The Dr. Hyman Show - The Real Reason You Age (And How to Slow It Down) | Dr. Eric Verdin
Episode Date: May 6, 2026We tend to think of heart disease, cancer, and Alzheimer’s as separate problems. But what if they all stem from the same underlying process? On this episode of The Dr. Hyman Show, I sit down with D...r. Eric Verdin, whose research, including work on compounds like urolithin A, is helping reshape how we think about aging and long-term health. We explore why aging may be the biggest driver of chronic disease and what that means for how you approach your health. Watch the full conversation on YouTube, or listen wherever you get your podcasts. We unpack: • How your immune system becomes both overactive and less effective over time • What chronic inflammation is doing inside your body and how to start bringing it back into balance • Why cellular energy and mitochondrial health are key to repair and recovery • How your microbiome shapes inflammation, immunity, and long-term health • The daily habits that impact longevity most and where people get it wrong This conversation reflects a shift in how we think about health, moving beyond treating disease to understanding what’s driving it in the first place. View Show Notes From This Episode Get Free Weekly Health Tips from Dr. Hyman https://drhyman.com/pages/picks?utm_campaign=shownotes&utm_medium=banner&utm_source=podcast Sign Up for Dr. Hyman’s Weekly Longevity Journal https://drhyman.com/pages/longevity?utm_campaign=shownotes&utm_medium=banner&utm_source=podcast Join the 10-Day Detox to Reset Your Health https://drhyman.com/pages/10-day-detox Join the Hyman Hive for Expert Support and Real Results https://drhyman.com/pages/hyman-hive This episode is brought to you by Timeline, Seed, BIOptimizers, BON CHARGE, Paleovalley and Big Bold Health. Visit timeline.com/drhyman for 20% off a subscription on top of the new starting price of $79. Go to seed.com/hyman and use code 20HYMAN to get 20% off your first month. Head to bioptimizers.com/hyman and use promo code HYMAN at checkout to save 15%. Head to boncharge.com/hyman and use code HYMAN for 15% off. Head to paleovalley.com/hyman to save 15% off your first order today. Go to bigboldhealth.com/drhyman and use code HYMAN15 to save 15% on your first order. (0:00) Biological age vs. cholesterol in heart disease and chronic disease risk (0:50) Introduction of Dr. Eric Verdin and his work (1:23) Sponsor: Brain Shaping Academy (1:51) Sponsor: Mitopure (2:54) Sponsor: Seed (3:48) Welcoming Dr. Eric Verdin and longevity framing (5:42) The geoscience hypothesis and modifying age as a risk factor (8:21) Early-stage interventions in aging and potential for life extension (9:56) Longevity skepticism and practical steps for today (11:20) Mitochondria, inflammation, and hallmarks of aging (17:20) Mitochondrial DNA, inflammation, and immune system aging (22:17) Innate vs. adaptive immunity and immune aging (28:47) Strategies to combat immune aging (33:07) Gut health, inflammation, and foundational elements of longevity medicine (38:20) Social connections, sociogenomics, and cellular energy in aging (46:29) Cellular repair systems and postbiotics (50:33) Sponsor: Paleo Valley (52:34) Sponsor: Big Bold Health (53:23) Urolithin A, immune rejuvenation, and longevity interventions (59:08) Longevity and functional medicine approaches (1:02:27) Big data, AI, and the evolution of medicine (1:04:26) Microbiome, diet, and gut health (1:06:14) Measuring biological age and biological clocks (1:09:37) Future of health monitoring and closing remarks
Transcript
Discussion (0)
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What really has changed in the last 20 years is that we can change your biological age to some degree.
Your cholesterol level is seven times less important than your age.
So imagine now that we're targeting aging what it's going to do in terms of impact on your risk for heart disease.
You say that the phenomena that drive aging is primary. The diseases are secondary.
Aging is the biggest risk factor for a whole series of conditions that we call heart attack, stroke, atherosclerosis, many forms of cancer, type 2 diabetes, Alzheimer's, Parkinson's, all of these diseases.
And so it really changes the paradigm of the way we've been taught medicine, which is to respond to all of these.
emergencies that occur, what I call Wachamol medicine.
If we targeted the underlying mechanisms of aging, we could extend like by 30 or 40 years.
So what do you do for helping your immune system age well?
That's really the way medicine is going to change.
Dr. Eric Burden is president and CEO of the Buck Institute for Research on Aging
and a globally recognized leader in aging in science, a physician, scientist with over 300
publications.
He studies the intersection of metabolism, immunity, and longevity, helping shape the future
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podcast. So good to have you again. I love talking to you. You're my favorite longevity guy because
you're like the legit guy. You do the studies. You published hundreds and hundreds of papers.
You do the real science.
You really understand this field more than I think most people out there.
And you're kind of willing to explore the margins and edges, which is great,
but you're also not holding us to the truth, which I really appreciate.
I'm delighted to be here, and I like you.
I'm a physician.
So I think, you know, I think it takes for us to have gone through the root of what it means
to deal with real lives to understand the implications of any statement that you make.
And so, you know, a number of people have taken to calling me the grandkids.
Rumpy men of longevity medicine.
I don't see you that way.
And I take this as a badge of honor because I would rather be sort of a little more conservative
than a little more adventurous.
Yeah, and I agree.
If I really want to know about something, I ask you.
So with that said, you know, one of the things I really love about your framing of longevity
because you're at the Buck Institute on aging is the framing around disease and aging.
you say that the phenomena that drive aging is primary.
The diseases are secondary,
and that if we can attack the primary features of aging,
which are not necessarily all inevitable,
that we can change the trajectory of disease in a far greater way.
I love that you ask that question
because it's a concept that came out of the Buck Institute.
It's a scientific term.
It's something we call the geoscience hypothesis,
and it was published about,
12 years ago by my colleagues, Gordon Lithcar was the leader of this, and it hasn't been
paid attention enough. So I will restate what it is. Aging is the biggest risk factor for a
whole series of conditions that we call heart attack, stroke, arthroscoposis, many forms of cancer,
type 2 diabetes, Alzheimer's, Parkinson's, all these diseases, osteoporosis, macular degeneration,
sarcopenia, the list, you know, the list goes, your response to COVID-19, your response to
your risk of pneumonia.
All of this is driven by aging.
When I went to medical school, which was already a long time ago, we were told, for example,
for heart attacks.
I think we're doing pretty good for a couple old guys.
And this work actually is helping.
There's a sense of urgency there.
You know, when you think about this and how medical school.
for heart attacks, the risk factors, most people can actually recite the risk factors, smoking,
physical inactivity, obesity, and so on. Those were in a box in my textbook of medicine as a
modifiable risk factor. There was another box, which was the unmodifiable risk factor, and that
was your age and your gender. Now, we're changing both. And so, but your age, what really has
changed in the last 20 years is that we can change your age to some degree.
Your biological age. Biological age. Not your chronological age. How many years you've lived.
I'm waiting for that. Yes.
