe a couple that
were a bit overweight, but it was rare.
You just didn't see it.
>> Yeah.
>> And then there would be these television
shows about people who were they used to
call, it's not a kind term, but they
would call it morbidly obese, you know,
and they'd remove them from a building
with a crane or something. It would be
like Heraldo would do an episode. So,
you were aware that it happened, but it
was really like these extremes of
pathology. Um, you just didn't really
see very very lots of very very
overweight people.
>> And back then, type 2 diabetes was
called adult onset diabetes. And for
reasons you're getting at, it's now not
called that because we we get, you know,
not high percentage, but a noticeable
percentage of of children and and
certainly teenagers who develop type 2
diabetes. Do you think it was all the
highly processed food industry? I
>> I I don't want to say anything was all
Yeah. But it certainly contributed.
Yeah.
>> And I I didn't I grew up with an adlib
access to Mountain Dew and um
>> Yeah.
>> Yeah. It was just a different time.
>> Yeah. School lunches used to be like a
sandwich with maybe a bag of chips
>> or a cookie.
>> Cookie. Yeah.
>> Like it was one or the other. you had to
pick, you know, and soda wasn't really a
you could get soda, but it was more like
a treat.
>> My high school, we had an alle cart
lunch, so you could buy like a
>> pretzel with nacho cheese dip. You could
just buy whatever you wanted. It wasn't
there was no standardized
>> here's a healthy meal.
>> So much has changed so fast, but it
looks like the error correction is
coming in and hopefully not only in the
form of GLPS. I mean, one of the reasons
I do this podcast is to try and take,
you know, showcase serious scientists
and clinicians who are like extolling
the the virtues of eating well healthily
for people of all ages. But all right,
re I've alluded to it so many times now,
it's almost seems like uh like I'm
teasing, but here we are. Reward,
reinforcement, uh enticement.
Most people are familiar with the word
dopamine. They think of it as pleasure.
most people thanks to Anna LMK's book
Dopamine Nation now and the book the
molecule of more uh which is also
excellent I um in my opinion that
dopamine is about craving wanting
motivation
>> um at least as much and probably more
than it is about pleasure
>> that's true yeah
>> so in the context of food and food
intake and nutrient intake and memory uh
what is the role of the reinforcement
pathway um what you and I call the miso
the liyic reward pathway.
>> This system which it the most basic
description of it would be a mid
midbrain vententral tegmental area to
the nucleus ccumbent. That's kind of the
the classic misostrial dopamine
projection. And this system is engaged
by palatable foods. So like liquid
sucrose um a highfat sucrossse
combination.
But there's a little bit more to it than
that. So you can get the system engaged
by a bland tasting healthy food when an
animal's food restricted or you can get
the the system engaged by by water when
an animal's water restricted or um even
a sodium deplete animal will show a a
dopamine release in this pathway to to
sodium consumption. So it's it's it's
very much dependent upon the the animal
state. Mhm.
>> That said, palatable foods tend to
tickle that pathway more so than what we
consider to be more healthy and and
bland foods.
>> And then of course um substances of
abuse tap into the same system. Um
albeit to a different degree, but it
it's definitely a common brain currency
for for things that we enjoy. So when I
hear you say that if we are food
restricted or we just haven't we're very
hungry have to be fasting that um bland
foods can activate the dopamine reward
pathway a reinforcement pathway excuse
me I'm trying to be more careful with my
language. I wonder whether eating highly
palatable foods or or even just sweet
foods changes our threshold for what we
consider reinforcing and and and
rewarding. I try to eat healthy and I
notice that I really love and crave
>> blueberries and uh I keep mentioning
them but that and other foods but if I
eat healthy foods and I like the way
they taste I find that I crave those
foods and I don't tend to crave other
foods presumably because I'm sad. I'm
not I'm not excessively hungry. But is
there a way that we can recalibrate this
system? It seems there is.
>> I think so. So I mean the examples
you're saying make make a lot of sense
and individuals who consume a lot of
sugar who stop consuming it or or
consume much less they they change their
preference. You know something that they
normally would have enjoyed is now too
sweet. So there's a lot of plasticity in
terms of what we want to eat
>> and that's based largely on what what we
choose to eat. We can we can we can
change that as you've described. Like
you probably weren't craving blueberries
when you were 12, maybe.
>> I mean, I've always liked fruit, but I
liked other stuff, too. And I It's not
like I actively avoid ice creams and
things like that, but I but I feel like
it's different with food than it is with
other reinforcing substances because if
somebody who really craves alcohol, who
really craves stimulants, is deprived of
those, and then gets a small amount of
it, I don't know that they say, "Oh,
that just I didn't like that
experience." Usually it's like they
really like that experience. But here it
seems we can rewire the the circuitry
toward healthier choices and maybe even
to the point where what used to be
rewarding is now aversive. And that is
how I feel about like the other day I
had a sip of a milkshake expecting it to
be like delicious. And I was like like I
felt like it was like
>> it is so unbelievably sweet. I felt like
I needed a palette cleanser afterwards.
And but there was a time when I really
enjoyed a vanilla milkshake and I bet if
I kept drinking that vanilla milkshake I
would start to enjoy it. Yeah.
