Shades of de Grey

de Gray. And this is someone who has sort of dedicated the second half of his professional life to figuring out how to defeat the symptoms of aging. You may have seen him in various mind expanding videos on the Internet. He's a uh, scraggly looking fellow with a gigantic beard.

He's kind of like a latter day rest sputant. David David step of Forbes called it his rip Van Winkle beard ever, which I really like, Every single article I have ever read had anything to do with him, had at least a part of a paragraph dedicated to this man's beard. And indeed it is impressive. His beard. It's like a tree. It is it is he he's got. He's been on Ted Talks. He's we've got it. We've

got a feature on him on Curiosity Project. And uh, it's because he has some pretty interesting ideas of how to combat the symptoms of aging. And he comes from this from a really interesting pathway because he didn't start

out as a biologist. He started out as computer scientist, specifically focusing our artificial intelligence, right, and he's never actually been well, I mean, he he has studied a lot of biology, but he's studied theoretical biology, and so he's sort of approaching this from the perspective of an engineer, which has some doctors and other people within the medical field concerned that perhaps it's an oversimplified you. But I'm

kind of getting ahead of myself. We should sort of talk or about his area of interest and and what it is he's trying to accomplish. So, first of all, you could say that he's a gerontologist in a way, that's someone who studies aging. So that's the whole area

of the study of aging is gerontology. And he is well, he formed this this this organization called the Strategies for Engineered Negligible Senescence that again sends send there you go with the acronym negligible senescence, and so senescence that means something. What does senescence mean? All right? Well, so, so cells, normal healthy cells go through a life process in three stages. First you've got normal healthy cell division, which is mitosis um.

And then eventually the cells will stop dividing and that's called senescence um. After that you have cell death, which is a poptosis. But that that comes later and and is debatably awesome for your right. So this idea of the negligible engineered sinescence or sentizens depending upon how it's pronounced, I honestly don't know. Uh. The idea here is that we are trying to find a way to to halt that that phase of of of an organism's life where the cells are no longer dividing in a healthy way

or they're dying off too early. Essentially, the ideas to try and preserve an organism's healthy state at the peak of its life. So, for example, the numbers that I tend to hear for a human according to the Aubrey de Gray stuff, is between the ages of five and twenty nine, right and there where you are in theory at your healthiest at least as far as you know

an average person is concerned. So, uh, it's all about trying to create this this uh solution or actually series of solution to maintain that kind of level of health uh indefinitely. And it may extend your life, it may not, but at any rate, what the the ideally, what it would do is allow you to have a healthy, active life throughout your life. Right. He said several times that that added lifespan is not the point of all of this.

It's it's really quality of life that he's looking for, right, Although he's also talked about how he would love to live to a thousands that he could read all the books he'd want to re I mean, he wants to see when when some of us, many of us, a few of us. I think we've already established that I'm planning on trading in Joe's immortality for double immortality for myself, as I recall from our previous podcast. More right, so, yeah,

I need to be twice as immortal. But he lays out the Gray lays out seven principle mechanisms of aging and or you can also think of this as different types of damage. This is interesting because I think most people don't think about what actually happens when we age. They don't realize it's just it's the cumulative effect of a series of processes, several biological processes exactly. And so any solution would not be, like I said, just one solution.

It would have to be multiple solutions to meet all the requirements to tou to cancel out these seven principles of aging. So what is aging at its core? Well, it's the way he breaks it down, because he's looking at aging as these various types of damage. He has the seven different types. The first three he lays out our types of cellular damage. The first is this loss of cells, the idea that you have cells that die and they aren't replicated, so there's not they're not being

replenished in any way. So you could have muscle loss, bone loss, that kind of thing. And a lot of these different types of damage that he talks about relate to specific kinds of disease is or or conditions that you are probably familiar with. So does this particular problem have anything to do with what I've heard of the

hay Flick limit. Yes, that would be the limit that was proposed by Dr Leonard hay Flick back in nineteen sixty five, and he he observed that that cell death process that I mentioned earlier, that apoptosis and this this is a natural process. It's really useful for you know, for us not having webbed hands um in because because embryos when when you're when you're going through development, UM, not all parts of you wind up being you. You know, it's we lose your tails, we lose the webbing between

our fingers, and so that's very useful for that. UM. Apoptosis goes on during menstruation. It's really great for fighting off viruses and cancers. UM. However, like Jonathan was saying, at a certain point, your cells are dying off and they're not being replenished, right, So that that's one thing that we would need to address. And he has he's named the various UH solutions, or at least the kind of overview of what the solution might be. Keeping in mind,

we don't have solutions for all this. If we did, we'd already know or at least we'd all be healthier. But it's sort of that he's named what the overall approach would have to be in order to you know, address this issue. So in this case he calls the this part replena sends each one having sends at the end of it, sc and s which is that acronym, So that that's the first one is the loss of cells, you know, figuring out how to make sure that cells continue.

