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Can We Slow Down Aging? · What's Your Problem?

0:15
Speaker 1: Pushkin. I'm Jacob Goldstein, and this is what's your problem.
0:33
Speaker 1: My guest today is Near Barzilai. Near is a physician
0:37
Speaker 1: and a researcher, and he runs the Institute for Gero
0:41
Speaker 1: Science at the Albert Einstein College of Medicine in New York.
0:45
Speaker 1: Near's problem is this, how can lifestyle changes and drugs
0:49
Speaker 1: slow the process of aging. In our conversation, Nier and
0:53
Speaker 1: I talk about the search for biological markers of aging,
0:57
Speaker 1: existing drugs that might reduce the risk of diseases associated
1:02
Speaker 1: with aging, and what he learned by studying the genes
1:05
Speaker 1: of people who lived to age one hundred and beyond. Also,
1:09
Speaker 1: we talk about the meaning and origin of the term
1:12
Speaker 1: gyo science. To start, I asked her how he decided
1:16
Speaker 1: to study the biology of aging.
1:18
Speaker 2: It actually happened young. It happened with my grandfather that
1:22
Speaker 2: walked with me every Saturday telling me about his life
1:27
Speaker 2: as a young person. And he was sixty eight. It's
1:30
Speaker 2: the year he died. He was looking old, fat, slow,
1:37
Speaker 2: and for me it always it almost became immediately clear
1:44
Speaker 2: that that's where I'm going, Okay, So it became the
1:48
Speaker 2: biggest question in biology of aging. When I went to
1:53
Speaker 2: my residency. I had an attending and whenever I presented
1:58
Speaker 2: the patient, he would stop me. I would say, this
2:02
Speaker 2: is a seventy five year old woman, and he would
2:05
Speaker 2: stop and say, but does she look younger than their age?
2:11
Speaker 2: And after a while you saw that it mattered. You
2:14
Speaker 2: can have a ninety year old guy and it comes
2:16
Speaker 2: to the emergency room and he has some infection and
2:18
Speaker 2: with some antibiotics, he'll be fine, and a seventy five
2:21
Speaker 2: year old woman that all her systems are totally gone,
2:24
Speaker 2: and you know, you know where she's going, and that
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Speaker 2: it's important in decision making. I want to say that
2:35
Speaker 2: this is thing that I think people intuitively understand that
2:39
Speaker 2: there's a biological age. I think it's more important to
2:43
Speaker 2: know that aging, this biology is what drives diseases. It's
2:50
Speaker 2: not that we get heart attacks and we become old.
2:53
Speaker 2: It's the opposite. We become old and that drives diseases.
2:57
Speaker 1: I mean, intuitively, we also know that, right you're much
3:01
Speaker 1: more likely to get a heart attack at seventy five
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Speaker 1: than at twenty five.
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Speaker 2: That's true, but let me give an example that you'll
3:08
Speaker 2: explain it better. You can be born with genes for Alzheimer's. Okay,
3:13
Speaker 2: there's a gene called apo E four. If you have
3:17
Speaker 2: two copies of these genes, you are really high risk
3:21
Speaker 2: of getting alzheimer at sixty or seventy and you'll be
3:24
Speaker 2: dead by the time you're eighteen. But when you're born,
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Speaker 2: you're not demented. And when you're one year or ten
3:31
Speaker 2: year of fifty year, you're not demented. You meet the
3:34
Speaker 2: biology of aging, the failure of our young biology in
3:39
Speaker 2: order to get those diseases. And it's important because we
3:44
Speaker 2: want to prevent your aging. And this is really the
3:48
Speaker 2: biggest issue that we're talking about.
3:51
Speaker 1: Now, tell me a little bit more about that.
3:54
Speaker 2: So it's based on the fact that around the world
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Speaker 2: in the last few decades, we not only went from
4:01
Speaker 2: hoping that there is something we can do, but we
4:04
Speaker 2: actually have a promise and we're at the stage of
4:07
Speaker 2: realizing a promise. And the promise is in what lifestyle
4:14
Speaker 2: decisions we make, what drugs are available right now to
4:18
Speaker 2: stunt aging, and the drugs that are being developed now
4:22
Speaker 2: and are going to make bigger impact.
4:26
Speaker 1: Well, so okay, so let's get into it. So here's
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Speaker 1: the three that I know. I feel like the big
4:31
Speaker 1: three in terms of what you're talking about, exercise, sleep, well,
4:40
Speaker 1: have friends, don't smoke, and eat whole fresh foods. That
4:46
Speaker 1: wasn't three, I know, I thought of two more in
4:49
Speaker 1: the middle.
4:50
Speaker 2: So what you don't do is okay, you know, don't smoke.
4:56
Speaker 2: There are four that every one in our field and
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Speaker 2: the longevity doctors and everyone would agree on. And that's exercise,
5:07
Speaker 2: its diet, sleep, and it's yeah, social connectivity. Okay. Each
5:13
Speaker 2: one of those have underlying biology of aging, and each
5:18
Speaker 2: one of them is really important when you're young or
5:22
Speaker 2: old to optimize. Okay, we used to say maximize, but optimize.
