Speaker 1: Brought to you by Toyota. Let's go places. Welcome to
Speaker 1: Forward Thinking. Hey there, welcome to the Forward Thinking, the
Speaker 1: podcast that looks at the future. It says, you're older
Speaker 1: than you've ever been, and now you're even older. I'm
Speaker 1: Jonathan Strick and I'm Joe McCormick. And so today you
Speaker 1: can probably guess that we're gonna be talking about aging,
Speaker 1: and specifically, since you probably know what kind of show
Speaker 1: this is, technological and scientific responses to aging. What do
Speaker 1: we do with the issue of aging as a as
Speaker 1: a techno scientific culture. Do we do we just let
Speaker 1: it happen and study how it happens? Heck, no, Joe,
Speaker 1: we do. We try to do something about it. We
Speaker 1: we we grab onto the sand and we make tracks
Speaker 1: with our fingers as the cold approach of time drags
Speaker 1: us ever onward toward oblivion. That's what we do. So,
Speaker 1: like a cat towards a cat carrying, let's mix some metaphors.
Speaker 1: I like it. So this isn't the first time we've
Speaker 1: talked about this. Back in June, we did a couple
Speaker 1: of episodes on various forms of technological immortality, though I
Speaker 1: think we were covering some other issues they're like, you know,
Speaker 1: would you want to have your consciousness put into a
Speaker 1: computer and stuff like that. Uh. And so one of
Speaker 1: the episodes was called who Wants to Live Forever? And
Speaker 1: the other one was more focused on something along the
Speaker 1: lines of what we're gonna be talking about today, which
Speaker 1: was the theories of the gerontologist Aubrey de Gray, and
Speaker 1: that podcast, quite stupidly, was called Shades of Degray. I
Speaker 1: think that was my choice here. I think that was
Speaker 1: my call. Well, we we're gonna be talking a lot
Speaker 1: about decay today. We talked about Degray in that episode,
Speaker 1: obviously quite extensively, and some of the stuff we're going
Speaker 1: to cover is probably going to be a little bit
Speaker 1: of a repetition of you know, it has been a minute,
Speaker 1: so we thought that we would revisit the topic. Also,
Speaker 1: I think that I think it's safe to say that
Speaker 1: all of us know how to speak better now. I
Speaker 1: was about to say talk better, and I caught myself
Speaker 1: more more good now ish. Uh So, Okay, So so
Speaker 1: today we're going to talk about the research being done,
Speaker 1: and then in the second part we're going to talk
Speaker 1: about the reasons why there's this ridiculously heated debate, or
Speaker 1: maybe not ridiculously like like, maybe it's a very human
Speaker 1: debate to be having about anti aging research and treatments
Speaker 1: and the whole perspective on the thing, because you hear
Speaker 1: so many different things from so many different groups, and
Speaker 1: who can you trust. We'll get to that in the
Speaker 1: next episode. For now, scientifically speaking, what is aging? It's
Speaker 1: kind of a good question. It's one of those things
Speaker 1: where you know it when you see it, but can
Speaker 1: you describe exactly what it is? Yeah, So here's the problem, right, Um,
Speaker 1: there is no full understanding in the realm of science
Speaker 1: of everything that goes into aging. We understand elements of aging,
Speaker 1: We understand some of the cause and effect of certain
Speaker 1: aspects of aging, but when you look at aging as
Speaker 1: an overall condition, we don't have a full understanding of
Speaker 1: what that is. Yeah. And one of the other things
Speaker 1: I would say is that you might have trouble with
Speaker 1: such a macroscopic effect as aging um in distinguishing causes
Speaker 1: from effects. For example, one thing we know is not
Speaker 1: a cause of aging, but you could say, since it correlates,
Speaker 1: is that aging is caused by hair turning gray. If
Speaker 1: you didn't understand that, it went the other way around.
Speaker 1: You could get confused on this point, and there are
Speaker 1: some issues where it's not quite so clear. And there
Speaker 1: are also some conditions and diseases that could end up
Speaker 1: exacerbating the effects of aging or perhaps replicating the effects
Speaker 1: of aging without itself being aging. So you know that
Speaker 1: that also throws in more confusion into the mix. Yeah,
Speaker 1: but one of the biggest concepts in aging is something
Speaker 1: that figures into what we talked about in that episode
Speaker 1: about Aubrey De Gray. Aubrey De Gray's program UH is
Speaker 1: a program for engineering negligible sinescence. What is sescence. Sinescence
Speaker 1: is the idea, and generally this this refers to growing
Speaker 1: old and deteriorating in power with age, but at the
Speaker 1: cellular level, senescence has a more specific definition. So your
Speaker 1: body tissues remain healthy and strong over the years by
Speaker 1: replenishing themselves through cell division. Cells divide and make new,
Speaker 1: brand new, happy, healthy cells out of the old cells.
Speaker 1: And that's great. It keeps your tissues refreshed. But when
Speaker 1: body cells cease their self replication, they stop making brand new,
Speaker 1: spanking new, happy, fresh little cells. This is known as senescence.
Speaker 1: It's also known as cells sort of going into retire ironment. Yeah,
Speaker 1: and that process leads into cell death. But why on
Speaker 1: earth would our bodies be coded to kill off cells.
Speaker 1: That seems like the opposite of what a body would
Speaker 1: want to do. Yeah. Uh, it is helpful in some situations,
Speaker 1: you know, when cells are too damage to continue functioning correctly,
Speaker 1: and so that that's the body's way of telling them
Speaker 1: to just just go out and quit. You've done enough,
Speaker 1: You're fine. Um or in the case of sing like cancer,
Speaker 1: it's really good to be able to just just be like,
Speaker 1: you know what, we don't really need you any here
Speaker 1: here anymore. We're doing okay. And certainly, if you didn't
Speaker 1: have senescence, if you didn't have this process, uh, if
Speaker 1: there was this unchecked method of cellular division, it could
Speaker 1: lead to things like cancer. However, if you have senescence
Speaker 1: body wide, then you're essentially saying that the cells have
Speaker 1: stopped dividing and now it's borrowed time because cells have lifespans. Yeah.