He's replenished. He's proposed stem cell therapy for that one as being kind of the leading Yeah, and in fact, stem cells are just kind of magic. They're unicorns. They're pretty much the They're made of unicorn nichols. That's a science fact, guy, So you can just buy that straight from a think geek. You get that canned unicorn meat you've got. That's not the way that works. Cells they're like the they're like the phenomena of medicine, right right exactly.

These are the cells that have the potential to develop into other types of cells. And depending upon what kind of stem cells you're talking about, the variety of cells they can turn into is very wide or very narrow, because not all stem cells are the kind where this this one proto cell could be anything. Some of them are. They can be any type of vascular tissue, that kind of thing. So it all depends on the type of

stem cell. But anyway, yes, he does say that that is one potential way we could meet this challenge, and in fact, from why I understand it might be one of those things that would be a requirement because some of the other solutions he's proposed would UH end up affecting us in such a way that we would have to have stem cell treatment in order to UH to to combat some of the side effects we could have from treatments from the other principles. This is where it

starts getting complicated. But we haven't even gotten into principle number two. You okay, let's go to number two. Thank you. Number two is that uh, there are two different version of this, so this is technically two and three. So number two is that you end up with too many cells because the cells don't die when they are supposed to UH. And that one he suggested a pop apop apopto sends this is so hard to say because of

the sens acronym at the end. That was the that was his solution or overview of what the solution would need to be to take care of that problem. And the other type was too many cells because these cells divide when they aren't supposed to, which sounds like cancer exactly. That's that's pretty much what cancer is. And so his overview of what the solution would have to be is called onco sens which oncology that makes sense, you know, sure, yeah, yeah,

because because cancer is actually pretty cool. I mean, not when you have it, obviously that's terrible, but um, but but the the way that cancer cells don't die is kind of terrific, and so people are doing a lot of studying into that to see if we can use that to extrapolate this idea that you can take something that is very harmful in one one manifestation, but find a way of applying some of that in a medicinal way in order to prolonged life. It's it's a fantastic

idea if we can make it work. I mean, we've seen this in other applications as well, not just with cancer, things like viruses. We've seen medicine used viruses in order to have uh nanomedicine delivered to particular parts. If you can reprogram them, then you can get them to do it. Yeah, exactly, that you can code of virus shell with a certain type of protein and theoretically it'll seek out the right kind of cells to deliver a cellular amount of of medication,

So you're dosing particular cells. So you know, we see this where we're using things that were at one point potentially hazardous or deadly, uh, in other ways to have to improve our lives. So that might work out, but we still have to figure out how to actually accomplish any of that. Well, not only that, but how do we actually stop the uncontrolled division? How do we stop the cancer part of cancer and utilize the beneficial aspects

while getting rid of the ones that are deadly? And uh, he's thinking about mainly things like a gene therapy as

an approach. And again that's one of those approaches that some people say may oversimplify the matter, although it's really kind of hard to say right now, because you can you can frame these approaches in such general language as for them to be um, they can fit any definition in a sense, you know, like if you if you just sit there and say, someday we will be able to do this, it's kind of hard to refute that. All right, Well, that's the three types of cellular damage,

but then there's three types of molecular damage. One of those is damage to DNA, specifically in mitochondria. These are the cellular powerhouses. This is an an energy element to the way cells live. They have their own DNA, mitochondrial

DNA and UH. Unlike the DNA that you find in a cell nucleus, which has some repair systems built up around it to help maintain that DNA's integrity, the mitochondrial DNA they don't have that kind of support system, so they are more vulnerable to various types of mutations, right and there they exist in a highly oxidized environment, which makes them even more susceptible to damage than a lot

of other little cellular bits. Right. So that's that's another one of the ones that he's identified, and Mito sends, which is probably the easiest one to pronounce, is his overview of the solution to that. Then you have two different types of molecular junk or garbage, depending depending upon which one you read, but in any case, it's unwanted molecules that begin to accumulate within an organism and some accumulates inside cells, which these are byproducts of cellular process

e is um. One example of this would be cardiovascular disease that it can manifest in that way. The approach that that Degray suggests is called liso sins. And then there's the molecular junk that accumulates outside a cell's wall, so in between cells, and this is created through metabolism uh and de Gray points out that the an example of this could be manifested in something like Alzheimer's or diabetes and h a millocin's or um. Yeah, and a millocent's is the name of the approach that you would

have to address this issue. So those are the three types of molecular damage, right, and and there are there are already processes going on inside your body that are that are taking care of some of this junk. The the licensome with within cells is the organ that kind of digests some of this junk, but it can't digest everything. And say, some of the therapy that he's suggesting is adding extra enzymes in there to drive the licensome to

to get rid of more stuff than it currently can. Right, Some of these molecules that get formed turned into stuff that cells just can't process, and so it just accumulates. That's why they call it junk. It's this idea of kind of like, ah, if you've ever lived with someone who is a hoarder, when you walk into the room and you just realize that tomorrow I will not be able to open this door. Uh, same sort of thing.

