Longer Life: What Does Science Say?

While the longevity field is filled with dubious claims and junk science, there have been some truly remarkable advances that will have an impact on how we can live longer and stay healthier. In this episode, Kara unpacks some of them with Dr. Eric Verdin, the president and CEO of the Buck Institute for Research on Aging in Novato, California. The Buck Institute was the first of its kind, and it’s at the forefront of all the latest research on longevity. Later she speaks to Dr. Vinod Balachandran, attending physician and director of The Olayan Center for Cancer Vaccines at Memorial Sloan Kettering in New York. He’ll explain his research into mRNA vaccines and their potential to treat and possibly cure pancreatic cancer. Questions? Comments? Email us at [email protected] or find us on YouTube, Instagram, TikTok, Threads, and Bluesky @onwithkaraswisher. Learn more about your ad choices. Visit podcastchoices.com/adchoices

Speaker names marked ? are inferred from speaking time and the show’s known hosts — they are not voice-verified.

• 0:12Kara Swisher?

  Hi, everyone. From New York Magazine and the Vox Media Podcast Network, this is On with Kara Swisher, and I'm Kara Swisher. When it comes to the science of living longer, there's so much garbage out there that it's easy to miss some of the truly remarkable things that are happening with scientific advancement around longevity. In this episode of our Hacking Longevity series, we'll go deep into the science behind some of the most promising medical developments happening right now, specifically when it comes to fighting pancreatic cancer. We'll speak with the leading researcher in that fight, Dr. Vinod Balachandran of the Memorial Sloan Kettering Cancer Center. But first, the bigger picture. I'm joined by Dr. Eric Verdin, the president and CEO of the Buck Institute for Research on Aging in Novato, California. The Buck Institute was the first research center of its kind, and it's at the forefront

• 0:57Kara Swisher?

  of what's going on in the field. Dr. Verdin has a medical background, of course. He also has an entrepreneurial take that I wish more doctors shared. I think it's really interesting to talk to all the various big names in this. Some of them are more scientific than others, and those are the ones I'm sticking with. But it's really important to understand all the differing viewpoints of where this is going, and that's what's necessary to moving forward, to have disagreement, and then move forward with actual scientific facts and, of course, measurements. It's a smart and interesting conversation, so stick around.

• 1:45Kara Swisher?

  Support for this show comes from The Guardian and their new show, Stateside, where journalists Kai Wright and Carter Sherman use the entire independent reporting resources of The Guardian to slow down the news and wrestle with the questions we all have about what is actually happening in the world. Join Kai and Carter three times a week as they utilize all the reporting resources The Guardian has across news, international coverage, climate, culture, wellness, and more. And The Guardian's not owned by a billionaire. They fearlessly report the facts without interference. Go to theguardian.com/stateside to learn more. And listen wherever you get your podcasts, or watch on YouTube. That's theguardian.com/stateside.

• 2:31Kara Swisher?

  Dr. Eric Verden, thank you for coming on.

• 2:34Speaker 01

  Thank you for having me.

• 2:35Kara Swisher?

  So you're at the forefront of some of the most interesting ideas in this field. So the first question, what is something about aging that would surprise the average person? And what people get wrong about aging?

• 2:48Speaker 01

  Wow, that's a big question.

• 2:51Kara Swisher?

  It is.

• 2:52Speaker 01

  What would surprise people is how much control you actually have over the way you're going to age at the end of your life. Many of us live through life sort of hoping for the best, flying blind mostly. This is the state of medicine today. And I think there's what I call a revolution happening in a way that we're finding out that the way you live can have an absolutely dramatic impact on how you're going to spend the later years of your life. And in some way, that's the message I've been trying to spread.

• 3:29Kara Swisher?

  You have.

• 3:30Speaker 01

  Because I think it's an incredibly optimistic and positive message versus a fatalistic sort of, you know, my parents didn't live very old, well, I might as well have another cigarette.

• 3:40Kara Swisher?

  Right, right. So what do people get wrong, would you say? Is that idea that you have to be sort of a decrepit person, no matter what happens? Like, it's just the way, it's inevitable kind of thing?

• 3:51Speaker 01

  Yeah, sort of a very fatalistic view of their own aging. What they get wrong also is the intensity of what needs to be done to actually get maximum benefits. And I tell people, you know, that as a very simple example, that walking 15 minutes every morning and every night is going to have a dramatic effect on everything in terms of how you age. Most people are not aware of this. They think, well, I have to eat perfectly, I have to sleep, I have to do everything perfectly. And my approach has been, everything that you do will help, especially at the early stages.

• 4:28Kara Swisher?

  So you're studying aging itself. What does it mean to study aging as a disease? Is that how, that's how you look at it? Explain that for people who don't understand what you're doing.

• 4:37Speaker 01

  And this is not something that everybody agrees on. I do not, I do not like the idea of calling aging a disease itself because it has a lot of implications. One very simple one is that if we start doing this, it means everybody at age twenty five is now disabled. Uh, I think aging is a normal process, but there are many different ways of aging. And the thing to know is that rather than calling it a disease, I call it a risk factor. It's the major risk factor for a whole series of conditions that your audience will be familiar with. Heart attack, stroke, uh, type two diabetes, macular degeneration, uh, hip fractures, uh, the list goes on and on.

• 5:20Kara Swisher?

  Can I, can I interject? How did you come to see aging itself as the root? Talk about how you got there.

• 5:26Speaker 01

  About twenty five years ago, thirty years ago, nineteen ninety five for most part. Uh, a whole series of discoveries pointed to the fact that aging was really much more strongly regulated than we had imagined. Before this, people thought aging is just something that happens. What we discovered is that there were really critical genes that changed the, the rate of aging. So we can make a single mutation in a small animal and really dramatically double its life expectancy. So that really changed the whole way of thinking of aging as something fatalistic that we could not control, that was random, to something that's actually pretty strictly regulated. And this regulation should imply the fact that if we could find drugs

• 6:10Speaker 01

  or interventions that targeted these regulatory points, we could really change the rate of aging. And when we started doing this, what we found is we could make animals live longer. So all of this work was done in small animal models, system, uh, mice and so on. But the animals not only lived longer, but they lived much healthier. That was really something that surprised us. And so they generated something called the Gerescience hypothesis. Uh, I want to step back for one second.

• 6:41Kara Swisher?

  Sure.

• 6:41Speaker 01

  The, the idea that we live today about double the time that we lived a hundred and fifty years ago. So, you know, eighteen fifty, we lived until around forty.

