Pod Insights StarTalk Podcast Medicine 3.0: Extending Human Lifespan with Dr. Peter Attia About this episode What’s the maximum human lifespan? Neil deGrasse Tyson and co-hosts Chuck Nice and Gary O’Reilly explore how to extend your longevity, the history of medicine, and how we can live better with author of Outlive: The Science & Art of Longevity, Dr. Peter Attia.
Transcript 10,070 words · 4 speakers
Speaker names marked ? are inferred from speaking time and the show’s known hosts — they are not voice-verified.
0:02 Neil deGrasse Tyson? Welcome to StarTalk, your place in the universe where science and pop culture collide. StarTalk begins right now.
0:14 Neil deGrasse Tyson? This is StarTalk Sports Edition. I'm your host Neil deGrasse Tyson, your personal astrophysicist. Got with me my co-host Gary, Gary Riley. How are you, man? Hey Neil, I'm good. All right, all right. When he's not otherwise announcing soccer, he is with us here on StarTalk. Former soccer pro, always good to have you there Gary. And of course Chuck Nice, Jack. Hey, former nothing. Former nothing, okay, that's why we have you. That's why you got me. That's why I'm available, former nothing. That's why you always, every time we call you, you're there, all right. For today's topic, we're thinking about human longevity and is it a good thing?
0:59 Neil deGrasse Tyson? What does it mean to live to 200 if you have a 200-year-old body, for example? So, we're gonna get to the bottom of that and with the obvious connections to how long can someone be at the top of their game athletically, just as an example? And so Gary, what have you put together for today's show?
1:19 Speaker 01 Let's meet our guest, Dr. Peter Attia, Stanford University School of Medicine, trained at Johns Hopkins in general surgery for five years. Founder of Early Medical, a practice that applies medicine 3.0, which we will be getting into shortly. Host of the podcast The Drive, author of Outlive: The Science of Longevity, and you'll love this one, once planned to take a PhD in aerospace engineering, so nerd alert.
1:46 Neil deGrasse Tyson? But he didn't?
1:47 Speaker 01 Uh, well, ask him, he may have done it.
1:51 Neil deGrasse Tyson? All right, the whole show, I'm gonna have to get on his case for not getting the PhD in aerospace engineering.
1:57 Speaker 01 But he may have it tucked up his sleeve somewhere, he's not wearing it.
2:00 Chuck Nice? He's a veritable Ponce de Leon, and you're talking about aerospace? Scott's teaching us to live forever.
2:07 Neil deGrasse Tyson? Good, very good point, and we all have to remember who Ponce de Leon is. The reference there, but yes, he's a Spanish explorer who went searching for the Fountain of Youth. And the reason why I know that is because I wrote a book report on him when I was in fifth grade, and so, you have it, okay?
2:25 Speaker 01 There you go.
2:27 Neil deGrasse Tyson? So Peter, welcome to StarTalk.
2:29 Speaker 03 Thanks for having me, guys.
2:30 Neil deGrasse Tyson? So Peter, is our human body really built, have the capacity to last longer than we are right now? And I ask, you know, it's a really obvious question, and it's not clear how obvious the answer will be, because I know we are living twice as long as we were 150 years ago or so, and we're living longer than, at least in heartbeats, than any other mammals on Earth. So we're doing something right, and you're thinking we could just keep at this?
3:05 Speaker 03 Yeah, I mean, I do think there is a limit to human lifespan. Where we are in relation to that limit, I don't think anybody knows, and I certainly don't think it's significantly longer than where we are. In other words, you know, when people talk about, oh, we're all gonna live to 200, or kids born today are gonna, you know, be effectively immortal, I just have a very hard time believing that. And of course, there's nothing that's black and white in science.
3:31 Neil deGrasse Tyson? Wait, wait, Peter, you're trying to sell a book called longevity. Could you say nicer things about living longer? We want to help you sell the book, Peter.
3:40 Chuck Nice? Yeah, exactly.
3:42 Speaker 03 Yeah, so remember longevity has two pieces to it. And you kind of alluded to this at the outset, right? But one of them is the lifespan piece. And that's the easier one for people to think about because it's binary. You're either alive or you're dead. You're respiring or you're not. But an equally important part of this, if not, I think more important, is the health span piece. And that that part's analog. And I think that's the part that is, you know, much more subject to the individual's views on the quality of their own life. And two people can have a very different set of metrics for what constitutes quality of life there. I think what's abundantly clear is that while our length of life has indeed doubled, as you stated, Neil, from about 40 to 80 since 1900,
4:24 Speaker 03 it's not clear that that has come with a doubling in the quality of life. So we've basically traded one set of problems for another. We've we've effectively solved the problem for the most part of acute death, largely brought on by infectious diseases and trauma.
4:40 Chuck Nice? Right.
4:41 Speaker 03 And we've shifted that over to chronic death, for which we don't actually have a great solution at this time.
4:48 Chuck Nice? Yeah.
4:49 Neil deGrasse Tyson? Ooh, chronic. So just to be clear about language here. So acute death would be you're alive one minute and you drop dead the next. And and and chronic death is you there's some long disease that puts you in the hospital for some time and then you die. Is that what you mean by those?
5:04 Speaker 03 Yeah, I mean, so so when you think of chronic diseases, you you think of what I kind of talk about as the four horsemen of disease, the atherosclerotic diseases, so heart disease, stroke, cancer, neurodegenerative disease such as Alzheimer's and Parkinson's. And then, of course, the whole cluster of metabolic diseases around type 2 diabetes, such as nonalcoholic fatty liver disease and insulin resistance, et cetera. Those things percolate for years and in some cases decades. And even when someone dies suddenly, for example, a person drops dead of a heart attack, that process was brewing inside their coronary arteries for decades.
5:39 Chuck Nice? You know, but didn't isn't it true that people didn't get a chance to experience chronic death? Uh, as short as maybe a hundred years ago. And that's because often, uh, external, uh, of forces intervened and, and, and affected life. You're talking about pandemic, something we just went through. You're, you're talking about all kinds of infectious diseases and, uh, and then also, uh, something as simple as breaking a hip or an arm. You, you die of an infection, like, you know, crap that we take for granted now killed everybody back in the day.
6:16 Speaker 03 That's exactly right.
6:17 Neil deGrasse Tyson? But I think that's what he's, he just said, Chuck. But the point is, but, but to Chuck's point, it's not that these are new problems that you cite, these chronic diseases. It's that we didn't live long enough to
6:29 Chuck Nice? We never got to them.
