Speaker 1: Brought to you by Toyota. Let's go places. Welcome to
Speaker 1: Forward Thinking. Hello everyone, and welcome to Forward Thinking, the
Speaker 1: audio podcast that looks at the future and s as well.
Speaker 1: We know where we're going, but we don't know where
Speaker 1: we've been. I'm Jonathan Strickland, I'm Lauren Volkeman, and I'm
Speaker 1: Joe McCormick. So today we wanted to talk about a
Speaker 1: guy who's had some fairly exciting and controversial ideas, Aubrey
Speaker 1: de Gray. And this is someone who has sort of
Speaker 1: dedicated the second half of his professional life to figuring
Speaker 1: out how to defeat the symptoms of aging. You may
Speaker 1: have seen him in various mind expanding videos on the Internet.
Speaker 1: He's a uh, scraggly looking fellow with a gigantic beard.
Speaker 1: He's kind of like a latter day rest sputant. David
Speaker 1: David step of Forbes called it his rip Van Winkle
Speaker 1: beard ever, which I really like, Every single article I
Speaker 1: have ever read had anything to do with him, had
Speaker 1: at least a part of a paragraph dedicated to this
Speaker 1: man's beard. And indeed it is impressive. His beard. It's
Speaker 1: like a tree. It is it is he he's got.
Speaker 1: He's been on Ted Talks. He's we've got it. We've
Speaker 1: got a feature on him on Curiosity Project. And uh,
Speaker 1: it's because he has some pretty interesting ideas of how
Speaker 1: to combat the symptoms of aging. And he comes from
Speaker 1: this from a really interesting pathway because he didn't start
Speaker 1: out as a biologist. He started out as computer scientist,
Speaker 1: specifically focusing our artificial intelligence, right, and he's never actually
Speaker 1: been well, I mean, he he has studied a lot
Speaker 1: of biology, but he's studied theoretical biology, and so he's
Speaker 1: sort of approaching this from the perspective of an engineer,
Speaker 1: which has some doctors and other people within the medical
Speaker 1: field concerned that perhaps it's an oversimplified you. But I'm
Speaker 1: kind of getting ahead of myself. We should sort of
Speaker 1: talk or about his area of interest and and what
Speaker 1: it is he's trying to accomplish. So, first of all,
Speaker 1: you could say that he's a gerontologist in a way,
Speaker 1: that's someone who studies aging. So that's the whole area
Speaker 1: of the study of aging is gerontology. And he is well,
Speaker 1: he formed this this this organization called the Strategies for
Speaker 1: Engineered Negligible Senescence that again sends send there you go
Speaker 1: with the acronym negligible senescence, and so senescence that means something.
Speaker 1: What does senescence mean? All right? Well, so, so cells,
Speaker 1: normal healthy cells go through a life process in three stages.
Speaker 1: First you've got normal healthy cell division, which is mitosis um.
Speaker 1: And then eventually the cells will stop dividing and that's
Speaker 1: called senescence um. After that you have cell death, which
Speaker 1: is a poptosis. But that that comes later and and
Speaker 1: is debatably awesome for your right. So this idea of
Speaker 1: the negligible engineered sinescence or sentizens depending upon how it's pronounced,
Speaker 1: I honestly don't know. Uh. The idea here is that
Speaker 1: we are trying to find a way to to halt
Speaker 1: that that phase of of of an organism's life where
Speaker 1: the cells are no longer dividing in a healthy way
Speaker 1: or they're dying off too early. Essentially, the ideas to
Speaker 1: try and preserve an organism's healthy state at the peak
Speaker 1: of its life. So, for example, the numbers that I
Speaker 1: tend to hear for a human according to the Aubrey
Speaker 1: de Gray stuff, is between the ages of five and
Speaker 1: twenty nine, right and there where you are in theory
Speaker 1: at your healthiest at least as far as you know
Speaker 1: an average person is concerned. So, uh, it's all about
Speaker 1: trying to create this this uh solution or actually series
Speaker 1: of solution to maintain that kind of level of health
Speaker 1: uh indefinitely. And it may extend your life, it may not,
Speaker 1: but at any rate, what the the ideally, what it
Speaker 1: would do is allow you to have a healthy, active
Speaker 1: life throughout your life. Right. He said several times that
Speaker 1: that added lifespan is not the point of all of this.
