Never Grow Old

this is, technological and scientific responses to aging. What do we do with the issue of aging as a as a techno scientific culture. Do we do we just let it happen and study how it happens? Heck, no, Joe, we do. We try to do something about it. We we we grab onto the sand and we make tracks with our fingers as the cold approach of time drags us ever onward toward oblivion. That's what we do. So, like a cat towards a cat carrying, let's mix some metaphors.

I like it. So this isn't the first time we've talked about this. Back in June, we did a couple of episodes on various forms of technological immortality, though I think we were covering some other issues they're like, you know, would you want to have your consciousness put into a computer and stuff like that. Uh. And so one of

the episodes was called who Wants to Live Forever? And the other one was more focused on something along the lines of what we're gonna be talking about today, which was the theories of the gerontologist Aubrey de Gray, and that podcast, quite stupidly, was called Shades of Degray. I think that was my choice here. I think that was my call. Well, we we're gonna be talking a lot

about decay today. We talked about Degray in that episode, obviously quite extensively, and some of the stuff we're going to cover is probably going to be a little bit of a repetition of you know, it has been a minute, so we thought that we would revisit the topic. Also, I think that I think it's safe to say that all of us know how to speak better now. I was about to say talk better, and I caught myself

more more good now ish. Uh So, Okay, So so today we're going to talk about the research being done, and then in the second part we're going to talk about the reasons why there's this ridiculously heated debate, or maybe not ridiculously like like, maybe it's a very human debate to be having about anti aging research and treatments and the whole perspective on the thing, because you hear so many different things from so many different groups, and who can you trust. We'll get to that in the

next episode. For now, scientifically speaking, what is aging? It's kind of a good question. It's one of those things where you know it when you see it, but can you describe exactly what it is? Yeah, So here's the problem, right, Um, there is no full understanding in the realm of science

of everything that goes into aging. We understand elements of aging, We understand some of the cause and effect of certain aspects of aging, but when you look at aging as an overall condition, we don't have a full understanding of what that is. Yeah. And one of the other things I would say is that you might have trouble with such a macroscopic effect as aging um in distinguishing causes from effects. For example, one thing we know is not a cause of aging, but you could say, since it correlates,

is that aging is caused by hair turning gray. If you didn't understand that, it went the other way around. You could get confused on this point, and there are some issues where it's not quite so clear. And there are also some conditions and diseases that could end up exacerbating the effects of aging or perhaps replicating the effects of aging without itself being aging. So you know that

that also throws in more confusion into the mix. Yeah, but one of the biggest concepts in aging is something that figures into what we talked about in that episode about Aubrey De Gray. Aubrey De Gray's program UH is a program for engineering negligible sinescence. What is sescence. Sinescence is the idea, and generally this this refers to growing old and deteriorating in power with age, but at the

cellular level, senescence has a more specific definition. So your body tissues remain healthy and strong over the years by replenishing themselves through cell division. Cells divide and make new, brand new, happy, healthy cells out of the old cells. And that's great. It keeps your tissues refreshed. But when body cells cease their self replication, they stop making brand new, spanking new, happy, fresh little cells. This is known as senescence.

It's also known as cells sort of going into retire ironment. Yeah, and that process leads into cell death. But why on earth would our bodies be coded to kill off cells. That seems like the opposite of what a body would want to do. Yeah. Uh, it is helpful in some situations, you know, when cells are too damage to continue functioning correctly, and so that that's the body's way of telling them to just just go out and quit. You've done enough,

You're fine. Um or in the case of sing like cancer, it's really good to be able to just just be like, you know what, we don't really need you any here here anymore. We're doing okay. And certainly, if you didn't have senescence, if you didn't have this process, uh, if there was this unchecked method of cellular division, it could lead to things like cancer. However, if you have senescence body wide, then you're essentially saying that the cells have

stopped dividing and now it's borrowed time because cells have lifespans. Yeah. And you know, if you think about it from the genetic perspective of your cells, you can see why this might be the case, because what is the purpose of your body Genetically speaking, It's not to be happy and healthy forever. It's to survive long enough to achieve prodigious sexual recombination. And uh and so, I mean, once you're beyond the age of sexual reproduction, what of what uses

it to your genes to just keep making your muscles strong? Yeah, we're really just biting our thumbs at our genes every day that we live without having healthy children. Yeah, yeah, I'm alright with that. Okay, so so, so, why why does senescence happen? Researchers think that on a cellular level, it happens because of this stuff called telomeres. Telomeres our our DNA caps on the end of your chromosomes that protect your DNA from wear and tear when cells divide.