Speaker 1: And you know, if you think about it from the
Speaker 1: genetic perspective of your cells, you can see why this
Speaker 1: might be the case, because what is the purpose of
Speaker 1: your body Genetically speaking, It's not to be happy and
Speaker 1: healthy forever. It's to survive long enough to achieve prodigious
Speaker 1: sexual recombination. And uh and so, I mean, once you're
Speaker 1: beyond the age of sexual reproduction, what of what uses
Speaker 1: it to your genes to just keep making your muscles strong? Yeah,
Speaker 1: we're really just biting our thumbs at our genes every
Speaker 1: day that we live without having healthy children. Yeah, yeah,
Speaker 1: I'm alright with that. Okay, so so, so, why why
Speaker 1: does senescence happen? Researchers think that on a cellular level,
Speaker 1: it happens because of this stuff called telomeres. Telomeres our
Speaker 1: our DNA caps on the end of your chromosomes that
Speaker 1: protect your DNA from wear and tear when cells divide.
Speaker 1: Geneticist Elizabeth Blackburn famously compare them to the little plastic
Speaker 1: caps on the end of shoelaces. Oh, I've heard Michia
Speaker 1: Cake you say the same thing. But I bet he
Speaker 1: got it from her. I I think I think she
Speaker 1: was the originator of that phrase. Now I'm terrified that
Speaker 1: I'm wrong. No, I bet, I bet, I bet that's
Speaker 1: the case. Okay, Uh, so, so you're you're you're telomeres
Speaker 1: unlike well, well, actually exactly like the plastic caps on
Speaker 1: the end of your shoeleases are also subject to the
Speaker 1: same wear and tear that happens to the DNA when
Speaker 1: your cells are dividing, so they get shorter after many
Speaker 1: cell divisions, and when they wear down enough, the cells
Speaker 1: that they're in stop dividing, and that is in essence,
Speaker 1: So when that happens to adult stem cells, that might
Speaker 1: be one of the critical factors of aging, because adult
Speaker 1: stem cells are the things that create new cells when
Speaker 1: you're when your tissues are damaged or or your your
Speaker 1: blood needs to be replaced, and they're usually just hanging
Speaker 1: out in a state of quiescence, a sort of like
Speaker 1: like yellow alert. Okay, so they're not actively creating new cells,
Speaker 1: and they don't themselves divide to create new stem cells
Speaker 1: unless some kind of damage happens. And there have been
Speaker 1: some studies that have shown that with age, or or
Speaker 1: possibly once having gone enough cell divisions, adult stem cells
Speaker 1: don't function as quickly or as completely as they used to,
Speaker 1: so your body is less able to replace and repair
Speaker 1: damage that gets done. And of course, when one thing
Speaker 1: gets damaged in one of our bodily systems, it reduces
Speaker 1: the function of other things, or you know, like weakens
Speaker 1: the structures needed to prevent further damage, like in osteoporosis. Right, Okay,
Speaker 1: that makes sense. However, there is a process of your
Speaker 1: cells that protects your telomeres, an enzyme called telomerase to telomerasemerase, telomerase, interesting,
Speaker 1: telomerase like telemachus. I like that you look at obviously,
Speaker 1: and I'm like, I want to cobb Well anyway, not kebabs.
Speaker 1: But telomerase or telomerase controls the generation and the formation
Speaker 1: and the length of your telomere, but not all of
Speaker 1: your cells make it, which is actually a good thing
Speaker 1: because cancer. But more more on that later on. Didn't
Speaker 1: that funny that cancer link just keeps coming up in
Speaker 1: this episode? Well, it's gonna come up a lot in general,
Speaker 1: not just in this episode, but in the following one.
Speaker 1: Because one of the things when you're talking about trying
Speaker 1: to find a way to counteract or even reverse aging,
Speaker 1: one of the big questions that comes up in everyone's
Speaker 1: mind is you're talking about regenerating tissue that is frighteningly
Speaker 1: close to the concept of uncontrolled cellular division, which is
Speaker 1: what cancer is made of. Exactly. Yeah, undifferentiated, uncontrolled growth.
Speaker 1: So yeah, so that that's an interesting avenue of research
Speaker 1: about what causes aging. But we've also got the issue
Speaker 1: of mitochondria, right, oh yeah, okay, so so our selves
Speaker 1: mitochondria definitely become less efficient as we age. UM and
Speaker 1: and my mitochondria if you guys don't remember, from like
Speaker 1: seventh grade biology or possibly from a wind in the door?
Speaker 1: Was that which which one did you guys ever met? Yeah? Yeah, yeah,
Speaker 1: she totally talked about mitochondria and one of those books
Speaker 1: at any rate. Um. But what mitochondria actually are are
Speaker 1: the organelles inside of ourselves that, among other things, chemically
Speaker 1: convert the nutrients that we take in into the molecules
Speaker 1: that our cells eat to gain the energy they need
Speaker 1: to do what they do. Yeah. I think the common
Speaker 1: way of expressing it is that they're the power plants
Speaker 1: of our selves exactly. Yeah. Yeah. They produce what is it,
Speaker 1: t um and so when mitochondria become less efficient, they
Speaker 1: produce less a tp Our cells can't do as much,
Speaker 1: and therefore our body's entire metabolic activity systems slows down.
Speaker 1: We have, you know, less nutrient transfer, fewer new cells,
Speaker 1: decreased immune response all that good stuff that goes into
Speaker 1: a young and healthy body. But of course all that,
Speaker 1: all that that and more tends to add up to
Speaker 1: these macroscopic effects that we see on the body as
Speaker 1: a whole. Oh sure, yeah, and we see plenty of those.
