August 13, 2026 • 36 mins
Nir Barzilai is a physician and a researcher at the Albert Einstein College of Medicine in New York, where he runs the Institute for Geroscience. Nir’s problem is this: How can we use lifestyle changes and drugs to slow the process of aging?
In this episode, Nir explains:
- The search for biological markers of aging
- The existing drugs that might reduce the risk of diseases associated with aging
- The four key lifestyle factors that every researcher in the field agrees on
- What he learned by studying the genes of people who lived to 100
- What “geroscience” means, and why it doesn’t have a Wikipedia page
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Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:15):
Pushkin. I'm Jacob Goldstein, and this is what's your problem.
My guest today is Near Barzilai. Near is a physician
(00:37):
and a researcher, and he runs the Institute for Gero
Science at the Albert Einstein College of Medicine in New York.
Near's problem is this, how can lifestyle changes and drugs
slow the process of aging. In our conversation, Nier and
I talk about the search for biological markers of aging,
(00:57):
existing drugs that might reduce the risk of diseases associated
with aging, and what he learned by studying the genes
of people who lived to age one hundred and beyond. Also,
we talk about the meaning and origin of the term
gyo science. To start, I asked her how he decided
to study the biology of aging.
Speaker 2 (01:18):
It actually happened young. It happened with my grandfather that
walked with me every Saturday telling me about his life
as a young person. And he was sixty eight. It's
the year he died. He was looking old, fat, slow,
and for me it always it almost became immediately clear
(01:44):
that that's where I'm going, Okay, So it became the
biggest question in biology of aging. When I went to
my residency. I had an attending and whenever I presented
the patient, he would stop me. I would say, this
is a seventy five year old woman, and he would
(02:05):
stop and say, but does she look younger than their age?
And after a while you saw that it mattered. You
can have a ninety year old guy and it comes
to the emergency room and he has some infection and
with some antibiotics, he'll be fine, and a seventy five
year old woman that all her systems are totally gone,
and you know, you know where she's going, and that
(02:28):
it's important in decision making. I want to say that
this is thing that I think people intuitively understand that
there's a biological age. I think it's more important to
know that aging, this biology is what drives diseases. It's
(02:50):
not that we get heart attacks and we become old.
It's the opposite. We become old and that drives diseases.
Speaker 1 (02:57):
I mean, intuitively, we also know that, right you're much
more likely to get a heart attack at seventy five
than at twenty five.
Speaker 2 (03:05):
That's true, but let me give an example that you'll
explain it better. You can be born with genes for Alzheimer's. Okay,
there's a gene called apo E four. If you have
two copies of these genes, you are really high risk
of getting alzheimer at sixty or seventy and you'll be
dead by the time you're eighteen. But when you're born,
(03:28):
you're not demented. And when you're one year or ten
year of fifty year, you're not demented. You meet the
biology of aging, the failure of our young biology in
order to get those diseases. And it's important because we
want to prevent your aging. And this is really the
biggest issue that we're talking about.
Speaker 1 (03:51):
Now, tell me a little bit more about that.
Speaker 2 (03:54):
So it's based on the fact that around the world
in the last few decades, we not only went from
hoping that there is something we can do, but we
actually have a promise and we're at the stage of
realizing a promise. And the promise is in what lifestyle
decisions we make, what drugs are available right now to
(04:18):
stunt aging, and the drugs that are being developed now
and are going to make bigger impact.
Speaker 1 (04:26):
Well, so okay, so let's get into it. So here's
the three that I know. I feel like the big
three in terms of what you're talking about, exercise, sleep, well,
have friends, don't smoke, and eat whole fresh foods. That
(04:46):
wasn't three, I know, I thought of two more in
the middle.
Speaker 2 (04:50):
So what you don't do is okay, you know, don't smoke.
There are four that every one in our field and
the longevity doctors and everyone would agree on. And that's exercise,
its diet, sleep, and it's yeah, social connectivity. Okay. Each
(05:13):
one of those have underlying biology of aging, and each
one of them is really important when you're young or
old to optimize. Okay, we used to say maximize, but optimize.
Speaker 1 (05:28):
So those are the ones that we sort of all know,
right Whether we do them or not is a different question,
because whose we all lots of people know that those
things are good, and it is remarkable how good they are, right, Like,
exercise is so good for so many things in non
obvious ways. Like sure, cardiovascular exercise is good for your heart,
(05:50):
that's obvious, but like, why does it make you less
likely to get cancer? This is an interesting question, right, Hey.
Speaker 2 (05:56):
I just answer that because those are affecting the biology
of aging a bold claim. Those are affecting the biology
of aging, and when I'm talking of biology of aging
is cellular aging. So cells all over the body will
will be younger or stay younger, and that's why you
(06:18):
get less cancer and less and less cardiovastro disease.
Speaker 1 (06:23):
When you say cellular age, what is the measure of
cellular age you're referring to?
Speaker 2 (06:29):
Let me say this way. There are twelve things that
we call hallmarks of aging. Okay, and I'm not going
to count them. I might give an example throughout.
Speaker 1 (06:40):
Give me one example. What's the what's a particularly robust example.
Speaker 2 (06:44):
Let's say that one of the problems is we have
a mechanism of garbage disposal in all our cells. And
this garbage disposal that's often called autophogy, or the scientists
will call it autophogy, takes junks that accumulate in our
cells because our selves is making mistakes in its production.
(07:07):
And it's taking those things that are really not helpful
and breaking them down to their component. It's going to
clean yoursels. Okay, Okay, that's what's going to happen now
every one of the hallmarks. What you have to show
is first of all, that it gets worse with aging. Second,
you can take a young model and make it old. Okay,
(07:31):
so it was done with autopogy. You knock out autophogy,
the mice are freaking out. They are becoming older at
a very young age. But more important, if you fix
it throughout aging, the mice are not only healthier overall healthier,
but they also live like twenty percent longer. Okay, So
(07:52):
that's how you become a hallmark. But the point is,
whenever you fix one of them, of those hallmarks, you
really fix also others. Okay. So it's you could take
one hallmark and show that it's very important, but you
can do it with each one of them. You don't
have to do it together. Not that doing it together
wouldn't be even better, but you don't have to do
(08:15):
it together.
Speaker 1 (08:15):
You're saying, if you fix one, that one working better
actually helps to fix the others, right.
Speaker 2 (08:21):
And you can see changes in the others.
Speaker 1 (08:23):
And so when you talk about these, you know lifestyle
changes like exercise, does your autophogy work better for longer?
That basically going.
Speaker 2 (08:37):
On exactly, And I'll give you another example. And I
can stay on autopogy because we don't have enough time
to cover the twelve. But how does so exercise fixes autophogy.
The hard one is diet. And I'll tell you why
I pick diet, because diet is something that's very individual.
(09:01):
It's it's it's really you know, if I take people
and say you should become vegetarians, they're going to which
proteins with carbohydrates, They're going to get fat or some
of them, and they're going to actually pay. Their health
is going to be worse. So it's very in the individual.