Geneticist Elizabeth Blackburn famously compare them to the little plastic caps on the end of shoelaces. Oh, I've heard Michia Cake you say the same thing. But I bet he got it from her. I I think I think she was the originator of that phrase. Now I'm terrified that I'm wrong. No, I bet, I bet, I bet that's

the case. Okay, Uh, so, so you're you're you're telomeres unlike well, well, actually exactly like the plastic caps on the end of your shoeleases are also subject to the same wear and tear that happens to the DNA when your cells are dividing, so they get shorter after many cell divisions, and when they wear down enough, the cells that they're in stop dividing, and that is in essence, So when that happens to adult stem cells, that might be one of the critical factors of aging, because adult

stem cells are the things that create new cells when you're when your tissues are damaged or or your your blood needs to be replaced, and they're usually just hanging out in a state of quiescence, a sort of like like yellow alert. Okay, so they're not actively creating new cells, and they don't themselves divide to create new stem cells

unless some kind of damage happens. And there have been some studies that have shown that with age, or or possibly once having gone enough cell divisions, adult stem cells don't function as quickly or as completely as they used to, so your body is less able to replace and repair damage that gets done. And of course, when one thing gets damaged in one of our bodily systems, it reduces the function of other things, or you know, like weakens

the structures needed to prevent further damage, like in osteoporosis. Right, Okay, that makes sense. However, there is a process of your cells that protects your telomeres, an enzyme called telomerase to telomerasemerase, telomerase, interesting, telomerase like telemachus. I like that you look at obviously, and I'm like, I want to cobb Well anyway, not kebabs.

But telomerase or telomerase controls the generation and the formation and the length of your telomere, but not all of your cells make it, which is actually a good thing because cancer. But more more on that later on. Didn't that funny that cancer link just keeps coming up in this episode? Well, it's gonna come up a lot in general, not just in this episode, but in the following one.

Because one of the things when you're talking about trying to find a way to counteract or even reverse aging, one of the big questions that comes up in everyone's mind is you're talking about regenerating tissue that is frighteningly close to the concept of uncontrolled cellular division, which is what cancer is made of. Exactly. Yeah, undifferentiated, uncontrolled growth. So yeah, so that that's an interesting avenue of research

about what causes aging. But we've also got the issue of mitochondria, right, oh yeah, okay, so so our selves mitochondria definitely become less efficient as we age. UM and and my mitochondria if you guys don't remember, from like seventh grade biology or possibly from a wind in the door? Was that which which one did you guys ever met? Yeah? Yeah, yeah, she totally talked about mitochondria and one of those books

at any rate. Um. But what mitochondria actually are are the organelles inside of ourselves that, among other things, chemically convert the nutrients that we take in into the molecules that our cells eat to gain the energy they need to do what they do. Yeah. I think the common way of expressing it is that they're the power plants

of our selves exactly. Yeah. Yeah. They produce what is it, t um and so when mitochondria become less efficient, they produce less a tp Our cells can't do as much, and therefore our body's entire metabolic activity systems slows down. We have, you know, less nutrient transfer, fewer new cells, decreased immune response all that good stuff that goes into a young and healthy body. But of course all that, all that that and more tends to add up to these macroscopic effects that we see on the body as

a whole. Oh sure, yeah, and we see plenty of those. Yeah right. So, for example, some of these macroscopic effects that we'll see, one of the most general ones tends to be a decrease in tissue elasticity. And this is this is pretty much body wide, but really we're talking about muscles and blood vessels in particular. Yeah. Yeah, it's the the collagen inside the little tiny molecules of proteins