Speaker 1: Yeah right. So, for example, some of these macroscopic effects
Speaker 1: that we'll see, one of the most general ones tends
Speaker 1: to be a decrease in tissue elasticity. And this is
Speaker 1: this is pretty much body wide, but really we're talking
Speaker 1: about muscles and blood vessels in particular. Yeah. Yeah, it's
Speaker 1: the the collagen inside the little tiny molecules of proteins
Speaker 1: that are folded up. Stop being as cool. Yeah, it's
Speaker 1: it's like if you you know, you got that that
Speaker 1: one pair of underwear you really should be tossing out.
Speaker 1: It just in't doing the job anymore. It's that elastic
Speaker 1: is all totally worn out. It's kind of sad when
Speaker 1: that that pair of underwear is actually representing something like,
Speaker 1: I don't know, your heart. That's a bad thing. Yeah,
Speaker 1: but if only science could replace it with a pair
Speaker 1: of means right. Bones also also come weaker. You lose
Speaker 1: bone mass faster than you are regenerating it, uh, and
Speaker 1: that can lead to osteoporosis, which is the more extreme
Speaker 1: version of that problem. You know, one thing I've heard
Speaker 1: expressed by some of the advocates of aging reversal technology
Speaker 1: is to think about it this way. Aging is the
Speaker 1: number one risk factor for almost every disease we know of.
Speaker 1: I'm not quite everyone, but the vast majority of them.
Speaker 1: And if you think about it like that, it kind
Speaker 1: of might tweak your understanding of whether or not we
Speaker 1: should do something about aging. Because if you had, say,
Speaker 1: if you said cigarette smoking was the number one risk
Speaker 1: factor for the majority of known diseases and conditions, I mean,
Speaker 1: it seems like you'd really want to do something to
Speaker 1: get people to stop smoking. It's it's like, well, obviously,
Speaker 1: don't smoke. That's terrific. So clearly you should stop aging.
Speaker 1: Just don't do it. Don't age, kids, don't age. My
Speaker 1: life's been doing that for years. She celebrates her twenty
Speaker 1: nine birthday every year. Oh that old joke, And you
Speaker 1: make that joke every year, don't you might? Okay, So,
Speaker 1: so one idea to keep in mind going forward, we
Speaker 1: are going to talk about some some new ideas and
Speaker 1: what to do about aging and in ways to counteract it.
Speaker 1: But one idea to keep in mind is also the
Speaker 1: difference between the concepts of life span and health span um.
Speaker 1: And so this is something that I think is recently
Speaker 1: something that doctors have started to talk about more. Lifespan,
Speaker 1: of course, is just time from birth until death. How
Speaker 1: many years do you Yeah, But health span is time
Speaker 1: until serious illness. And a lot of medical technology over
Speaker 1: the you know, past decades, has succeeded in extending the
Speaker 1: former without necessarily extending the ladder. So, in other words,
Speaker 1: life expectancy has increased, but but how long you remain
Speaker 1: healthy within that lifespan hasn't measurably increased at the same rate,
Speaker 1: or I should say, just increased at the same rate.
Speaker 1: It has certainly increased, there's no denying that, but it
Speaker 1: has an increased to the point where you would say, um,
Speaker 1: if the average life expectancy has gone up three years,
Speaker 1: the health span has not done that. Yeah, And so
Speaker 1: that's a thing that's important to keep in mind when
Speaker 1: you're talking about rejuvenation research. A lot of it is
Speaker 1: focused on extending quality of life and not just extending life,
Speaker 1: So maybe not even extending lifespan at all. Maybe that
Speaker 1: you know that that could happen, But perhaps the focus
Speaker 1: for at least some of the researchers is not let's
Speaker 1: see if we can get people to live to a
Speaker 1: hundred and twenty on a regular basis. It's let's see
Speaker 1: if we can make sure people maintain a good quality
Speaker 1: of life, a good healthy life, or more of their lifespan.
Speaker 1: I mean, think about it this way. Would you rather
Speaker 1: live to two hundred but for the second two hundred
Speaker 1: years you can't get out of bed? Or would you
Speaker 1: rather live to e ight but be healthy and fit
Speaker 1: the whole time can't or whoa, there's a lot of
Speaker 1: comic books in the universe, Like I could spend a
Speaker 1: solid decade or two just reading comics, and that's not
Speaker 1: even getting into nonfiction. But eventually you'd want to get
Speaker 1: out of bed, go line up to see the movie
Speaker 1: that's going to disappoint you. That's what digital downloads are for,
Speaker 1: all right. So let's talk about some of the research. Yeah, well, okay,
Speaker 1: So there are some avenues of research into rejuvenation or
Speaker 1: aging reversal that we have talked about in recent podcasts.
