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TECH007: Longevity Roadmap w/ Seb Bunney (Tech Podcast)
01:10:51
The episode dives into epigenetics, sirtuins, Yamanaka factors, and how AI may accelerate regenerative medicine—offering a glimpse at the future of human health.
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- [00:01]
Preston Pysh
You're listening to tip.
- [00:03]
Hey, everyone. Welcome to this Wednesday's release of Infinite Tech. Just this month, MIT Technology Review ran a story saying Ray Kurzweil believes we'll reach longevity escape velocity by 2032, the moment when medical progress starts adding years to our lives faster than we're aging. It's a bold claim and it raises a huge question. Are we actually that close to out running time? To dig into this, Seb Bunny and I are unpacking David Sinclair's book Lifespan. This is a book that's a landmark in longevity science that argues aging isn't inevitable, it's information loss that can be reversed. We'll cover the Yamanaka factors sirtuins nad plus the science of hormesis and explore what all of this means for living right now. This is surely an episode you will not want to miss. So without further ado, let's jump right into the book.
- [00:53]
Sponsor/Ad Voice
Foreign.
- [00:56]
Preston Pysh
You'Re listening to Infinite Tech by the Investors Podcast Network. Hosted by Preston Pysh. We explore bitcoin, AI, robotics, longevity, and other exponential technologies through a lens of abundance and sound money. Join us as we connect the breakthroughs shaping the next decade and beyond, empowering you to harness the future today. And now, here's your host, Preston Pysh.
- [01:25]
Foreign hey everyone. Welcome to Infinite Tech. I'm here with Seb Bunny and we've got another book for you guys. I'm super excited to cover this topic. I've always wanted to cover this topic on the show, but never had the opportunity to cover this topic on the show. We're talking about longevity, health, health, technology, like where this is all going. The book that we both read is called Lifespan by David Sinclair. And this book has been out for a few years, but it for me was just this really inspirational read on where the technology is moving when it comes to people being able to live longer. And, you know, if you're living a good life and you're pretty happy, you want to live longer. So I'm really excited to get into this. Seb Bunny, welcome back. What's your initial thoughts on this book?
- [02:19]
Seb Bunny
You know what? I would say that one, I'm super excited to talk about this and just see your perspective on the book. Two, I should be absolutely transparent and upfront. This is not my area of expertise. I had to do a ton of research to be able to really dig into the topic which we're going to discuss and how all of this kind of conversation around genetics and enzymes and such, how it all kind of like pieces Together. It took me definitely quite a bit of studying to kind of piece this together, but I'm super excited to discuss it.
- [02:47]
Preston Pysh
Amen. And if you're a doctor or you're in the medical, you know, industry, or you're a biologist, I apologize upfront. I deeply apologize for all the terminology that we are going to botch or just get wrong. But we're going to try our best here. So let's start off here. I was literally scrolling through X this morning and I see a post and Ray Kurzweil, everybody knows the technologist Ray Kurzweil, CTO at Google for decades. And the quote was, he expects to have longevity escape velocity by 2032. Meaning by 2032 the science is going to enable people to outpace what our death rate is. And that's not framed correctly, but we're actually going to have this technology in place to keep extending your life longer than what the average death rate is. So what do you think, Seb? Is this nonsense? Are we, you know, and we're going to get into the book and what the book is proposing is like how some of this is possible, but what's your just off the cuff gut feeling about some of these proclamations that we're hearing from people?
- [04:01]
Seb Bunny
My gut feeling, being absolutely transparent, is that. And I can dive into it a little bit more at the very end. I think it's good to kind of get the book out of the way. But my gut feeling is that I think we get caught up in the hype of things. And just as we've discussed in the monetary system, we tend to point to, well, this is the cause of inflation, this is the cause of the banking crisis. And in reality, we are dealing with a complex adaptive system that is almost impossible to be able to pinpoint these black and white stories about what causes something. And I think the same thing is true for lifespan, healthspan, longevity. I think sometimes we try to simplify a really complex topic and people have been talking about longevity and increasing lifespan for decades. And there's also some contradictory data which I'll dive into at the end that I find really interesting that kind of tends to argue that have we actually seen an increase in lifespan even over the last 2,000 years? But we'll leave that for a little bit. And yeah, I'm excited. And it's just, it's fun to dive into these other topics. And there's definitely technology in this world. There's definitely advancements in understanding that are supporting health for sure.
- [05:05]
Preston Pysh
Yeah. So David Sinclair, out of Harvard, the author of the book and his core thesis is that aging itself is a disease. And I think from a definition standpoint, he's trying to get this included as a disease so that the treatment and the way that it's handled from a health medical perspective is treated differently than it's currently approached. Because I think today it's like, well, they just got old and they died. And he's like, that's not good enough. We have to change the definition so that it's bucketed in as a disease like any other disease. And then you're going to get a lot more research dollars into it. You're just going to, like, unlock a whole lot more funding to really kind of dig way deeper into some of these things. Anything you want to add there, Seb, on why you think he's classifying it as that? But this was a really important part that kept coming up in the book. Is this redefinition of it being a disease itself. Aging is a disease itself.
- [06:04]
Seb Bunny
Absolutely. I think that he highlights it quite a few times throughout the book that essentially there are these hallmarks to aging, and he's like, genomic instability, telomere attrition, epigenetic alterations, all of these things that basically lead to aging. But he believes that we're focused on the symptom. And actually what leads to those things is kind of this information loss, which I'm sure we'll get into. But he thinks there's this upstream thing that we're not talking about, and if we can recognize and fix that upstream issue, then we may be able to increase longevity.