How do you choose diet and how you can actually
(09:23):
stick to a diet. So when I started my studies,
the experiment that worked in every lab, I took rats
and half of them got to eat whatever they wanted
and the other half I gave them forty percent less
food forty percent less food, so sixty percent of what
(09:44):
the others got. The rats that got sixty percent of
the food lived healthier and lived longer. What we did
is we gave the food in the morning to those animals,
and they were hungry, and they ate the food, and
they were then fasting for twenty three more hours. So
(10:04):
it wasn't only caloric restriction, it was also fasting. In fact,
when we gave them the food little bit throughout the day,
they were leaner, but they didn't live much longer, and
that led to this concept that a lot of us
are doing, including myself, which is intermittent fasting fast as
many hours as you can. Because what it does almost
(10:29):
the major thing that happened, it improves atophagy. This is
easy for most people to do, not for everyone. It's
easy for most people to do, and we don't know
if it extends life, but it certainly improves several factors
that you can look at, such as weight or metabolism
(10:49):
and other things.
Speaker 1 (10:50):
So we're talking at nine point thirty in the morning.
When was the last time you ate?
Speaker 2 (10:56):
I actually finished dinner at six pm yesterday because I
was traveling.
Speaker 1 (11:01):
What's your usual?
Speaker 2 (11:03):
It's usually eight in the evening when I finished dinner,
which brings me to noontime the next day. And what
I'm having. I'm having black coffee and I'm having you know, water,
but I'm not eating anything.
Speaker 1 (11:16):
How do you feel right now it's been fifteen hours
since you've eaten. How do you feel?
Speaker 2 (11:19):
I'll tell you the opposite. I was in Europe for
two weeks and sometimes I had breakfast, and in the
days that I had breakfast, I was just miserable, but
by noontime this is really and people in particular people
my age will tell you that they feel the benefit
(11:40):
on their basically cognition, their tiredness, their energy throughout the day.
Speaker 1 (11:48):
So you mentioned rats and fasting, and you mentioned mice
and autophogy, and you know there is that famous line
mice lie and primates exaggerate, Like to what extent have
these studies been validated in humans?
Speaker 2 (12:04):
I got a grant from our page together with Dan
Belski from Colombia.
Speaker 1 (12:09):
Our pages. The government basically it.
Speaker 2 (12:10):
Is the government right, and the government totally bought into
targeting aging and health spin but they funded us for
a simple reason. There are four drugs probably more that
we know target aging. And when you put those drugs
on cells, okay, they change the hallmarks of aging utophagy, Okay,
(12:36):
when you give them to animals, they live healthier and longer.
And in clinical studies, although those drugs were designed for
a certain disease, they also prevent other diseases. And although
they were developed for a certain disease, they prevented overall
mortality and not the disease specific mortality. So we take
(12:57):
studies that were already ended, and we're asking a simple question,
not only what are the biomarkers of aging, but which
one are changing with intervention?
Speaker 1 (13:09):
So what exactly is the study that you're doing.
Speaker 2 (13:13):
We we take blood samples that already exist because the
trials are done of four drugs, and we're looking at
what happened to each individual, whether he was on a
drug or on a placebol within the first year of therapy.
Speaker 1 (13:30):
And to be clear, when you say drugs blood samples,
do you mean the actual blood or you just mean
the tests that were done on those samples in previous tests.
Speaker 2 (13:37):
No, no, no, no, we have to do it's it's
totally new. We're taking the blood and using.
Speaker 1 (13:44):
So people store the blood from trials. These are trials
that are years old and the blood has just been
sitting there in the fridge waiting for you to come
in the free the freezer. Yeah, of course, and so
so and and the drugs are what theyre It's met foreman, rapamycin,
GLP one, some GLP one drug.
Speaker 2 (14:02):
And s GILT two inhebitors.
Speaker 1 (14:04):
What's that last one. I don't know what that last
one is.
Speaker 2 (14:07):
This is a very potent drug against aging. It's developed
for diabetes for sigia in volcana are the common name.
There are five five manufactures of this drug.
Speaker 1 (14:19):
So there's the blood in the freezer and you're taking
it out of the freezer and you're looking at these
twelve different hallmarks of aging and you're seeing how they
change over the course of the year and comparing those
changes for people in the drug arm of these trials,
in the treatment arm versus the people in the placebo arm.
Speaker 2 (14:36):
So for each individual before and after treatment, we're going
to have tons of data and we're going with AI
to reduce it to what is common for all those drugs,
what has commonly changed with treatment between all those drugs,
and this is likely to get to give us the
(14:56):
best clock to use in a clinical practice.
Speaker 1 (15:02):
And so basically, you want to find something that is
easy to measure or relatively easy to measure from a
blood test, say so that you can look in a
blood test and ideally find someone's biological age so to speak.
Speaker 2 (15:18):
Correct Again, we can do the biological age quite good now,
but what is change what has change when you actually
give a treatment that targets the age, that's the major point.
Speaker 1 (15:32):
But you're assuming that bigs into that assumption is that
all these drugs in fact slow aging. That like, that
is a conclusion that has to be true for this
study to make sense. Is that right?
Speaker 2 (15:45):
Well, it's the other way around. Those drugs did four
things right, each one of them. You put them in cells,
They make the cells younger. You give them to animal,
they live healthier and longer. You gave them already to people.
Those are our studies that had outcomes, and you show
that you give it for one thing and you prevented
(16:06):
other things, and that it changed overall mortality.
Speaker 1 (16:10):
That last part is that unambiguous. Like I wish I
knew the data better.
Speaker 2 (16:14):
Oh, like the studies, I mean, it's absolutely amazing. Let
me give you a flavor for the drug that you
didn't hear about as Gilty two inhibitors. S. GILTY two
inhibitors were developed for diabetes, and in the diabetes trial
it became apparent that they prevent cardiovas to disease and
kidney disease. Yeah, but then nephrologies came and did a
(16:37):
study and just to give you a taste, they took
four thousand people, half of them are placible and in
forty two non diabetic just people with impaired kidney function,
and in thirty two months they showed that they prevented
forty percent of deteriorating of kidney function, forty percent decrease
(16:57):
in cardiovas to disease, and forty percent decrease in overall mortality.
So it's circular. But what other explanation do you have
for a drug that actually changed the hallworks of agyp.
Speaker 1 (17:12):
We'll be back in just a minute. Shall we talk
about your genetics work?
Speaker 2 (17:28):
Sure?
Speaker 1 (17:30):
What have you learned from studying the genes of people
who live to one hundred?
Speaker 2 (17:35):
So first of all, I want to tell you that
my fear when I did the study was what if
I find that all those hundred years old have gotten
disease like everyone after the age of sixty, they got
disease and just lived longer with diseases. And what we
(17:56):
found is that they live twenty thirty years healthier. So
it's not only they lived longer, they live healthier, and
that wasn't really the big thing. The big thing is
that they had what we call a contraction of morbidity.
They will sick very little time at the end of
their lives. The CDC may rest in peace or be
(18:18):
resurrected whatever. The CDC have shown since nineteen ninety three
that people who die over the age of one hundred
have third of the medical cost in the last two
years of their own Interesting, then people who die at seven.
Speaker 1 (18:35):
So they die, they live a long time, and then
they die fast. That's the dream exactly.
Speaker 2 (18:40):
So that's what we want.
Speaker 1 (18:42):
Right, that's good news for people with the genes that
cause you to live a long time. Regarding your genetic studies,
I mean, is there any I don't know people in
my family don't live to one hundred, Like, am I screwed?
Does that matter for me that study?
Speaker 2 (18:59):
No, the opposite. You're the one who's going to benefit.