Speaker 1: One of them, for example, is if you remember our
Speaker 1: episode about the Future of blood, we talked about research
Speaker 1: into the rejuvenating effects of young blood. Now really, honestly
Speaker 1: that research has goes back centuries. Elizabeth. You have to
Speaker 1: believe the the sensational reports of Elizabeth Bathory. Yes, but no,
Speaker 1: that this is very interesting though it's yet another one
Speaker 1: of these things where we should always couch all coverage
Speaker 1: of aging reversal research with it. Let's not get carried
Speaker 1: away here, um that you know, there is there is
Speaker 1: some interesting research coming out and we want to keep
Speaker 1: an eye on it. But nobody's found the fountain of
Speaker 1: youth yet. But yeah, yeah, can we just never use
Speaker 1: that phrase again as a as a human species. I'm
Speaker 1: right there with you, Lauren. Okay, so, but but a
Speaker 1: quick refresher on the blood thing if you if you
Speaker 1: wanna full breakdown of this, you can go back and
Speaker 1: check out our episode on the Future of blood. But
Speaker 1: in short, multiple lines of research have shown that giving
Speaker 1: older animals infusions of blood from younger animals of the
Speaker 1: same species has rejuvenating effects on body tissues. And some
Speaker 1: of the experiments have been in what's called heterochronic parabiases,
Speaker 1: where you sew together to mice one young and one old,
Speaker 1: so that they share a circulatory system and a common
Speaker 1: pool of blood. That, yeah, that does sound creepy, but
Speaker 1: the results, it's an extreme measure, like I'm not going
Speaker 1: to sign up for that tomorrow, but the results. But
Speaker 1: the results have shown that the old mice have improved
Speaker 1: muscular and cognitive function and the they have younger looking
Speaker 1: tissues at a cellular level when continually exposed to the
Speaker 1: blood of young mice in this way. On the other hand,
Speaker 1: the young mice do not seem too fair as well
Speaker 1: from this procedure. Uh there there seems to be a
Speaker 1: sort of compensating not so great effect for them. But
Speaker 1: in some studies in rodents, they think they've isolated a
Speaker 1: protein called g DF eleven for growth differentiation factor eleven,
Speaker 1: as a major contributor to the rejuvenation effects. Though since
Speaker 1: the podcast on this we did, I think I've read
Speaker 1: a couple of articles questioning the primacy of g DF
Speaker 1: eleven as as the factor affecting this rejuvenation. Uh So,
Speaker 1: as you can tell from that, the research is still ongoing,
Speaker 1: and it would be premature to say that the blood
Speaker 1: of the young is this fountain of youth or whatever.
Speaker 1: We should have an alternative phrase, the hose of infancy.
Speaker 1: So health recommend nuts the spigot of infancy, spat of
Speaker 1: spigot of infancy, come on adolescence. I'm not sure if
Speaker 1: infancy is where I want to go back to. No,
Speaker 1: we will Benjamin Button all the way. I haven't seen
Speaker 1: that movie, so I don't know what that means better
Speaker 1: than my suggestion of prepubiscent dip. Wow. Okay, yes it
Speaker 1: is the spigot of health. Yeah. No, it is not
Speaker 1: necessarily been shown to be this A Researchers are usually
Speaker 1: quick to point out that the technique hasn't been shown
Speaker 1: to make animals immortal or even necessarily increase the lifespan.
Speaker 1: But what research we have seen is interesting, particularly with
Speaker 1: reference to potential treatment for specific diseases like Alzheimer's, where
Speaker 1: you might be able to see uh targeted rejuvenation of
Speaker 1: cells that have seen some kind of deterioration due to
Speaker 1: an age related disease. And so it could be that
Speaker 1: with some of these things we talked about today, they
Speaker 1: might not make you younger or make you live longer,
Speaker 1: but they might turn out to help with some particular
Speaker 1: disease which may or may not be age related. It
Speaker 1: kind of goes into something that we say on the
Speaker 1: show all the time, which is that, uh, scientific experimentation
Speaker 1: and exploration can lead to answers to questions that we
Speaker 1: weren't even specifically looking at at the time, and it
Speaker 1: requires very rigorous follow up to make certain that those
Speaker 1: answers are in fact valid. But it is well, yeah, no,
Speaker 1: I'm I'm sorry, I'm loving I I It just occurred
Speaker 1: to me that like that basically, like we are constantly
Speaker 1: just going like, well the answer is forty two. Well,
Speaker 1: I just think like if you if you were to
Speaker 1: do an experiment and you get an unexpected outcome, then
Speaker 1: obviously you need to uh re examine that and see
Speaker 1: if it's replicable and then get down to the question
Speaker 1: of what is it that's actually happening. Yeah. But another
Speaker 1: thing that this springs up is we sort of mentioned
Speaker 1: this earlier, but just to highlight it again, there are
Speaker 1: multiple different goals they're sort of encompassed by by rejuvenation research.
Speaker 1: One of them would be increasing lifespan. Another would be
Speaker 1: making old body tissues look like young body tissues and
Speaker 1: work as well as them. Yeah, like like a good
Speaker 1: uh you know, a good pair of kidneys or a
Speaker 1: good heart, all of that kind of stuff that does
Speaker 1: tend to decrease its efficiency over time. Yeah, and another
Speaker 1: thing would just be, uh doing this in a way
Speaker 1: that leads to a good quality of life. For example,
Speaker 1: we already know of one thing in animals that leads
Speaker 1: to increased lifespans, you know this caloric restriction. If you
Speaker 1: are willing to starve yourself too nearly to death on
Speaker 1: a constant basis annual, probably live longer in a laboratory setting. Unfoly,
Speaker 1: the thing that happens along with this, uh, this boost
Speaker 1: in longevity is a complete shutdown of the immune system.
Speaker 1: So if you're just wandering out around the world full
Speaker 1: of germs, then probably that's not going to fare very
Speaker 1: well for you. Oh yeah, that's a good thing to
Speaker 1: point out. But also it just sounds miserable. I mean,
Speaker 1: people don't want to live this way. No, I I
Speaker 1: certainly don't. Food is probably the most important thing to me. Um.
Speaker 1: This research, by the way, was from It was just
Speaker 1: published in March sixteen and it came out of the
Speaker 1: Leibnitz Institute on Aging out of Germany. And yeah, so
Speaker 1: uh so, so don't so don't totally restrict your calories
Speaker 1: down to nothing in the hopes of getting better longevity.
Speaker 1: It probably won't work. Well, maybe you should if you
Speaker 1: can live that way and want to live in the
Speaker 1: bubble boy suit and no, yeah, I mean it's very fetching, right, Yeah,
Speaker 1: this is is it living? If you can't snuggle with
Speaker 1: a dog on your face? It's interesting to me because
Speaker 1: that Clorican, the cloric intake research, that stuff that's been
Speaker 1: going on since like the nineteen thirties. Yeah, so this
Speaker 1: is uh, you know, it goes to show like that
Speaker 1: research began in the nineteen thirties, we're still looking into
Speaker 1: the effects today. That to me is a big indicator
Speaker 1: of how challenging it is. This this idea of how
Speaker 1: do we rejuvenate, how do we combat aging? It's not
Speaker 1: like it's a new question. It is something that has
Speaker 1: been going on for a while. So that's an interesting,
Speaker 1: uh note. I think I agree with you. But then again,
Speaker 1: there are also new technologies and techniques and bits of
Speaker 1: knowledge that are coming out that could be very well
Speaker 1: accelerating our our knowledge on how to combat aging. One
Speaker 1: of them, I think is this interesting idea of the
Speaker 1: clearing out of sinescence cells as one possible way to
Speaker 1: reverse the effects of aging. So I was reading about this.