that are folded up. Stop being as cool. Yeah, it's it's like if you you know, you got that that one pair of underwear you really should be tossing out. It just in't doing the job anymore. It's that elastic is all totally worn out. It's kind of sad when that that pair of underwear is actually representing something like, I don't know, your heart. That's a bad thing. Yeah, but if only science could replace it with a pair

of means right. Bones also also come weaker. You lose bone mass faster than you are regenerating it, uh, and that can lead to osteoporosis, which is the more extreme version of that problem. You know, one thing I've heard expressed by some of the advocates of aging reversal technology is to think about it this way. Aging is the number one risk factor for almost every disease we know of. I'm not quite everyone, but the vast majority of them.

And if you think about it like that, it kind of might tweak your understanding of whether or not we should do something about aging. Because if you had, say, if you said cigarette smoking was the number one risk factor for the majority of known diseases and conditions, I mean, it seems like you'd really want to do something to get people to stop smoking. It's it's like, well, obviously, don't smoke. That's terrific. So clearly you should stop aging.

Just don't do it. Don't age, kids, don't age. My life's been doing that for years. She celebrates her twenty nine birthday every year. Oh that old joke, And you make that joke every year, don't you might? Okay, So, so one idea to keep in mind going forward, we are going to talk about some some new ideas and what to do about aging and in ways to counteract it. But one idea to keep in mind is also the difference between the concepts of life span and health span um.

And so this is something that I think is recently something that doctors have started to talk about more. Lifespan, of course, is just time from birth until death. How many years do you Yeah, But health span is time until serious illness. And a lot of medical technology over the you know, past decades, has succeeded in extending the

former without necessarily extending the ladder. So, in other words, life expectancy has increased, but but how long you remain healthy within that lifespan hasn't measurably increased at the same rate, or I should say, just increased at the same rate. It has certainly increased, there's no denying that, but it has an increased to the point where you would say, um, if the average life expectancy has gone up three years,

the health span has not done that. Yeah, And so that's a thing that's important to keep in mind when you're talking about rejuvenation research. A lot of it is focused on extending quality of life and not just extending life, So maybe not even extending lifespan at all. Maybe that you know that that could happen, But perhaps the focus for at least some of the researchers is not let's see if we can get people to live to a

hundred and twenty on a regular basis. It's let's see if we can make sure people maintain a good quality of life, a good healthy life, or more of their lifespan. I mean, think about it this way. Would you rather live to two hundred but for the second two hundred

years you can't get out of bed? Or would you rather live to e ight but be healthy and fit the whole time can't or whoa, there's a lot of comic books in the universe, Like I could spend a solid decade or two just reading comics, and that's not even getting into nonfiction. But eventually you'd want to get out of bed, go line up to see the movie that's going to disappoint you. That's what digital downloads are for,

all right. So let's talk about some of the research. Yeah, well, okay, So there are some avenues of research into rejuvenation or aging reversal that we have talked about in recent podcasts. One of them, for example, is if you remember our episode about the Future of blood, we talked about research into the rejuvenating effects of young blood. Now really, honestly that research has goes back centuries. Elizabeth. You have to

believe the the sensational reports of Elizabeth Bathory. Yes, but no, that this is very interesting though it's yet another one of these things where we should always couch all coverage of aging reversal research with it. Let's not get carried away here, um that you know, there is there is some interesting research coming out and we want to keep an eye on it. But nobody's found the fountain of youth yet. But yeah, yeah, can we just never use that phrase again as a as a human species. I'm

right there with you, Lauren. Okay, so, but but a quick refresher on the blood thing if you if you wanna full breakdown of this, you can go back and check out our episode on the Future of blood. But in short, multiple lines of research have shown that giving older animals infusions of blood from younger animals of the

same species has rejuvenating effects on body tissues. And some of the experiments have been in what's called heterochronic parabiases, where you sew together to mice one young and one old, so that they share a circulatory system and a common pool of blood. That, yeah, that does sound creepy, but the results, it's an extreme measure, like I'm not going