• 6:52Speaker 01

  Right now, it's around eighty, most of the Western world. But it has come with an incredible burden of chronic disease. When I ask people, you know, who wants to live to a hundred, uh, very few hands will rise. Because people envision a future of disease.

• 7:08Kara Swisher?

  Right.

• 7:09Speaker 01

  And so what what we have found in animal models is that if we tinker with these aging pathways, these mechanisms that regulate aging, we make the animal live longer, but they also live much healthier.

• 7:21Kara Swisher?

  Right, without the onset of these chronic diseases that happen, right?

• 7:25Speaker 01

  Yes, and so they behave in many ways much more like the centenarians today. And centenarians not only live longer, they live much healthier. Your your typical centenarians will live until ninety five in good health, and then will have five years of a compressed morbidity.

• 7:40Kara Swisher?

  The things you're doing at the Buck Institute, explain for people what you do. And it's the Verdin Lab at the Buck Institute. You've been particularly studying the connection between aging and immunology. Uh, talk a little bit about that and the connection.

• 7:52Speaker 01

  Yeah, so first, the Buck Institute was founded in nineteen ninety nine on the heel of these discoveries that we we talked about. Uh, with a generous gift at Mrs. Beryl Buck. We, today, we have about three hundred employees working on all different aspects of aging and trying to really to do two things. One, understand the basic biology of aging, because we we've made huge progress, but there are still really big questions that we don't we don't fully understand. But also importantly, trying to bring all of this knowledge to humans. Because that's obviously, that's that's the goal, is to make all of us live longer better. But we we've been a clinical center, we have clinical trials going on.

• 8:36Speaker 01

  Uh, pretty much half of our faculty is focused on really bringing all this knowledge to humans. And so this will happen pretty quickly, within the next five years, I would say. We will have some of the first interventions for humans. Um, so the Verdin Lab itself, so I I have a dual role. I am, um, sort of CEO of the organization, I lead it, but also have my own lab, uh, and I focus on understanding the role of the immune system. The immune system seems to be one of the few organs, along with the central nervous system, that play a dominant role in aging. And so there's evidence, for example, that if you if you have a lesion only in the immune system, this will cause aging in the whole organism.

• 9:19Speaker 01

  Uh, and this is true also for the central nervous system. The other thing is aging in the immune system, I think, has not received the attention that it requires. And this was highlighted during the pandemic. Where your age, for example, was the major risk factor from dying from COVID. It's also the major risk factor from dying from influenza, the flu, from RSV, respiratory system virus. It's also, the immune system is a critical system that controls how you respond to cancer. So there's a whole series of aspects linked to aging that are controlled by the immune system. Uh, what I like personally as a model system to study is that it's readily accessible. We can, we can draw blood from, from your arm.

• 10:04Speaker 01

  And within an hour, we can really enumerate all the different cells. We can figure out what is the state of your immune aging. It's a system that we can intervene on by the same way. We can take cells out, we can modify it, we could put them back.

• 10:18Kara Swisher?

  Now, one of the things you've also focused on there, the issues around supplements is something I covered a little bit in the series, but not a lot. And some doctors think they're a waste of time and money. You don't dismiss them at all. You sell some supplements like the Juvenessence Metabolic Switch. Talk a little bit about why there's a lack of scientific consensus in this area. Because I, I suspected somewhere in the middle in terms of, there's a lot of influencers selling nonsensical stuff. And then there's some good stuff, a vitamin D, a vitamin K, for example. Talk a little bit about this, because I think one of the things that, the one question I've been asked by most people after the series was, what about supplements? And I was like, well, it's complicated. Let me.

• 11:01Speaker 01

  Yes.

• 11:02Kara Swisher?

  Don't buy it from Dr. Nobody, like, please don't, like.

• 11:06Speaker 01

  Yes.

• 11:07Kara Swisher?

  You know, Dr. Dr. Instagram, don't buy it from Dr. Instagram, but go ahead.

• 11:12Speaker 01

  I, I could not agree more. And I've been called sometimes the, the grumpy man of longevity medicine because of the science that I've taken, which is somewhat conservative. But probably a lot more open to, to the idea that, that most physicians would be. You know, I went to medical school and I was told most supplements don't do anything. I, I disagree with this. So first, there's a whole. World of what I call Instagram medicine.

• 11:39Kara Swisher?

  Yeah, Dr. Google. It used to be Dr. Google, now it's Instagram medicine.

• 11:43Speaker 01

  Okay. And so, you know, quite often you will find these influencers making big pronouncements on science that they've never been close to and promoting products for which they are being paid. And many of these products have some kind of relationship to aging from laboratory studies and so on. None of them, to this day, have been proven in humans. No. So that doesn't mean that I'm not taking any supplements. I do take supplements, quite a few, actually. I do take them in a way that is based on some of the data that I have seen and what I think is promising or not. So we live right now in this sort of netherworld

• 12:26Speaker 01

  where we have the supplements that have been documented to have big effects sometimes in animal models. And then we have humans where the barrier is much harder. So I advise people to, you know, there are some supplements that most people should take, as you mentioned, vitamin D. Most of us are deficient. Vitamin B12, quite a few of us are deficient. Omega fatty acid, we know that the Western diet is quite low in omega fatty acids in comparison, for example, to Japanese. Creatine is another supplement that really came out of the sports world and seems to have really big effects. Protein supplementation, in some cases, this would be my essential list. Magnesium helps a lot of people as well.

• 13:11Speaker 01

  So that would be my essential list. Then beyond this, there's a whole series of additional supplements that have shown promising results in animal models. And this is where it really depends on your sense and your risk-taking. My approach has been to introduce them one at a time and then to follow my numbers. And if I see your positive picture, I tend to continue.

• 13:38Kara Swisher?

  Give me an example of that.

• 13:40Speaker 01

  I'll give you an example of one that has been very controversial, NAD.

• 13:45Kara Swisher?

  Yeah, I was gonna ask you about that.

• 13:46Speaker 01

  Yeah, so NAD is a key molecule in metabolism. I've spent many years studying it. There is some evidence that NAD levels can decrease in many tissues, although there was just a paper came out this past week saying it doesn't decrease in blood. There's some evidence it decreases in several tissues. And so the idea has been, since it is so critical and it decreases during aging, why not try to bring it back to a normal level? And so two supplements have emerged out of these studies called NMN and NR, nicotinamide mononucleotide, nicotinamide riboside. And they do restore in animal models, NAD levels.