6:30 Neil deGrasse Tyson? Have them show up on
6:31 Speaker 03 Well, I would say, I would say there's, there's two things there. So everything you said is right, Chuck, that we, we basically, you know, didn't earn the right to die of chronic diseases back then because we didn't live long enough on average to have them. However, I think there's plenty of evidence that our current environment, while remarkable in many ways, right? Modernity has brought great things. With it, it's come at a cost. And the cost has been we eat too much, we don't exercise enough, we don't sleep enough, we're under too much chronic stress. And those things, I would argue, are also exacerbating the problem. So we have this ability to live longer and, uh, be more exposed to these things that therefore render us more susceptible to chronic disease.
7:14 Speaker 01 Doctor, are you suggesting that current medical science has been looking for the answers in the wrong places? Like treating symptoms and conditions rather than looking at the early identification and therefore preden- prediction and prevention? So is, is this, is this what you're calling medicine 3.0? Because that's a new terminology.
7:34 Speaker 03 No, what I'm, that's, that's what I'm calling medicine 2.0. So medicine 2.0 was a really successful playbook for treating the problems that were killing us. Basically for all of human history. And there are basically two huge things that catapulted us from medicine 1.0, which was basically kind of witchcraft and voodoo medicine into medicine 2.0. So the first is sort of Francis Bacon coming along in the late 17th century or mid 17th century, effectively coming up with a new frame of thinking about science. Right? So we collectively can sit here on this podcast today and take for granted something called the scientific method, which is that you, I don't need to state this to you guys,
8:18 Speaker 03 but you make an observation, right? You observe something in the natural world, you make an observation, you formulate a hypothesis, you design an experiment to test that hypothesis, you measure the results of the experiment against the prediction of the hypothesis and you correct. And we iterate and iterate and iterate. Well, people who are in science today take that for granted. There was a day that was as foreign to the world as an airplane was. So call that step one. Step two was more technical and it was basically the development of the light microscope. Those two things, separated by a couple hundred years, effectively allowed us a window into a world that then allowed us to create therapies, namely antimicrobial therapies and vaccines that allowed us to basically eradicate, for the most part, communicable diseases, infectious diseases.
9:03 Chuck Nice? Not in my child, not in my child, doctor. You keep your vaccines to yourself, okay? Trying to mind control my kid. You're not gonna mind control my kid. I'm telling you right now, pushing, you keep your politics to yourself.
9:20 Neil deGrasse Tyson? No, no, his vaccines don't have microchips in them.
9:22 Speaker 03 The polio vaccine had no microchips.
9:24 Neil deGrasse Tyson? Okay, I'm sorry, okay.
9:25 Speaker 03 So that playbook worked very well. The problem is the systems that were required for that system to work, for example, the randomized control trial. Don't work very well in treating cancer or preventing cancer or in preventing cardiovascular disease because of many factors that we don't have to get into now, but among them, the chronicity of those diseases and the time course and the complexity of the interventions used to prevent them. You see, it's really easy to do a randomized controlled trial in humans when the intervention is take this pill versus take this placebo. That works pretty well. Imagine I said, listen, guys, we're going to do an experiment where the next 30 years, these people need to eat exactly this way. These people need to eat exactly
10:08 Speaker 03 this people this way. These people need to exercise exactly this way. And then in 30 years, let's see how things are going. I mean, that experiment can't be done for so many reasons that it's not worth going into them. And therefore, we're stuck.
10:20 Chuck Nice? I think you just brought up something that is so important for people to understand. And I think we're saying it like a throwaway, which is, you know, your RCT. And RCT really revolutionized. That was kind of like a medical revolution. Because I think what people forget is that a lot of times, no matter how you get sick, your body sometimes will recover. A lot of times will recover. So there was a time where they were just like, eat some dirt. And then you would recover. And then they'd be like, see, dirt is the answer. So I mean, maybe you What does RCT mean?
10:56 Speaker 03 Randomized controlled trial. And I'm glad you brought that up, Chuck, because we are throwing that around without giving it its due course, which is, again, that's a big part of the scientific method. Randomization is essential to eliminate bias and to eliminate confounding and to determine causality. So causality is such an important thing in science. And without those tools, it's very difficult to establish causality. And that's why medicine 1.0 was all about bad humors, right? Elixirs, nonsense.
11:30 Chuck Nice? I know all about bad humor.
11:36 Neil deGrasse Tyson? Hey. Chuck, you're occasionally good for good humor.
11:39 Chuck Nice? Okay, thank you, Neil.
11:41 Neil deGrasse Tyson? Wait, wait, wait. So Peter, so what you're saying is, in modern times, since those experiments you described are not executable for many reasons, including, at some level, just the ethics of what it is to force someone in their life to do something that you think might give them cancer, but now you want to see if it actually does. So we're left with finding isolated populations in the world that might have those habits just as a matter of their culture, their religion, or their traditions. Is that...
12:11 Speaker 03 Yeah.
12:12 Neil deGrasse Tyson? And it should be able to work as well, right?
12:14 Speaker 03 Well, but not by itself, right? Because it still can't establish causality. So we still have this problem of, we have to get away from the gold standard and instead rely on a whole bunch of imperfect things and make inferences based on a lot of imperfect things. So, yes, we would still rely on epidemiology. Let's remember something. The relationship between cigarettes and lung cancer was never established using an RCT.
12:41 Chuck Nice? Right.
12:41 Speaker 03 It was established using epidemiology. But the epidemiology was so compelling there that we are very confident in establishing causality and making bold claims, policy-wise and medically, about those things.
12:54 Chuck Nice? We had a huge sample, too, you gotta remember, because frickin' everybody in the world smoked back then.
13:01 Speaker 03 Well, it's the sample size was less the issue. It's the magnitude of the hazard ratio and the dose response that probably played a greater role. In other words, it was the ability... So first of all, the hazard ratio was like 10, right? This is a log more than the hazard ratios we see with things like, you know, eating this food versus eating that food, where your hazard ratio is like 1.17 or something like that. And then you had the dose effect. So the more you smoked, the more likely you were. So there's this guy named Austin Bradford Hill, who was kind of the godfather of the statistical methods utilized to establish and understand RCTs. And he proposed these nine, basically, checks that you would run through your epidemiologic observations. And the more of those checks you had,
13:46 Speaker 03 the more confident you could be that causality was, in fact, underneath this correlation.
13:51 Chuck Nice? Cool. That's... that's cool.
13:54 Speaker 01 So doctor, the phrase "people get sick," right? Are we saying now that's the wrong way to look at it? The person gets sick, and I need to know that person because it's that person I'm treating. So therefore, I have to really have an intimate knowledge of that person because they might be presenting the same symptoms as the person in the bed next to them, but one's bacterial, one's viral. So the treatment for both is the same, one of them's not gonna cure, one's not gonna get better. So we need to have, is that what you're saying? We need to have that specific knowledge to treat that person?