But so that time machine. That changes that whole equation because what people fail to recognize is, you know,
imagine your cholesterol level, $20 billion industry with statins. You know, a lot of success,
actually mitigating, decreasing the risk for heart disease. Your cholesterol level is seven-time
less important than your age. So imagine now that we're targeting aging what it's going to do in
terms of impact on your risk for heart disease. Now, the beauty of the system is that you're not
only affecting heart disease, you're affecting everything. Everything. And so it really changes the
paradigm of the way we've been taught medicine, which is to respond to all of these emergencies that
occur, what I call Waccamol medicine, where you have a heart attack, we survive, we cure cancer,
and so on versus targeting the root core.
So think about a tree with all of these branches being diseases.
Now, we're going for the core.
The biggest risk factor, and that's aging.
Now, we are at early stage in trying to understand how this works.
How do we actually interfere with the aging process?
I think we can slow it down.
There's some early evidence that we might be able to revert.
And I think this is really what animates all of our work.
It's really the idea that we're going to be getting to the root core of all of these diseases.
That's how I think is root cause.
Like, how do we deal with root causes?
That's what functional medicine is, is root cause thinking.
And it's just a different way of thinking about things.
And I heard it said that if we cured cancer and heart disease
and we just got rid of them completely from the face of the planet,
we'd extend life by five to seven years.
And if we targeted the underlying mechanisms of aging,
we'd call the hallmarks of aging,
we could extend life by 30 or 40 years.
It's orders of magnitude more.
Totally agree.
Is that right?
Yeah, this seems to be, right now, based on what we know,
there seems to be a hard stop at 115, 120.
Very few people have gone, one person has gone to have one.
Madame Calman. And she smoked and she drank and she needed chocolate, but she didn't get married.
Yes. And some questions, some have questions, you know, the veracity of whether she was Madame Calman, her daughter, who was collecting social security benefit.
So there's been a lot of controversy, but, you know, a handful of people have lived about 115.
There's a hard stop at around 115. So imagine that everyone getting there. That's already, I imagine everybody getting to 95.
They would already be amazing.
So one of the reasons why sometimes, as we talked about, I'm called grumpy or unimaginative or not ambitious enough
as people feel that I should be projecting bigger numbers in terms of what we're going to be able to do in the future.
And we might, but the bottom line is no one can walk around and tell you, I'm going to lift to 140, 150.
We don't have any evidence for this.
So why even say this?
I mean, the don't die thing is not real?
No. No. You're not bent on that horse.
We're not even talking about immortality because that's a whole other ballgame.
You know, people talking about immortality say, I've said on a record, if you're looking for this, join a church, don't come to the longevity field.
Yeah, exactly. I'm really, we are focused on two things. One is, what can we do really to push the envelope very far?
But also, what can you do today?
Yeah.
Because that's really the most important thing, to modify the way we...
This is so important because right now, I mean, there's a lot of cool things happening
like Yamanaka factors and some big money behind researching ways of gene modification or inserting
transcription factors that regulate aging and can reverse biological.
Those are kind of sci-fi and there's some real money and research going on and that might do
something.
But right now, what you're saying, what I hear you're saying, is we can really look to getting
to at least 100 most people if we do all the things that we need to do, given what we know now.
We focus on the fundamental mechanism of aging, what people call the Hallmark
of aging, and we're going to kind of dive into one of them particular today, inflammation,
or what we call inflammation, or what we call inflame aging, is that all these are related,
they're all interconnected, they're not really all separate phenomena, they all kind of cross-talk,
and they influence each other, and there are some meta-frameworks that actually allow us to
kind of push the field of those hallmarks into health.
And I think that's kind of how I think about it.
And all the things that people are listening to and hearing about, whether it's saunas or,
you know, peptides or exercise or whatever.
whatever the modifications are or NMN or whatever the molecules are,
they're all affecting these fundamental systems.
And I think that's the kind of the home kind of core message I want to get today.
And with that framework, I want to dive into this concept of immune aging.
You look across all the diseases of aging.
They're all related to inflammation.
Brain aging is inflammation, Alzheimer's inflammation, cancer is inflammation, obesity's inflammation,
diabetes inflammation, heart disease inflammation.
Yeah, we're talking about a common core.
Right.
And there's a lot of ways to get to inflammation.
And when you have inflammation, it affects everything else.
It affects your mitochondria and your genes and your telomeres and your microbiome.
It's all connected, right?
So the cause and effect sometimes are not always clear, but the phenomena is really clear.
I can say a word about this.
One thing that's remarkable about inflammation, it's a normal response of your body.
So, you know, if you cut yourself, if you burn yourself, you're going to see the appearance of redness first, then there will be a bubble.
and then there's a whole repair process.
And you'll see the area where it's been burnt,
actually will stay inflamed.
Eventually, so this is what we call acute inflammation,
which is a normal response of your body to damage.
Eventually, that bubble is going to recede.
There'll be a crust.
The crust is going to fall.
And soon there'll be maybe a little redness.
And then eventually everything will be gone.
So that's inflammation at work.
because I think inflammation is a bad name,
something that's always bad.
Inflammation is critical.
This is our response to damage, to fix it.
The problem of aging is persistent inflammation.
Chronic sterile inflammation.
It's like chronic sterolence.
Yeah, and it stays on,
and what's remarkable, it becomes part of the problem.
So a body response that was there to actually heal
becomes part of the chronic response.
And so there's a lot of interest in trying to understand.
How does that, what's cause, what's effect?
as you mentioned, and how do we actually suppress it and eliminate it?
And I think that's key.
And I think, you know, as we, as we're younger, immune systems are very vigorous and they're
very good at fighting infections and kind of preventing cancer.
As we get older, it kind of switches a little bit.
Like we don't get so good at fighting cancer or preventing infections, right?
And so I want to unpack that a little bit.
But what I want to sort of create a little bit of a framework is a new concept that I think
people are going to hear about today, which is the link and the connection between
mitochondria and inflammation. They're often thought of as separate. There's like mitochondrial dysfunction
is one of the hallmarks and inflammation and, you know, inflammation is another one, but they're not
really separate. So I want to really frame that up as we're talking about this. So let's talk about
about this concept of how sort of cellular energy and mitochondrial function and inflammation and
immune aging are connected. Maybe I'll say a word about the hallmarks of aging first because I think
it will put everything into context. So this hallmarks of aging. So this hallmarks of
that you mentioned, mitochondrial function,
senescent cells, and all this,
was a way for the field to organize all of our different activities.
Everybody was doing research.
There was no organization.
A blind man in the elephant.
Exactly.
And so people sometimes were working on something similar.
They just did not call it the same.
So this hallmark of aging review was published
by Giedo Khrummer and his colleagues
and organized these molecular manufacturing
manifestation of aging. So that's what they are. The paper was published. It created a lot of
excitement because we were finally starting to think about a problem in all of its dimensions.
Yes. Okay. And so meetings were organized on mitophagy, on senescence, and so on. What people
fail to recognize is that biology is a series of incredibly intricate network. So there's not such a,
you can't put these hallmarks in need little boxes. That's what I was trying to say, yeah.