We don't have anything for those hundred years old, Okay,
because that's it. So two of those genes have already
been developed to drugs that past phase three trial.
Speaker 1 (19:14):
That that past phase three meaning the FDA is they're
up for approval at the FDA, right, Yeah, tell me
about those drugs.
Speaker 2 (19:21):
So one drug is called the CDP INHIBITORQUE. It's a
drug that basically increase your good cholesterol and decrease your
trigue glycerides. But that's only part of what it's doing.
Speaker 1 (19:36):
And so when they're doing a phase three trial of
this drug, what is the end point? What are they
actually trying to show that it does?
Speaker 2 (19:43):
So they're not doing it for aging. They came to
me because my studies showed that probably inhibiting CDP safe
because they are one hundred years old. Fourteen percent of
one hundred years old have these genes that increase their.
Speaker 1 (19:59):
As opposed to how many people in the population.
Speaker 2 (20:01):
At large three to four percent.
Speaker 1 (20:03):
Okay, so it's like four times as common or something. Right,
Is that drug being developed as a cardiovascular drug? Like,
what are they testing it for?
Speaker 2 (20:12):
It's been developed as a cardiovas or drug, but there's
evidence that it's also prevent cognitive decline, which was our
major claim around these drug.
Speaker 1 (20:24):
Are they testing it for that? That's a hard indication
to get.
Speaker 2 (20:26):
Yeah, yeah, they tested and their data.
Speaker 1 (20:29):
So you've talked about these promising drugs, most of which
are approved by the FDA for something met Foreman's approved
for diabetes, GLP one drugs are approved for weight loss.
I know that you've talked in the past about getting
a broader FDA approval. Specifically, you were trying to get
funding for this study called the tame trial where you
(20:51):
randomize people to get met foreman or placebo, and then
the idea was you would follow them for several years
and see if the people getting met foreman had a
lower rate of things like cardiovascular disease and cancer and
overall mortality, just do they die less. So is the
idea that if you do that study and you have
a positive outcome, like, what would the FDA say, what
(21:14):
would the indication be? Would it be give metform into
everybody over a certain age or what?
Speaker 2 (21:22):
No? No, the answer is no, because the study population
are people over the age of sixty five that are
already not doing not doing well. Not that people will
become centenarians.
Speaker 1 (21:37):
Okay, uh, because you need I mean for the study
to work, you need some people to get sick. Frankly,
if everybody on both sides stays healthy, you don't learn
anything exactly.
Speaker 2 (21:46):
And it doesn't make sense to take forty years old
and do the study and finish it in forty years
to ever result. It's but the FDA is working with
us on trying to get other indications that don't take
so long to.
Speaker 1 (22:06):
How long, how long and how big would that study
need to be to be properly powered.
Speaker 2 (22:11):
We had three thousand people for four years.
Speaker 1 (22:14):
That was the design.
Speaker 2 (22:15):
Yeah.
Speaker 1 (22:15):
And it's just hard to fund because this is a
generic drug. It's cheap, which is good if you want
to take it, but it's bad because there's no drug
company that can make a billion dollar selling it, so
they're not going to pay for the trial.
Speaker 2 (22:26):
Right, And we had funding, and then there was COVID
and then we lost, you know, the funding.
Speaker 1 (22:34):
Tell me about supplements.
Speaker 2 (22:37):
I'll start with a good thing. Supplements are good for
the economy.
Speaker 1 (22:41):
Yeah, okay, because people spend a lot of money on them. Yes,
you know.
Speaker 2 (22:44):
For me, supplement means that you measured something and it's
slow and you give it back, right, But that's not
how supplements are done. Supplements are pecking together one hundred
things or several things and giving you an also in
the bottle they say take two. Okay. There's no clinical
data on supplements. Okay. The FDA approves supplement not based
(23:08):
on clinical data. So what marketing of supplement is a
total hope? Okay, there's no promise. Not only that, the
most dangerous things is multi supplement that you take them together. Okay,
and you think they're additive, but they're antagonistic many times,
(23:29):
because if they're biologically important, you're going to find interactions
that you don't like. We actually know that people who
take multi supplements have increased mortality in spite of the
fact that they are the people who also exercise and
diet very often.
Speaker 1 (23:44):
When you say multi supplement, like a multi vitamin or
what do you.
Speaker 2 (23:47):
Mean like multi vitamins, let me ask.
Speaker 1 (23:52):
You another question. So the field that you are in
is full of and has always for all of history
been full of cranks and charlatan's. You're a doctor at
a medical school, Like, how do you deal with that?
And do your colleagues think you are a crank and
a charlatan?
Speaker 2 (24:11):
Respectfully, what you said was exactly the sentiment when I
got several major organizations to meet in New York and say, hey,
we have a lot of progress, and we have a
lot of noise.
Speaker 1 (24:23):
When was this? When was this?
Speaker 2 (24:25):
That was two years ago? Two years ago, and we
did something that's so unusual for a bunch of scientists.
We said, you know what, we really don't know what
to do. Why don't we take a branding company and
let them deal with it? And this is the best
thing we did because the branding company actually worked. It
(24:45):
was hundreds of thousands of dollars and we're still working
with them.
Speaker 1 (24:49):
It makes me nervous when you say branding company. I'm
asking you about cracks, Charlotte. Since you start telling me
about branding, it makes me nervous.
Speaker 2 (24:56):
But I think I'll make you I'll make you feel better.
And they said, first of all, you're using thirty different
terms to describe yourself. Yeah, okay, help spend, launch, avity, rejuvenation, gerontology, immortality,
you know, goes on and on, and that's very divisive.
(25:17):
So they said, hey, this is a problem. Second, they said, yeah,
you have an enemy and that's the noise. Okay, and
that's a good thing. Okay, that's a good thing because
you want to distinct yourself from the noise. The noise
are Charlotte Tan's snake oil, Brian Johnson, you know, things
(25:39):
like that. And they said, and for you, the best
name is gero science. And we said, oh, we like geroscience.
We always called ourselves gero scientists. But you know what,
gero scientists didn't pick up them. They said, yeah, because
you never marketed it. It's not even in a Wikipedia.
So we so with this branding company, we do several things.
(26:03):
First of all, like what we do now I talk
about geroscience. We changed the Academy that was the Academy
of Health and Lifespan Research to Academy of Geroscience, my
center that was the Insuite for Aging Research and the
Institute of Geroscience. We have a geoscience web now that
will feed all the organizations and all the people who
want to know everything. And we want to make it,
(26:25):
you know, like a real thing and not a divisive
thing or really distinct ourselves from from the noise.
Speaker 1 (26:33):
And in a sentence, what is geroscience?
Speaker 2 (26:38):
So the ideal of geroscience is that we target We
can target aging by by learning the science and improve
basically decrease the burden of diseases and increase increase the
health spen for everyone.
Speaker 1 (26:59):
Is there a Wikipedia page?
Speaker 2 (27:02):
Not yet?
Speaker 1 (27:02):
No, no, you can make a Wikipedia page.
Speaker 2 (27:04):
No no, no, no no, no, there will be soon.
But it's actually a process you can make. You can
make the Wikipedia page. But when it comes to things
like that, there's a committee and the committee now is
biased and we're spending actually twenty thousand dollars to show
the gero science is a real.