14:27 Speaker 03 Yeah, this is the next layer. This is now how we have to get to medicine 3.0 because what you've highlighted is a very important point that also gets lost in the culture of only the RCT is valuable. Keep in mind, the RCT takes a whole bunch of people who are heterogeneous.
14:45 Speaker 01 Right.
14:46 Speaker 03 And it finds the average outcome. So it spits out homogeneous from heterogeneous. And to your point, at the end of the day, any physician who's taking care of a human being will tell you that you can have exactly the situation you're having. And by the way, I'll go one step further. It's not just, well, these two are both sick, but it turns out one's viral and one's bacterial. It's like, no, no, no. These two people are having the exact same heart attack, or these two people have the exact same cancer, but there might be different factors about them that will make one susceptible to a treatment while the other is not.
15:18 Chuck Nice? Well, that's what's happening right now with genetics and cancer treatment right now, you know? So, wow.
15:26 Neil deGrasse Tyson? Well, wait, but all right, but getting back to the theme of this program, you're, all right, so suppose we do cure all that. At the end of the day, we live longer because we're not dying from those disease, but we're still getting older, right? And so is there a limit beyond susceptibility to disease that you think we will still confront? Is there another wave of things we will hit when we all live to 150? Oh my gosh, look what we're dying of now, all right? Because we got to live that long. Is this in our future?
16:05 Speaker 03 This is actually a pretty interesting debate within the aging community because what you're really asking, and I think it is the jugular question, is do we take a
16:16 Neil deGrasse Tyson? I love your medical analogy.
16:18 Chuck Nice? The jugular question, damn, that question just slipped my damn throat.
16:24 Chuck Nice? That's a dangerous question.
16:27 Neil deGrasse Tyson? Damn, okay. I'm loving, I love the extra vocabulary here. Okay, go on.
16:32 Speaker 03 So, independent of disease, what is aging? Now, there are these nine hallmarks of aging that, you know, obviously play a role in disease. So let's take one of them, for example, genomic instability. There's no mystery here that the older we get, the more we accumulate genetic mutations. Well, that directly feeds into at least one of the four horsemen, right? Cancer is fed by that. In fact, that's the sine qua non of cancer, right? Cancer arises when cells acquire somatic mutations, and those mutations produce a phenotype, meaning they produce a cell whose properties are two things.
17:13 Speaker 03 One, it no longer responds to cell cycle signaling, so it will grow in an unregulated manner. And two, it has the capacity to leave its site of origin.
17:21 Chuck Nice? So let me, just as a regular person, see if I understood what you just said there, because that was, that was a lot.
17:28 Speaker 03 There's nothing regular about you, but please continue.
17:30 Chuck Nice? But did you, did you just say, because this, and if I'm wrong, I'm wrong, I don't care. I'm just telling you what I heard, that cancer basically is already in you, but what happens is you're making a replica of yourself over the years. It gets to a point where you're replicating those cells, but they no longer, they kind of say, ah, I'm gonna break the rules. I don't care about the rules. I'm not going to generate or regenerate the way I should. So as a matter of fact, forget it. I'm gonna have a party, and I'm just, I'm gonna regenerate like crazy.
18:01 Speaker 03 Okay.
18:01 Chuck Nice? And, you know, and so basically, that's cancer.
18:05 Speaker 03 Yeah, think about it. If you, if a person gets colon cancer, like I'll just pick that because it's the third leading cause of cancer death, that grows out of colon cells that are in your body. And those are cells that have to reproduce constantly, because you're constantly sloughing off cells in your colon.
18:19 Chuck Nice? Wow.
18:20 Speaker 03 But the problem is, if one of those cells acquires a set of mutations that basically makes it deaf to the signals that tell them when to grow and when to stop, and acquires mutations that allows it to leave the colon and go somewhere else, all of a sudden, it grows and grows and grows, and everybody around is saying, hey dude, you gotta stop, you gotta stop, you gotta stop. He's like, I don't hear you, I don't hear you. I'm just gonna keep growing. And oh, by the way, I can leave and go to the liver and take up residence there. That's what's gonna kill you.
18:48 Chuck Nice? Look at that. Shoot.
18:50 Speaker 03 But let me go back to Neil's question, right? So you asked a question, Neil, well, what if you somehow figure out a way to cure all cancers? And what if you somehow figure out a way to cure heart disease? And what if you somehow figure out a way to not get Alzheimer's disease? Will we still age? And I think the answer is yes, right? I still think there are enough of these other processes that are going on where, for example, our mitochondria, which are the little, you know, energy-producing organelles of our cells, become less and less effective. And that will, for example, mean you are weaker, you have less energy, even absent a quote-unquote "disease." So I don't know, truthfully, which side of this debate I come down on, right?
19:32 Speaker 03 Is aging necessarily an implication of disease? Or is there an aged phenotype absent disease? I probably lean more towards that side of the philosophical debate, though.
19:42 Chuck Nice? Oh, now you just made me think of this. What happens? They say whatever doesn't kill you makes you stronger. Is it possible that it's just the opposite? That you get a disease, that disease makes you weaker? And then later on in life, you're actually weaker? Because it just weakened you? And now something else has come to attack you? And, you know, and that makes you, you know?
20:03 Speaker 03 I mean, I think there are examples of both, right? So the process you're describing in the first part of that statement is what we call hormesis, right? What doesn't kill you makes you stronger. So again, to bring it back to your favorite subject of vaccination, vaccination is a form of hormesis. We introduce a small amount of the virus. Sometimes we would disable it or whatever in the traditional sense. Let's ignore the mRNA vaccine. So we would give you kind of a deactivated or weakened virus or attenuated in some way. It makes you a little sick, right? But your body rises to that occasion. It develops a huge memory response to it. And the next time that virus shows up, you're ready to pounce it. Exercise is probably my favorite form of hormesis. In the short term, exercise does everything wrong to your body. It raises your heart rate, it raises your blood pressure,
20:47 Speaker 03 it lowers your heart rate variability, it induces stress hormones. Everything about exercise while you're exercising is unhealthy.
20:53 Neil deGrasse Tyson? It damages your muscles, right?
20:54 Speaker 03 Sure, yeah, it tears down muscle fibers. It's what your body... So if you're exercising for two hours a day, that two hours isn't what's making you healthy. What's making you healthy is the other 22 hours of the day when your body responds to that, adapts to that, and gets stronger as a result of that.
21:09 Chuck Nice? Hormesis.
21:10 Neil deGrasse Tyson? We've got to take a quick break. When we come back, we're going to see what role sleep plays in our health and longevity. And... What else we might have control over to live the life we hope we want to lead as we get older on StarTalk.