And so the reason I'm bringing this up, because when we think about, most people think about mitochondria, they think, oh, mitochondria, that's energy power for the cells.
Simplistic.
It's very simplistic because the mitochondria is also an incredible sensor for what's happening in terms of inflammation.
An example that I like, how does mitochondria connect to inflammation?
So if your mitochondria are not functioning well, they generate what we call radical oxygen species.
these RELLS, free radicals.
These free radicals are nasty.
They will by themselves create inflammation.
Your oxidants, so I would take antioxidants.
They have pro-oxidants.
That's where the whole theory of antioxidant came from.
That was Denham Harmon way back when, yeah.
Exactly.
Not recognizing that free radicals actually can also be positive.
They're cell signaling molecules.
So is inflammation.
Everything is like a signal, right?
Exactly.
And it can be too much or too little, and that's what the balance is the key.
Totally.
Having a lot of oxidative stress is not good, and you can tamping down, you're probably going to do yourself some good.
But you can't block it all because then you run into a whole series of other problems.
So that's one way by which if your mitochondria are not functioning well, you're going to create more oxidative stress.
Another way is mitochondria.
An oxidative stress least inflammation.
Exactly, a direct link.
Another way, which is actually fascinating where there's so much work going on right now, is you might be aware
that mitochondria have their own DNA.
Yeah.
Okay, so my mother.
Yeah, exactly.
Mitochondria are actually descendants of a bacteria that was absorbed by our cells and
form a whole kingdom called the Eukaryotes.
And so we have within our cells these bacteria that have their own little genome and they
replicate and they, you know.
And they look like a bacteria.
Yeah, exactly.
They look like a bacteria.
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Now, we have in our cells mechanism that allow us to recognize the presence of DNA in our cytoplasm.
Remember, DNA is normally in the nucleus of the cell.
The only way you can get DNA in your cytoplasm is for two reasons, either.
And so, baby, your cytoplasm is like the liquid inside your cell, like the cell is like a baggie.
Exactly.
And inside the baggies like your nucleus and the mitochondria, but there's also this squishy liquid and that's the cytoplasm.
Yeah.
Perfect.
I'm sorry for getting too technical.
But all of you...
I'll stop you if I got to translate.
All of your DNA is in the nucleus, and it should stay there.
So if your cell gets infected by a virus, there's a system in the cytoplas,
and I will recognize the presence of abnormal DNA.
Carviral DNA.
And it will activate an inflammatory response.
The same thing, if your mitochondria get damaged,
they start leaching out their DNA in the cytoplas.
that's also recognized as an inflammatory signal.
So the body does not know.
It says, oh, there's something wrong.
It doesn't recognize even your own mitochondria as you.
No.
It's a foreign mitochondria.
Yeah.
And so, that's a, this is a whole system called sea gas sting.
There's new inhibitors that are targeting this, that are showing amazing effects.
So again, a completely new different direction of research.
What other mechanism by which I'm trying to think?
I think this would be probably the two major.
But also inflammation is, and it also affects mitochondria.
So it bidirectional, right?
Yes.
If it's an inflammatory signal from your microbiome, for example, which is most people have
terrible bacteria, that can affect your mitochondria.
Or if there's an environmental toxin which creates an insult, the mitochondria,
that can also create inflammation because these are autogens, right?
When you age, for example, you know, your NAD levels decrease.
We've talked about this before.
together.
You go back and listen
our old podcast on NED.
Yes, NAD is critical,
for example, for mitochondrial
integrity and functions.
So as you age,
these mitochondria become tired.
They don't divide as well.
They're not cleared as well.
They don't generate as much energy.
So the whole series of problems
that are linked to the aging process
that makes your mitochondrial
a really essential pivot in all of this.
And the immune system is like any other system,
like your muscle system.
You don't have the same strength.
when you are young as when you are old, the same thing.
Your immune system is performing at a much lower level.
So let's kind of unpack the immune system starting there.
There's two parts, really.
There's the ancient generalized, like, carpet bombing immune system,
which is preserved, you know, in many, many species.
It's not so smart.
It's just like a kind of a fire bombing city,
as opposed to our kind of smart, targeted bombs.
And that's called the innate immune system or the ancient immune system.
And then there's the adaptive,
or that's also called the cell-mediated immune system,
which we learned in medical school,
which is meted by the T-cells.
And the B cells. And then there's the adaptive.
And then there's the adaptive immunity
or the antibody immune system
where we create specific targeted antibodies,
for example, against COVID.
When we check our COVID test,
that's what we're checking as antibodies.
Can you kind of unpack what those are,
what they do, and how they change as we age?
Great question.
So, so think about, again, two systems, innate,
first line of defense.
And I probably should everybody,
we're going to get to the news to use here.
I just want to kind of lay.
the groundwork here. Yeah. First line
of defense is the innate immune system.
It's a thing about
a country defending itself.
It would be the barbed wire at the
border, you know, just or maybe
a series of people who are
arming the border, making sure
nobody crosses. We talked
about DNA
in a cytoplasm, that's part of the
innate immune response. So there's a
whole series of receptors that
allow every cell to determine
whether something there's a danger
signal.
During aging, for example, we have a disruption of the gut barrier.
Some of the bacteria in our intestine can leach out into the blood, and they cause inflammation.
Simply that the disruption of your gut barrier will cause inflammation because some bacterial
product are leaching out across, again, in the blood, all of your cells see that,
and they think there's an infection, and so they activate the first line of response.
So that's inflammation, by the way,
is inflammation is that innate immune response.
The chronic sterile age-related inflammation.
Or acute as well.
You have damage, you burn yourself,
there's damaged tissue that's recognized by the innate immune system.
It starts repairing.
That part of the immune system,
as we age, becomes hyper-responsive.
It just sees problems where there's none.
And that's a whole concept of people have talked called inflammation.
That's what I was getting at when I said related to the aging.
So that's inflammation aging.
The second part of the immune system you mentioned is the adaptive, which is totally different.
It's actually an educated system.
It will learn from what it has been exposed to.
So imagine you get an infection with influenza with the virus.
The body will learn how to recognize it and it will develop specific tools, T cells and B cells,
that will make specific targets.
That's the basis for vaccination.
When you get a vaccination, you get a little dose of something.
The body learns how to recognize it,
and it will confer a protective response that will last sometimes a lifetime.
Yeah, like a measles vaccine, right?
Measles, vaccines, or even infection that you have when you were a kid,
herpesoster, you can have a chickenpox when you're a kid,
and for many people you actually have immunity for life,
although you should get your shingricks.
Single shot.
I hope we can talk about this because this is really fascinating in terms of the implication of some of these vaccinations.
And that system, the whole immune system that's adaptive, depends on, in part, from your thymus.
Thymus.
Yes.
Tymos is a gland that's called sweetbreads.
Exactly.
Some of us.
I have them the other night, forget her.
Yes.
I hope it's going to help my immune system, but I don't think it works like that.
No.
So that's exactly what it is.