- [06:38]
Preston Pysh
Yeah. So his big theory, his big breakthrough is this idea of the information theory of aging. And we've covered Claude Shannon's information theory on the show numerous times. We had the author of the book come on about Claude Shannon and just this idea of, like, how do you transmit information across, you know, a wire or through the air via signal, RF energy? And David Sinclair takes this idea of transmitting information or information loss and noise factors to biology and suggests that the reason we age is because it's a loss of information. Specifically, it's a loss of information for your epigenetics. And so when people hear some of this terminology, they're saying, well, Preston, I have no idea what you just said when you said a loss of information of your epigenetics. So what I'm going to try to do here is explain this from the ground up. And Preston, verbiage and feel free to step in if you feel like I'm stepping out way over my ski tips here. But okay, let's start here. You got your cell. And I think everybody's familiar with DNA. Okay, let me just. Let me explain it like this, because I think this is fun to frame it this way. So the typical human has about 3.3 billion base pairs in their DNA. So just think of it like genetic code. Like, you got all this software, all this code that's run, and it's 3.3 billion lines. Think of it like that. Interestingly, a tomato. Also, if you look at the DNA of a tomato, it's about 3 billion base pairs of DNA as well. So when a person hears that and they say, well, hold on a second. What do you mean? DNA of a tomato is the same, you know, length or lines of code as a human. And it just doesn't seem to make any sense. Like, how is that possible when you think of the complexity of a human. They got a brain, they got a heart, they got eyes, they can do all these things. They can communicate socially. And you're telling me that the code inside of the cell is of the same length as a tomato? Like, it just doesn't make any sense. This is where you step into the epigenetics of the DNA. So what is that? So think of the DNA as this big, long line of code, but what's actually needed inside of the code to read it and create, call it a heart cell or a neuron or the cell in your eye, these differentiations that are happening in your organs, and just all the different pieces that make up a human, how do you get those different pieces and parts out of those 3.3 billion base pairs in the DNA? And the way you do it is through what, you know, is referred to in the book as the epigenetic settings of the DNA. So just imagine, like, all of that line, all those lines of code are on a piece of paper. Let's say we had thousands and millions and millions of pieces of paper with all this genetic sequence, okay? And let's say you flip to page 50, and in order to create a heart cell, you need the genetic code on page 50. You need it on page 1 million, you need it on page whatever. And there's just very specific pages that. That's the code for making a heart cell. And then it's a whole different set of code or pages of that code that need to be read in order to create an eye cell. And the list goes on and on. For each organ, each cell type in the body, there's only Specific pages of the 3.3 billion that exist, you only need certain pages to read in order to do that. So when we say the epigenetics, what we're really saying is which pages of the 3.3 billion lines of code actually need to be turned on in order to be read? And so when you think about going back to this example between, you know, a tomato and a person having the same amount of genetic code, for all intensive purposes, the pages that are being read are the pages that are being flipped open in the book to be ready by. The transcription proteins are very specific and very different depending on what organism or person or thing is being built and constructed inside of the body. And so David Sinclair's book, so hopefully that provides a little bit of a background on, like, what epigenetic settings are. It's the pages that are open to be read. And this idea of the information theory of aging is as the cells replicate, they go through mitosis. As these cells are, you know, as you're living life, you're in year 20 versus year 40 versus year 60 of your life. As these cells have replicated the pages that are flipped open for these different things that need to continually be built and transcribed in order to create the proteins inside of the cells, that information of those epigenetic settings, which pages are flipped open, are changing very slightly. And instead of it being page 50 that was open, now it's page 50amp, page 49, which was never intended to be read, is also open. And as those transcription proteins go in there and they read that genetic code that it wasn't supposed to be reading, it's now producing and creating extra material inside of the cell. And this, this is creating noise that is not intended. And this is what's causing aging inside of anybody or any living thing. And so this is a really, like, for me, when I was reading this, I was just like, my mind was blown. I was like, this is so fascinating. It's so interesting. And it's pretty elegant, right? Like, it's pretty simple when you really kind of pull back and you think about, like, well, what would be the ramifications of this, of a heart cell that had certain settings, but now it has additional settings that are not supposed to be being read and being produced and being turned into proteins that were never intended to be turned into proteins inside of that cell, and how do you turn those off so that you can get it reset back to the initial epigenetic settings? Seb, am I out to lunch in the way that I'm describing This, or do you have anything else that can maybe help the listener piece this together? Especially the ones that have no background in biology?
- [12:55]
Seb Bunny
No, Preston, I think you absolutely crushed it. And I think for me, it had an analogy in the book around this kind of cd, CD player. And I struggled a little bit of the analogy, and so I didn't like it a little more.
- [13:05]
Preston Pysh
Yeah, I didn't like it, but I didn't.
- [13:07]
Seb Bunny
To me, it didn't make a ton of sense. And so I was thinking a little bit more, and I was like, I was really trying to understand this in terms of an analogy and the way that I interpret things. And again, like, correct me if I'm kind of misinterpreting this, but the way I see it is that by getting older isn't so much a kind of a hardware problem, it's a software problem. And so imagine if your body is a computer and your DNA is effectively the hardware. It's the physical machinery, and it's built upon, as you're talking about, these kind of four chemical bases, A, T, C, and G, which I think, what are they? Adenine, thymine, cytosine, and guanine. And I butchered those names.
- [13:43]
Preston Pysh
So better than I would have done. Better than I would have done.
- [13:47]
Seb Bunny
So all of our genetic information is made up of these four bases. Everything is made up of these four bases. And that information is remarkably stable. If you have a 1990s iMac, it's still the same 1990s iMac that the hardware is remarkably stable. They barely change over a lifetime. But then on top of that, you have the epigenome, which is what you're talking about, the epigenetics. And this is the software or the operating system that tells the computer what to do. And so it decides which programs to run, how to use the fan, how to basically enable this machinery to run. And so when it's saying which program is to run, from a DNA perspective, to your point, it's saying, well, this needs to be a skin cell, this needs to be a liver cell, this needs to be a brain cell. The problem is that over time, software starts to glitch and it introduces error on the hardware. So you get environmental stress, you get DNA damage, metabolic wear. And so the hardware itself is still fine, but the computer starts freezing, it starts misfiring, it starts having memory issues as to how it's meant to run. And that is what this guy, David Sinclair, kind of talks about is aging. It's not necessarily the loss of biological information. The computer itself is still Totally fine. It's more. It's forgetting how to run and operate efficiently. And his whole thesis is that if we can restore that software to its original kind of uncorrupted state, then we may be able to reboot the system and bring hardware back to its kind of full use. And that's kind of, in my mind, I see genetics as the hardware, and epigenetics is the software telling the hardware how to run. And that is where this understanding of aging comes about.
- [15:25]
Preston Pysh
Yeah. And to that example that you're providing, the software on the computer is what's telling it how to rejuvenate the hardware itself. So, like, let's say that the hard drive was getting old and decrepit. The software that's loaded onto that computer is providing the information to be able to self reinforce and self fix the hardware itself. So if the software gets corrupted, it's never going to be able to perform those tasks of the rejuvenation of the hardware. So really kind of like, fascinating insight. He does a really good job kind of explaining all of this stuff that makes it really accessible, which I loved about the book. Anything else that you wanted to cover on the information theory of aging before we kind of go on to, like, putting it into a little bit more context?