Speaker 1: There was a study published in Nature in by Mayo
Speaker 1: clinic researchers Darren Baker and Jan Van Deerson, and it
Speaker 1: was the latest to suggest that if you clear out
Speaker 1: sinescence cells from the body. Remember these are the cells
Speaker 1: who were talking about earlier. That are the retired cells.
Speaker 1: They're they're done dividing and making new happy cells. You
Speaker 1: if you clear those out of the body, you can
Speaker 1: rejuvenate tissue and perhaps live longer. So Baker and vin
Speaker 1: Jerson found that if you're able to remove sinescence cells
Speaker 1: from the bodies of mice, those mice live about twenty
Speaker 1: longer on average. So we mentioned these sinescence cells earlier.
Speaker 1: But what do they do once they sit around in
Speaker 1: the body so they retire. It turns out they have
Speaker 1: some not so friendly side effects. There might be beneficial
Speaker 1: effects to um. We can talk about those if you want,
Speaker 1: but they're believed to mostly just hang out and excrete
Speaker 1: molecules that harm other tissues and processes in the body.
Speaker 1: Basically molecules that lead to greater inflammation and greater rates
Speaker 1: of oxidation. Oxidation is rust It's not something you want
Speaker 1: inside your body. No, No, you don't want your inter
Speaker 1: cellular structures rusting. Nobody nobody wants that, or or or
Speaker 1: having happened to them. What happens to avocado dip left
Speaker 1: out too long as guaco? I think, I think I
Speaker 1: want that less than I want rusting. However, I do
Speaker 1: want guacamole, I don't. I always want glucomole um and research.
Speaker 1: Some researchers think at any rate that aging mitochondria have
Speaker 1: something to do with those molecules that are being released,
Speaker 1: tying it back to the mitochondria issue. Um there was
Speaker 1: there was a study published in the E m b
Speaker 1: O or possibly MBO journal um in uh just recently
Speaker 1: in but but so so back back to these mice though. Yeah,
Speaker 1: Actually I've read a good article about this research, the
Speaker 1: Clearing of senescence Cells that ed Young Road for the
Speaker 1: Atlantic in February, where he describes looking at two mice
Speaker 1: side by side, and one of them looks like a
Speaker 1: healthy adult mouse and the other one has quote graying
Speaker 1: for a hunched back and an eye that's been whitened
Speaker 1: by cataracts. So it sounds like it's seen better days.
Speaker 1: And yet these two mice are the same age. In fact,
Speaker 1: they're not just the same age, they're twins, genetic twins. Yeah,
Speaker 1: same age, same genes. It's one of them, an actor
Speaker 1: mouse that's portraying like the hunchback of Notre Dame. No
Speaker 1: it is it does not have Tom Savini mouse makeup
Speaker 1: on the mouse version of King Lear. Oh no, no, no, no,
Speaker 1: it's too Oh that would be so cute. Okay, please
Speaker 1: go ahead. Well, anyway, it's just that one of them,
Speaker 1: the healthy looking one, has undergone this procedure to clear
Speaker 1: out the retired senescence cells from its body. So to
Speaker 1: back up a little bit. In two thousand eleven, Baker
Speaker 1: and Van Jersen were part of a team that came
Speaker 1: up with this process for removing senescence cells from the body.
Speaker 1: So they genetically engineered the strain of mice that display
Speaker 1: aid congenital accelerated aging. These mice. You don't want to
Speaker 1: be one of these mice. They got old very fast. Uh,
Speaker 1: and also with a trait that would allow the researchers
Speaker 1: to administer a particular drug in order to induce the
Speaker 1: systemic destruction of all the retired cells from the body,
Speaker 1: and they found that when the mice received this drug,
Speaker 1: they became fitter, stronger, bigger, and healthier, and yet they
Speaker 1: still died early. Remember these were the rapid aging mice.
Speaker 1: But a more recent bit of research is that Baker
Speaker 1: and Van Deerson found that you could do the same
Speaker 1: thing with mice that were not genetically faded to rapid aging.
Speaker 1: You could do it to the regular old lab mice,
Speaker 1: and they found that if you use the same procedure
Speaker 1: to clear the senescent cells from middle aged mice twice
Speaker 1: a week, the mice also showed healthier tissue, less body fat,
Speaker 1: and just seemed fitter in general. Not only that, but
Speaker 1: as I mentioned earlier, they lived longer, longer on averager
Speaker 1: and average of I can't imagine how depressing that must
Speaker 1: be to be the elderly twin looking at the younger
Speaker 1: twin and just thinking that could have been me. Well,
Speaker 1: it's it comes back to my proposal for NASA to
Speaker 1: do the twin study again. That's what the Earth twin
Speaker 1: would say to to his or her returning astronaut twin.
Speaker 1: I mean, I'm sure that what the mice we're actually
Speaker 1: thinking was like squeak yeah, So let's let's talk beyond
Speaker 1: this experiment. What about Could this be something that's applicable
Speaker 1: to human beings not just to mice. Well we don't
Speaker 1: know yet, but that's the thing that obviously people want
Speaker 1: to find out. So researchers think that drugs could be
Speaker 1: developed to recognize the bio markers of sinescence cells, you know,
Speaker 1: the little flag that says I'm a retired cell in
Speaker 1: humans and selectively destroy those cells. So just to go
Speaker 1: in your body, only find the retired cells, not hurt
Speaker 1: the good cells the you want and get rid of them.