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Speaker 1: So those are the ones that we sort of all know,
5:32
Speaker 1: right Whether we do them or not is a different question,
5:34
Speaker 1: because whose we all lots of people know that those
5:39
Speaker 1: things are good, and it is remarkable how good they are, right, Like,
5:43
Speaker 1: exercise is so good for so many things in non
5:46
Speaker 1: obvious ways. Like sure, cardiovascular exercise is good for your heart,
5:50
Speaker 1: that's obvious, but like, why does it make you less
5:53
Speaker 1: likely to get cancer? This is an interesting question, right, Hey.
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Speaker 2: I just answer that because those are affecting the biology
6:00
Speaker 2: of aging a bold claim. Those are affecting the biology
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Speaker 2: of aging, and when I'm talking of biology of aging
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Speaker 2: is cellular aging. So cells all over the body will
6:14
Speaker 2: will be younger or stay younger, and that's why you
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Speaker 2: get less cancer and less and less cardiovastro disease.
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Speaker 1: When you say cellular age, what is the measure of
6:26
Speaker 1: cellular age you're referring to?
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Speaker 2: Let me say this way. There are twelve things that
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Speaker 2: we call hallmarks of aging. Okay, and I'm not going
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Speaker 2: to count them. I might give an example throughout.
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Speaker 1: Give me one example. What's the what's a particularly robust example.
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Speaker 2: Let's say that one of the problems is we have
6:48
Speaker 2: a mechanism of garbage disposal in all our cells. And
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Speaker 2: this garbage disposal that's often called autophogy, or the scientists
6:58
Speaker 2: will call it autophogy, takes junks that accumulate in our
7:03
Speaker 2: cells because our selves is making mistakes in its production.
7:07
Speaker 2: And it's taking those things that are really not helpful
7:11
Speaker 2: and breaking them down to their component. It's going to
7:15
Speaker 2: clean yoursels. Okay, Okay, that's what's going to happen now
7:20
Speaker 2: every one of the hallmarks. What you have to show
7:23
Speaker 2: is first of all, that it gets worse with aging. Second,
7:27
Speaker 2: you can take a young model and make it old. Okay,
7:31
Speaker 2: so it was done with autopogy. You knock out autophogy,
7:35
Speaker 2: the mice are freaking out. They are becoming older at
7:39
Speaker 2: a very young age. But more important, if you fix
7:42
Speaker 2: it throughout aging, the mice are not only healthier overall healthier,
7:48
Speaker 2: but they also live like twenty percent longer. Okay, So
7:52
Speaker 2: that's how you become a hallmark. But the point is,
7:55
Speaker 2: whenever you fix one of them, of those hallmarks, you
8:00
Speaker 2: really fix also others. Okay. So it's you could take
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Speaker 2: one hallmark and show that it's very important, but you
8:07
Speaker 2: can do it with each one of them. You don't
8:09
Speaker 2: have to do it together. Not that doing it together
8:12
Speaker 2: wouldn't be even better, but you don't have to do
8:15
Speaker 2: it together.
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Speaker 1: You're saying, if you fix one, that one working better
8:18
Speaker 1: actually helps to fix the others, right.
8:21
Speaker 2: And you can see changes in the others.
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Speaker 1: And so when you talk about these, you know lifestyle
8:29
Speaker 1: changes like exercise, does your autophogy work better for longer?
8:36
Speaker 1: That basically going.
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Speaker 2: On exactly, And I'll give you another example. And I
8:41
Speaker 2: can stay on autopogy because we don't have enough time
8:45
Speaker 2: to cover the twelve. But how does so exercise fixes autophogy.
8:53
Speaker 2: The hard one is diet. And I'll tell you why
8:56
Speaker 2: I pick diet, because diet is something that's very individual.
9:01
Speaker 2: It's it's it's really you know, if I take people
9:05
Speaker 2: and say you should become vegetarians, they're going to which
9:09
Speaker 2: proteins with carbohydrates, They're going to get fat or some
9:12
Speaker 2: of them, and they're going to actually pay. Their health
9:16
Speaker 2: is going to be worse. So it's very in the individual.
9:20
Speaker 2: How do you choose diet and how you can actually
9:23
Speaker 2: stick to a diet. So when I started my studies,
9:29
Speaker 2: the experiment that worked in every lab, I took rats
9:33
Speaker 2: and half of them got to eat whatever they wanted
9:37
Speaker 2: and the other half I gave them forty percent less
9:40
Speaker 2: food forty percent less food, so sixty percent of what
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Speaker 2: the others got. The rats that got sixty percent of
9:49
Speaker 2: the food lived healthier and lived longer. What we did
9:54
Speaker 2: is we gave the food in the morning to those animals,
9:57
Speaker 2: and they were hungry, and they ate the food, and
10:00
Speaker 2: they were then fasting for twenty three more hours. So
10:04
Speaker 2: it wasn't only caloric restriction, it was also fasting. In fact,
10:09
Speaker 2: when we gave them the food little bit throughout the day,
10:13
Speaker 2: they were leaner, but they didn't live much longer, and
10:16
Speaker 2: that led to this concept that a lot of us
10:19
Speaker 2: are doing, including myself, which is intermittent fasting fast as
10:24
Speaker 2: many hours as you can. Because what it does almost
10:29
Speaker 2: the major thing that happened, it improves atophagy. This is
10:34
Speaker 2: easy for most people to do, not for everyone. It's
10:37
Speaker 2: easy for most people to do, and we don't know
10:40
Speaker 2: if it extends life, but it certainly improves several factors
10:44
Speaker 2: that you can look at, such as weight or metabolism
10:49
Speaker 2: and other things.