21:42 Neil deGrasse Tyson? We're back, StarTalk, with Dr. Peter Attia, who is an expert on aging and longevity, a medical doctor, and he's written a book. And Peter, tell us the title of that book, the full title.
21:58 Speaker 03 Outlive: The Science and Art of Longevity.
22:01 Neil deGrasse Tyson? I love it, I love it. And of course, you're the host of the popular podcast, The Drive. And so, let me just lead off, something, a point I wanted to make earlier. There are people who don't fully embrace or understand the statistics of disease. So for example, if the press reports cancer rates are up relative to 50 years ago, how often is it that they're up because people are simply living longer and then have that susceptibility for having lived longer? So therefore, they shouldn't start wondering what's happening in their environment that could be giving them cancer?
22:41 Speaker 03 Yeah, it really comes down to how those things are reported. So as you know, there's, one way to think about this is through the lens of incidence, and another way is through the lens of prevalence. So, and then on top of that, so I think a better example, Neil, might actually be Alzheimer's disease, because that's the most clearly associated with aging. So, we would say that today, both the incidence and prevalence of Alzheimer's disease is significantly higher than it was, say, 50 years ago. And now the question becomes, what are the confounders there? Well, one really big confounder is not just that we're living a bit longer now, it's that we are much better in our diagnostic acumen.
23:23 Speaker 03 So, what would have been Alzheimer's disease 50 years ago was, mom's a little loopy and it's sort of, you know, she's a bit senile. Whereas now, we have diagnostic tools to make that distinction more clearly. That said...
23:38 Speaker 03 In every treatment that I've looked at, especially with respect to Alzheimer's disease, the incidence is indeed increasing, even when adjusted for age. So it does suggest that we are actually getting a little less healthy. But because medicine is also getting better, we're kind of stretching out extra years of life, albeit at probably a lower quality. So our lifespan, and to put it in the speak of what we discussed in the last segment, our lifespan is incrementally getting longer, while our health span is eroding, at least by my definition. Now, some people have a different definition of health span that is more, you know, frankly,
24:21 Speaker 03 I think not strenuous enough, which says it's the time of life you are free from disability and disease. I think that's a pretty useless definition, truthfully. I think we want to be more particular about cognitive and physical capacity.
24:34 Speaker 01 Doctor, we're going to jump into the neurodegenerative process and diseases because you cite that as one of the four horsemen of disease in your book.
24:43 Speaker 03 Wait, wait, wait, but we left off right at the end of the second segment, where he's talking about exercise being the best thing. So if I do my ab crunches or whatever, you know, and or my planks and I pump some iron and I, you know, run the track, I still don't live to 150.
25:03 Speaker 01 No.
25:04 Speaker 03 So what's up with that?
25:05 Chuck Nice? But it doesn't make a difference because I look, I look, I look amazing.
25:10 Speaker 01 Are you happy now? You feel better for that?
25:15 Speaker 03 Yes. You look good on the beach. Yes, okay. But exercise, I would argue, makes a bigger difference than any other intervention we have. So you have these interventions, like whether it be, you know, the right nutrition, exercise, sleep, etc. But the data would suggest that exercise has a bigger impact on your longevity than anything else. And the, you know, the two metrics that we have that are probably most rigorous to measure that is strength and cardiorespiratory fitness, peak cardiorespiratory fitness, something measured by VO2 max. Gary, you must have had a VO2 max back, the test done back in the day.
25:53 Speaker 01 We chiseled that on the side of the cave back in my day. It was just really prehistoric.
26:01 Speaker 03 Well, it, look, it's a test anybody could go and do, right? So y'all could go do this next week.
26:06 Speaker 01 So the thing is, doctor, I mean, as much as I do know, we have these, and you mentioned these guys before in the, in segment one, the mitochondria, because they're our little powerhouses, as far as I can see in my layman's terminology. But do they not diminish in terms of number and efficiency as we get older? And exercising, as you just, Neil just pointed out, you know, do my abs, pump my iron, run the track, but that doesn't help as much. So there has to be a way to exercise for efficiency.
26:41 Speaker 03 Well, it does, it does, though. Exercise, exercise does indeed improve mitochondrial efficiency, but it has to be the right kind of exercise. So for example, if that's your specific aim, you have to do it correctly. So a silly example would be if you tell me your objective is to have bigger biceps, it doesn't really matter if you do all the leg extensions in the world. And similarly, if you're telling me, as you should be, that you want to target mitochondrial efficiency, and I would argue we should, then you have to train in a way that targets that. And the way to do that is a type of training called zone two training. So zone two training is aerobic steady state activity that is
27:23 Speaker 03 right at the threshold of lactate production at the mitochondria. Now, for people who don't want to do what I like to do, which is actually measure lactate production while exercising, a very simple heuristic for doing this.
27:37 Speaker 03 Is assessing your perceived exertion during exercise and making sure you're at the following threshold, you are able to speak, but you don't want to.
27:46 Neil deGrasse Tyson? Wait, wait, wait, wait, let's get the vocabulary. So we have lactose, which is sort of a milk sugar.
27:52 Speaker 03 No lactate.
27:53 Neil deGrasse Tyson? But then we think of lactate acid.
27:55 Speaker 03 Yeah, yeah, they're totally different.
27:56 Chuck Nice? Lactate, lactate acid.
27:57 Neil deGrasse Tyson? Look, please, so let's help Chuck out here.
27:59 Chuck Nice? Let's help.
28:00 Neil deGrasse Tyson? Let's help out Chuck. And when I think of the lactate acid buildup in muscles that can work back against you if you reach that zone and lactose, which is a milk sugar.
28:10 Speaker 03 Right, that's right. That's right. Yeah. So lactate is a byproduct of anaerobic metabolism, which is just another way of saying, when your muscles are demanding energy at a rate that can't be met purely through the much more efficient but slow burning process of utilizing oxygen, what's called aerobic metabolism, you turn to this other method, which has the benefit of giving you ATP or energy very quickly, but with a nasty side effect, which is it's also starting to accumulate lactate. And if you can't tolerate that lactate buildup, which most of us can't at a high enough level, your exercise becomes limited. Now, what you want to do is increase the capacity
28:52 Speaker 03 of your mitochondria to develop ATP, to produce ATP at the highest work capacity possible. And to do that, you have to train right at that threshold. And as I said, you can, you can do this in a very technical way, but you can get 80% of the value just by saying, look, I'm going to go, you know, walk on a steep incline on the treadmill and I'm going to titrate that incline and speed until I'm right at the point where if my wife comes in and talks to me, I can talk with her a little, but I just don't want to. If you can't talk at all, you're beyond that. You're actually into too much lactate production and you're not going to get that training adaptation. And if you're too far below that, if it's actually easy to have a discussion, then you're not training hard enough.