Speaker 1: But as usual, there a few things we need to say.
Speaker 1: One of them is don't get carried away here. We
Speaker 1: we need to see this reproduced in other studies. And
Speaker 1: even then what works for mice and lab conditions won't
Speaker 1: necessarily mean humans can undergo the same procedure and regularly
Speaker 1: live to a hundred. But even if it's not useful
Speaker 1: in increasing general human lifespan, it might be useful in
Speaker 1: treating age correlated diseases like arthritis, heart disease in glucoma.
Speaker 1: Another drawback is already obvious from their research mice that
Speaker 1: had their sinescence cells cleared on a regular basis also
Speaker 1: displayed lower rates of healing from wounds, which is interesting
Speaker 1: going back to that immune system depression. Yeah, so it
Speaker 1: appears that the removal of these cells doesn't come without
Speaker 1: a cost. They they're sitting there having maybe a net
Speaker 1: negative effect on the body, but they also appear to
Speaker 1: do some things that are useful, and removing them counteracts
Speaker 1: those positive effects. Uh. And then another potential risk of course,
Speaker 1: yet again cancer. It just keeps coming up with rejuvenation technologies.
Speaker 1: Like we mentioned earlier, cancer is the uncontrolled, undifferentiated cell
Speaker 1: growth that we see. Any therapy that seems to unnaturally
Speaker 1: extend or accelerate cell growth seems at least in potential
Speaker 1: a cancer concern. One last thing from Young's article that
Speaker 1: I thought was really interesting is that he got a
Speaker 1: quote from Dr Norman Sharpless of the UNC Chapel Hills
Speaker 1: School of Medicine, who said the following quote, you take
Speaker 1: a drug reserve at all green tea, god knows what,
Speaker 1: And he's naming there a few of the things that
Speaker 1: have been called up in the research as potential anti
Speaker 1: aging drugs throughout the years. But he continues, you take
Speaker 1: that drug for thirty years and by the time you're eighty,
Speaker 1: you're actually seventy. That paradigm doesn't work in the real world.
Speaker 1: And I think I agree with him there. I mean,
Speaker 1: people don't want to take a drug their whole lives
Speaker 1: to see maybe some reduce staging over a long period
Speaker 1: of time. Right. Uh, he continues, people hate taking drugs,
Speaker 1: especially when they don't know it's helping them. And no
Speaker 1: farmer company would develop such a drug. If this paper
Speaker 1: is right, and he's talking about the Baker and Vandersen paper,
Speaker 1: suddenly you have a way of taking an old organism
Speaker 1: and making it physiologically younger. You go from a prevention
Speaker 1: paradigm to a treatment one that's something you can sink
Speaker 1: your teeth into. And I think he's got a good
Speaker 1: point there. I mean it it reacts to not just
Speaker 1: what a drug can do, but the different ways that
Speaker 1: we want to interact with medical technologies. It specifically speaks
Speaker 1: to a very American approach to medicine, this idea of
Speaker 1: treating a disease as opposed to trying to prevent one, right.
Speaker 1: And I think that we would be better off probably
Speaker 1: if we did the prevention more than the treatment. I mean,
Speaker 1: but you know what, when you really get down to it,
Speaker 1: a great way to prevent aging is to hide eight
Speaker 1: and eat vegetables and exercise. Sometimes I think I think
Speaker 1: if you, I think, if you look at it in
Speaker 1: the sense of, if you take this drug, you're still
Speaker 1: going to get old. It might take a little longer
Speaker 1: for you to feel like you're getting old than it
Speaker 1: would otherwise, But that's your personal experience. You wouldn't know otherwise, right,
Speaker 1: You know, your reality is whatever it is that you
Speaker 1: are doing. So and we've talked about that that bias
Speaker 1: on on the show before too, that the whole, the whole, like, well,
Speaker 1: it didn't not work. I'm still here, right, But but
Speaker 1: something where you take a drug and you feel younger,
Speaker 1: then you have something to compare the effects to you,
Speaker 1: Like I already know what being older than this feels like.
Speaker 1: So it's definitely one of those things where you can
Speaker 1: understand where someone's coming from if that seems more appealing
Speaker 1: to them, even if you were to demonstrate Yeah, but
Speaker 1: if you do this other approach, you're going to feel
Speaker 1: better for longer and you don't ever have to dial back.
Speaker 1: Right then, again, I would say that there is a
Speaker 1: quite obvious appeal to the reversal process for people who
Speaker 1: are already today in their sixties or seventies. There's appeal
Speaker 1: to me right now, and I'm in my forties. I
Speaker 1: guess to all of us, except those babies out there
Speaker 1: who are still in their prime. Huh, all right, Jonathan
Speaker 1: moans with hate. Look, I don't I don't hate young people.
Speaker 1: I just don't want to him a lawn. He just
Speaker 1: wants the spigot of health all to himself. I'm not
Speaker 1: going to deny your accusation. I'm just not going to
Speaker 1: acknowledge it. Okay. But but that avenue of research we
Speaker 1: just talked about is based on one type of approach
Speaker 1: to the aging problem. If you are looking at aging
Speaker 1: as an engineering problem and you want to fix it
Speaker 1: or reverse it, there are several approaches you could take.
Speaker 1: And this this is sort of the error corre acting problems, saying, oh,
Speaker 1: we've got we've got a build up of stuff we
Speaker 1: don't want in the body, or of errors or of damage,
Speaker 1: and we can go in and fix that somehow. But
Speaker 1: there is an entirely different way to look at it.
Speaker 1: Instead of saying going in and doing repairs, you could
Speaker 1: look at it from a genetic point of view. So,
Speaker 1: in other words, the instructions within our genes, if you
Speaker 1: could somehow rewrite those instructions so that the damage doesn't
Speaker 1: even happen in the first place, yeah, Or so that
Speaker 1: the cells in your body, by their very nature, executing
Speaker 1: their genetic instructions, will fix the problem themselves. And that's
Speaker 1: the genetic method. So one I one name that has
Speaker 1: come up in this way of looking at the aging
Speaker 1: problem is the geneticist George Church. So George Church runs
Speaker 1: a lab at Harvard Medical School, and he has made
Speaker 1: some very interesting predictions about aging research that I read about.