to sign up for that tomorrow, but the results. But the results have shown that the old mice have improved muscular and cognitive function and the they have younger looking tissues at a cellular level when continually exposed to the blood of young mice in this way. On the other hand, the young mice do not seem too fair as well from this procedure. Uh there there seems to be a

sort of compensating not so great effect for them. But in some studies in rodents, they think they've isolated a protein called g DF eleven for growth differentiation factor eleven, as a major contributor to the rejuvenation effects. Though since the podcast on this we did, I think I've read a couple of articles questioning the primacy of g DF

eleven as as the factor affecting this rejuvenation. Uh So, as you can tell from that, the research is still ongoing, and it would be premature to say that the blood of the young is this fountain of youth or whatever. We should have an alternative phrase, the hose of infancy. So health recommend nuts the spigot of infancy, spat of spigot of infancy, come on adolescence. I'm not sure if infancy is where I want to go back to. No,

we will Benjamin Button all the way. I haven't seen that movie, so I don't know what that means better than my suggestion of prepubiscent dip. Wow. Okay, yes it is the spigot of health. Yeah. No, it is not necessarily been shown to be this A Researchers are usually quick to point out that the technique hasn't been shown to make animals immortal or even necessarily increase the lifespan.

But what research we have seen is interesting, particularly with reference to potential treatment for specific diseases like Alzheimer's, where you might be able to see uh targeted rejuvenation of cells that have seen some kind of deterioration due to an age related disease. And so it could be that with some of these things we talked about today, they might not make you younger or make you live longer, but they might turn out to help with some particular

disease which may or may not be age related. It kind of goes into something that we say on the show all the time, which is that, uh, scientific experimentation and exploration can lead to answers to questions that we weren't even specifically looking at at the time, and it requires very rigorous follow up to make certain that those answers are in fact valid. But it is well, yeah, no, I'm I'm sorry, I'm loving I I It just occurred to me that like that basically, like we are constantly

just going like, well the answer is forty two. Well, I just think like if you if you were to do an experiment and you get an unexpected outcome, then obviously you need to uh re examine that and see if it's replicable and then get down to the question of what is it that's actually happening. Yeah. But another thing that this springs up is we sort of mentioned this earlier, but just to highlight it again, there are multiple different goals they're sort of encompassed by by rejuvenation research.

One of them would be increasing lifespan. Another would be making old body tissues look like young body tissues and work as well as them. Yeah, like like a good uh you know, a good pair of kidneys or a good heart, all of that kind of stuff that does tend to decrease its efficiency over time. Yeah, and another thing would just be, uh doing this in a way that leads to a good quality of life. For example, we already know of one thing in animals that leads

to increased lifespans, you know this caloric restriction. If you are willing to starve yourself too nearly to death on a constant basis annual, probably live longer in a laboratory setting. Unfoly, the thing that happens along with this, uh, this boost in longevity is a complete shutdown of the immune system. So if you're just wandering out around the world full of germs, then probably that's not going to fare very well for you. Oh yeah, that's a good thing to

point out. But also it just sounds miserable. I mean, people don't want to live this way. No, I I certainly don't. Food is probably the most important thing to me. Um. This research, by the way, was from It was just published in March sixteen and it came out of the Leibnitz Institute on Aging out of Germany. And yeah, so uh so, so don't so don't totally restrict your calories down to nothing in the hopes of getting better longevity.

It probably won't work. Well, maybe you should if you can live that way and want to live in the bubble boy suit and no, yeah, I mean it's very fetching, right, Yeah, this is is it living? If you can't snuggle with a dog on your face? It's interesting to me because that Clorican, the cloric intake research, that stuff that's been going on since like the nineteen thirties. Yeah, so this is uh, you know, it goes to show like that research began in the nineteen thirties, we're still looking into

the effects today. That to me is a big indicator of how challenging it is. This this idea of how do we rejuvenate, how do we combat aging? It's not like it's a new question. It is something that has been going on for a while. So that's an interesting, uh note. I think I agree with you. But then again, there are also new technologies and techniques and bits of knowledge that are coming out that could be very well

accelerating our our knowledge on how to combat aging. One of them, I think is this interesting idea of the clearing out of sinescence cells as one possible way to reverse the effects of aging. So I was reading about this. There was a study published in Nature in by Mayo clinic researchers Darren Baker and Jan Van Deerson, and it was the latest to suggest that if you clear out sinescence cells from the body. Remember these are the cells who were talking about earlier. That are the retired cells.