It shrinks as we get older. It shrinks as we get older. By the time you reach 50, most of us, it's gone.
Now, the problem when you do this is you're not able to generate the new cells. So you are living with
the number of cells that you had at age 50. And these cells dwindles slowly over time so that
your immunity, your ability to mount a new immune response will decrease. So that vaccinations are
given mostly when you're young. And you get older, your ability to mount.
of vaccination response,
decrease.
You don't respond as well as the vaccines.
You don't respond.
And for example, if you get a flu shot,
you're going to get actually a specific flu shot
for elderly, older individuals
that will try to trigger your immune system more forcefully.
And so this failure of adaptive immunity as you age
is one reason why we saw during COVID-19
in the risk of death increasing so much during age,
as a function of aging,
aging. This is why 30,000 people, I believe, still die from influenza every year. The same thing
with RSV. So there is an epidemic that no one talks about, which is the fact that older
individual die from viral and pneumonia, all these infections at much higher frequency than
younger ones. So there's a lot of interest in the aging field to try to say, how can we mitigate
this? Can we restore the thymus? Can we understand what makes the thymus? Can we understand what makes a
times go away and so on.
It's almost like the worst of two worlds. On one hand, the innate immune system starts to be
overactive and more indiscriminate and creates this low-grade chronic sterile inflammation that
we call inflammation. And at the same time, are anybody levels or are less able to mount
in response to their cells that do anybody, they're less able to mount a response to invaders.
And so we can't fight cancer. We can't fight infections as well. And so we get all these different
problems. That's a great point. You can respond to a vaccine in the same way. As you mentioned,
the immune system, the adaptive immune system, plays an important rule for what we call a tumor
surveillance. So it goes around the tissue and it tries to determine, is a cell acting funny?
Is it synestine? Is it a zombie cell? If it's a zombie cells, we'll try to eliminate it.
So there are many mechanisms by which the immune system participate in our health.
One last point is the fact that these two immune systems do not function independently from one another.
Right.
System is really smart.
So the innate immune system, when it's activated, actually provides the help to educate the adaptive immune system.
And so if you have a chronically active innate immune system, that doesn't jive well with the adaptive.
So the whole system degrades as we age.
And so as people are listening to, well, this isn't good news, right?
The immune system ages.
You can't mount responses to infection surfact cancer.
You get this chronic inflammation that creates a downstream cascade that leads to all these chronic age-related diseases.
What do we do about it? How do we manage that? Is there a way to kind of reduce inflammation or to stop the inflammation or to improve immune response? How do we do that, given what we know in longevity now? Because immune aging is what we're talking about.
Yes, it's very hard to sort of, first thing I should say also why immune aging is so important. There's evidence that if you induce aging only in the immune system and we can do this in mice. Okay, so you can make a,
a lesion only in the immune system.
That will induce organismal aging.
So it will not just induce aging of the immune system.
It will induce secondary aging in the other organs.
And so that's been shown in two different studies.
So it's real data in mice.
Creating these artificial tools that we have,
he can make only a lesion in the immune systems,
which means the immune system as a dominant role.
in our aging.
That has been proven in another way.
You might have heard about the new clocks
that Tony Whisker-ray has generated,
these organ-specific proteomics clock.
Okay, so you can now...
Is that generation labs?
It's a Vero.
A Vero.
Vero labs.
Yeah, yeah.
That's right.
So what this company and Tony's work have shown
is that they now can draw,
from a blood jar,
they can measure a series of proteins
that are circulating,
that are reflective of the activity and the health of all organs.
So they can determine...
Your organ clock, how old your brain is, how your heart, your kidneys,
because obviously, you know, you can be an incredible health in your whole organism.
If your brain health is 20 years ahead, you're going to be not doing so well.
So there's always that sort of rate-limiting organ that could be causing all of the problems.
So we want not to age at an accelerated rate in any organs.
But what his data, they've gone back and analyzed 50,000 people from UK Biobank, huge data set from England.
And they found that there are two organs that are predictive of your demise in terms of your lifespan.
It's the immune system and it's the brain.
And it's not that surprising because there are the two organs that are distributed.
They're the sensory organs.
Yeah.
And your brain, you know, your brain has ramification and the whole organ is your nerves, your brain does not just sit in the cranium.
It sends nerves to the whole body for muscle, but also to your organs and so on.
So same for the immune system.
It's not only sitting in your lymph nodes.
It's in your skin.
It's in your liver.
It's in your gut.
Half of your immune system is actually in your gut.
So that means that all of this data in aggregates mean that maintaining immune health is really critical.
And it's going to be one of these, you know, we used to think as physicians that the critical organ for survival was your heart.
because half of the population was dying of heart attack,
and we still have that problem.
But beyond this, let's say we can cure heart attacks
as I think we will in the near future.
But also that's related to inflammation.
Yes, but we, that's also,
so maintaining immune health is going to be really critical.
Well, you make an interesting point,
because the way I think about the brain and the immune system
is the brain is the sensory organ for macroscopic things.
The immune system is the sensory organ for microscopic things.
So they're kind of mirrors.
They're very, very important in maintaining tissue integrity and so on.
So what do you do for helping your immune system age well?
Dr. Burden.
That's a tough one.
So I think.
Or at least better phrase, what do you think the science best says we should do?
Yes.
First, we have to mitigate inflammation, okay?
Because I think, as we talked about, inflammation is not only a response, it becomes
the driver.
Yeah.
And there are lots of sort of self-ampifying loops that have.
happen there. If your immune system becomes activated, it can actually induce that. It can try to
repair, but eventually it can actually cause damage. The solution becomes the problem. The solution
becomes the problem. And so mitigating this inflammation is key. And one area, for example,
that I think there are multiple areas that we can talk about. Gut health, I think, is critical in this
respect for me. And I tell people, this is something that not enough people are talking about in the
longevity field. And actually, the people who are talking about it, I think, focus on a lot of the
wrong things. A lot of focus on probiotics. And I think we should be focusing on prebiotics and
postbiotics. And I'm happy to. I want to get into that. That's a topic we're going to get to.
That's a great one for me. And one that I think we're not talking about enough. And if you ask most
doctors, how do you create a healthy gut? They have no idea. Yes. And there's a way to do it.
I mean, that's what functional medicine might the joke about me where at my old job at Canyon Ranch was
I was Dr. C.
Every poop, because I wanted to look at every still test,
look at every microbiome, see what's going on,
reset the gut as a way of treating all these kinds of diseases.
Agreed. Totally agree.
And I think for most people,
totally unaware.
And, you know, the only thing they think about this is
when you walk into a whole food,
there's a fridge full of probiotics that I said,
I wouldn't go near those if I were you,
because we don't, except maybe for Archimansia,
most of those, we don't know how to use them
or maybe like to basilus.
And your diet is what creates your microbiome.
Exactly.
For the main reason, and you're focusing on prebiotics.
These are foods, whether it's asparagus or juice from artichokes or plantains.
These are things we can eat that actually feed the good bugs.
I agree.
Or if you're not able, and actually the evidence points to the fact that most of us,
prebiotics would be all fiber.