Speaker 1: It's it's really quality of life that he's looking for, right,
Speaker 1: Although he's also talked about how he would love to
Speaker 1: live to a thousands that he could read all the
Speaker 1: books he'd want to re I mean, he wants to
Speaker 1: see when when some of us, many of us, a
Speaker 1: few of us. I think we've already established that I'm
Speaker 1: planning on trading in Joe's immortality for double immortality for myself,
Speaker 1: as I recall from our previous podcast. More right, so, yeah,
Speaker 1: I need to be twice as immortal. But he lays
Speaker 1: out the Gray lays out seven principle mechanisms of aging
Speaker 1: and or you can also think of this as different
Speaker 1: types of damage. This is interesting because I think most
Speaker 1: people don't think about what actually happens when we age.
Speaker 1: They don't realize it's just it's the cumulative effect of
Speaker 1: a series of processes, several biological processes exactly. And so
Speaker 1: any solution would not be, like I said, just one solution.
Speaker 1: It would have to be multiple solutions to meet all
Speaker 1: the requirements to tou to cancel out these seven principles
Speaker 1: of aging. So what is aging at its core? Well,
Speaker 1: it's the way he breaks it down, because he's looking
Speaker 1: at aging as these various types of damage. He has
Speaker 1: the seven different types. The first three he lays out
Speaker 1: our types of cellular damage. The first is this loss
Speaker 1: of cells, the idea that you have cells that die
Speaker 1: and they aren't replicated, so there's not they're not being
Speaker 1: replenished in any way. So you could have muscle loss,
Speaker 1: bone loss, that kind of thing. And a lot of
Speaker 1: these different types of damage that he talks about relate
Speaker 1: to specific kinds of disease is or or conditions that
Speaker 1: you are probably familiar with. So does this particular problem
Speaker 1: have anything to do with what I've heard of the
Speaker 1: hay Flick limit. Yes, that would be the limit that
Speaker 1: was proposed by Dr Leonard hay Flick back in nineteen
Speaker 1: sixty five, and he he observed that that cell death
Speaker 1: process that I mentioned earlier, that apoptosis and this this
Speaker 1: is a natural process. It's really useful for you know,
Speaker 1: for us not having webbed hands um in because because
Speaker 1: embryos when when you're when you're going through development, UM,
Speaker 1: not all parts of you wind up being you. You know,
Speaker 1: it's we lose your tails, we lose the webbing between
Speaker 1: our fingers, and so that's very useful for that. UM.
Speaker 1: Apoptosis goes on during menstruation. It's really great for fighting
Speaker 1: off viruses and cancers. UM. However, like Jonathan was saying,
Speaker 1: at a certain point, your cells are dying off and
Speaker 1: they're not being replenished, right, So that that's one thing
Speaker 1: that we would need to address. And he has he's
Speaker 1: named the various UH solutions, or at least the kind
Speaker 1: of overview of what the solution might be. Keeping in mind,
Speaker 1: we don't have solutions for all this. If we did,
Speaker 1: we'd already know or at least we'd all be healthier.
Speaker 1: But it's sort of that he's named what the overall
Speaker 1: approach would have to be in order to you know,
Speaker 1: address this issue. So in this case he calls the
Speaker 1: this part replena sends each one having sends at the
Speaker 1: end of it, sc and s which is that acronym,
Speaker 1: So that that's the first one is the loss of cells,
Speaker 1: you know, figuring out how to make sure that cells continue.
Speaker 1: He's replenished. He's proposed stem cell therapy for that one
Speaker 1: as being kind of the leading Yeah, and in fact,
Speaker 1: stem cells are just kind of magic. They're unicorns. They're
Speaker 1: pretty much the They're made of unicorn nichols. That's a
Speaker 1: science fact, guy, So you can just buy that straight
Speaker 1: from a think geek. You get that canned unicorn meat
Speaker 1: you've got. That's not the way that works. Cells they're
Speaker 1: like the they're like the phenomena of medicine, right right exactly.
Speaker 1: These are the cells that have the potential to develop
Speaker 1: into other types of cells. And depending upon what kind
Speaker 1: of stem cells you're talking about, the variety of cells
Speaker 1: they can turn into is very wide or very narrow,
Speaker 1: because not all stem cells are the kind where this
Speaker 1: this one proto cell could be anything. Some of them are.