They're they're done dividing and making new happy cells. You if you clear those out of the body, you can rejuvenate tissue and perhaps live longer. So Baker and vin Jerson found that if you're able to remove sinescence cells from the bodies of mice, those mice live about twenty longer on average. So we mentioned these sinescence cells earlier. But what do they do once they sit around in the body so they retire. It turns out they have some not so friendly side effects. There might be beneficial

effects to um. We can talk about those if you want, but they're believed to mostly just hang out and excrete molecules that harm other tissues and processes in the body. Basically molecules that lead to greater inflammation and greater rates of oxidation. Oxidation is rust It's not something you want inside your body. No, No, you don't want your inter cellular structures rusting. Nobody nobody wants that, or or or having happened to them. What happens to avocado dip left

out too long as guaco? I think, I think I want that less than I want rusting. However, I do want guacamole, I don't. I always want glucomole um and research. Some researchers think at any rate that aging mitochondria have something to do with those molecules that are being released, tying it back to the mitochondria issue. Um there was there was a study published in the E m b O or possibly MBO journal um in uh just recently

in but but so so back back to these mice though. Yeah, Actually I've read a good article about this research, the Clearing of senescence Cells that ed Young Road for the Atlantic in February, where he describes looking at two mice side by side, and one of them looks like a healthy adult mouse and the other one has quote graying for a hunched back and an eye that's been whitened by cataracts. So it sounds like it's seen better days. And yet these two mice are the same age. In fact,

they're not just the same age, they're twins, genetic twins. Yeah, same age, same genes. It's one of them, an actor mouse that's portraying like the hunchback of Notre Dame. No it is it does not have Tom Savini mouse makeup on the mouse version of King Lear. Oh no, no, no, no, it's too Oh that would be so cute. Okay, please go ahead. Well, anyway, it's just that one of them, the healthy looking one, has undergone this procedure to clear out the retired senescence cells from its body. So to

back up a little bit. In two thousand eleven, Baker and Van Jersen were part of a team that came up with this process for removing senescence cells from the body. So they genetically engineered the strain of mice that display aid congenital accelerated aging. These mice. You don't want to

be one of these mice. They got old very fast. Uh, and also with a trait that would allow the researchers to administer a particular drug in order to induce the systemic destruction of all the retired cells from the body, and they found that when the mice received this drug, they became fitter, stronger, bigger, and healthier, and yet they still died early. Remember these were the rapid aging mice.

But a more recent bit of research is that Baker and Van Deerson found that you could do the same thing with mice that were not genetically faded to rapid aging. You could do it to the regular old lab mice, and they found that if you use the same procedure to clear the senescent cells from middle aged mice twice a week, the mice also showed healthier tissue, less body fat,

and just seemed fitter in general. Not only that, but as I mentioned earlier, they lived longer, longer on averager and average of I can't imagine how depressing that must be to be the elderly twin looking at the younger twin and just thinking that could have been me. Well, it's it comes back to my proposal for NASA to do the twin study again. That's what the Earth twin would say to to his or her returning astronaut twin.