• 14:29Speaker 01

  And in animal models, they show very strong effect. In my lab, in many labs, actually. And so that has led to a whole industry of companies selling NR and NMN. And here's the downside. Many of the clinical studies that have been done in humans have really not shown very significant

• 14:48Kara Swisher?

  That's right.

• 14:48Speaker 01

  beneficial effect. And so right now, we live in this nether world where people don't know what to do. Should I continue? Should I not? In my lab, for example, we've done some work trying to understand why do NAD levels decrease in the first place? And what we found is that there's a molecule called CD38, which increases during aging. And this molecule, CD38, churns through NAD. So based on that data, I would say that the proper approach, the problem would be to block CD38. And we have, we have some novel drugs that are doing this, rather than pouring more water, more in.

• 15:25Kara Swisher?

  Let's go through some others then, because there really are out there, like rapamycin had a moment, especially off-label use of it. Talk a little bit about that.

• 15:35Speaker 01

  So rapamycin is not a supplement. That's an important distinction. It's a real medicine. Rapamycin targets a protein called mTOR.

• 15:44Speaker 01

  Mechanistic target of rapamycin. So and mTOR is a critical protein in metabolism and in aging. The data in animal model says that rapamycin is the strongest molecule that we have in an experimental setting to increase lifespan. Okay, so it's been tested in multiple species, all the way from yeast to mice to fruit flies. Everywhere it increases lifespan and health span. So what's interesting also is that rapamycin is already an approved drug in humans. It's used actually in to immunosuppress patients who receive a transplant.

• 16:26Speaker 01

  So what the field has proposed and what a number of people have jumped on is the idea, well, let's take rapamycin at low dose and take a bet, because it is a bet. We don't have the clinical trials that demonstrate that it is actually working. So and those those trials should be done and will be done. What we don't know is the proper dose. Obviously, you don't want to get and use it at a level which is immunosuppressive, because that's going to have a whole series of the bad complications. But maybe at lower dose, you're gonna get some benefit. I have taken it, and so have a number of people.

• 17:04Kara Swisher?

  Yeah.

• 17:05Speaker 01

  Many of us have stopped.

• 17:07Kara Swisher?

  Stopped, that's correct.

• 17:08Speaker 01

  Yes. And I tell you, the reason why I stopped personally is that I could not see any difference in any of my numbers. The fact that I stopped doesn't mean anything by itself. The fact that Brian Johnson stopped doesn't mean anything either. But I think what we need, again, here.

• 17:24Kara Swisher?

  Gold standard clinical trial, which I was arguing with Brian about. I'm like, why don't you just do the trials? Like, you can talk about it all you want. Another thing that I've noticed is a lot of biological age tests. By the way, my source scores came out excellent. But I find a lot of them are a waste of money, too. Again, another these things, Brian does them, a bunch of people, and I'm like, they don't really say a lot. How do you feel about them?

• 17:48Speaker 01

  They say, I think, probably a lot that we don't know how to interpret them.

• 17:51Kara Swisher?

  Yeah, that's a very good way of putting it, yeah.

• 17:53Speaker 01

  I think we are in discovery mode right now, so every week there's another of these clocks being discovered. The biggest group is the so-called epigenetic clocks. Steve Horvath was the one who did it first. There's probably fifty or sixty of them, different. If you send one blood sample to many of those, I did this, my number came back from forty to sixty-eight.

• 18:17Kara Swisher?

  Mine too, mine too, all different.

• 18:20Speaker 01

  Of course, I like the company that tells me I'm forty and if I had only done one test and it had been that one, I could be sort of deluding myself that I'm forty years old. So the way I look at them is that they are incredible tools. They will be important in the future, but they are right now experimental tools.

• 18:38Kara Swisher?

  Let's go through a few more cellular rejuvenation.

• 18:41Speaker 01

  A very exciting area of biology, late nineties, early two thousand. A colleague of mine, when I was at the Glazier Institute at UCSF, Shinya Yamanaka, discovered a few factors, called the Yamanaka factors, that were able to take a somatic cells, the skin cells, nerve cells, brain cells, and bring it back to what we call a pluripotent stem cell. That is a cell that has the potential to become a whole organism. So this showed incredible plasticity of a process that we thought was irreversible. So our vision before was that when you are a muscle cell, you stop being a muscle cell forever. And it showed the idea that you could actually bring it back all the way.

• 19:25Speaker 01

  Now, there is something that happens when we are born is that we're not being as old as our parents were. Every time a baby gets born, there's a resetting at zero, which, when you think about it, it is in some ways remarkable because this has been going on for billions of years. So what a colleague put these two observations together and said, what about if we would use the Yamanaka factor to bring you back a little bit closer to being a baby? Would that actually make you younger? And so they introduced the Yamanaka factor in mice, and lo and behold, they were able to show that these mice were rejuvenated. They seemed to be living younger.

• 20:08Speaker 01

  And so this led to the creation of a whole series of new laboratories and companies. Altos is probably the most visible one.

• 20:18Speaker 01

  That are exploring the possibility of testing these yarmulke factors or variation of them to actually do what we call reprogramming.

• 20:28Kara Swisher?

  So a couple more, longevity, escape velocity. Explain for people what this is.

• 20:33Speaker 01

  Yeah, so over the last 150 years,

• 20:38Speaker 01

  we've gained two years every decade, two years of extra lifespan. So now let's just imagine for an instant that every decade we would gain not two years, but 10 years. That would mean our science would go as fast as we are aging. If we were able to gain 10 years every decade, then, you know, another 10 years will pass and we will get another 10 years. This is the road to immortality. That's the way this is being presented.

• 21:06Kara Swisher?

  Presented. How do you feel about this?

• 21:12Speaker 01

  I've said that if you're looking for immortality, then come to the longevity field, join the church.

• 21:18Kara Swisher?

  Yeah.

• 21:18Speaker 01

  And there's no disrespect to religion. It's just, these are different spaces. I think as a scientist, we should never talk about immortality. It's just not, I don't know frankly, if it's desirable. I think a long, healthy life definitely is. And even I'm open to the idea of much, much longer healthy life. But when we talk about immortality, for me, we talk about first, something for which we have absolutely no evidence. And I know the concept of longevity, escape velocity is cute. It just, it just helps you to visualize how this might happen. Now, one thing that I always bring up as a counter argument to this whole immortality point of view is that

• 22:02Speaker 01

  this seems to be a very hard limit at about 115 for human to live. Now, it doesn't mean that we will never be able to change it, but I haven't heard anyone bring sort of an argument of how we're going to be able to do this.