Speaker 1: They can be any type of vascular tissue, that kind
Speaker 1: of thing. So it all depends on the type of
Speaker 1: stem cell. But anyway, yes, he does say that that
Speaker 1: is one potential way we could meet this challenge, and
Speaker 1: in fact, from why I understand it might be one
Speaker 1: of those things that would be a requirement because some
Speaker 1: of the other solutions he's proposed would UH end up
Speaker 1: affecting us in such a way that we would have
Speaker 1: to have stem cell treatment in order to UH to
Speaker 1: to combat some of the side effects we could have
Speaker 1: from treatments from the other principles. This is where it
Speaker 1: starts getting complicated. But we haven't even gotten into principle
Speaker 1: number two. You okay, let's go to number two. Thank you.
Speaker 1: Number two is that uh, there are two different version
Speaker 1: of this, so this is technically two and three. So
Speaker 1: number two is that you end up with too many
Speaker 1: cells because the cells don't die when they are supposed
Speaker 1: to UH. And that one he suggested a pop apop
Speaker 1: apopto sends this is so hard to say because of
Speaker 1: the sens acronym at the end. That was the that
Speaker 1: was his solution or overview of what the solution would
Speaker 1: need to be to take care of that problem. And
Speaker 1: the other type was too many cells because these cells
Speaker 1: divide when they aren't supposed to, which sounds like cancer exactly.
Speaker 1: That's that's pretty much what cancer is. And so his
Speaker 1: overview of what the solution would have to be is
Speaker 1: called onco sens which oncology that makes sense, you know, sure, yeah, yeah,
Speaker 1: because because cancer is actually pretty cool. I mean, not
Speaker 1: when you have it, obviously that's terrible, but um, but
Speaker 1: but the the way that cancer cells don't die is
Speaker 1: kind of terrific, and so people are doing a lot
Speaker 1: of studying into that to see if we can use
Speaker 1: that to extrapolate this idea that you can take something
Speaker 1: that is very harmful in one one manifestation, but find
Speaker 1: a way of applying some of that in a medicinal
Speaker 1: way in order to prolonged life. It's it's a fantastic
Speaker 1: idea if we can make it work. I mean, we've
Speaker 1: seen this in other applications as well, not just with cancer,
Speaker 1: things like viruses. We've seen medicine used viruses in order
Speaker 1: to have uh nanomedicine delivered to particular parts. If you
Speaker 1: can reprogram them, then you can get them to do it. Yeah, exactly,
Speaker 1: that you can code of virus shell with a certain
Speaker 1: type of protein and theoretically it'll seek out the right
Speaker 1: kind of cells to deliver a cellular amount of of medication,
Speaker 1: So you're dosing particular cells. So you know, we see
Speaker 1: this where we're using things that were at one point
Speaker 1: potentially hazardous or deadly, uh, in other ways to have
Speaker 1: to improve our lives. So that might work out, but
Speaker 1: we still have to figure out how to actually accomplish
Speaker 1: any of that. Well, not only that, but how do
Speaker 1: we actually stop the uncontrolled division? How do we stop
Speaker 1: the cancer part of cancer and utilize the beneficial aspects
Speaker 1: while getting rid of the ones that are deadly? And uh,
Speaker 1: he's thinking about mainly things like a gene therapy as
Speaker 1: an approach. And again that's one of those approaches that
Speaker 1: some people say may oversimplify the matter, although it's really
Speaker 1: kind of hard to say right now, because you can
Speaker 1: you can frame these approaches in such general language as
Speaker 1: for them to be um, they can fit any definition
Speaker 1: in a sense, you know, like if you if you
Speaker 1: just sit there and say, someday we will be able
Speaker 1: to do this, it's kind of hard to refute that.