Speaker 1: Speaking to Joel Aichenbach of the Washington Post, Church has
Speaker 1: said that new breakthroughs in genetics and gene editing will
Speaker 1: make it possible to reverse aging and humans. And he
Speaker 1: even predicts, quote, in just five or six years, he's
Speaker 1: going to be able to reverse the aging process in
Speaker 1: human beings. And he seems to be speaking out of
Speaker 1: personal experience based on the research that's going on in
Speaker 1: his lab. This is obviously a really bold claim. But
Speaker 1: five or six years, I mean, that sounds kind of crazy.
Speaker 1: But I do want to point out Church is not
Speaker 1: just some whacko on the Internet. And he's not a
Speaker 1: quack because he's a very well respected geneticist who has
Speaker 1: been working in the field for years. He uh, I
Speaker 1: know he. I think he was one of the founders
Speaker 1: of the Human Genome Project, or one of the organizers
Speaker 1: at least. So so what's so, what's he proposing? So
Speaker 1: he's talking about gene therapy. Basically, it sounds like his
Speaker 1: experiments so far based on gene manipulation gene therapy not
Speaker 1: just for curing specific diseases, but for reversing aging itself.
Speaker 1: Whereas most research and rejuvenation is aimed at counteracting the
Speaker 1: effects of aging, these would be doing what we were
Speaker 1: just talking about, addressing the genetic root causes of aging
Speaker 1: in cells. So Church claims that he's already demonstrated aging
Speaker 1: reversal on smaller animals in the lab, and the next
Speaker 1: step is translating these results to larger animals and human trials.
Speaker 1: I found some good quotes from an article in the
Speaker 1: San Diego Union Tribune covering his Future of Genomic Medicine
Speaker 1: conference speech in sixteen, where Church said a few things
Speaker 1: that seemed very interesting to me. One of them is
Speaker 1: quote if we could take one of my skin cells
Speaker 1: and turn it into an embryo like cell and turn
Speaker 1: it back into a skin cell, it is reset almost
Speaker 1: all of the developmental indications of age. We have sixty
Speaker 1: five gene therapies that are being tested in mice and
Speaker 1: larger animals. If they go well, we will go straight
Speaker 1: into human trials that could be as little as two years.
Speaker 1: He said this in essentially the I T crowd approach
Speaker 1: of turning it off and on again. It is control
Speaker 1: all delete on your cells and it refreshes it. Yeah.
Speaker 1: And and so he talks very interestingly. I like his
Speaker 1: thinking here about why he uses the term reversal for
Speaker 1: aging instead of curing aging or stalling aging. Uh. He says,
Speaker 1: I don't think it's about stalling or curing. It's about reversing.
Speaker 1: Curing gives you the impression of immortality, which is not
Speaker 1: necessarily what is being proposed. Uh. Stalling gives you the
Speaker 1: impression that you'll be eighty five forever, which is not great.
Speaker 1: And we sort of mentioned that earlier in the show. Uh.
Speaker 1: And So the last thing he says that I think
Speaker 1: is interesting is he says, quote, reversal is something that's
Speaker 1: been demonstrated in a number of different animals in a
Speaker 1: number of different ways. I think that's going to translate
Speaker 1: into larger animals and humans. We won't know until we try,
Speaker 1: But we're trying sixty five different genes in different combinations
Speaker 1: to see if we can reproduce the aging reversal that
Speaker 1: we've seen in small animals. We don't know what age
Speaker 1: reversal would mean in terms of human years. Animals have
Speaker 1: had their life extended by factors to to ten. That
Speaker 1: seems to be too good to be true for humans. Yeah,
Speaker 1: I think, uh, you know, living to sixty might be
Speaker 1: a bit much. Yeah, unless you're an evil wizard so
Speaker 1: many comic books. Uh huh. So, despite the fact, I
Speaker 1: did want to point out that he's not just some
Speaker 1: whacko on the internet. This is a respected scientist. But
Speaker 1: at the same time, you can't just take it on
Speaker 1: one scientists authority that like, oh, yeah, he's got it. Yeah,
Speaker 1: so he go home. Now, obviously he has a very
Speaker 1: optimistic prediction, but it is interesting to hear this. Yeah,
Speaker 1: I mean it's there. Obviously, there are a lot of
Speaker 1: questions to ask to like, would this approach also stave
Speaker 1: off the age related diseases, that we're that we've talked
Speaker 1: about some things, or would it just be like like
Speaker 1: seven hundred years of Alzheimer's Right, it seems to be
Speaker 1: that he's got the idea of the health span in mind,
Speaker 1: because he's talking about not just forestalling death, but being
Speaker 1: able to rejuvenate the tissues. Yeah. Yeah, I think a
Speaker 1: lot of um, and we'll talk more about this in
Speaker 1: the second episode, but I think a lot of of
Speaker 1: experts in the field of aging are skeptical or or
Speaker 1: reluctant to endorse such a bold claim. I mean on
Speaker 1: the face of it, because, as we said at the
Speaker 1: top of the episode, it's such a complicated issue that
Speaker 1: it may very well be that something you did not
Speaker 1: anticipate is still in a problem, like one of these
Speaker 1: age related diseases. And it may be that you have
Speaker 1: very healthy tissues overall, but that you're still prone to
Speaker 1: these other issues. Yeah, but you know your your immune
Speaker 1: system craps out or you have cancer and wind up
Speaker 1: looking like the character from the end of Akira and
Speaker 1: that's all bad. Um. But uh, why did I just
Speaker 1: make myself think about that? So I hope this guy's right.