• 22:17Kara Swisher?

  Last one, and then I have some big picture things to finish up on fasting. This is one I believe you personally do. This is one I wish I could do. I never seem to be able to pull it off. But I do. These have, these are very clearly proven scientific benefits from fasting, although I'm so tired of listening to tech people talk to me about it obsessively, and that's a different thing. That's just shortening my life by wasting my time. But talk a little bit about it, because this is an area that sort of became a trend and then fell out of trend in a weird way.

• 22:48Speaker 01

  Yeah, I'll tell you how it started. I mean, one of the oldest and most robust way to increase lifespan in almost every animal species that has been tested in is calorie restriction, so decreasing calorie input. So here comes fasting, which is a sort of a minimized version of calorie restriction. So there are many ways to do fasting that would induce the same response. I favor a concept that's been advanced by my friend and colleague Sachinandha Panda, which is called a time-restricted eating. So most of us are eating for 16 hours in a day and fasting for eight hours while we sleep.

• 23:31Speaker 01

  The whole idea is to get as close to possible to the invert, which is eating in an eight-hour window and fasting for 16. Now, again, we started the interview by this whole idea that, you know, people have sort of absolute disversions of everything. If you're doing 16, eight today, eating for 16 hours, and you decrease this to 12, you would already do yourself some good. So I tell, you know, and I'd be curious to hear what has been your difficulty of trying this, for example?

• 24:01Kara Swisher?

  Probably the presence of, the availability is the problem for most people.

• 24:07Speaker 01

  I agree. No, I agree. It's just, I, you know, my approach has been to do this progressively. If you're eating for 16 hours, decrease it to 14 for a month, and then decrease it to 12 for a month, then decrease it to 10, and eventually, soon enough, you'll be able to do it. There are issues. Women have a totally different response to fasting, depending on where they are in their menstrual cycle, so this is something always to consider.

• 24:38Speaker 01

  There are also alternative ways of fasting. By the way, there are many sort of traditions that that have these fasting periods. You know, think about Lent, think about.

• 24:48Kara Swisher?

  Yes, they do. My grandmother.

• 24:50Speaker 01

  Yeah, exactly. So this is this is not something that we even that we.

• 24:54Kara Swisher?

  No, not at all. No, no, my son's doing the no eating after dark, although I'm like, summer. What do you do in the summer? Like.

• 25:00Speaker 01

  Yes.

• 25:01Kara Swisher?

  It's actually he's lost a lot of weight doing it. That's how he's doing it. Um, let me finish up by talking sort of the bigger picture. As we've been talking, one of the things that's very clear, there's a lot of noise around longevity science, and especially now with, as you noted, the charlatanism online, a lot of it, some of it good, some of it junk, um, but loud and and noisy. And of course, uh, as part of the series, I've been doing a lot of reporting on the people who are most obsessed with it have been the people I were covering for years, a lot of the tech billionaires who are also involved in AI and various things like that. As you said, you've been called the grump grump because you're so conservative with this stuff. I'd love to to sort of you to contrast the pushing towards this and at the same time

• 25:45Kara Swisher?

  with all this incredible scientific promise, no question, that's one of the things that's been the biggest takeaway. But is it okay if it starts as a narcissistic pursuit rather than something that's for all of us? How do you shift it to all of us, to the wider population, which is where you really want to see longevity increases?

• 26:05Speaker 01

  I I'm really glad you're bringing this up because, uh, first, we do receive money from billionaires. And I have nothing against the idea.

• 26:15Kara Swisher?

  Right, take it.

• 26:15Speaker 01

  I I actually find it admirable that they give their money. And and I, you know, there's a number of people, especially in Europe, have conflated these sort of narcissistic billionaire and their desire to live forever. And there's, you know, I I read these articles and they make me mad because I think they don't reflect the reality. The billionaires that are giving money, I think, are doing it, of course, out of self-interest. There's nothing wrong with this, but they're doing it also of a long tradition of philanthropy that exists in the US. So there's nothing intrinsically evil about.

• 26:49Speaker 01

  You know, Sergey Brin and all of the others, you know, giving money to longevity research.

• 26:55Kara Swisher?

  No, not at all.

• 26:55Speaker 01

  That being said, it also creates a problem for us because it creates this perception that we are only about increasing longevity for rich people.

• 27:05Kara Swisher?

  Rich people, right.

• 27:06Speaker 01

  And this is compounded by the fact that many of the longevity clinics that are opening today are actually catering to a

• 27:13Kara Swisher?

  Yes, a small

• 27:14Speaker 01

  elite wealthy clientele. This is, again, this is nothing new. When Elon Musk built the first Tesla, it cost a hundred and fifty thousand dollars, you know, and eventually he built a mass market car that cost thirty five thousand dollars. And so it will go for longevity medicine, which is a whole new discipline that we're building. And this is really something that people misunderstand in terms of my intent. When it comes to humans, it's nice to talk about longevity escape velocity, but it should not obscure the fact that we have a lot of work that we can do today to make people live healthier.

• 27:49Kara Swisher?

  Correct, yeah.

• 27:50Speaker 01

  Longer now. And so this is really where I feel the passion that the longevity field should not only be about extreme longevity, it should also be about health span.

• 27:59Kara Swisher?

  I mean, my last question is a bit of a curve ball from the last one. I know you're a racing fan, auto racing. There's a model on your shelf, I see, and I know you actually drive some of these race cars.

• 28:11Kara Swisher?

  Life's work is about extending human life. Talk about why you do this.

• 28:16Speaker 01

  Yes, first, racing itself is a dangerous sport, but it is also, many of us have an image of it that's colored by what racing was in the seventies and eighties, where every year two pilots would die in the Formula One championship. It's still a dangerous sport, but it's not more dangerous than diving. Or, you know, I have a number of friends who were road biking, who would get hit by cars. So it is, it's amateur racing, and when the time comes to really, you know, make a pass that is going to hurt your friend or your car, I think we all think about it. Personally, I thrive in these moments when I'm right at the edge where

• 28:59Speaker 01

  Focus and the concentration needs to be absolute. You get into this flow state.

• 29:04Kara Swisher?

  Uh huh.

• 29:04Speaker 01

  Racing also, for most people do not appreciate is an extremely physical sport. So for me, it's a motivation for to staying in shape. Uh, and frankly, the community of, of people that I race with is incredible. So it, it meets actually many of the ingredients that I tell people. Yeah. So physical sport, uh, it's a community, uh,

• 29:27Kara Swisher?