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Speaker 1: So we're talking at nine point thirty in the morning.
10:53
Speaker 1: When was the last time you ate?
10:56
Speaker 2: I actually finished dinner at six pm yesterday because I
11:00
Speaker 2: was traveling.
11:01
Speaker 1: What's your usual?
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Speaker 2: It's usually eight in the evening when I finished dinner,
11:06
Speaker 2: which brings me to noontime the next day. And what
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Speaker 2: I'm having. I'm having black coffee and I'm having you know, water,
11:14
Speaker 2: but I'm not eating anything.
11:16
Speaker 1: How do you feel right now it's been fifteen hours
11:18
Speaker 1: since you've eaten. How do you feel?
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Speaker 2: I'll tell you the opposite. I was in Europe for
11:24
Speaker 2: two weeks and sometimes I had breakfast, and in the
11:27
Speaker 2: days that I had breakfast, I was just miserable, but
11:32
Speaker 2: by noontime this is really and people in particular people
11:37
Speaker 2: my age will tell you that they feel the benefit
11:40
Speaker 2: on their basically cognition, their tiredness, their energy throughout the day.
11:48
Speaker 1: So you mentioned rats and fasting, and you mentioned mice
11:53
Speaker 1: and autophogy, and you know there is that famous line
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Speaker 1: mice lie and primates exaggerate, Like to what extent have
12:01
Speaker 1: these studies been validated in humans?
12:04
Speaker 2: I got a grant from our page together with Dan
12:07
Speaker 2: Belski from Colombia.
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Speaker 1: Our pages. The government basically it.
12:10
Speaker 2: Is the government right, and the government totally bought into
12:15
Speaker 2: targeting aging and health spin but they funded us for
12:20
Speaker 2: a simple reason. There are four drugs probably more that
12:25
Speaker 2: we know target aging. And when you put those drugs
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Speaker 2: on cells, okay, they change the hallmarks of aging utophagy, Okay,
12:36
Speaker 2: when you give them to animals, they live healthier and longer.
12:40
Speaker 2: And in clinical studies, although those drugs were designed for
12:43
Speaker 2: a certain disease, they also prevent other diseases. And although
12:49
Speaker 2: they were developed for a certain disease, they prevented overall
12:53
Speaker 2: mortality and not the disease specific mortality. So we take
12:57
Speaker 2: studies that were already ended, and we're asking a simple question,
13:02
Speaker 2: not only what are the biomarkers of aging, but which
13:06
Speaker 2: one are changing with intervention?
13:09
Speaker 1: So what exactly is the study that you're doing.
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Speaker 2: We we take blood samples that already exist because the
13:18
Speaker 2: trials are done of four drugs, and we're looking at
13:23
Speaker 2: what happened to each individual, whether he was on a
13:26
Speaker 2: drug or on a placebol within the first year of therapy.
13:30
Speaker 1: And to be clear, when you say drugs blood samples,
13:32
Speaker 1: do you mean the actual blood or you just mean
13:34
Speaker 1: the tests that were done on those samples in previous tests.
13:37
Speaker 2: No, no, no, no, we have to do it's it's
13:39
Speaker 2: totally new. We're taking the blood and using.
13:44
Speaker 1: So people store the blood from trials. These are trials
13:46
Speaker 1: that are years old and the blood has just been
13:48
Speaker 1: sitting there in the fridge waiting for you to come
13:50
Speaker 1: in the free the freezer. Yeah, of course, and so
13:54
Speaker 1: so and and the drugs are what theyre It's met foreman, rapamycin,
13:59
Speaker 1: GLP one, some GLP one drug.
14:02
Speaker 2: And s GILT two inhebitors.
14:04
Speaker 1: What's that last one. I don't know what that last
14:06
Speaker 1: one is.
14:07
Speaker 2: This is a very potent drug against aging. It's developed
14:11
Speaker 2: for diabetes for sigia in volcana are the common name.
14:15
Speaker 2: There are five five manufactures of this drug.
14:19
Speaker 1: So there's the blood in the freezer and you're taking
14:21
Speaker 1: it out of the freezer and you're looking at these
14:23
Speaker 1: twelve different hallmarks of aging and you're seeing how they
14:26
Speaker 1: change over the course of the year and comparing those
14:28
Speaker 1: changes for people in the drug arm of these trials,
14:33
Speaker 1: in the treatment arm versus the people in the placebo arm.