Speaker 1: All right, Well, that's the three types of cellular damage,
Speaker 1: but then there's three types of molecular damage. One of
Speaker 1: those is damage to DNA, specifically in mitochondria. These are
Speaker 1: the cellular powerhouses. This is an an energy element to
Speaker 1: the way cells live. They have their own DNA, mitochondrial
Speaker 1: DNA and UH. Unlike the DNA that you find in
Speaker 1: a cell nucleus, which has some repair systems built up
Speaker 1: around it to help maintain that DNA's integrity, the mitochondrial
Speaker 1: DNA they don't have that kind of support system, so
Speaker 1: they are more vulnerable to various types of mutations, right
Speaker 1: and there they exist in a highly oxidized environment, which
Speaker 1: makes them even more susceptible to damage than a lot
Speaker 1: of other little cellular bits. Right. So that's that's another
Speaker 1: one of the ones that he's identified, and Mito sends,
Speaker 1: which is probably the easiest one to pronounce, is his
Speaker 1: overview of the solution to that. Then you have two
Speaker 1: different types of molecular junk or garbage, depending depending upon
Speaker 1: which one you read, but in any case, it's unwanted
Speaker 1: molecules that begin to accumulate within an organism and some
Speaker 1: accumulates inside cells, which these are byproducts of cellular process
Speaker 1: e is um. One example of this would be cardiovascular
Speaker 1: disease that it can manifest in that way. The approach
Speaker 1: that that Degray suggests is called liso sins. And then
Speaker 1: there's the molecular junk that accumulates outside a cell's wall,
Speaker 1: so in between cells, and this is created through metabolism
Speaker 1: uh and de Gray points out that the an example
Speaker 1: of this could be manifested in something like Alzheimer's or
Speaker 1: diabetes and h a millocin's or um. Yeah, and a
Speaker 1: millocent's is the name of the approach that you would
Speaker 1: have to address this issue. So those are the three
Speaker 1: types of molecular damage, right, and and there are there
Speaker 1: are already processes going on inside your body that are
Speaker 1: that are taking care of some of this junk. The
Speaker 1: the licensome with within cells is the organ that kind
Speaker 1: of digests some of this junk, but it can't digest everything.
Speaker 1: And say, some of the therapy that he's suggesting is
Speaker 1: adding extra enzymes in there to drive the licensome to
Speaker 1: to get rid of more stuff than it currently can. Right,
Speaker 1: Some of these molecules that get formed turned into stuff
Speaker 1: that cells just can't process, and so it just accumulates.
Speaker 1: That's why they call it junk. It's this idea of
Speaker 1: kind of like, ah, if you've ever lived with someone
Speaker 1: who is a hoarder, when you walk into the room
Speaker 1: and you just realize that tomorrow I will not be
Speaker 1: able to open this door. Uh, same sort of thing.
Speaker 1: These cells get bogged down with lots of molecules that
Speaker 1: they cannot deal with, and then eventually that causes problems
Speaker 1: outside of your cells. The the immune system process, it's
Speaker 1: called phagocytosis, that's supposed to take care of this, and
Speaker 1: it and it does to a certain extent, but just
Speaker 1: from the root, like eating, you've got some cells that
Speaker 1: come and eat up the junk exactly. Yeah. Yeah, but
Speaker 1: and and so his his proposition is to kind of
Speaker 1: chemically amp up that process. Right. And then the final principle.
Speaker 1: So we've got the three types of cellular damage, three
Speaker 1: types of molecular damage. The final principle is called cross linking.
Speaker 1: And this has to do with tissue. So you have
Speaker 1: tissues that that hold things into place, kind of give
Speaker 1: a shape, sort of a scaffolding, if you will, for
Speaker 1: various types of so that all your cells aren't just
Speaker 1: floating free within your body, right, You're not just a
Speaker 1: big lobby massive cells. It's very important as far as
Speaker 1: I'm concerned, But they're supposed to be there's in most cases,
Speaker 1: they're supposed to be elastic, right, So the idea being
Speaker 1: that they can, uh, they can change in shape and
Speaker 1: uh and maintain and organisms. Uh. Yeah, that's why you
Speaker 1: can can push on your skin and have it bounce back. Yeah,
Speaker 1: it's or it's why your your tendons will hold your
Speaker 1: muscles in place but not restrict them so that you
Speaker 1: can't actually flex them that sort of thing, or your
Speaker 1: heart muscles as well. I mean, it's it's important stuff.
Speaker 1: But the problem is that as you age, uh, there
Speaker 1: are these proteins that can form cross links between a
Speaker 1: tissues lattice like structure, which then gives it rigidity. So
Speaker 1: something that was once elastic becomes more stiff and rigid
Speaker 1: as time goes on, and this obviously can inhibit it's
Speaker 1: your your various organs ability to do their jobs. So
Speaker 1: that's something else that has to be addressed as you age.