29:36 Speaker 03 So that's a very specific example where you use exercise in a very targeted way to train a very specific adaptation.
29:44 Chuck Nice? So what is it then that there's so much around this HIIT training, this high intensity training? So that it's like, kind of like what you say, except you do exceed the threshold, but only for short bursts and then rest, recover, do it again. What's the difference there?
30:05 Speaker 03 Significant difference. There's nothing wrong with HIIT training, but it really comes out of a sort of human condition of looking for the minimum effective dose for everything. So if someone says, "Look, I've only got 30 minutes a week that I'm willing to exercise. How can I make the best use of it?" Then yeah, you're probably, if you're truly going to draw that line in the sand and say, "I'm only willing to do 30 minutes a week," yeah, you're probably better off doing 10-minute short bursts of brutal activity three times a week.
30:36 Chuck Nice? Gotcha.
30:36 Speaker 03 What I'm saying is, let's put that caveat, or constraint, rather, aside, and say, "What's actually the best thing to be doing?" And the data would suggest probably at least three, if not four, hours a week of just that kind of steady-state cardio. And then we have to talk about the strength training and some of the higher-intensity stuff as well. And before you all say, "Who the hell has time for that?" I would argue, if you're in the business of trying to live longer and live as well as possible, you have to ask yourself the question, "What's more important?"
31:04 Chuck Nice? Wow.
31:05 Speaker 01 So, doctor, when your patients come to you and you explain the Zone 2 exercise and the benefits therein, why do you advise them to do the VO2 Max training as well? What is the synergy between the two of them that's so effective?
31:20 Neil deGrasse Tyson? Tell us what VO2 Max is.
31:22 Speaker 03 Sure, sure. So VO2 Max is this test that measures literally the maximum amount of oxygen your muscles can utilize. And to do that, you're strapped up to this mask and you're put into a very stressful situation, usually on a bike or a treadmill, and you are pushed until you fail. And during that period of time, these sensors, so there's an O2 sensor and a CO2 sensor on the mask, it will basically tell you, "This is the maximum amount of oxygen you were able to consume in liters per minute." So it's calculating something known as the ventilatory rate of oxygen consumption. And the bigger that number...
32:01 Neil deGrasse Tyson? That's what the V stands for, ventilatory?
32:03 Speaker 03 Yeah, the V is ventilatory, right. So VO2 Max is ventilatory rate of oxygen consumption. So it's technically V. O2 Max.
32:11 Speaker 03 And so the bigger that number, the fitter you are and the longer you live. In fact, there is no metric we have that is more correlated with lifespan than VO2 max.
32:24 Speaker 01 So, Doctor, if I don't live in a $50 million penthouse apartment and have a Peloton and have an elevator that goes up to my room.
32:34 Speaker 03 I don't think you need to live in that apartment anymore to have a Peloton.
32:37 Speaker 01 Yeah, right, nice. Thanks for the tip. Yeah, exactly. Exactly. What are we missing? Chuck, let's get busy. So the thing, the hidden thing is, I've got a bad knee, my hip plays me up. Stuff's not easy for me to do. This is why I don't live on the penthouse, because the elevator gets broken and I can't walk all those flights of stairs. So what are we trying to do? Because, you know what? Life takes a bite out of us. It doesn't allow us to be as perfectly fit as we once were or we'd like to be. So how are people working around these sort of impediments to get to where they need to be?
33:12 Neil deGrasse Tyson? Plus, I want to hear more about sleep, too, in this segment. So make sure that falls in here somehow.
33:16 Speaker 01 Yeah.
33:18 Speaker 03 So, look, I think one has to come up with ways to get the circulatory system moving. So if a person says, "Look, I can't walk on a treadmill or I can't climb stairs", then maybe they can get on a bike where there's less impact. Or if that doesn't work, maybe they can be in a pool or on a rowing machine. But unfortunately, this type of activity has to be done. And if injuries are preventing all of that, then those injuries have to be addressed. You know, that's, that is an important part of living longer is being free of pain. That factors in very heavily to my definition of health span at least, where freedom from pain is a pursuit.
33:56 Chuck Nice? Yeah. And most people do not follow up on injury. Most of us have received some type of injury in life, and then they don't follow up on the rehab for that injury properly. And then I just recently found out that no injury heals. It just, it just stops hurting until you're 49 years old.
34:22 Neil deGrasse Tyson? That how that works, Chuck?
34:23 Chuck Nice? It never, it did not heal. It just stopped hurting. And then all of a sudden, one day, you're like, why is this hurting again? And, uh, yeah, it's because you didn't do the rehab, you big dummy.
34:35 Neil deGrasse Tyson? So Chuck is writing a book, all the shit that happens to you when you turn 50.
34:40 Chuck Nice? It'll be out next year, people.
34:41 Speaker 01 So, all right, so, Doc, I used to have one coach who would say, the harder you work, the harder you have to rest. And for years, no one gave a damn, right? But now, you have got athletes wandering around with wrist ornaments that will tell their medical team how much sleep they got, the quality of sleep they had. Now, if it's good enough for elite athletes, it's surely doing something special. So what is the whole secret behind getting sleep? Because we've kind of ignored it for most of our lives, really.
35:19 Neil deGrasse Tyson? Yeah, no one even thought about it, yeah.
35:20 Speaker 03 Yeah, and, and look, I did till about 10 years ago, I was very much of the mindset that I'll, I'll sleep when I'm dead. But I think the science is pretty unequivocal here. And, and so too, if you just, once in a while, it's nice when evolution makes such an obvious statement, which is, why did evolution not get rid of this thing that kept us unconscious a third of our lives, unable to hunt for food, reproduce, fend ourselves against danger? I mean, so, so there's, there's a pretty compelling case for why we and every other species on this planet requires sleep.
35:51 Chuck Nice? It's a great point.
35:52 Speaker 03 So.
35:53 Neil deGrasse Tyson? And, and I've joked about this, where aliens come to Earth and say, what? These humans are semi-comatose for one-third of the rotation of their planet? Like, what's up with that? They, they would be completely stupefied by it, just with, and we take it all for granted, right? So, so, so tell me, what, what's it doing for us?
36:12 Speaker 03 It turns out it's doing a lot, right? So it's not just restoring things in your brain. So one of the most important functions of sleep is basically cleaning up debris through the, what's called the glymphatic system. So Matthew Walker uses this analogy of picture your brain as Manhattan, where the streets represent the area between cells and at night, the street sweepers are coming out and getting the trash out of those areas. It's also a time when you consolidate memory, right? You can't consolidate memory or new skill absent sleep. It's also a time when some of the most important hormones in your body are being synthesized, or at least the signals that tell those hormones to be made.