  Something new?

• 29:28Speaker 01

  cognition, uh, excitement. So these are all the things, you know, I'm going to race this weekend, by the way, in a Mini Cooper.

• 29:35Kara Swisher?

  Yeah. Oh, wow.

• 29:36Speaker 01

  And, uh, this big race with about 30 Mini Coopers, which is going to be total, total fun.

• 29:42Kara Swisher?

  Where is that?

• 29:43Speaker 01

  That's at, uh, at Sonoma Raceway.

• 29:45Kara Swisher?

  Oh, wow.

• 29:46Speaker 01

  It's this whole weekend. The Velocity Invitational is an amazing event. It's the largest sort of a vintage racing, uh, event.

• 29:53Kara Swisher?

  That's a great, that's a great racetrack up there in Sonoma.

• 29:55Speaker 01

  Absolutely.

• 29:56Kara Swisher?

  It's really fun. I, I'm just teasing you on this because I think it's great. I think it's great to do things like that, um, to have a hobby. Anyway, I really appreciate it, Eric.

• 30:05Speaker 01

  Thank you, Kara.

• 30:09Kara Swisher?

  We'll be back in a minute.

• 30:20Kara Swisher?

  Support for this show comes from The Guardian. Trying to locate news sources that reliably separate fact from fiction can seem like looking for a needle in a haystack these days. Social media feeds, cable news and subscription based news outlets might be able to give you one version of the news, but not in the way that you need. You want news fast, but slow enough to actually absorb the information. Stateside with Kai Wright and Carter Sherman is here to do just that. The podcast tries to slow down the news and wrestle with the questions regarding the world at large at your own pace. Three times a week, hosts Kai Wright and Carter Sherman bring their expertise together to showcase different and engaging perspectives regarding the world today. They will use their collective knowledge to discuss the news, international affairs,

• 31:03Kara Swisher?

  climate, culture, sports, lifestyle, fashion and wellness. Plus, The Guardian wants to emphasize they're not billionaire owned, meaning they're free to report the whole picture without interference. Go to theguardian.com/stateside to learn more and listen wherever you get your podcasts or watch on YouTube starting May 13th.

• 31:23Kara Swisher?

  Doctors and scientists are making truly remarkable progress against aging and disease, and we're going to go deep on one of the most promising areas of research right now, fighting pancreatic cancer. Researchers have really upended our understanding of how to treat pancreatic cancers, and one of the ways they're testing is using vaccines to treat cancers that have already developed. It's early days, but it has all the hallmarks of a huge breakthrough. I think one of the things that's been exciting is to see all the excitement around these mRNA technology solutions for pancreatic cancer, when there's been such a backlash against vaccine among the general populace. But most people understand that this is a game changer, and I just have paid a lot of attention, as I've known

• 32:05Kara Swisher?

  a lot of people who've died of pancreatic cancer, or lung cancer, or cancers that are much harder to treat, even as they've made strides in other cancers, such as breast cancer and colon cancer, which is amazing. One of the people leading the work is my next guest, Dr. Vinod Balachandran. He runs the Oleon Center for Cancer Vaccines at Memorial Sloan Kettering Cancer Center. He's a surgeon and a scientist, which is a rare combination. He has taken an unusual and very promising approach to his work. Vinod, thank you for coming on, on.

• 32:37Speaker 02

  Thanks for having me, Kara.

• 32:38Kara Swisher?

  All right, you're a surgeon, and you also run a lab. And for people who don't know, that's an incredibly rare combination, partly because the demands of even one of those are hard to manage. Explain how that happened.

• 32:48Speaker 02

  Sure. So the specific disease that I take care of is pancreatic cancer. And you may know pancreatic cancer is projected to become the second-leading cause of cancer death in the United States next year. So more deaths from pancreatic cancer than many of the other common cancers, such as breast cancer, prostate cancer, ovarian cancer, melanoma, second only to lung. And part of the reason for this is because the current treatments that we have for this disease, which include surgery, chemotherapy, and radiation are

• 33:25Speaker 02

  sort of still last generation, if you will. And the recent advances in oncology drugs, which there have been many, have not really impacted pancreatic cancer in a way that we would like. So when I Started out as a junior faculty member to try to make a difference in cancer, which really has very high unmet need and patients really need help. I really wanted to spend time in the laboratory to be able to do this as I felt this was probably where we would be able to make.

• 34:00Kara Swisher?

  Because, as you said, the treatments were so last generation, essentially.

• 34:05Speaker 02

  That's right. We think the most exponential advances here would come with scientific discoveries and application, and that really has to come from the lab.

• 34:14Kara Swisher?

  So explain why pancreatic and lung cancer also, and I've known both, both the people who've had cancer, who've had both those things have died of those things. I was thinking of Susan Wojcicki, who used to run YouTube and was an early Google executive, and then a friend of mine who died of pancreatic cancer. Everybody else seems to be okay who's gotten cancer, which is, explain why those are so vexing.

• 34:39Speaker 02

  Number one, it's very difficult to detect it early. So early detection, which has made significant progress in many other cancers, such as colon cancer, breast cancer, we don't have this for pancreatic cancer. And even when you detect it early, the treatments that we have are not as effective as other cancer types. So because of this, the mortality rate from pancreatic cancer now at five years still ranges on the order of approximately 90%.

• 35:13Kara Swisher?

  Yeah.

• 35:14Speaker 02

  So only about 10% of patients really survive long term.

• 35:18Kara Swisher?

  Long term. So your work on developing vaccines that will treat cancer is groundbreaking. It's something I remember talking to the German couple who had started the, some of the mRNA stuff around cancer, and it became a COVID vaccine. So most people know mRNA through COVID, but in fact, it was aimed at cancer initially, as I recall. But I want to get into the science of it, but first, provide some context for people who don't know how vaccines were targeted to do this.

• 35:43Speaker 02

  Vaccines, in short, perhaps you could describe them as the most impactful.

• 35:51Speaker 02

  Medicine in human history to improve health. And the way they work is by teaching the body to recognize what is foreign. So by delivering a small piece of a virus or a bacteria. So when or if they come, we already have a powerful immune system that knows that these agents are foreign and thereby can kill them. And these vaccines, the ones that we sort of commonly know about for influenza, COVID, others, these are given to healthy individuals to prevent future potential disease.