14:36
Speaker 2: So for each individual before and after treatment, we're going
14:40
Speaker 2: to have tons of data and we're going with AI
14:44
Speaker 2: to reduce it to what is common for all those drugs,
14:49
Speaker 2: what has commonly changed with treatment between all those drugs,
14:54
Speaker 2: and this is likely to get to give us the
14:56
Speaker 2: best clock to use in a clinical practice.
15:02
Speaker 1: And so basically, you want to find something that is
15:06
Speaker 1: easy to measure or relatively easy to measure from a
15:10
Speaker 1: blood test, say so that you can look in a
15:12
Speaker 1: blood test and ideally find someone's biological age so to speak.
15:18
Speaker 2: Correct Again, we can do the biological age quite good now,
15:23
Speaker 2: but what is change what has change when you actually
15:27
Speaker 2: give a treatment that targets the age, that's the major point.
15:32
Speaker 1: But you're assuming that bigs into that assumption is that
15:37
Speaker 1: all these drugs in fact slow aging. That like, that
15:40
Speaker 1: is a conclusion that has to be true for this
15:43
Speaker 1: study to make sense. Is that right?
15:45
Speaker 2: Well, it's the other way around. Those drugs did four
15:48
Speaker 2: things right, each one of them. You put them in cells,
15:52
Speaker 2: They make the cells younger. You give them to animal,
15:55
Speaker 2: they live healthier and longer. You gave them already to people.
15:59
Speaker 2: Those are our studies that had outcomes, and you show
16:03
Speaker 2: that you give it for one thing and you prevented
16:06
Speaker 2: other things, and that it changed overall mortality.
16:10
Speaker 1: That last part is that unambiguous. Like I wish I
16:13
Speaker 1: knew the data better.
16:14
Speaker 2: Oh, like the studies, I mean, it's absolutely amazing. Let
16:18
Speaker 2: me give you a flavor for the drug that you
16:21
Speaker 2: didn't hear about as Gilty two inhibitors. S. GILTY two
16:25
Speaker 2: inhibitors were developed for diabetes, and in the diabetes trial
16:29
Speaker 2: it became apparent that they prevent cardiovas to disease and
16:33
Speaker 2: kidney disease. Yeah, but then nephrologies came and did a
16:37
Speaker 2: study and just to give you a taste, they took
16:40
Speaker 2: four thousand people, half of them are placible and in
16:44
Speaker 2: forty two non diabetic just people with impaired kidney function,
16:49
Speaker 2: and in thirty two months they showed that they prevented
16:53
Speaker 2: forty percent of deteriorating of kidney function, forty percent decrease
16:57
Speaker 2: in cardiovas to disease, and forty percent decrease in overall mortality.
17:01
Speaker 2: So it's circular. But what other explanation do you have
17:05
Speaker 2: for a drug that actually changed the hallworks of agyp.
17:12
Speaker 1: We'll be back in just a minute. Shall we talk
17:26
Speaker 1: about your genetics work?
17:28
Speaker 2: Sure?
17:30
Speaker 1: What have you learned from studying the genes of people
17:33
Speaker 1: who live to one hundred?
17:35
Speaker 2: So first of all, I want to tell you that
17:38
Speaker 2: my fear when I did the study was what if
17:42
Speaker 2: I find that all those hundred years old have gotten
17:47
Speaker 2: disease like everyone after the age of sixty, they got
17:51
Speaker 2: disease and just lived longer with diseases. And what we
17:56
Speaker 2: found is that they live twenty thirty years healthier. So
18:03
Speaker 2: it's not only they lived longer, they live healthier, and
18:06
Speaker 2: that wasn't really the big thing. The big thing is
18:09
Speaker 2: that they had what we call a contraction of morbidity.
18:12
Speaker 2: They will sick very little time at the end of
18:14
Speaker 2: their lives. The CDC may rest in peace or be
18:18
Speaker 2: resurrected whatever. The CDC have shown since nineteen ninety three
18:25
Speaker 2: that people who die over the age of one hundred
18:28
Speaker 2: have third of the medical cost in the last two
18:31
Speaker 2: years of their own Interesting, then people who die at seven.
18:35
Speaker 1: So they die, they live a long time, and then
18:37
Speaker 1: they die fast. That's the dream exactly.
18:40
Speaker 2: So that's what we want.
18:42
Speaker 1: Right, that's good news for people with the genes that
18:45
Speaker 1: cause you to live a long time. Regarding your genetic studies,
18:49
Speaker 1: I mean, is there any I don't know people in
18:54
Speaker 1: my family don't live to one hundred, Like, am I screwed?
18:57
Speaker 1: Does that matter for me that study?
18:59
Speaker 2: No, the opposite. You're the one who's going to benefit.
19:03
Speaker 2: We don't have anything for those hundred years old, Okay,
19:06
Speaker 2: because that's it. So two of those genes have already
19:10
Speaker 2: been developed to drugs that past phase three trial.
19:14
Speaker 1: That that past phase three meaning the FDA is they're
19:17
Speaker 1: up for approval at the FDA, right, Yeah, tell me
19:20
Speaker 1: about those drugs.