36:54 Speaker 03 So for example, testosterone, while it's not made in the brain, is made in response to something called follicular stimulating hormone or follicle stimulating hormone and luteinizing hormone. Those are maximally produced at night, as is growth hormone and things like that. But it also regulates very important things, which is easier. And sometimes there's things we don't fully understand how it's doing it, but we can see experimentally when you, even for a short term, deprive sleep, you can induce a horrible physiologic state. And the most obvious example to me is that of insulin resistance. This is the precursor to type 2 diabetes. Just a week of significant sleep deprivation, taking normal, healthy people and restricting them down to four and a half hours per night will induce a state of profound insulin resistance in about a week.
37:39 Speaker 03 So you get the sense, even without fully understanding mechanistically how this is happening, that disruptions of sleep lead to horrible consequences, both above and below the neck.
37:49 Speaker 01 So with shift workers, with shift workers who work those awfully unsocial hours, they must be at phenomenal risk of having all sorts of problems.
37:59 Speaker 03 Well, unless they sleep during the day. I mean, they can still sleep during the day.
38:02 Speaker 01 No, but it's, you're not, your body's programmed to do it at a certain time of the day and all of a sudden you're turning that on its head.
38:09 Chuck Nice? Can you, well, the question is, the question is, can you change your circadian rhythm? Is that possible?
38:14 Speaker 03 You can, but it requires a lot of manipulation of light. So one of the, there's three basic driving forces for sleep. One is cortisol, one is light, and one is adenosine. So we could talk about all of them, but let's just talk about the light one. The light one is sensed through something called a pineal gland right behind the eyes. And so. All that gland is basically trying to ascertain is when is it getting dark enough that I can start secreting melatonin, which is a pro-sleep hormone? So, one of the challenges that a shift worker is going to have if they're not paying attention to it is, how do I make sure when I sleep, I create enough of a darkness environment that I get that hormone to be produced to shift my physiologic state?
38:58 Speaker 03 And by the way, that means that they need light when they're working. And it has to be kind of the right kind of light. And unfortunately, there's no perfect substitute for sunlight.
39:06 Chuck Nice? Well, and once again, doctor, I know you went to med school and everything, but the penile gland is much lower in the body.
39:14 Speaker 01 Anyway.
39:19 Neil deGrasse Tyson? Chuck has his own medical school.
39:22 Speaker 01 School of Medicine. And it exists below the waistline as well.
39:30 Neil deGrasse Tyson? We're going to take a quick break, but when we return for our third and final segment, we're going to get deeper into sort of our neurological health, emotional health, other dimensions of what we will care about as we get older here on StarTalk. We're back on StarTalk Sports Edition, completely devoted to longevity. And we've got in-house as our expert, Dr. Peter Attia, and he is host of the podcast, The Drive. And he's, he's got a book out. And again, tell us about your book, Peter.
40:14 Speaker 03 It's called Outlive: The Science and Art of Longevity.
40:18 Neil deGrasse Tyson? Yeah, I love that title. So Gary, keep us going here. What's next up? What have you teed up?
40:24 Speaker 01 All right, so we kind of touched on in segment one, the four horsemen of disease, you know, all these things that fight us in our aging battle. So I thought maybe we'd kind of try and saddle one up and ride it a little bit harder and find out a bit more. And that would be neurodegenerative disease, because I think as we get older, a lot of people's biggest fear is, you know what?
40:49 Speaker 01 Is my head gonna be really good? Or am I gonna lose the plot? What's going on? So there has to be a way, because once you get to that Alzheimer's, and I sadly lost my father to dementia, once it gets to a certain point, this train only goes in one direction. But is there? Is there a way in the future we can successfully battle something like this?
41:10 Neil deGrasse Tyson? Or prevent it? Yeah.
41:12 Speaker 03 Well, I think that's, that's again, the important distinction. And I'll be honest with you. I'm far more optimistic in our capacity to prevent, or at a minimum significantly delay the onset of Alzheimer's disease, than I am in our capacity to treat it once it takes hold. And part of the problem is just that protein folding is a really common problem. So the easiest example, and admittedly, this is an oversimplification, is why does an egg change color when you cook it? Like, why does the white part of the egg?
41:48 Neil deGrasse Tyson? I think that's one of the most fascinating things in the kitchen. Between you and me, I'd just say, here's a transparent fluid.
41:54 Speaker 03 Yep.
41:55 Neil deGrasse Tyson? And it bada bing, turns white, exposed to heat. It's like, we should marvel at that more often than we do.
42:01 Speaker 03 And so here's the equally remarkable thing, Neil, which is why can we never go back from white to clear? So, so basically, like, there's a real problem with folding and unfolding proteins. And once you move in that direction, where the, so the main protein, of course, like, you have albumin and things like that inside the egg protein. Once you apply heat, you're basically changing the shape of the protein, and it fails to be translucent anymore. And something very similar is kind of happening in the brain, right? Which is, as the amyloid beta plaques and the neurofibular tangles are wreaking havoc in the neurons,
42:43 Speaker 03 it does not appear to be reversible, any more than it appears reversible, to take a white egg and return it back to a clear egg. So. I think that if we're going to see successful pharmacotherapy, it's going to have to be applied very early. And that's why I think today what's exciting is the development of biomarkers that are being applied to high-risk individuals before they have symptoms, but identifying the seeds of problem. So let's use an analogy in cardiovascular disease. I don't want to wait until you're having chest pain or, God forbid, a heart attack to interfere with drugs that lower cholesterol. Instead, what I'd rather do is say, look,
43:27 Speaker 03 I can measure your cholesterol and I know it's high and I know what that's going to do. And if I really need to convince myself, I could look at a CT scan of your coronary arteries and realize that, oh, by the way, you're already accumulating soft plaque. So similarly-
43:39 Neil deGrasse Tyson? So how do you know if someone is susceptible to Alzheimer's if they don't yet have symptoms?
43:43 Speaker 03 I think the two most important ways are family history. So that's a big predictor. And then the second-
43:50 Neil deGrasse Tyson? Genetics.
43:50 Speaker 03 Yeah, and then the second is genetics.
43:52 Chuck Nice? Oh, I'm screwed.
43:53 Speaker 03 There's a gene-
43:54 Neil deGrasse Tyson? It's the same thing. That's the same thing.
43:55 Chuck Nice? Family history is indicative-
43:57 Speaker 03 Not necessarily, not necessarily. Because there are many people who get this that are not getting it through the gene that we are most commonly measuring. So the gene I'm referring to is called ApoE. So Apolipoprotein E is the gene. And this is an unusual gene in that it has three isoforms. So most genes just exist in one form. So for example, the LPA gene or the ApoB gene, there's just one. We all have the same one. The ApoE gene used to only exist in an isoform called E4. That was the one that we historically had for thousands of years. And about 200,000 years ago, another one showed up called the ApoE3 isoform. And then about 25,000 years ago, the ApoE2 one showed up.