I mean, I'm sure that what the mice we're actually thinking was like squeak yeah, So let's let's talk beyond this experiment. What about Could this be something that's applicable to human beings not just to mice. Well we don't know yet, but that's the thing that obviously people want to find out. So researchers think that drugs could be developed to recognize the bio markers of sinescence cells, you know, the little flag that says I'm a retired cell in

humans and selectively destroy those cells. So just to go in your body, only find the retired cells, not hurt the good cells the you want and get rid of them. But as usual, there a few things we need to say. One of them is don't get carried away here. We we need to see this reproduced in other studies. And even then what works for mice and lab conditions won't necessarily mean humans can undergo the same procedure and regularly

live to a hundred. But even if it's not useful in increasing general human lifespan, it might be useful in treating age correlated diseases like arthritis, heart disease in glucoma. Another drawback is already obvious from their research mice that had their sinescence cells cleared on a regular basis also displayed lower rates of healing from wounds, which is interesting going back to that immune system depression. Yeah, so it appears that the removal of these cells doesn't come without

a cost. They they're sitting there having maybe a net negative effect on the body, but they also appear to do some things that are useful, and removing them counteracts those positive effects. Uh. And then another potential risk of course, yet again cancer. It just keeps coming up with rejuvenation technologies. Like we mentioned earlier, cancer is the uncontrolled, undifferentiated cell

growth that we see. Any therapy that seems to unnaturally extend or accelerate cell growth seems at least in potential a cancer concern. One last thing from Young's article that I thought was really interesting is that he got a quote from Dr Norman Sharpless of the UNC Chapel Hills School of Medicine, who said the following quote, you take a drug reserve at all green tea, god knows what, And he's naming there a few of the things that have been called up in the research as potential anti

aging drugs throughout the years. But he continues, you take that drug for thirty years and by the time you're eighty, you're actually seventy. That paradigm doesn't work in the real world. And I think I agree with him there. I mean, people don't want to take a drug their whole lives to see maybe some reduce staging over a long period of time. Right. Uh, he continues, people hate taking drugs, especially when they don't know it's helping them. And no

farmer company would develop such a drug. If this paper is right, and he's talking about the Baker and Vandersen paper, suddenly you have a way of taking an old organism and making it physiologically younger. You go from a prevention paradigm to a treatment one that's something you can sink your teeth into. And I think he's got a good point there. I mean it it reacts to not just what a drug can do, but the different ways that

we want to interact with medical technologies. It specifically speaks to a very American approach to medicine, this idea of treating a disease as opposed to trying to prevent one, right. And I think that we would be better off probably if we did the prevention more than the treatment. I mean, but you know what, when you really get down to it, a great way to prevent aging is to hide eight

and eat vegetables and exercise. Sometimes I think I think if you, I think, if you look at it in the sense of, if you take this drug, you're still going to get old. It might take a little longer for you to feel like you're getting old than it would otherwise, But that's your personal experience. You wouldn't know otherwise, right, You know, your reality is whatever it is that you are doing. So and we've talked about that that bias on on the show before too, that the whole, the whole, like, well,

it didn't not work. I'm still here, right, But but something where you take a drug and you feel younger, then you have something to compare the effects to you, Like I already know what being older than this feels like. So it's definitely one of those things where you can understand where someone's coming from if that seems more appealing to them, even if you were to demonstrate Yeah, but if you do this other approach, you're going to feel better for longer and you don't ever have to dial back.

Right then, again, I would say that there is a quite obvious appeal to the reversal process for people who are already today in their sixties or seventies. There's appeal to me right now, and I'm in my forties. I guess to all of us, except those babies out there who are still in their prime. Huh, all right, Jonathan moans with hate. Look, I don't I don't hate young people. I just don't want to him a lawn. He just wants the spigot of health all to himself. I'm not

going to deny your accusation. I'm just not going to acknowledge it. Okay. But but that avenue of research we just talked about is based on one type of approach to the aging problem. If you are looking at aging as an engineering problem and you want to fix it or reverse it, there are several approaches you could take. And this this is sort of the error corre acting problems, saying, oh, we've got we've got a build up of stuff we don't want in the body, or of errors or of damage,

and we can go in and fix that somehow. But there is an entirely different way to look at it. Instead of saying going in and doing repairs, you could look at it from a genetic point of view. So, in other words, the instructions within our genes, if you could somehow rewrite those instructions so that the damage doesn't even happen in the first place, yeah, Or so that the cells in your body, by their very nature, executing their genetic instructions, will fix the problem themselves. And that's