19:21
Speaker 2: So one drug is called the CDP INHIBITORQUE. It's a
19:27
Speaker 2: drug that basically increase your good cholesterol and decrease your
19:32
Speaker 2: trigue glycerides. But that's only part of what it's doing.
19:36
Speaker 1: And so when they're doing a phase three trial of
19:39
Speaker 1: this drug, what is the end point? What are they
19:41
Speaker 1: actually trying to show that it does?
19:43
Speaker 2: So they're not doing it for aging. They came to
19:47
Speaker 2: me because my studies showed that probably inhibiting CDP safe
19:53
Speaker 2: because they are one hundred years old. Fourteen percent of
19:56
Speaker 2: one hundred years old have these genes that increase their.
19:59
Speaker 1: As opposed to how many people in the population.
20:01
Speaker 2: At large three to four percent.
20:03
Speaker 1: Okay, so it's like four times as common or something. Right,
20:07
Speaker 1: Is that drug being developed as a cardiovascular drug? Like,
20:11
Speaker 1: what are they testing it for?
20:12
Speaker 2: It's been developed as a cardiovas or drug, but there's
20:16
Speaker 2: evidence that it's also prevent cognitive decline, which was our
20:21
Speaker 2: major claim around these drug.
20:24
Speaker 1: Are they testing it for that? That's a hard indication
20:26
Speaker 1: to get.
20:26
Speaker 2: Yeah, yeah, they tested and their data.
20:29
Speaker 1: So you've talked about these promising drugs, most of which
20:33
Speaker 1: are approved by the FDA for something met Foreman's approved
20:37
Speaker 1: for diabetes, GLP one drugs are approved for weight loss.
20:41
Speaker 1: I know that you've talked in the past about getting
20:43
Speaker 1: a broader FDA approval. Specifically, you were trying to get
20:47
Speaker 1: funding for this study called the tame trial where you
20:51
Speaker 1: randomize people to get met foreman or placebo, and then
20:54
Speaker 1: the idea was you would follow them for several years
20:57
Speaker 1: and see if the people getting met foreman had a
21:00
Speaker 1: lower rate of things like cardiovascular disease and cancer and
21:03
Speaker 1: overall mortality, just do they die less. So is the
21:07
Speaker 1: idea that if you do that study and you have
21:10
Speaker 1: a positive outcome, like, what would the FDA say, what
21:14
Speaker 1: would the indication be? Would it be give metform into
21:17
Speaker 1: everybody over a certain age or what?
21:22
Speaker 2: No? No, the answer is no, because the study population
21:27
Speaker 2: are people over the age of sixty five that are
21:30
Speaker 2: already not doing not doing well. Not that people will
21:35
Speaker 2: become centenarians.
21:37
Speaker 1: Okay, uh, because you need I mean for the study
21:39
Speaker 1: to work, you need some people to get sick. Frankly,
21:42
Speaker 1: if everybody on both sides stays healthy, you don't learn
21:45
Speaker 1: anything exactly.
21:46
Speaker 2: And it doesn't make sense to take forty years old
21:49
Speaker 2: and do the study and finish it in forty years
21:53
Speaker 2: to ever result. It's but the FDA is working with
21:57
Speaker 2: us on trying to get other indications that don't take
22:03
Speaker 2: so long to.
22:06
Speaker 1: How long, how long and how big would that study
22:08
Speaker 1: need to be to be properly powered.
22:11
Speaker 2: We had three thousand people for four years.
22:14
Speaker 1: That was the design.
22:15
Speaker 2: Yeah.
22:15
Speaker 1: And it's just hard to fund because this is a
22:17
Speaker 1: generic drug. It's cheap, which is good if you want
22:20
Speaker 1: to take it, but it's bad because there's no drug
22:22
Speaker 1: company that can make a billion dollar selling it, so
22:24
Speaker 1: they're not going to pay for the trial.
22:26
Speaker 2: Right, And we had funding, and then there was COVID
22:29
Speaker 2: and then we lost, you know, the funding.
22:34
Speaker 1: Tell me about supplements.
22:37
Speaker 2: I'll start with a good thing. Supplements are good for
22:39
Speaker 2: the economy.
22:41
Speaker 1: Yeah, okay, because people spend a lot of money on them. Yes,
22:44
Speaker 1: you know.
22:44
Speaker 2: For me, supplement means that you measured something and it's
22:49
Speaker 2: slow and you give it back, right, But that's not
22:52
Speaker 2: how supplements are done. Supplements are pecking together one hundred
22:56
Speaker 2: things or several things and giving you an also in
22:59
Speaker 2: the bottle they say take two. Okay. There's no clinical
23:04
Speaker 2: data on supplements. Okay. The FDA approves supplement not based
23:08
Speaker 2: on clinical data. So what marketing of supplement is a
23:14
Speaker 2: total hope? Okay, there's no promise. Not only that, the
23:19
Speaker 2: most dangerous things is multi supplement that you take them together. Okay,
23:25
Speaker 2: and you think they're additive, but they're antagonistic many times,
23:29
Speaker 2: because if they're biologically important, you're going to find interactions
23:33
Speaker 2: that you don't like. We actually know that people who
23:36
Speaker 2: take multi supplements have increased mortality in spite of the
23:40
Speaker 2: fact that they are the people who also exercise and
23:43
Speaker 2: diet very often.