Speaker 1 (27:25):
Say, convinced the Wikipedia committee. Yeah, wow, Like, do you
need a newspaper reporter to use the word in the
in the you know, in the Wall Street Journal, in
the New York Times? That is that what you need.
Speaker 2 (27:37):
But it was effective because when I called ourselves gero science,
when I talked about it, several editors have changed the
name of the article to anti aging because they said,
we don't know what's gero science, but anti aging.
Speaker 1 (27:50):
What do you think about the phrase anti aging?
Speaker 2 (27:53):
So first of all, we're not anti the aging, but
it is used much more commonly for non scientific fact
than for science. And so we actually we we actually
trying to make it worse, really for people to know
that whoever called themselves anti aging and there's no gero
(28:15):
signs behind that. Yeah, it's going to be bad.
Speaker 1 (28:23):
We'll be back in a minute with the lightning round. Okay,
let's finish with a lightning round a little bit more random.
What one thing you do, even though it may shorten
(28:46):
your life.
Speaker 2 (28:49):
So I'm doing the sixteen hour fast, but I'm a foodie. Okay,
so after the sixteen hours fast, I really don't care
what I got interesting?
Speaker 1 (29:03):
What was the last really unhealthy but delicious thing that
you ate?
Speaker 2 (29:09):
Black forest cake? I have a black forest cake, also
with ice cream.
Speaker 1 (29:16):
Yes, ice cream is so good. Do you have a
favorite really really old person, like from the Old Testament
or from mythology.
Speaker 2 (29:29):
I'm talking about Metusilla because he supposedly leave nine hundred
and sixty nine years And the people who are very
orthodox in religions, whether Christians or Jews, believe every word
in the Bible, right, But when you ask them, did
(29:49):
Metusla leave nine hundred and sixty nine years? Ah, they
didn't know how to count.
Speaker 1 (29:55):
Well, I don't know that particular story. I mean one
thing that's interesting to me, Like in the Old Testament,
people are just old. Noah's hundreds of years old, whatever.
But you know, the myths and the stories that focus
in particular on in more mentality especially, it's often bad, right,
somebody lives forever and it's terrible to live forever, which
(30:16):
is interesting in the context of this conversation.
Speaker 2 (30:20):
Right, And you know, there's a whole people who are immortalists,
and that's very different from me. Okay, I'm not immortalist.
In fact, I'm saying what to live a billion more years?
How many you know, presidents do you have to suffer through? Yeah,
I'm tired a little bit. Immortality. Immortality is a belief,
(30:44):
and people realize now that this is not going to
happen in their lifetime, and what they are turning into
is freezing.
Speaker 1 (30:53):
Yeah, that's been around for a while. Cryogenics like cryogenous
that one seems very crankish to me.
Speaker 2 (31:00):
Well, but it relieves them in their mind they're dealing
with their immortality.
Speaker 1 (31:06):
So I read this interview with you where you talked
about the fact that people with Alzheimer's disease sometimes will
respond to music that they know from earlier in their life,
and that you actually started making an Alzheimer's playlist for yourself.
What's on the playlist?
Speaker 2 (31:23):
So usually the playlist for those people are of their
most earlier memories as young adults, right when you were
kind of a kid, when you were in high school,
when you were in college. And so for me, it's
really the sixties seventies.
Speaker 1 (31:41):
It's a great era. It's my favorite era.
Speaker 2 (31:44):
In a lot of ways that are taking and my
kids are saying, you know, when you have Alzheimer's, mom
would leave you, not because she doesn't like you, but
because she wouldn't stand the music.
Speaker 1 (31:58):
So, from your work with people who've lived past one hundred,
I'm curious, what's one thing that you've learned that's not
related to health.
Speaker 2 (32:08):
Will they have a belief in what makes them leave
two hundred? And they could adopt the belief because they
actually had genes, which means they were protected from everyone.
Speaker 1 (32:21):
What actually made them lift two hundred is their genes,
not the fact that they play golf every Wednesday or whatever.
Speaker 2 (32:27):
So I have a woman who died at the age
one hundred and ten, and she smoked for ninety five years,
and she thinks it's because of cigarettes. She said, the
four doctors that told her to stop smoking, they died.
Speaker 1 (32:41):
Yes, yes, Okay. Of all the things we've talked about,
If there's only one thing I do to live a longer,
healthier life, what should I do?
Speaker 2 (32:52):
You know? I think at the end it's all individualized.
Will be able to see what is the one thing
you do. Look, I'm looking at you. It looks to
me like that your BMI is normal. It looks to
me that you're probably exercising. So I don't know, you
have to tell me what you don't do, and I'll
(33:12):
pick one.
Speaker 1 (33:12):
Yeah, that's really because I was hoping you'd say exercise,
because I was like, oh, yeah, that's the what I got.
I'm not a great sleeper. I don't know, you know,
I don't look at my phone. Whatever I do the
things they say to do, I just don't tend to
sleep that well.
Speaker 2 (33:27):
So with sleep, there there are two things. One is
for the young people and one is for the old.
For the young people, stop bingch watching. Okay, a lot
of the sleep deprivation is self inflicted. Right, you need
eight hours. You should strive for eight hours sleep, and
so that means that you have to plan which are
(33:49):
the eight hours for the older one or older one
than young. So for you and me, it's eight hours
in a dark room without electronic Okay, you're not going
to sleep the eight hours I sleep for some reason,
no matter what happen. I travel around the world. I'm
(34:10):
just like, I sleep six hours and forty minutes no
matter what. But if I sleep less, it's not going
to be good. But what I'm doing that's different than you.
I have a feet, bit, you can have a ring,
and you can actually measure because it's possible that you'll
find that your ram sleep and deep sleep are long
(34:32):
enough and you don't need the sleep, and you're not
going to feel tired, even if you feel that you
didn't sleep well.
Speaker 1 (34:39):
So you're saying it's important to be in bed in
the dark for eight hours, but it's okay to not
sleep the whole time. Right, So do you lie in
bed for an hour and twenty minutes every night not sleeping?
Speaker 2 (34:53):
That's pretty much what happens. I'm spending time trying to
fall asleep and trying to stay asleep.
Speaker 1 (35:00):
Yes, anything else we should talk about, just.
Speaker 2 (35:05):
The one thing that's important to know that aging, that
what what we're doing is not only for older adults.
People who survive cancer are aging rapidly because we give
them chemotherapy and radiation. Right. I don't know if you
know cancer survivors, but they usually are doing badly after
they recover, so they need help. People with HIV have
(35:28):
diseases ten years younger than their ages. Down syndrome is
an aging syndrome. Disabled people, you know, need help. And
if we're going to Mars, if this is for some people,
it's very important. I think this world is beautiful we
need to repair it. But if you go to Mars,
you're not going to get there before we stopped aging,
(35:50):
because you'll be sick on the way there and you're
never coming back.
Speaker 1 (35:55):
Thank you very much for your time. I really appreciate it.
Speaker 2 (35:58):
Thank you very much.
Speaker 1 (36:06):
Your Barselai is a physician and he runs it's the
Institute for Geroscience at the Albert Einstein College of Medicine.