And most of us actually have an inadequate intake in our modern way of eating of fiber.
And so I tell people, you know, if you have to supplement, supplement.
but there are a growing number of good supplements that you can take.
I mean, it's staggering when you look at the historical fiber intake of hunter-gatherers.
It was estimated to be 150 grams of fiber a day.
We ate at 15.
And the average American, we should be trying to get to 30 by 40, 50, at least, you know.
My wife is from Germany, and I suspect you've traveled there when you eat a slice of bread from Germany.
Yeah, you need a meat slicer.
I visited a friend of mine in Germany when I was like 20-something, and she had one of those like deli meat slices in her kitchen.
I'm like, what is it for?
For cutting the bread?
Because a knife doesn't work.
Yes.
It's dense.
And that bread is, you know, but the other way is this bread also will force you to chew
and will get you a large jaw which will stop sleep apnea.
So there's a lot of interesting things in terms of the fact that our diet has become almost like semi-liquid.
Yeah.
Creates all of these problems in terms of facial features and so on.
That was the work of the dentist who went around.
I forget his name right now, the guy who went around and said all the indigenous cultures and looked at all the teeth and the teeth.
I mean, you know, I was in Africa and I saw the gorillas and I got to go to the museum and I got to see all the gorilla skulls.
Perfect teeth. Like, they have perfect teeth. They don't need dentures. They don't need, you know, they don't need braces. I mean, it was amazing to see.
And I was like, wait, that their diet is what's driving their dentition and their dentition is driving their health.
Absolutely. I'm reading James Nestor's book, Breathe. Yeah.
or breath.
I don't know.
And there's a whole chapter on this.
There's this sort of adventurer who was one the first one to actually visit American Native Indians.
And what was one of the things that struck him the most is the teeth of all of these Native Indians were absolutely perfect, no crooked.
They didn't have to remove wisdom tea.
They didn't have to do anything.
So that's a fascinating aspect of it.
But I think the two are linked.
So this idea that we're eating a semi-liquid diet, soft bread, soft everything versus chewing a heart
has implication not only in terms of our microbiome, but also our tooth structure, our ability to breathe through our nose and so on.
So whole foods, fiber is the root of everything.
Yeah.
So phytochemicals, fiber, whole foods, getting rid of processed food, sugar, all that's going to be the biggest lever for inflammation, stress, sleep, removing toxins.
These are the things that I think about.
Do you think about those?
Is there anything else?
This is the foundation.
And I think, you know, I...
Sleep, stress, exercise, food, toxins.
Human connection.
Human connection, yeah.
All of those is for me, the foundation of longevity medicine.
And, you know, it's people, I've argued, well, this is not sexy.
This is not what people want.
They want supplements.
They want drugs.
They want a shortcut.
And I'm all for shortcuts, but I believe it just doesn't work.
And we, and also, plus none of these.
shortcuts have been proven. The rest of everything else has been proven, the effect of physical
activity and so on. So the stance that I've taken lately sort of social media and talking is
one that is a bit contrarian to what some my colleagues are advancing in the longevity
field. I'm as excited by, as anybody, by what we're going to be doing 20 years from now,
but let's not forget where the foundation is. And we can create so many problems that are so
easily solvable as a society. Not everything needs a pill. Yeah, one of the most interesting studies
I ever saw was it was a whole field of sociogenomics, which I kind of came up with on the term myself,
because I kind of saw Paul Farmer's work in Haiti and how he helped people and using community
health workers to help. And I just came up with this concept. And then I started researching it.
And I was like, wait, there's a whole literature on how our social connections affect our immune
system. And that if you're in a loving, connected relationship or in an interaction, it's going to
reduce inflammation. But if you're in a conflictual, literally inflamed relationship, it's going to
create inflammation. I love that whole aspect. Yeah, it's really interesting. And it's more cuddle
puddles. It's incredibly frustrating for me that we know from the happiness studies, for example,
that the biggest factor determining your longevity is your social connections.
The number of loving relationship you have, your sense of purpose.
The problem is that these are also the hardest one to study, especially in animal models.
I can go ask a mouse what its sense of purpose is, you know, living in a little plastic box and eating the same food that looks totally disgusting.
So there is, you know, we've been talking actually at the back about creating a center for a psychobiology of aging, which would really try to, at the end, everything is driven by,
molecular mechanism. I mean, we are biochemical feature. Could you reproduce like a whole natural mouse
environment? You know, like dirt. People are doing this. Yeah. Kind of interesting. Like a cage.
They're creating these like really, and you know, we study longevity, by the way, in these mice that live
like, you know, these prisoners. I mean, they, they're alone in their cage. There's no distraction.
There's nothing to do. The food is there all the time. It doesn't taste good. Imagine, I mean,
the mice, I'm sure, have the same needs that we do in terms of having a different.
diversified environment and so on. So there's a whole group of people thinking that we should create these. And maybe, you know, the drugs that we find that work in mice would be a lot more relevant to what we have to do in you.
Amazing. All right. This is so good. So I think we kind of got a good dive on the immune system. Let's kind of switch over to mitochondria and help us understand how mitochondria and cellular energy are so central to aging. Because to me, they're kind of like the final common pathway that goes wrong. And inflammation is causing them to make.
out function. And how do we, how do we understand how that's occurring and why and what we can do
about it? Yes, so where do we start? Let's start with like, why are mitochondria and solar energy
is so important to aging? The big reason that everyone knows is the, most people agree on is the
energy, energy requirement. So everything that we do is dependent on energy. People think about
moving your arms, thinking.
Everything that we do is depending on generating energy.
Typically, we get that energy from our food.
So we're able to extract energy from the food.
The place where that energy conversion happens is in the mitochondria.
Most of our energy generation happens in the mitochondria.
We also know that as we...
So all of these activities, think,
moving,
are the two major ones.
But there's a whole other aspect
of energy
that most people do not appreciate
is that repair.
So we are constantly subjected
to toxic insults, yeah.
Okay, we talked about
the free radicals.
That would induce damage.
Damage in our proteins,
damage in our DNA,
damage into our membranes.
All of these lesions,
these damage have to be repaired.
So we,
have in our cells little monitoring mechanism that constantly look at everything, make sure
everything is fixed. As soon as a reason, sensors. As soon as something is seen to be damaged,
a whole crew is sent to repair it and fix it. For example, I'll give you an example of DNA damage.
Your DNA is the code that encodes every one of our cells. It stands the reason that if you're making
a damage and you're creating a mutation,
you have the potential to change the code.
Essentially, so if you allow this to happen all the time,
eventually the whole system is going to go awry.
So there are human mutants who are people who carry a mutation from their parents
where they are not able to repair DNA damage.
They typically live until 20.
You're the progeria patients?
Yeah, some of these progerias.
So there's a whole series of syndromes,
xenodermopigmentosum, ataxia tel-injectasia,
The whole series of these DNA damage repair, all really tough disease to live with, many of them with very shorten lifespan.
So that highlights how important all of these repair pathways.