23:44
Speaker 1: When you say multi supplement, like a multi vitamin or
23:47
Speaker 1: what do you.
23:47
Speaker 2: Mean like multi vitamins, let me ask.
23:52
Speaker 1: You another question. So the field that you are in
23:59
Speaker 1: is full of and has always for all of history
24:01
Speaker 1: been full of cranks and charlatan's. You're a doctor at
24:05
Speaker 1: a medical school, Like, how do you deal with that?
24:09
Speaker 1: And do your colleagues think you are a crank and
24:10
Speaker 1: a charlatan?
24:11
Speaker 2: Respectfully, what you said was exactly the sentiment when I
24:15
Speaker 2: got several major organizations to meet in New York and say, hey,
24:20
Speaker 2: we have a lot of progress, and we have a
24:22
Speaker 2: lot of noise.
24:23
Speaker 1: When was this? When was this?
24:25
Speaker 2: That was two years ago? Two years ago, and we
24:27
Speaker 2: did something that's so unusual for a bunch of scientists.
24:31
Speaker 2: We said, you know what, we really don't know what
24:35
Speaker 2: to do. Why don't we take a branding company and
24:39
Speaker 2: let them deal with it? And this is the best
24:42
Speaker 2: thing we did because the branding company actually worked. It
24:45
Speaker 2: was hundreds of thousands of dollars and we're still working
24:48
Speaker 2: with them.
24:49
Speaker 1: It makes me nervous when you say branding company. I'm
24:52
Speaker 1: asking you about cracks, Charlotte. Since you start telling me
24:55
Speaker 1: about branding, it makes me nervous.
24:56
Speaker 2: But I think I'll make you I'll make you feel better.
25:00
Speaker 2: And they said, first of all, you're using thirty different
25:05
Speaker 2: terms to describe yourself. Yeah, okay, help spend, launch, avity, rejuvenation, gerontology, immortality,
25:13
Speaker 2: you know, goes on and on, and that's very divisive.
25:17
Speaker 2: So they said, hey, this is a problem. Second, they said, yeah,
25:21
Speaker 2: you have an enemy and that's the noise. Okay, and
25:26
Speaker 2: that's a good thing. Okay, that's a good thing because
25:29
Speaker 2: you want to distinct yourself from the noise. The noise
25:33
Speaker 2: are Charlotte Tan's snake oil, Brian Johnson, you know, things
25:39
Speaker 2: like that. And they said, and for you, the best
25:42
Speaker 2: name is gero science. And we said, oh, we like geroscience.
25:47
Speaker 2: We always called ourselves gero scientists. But you know what,
25:51
Speaker 2: gero scientists didn't pick up them. They said, yeah, because
25:53
Speaker 2: you never marketed it. It's not even in a Wikipedia.
25:58
Speaker 2: So we so with this branding company, we do several things.
26:03
Speaker 2: First of all, like what we do now I talk
26:05
Speaker 2: about geroscience. We changed the Academy that was the Academy
26:08
Speaker 2: of Health and Lifespan Research to Academy of Geroscience, my
26:12
Speaker 2: center that was the Insuite for Aging Research and the
26:14
Speaker 2: Institute of Geroscience. We have a geoscience web now that
26:19
Speaker 2: will feed all the organizations and all the people who
26:22
Speaker 2: want to know everything. And we want to make it,
26:25
Speaker 2: you know, like a real thing and not a divisive
26:29
Speaker 2: thing or really distinct ourselves from from the noise.
26:33
Speaker 1: And in a sentence, what is geroscience?
26:38
Speaker 2: So the ideal of geroscience is that we target We
26:41
Speaker 2: can target aging by by learning the science and improve
26:49
Speaker 2: basically decrease the burden of diseases and increase increase the
26:54
Speaker 2: health spen for everyone.
26:59
Speaker 1: Is there a Wikipedia page?
27:02
Speaker 2: Not yet?
27:02
Speaker 1: No, no, you can make a Wikipedia page.
27:04
Speaker 2: No no, no, no no, no, there will be soon.
27:09
Speaker 2: But it's actually a process you can make. You can
27:12
Speaker 2: make the Wikipedia page. But when it comes to things
27:15
Speaker 2: like that, there's a committee and the committee now is
27:18
Speaker 2: biased and we're spending actually twenty thousand dollars to show
27:22
Speaker 2: the gero science is a real.
27:25
Speaker 1: Say, convinced the Wikipedia committee. Yeah, wow, Like, do you
27:30
Speaker 1: need a newspaper reporter to use the word in the
27:33
Speaker 1: in the you know, in the Wall Street Journal, in
27:35
Speaker 1: the New York Times? That is that what you need.
27:37
Speaker 2: But it was effective because when I called ourselves gero science,
27:41
Speaker 2: when I talked about it, several editors have changed the
27:44
Speaker 2: name of the article to anti aging because they said,
27:47
Speaker 2: we don't know what's gero science, but anti aging.