• 36:35Speaker 02

  Now for cancer, this has been a significant challenge for many reasons. The first being that it's easier to teach our immune system to recognize, let's say, a virus or a bacteria as foreign, because this, it already wants to do that. Cancers derive from our own tissues, so they are in fact self. And our immune system is in fact hardwired to not recognize our own bodies as foreign. So to be able to teach the immune system to recognize specifically the portions of a cancer that are foreign compared to normal tissues is a fundamental scientific challenge.

• 37:14Speaker 02

  But in, in recent decades, we have made several significant breakthroughs in understanding, how does the immune system recognize cancer as foreign? And how can we teach it to do this in a really effective way to make cancer vaccines? And this has really been quite exciting.

• 37:31Kara Swisher?

  Right. So talk about the, the most common therapies right now for pancreatic cancer. Right at the second, if you found out you got it, what would you go through? What would be the ways they would move through, through various therapies? And I know there's several that they do.

• 37:44Speaker 02

  So in scenarios where the tumors are detected early, meaning sort of confined to the pancreas without any signs of spread outside the pancreas. The treatments include removal with surgery and usually chemotherapy afterwards to prevent it from coming back after surgery. In scenarios where the tumor is either not removable with surgery or has spread outside of the pancreas, the treatments include chemotherapy and/or radiation. However, in recent years, there have been significant breakthroughs in using the more

• 38:28Speaker 02

  modern waves of oncology drugs to be able to target pancreatic cancer. Number one being immune therapy, which is sort of what we've been working on, vaccines. And a second being these targeted therapies, which sort of target the specific mutation that is found in pancreatic cancer using drugs. These are called the KRAS inhibitors. So I think even though our current treatments are still perhaps the last generation, there have been significant improvements in recent years.

• 39:00Kara Swisher?

  What are the drawbacks to most of these?

• 39:02Speaker 02

  Well, I mean, I think the central drawback here is we want them, we want drugs that work better.

• 39:11Kara Swisher?

  Yeah. They don't work.

• 39:13Speaker 02

  Yeah, they don't work. Yeah, yeah, we want things that work a lot better than this. We want to, we want cure. You know, this is of course a word that oncologists use sparingly, but certainly this is what we would want to achieve. And it's interesting because the, the story of the vaccines for pancreatic cancer really emerged from the few patients that naturally sort of affect cure. Meaning although about 90% of pancreatic cancer patients die with current treatments, not everybody does. And there's a rare 10% that survive long term. So about a decade ago, we began studying these rare survivors

• 39:58Speaker 02

  of pancreas cancer, long-term survivors, to try to understand, well, how are they doing this? And how could we replicate this in a therapy?

• 40:06Kara Swisher?

  Right.

• 40:07Speaker 02

  And what we learned is that these patients, we believe their immune systems are able to naturally recognize their cancers in a very potent way.

• 40:18Speaker 02

  That allows these patients to survive so long. So this led us to this idea that if this is sort of happening in the best case scenario.

• 40:27Kara Swisher?

  You can facilitate it via vaccines.

• 40:29Speaker 02

  How could we teach other patients' immune system to recognize their cancer? Just like it's happening in these rare survival.

• 40:34Kara Swisher?

  And cancer researchers had traditionally not looked at it this way, correct?

• 40:38Speaker 02

  Right. And also for immune therapy, I think pancreas cancer was considered perhaps one of the toughest cancers for immune therapy, which the vaccines would fall under this category. And perhaps there was also a question whether an immune therapy or a vaccine would ever be possible for a cancer like pancreas cancer.

• 41:00Kara Swisher?

  This is a series about longevity, so it's also a series about aging itself. And is pancreatic cancer one of the diseases you're more likely to have the older you have? Or how does aging factor into how you approach the disease?

• 41:12Speaker 02

  Yeah, so it is a disease that is found or typically occurs in the age range of 60s to 70s. So it is not something that some would refer to as a young person cancer. But the incidence of pancreas cancer in the United States is also slowly increasing.

• 41:36Kara Swisher?

  Yes, it is. It's low cancer.

• 41:38Speaker 02

  Yeah, so I think it is a significant national and global health challenge to be able to try to find effective drugs, medicines that can help treat, cure these patients of this really terrible.

• 41:56Kara Swisher?

  As the age range wafts down.

• 41:58Speaker 02

  That's right, because the population is going to continue to.

• 42:01Kara Swisher?

  Is there a reason why? Or is there something that scientists are looking at as why that's the case?

• 42:06Speaker 02

  Yeah, the etiology, like why does it happen? Why do you patients get pancreas cancer?

• 42:12Kara Swisher?

  And why is it increasing?

• 42:14Speaker 02

  Why is it increasing? Yeah, it's not clear. There's not one sort of magic bullet, I think, that would explain this.

• 42:38Kara Swisher?

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• 43:22Kara Swisher?

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• 43:51Kara Swisher?

  So let's walk through the research you're doing. There's something interesting about your approach as you described. You decide to focus on the outliers, the small percentage of people who do better from existing treatments. Talk about why you do that, and what did you find in your hypothesis of how to replicate the success these patients had?

• 44:09Speaker 02

  Yeah, I think this goes back to one of the first questions that you asked about, you know, being a physician scientist and how, how does that really help? I think this, this was something that I had encountered as a surgeon taking care of patients with pancreas cancer. You see these patients who come into your clinic that get the same treatments as everyone else, but they survive long-term. And it immediately strikes you as, well, why is that happening? Maybe we could try to understand what's happening in these patients because they, they're doing great. We want everyone to sort of do great just like them. And essentially, fast forward after us studying a huge cohort of these rare survivors

• 44:54Speaker 02

  and comparing them to other patients who had pancreas cancer but that didn't survive that long, what we found is that these patients, when they develop their tumors, their tumors are infiltrated by many more immune cells. So specifically, a type of immune cell called a T cell, which protects the body against viruses and cancer. So these patients' tumors, they have about 12 times more T cells.

• 45:21Kara Swisher?

  That show up here.

• 45:22Speaker 02

  That show up in the tumor compared to other patients.

• 45:26Kara Swisher?

  Looking to attack the cancer.

• 45:27Speaker 02

  Exactly. So this led us to this question, oh, these T cells are seeing something. What are they seeing? Because if we could find out how they are able to potentially recognize these patients' cancer as foreign, maybe we can teach other patients' T cells to recognize their cancers in a manner very similar.

• 45:45Kara Swisher?