- [16:16]
Seb Bunny
Yeah. So what I found was really fascinating is that, like, once he kind of breaks down the information theory of aging, he then goes into, well, how did he get to this theory? And he starts talking about yeast. And so at first you're just like, what has yeast got to do with humans? And what you realize is that yeast ages in one week. Humans obviously take decades. And so you are able to effectively rapidly test longevity ideas on yeast, which is obviously not possible in humans. And if we can't obviously create some form of longevity mechanism, a way to extend a yeast life, how are we ever going to be able to do that in a human? And so I think they recognize this. And this wasn't even necessarily even just David Sinclair. There's a whole backstory to yeast. And that's what I found was really, really fascinating. So when it comes to yeast, what he starts talking about is, in the 1940s and 50s, yeast becomes like a model organism. All of these researchers start diving into how yeast is aging, and what they realize is this guy Robert Mortimer and John Johnston. What they realize is the mother yeast cells can only divide a finite number of times before they're dying. So this is like the first measurable model of cellular aging. And then from there, in the 80s and 90s they find out that actually there are genes related to aging. And these are called the sir, the silent information regulator genesis. And you can think of. And again, like, feel free to step in, Preston, if I'm butchering this. The silent information regulator genes I found so fascinating, and we can dive into more depth on this. But basically the way that they essentially work is these genes have kind of two roles. Essentially what they'll do is these silent information regulated genes will sit on the DNA and they will prevent that DNA, that information from being read and turning a cell into, say, a liver cell when it's in the brain, or if you're in the liver, turning that cell into a kidney cell. And that's when you start to get mutations, metastases, and all of these other issues. But at the same time, they also do something else, which is in the event you have a DNA break, you have some form of genetic issue, they will leave where they're located, they will move to that area and they'll start to repair that break. And then once they're done, they'll go back to the DNA place where they were shutting down this information from kind of a turning into a liver cell, a brain cell. They will kind of turn that information back off again. And so anyway, it will return back to its original spot and it will silence those genes again, preventing that gene from that DNA from expressing in a certain direction. And so this was in the 80s or 90s. And so this is the silent information regulated genes. Now we're going to talk about this more because these SIR genes were essentially the backbone for this whole idea of aging that David Sinclair talks about. So that was in the. Going up to the 80s and into the 90s. This is where David Sinclair kind of enters the frame. And so he starts looking at how to kind of age things prematurely. And he figures out that there's these yeast mutants that basically have this mutation, and he's able to age them prematurely, hinting at there's some universal aging mechanism. And then in 97 through 99, he recognizes that, you know what, if they're able to go in and over express these SIR genes, it's able to reduce and extend, sorry, reduce DNA damage and extend the lifespan by up to 30% in this yeast. And so this was profound. And he kind of gets to this in about probably one third, one quarter of the way into the book, is that there are ways to be able to extend the lifespan of yeast. And to me, that's when the book starts to get really interesting because it starts diving into the technicalities of like, well, how is it actually doing this? I'm curious to hear if you have any thoughts on that person.
- [20:09]
Preston Pysh
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- [21:42]
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- [24:04]
Preston Pysh
All right, back to the show. The thing that I took away when he started there was like, this guy's a first principled thinker and the approach that they're taking to try to solve this is very first principle. It's like, let's go back to the essence or the start of life itself, which was, you know, the swamp sludge. Let's see how it all started and how the mechanics of growth or contraction of self preservation interacts. And what are those triggers or what are those cueings that are causing life to want to expand or contract or just preserve itself? And so by starting there I was just kind of like, and he does a really good job of framing this in the book, way better than probably Seb and I have done, as we're just kind of sporadically talking about all the different ideas in the book. It's laid out really well in the book and organized in a really thoughtful way to kind of walk you through how he's arrived at a lot of the these theories. One of the things that I also thought was really well done in the book was how he was walking through his proof of this information theory of Aging. And one of the things that he talks about is this idea of an epigenetic clock. And so what he's saying is if aging is truly information loss, okay? And going back to this idea of the book, right, you got this big giant book of all the code, the genetic code, the DNA. And if to make a heart sell, it is page 50 and page 500 and page 5000 and just name out those very specific pages in the code that have to be read to create that heart cell. His opinion is if it's truly an information loss that's occurring and other pages are accidentally getting opened and getting read, we should be able to peer into a cell and look at the epigenetics and determine how old something is just based off of, and this is called methylation, the methylation of the DNA. And what he found is that when they did this and they go in and they do it an audit of the entire DNA and they see how much of the DNA is supposed to be opened for a specific cell type versus what is actually opened. They were able to pinpoint the age of the rat that they were doing a lot of this testing on. They were able to pinpoint that with a lot of accuracy. And you can even do an epigenetic clock test on a human. And what they're finding is that the accuracy of the test is one of the best markers of a person's actual health. Because somebody might be 40 years old, but when they go in there and they do this epigenetic clock test, the person might have the age of a 30 year old because their DNA is so in good working order and hasn't been. The files haven't been corrupted. So if you ever go into like a longevity clinic, I think a lot of them are starting to roll out these epigenetic test clock tests to kind of see where you're at versus where they think they can get you as far as dialing back a lot of the corruption that's happened in your epigenetics.
- [27:01]
Seb Bunny
No, I think you're absolutely spot on. And I think that one of the interesting points that he talks about his, like, obviously he needed to prove his information theory of aging. And so you can almost prove it in reverse, which is if we believe that it's this noise which is creating aging, well, how do we test that? And so they ended up using, I think they call it the DNA scratch test. They ended up using crispr. And I'm going to butcher if I try and explain crispr, but basically for anyone who can explain it Better. We would love that. Go and explain it on Twitter. Crispr. From my understanding, they would go into the DNA and they would make precise edits, and they would create these spikes in the DNA of these young mice, mimicking decades of accumulated DNA damage, but without actually introducing any mutations. And the result is that the mice ended up aging rapidly, and they showed gray hair, fragility, organ decline, even though their DNA sequence, the hardware was kind of unchanged. They just added in all of this noise.
- [28:01]
Preston Pysh
And then I would say, yeah, basically my take, and I might be wrong too, Seppit. They use CRISPR to go there and open up additional pages in the cell in the DNA book, right? To have more noise factors, just like what the theory suggests should make the species look old. And when they did this with a rat, it started getting gray hairs and it was, you know, decrepit and basically was just acting like a rat that was on its deathbed by going in and performing this epigenetic methylation of the DNA.
- [28:34]
Seb Bunny
We're going to take a little bit of a tangent and come back to the mouse here for a second. But what is fascinating is the book starts going into these things called Yamanaka genes. And this Dr. Shinya Yamanaka, in 2006, he basically discovered these four genes. And these four genes were kind of the OCT4 gene, the SOX2 gene, the KLF4 gene, and the CMYC gene. And this is where it just kind of blew my mind, because I always believed once a stem cell had grown into some form of specialized cell, a liver cell, a brain cell, there's no way to reverse that aging back into a stem cell, an unspecialized cell. And this doctor basically found out, well, actually, through these genes tinkering with these genes, you can reset them back to their embryonic state, their unspecialized state. And it actually ended up winning the Nobel Prize in 2012. But what is fascinating is that Sinclair had kind of dug into these Yamanaka genes and wanted to test this on these mice. And so this mouse that they had aged rapidly, well, they went back and rebooted the epigenetics software using these Yamanaka genes, and they were able to reverse the signs of aging. And so you're just like, that is. To me, that was mind blowing.