27:50
Speaker 1: What do you think about the phrase anti aging?
27:53
Speaker 2: So first of all, we're not anti the aging, but
27:57
Speaker 2: it is used much more commonly for non scientific fact
28:03
Speaker 2: than for science. And so we actually we we actually
28:09
Speaker 2: trying to make it worse, really for people to know
28:11
Speaker 2: that whoever called themselves anti aging and there's no gero
28:15
Speaker 2: signs behind that. Yeah, it's going to be bad.
28:23
Speaker 1: We'll be back in a minute with the lightning round. Okay,
28:36
Speaker 1: let's finish with a lightning round a little bit more random.
28:43
Speaker 1: What one thing you do, even though it may shorten
28:46
Speaker 1: your life.
28:49
Speaker 2: So I'm doing the sixteen hour fast, but I'm a foodie. Okay,
28:56
Speaker 2: so after the sixteen hours fast, I really don't care
29:00
Speaker 2: what I got interesting?
29:03
Speaker 1: What was the last really unhealthy but delicious thing that
29:06
Speaker 1: you ate?
29:09
Speaker 2: Black forest cake? I have a black forest cake, also
29:15
Speaker 2: with ice cream.
29:16
Speaker 1: Yes, ice cream is so good. Do you have a
29:20
Speaker 1: favorite really really old person, like from the Old Testament
29:25
Speaker 1: or from mythology.
29:29
Speaker 2: I'm talking about Metusilla because he supposedly leave nine hundred
29:36
Speaker 2: and sixty nine years And the people who are very
29:41
Speaker 2: orthodox in religions, whether Christians or Jews, believe every word
29:47
Speaker 2: in the Bible, right, But when you ask them, did
29:49
Speaker 2: Metusla leave nine hundred and sixty nine years? Ah, they
29:52
Speaker 2: didn't know how to count.
29:55
Speaker 1: Well, I don't know that particular story. I mean one
29:58
Speaker 1: thing that's interesting to me, Like in the Old Testament,
30:00
Speaker 1: people are just old. Noah's hundreds of years old, whatever.
30:03
Speaker 1: But you know, the myths and the stories that focus
30:06
Speaker 1: in particular on in more mentality especially, it's often bad, right,
30:12
Speaker 1: somebody lives forever and it's terrible to live forever, which
30:16
Speaker 1: is interesting in the context of this conversation.
30:20
Speaker 2: Right, And you know, there's a whole people who are immortalists,
30:25
Speaker 2: and that's very different from me. Okay, I'm not immortalist.
30:29
Speaker 2: In fact, I'm saying what to live a billion more years?
30:33
Speaker 2: How many you know, presidents do you have to suffer through? Yeah,
30:38
Speaker 2: I'm tired a little bit. Immortality. Immortality is a belief,
30:44
Speaker 2: and people realize now that this is not going to
30:48
Speaker 2: happen in their lifetime, and what they are turning into
30:52
Speaker 2: is freezing.
30:53
Speaker 1: Yeah, that's been around for a while. Cryogenics like cryogenous
30:57
Speaker 1: that one seems very crankish to me.
31:00
Speaker 2: Well, but it relieves them in their mind they're dealing
31:04
Speaker 2: with their immortality.
31:06
Speaker 1: So I read this interview with you where you talked
31:08
Speaker 1: about the fact that people with Alzheimer's disease sometimes will
31:13
Speaker 1: respond to music that they know from earlier in their life,
31:16
Speaker 1: and that you actually started making an Alzheimer's playlist for yourself.
31:21
Speaker 1: What's on the playlist?
31:23
Speaker 2: So usually the playlist for those people are of their
31:28
Speaker 2: most earlier memories as young adults, right when you were
31:33
Speaker 2: kind of a kid, when you were in high school,
31:36
Speaker 2: when you were in college. And so for me, it's
31:40
Speaker 2: really the sixties seventies.
31:41
Speaker 1: It's a great era. It's my favorite era.
31:44
Speaker 2: In a lot of ways that are taking and my
31:47
Speaker 2: kids are saying, you know, when you have Alzheimer's, mom
31:50
Speaker 2: would leave you, not because she doesn't like you, but
31:54
Speaker 2: because she wouldn't stand the music.
31:58
Speaker 1: So, from your work with people who've lived past one hundred,
32:01
Speaker 1: I'm curious, what's one thing that you've learned that's not
32:05
Speaker 1: related to health.
32:08
Speaker 2: Will they have a belief in what makes them leave
32:15
Speaker 2: two hundred? And they could adopt the belief because they
32:18
Speaker 2: actually had genes, which means they were protected from everyone.
32:21
Speaker 1: What actually made them lift two hundred is their genes,
32:23
Speaker 1: not the fact that they play golf every Wednesday or whatever.
32:27
Speaker 2: So I have a woman who died at the age
32:31
Speaker 2: one hundred and ten, and she smoked for ninety five years,
32:34
Speaker 2: and she thinks it's because of cigarettes. She said, the
32:38
Speaker 2: four doctors that told her to stop smoking, they died.