44:43 Neil deGrasse Tyson? What were the cavemen doing to make this?
44:45 Chuck Nice? Whatever, whatever they were doing, they were like, we gotta forget this mess.
44:49 Speaker 03 Well, it's interesting. Here's a great example of going back to what we talked about earlier, right? The ApoE4 gene, which was the one that our ancestors had forever, is the high-risk Alzheimer's gene.
44:59 Chuck Nice? Ah, okay.
45:01 Speaker 03 But it served a very important purpose, which is it probably helped us against infectious diseases.
45:10 Chuck Nice? Gotcha.
45:11 Speaker 03 So it was probably a very good gene to have when you were young, especially for most of human history, when you were much more likely to die from infectious diseases. But it turns out to not be as good a gene to have.
45:22 Chuck Nice? When you're old.
45:23 Speaker 03 Given that you don't need help with your genes to fight infectious diseases anymore. We have so many other technologies. What we need is help not getting Alzheimer's disease. So 25-
45:31 Neil deGrasse Tyson? This is like sickle cell and malaria.
45:33 Speaker 03 That's exactly right. Yep.
45:34 Neil deGrasse Tyson? The sickle cell will kill you, but it keeps you alive long enough to not get malaria. Right? And so these interesting biological trade-offs in our life expectancy historically.
45:44 Speaker 03 And it's a little bit different, right? Because sickle cell is, if you have, you have to have two copies of the gene to have the phenotype.
45:51 Chuck Nice? Right.
45:52 Speaker 03 And that would be negative under any circumstance. It's if you have one copy of the gene-
45:57 Neil deGrasse Tyson? Oh, there it is. Of course.
45:58 Speaker 03 That you're protected from malaria and you don't have the phenotype. And that probably explains why that trait has stuck around forever as opposed to a disease that kills people young.
46:07 Chuck Nice? When you say two copies, just for clarification, you mean that both people have to pass the same gene at the same time to the, to the recipient? Is that what you mean?
46:16 Speaker 03 That's in the case of sickle cell. You get, you get one from each parent.
46:19 Chuck Nice? One from each parent. Like, okay.
46:20 Speaker 03 Going back to Alzheimer's, one thing to keep in mind is the ApoE4 gene is quite different in the sense that there's no evolutionary pressure to get rid of that gene because it doesn't interfere with reproductive fitness at all.
46:31 Chuck Nice? Right.
46:32 Speaker 03 So this gene is here to stay, you know, absent like, you know, sci-fi CRISPR stuff where we just get rid of it. But the point is, people who have that gene, depending on if they have one or two copies, are at an increased risk for Alzheimer's disease. So if you have one copy of the ApoE4 gene and one copy of either two or three, your risk is about twofold higher.
46:55 Speaker 03 Maybe as high as three.
46:56 Speaker 01 Doctor, we've exercised our bodies, right? For the aim of longevity. Now, if someone and their blood work presents with markers that you think might be predisposed towards dementia, Alzheimer's, do we then not engage in some sort of cognitive skill exercise that is working for our minds as much as we do to exercise correctly for our bodies?
47:20 Neil deGrasse Tyson? So is the brain a muscle in this regard?
47:22 Speaker 03 Yeah. Not exactly the same, but there is an analogy. But first of all, exercise is still the most important intervention we have for brain health as well. So that shouldn't be forgotten. So the exercise you're doing for your body is also for your brain, both in terms of reducing inflammation, increasing growth factors such as brain-derived neurotropic factor, BDNF, increasing cardiovascular fitness, which in turn increases vascular fitness. Remember, a lot of dementia is exacerbated by microvascular disease. Anything that deprives... So just take a step back. The brain is like 2% of your body weight and 25% of your metabolic demand.
48:06 Speaker 03 So just kind of reflect on that for a moment. So anything that compromises any bit of its metabolic fitness is disastrous. And that's why small vessel disease, type 2 diabetes, anything that compromises that aspect of the brain is devastating with respect to dementia. And so, exercise helps that.
48:28 Neil deGrasse Tyson? To translate your phrase, it's 25% of our metabolic demand. What you mean is, of all your calorie intake, your body's using one-fourth... Your brain is taking one-fourth of it, and the rest goes to the rest of your body.
48:41 Speaker 03 That's right. And despite it only weighing 2%.
48:44 Chuck Nice? Well, some of our brains are doing that.
48:48 Neil deGrasse Tyson? Despite it being only 2% of your body?
48:49 Chuck Nice? Yeah, I know some people that their brain is 2% of their body weight and is probably only doing about 2% of the metabolic demand.
48:59 Speaker 03 So to your question, Gary, then, let's talk about where brain games fit into this, right? So the available evidence suggests that...
49:07 Neil deGrasse Tyson? Brain games are commercial for Chuck, who hosts Brain Games on the road.
49:10 Chuck Nice? It was two on the nose when he said, "Let's figure out where brain games fit in." I'll tell you where it fits in. You can watch it on Nat Geo, the card on Disney+. Where Chuck Nice is the host.
49:21 Neil deGrasse Tyson? Chuck Nice is the host. Brain Games on the road. Okay.
49:24 Chuck Nice? There you go.
49:24 Neil deGrasse Tyson? There's a, there's a unanticipated commercial for Chuck. Okay. Continue, Peter.
49:31 Speaker 03 So it turns out that cognitive reserve is just as important to the brain as physical reserve is to the body and what we call movement reserve. So if you take 10 people and you line them up in the order of their physical or movement capacity. So you've got one person who just kind of sits down all day and does nothing. And at the other end of the spectrum, you've got the most sophisticated ballroom dancer of all time who can spin and flip and do all sorts of things. You, you can basically assume that they're going to have that relationship towards their ability to mitigate movement disorders such as Parkinson's disease. In other words, the more movement reserve you have, the, the longer you can
50:13 Speaker 03 tolerate the insult of the neurodegeneration before you start showing symptoms. And the same is true with dementia. So the higher your cognitive reserve, the longer you go before you will experience symptoms. And so the question is, what type of brain activities boost cognitive reserve? And I think contrary to what people had hoped, it's not playing, you know, doing, you know, Sudoku or playing, you know, crossword puzzles or things like that. Like, those things are very narrow in what they're doing for your brain and they tend to just make you better at those things. Whereas doing something very complicated, doing, you know, doing much more cognitively complicated tasks.
50:56 Chuck Nice? Like learning a new language or learning to play the guitar or something like that?
51:01 Speaker 03 Exactly. Doing things that have many more moving pieces and requires much more of the brain, those do tend to boost cognitive reserve and therefore give us some protection against cognitive decline.