>> So I'm not sure people understand the
plasticity of the system. So is it about
the amount of dopamine is the is the
threat like the upper threshold set by
the most potent things like speed
milkshakes you know and uh banana split.
And then if you don't eat those, so you
don't consume those or or take those
substances, then then you can get to
that same high threshold with healthy
choices. Or is it that that the lower
threshold just starts at
>> that? I don't know. I don't think those
those careful studies haven't haven't
really been done.
>> I mean, there's ways to to measure with
PET, dopamine, a proxy of dopamine
binding in the human brain.
>> In animals, we have really nice tools. I
mentioned the acetyloline sensors with
fiber photometry. We also use dopamine
sensors in my lab. So we we can record
dopamine release again when the animals
are awake and and doing things. We
haven't looked at the question you're
getting at is how plastic is that
system. Um the most extreme example of
the plasticity of that system is with
like a conditioned taste aversion.
Right? So if you have an animal who
normally they consume sucrose, they will
get dopamine release in that pathway
either when exposed to a cue that
predicts that sucrose is forthcoming or
the actual consumption of the sucrose.
But then if you subsequently treat the
or train the animal that that sucrose
consumption is associated with um
malaise. So inject like a a compound
that makes the animals uncomfortable for
a few minutes. they attribute that
feeling to consuming the sucrossse. With
that kind of training, you will
eliminate that dopamine response that
you see uh to sucrossse. So that's just
the most extreme example of the
plasticity of this system. Humans have
tried to use the aversion approach to
learning. basically giving people things
that make them feel sick or electrically
shocking them to try and rewire
everything from uh these are not ethical
studies but people in the in the old
days like the 60s and 70s they tried to
use this to like conversion therapy
right for for uh sexual orientation
obviously terrible um and fortunately
that's illegal uh now but the but
>> I'm not aware of any like really good
studies showing that people will quit
smoking if they're like electrically
shocked when they pick up a cigarette.
My my understanding of these studies,
maybe this is not true, but I I was told
by somebody who worked in this general
area, that people uh basically just
figure out how to endure the shock. Like
that's how rewarding nicotine is. And I
I I wonder if there's something going on
with the processed food um aspect, too,
because
>> I don't know that people really enjoy
those foods. I feel like there is when
we hear that they're addictive. I don't
know that that's the proper word, but
they are impairing people's health, but
there seems to be this thing where
people get into this kind of like it's
not pleasure. It's not ahidonia, but
it's this kind of like mind I don't want
to say mindless, but there's there's
some no man's land of eating and
consuming not getting the thing they're
looking for. That looks a lot like
addiction. that looks like chronic drug
use, but it's not like they're getting
high off the food.
>> Yeah. I mean, it's tricky making the the
comparisons because yeah, there's a
common currency in the brain for
substance abuse and and palable foods,
but you have to eat every day, you know,
like this isn't it's not a a choice like
>> and there's a lot of controversy in in
whether there can be an addiction to
food. And I'm not going to take a side
on either either side of that one, but
if you look at the the DSM criteria for
substance abuse or addiction, you can
make an argument that there is food
addiction based on those criterion. But
that doesn't mean that it's the same
thing.
>> Yeah. Continued use continued harm to
self or others. Um yeah, inability
stopped desite despite desire to these
kinds of things. Late last year, there
was a really interesting set of videos
that were authenticated. The discussion
was should um food stamps be you uh
allowed to be used to uh purchase soda
and someone from the um American Heart
Association was asked on this panel,
what do you think? Do you think soda is
healthy? And they and they did this
incredible but really dismaying in my in
my opinion tap dance around well you
know in the context of this and then
this and I mean they did everything they
could to avoid answering the question
basically
>> sugar lobby's very powerful
>> yes or has been historically
>> are these health associations like the
American Heart Association are they
really like in bed with the sugar lobby
to me that seems a little bit like a
like a movie um that I'm hoping isn't
real but in the end they I think they
took uh soda off the the list of things
that could be purchased with these
stamps. I I believe that's the outcome
because there was enough social pressure
because of social media and this just
went wild. But is it really the case
that our medical industry is in bed with
the processed food industry? I mean,
hospitals have some of the worst food in
the world. Not Stanford Hospital, but
I'm sure not USC hospital.
>> Definitely not US. Definitely not.
>> But but many hospitals you go in and the
goal is to get people many calories for
very little money. And that's
understandable why they feel they need
to do that. Um, but you just go, "Oh my
god, the the nutrition here is just
dreadful and this is a hospital." So my
mind goes to like, it might be true, but
is it true? Do we know?
>> It certainly seems possible.
>> Um, I mean, I've, as someone who's
researched the negative impacts of sugar
consumption, I've I've had a few brushes
myself with with the sugar lobby early
in my career. Have they you've had
someone
tailing your car? That's kind of
>> not quite to that level.
>> Okay.
>> Or a public facing statements, but um
>> but yeah, to the extent that that's
influencing our policy, I don't know.
>> So you've had the sugar industry giving
you basically.