Just a quick note, we're going to be taking the
next couple weeks off. We're going to be back after
that with more episodes of What's Your Problem. Please email
us at problem at pushkin dot fm. Tell us what
kinds of shows we should do more of or less
of our particular people you think would be good on
(36:27):
the show. You can also find me on x and
on LinkedIn. Our show is produced by Gabriel Hunter Chang
and Trina Menino. Our editor is Lydia Jane Kott, and
our engineer is Sarah Buguer. I'm Jacob Goldstein.
Pushkin. I'm Jacob Goldstein, and this is what's your problem.
My guest today is Near Barzilai. Near is a physician
(00:37):
and a researcher, and he runs the Institute for Gero
Science at the Albert Einstein College of Medicine in New York.
Near's problem is this, how can lifestyle changes and drugs
slow the process of aging. In our conversation, Nier and
I talk about the search for biological markers of aging,
(00:57):
existing drugs that might reduce the risk of diseases associated
with aging, and what he learned by studying the genes
of people who lived to age one hundred and beyond. Also,
we talk about the meaning and origin of the term
gyo science. To start, I asked her how he decided
to study the biology of aging.
Speaker 2 (01:18):
It actually happened young. It happened with my grandfather that
walked with me every Saturday telling me about his life
as a young person. And he was sixty eight. It's
the year he died. He was looking old, fat, slow,
and for me it always it almost became immediately clear
(01:44):
that that's where I'm going, Okay, So it became the
biggest question in biology of aging. When I went to
my residency. I had an attending and whenever I presented
the patient, he would stop me. I would say, this
is a seventy five year old woman, and he would
(02:05):
stop and say, but does she look younger than their age?
And after a while you saw that it mattered. You
can have a ninety year old guy and it comes
to the emergency room and he has some infection and
with some antibiotics, he'll be fine, and a seventy five
year old woman that all her systems are totally gone,
and you know, you know where she's going, and that
(02:28):
it's important in decision making. I want to say that
this is thing that I think people intuitively understand that
there's a biological age. I think it's more important to
know that aging, this biology is what drives diseases. It's
(02:50):
not that we get heart attacks and we become old.
It's the opposite. We become old and that drives diseases.
Speaker 1 (02:57):
I mean, intuitively, we also know that, right you're much
more likely to get a heart attack at seventy five
than at twenty five.
Speaker 2 (03:05):
That's true, but let me give an example that you'll
explain it better. You can be born with genes for Alzheimer's. Okay,
there's a gene called apo E four. If you have
two copies of these genes, you are really high risk
of getting alzheimer at sixty or seventy and you'll be
dead by the time you're eighteen. But when you're born,
(03:28):
you're not demented. And when you're one year or ten
year of fifty year, you're not demented. You meet the
biology of aging, the failure of our young biology in
order to get those diseases. And it's important because we
want to prevent your aging. And this is really the
biggest issue that we're talking about.
Speaker 1 (03:51):
Now, tell me a little bit more about that.
Speaker 2 (03:54):
So it's based on the fact that around the world
in the last few decades, we not only went from
hoping that there is something we can do, but we
actually have a promise and we're at the stage of
realizing a promise. And the promise is in what lifestyle
decisions we make, what drugs are available right now to
(04:18):
stunt aging, and the drugs that are being developed now
and are going to make bigger impact.
Speaker 1 (04:26):
Well, so okay, so let's get into it. So here's
the three that I know. I feel like the big
three in terms of what you're talking about, exercise, sleep, well,
have friends, don't smoke, and eat whole fresh foods. That
(04:46):
wasn't three, I know, I thought of two more in
the middle.
Speaker 2 (04:50):
So what you don't do is okay, you know, don't smoke.
There are four that every one in our field and
the longevity doctors and everyone would agree on. And that's exercise,
its diet, sleep, and it's yeah, social connectivity. Okay. Each
(05:13):
one of those have underlying biology of aging, and each
one of them is really important when you're young or
old to optimize. Okay, we used to say maximize, but optimize.
Speaker 1 (05:28):
So those are the ones that we sort of all know,
right Whether we do them or not is a different question,
because whose we all lots of people know that those
things are good, and it is remarkable how good they are, right, Like,
exercise is so good for so many things in non
obvious ways. Like sure, cardiovascular exercise is good for your heart,
(05:50):
that's obvious, but like, why does it make you less
likely to get cancer? This is an interesting question, right, Hey.
Speaker 2 (05:56):
I just answer that because those are affecting the biology
of aging a bold claim. Those are affecting the biology
of aging, and when I'm talking of biology of aging
is cellular aging. So cells all over the body will
will be younger or stay younger, and that's why you
(06:18):
get less cancer and less and less cardiovastro disease.
Speaker 1 (06:23):
When you say cellular age, what is the measure of
cellular age you're referring to?
Speaker 2 (06:29):
Let me say this way. There are twelve things that
we call hallmarks of aging. Okay, and I'm not going
to count them. I might give an example throughout.
Speaker 1 (06:40):
Give me one example. What's the what's a particularly robust example.
Speaker 2 (06:44):
Let's say that one of the problems is we have
a mechanism of garbage disposal in all our cells. And
this garbage disposal that's often called autophogy, or the scientists
will call it autophogy, takes junks that accumulate in our
cells because our selves is making mistakes in its production.
(07:07):
And it's taking those things that are really not helpful
and breaking them down to their component. It's going to
clean yoursels. Okay, Okay, that's what's going to happen now
every one of the hallmarks. What you have to show
is first of all, that it gets worse with aging. Second,
you can take a young model and make it old. Okay,
(07:31):
so it was done with autopogy. You knock out autophogy,
the mice are freaking out. They are becoming older at
a very young age. But more important, if you fix
it throughout aging, the mice are not only healthier overall healthier,
but they also live like twenty percent longer. Okay, So
(07:52):
that's how you become a hallmark. But the point is,
whenever you fix one of them, of those hallmarks, you
really fix also others. Okay. So it's you could take
one hallmark and show that it's very important, but you
can do it with each one of them. You don't
have to do it together. Not that doing it together
wouldn't be even better, but you don't have to do
(08:15):
it together.
Speaker 1 (08:15):
You're saying, if you fix one, that one working better
actually helps to fix the others, right.
Speaker 2 (08:21):
And you can see changes in the others.
Speaker 1 (08:23):
And so when you talk about these, you know lifestyle
changes like exercise, does your autophogy work better for longer?
That basically going.
Speaker 2 (08:37):
On exactly, And I'll give you another example. And I
can stay on autopogy because we don't have enough time
to cover the twelve. But how does so exercise fixes autophogy.
The hard one is diet. And I'll tell you why
I pick diet, because diet is something that's very individual.
(09:01):
It's it's it's really you know, if I take people
and say you should become vegetarians, they're going to which
proteins with carbohydrates, They're going to get fat or some
of them, and they're going to actually pay. Their health
is going to be worse. So it's very in the individual.
How do you choose diet and how you can actually
(09:23):
stick to a diet. So when I started my studies,
the experiment that worked in every lab, I took rats
and half of them got to eat whatever they wanted
and the other half I gave them forty percent less
food forty percent less food, so sixty percent of what
(09:44):
the others got. The rats that got sixty percent of
the food lived healthier and lived longer. What we did
is we gave the food in the morning to those animals,
and they were hungry, and they ate the food, and
they were then fasting for twenty three more hours. So
(10:04):
it wasn't only caloric restriction, it was also fasting. In fact,
when we gave them the food little bit throughout the day,
they were leaner, but they didn't live much longer, and
that led to this concept that a lot of us
are doing, including myself, which is intermittent fasting fast as
many hours as you can. Because what it does almost
(10:29):
the major thing that happened, it improves atophagy. This is
easy for most people to do, not for everyone. It's
easy for most people to do, and we don't know
if it extends life, but it certainly improves several factors
that you can look at, such as weight or metabolism
(10:49):
and other things.