- [29:43]
Preston Pysh
Mind blowing. People hear stem cells all the time, and I would imagine most listeners kind of know what that is, but if not, I'm just going to quickly explain it. Think of a stem cell as the DNA sequence, and it's open to become any Type of specialized cell. So it could become a liver cell, it could become an, you know, a neuron, it could become whatever. And so because it doesn't have any epigenetics set, it's not saying read page 50, read page 1000. It's saying you can read any page and become any type of cell you want. That's what a stem cell is. And so this is called differentiation of a cell. Once it starts to differentiate itself as a skin cell, or you name it inside the, when the pages, the book is wide open as a stem cell, but as it starts to differentiate, all those pages start to get closed and only a select number of pages are open to be read and transcribed. So to Seb's point here about the Yamanaka factors, these three genes inside the sequence are almost like a reset button to push the book so that it's wide open to become anything again and become a stem cell again.
- [30:53]
Seb Bunny
And the analogy I think David Sinclair gives is imagine a marble sitting in a mountain range. All marbles start out at the top of the mountain range, unspecialized, but as they kind of roll down the mountain down into a valley, they become specialized. And the problem is, up until this point of these Yamanaka genes being discovered, we just assumed that it was kind of a one way trajectory. Once the marbles are down in the valley, how are you getting them back up the hill and then crossing over into another valley? We thought that was impossible. And so this, to me, I had no idea this was possible. And it really opened my eyes. And it shows a whole bunch throughout the book. It gives a whole bunch of studies in which they've done most of them on mice, but some of them they've mentioned even with some humans, but most of them have been on mice. They did an eye regeneration study. They even had ones where they had old female mice that were infertile. And they were able to restore eggs after like chemotherapy and everything through a similar approach. So to me, I'm just like this. I had no idea this was possible.
- [31:54]
Preston Pysh
Not only are the Amanaka factors really important in the grand scheme of things as far as being able to reset the cell back to this stem cell state, which would enable it to differentiate in any way that it wants, there's also a thing called sirtuin proteins or enzymes. And what the sirtuin proteins and enzymes do is they're able to go in and update or fix the existing settings. So if there was damage to the DNA, if there was damage to, it can go in and unmethylate certain histone tails so that the epigenetics reset in the right way. But these are two. And I put it into two different camps here you got the sirtuin proteins which are going and kind of fixing what's already there. And then you have the Yamanaka factors. And these are four specific genes that enable the DNA to go reset completely back to the stem cell. So he talks about a lot of these and he talks about a lot of the research that's happening. Because the sirtuin proteins, there's seven different types and goes on and on. It gets very technical. But I would just put those two camps or those two factors as where a lot of his research, or at least the research that he talks about in the book comes from.
- [33:07]
Seb Bunny
And I think you made a really good point and that is being able to break those two things into two different areas. And I think that you've got obviously these Yamanaka factors are four genesis and then you've got these pathways. Then I would even add two more to that because he talks about the sirtuins. And the sirtuins are named after. As I mentioned, when it came to yeast, there were these. Sir, sir, silent information regulator. These are enzymes which sit on the DNA and preventing it from expressing or it goes and repairs DNA. And so you've got sirtuins which are basically these enzymes and it's the body's longevity managers or maintenance crew. So they're basically there's these seven various enzymes which being found in humans and their job is essentially just to stabilize the DNA, repair the DNA and then make sure certain genes are properly switched on and off and how they work. And this is where again, it just opened my mind. They rely on a molecule called nad, nicotinamide, adenine and I'm not even going to die. Nucleotide. I cannot pronounce any of these chemistry. Useless at it.
- [34:14]
Preston Pysh
This episode is part comedy too. We're just trying to make sure you all are entertained. Go ahead, Se.
- [34:19]
Seb Bunny
And so you've basically, they rely on nad. NAD is what fuels these sirtuins. And when levels of NAD in the body are high, as they are in youth or during like fasting and exercise, satuans basically become active and they repair damaged DNA and they silence genes. But when they falter as we age, and as we age, we also see our NAD levels decline sharply by about half by midlife. These sirtuins just can't keep up. And without this nad, genes start to lose coordination, DNA repair slows and cells Begin to basically just forget their identity. And so you basically got these sirtuins and then you got two more which he talks about. One of them is called mtor. Mtor, which is basically the mechanistic target of rapamycin. Side tangent. I've found that the hardest part about reading these books is, is once you actually understand how they work, it's not actually that complex, but the words themselves, because you never come across these words, my mind is just lost half the time. So what are they talking about again? Yeah, so I've got to go back and actually figure out like, just trying to understand how they work. And so MTOR is basically the body's growth switch. And so MTOR tells cells when to grow and when to divide. And so when nutrients are plentiful. So if you're eating a lot, MTOR is active and it signals the body to store energy, make proteins, go and build tissue. However, when it's overactive, you can get like constant activation from this is like overeating frequent meals. I think this is what we're happening, what's happening globally. We've just got an abundance of food and then it keeps cells in this growth mode, which then can accelerate aging, lead to like cancer and all of those other things. And we're able to turn MTOR off through things like fasting, low protein intake or the drug rapamycin. And so when we're turning it off, that's when it's able to help with like maintenance, repair. And so the final one, and I'll summarize these after just so kind of bring it back full circle, is we have this other one called ampk, and this is kind of the body's energy sensor. And so this activates when cellular energy is low again during like fasting, exercise, cold exposure. And essentially what it does is it switches the body into energy saving mode, which increases fat burning and insulin sensitivity and boost mitochondrial health. And so going back to kind of what we were just discussing, you've effectively got these kind of two areas. You've got these genes. The genes themselves are absolutely necessary for kind of like governing aging in the cells. And you're able to reset cells back to their unspecialized state, as Preston, you were discussing. But then at the same time, you've got these pathways which then help do this. And that is through the sirtuins, which is their kind of longevity managers and maintenance crew, mtor, which is kind of the body's growth switch. And then you've also got the ampk, which is like the body's energy sensor. And so this is kind of, I think the foundation of the book is diving into these kind of different areas and how to test for these things and what to do in humans to be able to activate or deactivate certain areas.