We also have systems to repair unfolded proteins.
Remember, proteins is a string of amino acid.
It has to be folded in an extremely precise manner to function.
If it becomes a little unfolded, all of a sudden, it's creating problems.
And that's one of the hallmarks of aging is protein damage.
Yes, protein, proteostasis, the idea of maintaining all of your protein in good shape.
Again, there's a whole series of enzyme that we call chaperones that are sent.
If something is unfolded, they're sent.
But all of this refolding takes energy.
And so our body always makes this calculus, okay, what do I repair?
What do I not repair?
And so we try to repair as much as we can, but there's an energy cost to this.
Okay?
So you also have to move.
You know, so the difficulty for a living organism is how much energy do I allocate to repairing everything perfectly or what can I live with and still move, still hunt, still procreate, still.
So this antagonism between repair and reproduction is really at the root of aging.
And so as we age, the mechanism of production of this energy starts become limited.
We mentioned, these bacteria are, these mitochondria become old.
But there's a way to repair them and renew them, right?
That's the key.
So there's actually a special repair system just to get rid of old mitochondria that are damage.
It's called mitophagy.
Yeah, it's like autophagy, but it's for your mitochondria.
Autopathy is where you kind of eat yourself and clean yourself up.
And autophagy is activated when you're resting and actually allows you at night to actually repair a lot of the damage.
And what's amazing about autophagy is that it's a self-eating mechanism that specifically targets what's been damaged.
So imagine you're not eating, so you still need energy.
And that energy now has to come from the inside.
Your system has a mechanism that goes to clean up the attic first.
It doesn't destroy the kitchen.
It goes into the attic and say, okay, what's all the garbage here that I can still resell and make a profit without actually touching the kitchen?
So, and mitophagy is an arm of this that selectively targets defective mitochondria because they are so central.
But like everything during aging, so what is aging?
The progressive accumulation of damage.
Even though we have all these repair mechanisms, we don't repair perfectly.
We've repaired pretty good.
During our 20s, the rate of repair is such that if we work to continue repairing at the same rate, we would lift to a thousand years old.
So during our 20s, we're actually doing incredibly well.
The problem is as a little damage accumulates over time,
eventually some of the damage might actually target the repair mechanism.
And we know aging is not a linear process.
It accelerates.
The older you get, the faster your aging process.
And so the whole idea of activating, reactivating mitophagy.
Because eventually as you get old,
mitophagy becomes limiting as well.
It doesn't function as well.
So.
Clean up system.
Your garbage men get old.
Exactly.
Exactly.
That's right.
When I think about about this, it's, it's such an important kind of framework to think about the sort of
energy of the cell, because it really runs everything.
Yes.
And we kind of do know that everything that impacts aging also impacts the mitochondria and vice versa.
And there are levers, though, to really take care of your mitochondria.
We talked about NAD on our last podcast.
but there's other compounds that induce mitophagy and that are,
we mentioned postbiotics earlier,
which are essentially compounds that you eat from food,
they get metabolized by your bacteria,
and they produce downstream molecules that have function in the body,
which I think is a miracle,
just when you think conceptually about it,
that you eat stuff,
and then it creates like a literally a medicine
that turns on different signaling systems in your body
to help you repair, renew.
And I think, from my perspective,
it sounds like you think the same way. When I think about aging, I think, you know, the body has
these innate systems of repair, renewal, regeneration. We just burden them and we don't take care of them.
Yes. And that's why we age faster. And instead of focusing on treating disease, if we focus more on
our regenerative renewal and repair systems, we do a lot better. And so the way in is through some of these
food molecules. And I call it, I have a joke. I call it a symbiotic phyto-adaptation. We
symbolically evolved with plants and use their compounds to regulate our biology.
because we're lazy.
Like, we don't make vitamin C, so we get vitamin C from food.
We don't make, for example, one of these post-botics called urolithine,
so we make it from pomegranate or other elagiotanins that are in, you know, walnuts or berries
or whatever.
So kind of help us understand how, for example, this molecule of uralithinae, which you published
on, and we'll link to the papers in the show notes, and which I, by the way, take every day
because the literature is impressive on it.
What does it do, and why is it getting so much attention now?
And we've kind of learned about it more in the context of exercise,
improving, you know, exercise capacity, V-O-2 max and fitness and muscle health and mitochondria health.
But it does have a linked to immune system. So what is it and how is it linked to these things
that we just talked about? I'm wrapping back up with immune function, the gut, and mitochondria,
because it's like one thing. It's a really cool story because it's one really, I would call it,
of sort of a human ingenuity. And so in some way, we've known for a long time that pomegranate juice
is actually healthy for people.
And there's a whole, you know,
there have been studies showing
that consumption of pomegranate juice
is actually confer some health benefits.
What was not clear is what the mechanism.
So subscientists, a good friend of mine,
Yoran Aurek, who works in Lausanne,
actually went and looked for what is in pomegranate juice.
And they found these illegitans,
these compounds.
What they also realized is that these compounds
are not acting by themselves.
they are actually metabolized by your microbiome.
And the product that is made by your microbiome is called urolithin A.
Okay, now the catch is only about 35 to 40% of people is microbiome,
because remember all of our microbiomes are different.
And some 60% of people's microbiome is not able to make that conversion.
But we've trashed them because of our diet, because of antibiotics,
because of, you know, toxins, all this stuff.
So we kind of...
Having a rich, you know, most of us have more than a thousand different species of bacteria in our guts.
And the problem, the complicating factor is most of us have different species.
So you cannot compare your microbiome and mine, even though we might both be very healthy.
They can change.
Like, I've seen the same, you have people on a vegan diet or feel like meat, paleo diet,
and their microbiomes living in the same personal change.
Yeah.
We don't know how to read it well.
but we know certainly what upstream factors can actually yield a really complex and rich microbiome.
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Yeah, so this is a clear example of where
human ingenuity has been able to identify
a single molecule, urolithin A,
that is the result of a input
from a food product,
from a plant, permigranite juice,
it gets transformed by a fraction of us
into a product that has immense benefits.
So a company was founded based on this,
Amazonis,
that actually sells this product,
and has, we've been working with them.
I say, full disclosure, I sit on the board of that company as a scientific advisor,
but I always tell people, I don't sit on the board of supplement company
if I don't believe in the science, and if they're not willing to actually conduct clinical trials.
And one thing I think is commendable for Amazon is they've been going through clinical trials one at a time
to actually document and prove the efficacy of what.
I agree.
And they're a sponsor of the podcast, and that's why also I don't let everybody's
sponsor my podcast. You mentioned all of you will ask me because I think I want stuff that I know has
legitimate size behind it. And this is published in major journals like New England Journal or Jam or
other cells. So I think I think this is important. So to me, you know, I'm not opposed to
supplements, but we have to apply to them the same kind of standards that we've applied to generating
all of the drugs that we have. And that's how medicine has moved forward. So that being said,
you know, we've worked with them on a couple of studies. We still have another study going on with
them. So urolithin A has this remarkable ability to activate mitophagy. And mitophagy is not sort of the,
you know, as the term implies, it's eating mitochondria, but it doesn't eat them discriminately. It
eats the old defective mitochondria, which is absolutely remarkable. So when you do this, actually,
one of the study that we've done was looking at the human immune system of all the people on
urolithin A, and what we found is a really actually significant effect.