Speaker 1: And the overall process that he names in this one
Speaker 1: is called glyco sends. So those are the seven principles
Speaker 1: of aging, the various symptoms of aging that he wants
Speaker 1: to try and eliminate through various means and uh, and
Speaker 1: some of them scientists I think agree, are more reasonable
Speaker 1: than others. Some of them, I think some scientists and
Speaker 1: doctors would say, are oversimplifications of the problem, or at
Speaker 1: least the solutions are so vague as to not be
Speaker 1: practical in the foreseeable future. So I remember a while
Speaker 1: back he was challenging people to disprove this wasn't he Yeah,
Speaker 1: he had his Methuselah project. And also there was a
Speaker 1: the magazine Technology Review, which comes from Might heat Uh.
Speaker 1: They got together and put up ten thousand dollars each
Speaker 1: the twenty dollars total as a challenge to anyone who
Speaker 1: could draw up a an explanation that would disprove the
Speaker 1: SINS approach, saying that is there something that's been overlooked,
Speaker 1: or is there a fundamental flaw, or is there something
Speaker 1: about this approach that is simply not likely or feasible.
Speaker 1: And they received I think they received seven or eight responses,
Speaker 1: but only a few of them were considered, only a
Speaker 1: few of them actually met the requirements that were set
Speaker 1: out by the challenge, and ultimately the judges, who were impartial,
Speaker 1: came to the conclusion that no one had presented a
Speaker 1: a any finite yeah, anything that would actually say yeah,
Speaker 1: this disproves. So no one won the prize. However, it's
Speaker 1: not exactly a slam dunk win for Degray either, because
Speaker 1: they also said that, uh, you haven't really defined this
Speaker 1: in a way that is very scientific, right. It's not
Speaker 1: like a sign yet. It's not a scientific hypothesis that
Speaker 1: you can set out to clinically disproved, right, So I
Speaker 1: want to read a couple of little comments that we're
Speaker 1: actually not little, so a couple of significant comments that
Speaker 1: one of the judges said is Nathan Mervhold who who
Speaker 1: said this at issue is the conflict between the scientific
Speaker 1: process and the ambiguous status of ideas that have not
Speaker 1: yet been subjected to that process. The scientific process requires
Speaker 1: evidence through independent experimentation or observation in order to accord
Speaker 1: credibility to a hypothesis. SINS is a collection of hypotheses
Speaker 1: that have mostly not been subjected to that process and
Speaker 1: thus cannot rise to the level of being scientifically verified. However,
Speaker 1: by the same token, the ideas of SINS have not
Speaker 1: been conclusively disproved. SINS exists in a middle ground of
Speaker 1: yet to be tested ideas that some people may find intriguing,
Speaker 1: but which others are free to doubt. And he goes
Speaker 1: on quite a bit more says that that Sends as
Speaker 1: many unsupported claims and is certainly not scientifically proven. Uh.
Speaker 1: I personally would be surprised if Degray is correct in
Speaker 1: the majority of his claims. However, I don't think that
Speaker 1: the people who submitted the rebuttals have provided that Sends
Speaker 1: is false. That would require more research. In some cases,
Speaker 1: SINS makes claims that run parallel to existing research while
Speaker 1: being more sensational. Future investigation into those areas will almost
Speaker 1: certainly illuminate the controversy. Except this was England, so it
Speaker 1: might have been controversy. But ut at any rate, uh,
Speaker 1: it goes others people had similar things to say. Another person,
Speaker 1: Craig Venter, said, uh that in my view, the critics
Speaker 1: have not demonstrated that SINS is unworthy of discussion, but
Speaker 1: the propo oponents of sense have not made a compelling
Speaker 1: case for it. So, in other words, nobody came out
Speaker 1: looking great out of that experience. From a little bit
Speaker 1: that I've heard Aubrey de Gray talking, I've gotten the
Speaker 1: impression that he's very concerned with UM keeping possibilities open.
Speaker 1: I get the impression that his main objective is to
Speaker 1: get people to think about things that they might otherwise
Speaker 1: not think about. I would agree with that. I think
Speaker 1: that he has his concern well. He often says that
Speaker 1: he thinks, if if we really dedicate a lot of
Speaker 1: resources to looking at ways of defeating the symptoms of aging,
Speaker 1: then in the case of mice, because this is really
Speaker 1: why he's talking about right now, is just experimenting with
Speaker 1: mice and not on people yet, but that if we
Speaker 1: were to really constant I mean it's important thing, but
Speaker 1: that he would concentrate. If we really concentrate, we might
Speaker 1: be able to crack the the problem within ten years.