Speaker 1: But but if he's not. It wouldn't be the first
Speaker 1: time we've heard a scientist, even a very respected sign scientists,
Speaker 1: maybe speak with some overconfidence about how their their findings
Speaker 1: are going to be applied. Sure well, and and it's
Speaker 1: especially um, I've done more research into the into the
Speaker 1: cellular half of the argument, and or the fix it
Speaker 1: half of the argument, or that not fix it genetically
Speaker 1: half of the argument. It all kind of blurs together.
Speaker 1: But but yeah, and and especially the kind of timetable
Speaker 1: that seems like that side of the science is on
Speaker 1: is very much longer term than the genetic side, and
Speaker 1: a lot of other stuff that I've read about the
Speaker 1: genetics seems like it's very much longer term than that.
Speaker 1: And um, and most of the research in fact that
Speaker 1: I've that I've read is still so much in the
Speaker 1: exploratory phase. They're they're still really looking into those specific
Speaker 1: intracellular processes and lifestyle choices that cause aging. Right. Well,
Speaker 1: one of the things I should say is that some
Speaker 1: of these comments Church made seemed to be in the
Speaker 1: context of talking about what has been made possible through
Speaker 1: the Crisper gene editing across us, which, of course, as
Speaker 1: we've talked about on the show before. Didn't didn't. Uh,
Speaker 1: It wasn't like we just recently invented how to edit genes.
Speaker 1: We've been able to edit jeans for a long time.
Speaker 1: It just suddenly got way easier and way cheaper. Our
Speaker 1: toolboxes massively expanded and downgraded in terms of cost. And
Speaker 1: so you can always look at the possibility of new
Speaker 1: techniques for research emerging that could rapidly accelerate the progress
Speaker 1: of research absolutely. Um one one thing that I that
Speaker 1: I wanted to mention when one study that I ran
Speaker 1: across that looked promising to me in the long one
Speaker 1: in the long run, was was research into um the
Speaker 1: rate at which different bodily proteins oxidized and and this
Speaker 1: this is this is a slow burn. But follow along
Speaker 1: with me. So we're back to the rust slash guacamole
Speaker 1: e exactly. Yeah, yeah, yeah, we're back to resting in
Speaker 1: guacamole um. So, so, proteins within our cells are damaged
Speaker 1: by oxidation at different rates, and oxidation occurs at an
Speaker 1: increased rate in older cells. So a team out of
Speaker 1: Stony Brick University published findings about about what types of
Speaker 1: proteins are are affected by oxidation the most. Uh. They
Speaker 1: looked at a whole bunch of them, they crunched all
Speaker 1: the data, and they they published an article in the
Speaker 1: journal Structure in February of and what they found was
Speaker 1: that some of the proteins, like like twenty of the
Speaker 1: proteins that are already associated with aging are the most
Speaker 1: likely to be affected by oxidation. UM. They're they're short,
Speaker 1: highly charged molecule chains, and they unfold relatively quickly when
Speaker 1: exposed to that type of damage and UM as as
Speaker 1: we've talked about a bit in the Crisper episode and
Speaker 1: a bit in other genetic episodes genetic related episodes. UH,
Speaker 1: the folding of proteins is this very kind of mysterious
Speaker 1: thing that science is sort of just working out and
Speaker 1: has very much to do with how those proteins function.
Speaker 1: UM and specifically, UH telomerase is one of the proteins
Speaker 1: that is the most affected by oxidation. UM. Others include
Speaker 1: proteins with known links to memory loss and cancer. So
Speaker 1: this type of research, you know, like like right now
Speaker 1: they're just going like we found this cool thing, check
Speaker 1: it out. Yeah, and that, But the the important part
Speaker 1: is that this is another example of one more kind
Speaker 1: of chip away at the mystery of what aging is,
Speaker 1: and a lot of of people in the medical field
Speaker 1: argue that that deeper understanding is really what we require
Speaker 1: if we are to have any hope of actually combating
Speaker 1: or reversing aging in the first place. Absolutely, and uh
Speaker 1: and I think I think that that brings us to
Speaker 1: our to our kind of a breakpoint on this topic,
Speaker 1: because because now we are entering the realm of of
Speaker 1: what kind of what kind of products are out there,
Speaker 1: what kind of people are talking about, different philosophies of
Speaker 1: how you you can get better by maybe spending some
Speaker 1: money on some things. Right, there's, um, there's a whole
Speaker 1: world of scientists yelling at each other and shaking fists
Speaker 1: and throwing shoes about this very very topic. And we're
Speaker 1: going to cover that in our next episode because I
Speaker 1: think it's a very interesting way of looking at how
Speaker 1: even in the scientific community you can have very deep
Speaker 1: disagreements bordering sometimes on outright fighting about the subject. And
Speaker 1: and what does that mean? And could it be possible
Speaker 1: that you've got one side that's following a very scientific
Speaker 1: approach and one side that perhaps is being pseudo scientific,
Speaker 1: or is that an unfair accusation. Is it truly just
Speaker 1: a hatfield and McCoy is kind of things? Is it
Speaker 1: just misunderstandings all around? Right? Could it be that that
Speaker 1: scientists who have hitched their their trailer over to one
Speaker 1: particular vehicle saying this is the way I believe that
Speaker 1: aging UH operates in and this is how we're going
Speaker 1: to have to address it. Is it just that they
Speaker 1: have a fundamental disagreement with another camp and that's what's
Speaker 1: led to these these issues. That's what we're going to
Speaker 1: explore in our next episode. So guys, if you have
Speaker 1: suggestions for future episodes, whether it's a two parter like
Speaker 1: what we're doing this week or something totally different, you
Speaker 1: should let us know. Get in touch with us. Our
Speaker 1: email address is f W Thinking at how stup works
Speaker 1: dot com, or you can drop us a line on
Speaker 1: Twitter or Facebook. Our Twitter handle is f W Thinking,
Speaker 1: or drop us a line on Facebook. The the you know,
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