Even within one month of administration of uralithin A, we saw some, I would say, what anybody
would call a rejuvenation of the immune system.
I mean, I think, you know, early on when I looked at the data, this is years ago, I got
excited about it, I saw a reduction in CRP, which is a very crude marker of inflammation.
And we measure with function help, but there's even better markers.
But one of the things that you looked at that indicated that it,
it helped to reduce the inflammation process.
Yeah, actually, in our case, we, well, some cytokines,
we measured the presence of different cytokines,
TNF alpha, IL-6, IL-1,
and I don't remember exactly which ones were changed,
but some of them were.
And cytokines are the mess intermolecules of the immune system.
Exactly, and the IL-1, IL-6, TNF alpha,
are pro-inflammatory molecules,
so the higher the level, you know, the higher inflammation.
What we focused on in my lab with our core at the buck
was on looking at the adaptive immune system.
And what we saw was actually quite interesting.
We saw an increase in naivety cells.
So these are the precursors that are really critical
at generating an adaptive immune response.
We saw a whole series of other changes.
And just in English,
naivet cells are kind of cells that haven't made the antibodies yet.
They haven't kind of...
They haven't been activated to develop.
antibody. The T cells and the B cells would be making the antibody. So these are the T cells.
They cause the B cells to make the antibody. They help. But they also by themselves can generate
what we call cytotoxic T cells, CD8 T cells, which are the other, so the innate immune system,
the adaptive immune system has two arms, T cells and B cells. The T cells are making, actually,
they can kill bad cells. The B cells can actually secrete the
antibodies which help in the immune response. And so the uralithanae works on the T cells?
It worked on the T cells and actually increased the ability of these T cells to recognize their
targets. Now, this has implication not only for the person who's thinking this, but think about,
you might have heard about the CARE T cells that are used now for cancer cells, where we can
extract T cells from a patient and educate them to selectively kill tumor cells. And the problem
is that as you get older,
your ability to make,
to re-educate these T cells goes down.
And so this would have even application for cancer.
Yeah.
Because they did it in vitro
and show that these car T cells
were actually more effective.
So it makes immunotherapy work better
if you improve and rejuvenate your T cells
before you start to sort of target them
for cancer.
That's amazing.
So how does your own antenna affect
like the whole process of longevity,
the muscle, the inflammation?
Like what do we know about it?
mitochondria are not just present in the immune system.
They're present in every cell.
And so think about the concept of the top.
Except for red cells.
Except the red cells, exactly.
Yeah, they don't have a nucleus.
They don't have mitochondrial.
I think they have mitochondrial.
When we think about mitochondrial function,
it's not restricted to the immune system.
It's pretty much every cell that has to balance repair
and dividing and moving forward.
So when we think about urolithin effect,
they're going to be pretty much across the whole organism.
And I mean, we've focused so far on the muscle
where we could see increase endurance
in people actually on humans on urolithine A.
We've seen increased immune responsiveness.
My prediction is that when we start looking in the brain,
we might see increased performance,
increased memory and so on.
Not been proven yet,
but this is a molecule that's not just targeting
the immune system or an organism.
You call it pleotropic.
It's pleotropic, and I think my prediction, I don't think this has been shown yet,
but you can imagine that it would have real anti-aging effect.
Yeah, I mean, I think this is interesting because we often look at drugs or affect a single target.
There are a single molecule, a single receptor, a single target.
You know, when you look at, you know, these longevity interventions,
they have diverse effects across all these different systems.
So a compound like uralithinae has many different effects across the system.
That's an important point.
And it goes back to this whole idea of what we talked about geroscience.
What does geroscience really mean when we talk about aging being at the root of everything?
Like geriatrics, like gerontology.
Yeah, that's the root of it.
But it's the root of it.
That's what that means.
There's another example because the way we practice medicine is based on a model that dates back to the 17th century when we discover organs.
You know, you go see a heart doctor.
You go see a neurologist.
there's a National Institutes of Health,
which has a national heart, blood, and lung institute.
It's a national institute of organs.
Exactly.
So, first, I mean, it's a National Institute.
It's not a National Institute of Health,
the National Institute of Disease.
And second, it's based on a 17th century model.
Now, when we talk about urolithin A,
it's not that it's going to help your immune system.
It's going to help everything.
Same thing, think about rapamycin,
which is another darling from the longevity field.
It's target called Tor, target of rapamycin, is not only in the immune system.
It's in your brain.
It's in your muscle.
So when you give rapamycin to someone, you're not affecting just the immune system.
You're affecting pretty much the whole organism.
And that's the shift that longevity medicine is doing from sort of organ-based reactive model
to a sort of system-based proactive.
Yeah, you treat the system, not the symptoms or the diseases.
That's essentially what functional medicine is.
It's what I've been doing for 30 years.
It actually works really amazingly well.
You really get to the root cause, like you were talking about the root, not the branches and the leaves.
And that's even the paradigm we used to describe what functional medicine is.
We treat the root in the trunk, not the leaves and the branches.
As a physician, I've been a fan of this approach of medicine.
I think what longevity has done is to add a little bit of a more exciting aspect, frankly.
And I agree.
I think my hope is that this is a reintroduction of many of the concept of functional medicine through the eye of longevity.
And for some reason, it's resonating more with people.
It's become kind of, you know, longevity has become sort of a buzzword, which scares me also to some degree.
But I think it's a wave that we should ride because it will in the end change the care for patients and make it much.
I agree.
And I think, you know, the way I think about functional medicine is a heuristic.
It's just a tool that we use to think about things.
It's not the thing itself because we're trying to describe the human body is infinitely complex,
but we're trying to organize it, just like we organize the hallmarks of aging.
But when you look at the functional systems that we describe in functional medicine,
they almost map perfectly across the hallmarks of aging.
Mitochondria, microbiome, you know, nutrient sensing, all these things are all part of this.
And so we may improve that model and it becomes smarter and smarter.
especially as we start to dive into the complex biology that we barely have scratched the surface
of proteomics and transcriptomics and metabolomics and the microbiomics and the whole that's like,
you know, at Function Health we do like 160 biomarkers at first flush and there's more you can add on.
But there's literally thousands and tens of thousands of genes and, you know, millions of variations in your genetics.
And there's tens of thousands of proteins and there's, you know, there's thousands of metabolites.
And it's almost like incomprehensible.
But now with big data science and with AI, we can start to make sense of this.
I could not agree more.
And I think this is...
Because no, I matter how smart you and I are, we'll never get to understand it at all.
No.
And, you know, we're generating data right now in patients at a rate that is beyond anybody's comprehension.
And I'm always comparing, you know, the state of medicine today.
And I'm a physician, so this is not a condemnation of medicine.
This is just recognizing what it's doing.