- [37:17]
Preston Pysh
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- [40:41]
Preston Pysh
All right, back to the show. I'm going to use an example that I read from not this book, but a different book that really kind of helped me understand this idea of growth versus the cell kind of hunkering down and optimizing itself. The author of the book was Bruce Lipton. He has a book called Biology of Belief. I think there's another one called the wisdom of your cells. And in the book he provided an example that I think everybody can kind of wrap their head around. And I might mess up the example because I read this book long time ago, but it went something like this where he was saying, imagine a farmer that's there, you know, working in his fields because the sun's out, there's no storms, there's nothing to be worried of. He's out there, he's harvesting, he's doing all this work, he's in growth mode. Now imagine that there is a loudspeaker in the town that alerts him when there might be bombers that are coming overhead. So he hears the alert, get inside, hunker down, get safe. And so the farmer goes into a bunker, he closes the hatch, he goes in there, he has no idea how long it's going to take. But while he's in there, he's trying to do things that allow himself to self optimize. He's coming up the plans of like when he's going to harvest, he's going to come up with the plans on where he's going to store all of his crops. He's going to do all of these like self reflective type things as he's hunkered down because there's fear and there's concern in the environment, in the outside world that he is trying to always operate in and trying to grow within. And Lipton used this example as a way for you to kind of understand how the cell operates and how the cell, every cell in your body is functioning. If you are experiencing hardship, let's say you don't have any food, let's say you're lacking water, let's say you're, you've just run a marathon, right? You name it, stress. The cells in your body are kicking into efficiency mode. How can I operate most efficiently? How can I fix the damage inside of the cell? How can I do these types of activities that it can't do when it's expanding or transcribing the DNA in order to build new proteins and expand its growth? Right. And what he says is this back and forth where the cell is basically cleaning up itself and having this time to reset is actually extremely healthy. And David Sinclair in his book is talking about these sirtuin proteins that then go. And the enzymes, the seven enzymes that go there and kind of clean up the cell and fix the damage that's been done in the cell. The cueing for this, for these sirtuin proteins comes from stress. It comes from hormesis, the stress inside the cell. And so this could be through fasting. This is why he's promoting the idea of fasting. Eat in an eight hour window, go out there, experience cold exposure, experience heat stress, go into a sauna, go exercise. All of these types of things are actually very healthy if you do it in somewhat moderation. Do you want to go out there and not eat for a week? That's probably not healthy. Do you want to go out there and not eat for, you know, maybe a day? That might actually be a really healthy thing to do from time to time because it's forcing your cells, all the cells in your body to go in there and optimize. But yeah. Anything to add on, on that?
- [44:15]
Seb Bunny
No, I think you nail it. I think you're so good at being able to articulate these complex ideas and I think that's a perfect analogy. He essentially just talks about kind of these four different areas which make a big difference and that is eat less. To your point, it is plant heavy foods. And this is something that we can talk about at the end. I tend to disagree with somewhat and I think there's a lot of evidence support it. He is more vegetarian, plant based. And then you've got the Fasting, time, restricted eating, and then the cold and heat exposure. And the idea behind a lot of this stuff is essentially that hormesis idea. It's that you want to stress the body. Stress is good because it puts the cells into kind of cellular repair. Again, I can't stress people that are listening to this. To me, I would say what was so fascinating about this book is just understanding these sirtuins. I had no idea that we essentially have. We've got obviously our DNA, and these sirtuins sit on top of the DNA, preventing it from expressing in certain ways. As I mentioned at this part, and I'm repeating this because I think it's really important to understand, because I would say it was the biggest takeaway from the book for me is just how these satuins work, that they'll sit on the DNA preventing it from expressing in certain ways. And so you don't want a liver cell in the brain that's going to create massive issues. And so the sirtuins will sit on the DNA preventing that cell from expressing as a liver cell. However, at the same time, when there starts to be genetic damage, those sirtuins leave their little outpost. They go and repair that genetic damage. However, while they're gone, many times that cell can start to have issues. It can start to express as things that it doesn't want to be in that area of the body, which is what leads to a lot of this decline in health and aging and such. And then the moment it's repaired that DNA, it goes back to its little outpost and then silences that gene. The problem is, as we get older and we get more and more DNA issues throughout the body, and our sirtuins leave their little outposts, they're no longer preventing the DNA from expressing in certain ways. And so we start to get mutations, we start to get tumors, we start to get all of these other health issues. And sometimes the sirtuins, from my understanding, can also get lost on their way home and they can't find their way back to where they initially were. And so this is where essentially what he's been doing is how do we stimulate more sirtuins or to increase their activity. And that is all through, as I mentioned previously, nad. And if we can get more nad, that fuels the sirtuins, which helps with repairing DNA and it helps with preventing genes from expressing in ways that we don't want them to be expressing. And that is just what I found really, really fascinating. And so ultimately, going back to kind of what you were talking about, Preston I think he very much recommends focusing, eating less, plant heavy fasting, time restricted eating, and cold and heat exposure. And that helps support his body's natural repair mechanisms.
- [47:01]
Preston Pysh
Yes. Let's talk about what I found to be a really interesting part of the book, which was this, where they took the optical nerve on the rat. So going back to this idea that they were making the rats older, the mice older, by adjusting their epigenetics through CRISPR to prove that they could create age, or is someone aging faster? And Sinclair had this comment in the book, if I can give you age, if I can increase your age, then I should also be able to take the age away. And for him, the way to prove this, I guess there's a test in this community where they can go. They can perform surgery on a mouse of its optical nerve. The optical nerve connects the eye to the brain. It sends the signal back to the brain so that the mouse can see. And what they do is they perform a surgery where they go in, they pinch this optical nerve to cause damage. And the optical nerve is one of the parts of the body that cannot rejuvenate itself. So once this damage is done, it's irreversible, or at least it always has been irreversible. So what they did is they did this surgery, caused the optical nerve to have damage through pinching it, and they crushed it. And then they went to these Yamanaka factors, these four genes. And my understanding is they. They used three of the genes and they pulsed the genes so that they were only being transcribed occasionally. It wasn't like it was full on because there's issues with it becoming cancerous if they can just constantly have these turned on, because basically the cells in that region basically reset to a stem cell. There's no differentiation, and the cell has no idea what to be or what to do. So what they did is they pulsed it, they did it through, forcing the mice to drink some water occasionally with. I forget what they had in the water that caused these four genes, or, I'm sorry, three of the four Yakimoto genes to basically reset the epigenetics of the cells in the optical nerve. And so when they did this, it was provable that they were actually able to restore the eyesight of the mice. And so this was kind of a really big point in the book where they're proving that depending on how they're able to access these Yamanaka factors, they're actually able to reverse aging and bring something, basically a full reset back to the cells. Now, does this mean that they can turn back the clock and let's say you're 60 years old and now all of a sudden that they can make you 40? I think the answer is that's what they're trying to do, but they're not there yet. But they're experimenting with really crazy ideas like this that almost seem like it's out of a fiction novel. And it seems to be moving there very quickly. Going back to the original comment that we had at the start of the show when we said about the MIT Ray Kurzweil comment that we're going to be at the longevity escape velocity by 2032. You know, a lot of this research and a lot of the things that we're talking about, I think some of these things are five years old to seven years old. Some of these studies that have been done. So there's been a lot of progress. I'm kind of curious your thoughts on AI just accelerating so much of this, because when it comes to the terminology. Right, like to your point, Sep, I'm with you 100%. I think everybody in the audience is with you 100%, especially if they're not in, you know, the medical or biology space. Piecing this all together for something that is so complex and so terminology heavy, AI, I think, is going to just eat through so much of that chaos and confusion with ease, and it's going to lead to insights that I don't even think that we can possibly. And maybe that's why, you know, you have Ray Kurzweil, he's really good at seeing a systems of systems kind of culmination of how everything kind of vectors into an accelerated timeline because of these additional factors like AI. What are your thoughts? Do you think that that's going to play a huge part in a lot of this moving forward?