Speaker 1 (10:50):
So we're talking at nine point thirty in the morning.
When was the last time you ate?
Speaker 2 (10:56):
I actually finished dinner at six pm yesterday because I
was traveling.
Speaker 1 (11:01):
What's your usual?
Speaker 2 (11:03):
It's usually eight in the evening when I finished dinner,
which brings me to noontime the next day. And what
I'm having. I'm having black coffee and I'm having you know, water,
but I'm not eating anything.
Speaker 1 (11:16):
How do you feel right now it's been fifteen hours
since you've eaten. How do you feel?
Speaker 2 (11:19):
I'll tell you the opposite. I was in Europe for
two weeks and sometimes I had breakfast, and in the
days that I had breakfast, I was just miserable, but
by noontime this is really and people in particular people
my age will tell you that they feel the benefit
(11:40):
on their basically cognition, their tiredness, their energy throughout the day.
Speaker 1 (11:48):
So you mentioned rats and fasting, and you mentioned mice
and autophogy, and you know there is that famous line
mice lie and primates exaggerate, Like to what extent have
these studies been validated in humans?
Speaker 2 (12:04):
I got a grant from our page together with Dan
Belski from Colombia.
Speaker 1 (12:09):
Our pages. The government basically it.
Speaker 2 (12:10):
Is the government right, and the government totally bought into
targeting aging and health spin but they funded us for
a simple reason. There are four drugs probably more that
we know target aging. And when you put those drugs
on cells, okay, they change the hallmarks of aging utophagy, Okay,
(12:36):
when you give them to animals, they live healthier and longer.
And in clinical studies, although those drugs were designed for
a certain disease, they also prevent other diseases. And although
they were developed for a certain disease, they prevented overall
mortality and not the disease specific mortality. So we take
(12:57):
studies that were already ended, and we're asking a simple question,
not only what are the biomarkers of aging, but which
one are changing with intervention?
Speaker 1 (13:09):
So what exactly is the study that you're doing.
Speaker 2 (13:13):
We we take blood samples that already exist because the
trials are done of four drugs, and we're looking at
what happened to each individual, whether he was on a
drug or on a placebol within the first year of therapy.
Speaker 1 (13:30):
And to be clear, when you say drugs blood samples,
do you mean the actual blood or you just mean
the tests that were done on those samples in previous tests.
Speaker 2 (13:37):
No, no, no, no, we have to do it's it's
totally new. We're taking the blood and using.
Speaker 1 (13:44):
So people store the blood from trials. These are trials
that are years old and the blood has just been
sitting there in the fridge waiting for you to come
in the free the freezer. Yeah, of course, and so
so and and the drugs are what theyre It's met foreman, rapamycin,
GLP one, some GLP one drug.
Speaker 2 (14:02):
And s GILT two inhebitors.
Speaker 1 (14:04):
What's that last one. I don't know what that last
one is.
Speaker 2 (14:07):
This is a very potent drug against aging. It's developed
for diabetes for sigia in volcana are the common name.
There are five five manufactures of this drug.
Speaker 1 (14:19):
So there's the blood in the freezer and you're taking
it out of the freezer and you're looking at these
twelve different hallmarks of aging and you're seeing how they
change over the course of the year and comparing those
changes for people in the drug arm of these trials,
in the treatment arm versus the people in the placebo arm.
Speaker 2 (14:36):
So for each individual before and after treatment, we're going
to have tons of data and we're going with AI
to reduce it to what is common for all those drugs,
what has commonly changed with treatment between all those drugs,
and this is likely to get to give us the
(14:56):
best clock to use in a clinical practice.
Speaker 1 (15:02):
And so basically, you want to find something that is
easy to measure or relatively easy to measure from a
blood test, say so that you can look in a
blood test and ideally find someone's biological age so to speak.
Speaker 2 (15:18):
Correct Again, we can do the biological age quite good now,
but what is change what has change when you actually
give a treatment that targets the age, that's the major point.
Speaker 1 (15:32):
But you're assuming that bigs into that assumption is that
all these drugs in fact slow aging. That like, that
is a conclusion that has to be true for this
study to make sense. Is that right?
Speaker 2 (15:45):
Well, it's the other way around. Those drugs did four
things right, each one of them. You put them in cells,
They make the cells younger. You give them to animal,
they live healthier and longer. You gave them already to people.
Those are our studies that had outcomes, and you show
that you give it for one thing and you prevented
(16:06):
other things, and that it changed overall mortality.
Speaker 1 (16:10):
That last part is that unambiguous. Like I wish I
knew the data better.
Speaker 2 (16:14):
Oh, like the studies, I mean, it's absolutely amazing. Let
me give you a flavor for the drug that you
didn't hear about as Gilty two inhibitors. S. GILTY two
inhibitors were developed for diabetes, and in the diabetes trial
it became apparent that they prevent cardiovas to disease and
kidney disease. Yeah, but then nephrologies came and did a
(16:37):
study and just to give you a taste, they took
four thousand people, half of them are placible and in
forty two non diabetic just people with impaired kidney function,
and in thirty two months they showed that they prevented
forty percent of deteriorating of kidney function, forty percent decrease
(16:57):
in cardiovas to disease, and forty percent decrease in overall mortality.
So it's circular. But what other explanation do you have
for a drug that actually changed the hallworks of agyp.
Speaker 1 (17:12):
We'll be back in just a minute. Shall we talk
about your genetics work?
Speaker 2 (17:28):
Sure?
Speaker 1 (17:30):
What have you learned from studying the genes of people
who live to one hundred?
Speaker 2 (17:35):
So first of all, I want to tell you that
my fear when I did the study was what if
I find that all those hundred years old have gotten
disease like everyone after the age of sixty, they got
disease and just lived longer with diseases. And what we
(17:56):
found is that they live twenty thirty years healthier. So
it's not only they lived longer, they live healthier, and
that wasn't really the big thing. The big thing is
that they had what we call a contraction of morbidity.
They will sick very little time at the end of
their lives. The CDC may rest in peace or be
(18:18):
resurrected whatever. The CDC have shown since nineteen ninety three
that people who die over the age of one hundred
have third of the medical cost in the last two
years of their own Interesting, then people who die at seven.
Speaker 1 (18:35):
So they die, they live a long time, and then
they die fast. That's the dream exactly.
Speaker 2 (18:40):
So that's what we want.
Speaker 1 (18:42):
Right, that's good news for people with the genes that
cause you to live a long time. Regarding your genetic studies,
I mean, is there any I don't know people in
my family don't live to one hundred, Like, am I screwed?
Does that matter for me that study?
Speaker 2 (18:59):
No, the opposite. You're the one who's going to benefit.
We don't have anything for those hundred years old, Okay,
because that's it. So two of those genes have already
been developed to drugs that past phase three trial.
Speaker 1 (19:14):
That that past phase three meaning the FDA is they're
up for approval at the FDA, right, Yeah, tell me
about those drugs.