Speaker 1: So if we don't really concentrate, if we take our time,
Speaker 1: it may be more like forty and if we're really
Speaker 1: not interested in it might take one hundred. Uh. Now, personally,
Speaker 1: I think a lot of his concerns are going to
Speaker 1: be taken care of just from other disciplines that are
Speaker 1: also working on similar problems, right, I mean, you have
Speaker 1: the whole field of oncology that's working on the cancer problem,
Speaker 1: and it may be that the solution is very similar
Speaker 1: to the one that degree proposes, or it may be
Speaker 1: something totally different. But uh, I think that if you're
Speaker 1: looking as a unified discipline, yes, it's going to be
Speaker 1: one of those things that you know might be a
Speaker 1: tough sell just because it sounds a little outlandish when
Speaker 1: you first think about it, like I want to to
Speaker 1: stop to halt the process of aging or or the
Speaker 1: symptoms of aging, if you prefer. But I do think
Speaker 1: there are plenty of different disciplines out there that are
Speaker 1: working on these individual pieces and that's going to continue.
Speaker 1: And absolutely, and there's there's already, I mean there's there's
Speaker 1: a bunch of examples from nature of animals that don't
Speaker 1: quite behave the way that that aging says that they should.
Speaker 1: Oh yeah, I mean well, i'd say one fact that
Speaker 1: is in de grace favor is that, um, that senescence
Speaker 1: is or that you know, normal rate, the kind of
Speaker 1: senescence that humans experience is not a guarantee across the
Speaker 1: entire animal kingdom. Um, like you could. Uh. Well, for
Speaker 1: so for a while you may have seen this, there
Speaker 1: were these claims going around the internet that lobsters are immortal.
Speaker 1: Have you heard this? Yeah, I I remember hearing that
Speaker 1: phrase somewhere, and I never looked into it because I
Speaker 1: just got jealous. I also kept on imagining and they're
Speaker 1: just a lobster immortals battling it out until one of
Speaker 1: them's lives. Yeah, there can be only one lobster. That's
Speaker 1: another highlander joke. I think I made one in the
Speaker 1: last podcast to several Uh no, well, it turns out
Speaker 1: this isn't exactly true. Um, so it's not. We don't
Speaker 1: have any evidence. As far as I can tell just
Speaker 1: from my research, we don't have any evidence that lobsters
Speaker 1: can live forever. Um, but we do have but we
Speaker 1: keep eating them. They're so delicious. That's the trouble. Every
Speaker 1: time we try to study them, the scientists end up
Speaker 1: getting some butter. They should just have made do it
Speaker 1: because I'm allergic to lobsters. Oh wow, so you could
Speaker 1: get a grant. Yeah yeah, um, but no. So okay,
Speaker 1: here's what is interesting about lobsters. So um, they we
Speaker 1: we don't have any evidence that they would live forever
Speaker 1: if they weren't killed by you know, some fish eating
Speaker 1: them or something like that. But we do have evidence
Speaker 1: that they have much slower sin essence than we see
Speaker 1: in lots of other creatures and um, and basically it's
Speaker 1: worth a lot more research into looking at the ways
Speaker 1: that lobsters age or don't age and and seeing what
Speaker 1: actually happens. So we don't know enough about that. One
Speaker 1: thing I was reading that it's apparently just kind of
Speaker 1: difficult to track lobsters and dint move that fast. Um
Speaker 1: but uh and I mean i'd have to imagine that
Speaker 1: you interfere with their life processes when you remove them
Speaker 1: from the ocean and stuff like that. But also, um,
Speaker 1: but they do, like say, they continue to grow. That
Speaker 1: so a really old lobster the way we we grow
Speaker 1: until a certain age I don't know, you know, in
Speaker 1: the twenties or something like that, and then we start shrinking. Well,
Speaker 1: we might grow horizontally, but we we overall, we don't.
Speaker 1: We don't continue to get stronger. I mean a lobster might,
Speaker 1: and and some other uh decapods that live in the water. Uh,
Speaker 1: they do the same thing as they get older. They
Speaker 1: just get bigger and bigger and more powerful, and they
Speaker 1: don't lose function the way we do when we age. Um.