>> Yeah. Early in my career, we had a it
wasn't even published yet. It was from
our early life sugar model that I talked
about earlier where um there was a press
release. It wasn't through me trying to
get it noticed. It just got picked up
for something. And when you get pressed,
that's when the sugar lobby, for lack of
a better term, may
>> have a forward public statement about
that particular study
>> to try and protect themselves.
>> Exactly. And and generally, it's not a a
that's a great study
>> um kind of comment, but um that was a
long time ago.
>> Yeah. Don't worry, you're safe.
Actually, by saying this here, you're
actually safer now. Also the world's
changed and nobody tr nobody trusts big
institutions anymore especially medical
related institutions which in many ways
is both good and bad right yeah because
uh you know you're right god forbid
someone has to have surgery you want an
excellent surgeon like you can't just
like you can't just uh like health and
wellness that you know but but the um
and on and on but um it's I do think
we've experienced a tide change now I
think the United States is really um on
board that things need to change. In
fact, um this week we have an episode
out with Michael Pollen who's written
extensively about the food industry and
plants and and health and um and he
actually was very it was really
remarkable. I'll provide a link to this
that one segment in the caption for
anyone that wants to see it. He he
really said he's like in order to move
the health of this country forward there
it needs to be a bipartisan effort. like
the fact that there's an emphasis on
improving nutrition, but it really just
focused on food dyes and he wasn't so
thrilled about that. But then he
actually tipped his hat to some of the
things that the administration has been
doing. But then also pointed out some of
the things that they were doing like
related to liberating the use of
pesticides that was not good. So he has
a very balanced view of this and I and
he makes and is able to say we need to
get away from the politics if we ever
want to move forward and be a an
actually healthy country. I think we
still have a long ways to go.
>> We do. But there's hope.
>> There's hope.
>> And you and I are young enough and our
gut microbiomes hopefully are healthy
enough that we will remember what we
need to know moving forward. And and
there's this whole other generation of
young kids that grew up. I'm I'm
realizing like thinking about food,
nutrition, exercise, sure, through the
fire hose of social media where there's
a lot of like bad information too, but
they many many of them think about
taking really good care of themselves.
And if they grew up in a home where that
wasn't a priority, they think about it
and they're helping people. And I like
to think that things are changing. Uh
before we wrap, I do have uh a question
about oxytocin.
>> Yeah. Most of us think of oxytocin as
the loveydvey
>> loveydvey um hormone neurom modulator.
Educate us on the role of oxytocin in
the context of food intake and
nutrition.
>> It's been known for quite some time that
that oxytocin
can reduce appetite and food intake. And
through careful studies from uh Harvey
Grill and others, we have identified the
brain stem as being the the most robust
target of oxytocin signaling to reduce
food intake.
>> Um so oxytocin is uh released or created
in the PVH and the hypothalamus released
into the circulation but also there's
projections from oxytocin producing
neurons throughout the brain. And some
of those neurons project to directly to
the brain stem.
>> And that system seems to be an important
system for reducing food intake mainly
through the level of meal size. So
making meal size smaller,
>> increasing satiation. We had a a study
recently where we were looking at its
role in the hippocampus.
And in this case, we found some results
that were a little bit surprising, I
should say. Um there's a phenomenon in
in human humans that rodents also show.
It's called the social facilitation of
eating. So if you and I are if you're
eating alone, you might eat less than if
you're eating with a group of people.
And if those people are familiar to you,
you're going to eat more than if they
were unfamiliar. So that's kind of the
the um the gist of the phenomenon. And
we can model this in rodents. And we
found that that phenomenon requires
oxytocin signaling in the hippocampus.
So if we genetically turn down the
signal um the animals don't show that
effect.
>> So this is kind of a different role for
oxytocin because under these conditions
in this brain region it's actually
promoting intake
>> in a social context.
>> So I think it's it's really complicated
like most things in the brain are. Um
but historically the it's been a unit
unidirection that oxytocin in the brain
reduces food intake. Um but some of
recent findings from our lab and others
are saying well maybe yeah but it might
depend on the the social context for
example and where the signal is getting
to. Well Scott thank you so much for
coming and sharing your mechanistic
data. I love that you're highly
mechanistic offline. And I want to know
the the literal organization of these uh
colonergic aerence to the hippocampus
cuz I think that's more of a aicionado
question. But it's clear that you're
studying a really really important
system for the health of all humans and
especially right now with the highly
processed food thing, but also the GLPs
and also the this explosion of
discoveries on the microbiome and the
positive explosion of people that are
interested in doing what they can for
their brain and bodily health. you're
you're clearly in the right area.
Evidenced by the fact that I said if you
had a vault,
>> what uh of money, what would you study?
And you're like, what I'm doing right
now. So, you're clearly in uh in the
right um laboratory which you run. So,
thank you. Thank you for doing the work
that you do. And it's not lost on me and
it shouldn't be lost on the audience
that you do that work with taxpayer
dollars. So, you're working on our
behalf for our health. So, and you're
very busy. So, thanks for coming here
today. Appreciate you.
>> Thank you very much. Appreciate it. It's
been fun.
>> Great. Next time, bring your dog.
>> I will. Awesome.
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