- [51:09]
Seb Bunny
I believe so, because I think the way I look at it, and similar to what you just mentioned, is part of the learning curve is not actually the complexity of what's happening. It's the language to be able to actually piece everything together. So half the time I'm going back and being like, wait, wait, what is NAD again? What is NAD doing in the cell? And so although you understand this stuff, it's just, it's essentially like learning a whole new language. But once you've learned that language, it's not that much different communicating in English as it is to communicating Spanish. You just got to understand the terminology. And I think going back as well to some of these studies, it really, it opened my eyes as to what was possible, I mentioned it very briefly previously. They were also looking at fertility in mice. And one of the things is this kind of common held belief in society today. Women are born with a finite amount of eggs. And as you age, the amount of eggs you have slowly die off. They become unusable. We see infertility. What he was able to do is he put female mice through chemotherapy and they'd lost all of their viable eggs. And he called this mouse a pause. And then they were given something called nmn. And NMN is the precursor to nad. I dug into this a little more because I didn't quite understand it. Which is necessary. Oh, nad, which is necessary for these sirtuins. It feeds the sirtuins to be able to remember silence genes and go and repair DNA breaks. Well, nmn, if you actually take nmn, it's the precursor to NAD production in the body so that it actually feeds the twins. If we just go and take nad, from my understanding, when it enters the gut, most of it just gets destroyed. We can't actually absorb most of the NAD when we go and take it through supplement levels. So they were feeding these mice NMN and which is boosting these NAD levels. And then what was happening is these infertile mice were regaining fertility and some even produced offspring. Again, you're just like, that is mind blowing. And if I remember correctly, in the story, one of his friends or family member, so don't quote me on this, he ended up recommending, I think she was going through menopause or something like that, and he recommended NMN to her and she actually went back and started having a period again. And so you're just like, this is freaking fascinating. And so I think the world around longevity is definitely an interesting space. And I think there's some beliefs, such as the fact that we have a finite amount of eggs, that I think we're increasingly going to see studies that allow us to reverse that.
- [53:37]
Preston Pysh
Yeah, I don't think that we have any idea how crazy some of this is about to get. I think in the coming decade it's going to get pretty wild.
- [53:45]
Seb Bunny
So for those that are listening to the podcast, you just showed a container of. Was that nmn?
- [53:50]
Preston Pysh
That's why we laughed. If you were just listening to the audio, you just heard us burst out laughing and we just kept talking. I've been taking since I read this book, you know, I read this book years ago, but since I read the book, I've been actually taking NMN ever since I read it. Probably two Years ago or whenever.
- [54:06]
Seb Bunny
Did you notice a difference?
- [54:07]
Preston Pysh
No, I. I don't notice a difference at all. But, you know, in the book, my big thing was, is if I was feeling any different, like in a bad way or upset stomach or whatever, like, I was going to stop immediately. But I think the thing that surprised me most was how I don't feel anything at all. Just for reference in the book, David Sinclair says that he has his father taking nmn and you know, whether it has a longer life span, you know, enhancement, I don't know. I don't know. But I've been taking it. And this boosts going to Seb's point. This boosts your sirtuin protein. Supposedly it's boosting your sirtuin proteins to repair, you know, your cell. It's a precursor to. You get a very similar effect if you do these hard things that we were talking about earlier, which was eat less, go out there, sit in a. In a sauna, go do a cold plunge. You do these types of things and you're kind of creating the same NAD plus levels and signaling to your cells to repair themselves. So you can just do the free version of that by. By stressing yourself a bit, and then you don't even have to take bills. But I've been trying.
- [55:22]
Seb Bunny
Like, this brings me to the pushback on a lot of this longevity stuff, is that we're always looking for a pill for something.
- [55:28]
Preston Pysh
Yeah, right.
- [55:29]
Seb Bunny
People don't like doing the work.
- [55:31]
Preston Pysh
Yeah.
- [55:32]
Seb Bunny
People want to skip the work in order to be able to just take some form of pill that gets the benefits. People want to be able to have the benefits of the gym without going to the gym. And so it's just like, I think there's countless studies which are showing the amazing benefits of sauna, cold plunge, restrictive eating, those kind of things. But people don't like discomfort. That's the problem. Yeah.
- [55:54]
Preston Pysh
Amen.
- [55:54]
Sponsor/Ad Voice
Yeah.
- [55:55]
Preston Pysh
That is the issue. What are your thoughts on. Let's say you can dial back the clock. Let's say that people want to tap into these Yamanaka factors and they can knock 10 years off their life and reset and they start, you know, the wrinkles start going away and whatever. So what are your thoughts? Like, you know, Sinclair talks about this in the book. He goes and he does all these different speaking tours. He asked the audience, you know, what are your thoughts if you could live to 120? And he frames the question this way, like, if you could live to 120, 130. And everybody in the audience, for all Intents and purposes are just like, oh, God, no, I wouldn't want to do that. And he says that a lot of the stigmatism around, like, not wanting to live longer is people equate. Once I'm 100, I'm literally in a wheelchair or I am, you know, going around with a walker, and I'm not living a life that I want to live where I have full mobility to do and act the way I was when I was 30. And Sinclair's kind of making the argument, well, what if you could. What if you could have full mobility, full cognitive control and all these types of things at 100 or 110, would you still want to live longer? And it just kind of throws people into this cognitive, like, confused state of, like, not even really fully knowing if that's what they want. And I think this goes to a bigger point, but I'm going to pause right there and just kind of get your thoughts, Seb.