32:41
Speaker 1: Yes, yes, Okay. Of all the things we've talked about,
32:46
Speaker 1: If there's only one thing I do to live a longer,
32:49
Speaker 1: healthier life, what should I do?
32:52
Speaker 2: You know? I think at the end it's all individualized.
32:55
Speaker 2: Will be able to see what is the one thing
32:58
Speaker 2: you do. Look, I'm looking at you. It looks to
33:01
Speaker 2: me like that your BMI is normal. It looks to
33:04
Speaker 2: me that you're probably exercising. So I don't know, you
33:08
Speaker 2: have to tell me what you don't do, and I'll
33:12
Speaker 2: pick one.
33:12
Speaker 1: Yeah, that's really because I was hoping you'd say exercise,
33:15
Speaker 1: because I was like, oh, yeah, that's the what I got.
33:18
Speaker 1: I'm not a great sleeper. I don't know, you know,
33:22
Speaker 1: I don't look at my phone. Whatever I do the
33:23
Speaker 1: things they say to do, I just don't tend to
33:25
Speaker 1: sleep that well.
33:27
Speaker 2: So with sleep, there there are two things. One is
33:31
Speaker 2: for the young people and one is for the old.
33:33
Speaker 2: For the young people, stop bingch watching. Okay, a lot
33:37
Speaker 2: of the sleep deprivation is self inflicted. Right, you need
33:43
Speaker 2: eight hours. You should strive for eight hours sleep, and
33:47
Speaker 2: so that means that you have to plan which are
33:49
Speaker 2: the eight hours for the older one or older one
33:53
Speaker 2: than young. So for you and me, it's eight hours
33:58
Speaker 2: in a dark room without electronic Okay, you're not going
34:04
Speaker 2: to sleep the eight hours I sleep for some reason,
34:08
Speaker 2: no matter what happen. I travel around the world. I'm
34:10
Speaker 2: just like, I sleep six hours and forty minutes no
34:13
Speaker 2: matter what. But if I sleep less, it's not going
34:18
Speaker 2: to be good. But what I'm doing that's different than you.
34:21
Speaker 2: I have a feet, bit, you can have a ring,
34:25
Speaker 2: and you can actually measure because it's possible that you'll
34:28
Speaker 2: find that your ram sleep and deep sleep are long
34:32
Speaker 2: enough and you don't need the sleep, and you're not
34:35
Speaker 2: going to feel tired, even if you feel that you
34:37
Speaker 2: didn't sleep well.
34:39
Speaker 1: So you're saying it's important to be in bed in
34:43
Speaker 1: the dark for eight hours, but it's okay to not
34:45
Speaker 1: sleep the whole time. Right, So do you lie in
34:48
Speaker 1: bed for an hour and twenty minutes every night not sleeping?
34:53
Speaker 2: That's pretty much what happens. I'm spending time trying to
34:58
Speaker 2: fall asleep and trying to stay asleep.
35:00
Speaker 1: Yes, anything else we should talk about, just.
35:05
Speaker 2: The one thing that's important to know that aging, that
35:08
Speaker 2: what what we're doing is not only for older adults.
35:11
Speaker 2: People who survive cancer are aging rapidly because we give
35:15
Speaker 2: them chemotherapy and radiation. Right. I don't know if you
35:19
Speaker 2: know cancer survivors, but they usually are doing badly after
35:22
Speaker 2: they recover, so they need help. People with HIV have
35:28
Speaker 2: diseases ten years younger than their ages. Down syndrome is
35:32
Speaker 2: an aging syndrome. Disabled people, you know, need help. And
35:37
Speaker 2: if we're going to Mars, if this is for some people,
35:40
Speaker 2: it's very important. I think this world is beautiful we
35:44
Speaker 2: need to repair it. But if you go to Mars,
35:46
Speaker 2: you're not going to get there before we stopped aging,
35:50
Speaker 2: because you'll be sick on the way there and you're
35:53
Speaker 2: never coming back.
35:55
Speaker 1: Thank you very much for your time. I really appreciate it.
35:58
Speaker 2: Thank you very much.
36:06
Speaker 1: Your Barselai is a physician and he runs it's the
36:09
Speaker 1: Institute for Geroscience at the Albert Einstein College of Medicine.
36:14
Speaker 1: Just a quick note, we're going to be taking the
36:15
Speaker 1: next couple weeks off. We're going to be back after
36:17
Speaker 1: that with more episodes of What's Your Problem. Please email
36:20
Speaker 1: us at problem at pushkin dot fm. Tell us what
36:23
Speaker 1: kinds of shows we should do more of or less
36:25
Speaker 1: of our particular people you think would be good on
36:27
Speaker 1: the show. You can also find me on x and
36:29
Speaker 1: on LinkedIn. Our show is produced by Gabriel Hunter Chang
36:33
Speaker 1: and Trina Menino. Our editor is Lydia Jane Kott, and
36:36
Speaker 1: our engineer is Sarah Buguer. I'm Jacob Goldstein.