Speaker 1: I saw one study that suggested a link. They said,
Speaker 1: so the the slow sinescence of lobsters might be UM
Speaker 1: linked to high telomeraise activity that you can detect all
Speaker 1: throughout their body tissues at any age. And telomeraise UM
Speaker 1: essentially it's a it's a protein created by telomeres, which
Speaker 1: are those those end caps two DNA strands, right, that
Speaker 1: get a little shorter every time a cell divides, And
Speaker 1: so once that cap goes down to nothing, that's pretty
Speaker 1: much that's that's like the end for that cell, right right,
Speaker 1: That's that's what triggers that cell death supposedly. Yeah, so
Speaker 1: they have a high telomerase activity all throughout the body
Speaker 1: UM and maybe that that prevents some of that that
Speaker 1: yeah effecture UM. But not just lobsters. Actually, there are
Speaker 1: some things that come closer to that that immortality claim, like,
Speaker 1: for example, the polyps called hydras. You heard about these
Speaker 1: tiny little things and apparently they can live as far
Speaker 1: as we know, they can seem to live forever for
Speaker 1: all we can tell. Yeah, they just keep going. Uh.
Speaker 1: There's also the immortal jellyfish. I've heard about that one.
Speaker 1: To Autopsis Dorney, I'm glad that you said it, because
Speaker 1: I wasn't willing to to attempt to that one. UM.
Speaker 1: It seems to uh to reverse its life cycle back
Speaker 1: to the polyp stage and then grow again, and they
Speaker 1: think that it does this through um. During that rejuvenation,
Speaker 1: it undergoes cellular trans differentiation, which is what happens in
Speaker 1: stem cells. Interesting. So so, yeah, that's exactly right. The
Speaker 1: the jellyfish, as far as we can tell, can do
Speaker 1: this indefinitely. We don't know of any point at which
Speaker 1: it has to stop. And yeah, and it's apparently kind
Speaker 1: of an issue. It can take over large segments of
Speaker 1: the ocean, and it can apparently grow in any ocean
Speaker 1: that it wants to. And it's immortal, so I mean,
Speaker 1: you know, it's running around with swords and just killing everything.
Speaker 1: I wonder if that what you just said has any
Speaker 1: application to the idea of humans being able to live forever. Well,
Speaker 1: I mean, there's definitely been a lot of scientific inquiry
Speaker 1: into the matter, but it's bioethical. What I was referring
Speaker 1: to was the fact that you said that they can
Speaker 1: expand population wise if they're not dying off. Yeah, well
Speaker 1: that was kind of what our whole discussion was in
Speaker 1: our last podcast too. Well, he had the whole section
Speaker 1: on that and de Gray for his his he pretty
Speaker 1: much doesn't acknowledge, or doesn't acknowledge is probably the wrong word.
Speaker 1: He doesn't focus on the questions of things like population
Speaker 1: or any of those other or political matters. He's looking
Speaker 1: specifically at an engineering problem. Yeah, I've I've read him
Speaker 1: make make comments that are kind of like, well, like,
Speaker 1: clearly people will just stop having kids and that'll be great,
Speaker 1: And I'm like, well, I'm not sure. Okay, that's one. Okay,
Speaker 1: if you want to stick up in his defense for
Speaker 1: a second, it might be worth saying that, um, even
Speaker 1: if there could be negative implications to this, we at
Speaker 1: least want to have the option right now. His his
Speaker 1: point is that he says, look, why are you if
Speaker 1: you're sitting there saying that that young that children are
Speaker 1: at our disadvantage, or that that this is harming children
Speaker 1: in some way by by telling people not to have kids. Uh.
Speaker 1: He turns that around and saying, well, why are you
Speaker 1: saying that old people need to die? That's that's kind
Speaker 1: of his the way he turns that around, like, that's
Speaker 1: agi you're saying that old people need to die so
Speaker 1: that we can make room for young people. And it's
Speaker 1: also certainly true that there are a lot of biological
Speaker 1: limits that if you go back to certain points in history,
Speaker 1: I mean, people would just have to accept as, yeah,
Speaker 1: this is just what life is. You. You know, you die,
Speaker 1: most half of babies die before their five or something
Speaker 1: like that. Yeah, yeah, you know, just a couple of
Speaker 1: cent centuries ago, the human lifespan was only what like
Speaker 1: forty years. Yeah, but then that was because including infant
Speaker 1: mortal that if you if you live past the age
Speaker 1: of twenty one, there was a good chance you're going
Speaker 1: to see the right But but you had to live
Speaker 1: to one first. The point I'm making is that just
Speaker 1: because something is basically the way things are, doesn't mean
Speaker 1: that we'll always see it that way. I mean, that's true.