Speaker 2 (19:21):
So one drug is called the CDP INHIBITORQUE. It's a
drug that basically increase your good cholesterol and decrease your
trigue glycerides. But that's only part of what it's doing.
Speaker 1 (19:36):
And so when they're doing a phase three trial of
this drug, what is the end point? What are they
actually trying to show that it does?
Speaker 2 (19:43):
So they're not doing it for aging. They came to
me because my studies showed that probably inhibiting CDP safe
because they are one hundred years old. Fourteen percent of
one hundred years old have these genes that increase their.
Speaker 1 (19:59):
As opposed to how many people in the population.
Speaker 2 (20:01):
At large three to four percent.
Speaker 1 (20:03):
Okay, so it's like four times as common or something. Right,
Is that drug being developed as a cardiovascular drug? Like,
what are they testing it for?
Speaker 2 (20:12):
It's been developed as a cardiovas or drug, but there's
evidence that it's also prevent cognitive decline, which was our
major claim around these drug.
Speaker 1 (20:24):
Are they testing it for that? That's a hard indication
to get.
Speaker 2 (20:26):
Yeah, yeah, they tested and their data.
Speaker 1 (20:29):
So you've talked about these promising drugs, most of which
are approved by the FDA for something met Foreman's approved
for diabetes, GLP one drugs are approved for weight loss.
I know that you've talked in the past about getting
a broader FDA approval. Specifically, you were trying to get
funding for this study called the tame trial where you
(20:51):
randomize people to get met foreman or placebo, and then
the idea was you would follow them for several years
and see if the people getting met foreman had a
lower rate of things like cardiovascular disease and cancer and
overall mortality, just do they die less. So is the
idea that if you do that study and you have
a positive outcome, like, what would the FDA say, what
(21:14):
would the indication be? Would it be give metform into
everybody over a certain age or what?
Speaker 2 (21:22):
No? No, the answer is no, because the study population
are people over the age of sixty five that are
already not doing not doing well. Not that people will
become centenarians.
Speaker 1 (21:37):
Okay, uh, because you need I mean for the study
to work, you need some people to get sick. Frankly,
if everybody on both sides stays healthy, you don't learn
anything exactly.
Speaker 2 (21:46):
And it doesn't make sense to take forty years old
and do the study and finish it in forty years
to ever result. It's but the FDA is working with
us on trying to get other indications that don't take
so long to.
Speaker 1 (22:06):
How long, how long and how big would that study
need to be to be properly powered.
Speaker 2 (22:11):
We had three thousand people for four years.
Speaker 1 (22:14):
That was the design.
Speaker 2 (22:15):
Yeah.
Speaker 1 (22:15):
And it's just hard to fund because this is a
generic drug. It's cheap, which is good if you want
to take it, but it's bad because there's no drug
company that can make a billion dollar selling it, so
they're not going to pay for the trial.
Speaker 2 (22:26):
Right, And we had funding, and then there was COVID
and then we lost, you know, the funding.
Speaker 1 (22:34):
Tell me about supplements.
Speaker 2 (22:37):
I'll start with a good thing. Supplements are good for
the economy.
Speaker 1 (22:41):
Yeah, okay, because people spend a lot of money on them. Yes,
you know.
Speaker 2 (22:44):
For me, supplement means that you measured something and it's
slow and you give it back, right, But that's not
how supplements are done. Supplements are pecking together one hundred
things or several things and giving you an also in
the bottle they say take two. Okay. There's no clinical
data on supplements. Okay. The FDA approves supplement not based
(23:08):
on clinical data. So what marketing of supplement is a
total hope? Okay, there's no promise. Not only that, the
most dangerous things is multi supplement that you take them together. Okay,
and you think they're additive, but they're antagonistic many times,
(23:29):
because if they're biologically important, you're going to find interactions
that you don't like. We actually know that people who
take multi supplements have increased mortality in spite of the
fact that they are the people who also exercise and
diet very often.
Speaker 1 (23:44):
When you say multi supplement, like a multi vitamin or
what do you.
Speaker 2 (23:47):
Mean like multi vitamins, let me ask.
Speaker 1 (23:52):
You another question. So the field that you are in
is full of and has always for all of history
been full of cranks and charlatan's. You're a doctor at
a medical school, Like, how do you deal with that?
And do your colleagues think you are a crank and
a charlatan?
Speaker 2 (24:11):
Respectfully, what you said was exactly the sentiment when I
got several major organizations to meet in New York and say, hey,
we have a lot of progress, and we have a
lot of noise.
Speaker 1 (24:23):
When was this? When was this?
Speaker 2 (24:25):
That was two years ago? Two years ago, and we
did something that's so unusual for a bunch of scientists.
We said, you know what, we really don't know what
to do. Why don't we take a branding company and
let them deal with it? And this is the best
thing we did because the branding company actually worked. It
(24:45):
was hundreds of thousands of dollars and we're still working
with them.
Speaker 1 (24:49):
It makes me nervous when you say branding company. I'm
asking you about cracks, Charlotte. Since you start telling me
about branding, it makes me nervous.
Speaker 2 (24:56):
But I think I'll make you I'll make you feel better.
And they said, first of all, you're using thirty different
terms to describe yourself. Yeah, okay, help spend, launch, avity, rejuvenation, gerontology, immortality,
you know, goes on and on, and that's very divisive.
(25:17):
So they said, hey, this is a problem. Second, they said, yeah,
you have an enemy and that's the noise. Okay, and
that's a good thing. Okay, that's a good thing because
you want to distinct yourself from the noise. The noise
are Charlotte Tan's snake oil, Brian Johnson, you know, things
(25:39):
like that. And they said, and for you, the best
name is gero science. And we said, oh, we like geroscience.
We always called ourselves gero scientists. But you know what,
gero scientists didn't pick up them. They said, yeah, because
you never marketed it. It's not even in a Wikipedia.
So we so with this branding company, we do several things.
(26:03):
First of all, like what we do now I talk
about geroscience. We changed the Academy that was the Academy
of Health and Lifespan Research to Academy of Geroscience, my
center that was the Insuite for Aging Research and the
Institute of Geroscience. We have a geoscience web now that
will feed all the organizations and all the people who
want to know everything. And we want to make it,
(26:25):
you know, like a real thing and not a divisive
thing or really distinct ourselves from from the noise.
Speaker 1 (26:33):
And in a sentence, what is geroscience?
Speaker 2 (26:38):
So the ideal of geroscience is that we target We
can target aging by by learning the science and improve
basically decrease the burden of diseases and increase increase the
health spen for everyone.
Speaker 1 (26:59):
Is there a Wikipedia page?
Speaker 2 (27:02):
Not yet?
Speaker 1 (27:02):
No, no, you can make a Wikipedia page.
Speaker 2 (27:04):
No no, no, no no, no, there will be soon.
But it's actually a process you can make. You can
make the Wikipedia page. But when it comes to things
like that, there's a committee and the committee now is
biased and we're spending actually twenty thousand dollars to show
the gero science is a real.
Speaker 1 (27:25):
Say, convinced the Wikipedia committee. Yeah, wow, Like, do you
need a newspaper reporter to use the word in the
in the you know, in the Wall Street Journal, in
the New York Times? That is that what you need.