the genetic method. So one I one name that has come up in this way of looking at the aging problem is the geneticist George Church. So George Church runs a lab at Harvard Medical School, and he has made some very interesting predictions about aging research that I read about. Speaking to Joel Aichenbach of the Washington Post, Church has said that new breakthroughs in genetics and gene editing will

make it possible to reverse aging and humans. And he even predicts, quote, in just five or six years, he's going to be able to reverse the aging process in human beings. And he seems to be speaking out of personal experience based on the research that's going on in his lab. This is obviously a really bold claim. But five or six years, I mean, that sounds kind of crazy. But I do want to point out Church is not

just some whacko on the Internet. And he's not a quack because he's a very well respected geneticist who has been working in the field for years. He uh, I know he. I think he was one of the founders of the Human Genome Project, or one of the organizers at least. So so what's so, what's he proposing? So he's talking about gene therapy. Basically, it sounds like his experiments so far based on gene manipulation gene therapy not just for curing specific diseases, but for reversing aging itself.

Whereas most research and rejuvenation is aimed at counteracting the effects of aging, these would be doing what we were just talking about, addressing the genetic root causes of aging in cells. So Church claims that he's already demonstrated aging reversal on smaller animals in the lab, and the next step is translating these results to larger animals and human trials.

I found some good quotes from an article in the San Diego Union Tribune covering his Future of Genomic Medicine conference speech in sixteen, where Church said a few things that seemed very interesting to me. One of them is quote if we could take one of my skin cells and turn it into an embryo like cell and turn it back into a skin cell, it is reset almost all of the developmental indications of age. We have sixty five gene therapies that are being tested in mice and

larger animals. If they go well, we will go straight into human trials that could be as little as two years. He said this in essentially the I T crowd approach of turning it off and on again. It is control all delete on your cells and it refreshes it. Yeah. And and so he talks very interestingly. I like his thinking here about why he uses the term reversal for aging instead of curing aging or stalling aging. Uh. He says, I don't think it's about stalling or curing. It's about reversing.

Curing gives you the impression of immortality, which is not necessarily what is being proposed. Uh. Stalling gives you the impression that you'll be eighty five forever, which is not great. And we sort of mentioned that earlier in the show. Uh. And So the last thing he says that I think is interesting is he says, quote, reversal is something that's been demonstrated in a number of different animals in a number of different ways. I think that's going to translate

into larger animals and humans. We won't know until we try, But we're trying sixty five different genes in different combinations to see if we can reproduce the aging reversal that we've seen in small animals. We don't know what age reversal would mean in terms of human years. Animals have had their life extended by factors to to ten. That seems to be too good to be true for humans. Yeah, I think, uh, you know, living to sixty might be a bit much. Yeah, unless you're an evil wizard so

many comic books. Uh huh. So, despite the fact, I did want to point out that he's not just some whacko on the internet. This is a respected scientist. But at the same time, you can't just take it on one scientists authority that like, oh, yeah, he's got it. Yeah, so he go home. Now, obviously he has a very optimistic prediction, but it is interesting to hear this. Yeah,

I mean it's there. Obviously, there are a lot of questions to ask to like, would this approach also stave off the age related diseases, that we're that we've talked about some things, or would it just be like like seven hundred years of Alzheimer's Right, it seems to be that he's got the idea of the health span in mind, because he's talking about not just forestalling death, but being

able to rejuvenate the tissues. Yeah. Yeah, I think a lot of um, and we'll talk more about this in the second episode, but I think a lot of of experts in the field of aging are skeptical or or reluctant to endorse such a bold claim. I mean on the face of it, because, as we said at the top of the episode, it's such a complicated issue that it may very well be that something you did not anticipate is still in a problem, like one of these

age related diseases. And it may be that you have very healthy tissues overall, but that you're still prone to these other issues. Yeah, but you know your your immune system craps out or you have cancer and wind up looking like the character from the end of Akira and that's all bad. Um. But uh, why did I just make myself think about that? So I hope this guy's right.

But but if he's not. It wouldn't be the first time we've heard a scientist, even a very respected sign scientists, maybe speak with some overconfidence about how their their findings are going to be applied. Sure well, and and it's especially um, I've done more research into the into the cellular half of the argument, and or the fix it half of the argument, or that not fix it genetically half of the argument. It all kind of blurs together.