- [57:21]
Seb Bunny
So there's so many different ways you can take this. And the first thing I'll say is that I think you can look at it purely from a selfish perspective. And it's like, for sure, let's just go extend life. As long as I'm expanding my, as he calls it, his health span, the difference between lifespan and health span, and I think as long as my health span is matching somewhat of my lifespan, then I'm actually living a quality life and I'm able to go and do things I do not want to be a vegetable laying in a bed, unable to do anything. Poor memory. That just does not interest me. And so you could say at the base of it, if you're kind of thinking about it from a purely selfish perspective, it sounds great. However, there's a couple of things that kind of come to mind. First off, I think that it's actually the finality of life that gives value to life. It's because we only have a finite amount of time on this earth that actually allows us to enjoy these amazing moments. Whereas if I live to 500, if I live to a thousand, you can pretty much go experience most careers, you can go dive down most rabbit holes, and I think you'd lose a lot of interest in life. And I think that the other thing that's interesting is I went and dug into a handful of studies and one in particular, there's a guy called Samuel ellis, and in 2018, he followed 52 different species and found post reproductive stages are rare in mammals. And there's essentially, it's only humans, and there's a couple of toothed whales that have post reproductive life. And you could argue that this isn't accidental. It's that evolution tends to favor lifespans just long enough to ensure successful reproduction and survival of the offspring. But once that job is done, continued existence offers very diminishing evolutionary returns because you're obviously now consuming resources that could be for the next generation and are necessary for that generation to survive. And so I think there's an adaptability issue that arises with longevity around. As older generations kind of pass on, newer ones emerge that are better suited to the current environment. And the longer species live, the more ossified I think they become, both biologically and behaviorally. And we even see this in the financial world, the S&P 500. The average age of a company in The S&P 500 today, if you look 100 years ago, was like 50 years. Today it's like nine years or something like that. It's dropping so rapidly because it's so easy to become ossified. And I think that as a species, if we want humanity to thrive, I would argue that longevity is probably not going to be the way for humanity to thrive. It's actually probably just maintaining whatever lifespan we're meant to be born with because it allows us to adapt to our environment. And the final point that I'll mention along those lines is that I think that a lot of this longevity space evolved out of fear. If we look at the difference between western medicine and eastern medicine, well, pre current modern medicine, when the eastern side of things like if you got ill, you got a terminal illness, you're going to die within a few months. And so a lot of people experienced and saw their elders kind of pass on very rapidly. And so they spent a lot of time with their elders. They passed on wisdom. Death was a part of life. But I think that as we've got better at being able to extend life, but not necessarily health, we see people that live for another 15, 20 years with Alzheimer's and tumors and they're suffering and the quality of life is just not, not there. And so we've now got this fear of death. People in the western world are so scared of death because they just don't see it. And we end up putting a lot of these elderly people in homes. Yeah, we essentially just kind of lock them up. We don't see them, we don't experience death. So I think that a lot of life today we are fearful of death. So we want to constantly extend life. But I don't necessarily think that's the reason why we should be extending life. And I'm curious to hear your thoughts.
- [61:04]
Preston Pysh
I just think at the core, if a person doesn't feel like they're providing value to society, like, what's the point? What's the point of extending your life? Because deep down inside, I don't think people are going to be happy if they don't feel like they're contributing in some way, some fashion, or feel like they're providing some type of service or productivity to society. You get bored, you get stagnant, you just get unsatisfied. You hear this all the time with people that make a bunch of money all the time. People say, oh, Yeah, I made $50 million or whatever the number is. And then they're like, and I sold my business. And, like, I just didn't really know what to do after that. And I was just deeply dissatisfied for quite a period in my life. And I think that when you think of a person that's really older and of age, a lot of that comes from just not physically being able to do anything. They're just kind of. They've become a victim of their own environment because they just can't even really get around and be mobile and do things. So how can they create value to society? At that point, they're cognitively declined. It's really hard to compete. They've got their friends and whatnot, but at the same time, they're just kind of ready to go. It's not that they want to go, but it's not like they're upset about it at the same time. And I think a lot of it comes down to just your happiness of feeling like you're contributing something new to the world or something novel to the world.
- [62:33]
Seb Bunny
A few years back, I remember looking into, and don't quote me on this, I remember looking into the oldest working individual in the uk, and if I remember correctly, this guy has basically smoked since he was 15 years old. He finishes work, he goes down the pub and has a pint and, sorry, eats fish and chips, which are basically just cooked in seed oils. And this guy was 106 or something like that, and he's still working full time. And you're just like, this guy's just defied everything that we've been discussing in the whole idea of longevity. And so then you ask, you're like, well, what is at the root of this? And I think sometimes we're trying to alter ourselves on a cellular level. Yet what if it's. And to your point, what if it's actually got. If you want to extend life, it's not about the cellular level. It's about finding purpose. And if you ever read the book Man's Search For Meaning, by Viktor Frankl, who was kind of In World War II, he talks about how the tension between what a man has achieved and what they want to achieve is what basically allows us to survive. And there's people. There was. I think one of the analogies or one of the examples he gives in the book is there was this guy that was. Had been in one of these camps for. During World War II, had been in one of these heinous camps for multiple years. And what had kept him alive is knowing that if he's able to get out of this camp, he's going to go find his wife. And he ends up finding out that his wife had been killed and he dies the next day. And you wonder. You're like, that was just hope keeping him alive. It was his mental perseverance keeping him alive. And so I think that we can change ourselves on a cellular level as much as we want. But in the end, the most important factor, and this goes back to your point, Preston, is purpose. It's like actually feeling like we're creating value in society. Because even if we may be healthy, even if we may be able to extend longevity and stuff, if we don't have purpose in life, what is the point?
- [64:21]
Preston Pysh
Yeah, I think a lot of people just don't want to reinvent themselves, too, because it's a lot of work. Right. It goes back to, like, the difficulty of sitting in a cold plunge or getting into. Some people can't stand it, other people like it. But I think when you think about adding value, the world is a super competitive place. And a lot of the times people want to be in control of whatever they're creating. And a lot of jobs, you're not in control. You're just answering to somebody else. That's telling you. And so if you've worked that job for somebody else and you've never really even had the opportunity to create something yourself because it's super hard and super competitive as you get older and you've gone through this and you're 80, 90, 100 years old, I think a lot of people may not want to keep battling the competition to add value. They're just kind of done. They're tapped out. I don't know, maybe that's a pessimistic way to look at it, but I think there are going to be some people that enjoy the hell out of that competition and they're going to want to keep going. Right.
- [65:23]
Seb Bunny
One thing that I found really interesting is a little while back I read a book called Deep Nutrition. And this lady, Catherine Shanahan, this book I highly recommend for anyone who's kind of diving into the health side of things, the food side of things. And she mentioned a study, and I had to go back through her notes to try and find this study. One of the things she mentioned is they did this study in 1994 called Length in Life in the Ancient World, a controlled study. And they basically looked at Rome between the years of 650 BC and 602 AD. So this is like a. A thousand year, no, 1200 year period. And they looked just at males. They removed infant mortality, they removed people that were assassinated through the death penalty, and they removed death in battle. And what they found is that the average person in Rome during that time was living between 75 to 80 years old. And you're just like wild. So when you remove these other issues, infant mortality, death penalty, death in battle. Well, now let's compare that to the US today. Well, in 2023, and I had a look up this yesterday, the CDC, the Center for Disease Control, says that the average male in the US in 2023 lived to 75.8 years old. Now, if you remove infant mortality from that, which in the US is like six deaths per, I think it was like 1,000 or 10,000 or something. And so if you remove infant mortality from that, it increases it to 76.2. Well, 76.2 is no longer than what the Romans were living once you remove out those factors. And so this is where I think you start to look at the incentives. And there is an incentive for pharma and the medical industry to push that. We have been aging that we have been able to increase the average age of the individual in the face of all of these things that are going on in the world. But in reality, I think there are some studies that would say that's not necessarily true. And I think that what you can also say is that the health of the general population today, from over the last, say, 50 years, we've seen rising rates of diabetes, we have seen rising rates of allergies, chronic illness, all of these things. I would not say that the average person is healthy. And so that's where I tend to think that if you're looking at the journal data, the scientific journals, a lot of this stuff, when you start going down these rabbit holes, is curated A lot of it is manipulated. And I would argue that when you start looking at the data from a different perspective, we may not have increased lifespan to the extent that we might believe we have increased lifespan. I don't know what your thoughts are on that.