Speaker 2 (27:37):
But it was effective because when I called ourselves gero science,
when I talked about it, several editors have changed the
name of the article to anti aging because they said,
we don't know what's gero science, but anti aging.
Speaker 1 (27:50):
What do you think about the phrase anti aging?
Speaker 2 (27:53):
So first of all, we're not anti the aging, but
it is used much more commonly for non scientific fact
than for science. And so we actually we we actually
trying to make it worse, really for people to know
that whoever called themselves anti aging and there's no gero
(28:15):
signs behind that. Yeah, it's going to be bad.
Speaker 1 (28:23):
We'll be back in a minute with the lightning round. Okay,
let's finish with a lightning round a little bit more random.
What one thing you do, even though it may shorten
(28:46):
your life.
Speaker 2 (28:49):
So I'm doing the sixteen hour fast, but I'm a foodie. Okay,
so after the sixteen hours fast, I really don't care
what I got interesting?
Speaker 1 (29:03):
What was the last really unhealthy but delicious thing that
you ate?
Speaker 2 (29:09):
Black forest cake? I have a black forest cake, also
with ice cream.
Speaker 1 (29:16):
Yes, ice cream is so good. Do you have a
favorite really really old person, like from the Old Testament
or from mythology.
Speaker 2 (29:29):
I'm talking about Metusilla because he supposedly leave nine hundred
and sixty nine years And the people who are very
orthodox in religions, whether Christians or Jews, believe every word
in the Bible, right, But when you ask them, did
(29:49):
Metusla leave nine hundred and sixty nine years? Ah, they
didn't know how to count.
Speaker 1 (29:55):
Well, I don't know that particular story. I mean one
thing that's interesting to me, Like in the Old Testament,
people are just old. Noah's hundreds of years old, whatever.
But you know, the myths and the stories that focus
in particular on in more mentality especially, it's often bad, right,
somebody lives forever and it's terrible to live forever, which
(30:16):
is interesting in the context of this conversation.
Speaker 2 (30:20):
Right, And you know, there's a whole people who are immortalists,
and that's very different from me. Okay, I'm not immortalist.
In fact, I'm saying what to live a billion more years?
How many you know, presidents do you have to suffer through? Yeah,
I'm tired a little bit. Immortality. Immortality is a belief,
(30:44):
and people realize now that this is not going to
happen in their lifetime, and what they are turning into
is freezing.
Speaker 1 (30:53):
Yeah, that's been around for a while. Cryogenics like cryogenous
that one seems very crankish to me.
Speaker 2 (31:00):
Well, but it relieves them in their mind they're dealing
with their immortality.
Speaker 1 (31:06):
So I read this interview with you where you talked
about the fact that people with Alzheimer's disease sometimes will
respond to music that they know from earlier in their life,
and that you actually started making an Alzheimer's playlist for yourself.
What's on the playlist?
Speaker 2 (31:23):
So usually the playlist for those people are of their
most earlier memories as young adults, right when you were
kind of a kid, when you were in high school,
when you were in college. And so for me, it's
really the sixties seventies.
Speaker 1 (31:41):
It's a great era. It's my favorite era.
Speaker 2 (31:44):
In a lot of ways that are taking and my
kids are saying, you know, when you have Alzheimer's, mom
would leave you, not because she doesn't like you, but
because she wouldn't stand the music.
Speaker 1 (31:58):
So, from your work with people who've lived past one hundred,
I'm curious, what's one thing that you've learned that's not
related to health.
Speaker 2 (32:08):
Will they have a belief in what makes them leave
two hundred? And they could adopt the belief because they
actually had genes, which means they were protected from everyone.
Speaker 1 (32:21):
What actually made them lift two hundred is their genes,
not the fact that they play golf every Wednesday or whatever.
Speaker 2 (32:27):
So I have a woman who died at the age
one hundred and ten, and she smoked for ninety five years,
and she thinks it's because of cigarettes. She said, the
four doctors that told her to stop smoking, they died.
Speaker 1 (32:41):
Yes, yes, Okay. Of all the things we've talked about,
If there's only one thing I do to live a longer,
healthier life, what should I do?
Speaker 2 (32:52):
You know? I think at the end it's all individualized.
Will be able to see what is the one thing
you do. Look, I'm looking at you. It looks to
me like that your BMI is normal. It looks to
me that you're probably exercising. So I don't know, you
have to tell me what you don't do, and I'll
(33:12):
pick one.
Speaker 1 (33:12):
Yeah, that's really because I was hoping you'd say exercise,
because I was like, oh, yeah, that's the what I got.
I'm not a great sleeper. I don't know, you know,
I don't look at my phone. Whatever I do the
things they say to do, I just don't tend to
sleep that well.
Speaker 2 (33:27):
So with sleep, there there are two things. One is
for the young people and one is for the old.
For the young people, stop bingch watching. Okay, a lot
of the sleep deprivation is self inflicted. Right, you need
eight hours. You should strive for eight hours sleep, and
so that means that you have to plan which are
(33:49):
the eight hours for the older one or older one
than young. So for you and me, it's eight hours
in a dark room without electronic Okay, you're not going
to sleep the eight hours I sleep for some reason,
no matter what happen. I travel around the world. I'm
(34:10):
just like, I sleep six hours and forty minutes no
matter what. But if I sleep less, it's not going
to be good. But what I'm doing that's different than you.
I have a feet, bit, you can have a ring,
and you can actually measure because it's possible that you'll
find that your ram sleep and deep sleep are long
(34:32):
enough and you don't need the sleep, and you're not
going to feel tired, even if you feel that you
didn't sleep well.
Speaker 1 (34:39):
So you're saying it's important to be in bed in
the dark for eight hours, but it's okay to not
sleep the whole time. Right, So do you lie in
bed for an hour and twenty minutes every night not sleeping?
Speaker 2 (34:53):
That's pretty much what happens. I'm spending time trying to
fall asleep and trying to stay asleep.
Speaker 1 (35:00):
Yes, anything else we should talk about, just.
Speaker 2 (35:05):
The one thing that's important to know that aging, that
what what we're doing is not only for older adults.
People who survive cancer are aging rapidly because we give
them chemotherapy and radiation. Right. I don't know if you
know cancer survivors, but they usually are doing badly after
they recover, so they need help. People with HIV have
(35:28):
diseases ten years younger than their ages. Down syndrome is
an aging syndrome. Disabled people, you know, need help. And
if we're going to Mars, if this is for some people,
it's very important. I think this world is beautiful we
need to repair it. But if you go to Mars,
you're not going to get there before we stopped aging,
(35:50):
because you'll be sick on the way there and you're
never coming back.
Speaker 1 (35:55):
Thank you very much for your time. I really appreciate it.
Speaker 2 (35:58):
Thank you very much.
Speaker 1 (36:06):
Your Barselai is a physician and he runs it's the
Institute for Geroscience at the Albert Einstein College of Medicine.
Just a quick note, we're going to be taking the
next couple weeks off. We're going to be back after
that with more episodes of What's Your Problem. Please email
us at problem at pushkin dot fm. Tell us what
kinds of shows we should do more of or less
of our particular people you think would be good on
(36:27):
the show. You can also find me on x and
on LinkedIn. Our show is produced by Gabriel Hunter Chang
and Trina Menino. Our editor is Lydia Jane Kott, and
our engineer is Sarah Buguer. I'm Jacob Goldstein.
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