You go see your doctor and you have maybe 20.
20 measurements or typical annual visit, 20 or 30 measurements.
And that's what most people will rely on.
They're inoglobin A1C, they're LDL, not even APOB.
They're fasting blood sugar, maybe they're A1C and so on.
You're lucky if you get an A1C.
Yes.
And so anesthetoscope, you know, and a little bit sort of something that we used to.
17th century medicine.
Something that we used to do, you know, 50 years ago when we were being trained.
Today, I mean, we can generate out of a single blood draw hundreds of thousands of different data points.
And I think a lot of the work that we're doing at the buck right now is trying to integrate all of this data because we're generating it with AI.
Yeah. Making sense of it.
Yeah, making sense of it.
So these are early days, but I cannot help to be incredibly optimistic of the fact that in 10 to 20 years we will do, we're starting.
you know, you're starting with function health, others in different ways, really to generate a lot more data.
Yeah, we've got like 80 million biomarkers we've tested in the first few years and we're just getting started.
And, you know, I remember sitting on a panel at Cleveland Clinic with Stan Hazen, who's a cardiologist who's studied the microbiome and its effect on heart disease.
And I said, Stan, how many of the metabolites in your blood do you think come from the microbiome?
And he's like, I think probably a third, which blew my mind.
true or not. But, you know, when you think about that, it's like our microbiome, like you said earlier,
is a completely neglected area of medicine. You know, gastroenterologist don't even pay attention to it.
Well, I'll tell you, another piece of data, which I keep reminding myself of, is half of your immune
system. So your immune system is distributed across the whole body, but half of it isn't the
intestines. Yeah. Pires patches, yeah. Why? Because it's where you're interfacing with the outside
world. You're basically one cell. You're one cell away from a sewer.
So on the other side of your intestinal lining, which is one cell thick, you know, is on the inside is like a sewer.
And on the other side is your bloodstream and your immune system to kind of help take care of you.
So imagine now what you put in in terms of fibers, in terms of your food and all of this has a direct impact not only on the bacteria, your microbiome.
I think about the microbiome as an organ, frankly.
This is an additional organ in terms of weight.
It's pounds.
That's three to five pounds.
People don't realize these are pounds.
This is a big...
Pounds of poop.
Pounds of poop.
And all of these bacteria are digesting your food.
Many cases, they're predigests what you've eaten.
They're generating all of these secondary products.
All of these products go into the wall of the intestine, and they educate your immune system.
So this interface there is really, I would say, one of the still big black box of what...
It's interesting.
And in functional medicine, we've been testing organic acids for years.
And part of the things that show up in your urine are metabolites of things that are happening
in your gut.
So we can tell if there's yeast overgrowth, if there's bad bacteria, if there's things that are
going on.
It's quite interesting.
And we treat people based on that.
And it's pretty cool all stuff.
I mean, Eric, this is such a great conversation.
I actually want to talk to you more.
I'm not going to do a three-hour podcast with you this time.
We're going to break it up.
I want to talk about some of your new research going forward.
I think we're going to maybe do another podcast on this because it's a whole topic in
of itself, which is how do we do we?
measure biological age. And I'm just going to set this stage and I want people to come back and
listen to the next podcast. But we are trying to figure out, when we say we, the scientific community
is trying to figure out, is there a metric we can use to look at interventions to see if it's working?
Like if you say, oh, this molecule or this exercise or this thing, if we do it, will you reverse
your biological age? And there's a lot of clocks out there. A lot of people are doing this.
We use one in function, which is based on Morgan Libbyn's sort of calculation in biological age.
And it's, you know, it's an approximation.
And I say, you know, if you do the same clock over and over, you're going to get the same kind of variation.
But they all widely differ.
And one clock you were 29, when you're 689.
And they're like, same big I see.
And I'm like, man, I don't like the one that says I'm 70.
I like the one that says I'm 39, you know, but you've kind of done some more research on this.
I'm just going to set the stage of looking at the clock that has to do with your naive T cells.
And this seems to be more of a stable clock that you can kind of track.
It doesn't vary so much.
So we're going to come back and do a podcast on that.
I'm super excited about it.
We're going to put a link to the show notes.
We're going to do a full show on clocks.
Yeah, I think it's really, you know,
if I can say one more thing about these clocks,
why is that important?
As we move from this reactive to proactive medicine,
you know, the way we, most people live their life is they have their lifestyle.
Their spouse or their children might tell them,
you know, let's try to do this.
and exercise more.
Everybody's living their life,
flying, what I call flying blind.
You have your doctor's visit annually.
You might get a few samples.
But eventually, you know,
you get into your 50s, your 60s.
If you're lucky and you've done the right thing,
you're going to go right through.
If not, you get a heart attack.
And so the question that this whole new reinvention of medicine,
functional medicine,
longevity medicine, is reoccupying itself,
is this, can we accompany you starting at age
20, 25, measure you every, no, maybe every day using wearables, using blood sampling.
You know, the technology is going so quickly.
I don't know how we're going to be doing this.
The idea for me is really this constant monetary.
Nobody would fly a plane blind today.
We have incredible, but we fly our-ephotic medicine is just doesn't make sense.
We fly our health blind.
Yeah.
And we go to the doctor, we're nervous, our blood pressure is too high.
we go home, maybe it's too low.
So this whole idea of everyday measurement,
hopefully in a way that's totally invisible to you,
is the future.
And so these clocks represent sort of the integration
of many of these variables that are going to tell you
you're flying not completely blind.
It looks at age 30 that you're on your way
to getting a heart attack at age.
We can do this now.
15 years in advance, we can identify the first signature of disease.
And then correct, so we don't hit the mountain
with our plane. We're actually correct and we go a little higher, we go a little to the left or to the right. That's
really the way medicine is going to change. And I think the clock, for me at this point, are an incredibly
promising direction. Yeah, it's true. And I think what you're saying is right. I mean,
episodic care, waiting until you have something, doesn't make any sense. And I think that's really
our mission. Function Health has actually helped people to create a longitudinal data set with continuous
measurements or more frequent measurements, continuous
to wearables, for example, whether it's
a ring or a watch or something or
a band, or
even continuous glucose monitors,
and there's going to be more monitoring like that.
Plus regular blood testing and
scanning allows you to create a comprehensive picture
and actually detect signals early,
these early warning signs, decades
before you ever see a problem.
And I think that's what's exciting to me
for every aspect of aging and every
chronic disease. And we're getting there, whether it's cancer,
heart disease, Alzheimer's, diabetes, we can
see it coming a mile away. And that's, that's, you know, what I get excited about. Yeah, same for me.
So thanks so much, Eric. Thanks for doing your work. And great to see you again. And we'll have you
back soon. Likewise. Thank you. If you love this podcast, please share it with someone else you think
would also enjoy it. You can find me on all social media channels at Dr. Mark Hyman. Please reach out.
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Thank you so much again for tuning in.
We'll see you next time on the Dr. Hyman Show.
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my work at Cleveland Clinic, and Function Health, where I am chief medical officer.
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