51:14 Neil deGrasse Tyson? How about learning a musical instrument?
51:16 Speaker 03 I think it seems that that's probably in the take, but once you get pretty good, it's easier, I think, for people to kind of tone down the learning. So a lot of it also has to do with how deliberate a person is and how much the thing about. So one of my hobbies is driving a race car. And, you know, for me, that's cognitively insanely challenging.
51:35 Neil deGrasse Tyson? Okay.
51:35 Chuck Nice? Yeah. It would have to be, yeah.
51:38 Speaker 01 All right, Doc, so if we helicopter, because you know, you are so close to this, you know, it's right there in front of your face. So if we helicopter out, do we find all of these things are somehow interconnected and independent, interdependent on each other for a success? In terms of, it's okay for me, my body's good. You know, I'm 20 years younger than my actual sell-by date, but my brain's not there, so I need to do something. And is it all connected or that they just sit separately?
52:11 Speaker 03 If you're referring to the interventions that we do, whether it be exercise, sleep, stress management, I think they are all connected. And, you know, I'll give you an example, right? If you're, if you're doing everything wonderfully, if you're, if you're following like, say, Peter, it is prescription on exercise, but you're sleeping four hours a night and you're checking your email all night and living on social media, getting bothered by it. Yeah, it's actually going to impair your capacity to reap the benefits of that domain. So it's, it's better to be kind of a seven out of 10 on everything than a 10 out of 10 on one of them and then zero out of 10 on another.
52:49 Chuck Nice? Interesting, interesting. Well-balanced life, well-balanced diet, well-balanced everything.
52:54 Neil deGrasse Tyson? I'm a fan of moderation, but only in moderation.
52:57 Speaker 03 Me too.
52:58 Neil deGrasse Tyson? Personally.
52:59 Speaker 03 My, my swim team had T-shirts made for me one day that said, moderation is the only thing worth doing in moderation.
53:05 Chuck Nice? Yeah.
53:06 Neil deGrasse Tyson? Exactly.
53:07 Speaker 01 All right, the one, okay, Doctor, the one thing we haven't really touched on is nutrition, I'll call it nutrition. And then you have a phrase, nutritional biochemistry, which doesn't seem to be as much fun as me saying eating and enjoying. So what are we saying here?
53:25 Neil deGrasse Tyson? And I'd like to, I'd like to slip in there, just Peter, to get your fast reaction. Almost everyone I've ever met who said they became a vegetarian and never felt better.
53:40 Neil deGrasse Tyson? In their changeover to become vegetarian, it included the onset of an exercise regimen. And I'm intrigued by this because I, along with you, only you know it from experiments, I know it just from my own life, that I've never felt better than when I exercise, no matter what I eat. No matter how much I... The eating is secondary tertiary to the value that the exercise brings to my body. So how many people are misunderstanding what are the forces driving on how they feel with exercise relative to their diet?
54:17 Speaker 03 Yeah, you've hit the nail on the head, Neil. Most of the nutrition research is so heavily flawed in its epidemiology by these healthy user biases. And you're right, so there's no, virtually no epidemiologic study that wouldn't suggest that vegetarians are healthier than meat-eating people. However, these studies are simply incapable of correcting for the fact that people who select a vegetarian diet make many other changes. First of all, you're selecting just a different group of people. There's no randomization to make that happen. But you're selecting people who are then saying, I'm so health-conscious that I'm willing to give up this thing. It's not easy to give up, right? It's so ubiquitous. And in exchange, you know, or as a result of that, rather, I'm going to do a lot of things that are healthy.
55:02 Speaker 03 I'm going to be more mindful of my exercise, my stress. Yes, exactly.
55:06 Neil deGrasse Tyson? It's a life shift. Yeah.
55:08 Speaker 03 Yeah, so that's absolutely correct. And by the way, that comes back to Gary's point. Why do I want to talk about nutritional biochemistry? Because I never want to talk about diets. I can't stand talking about diets. It makes me sick. And all I want to do is just talk about amino acids, fatty acids, carbohydrates. How do these things work? What does energy balance mean? Why does it matter?
55:32 Chuck Nice? But once you put that all together, you end up with a diet.
55:35 Speaker 03 Yeah, except I think that I think it doesn't need to, I mean, the problem with diets is it becomes, so look, food is already an emotional topic for everyone. It's probably one of the reasons why I think these diets become so tribal.
55:47 Chuck Nice? I see what you're saying.
55:47 Speaker 03 It's a part of how we identify.
55:48 Chuck Nice? I get what you're saying.
55:50 Speaker 03 Yeah, so instead, I just want to say, look.
55:51 Neil deGrasse Tyson? Yeah, you become in-group, out-group.
55:53 Chuck Nice? Right.
55:53 Speaker 03 That's right.
55:54 Chuck Nice? Yeah, because really, a diet is whatever you're putting in your body, that is your diet, period, you know? So, so I see what you're saying is, once you divorce yourself from, you know, the emotion, from the social aspect of the diet, from what Neil just said, the in-group, out-group crap, once you break it down to just what, now you can talk about it in such a way where it is truly just nutrition.
56:24 Speaker 03 That's right, yeah, so let's ask the question.
56:26 Neil deGrasse Tyson? At the end of the day, you're eating protein, carbohydrates, and fat.
56:27 Speaker 03 That's right.
56:27 Chuck Nice? Right.
56:27 Speaker 03 Yeah, that's it.
56:28 Chuck Nice? That's it.
56:29 Speaker 03 Okay. And alcohol. Alcohol is the fourth macronutrient, right? So those are your, those are your four things. And I'm not, I'm not suggesting you consume much from that group, but, but we need to acknowledge that there are some people who are getting 25% of their calories from alcohol.
56:45 Chuck Nice? You, my friend, are my favorite doctor ever.
56:47 Neil deGrasse Tyson? But on that happy note, we actually have to, we've run out of time. Okay, right, quickly, Peter, what we will do is go out and buy Peter's book, Outlive: The Science of Longevity, where we will learn how to tackle and navigate all of the bad hands that are dealt us, and for what it is to be human and to get older. Peter, it's been a delight to have you on this show.
57:10 Speaker 03 Thank you for having me, gentlemen.
57:12 Neil deGrasse Tyson? All right, and Chuck and, Chuck and Gary, always good to have you there as my co-host.
57:18 Speaker 03 Thank you.
57:18 Neil deGrasse Tyson? All right. Neil deGrasse Tyson here, your personal astrophysicist, as always, bidding you to keep looking up.
Previous Cosmic Queries – Understanding Infinity with Stephon Alexander Next Cosmic Queries – Building Space Civilizations with Ariel Ekblaw Page updated September 28, 2026 · transcript and summary are machine-generated