  So what's the chief challenges in using vaccines to attack cancer cells?

• 45:49Speaker 02

  One challenge is what we've been talking about here, which is, well, what do you put in it? The antigen, meaning what do you encode in the vaccine that can allow the immune system to recognize?

• 46:03Kara Swisher?

  To take instructions.

• 46:04Speaker 02

  Yeah, the instructions, the code. So here, what we found was in pancreas cancer, in fact, it is, these red flags, these code, the codes really are derived from mutations. And this was a bit surprising to the community, I think, because pancreas cancer is a cancer which generally has very few of these mutations. So the thinking had been that, oh, it has too few mutations, therefore, a vaccine perhaps may not be possible because there's just no, there's no instructions there. So the immune system would not really be able to see pancreas cancer as foreign because the mutations just don't arise.

• 46:46Kara Swisher?

  But they are there.

• 46:47Speaker 02

  But they're there, right. You just need to find the right ones. And then what we found was that these mutations were, in fact, individual to each person's cancer. So the instructions.

• 46:58Kara Swisher?

  Have to be different for each person.

• 47:00Speaker 02

  Are different for each person's cancer. So this would require individualized vaccines.

• 47:05Kara Swisher?

  Right.

• 47:06Speaker 02

  And this is where mRNA comes in, because in 2000, this is in 2017, well before the pandemic, we felt. That the best technology for this rapid custom cancer vaccination that clinic was to use RNA.

• 47:18Kara Swisher?

  Yes, exactly. And mRNA, M stands for messenger, for people who don't know. So the idea among cancer doctors was this isn't, a vaccine doesn't going to work for this cancer, even if it worked for an infection, that this, this couldn't happen because there's no message to send essentially.

• 47:37Speaker 02

  Right.

• 47:37Kara Swisher?

  Correct.

• 47:37Speaker 02

  Cancer vaccines are hard as it is. They haven't even worked for cancers where we know the immune system can recognize it really well, such as, for example, melanoma or lung. So why would it even work in pancreas cancer when it is the toughest of all cancers?

• 47:56Kara Swisher?

  Right.

• 47:57Speaker 02

  We don't actually think the immune system can actually even see it as foreign.

• 48:00Kara Swisher?

  Right, exactly.

• 48:01Speaker 02

  This would be the last place that this is going to work.

• 48:03Kara Swisher?

  So, explain for people who don't understand how a cancer vaccine is different from, say, a flu vaccine, which is infectious, or an HPV vaccine to prevent cervical cancer. Explain the difference of what's happening there.

• 48:16Speaker 02

  I think this is a important point because we use the term vaccines for both infectious disease vaccines and cancer vaccines, but there are some important differences. Number one, for infectious disease vaccines, for influenza, flu, COVID, these vaccines are given to patients who are healthy.

• 48:38Kara Swisher?

  Mm-hmm.

• 48:39Speaker 02

  So it is given to healthy people to prevent future disease. For cancer, nearly all cancer vaccines are given to patients who have cancer.

• 48:52Kara Swisher?

  Cancer.

• 48:52Speaker 02

  As a therapy.

• 48:53Kara Swisher?

  Versus a...

• 48:54Speaker 02

  Versus prevention.

• 48:56Kara Swisher?

  Prophylactic. So, could you, could you use it as a prophylactic? Could you put it into people so they, so the cancer doesn't develop ever?

• 49:05Speaker 02

  This would be the holy grail in the future that we're all sort of trying to work towards. We think to get there, we need to understand how to do it.

• 49:14Kara Swisher?

  When, when you're going in.

• 49:15Speaker 02

  When you already have it.

• 49:17Kara Swisher?

  Right.

• 49:17Speaker 02

  Right. And this will give us instructions on how to perhaps take it to prophylaxis.

• 49:20Kara Swisher?

  So could you explain the difference for people to understand how this vaccine works and specifically how mRNA technology comes into play?

• 49:29Speaker 02

  So what we had learned from our work is that these vaccines for pancreas cancer, we hypothesized, we thought that you would have to make them individually for each patient's tumor because the instructions were encoded individually in each patient's tumor. So the way in this clinical trial that we ran in pancreas cancer here at Sloan Kettering in New York is that we perform surgery to remove the tumors. And then within 72 hours, we ship the tumors to our colleagues in Germany. And they do the genetic analysis of the tumor. They find the instructions and then they encode the instructions into messenger RNA

• 50:11Speaker 02

  or mRNA and make an individualized or bespoke vaccine.

• 50:17Kara Swisher?

  That's specific to this person.

• 50:19Speaker 02

  Specific for this individual.

• 50:21Kara Swisher?

  And it has to be, there aren't commonalities between these, correct? Is that at this moment?

• 50:26Speaker 02

  Yes. Well, in this trial, we tested it from a personalized fashion. There are other clinical trials that are also testing the question that you're asking, meaning do you have to do this individualization?

• 50:41Kara Swisher?

  For each person, right.

• 50:42Speaker 02

  Right. We don't actually know the answer, whether one is better than the other, but we will find out in upcoming years.

• 50:48Kara Swisher?

  So talk about the other tech that's being used. And for example, what role AI is playing or anything, anything else? What is the tech that is used in this, in mRNA technology?

• 51:00Speaker 02

  So you were asking earlier about why, why is there so much excitement about mRNA? And I think one of, one reason is, number one, when you have to do an individualized vaccine, you need a platform that can go from sequence to drug really fast. We're talking weeks. The mRNA technology allows us to go very, very quickly. So that's one advantage. And this is a contrast from, from other technologies that we have used in the past, which took much longer.

• 51:34Kara Swisher?

  But you have to cook essentially.

• 51:36Speaker 02

  Yeah. The second thing is that we think the technology is very potent, meaning.

• 51:44Speaker 02

  Not only can it make a fast vaccine, it is makes a very, very strong immune response against cancers which have been historically considered really tough to make an immune response against, like pancreas cancer. So in our trial, what we found is that when we give these vaccines, it makes an enormous amount of T cells in the peripheral blood. And not only can you make a really strong immune response, these cells last for, we think, perhaps even years to decades in patients.

• 52:20Kara Swisher?

  And, and you, you use AI how in this?

• 52:22Speaker 02

  Right, so the, the, the front end of it was where we do the genetic analysis and we find the red flags and we decide which red flags have to go into the instructions. This science is not fully matured yet. And this is where AI comes in, we think, because we think there are patterns of the best instructions for different cancer types, perhaps. So by learning more and more of what these patterns look like, we can then sort of go to an automated, best case selection of the targets here, the instructions, and be able to make.