- [67:55]
Preston Pysh
Yeah, I think to date, I think you're exactly right. I don't think that there's anything that's. Especially comparing the metric back to Rome. Right. Like, that's crazy. It doesn't surprise me, though. It doesn't surprise me. I think that when you look at Western diet right now, I think that's one of the reasons why it's as bad as it is. But I think I kind of suspect in the coming decade or two that we're going to really start to see the glass ceiling get shattered with respect to the ages that we see people start living, especially if people are eating appropriately and you kind of lean into some of this technology that I think we're really starting to deeply understand of how the body actually functions and how it regulates itself.
- [68:39]
Seb Bunny
I think it'll be interesting over the next, say, 50 years.
- [68:42]
Preston Pysh
Yeah.
- [68:43]
Seb Bunny
So, Preston, when you hit 100 and when I hit 80, we'll have a look back and listen to this episode and see what's happening.
- [68:50]
Preston Pysh
What are you implying here, sir? What are you implying? I'm turning red.
- [68:55]
Seb Bunny
Okay.
- [68:55]
Preston Pysh
That's all I had. Is there anything else you want to cover on this particular one, Seb?
- [68:59]
Seb Bunny
I did a little bit of research, again, because I like to try to understand, like, what is the accuracy of this information. And I think to be able to be fair to the science, what's interesting is there are actually quite a lot of studies that go against what lifespan has also been saying. And so there was a guy, specifically Charles Brenner, and he did a whole bunch of studies on this stuff. And one of the things he found is in yeast, sirtuin genes help only 1 in 5 million cells live longer. And across the whole batch of 5 million cells, they actually shortened lifespan. Lifespan extension effect in yeast is statistically negligible. There was another study that looked at. In 2011, researchers from seven institutions published that sirtuin genes do not extend lifespan in worms or flies. And then there was basically just a whole other bunch of results that there was a lot of media bias. While the positive results made global headlines, a lot of the negative results were not published. And so there's a bit of selective storytelling. And so overall, and I'm curious to hear your thoughts, I thought the book was really fascinating, and I think that from deepening my understanding about how our body thinks about repair, how our body thinks about aging. It opened my eyes massively. However, I would say that the author, it sounds like he's very much bought into the medical industry, the pharmaceutical industry, and as a result of that, he's citing things like, well, he wants to be vegan. Vegetarian is best. But now we're starting to see a lot of the literature coming out, which is disproving a lot of the historical literature, because you realize that historical literature has been born and paid for by certain corporations and entities that benefit from that narrative. So I think that there's definitely fascinating points that you can dig into throughout the book, but I think there's some interesting points as well, which I think aren't necessarily backed up by current understanding of food and health and such. But overall, I thought it was a really super interesting book.
- [70:55]
Preston Pysh
Yeah, I would say on the contrarian point, to kind of add some to what you're saying. Number one, he has a lot of investments in a lot of these companies that are, you know, working in some of these areas. The other thing that I had heard this was years ago was that the book was somewhat of a fundraising tour to raise money for his lab and the research that he was doing to get more money there. The point on the s. The enzymes was really interesting because I never even thought about that life or the time of the algae and whether, you know, statistically being able to prove whether that's actually extending it or not because it's such a short span of time, I never even thought about that. But that's a really interesting point of view. The one thing that I think is, for whatever reason, I just really buy into it. This idea that it's based. The aging is based on information loss. I just totally buy into it. Like, the way he lays it out in the book, it just intuitively makes sense. It seems to be simple enough to actually represent what's probably taking place. And I think that the loss of information with respect to the epigenetics, I think they're onto something really, really big with that simple idea. But, you know, as we know, the body is so freaking complex. And I guess that's why I'm kind of excited for them to kind of stick AI on it and to assist in some of the further research and where it might be all going in the future.
- [72:23]
Seb Bunny
But this is where I think it'll be interesting to see. Like, this is all very multifactorial, so we may be able to go in and reverse aging in some of these cells. But if a person doesn't have a desire to live, is their life still going to come to an end? And so I think that that's where it's really interesting is weighing up all of these different ideas and purpose and spirituality. And all of this stuff, I think, is really, really fascinating. But again, it's definitely an interesting book to read, and I definitely recommend people giving it a read. And some of the stories, some of the examples of what they're doing in mice is mind blowing.
- [72:55]
Preston Pysh
One other thing that I'll say, having gone to a bitcoin conferences and meetups and talking to a lot of bitcoiners. Bitcoiners love talking about longevity. Like, you can throw around a lot of these terms that we were talking about on this show, and most people in the bitcoin space are like, oh, yeah, yeah, yeah, I know all about that. And then they go off on their tangent. And I don't know if that's been your experience, Seb, but that's been my experience talking to bitcoiners, as they're totally into this stuff.
- [73:22]
Seb Bunny
Absolutely.
- [73:22]
Preston Pysh
Yeah. Anyway, just a side note, that's all we have for you guys. I apologize if our terminology is off. Our examples we provided weren't helpful. We were trying. We had fun recording it. Personally, I had fun recording this, and we really appreciate you guys tuning in. And if you have any good longevity books or any new insights into this space, we would love to cover it more. I love learning about this kind of stuff. And, Seb, give people a handoff to anything that you want to promote or talk about.
- [73:54]
Seb Bunny
Cool. Thanks, Preston. Yeah. And again, like, I really appreciate everyone just giving this a listen. And just as Preston mentioned, I apologize we butchered some of the explanations. A lot of this stuff, I feel like you guys are going to be learning alongside Preston and I.
- [74:08]
Preston Pysh
Absolutely.
- [74:09]
Seb Bunny
And I highly recommend, like, giving the book a read and really just trying to dig in and think about what it is that they're saying. Because I've found that actually having to speak about this together on this podcast has hugely improved my understanding of these topics. It may not seem like that, but it has hugely improved my understanding of these topics. And so highly recommend taking notes, going and digging into this stuff. And if you don't quite understand something, Type it into YouTube, type it into AI. These days, AI has blown me away. You just ask a question, I don't quite understand this. Can you explain it to me and give me an analogy? And it just lays out phenomenal examples. But if anyone wants to find me, you can find me at just Sebunny B u n n e y on Twitter. And then you've got my website, saidbunny.com, which you can find my books that didn't cost money and such. But again, as always, I appreciate you guys giving it a listen. And thanks a lot, Preston, for having me on.
- [74:57]
Preston Pysh
Okay, until next week. Thanks for listening.
- [75:01]
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