Speaker 1: It could be in the future people would look back
Speaker 1: and be like, oh my god, what was wrong with
Speaker 1: these people? They just accepted that aging was inevitable. I mean,
Speaker 1: what a horrible way to live. And that's another thing
Speaker 1: that he points out. And really, ultimately my view is
Speaker 1: that even if you were to disprove the sense approach,
Speaker 1: even if you were to even not maybe not disprove it,
Speaker 1: but at least say that it's unrealistic or it's too
Speaker 1: narrowly focused or or the solutions that have been proposed
Speaker 1: are far more complicated than what we expect. And I
Speaker 1: would keep in mind, you know, his approach right now
Speaker 1: is looking at mice and that once, even if we
Speaker 1: do figure out how to make it work for mice,
Speaker 1: we may never figure out how to make it work
Speaker 1: for people. But let's say that, uh that all of that,
Speaker 1: you know, you can just put that aside. The interesting
Speaker 1: thing to me is that if we do tackle this problem,
Speaker 1: even if we don't ultimately figure out how to completely
Speaker 1: eliminate the symptoms of aging, we will very likely learn
Speaker 1: other ways that can help us improve quality of life.
Speaker 1: It may not mean that you will be like a
Speaker 1: twenty five year old when you hit age seventy, but
Speaker 1: you might have, you know, a greater resistance to certain
Speaker 1: types of diseases that otherwise you might be vulnerable to.
Speaker 1: So I think that that it's a very valuable line
Speaker 1: of inquiry, no matter what, what do we always say
Speaker 1: around here, Yeah, you know, it may not work, but
Speaker 1: still learn something along the way. Yeah, exactly. I mean
Speaker 1: that's I know, we we bring that point up and
Speaker 1: just about every podcast, but I really do believe that's true.
Speaker 1: I would much rather that people seriously look into this,
Speaker 1: because best case scenario, it works. The worst case scenario
Speaker 1: we learn stuff. Our worst case scenario is a cure
Speaker 1: for cancer. That's that's still pretty good. Yeah yeah, now, now, truly,
Speaker 1: the worst case scenario is not looking into it at
Speaker 1: all and just accepting that what we've got is what
Speaker 1: we've got and that's it. But uh, I don't Fortunately,
Speaker 1: the human history is filled with people who refused to
Speaker 1: take that position, and I suspect that will continue. Uh.
Speaker 1: I mean, I I just know some people that's all yeah,
Speaker 1: one or two, and they tend to be no, no,
Speaker 1: These these are the people who are like, no, I'm
Speaker 1: not accepting this. So anyway, I'm sure everyone else there
Speaker 1: knows someone like that. If you guys have suggestions for
Speaker 1: future topics that we should cover in Forward Thinking, I
Speaker 1: invite you to share the information with us, because otherwise
Speaker 1: we're just gonna have to keep on guessing until we
Speaker 1: finally cover how how telepathy is going to work in
Speaker 1: the future. Yeah, well that's probably you know, off of
Speaker 1: always I can't see it just yet. There are seven
Speaker 1: steps to telepathy. Yeah, yeah, I'll tell you about them
Speaker 1: after the show. I think it's years off and an
Speaker 1: excellent and excellent guest there, Lauren, that's a number I'd
Speaker 1: print that all right. Anyway, The important thing is that
Speaker 1: I need you to send email or get in touch
Speaker 1: with us in some other way because I have not
Speaker 1: developed telepathy yet. So if you want to say as
Speaker 1: an email, that address is FW Thinking at Discovery dot
Speaker 1: com or go to f W thinking dot com. We
Speaker 1: have links there to our social media, so you can
Speaker 1: get in touch with us on Facebook, on Twitter, on
Speaker 1: Google Plus. Let's know what you think, Let's know what
Speaker 1: you want to hear. Uh. You can also read up
Speaker 1: on our blogs. You can watch the videos. You can
Speaker 1: listen to other episodes of the podcast. There Everything you
Speaker 1: would ever want right there after thinking everything absolutely is
Speaker 1: right there after What you Thinking dot Com. I'm just
Speaker 1: saying everything. Stop giving more examples, guys. That's we look
Speaker 1: forward to talking to you again, really say. For more
Speaker 1: on this topic and the future of technology, visit forward
Speaker 1: thinking dot com brought to you by Toyota. Let's Go
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