But but yeah, and and especially the kind of timetable that seems like that side of the science is on is very much longer term than the genetic side, and a lot of other stuff that I've read about the genetics seems like it's very much longer term than that. And um, and most of the research in fact that I've that I've read is still so much in the exploratory phase. They're they're still really looking into those specific

intracellular processes and lifestyle choices that cause aging. Right. Well, one of the things I should say is that some of these comments Church made seemed to be in the context of talking about what has been made possible through the Crisper gene editing across us, which, of course, as we've talked about on the show before. Didn't didn't. Uh, It wasn't like we just recently invented how to edit genes. We've been able to edit jeans for a long time.

It just suddenly got way easier and way cheaper. Our toolboxes massively expanded and downgraded in terms of cost. And so you can always look at the possibility of new techniques for research emerging that could rapidly accelerate the progress

of research absolutely. Um one one thing that I that I wanted to mention when one study that I ran across that looked promising to me in the long one in the long run, was was research into um the rate at which different bodily proteins oxidized and and this this is this is a slow burn. But follow along with me. So we're back to the rust slash guacamole e exactly. Yeah, yeah, yeah, we're back to resting in

guacamole um. So, so, proteins within our cells are damaged by oxidation at different rates, and oxidation occurs at an increased rate in older cells. So a team out of Stony Brick University published findings about about what types of

proteins are are affected by oxidation the most. Uh. They looked at a whole bunch of them, they crunched all the data, and they they published an article in the journal Structure in February of and what they found was that some of the proteins, like like twenty of the proteins that are already associated with aging are the most

likely to be affected by oxidation. UM. They're they're short, highly charged molecule chains, and they unfold relatively quickly when exposed to that type of damage and UM as as we've talked about a bit in the Crisper episode and a bit in other genetic episodes genetic related episodes. UH, the folding of proteins is this very kind of mysterious thing that science is sort of just working out and has very much to do with how those proteins function.

UM and specifically, UH telomerase is one of the proteins that is the most affected by oxidation. UM. Others include proteins with known links to memory loss and cancer. So this type of research, you know, like like right now they're just going like we found this cool thing, check

it out. Yeah, and that, But the the important part is that this is another example of one more kind of chip away at the mystery of what aging is, and a lot of of people in the medical field argue that that deeper understanding is really what we require if we are to have any hope of actually combating

or reversing aging in the first place. Absolutely, and uh and I think I think that that brings us to our to our kind of a breakpoint on this topic, because because now we are entering the realm of of what kind of what kind of products are out there, what kind of people are talking about, different philosophies of how you you can get better by maybe spending some money on some things. Right, there's, um, there's a whole world of scientists yelling at each other and shaking fists

and throwing shoes about this very very topic. And we're going to cover that in our next episode because I think it's a very interesting way of looking at how even in the scientific community you can have very deep disagreements bordering sometimes on outright fighting about the subject. And and what does that mean? And could it be possible that you've got one side that's following a very scientific approach and one side that perhaps is being pseudo scientific,

or is that an unfair accusation. Is it truly just a hatfield and McCoy is kind of things? Is it just misunderstandings all around? Right? Could it be that that scientists who have hitched their their trailer over to one particular vehicle saying this is the way I believe that aging UH operates in and this is how we're going to have to address it. Is it just that they have a fundamental disagreement with another camp and that's what's led to these these issues. That's what we're going to

explore in our next episode. So guys, if you have suggestions for future episodes, whether it's a two parter like what we're doing this week or something totally different, you should let us know. Get in touch with us. Our email address is f W Thinking at how stup works dot com, or you can drop us a line on Twitter or Facebook. Our Twitter handle is f W Thinking, or drop us a line on Facebook. The the you know, just search fw Thinking in the little search field will

pop right up. You can leave us a message there and we will talk to you again really soon. For more on this topic and the future of technology, visit Forward Thinking dot Com Problems Brought to you by Toyota. Let's go places