• 52:59Kara Swisher?

  And it would see things you wouldn't see as quickly, essentially, if at all.

• 53:02Speaker 02

  That's right.

• 53:03Kara Swisher?

  If, if at all. As you said, you've been running a trial of a small patient group, just 16 people of an mRNA-based pancreatic cancer vaccine that's showing promise. Back in April, Memorial St. Kettering announced that eight of, uh, eight patients whose immune system responded to the vaccine, seven, nearly 90%, were still alive four to six years after the surgery. Talk about the significance of that, because before there'd be an outlier, right? This is a lot of outliers, all of a sudden. And what happens next in testing the treatment after that?

• 53:35Speaker 02

  It was what we call a phase one clinical trial, where the purpose of the trial is really to understand whether the drug is safe, whether you can make it in time and deliver it to patients, and whether it does what we think. It should do, which is make a good immune response. And it wasn't really specifically designed to understand whether the drug can make people live longer. Because this requires what we call a randomized trial where some patients get the drug, some patients don't get the drug. However, in this trial, what we found was a sort of a stark dichotomy, namely, if you

• 54:20Speaker 02

  made an immune response, most patients lived. And if you didn't make an immune response, most patients died. And it was perhaps very close to black and white, as you might get in a trial. So I think that, like you said, was a bit striking to us in a very unexpected way, that perhaps these vaccines could be quite important in preventing pancreas cancers from coming back after surgery.

• 54:49Kara Swisher?

  Does this have implications of other cancers? And is it that if you can solve this one, I know every cancer is different, I'm aware of that, but why is this the cancer you wanted to make? It to show the most vexing cancer of the treatment cancer? Or does it have implications for the others?

• 55:06Speaker 02

  So our idea here was if we could crack the toughest here, perhaps this would provide a blueprint to crack the rest. And we're excited now to see that there's lots of clinical trials now using these concepts or testing these concepts.

• 55:22Kara Swisher?

  Breast cancer or colon cancers.

• 55:25Speaker 02

  Right.

• 55:25Kara Swisher?

  You explained mRNA piece of this, but the technology itself is under attack. Health and Human Services Secretary RFK Jr. recently pulled back a half a billion dollars in funding for mRNA vaccines. Talk a little bit about how, where you're doing this groundbreaking technology, which everyone's very excited about, you're operating in an environment that's been hostile to it. Now, it may not last. Look, these things have happened before, but it's not the greatest time to have these incredible breakthroughs at a time when the hostility towards even a basic flu vaccine is at an all time high.

• 55:59Speaker 02

  Yeah, I mean, I think the current moment that we are in, particularly for cancer vaccines, is a really, really exciting moment because perhaps we now know, after many decades of study, how to make an effective cancer vaccine, or one of the toughest of cancers, pancreas cancer. And what that unlocks is, well, what other cancers could the technology be used for?

• 56:30Kara Swisher?

  Exactly.

• 56:30Speaker 02

  And for us to go there, we need broad scale testing of these drugs in patients with more deadly cancers like pancreas cancer. And it's been exciting to see that actually the National Cancer Institute has launched a national cancer vaccine plan. This is a public-private partnership to be able to develop a national cancer vaccine roadmap to allow and enable this testing.

• 57:01Kara Swisher?

  But what has happened on the government level is this had an impact. A lot of mRNA researchers I talked to said it set us back decades in terms of different things they were working on. I was up at Johns Hopkins, I was at Penn, and all of them have the same. This government attack on mRNA technology has to stop at this, at this point because you're at the cusp of these breakthroughs.

• 57:25Speaker 02

  Right. I mean, I think you're bringing up the point that, well, we want the government to be able to actually invest in it. Invest in it so that we can expand into broader testing. And it's been exciting to see that they are investing in it now.

• 57:40Kara Swisher?

  What would you like from the government more to do this? What would you, or from private companies? Because other countries are also working on these things, China in particular, for example.

• 57:51Speaker 02

  It's essentially what we were just talking about, like what do we actually need at this moment in time? And I think what we really need is broad scale testing in clinical trials across the country. To answer the questions of, well, what other cancers could be vaccine suited? These would all require, we think, not just the federal government, but we also need really cross-sector support from all of the sectors, public, private, industry, philanthropy, academia, federal government. This is a moment where everyone has to come together.

• 58:30Kara Swisher?

  Right.

• 58:30Speaker 02

  To be able to try to really invest and tackle these questions as, as a collective team.

• 58:35Kara Swisher?

  So, final question for you. You said once in an interview that you like solving problems that have a definitive answer, math problems, physics problems. When you think about that, you're picking something that. People did not think had a definitive answer. And you firmly believe that this is a solvable problem.

• 58:52Speaker 02

  For pancreas cancer, you do.

• 58:54Kara Swisher?

  Mm hmm.

• 58:54Speaker 02

  I think it is solvable, yes. And in fact, I think perhaps maybe even in our lifetime, we're going to see major solutions for this cancer, which would be a huge change because over the past five decades plus, we have not really seen much change. But change is, I think, upon us now.

• 59:18Kara Swisher?

  Absolutely. I'm going to ask you one actual final question. Hundred years from now, what is the treatment? From you just, you're not going to be here. I'm not going to be here. Just be creative.

• 59:29Speaker 02

  Right now, one in three Americans will have cancer in their lifetime. And so it is a huge, huge national and global health crisis. But hundred years from now, I hope we will be in a society where the cancer does not exist.

• 59:44Kara Swisher?

  Yeah, yeah. Well, we'll see. We'll see about that. But that would be a great way to to end it. Anyway, thank you so much, Vinod. I really appreciate it. And congratulations on these these breakthroughs you've had. They are exciting people, very much so, which is great.

• 59:58Speaker 02

  Thank you, Kara, for having me.

• 1:00:07Kara Swisher?

  Today's show was produced by Tracy Hunt, Emma McNamara, and Dave Shaw. Nishat Kurwah is Vox Media's executive producer of podcasts. Our engineers are Jim Mackel and Steve Bone. And our theme music is by Trackademics. If you're already following the show, you're about to achieve longevity escape velocity. If not, you're stuck with the rest of us mortals. Go wherever you listen to podcasts, search for On with Kara Swisher and hit follow. Thanks for listening to On with Kara Swisher from Podium Media, New York Magazine, the Vox Media Podcast Network, and us. We'll be back on Monday.

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