These cells get bogged down with lots of molecules that they cannot deal with, and then eventually that causes problems outside of your cells. The the immune system process, it's called phagocytosis, that's supposed to take care of this, and it and it does to a certain extent, but just from the root, like eating, you've got some cells that come and eat up the junk exactly. Yeah. Yeah, but and and so his his proposition is to kind of

chemically amp up that process. Right. And then the final principle. So we've got the three types of cellular damage, three types of molecular damage. The final principle is called cross linking. And this has to do with tissue. So you have tissues that that hold things into place, kind of give a shape, sort of a scaffolding, if you will, for various types of so that all your cells aren't just floating free within your body, right, You're not just a

big lobby massive cells. It's very important as far as I'm concerned, But they're supposed to be there's in most cases, they're supposed to be elastic, right, So the idea being that they can, uh, they can change in shape and uh and maintain and organisms. Uh. Yeah, that's why you can can push on your skin and have it bounce back. Yeah, it's or it's why your your tendons will hold your muscles in place but not restrict them so that you can't actually flex them that sort of thing, or your

heart muscles as well. I mean, it's it's important stuff. But the problem is that as you age, uh, there are these proteins that can form cross links between a tissues lattice like structure, which then gives it rigidity. So something that was once elastic becomes more stiff and rigid as time goes on, and this obviously can inhibit it's your your various organs ability to do their jobs. So that's something else that has to be addressed as you age. And the overall process that he names in this one

is called glyco sends. So those are the seven principles of aging, the various symptoms of aging that he wants to try and eliminate through various means and uh, and some of them scientists I think agree, are more reasonable than others. Some of them, I think some scientists and doctors would say, are oversimplifications of the problem, or at least the solutions are so vague as to not be

practical in the foreseeable future. So I remember a while back he was challenging people to disprove this wasn't he Yeah, he had his Methuselah project. And also there was a the magazine Technology Review, which comes from Might heat Uh.

They got together and put up ten thousand dollars each the twenty dollars total as a challenge to anyone who could draw up a an explanation that would disprove the SINS approach, saying that is there something that's been overlooked, or is there a fundamental flaw, or is there something about this approach that is simply not likely or feasible.

And they received I think they received seven or eight responses, but only a few of them were considered, only a few of them actually met the requirements that were set out by the challenge, and ultimately the judges, who were impartial, came to the conclusion that no one had presented a a any finite yeah, anything that would actually say yeah,

this disproves. So no one won the prize. However, it's not exactly a slam dunk win for Degray either, because they also said that, uh, you haven't really defined this in a way that is very scientific, right. It's not

like a sign yet. It's not a scientific hypothesis that you can set out to clinically disproved, right, So I want to read a couple of little comments that we're actually not little, so a couple of significant comments that one of the judges said is Nathan Mervhold who who said this at issue is the conflict between the scientific process and the ambiguous status of ideas that have not

yet been subjected to that process. The scientific process requires evidence through independent experimentation or observation in order to accord credibility to a hypothesis. SINS is a collection of hypotheses that have mostly not been subjected to that process and thus cannot rise to the level of being scientifically verified. However, by the same token, the ideas of SINS have not

been conclusively disproved. SINS exists in a middle ground of yet to be tested ideas that some people may find intriguing, but which others are free to doubt. And he goes on quite a bit more says that that Sends as many unsupported claims and is certainly not scientifically proven. Uh. I personally would be surprised if Degray is correct in the majority of his claims. However, I don't think that the people who submitted the rebuttals have provided that Sends

is false. That would require more research. In some cases, SINS makes claims that run parallel to existing research while being more sensational. Future investigation into those areas will almost certainly illuminate the controversy. Except this was England, so it might have been controversy. But ut at any rate, uh,

it goes others people had similar things to say. Another person, Craig Venter, said, uh that in my view, the critics have not demonstrated that SINS is unworthy of discussion, but the propo oponents of sense have not made a compelling case for it. So, in other words, nobody came out looking great out of that experience. From a little bit that I've heard Aubrey de Gray talking, I've gotten the impression that he's very concerned with UM keeping possibilities open.

I get the impression that his main objective is to get people to think about things that they might otherwise not think about. I would agree with that. I think

that he has his concern well. He often says that he thinks, if if we really dedicate a lot of resources to looking at ways of defeating the symptoms of aging, then in the case of mice, because this is really why he's talking about right now, is just experimenting with mice and not on people yet, but that if we were to really constant I mean it's important thing, but that he would concentrate. If we really concentrate, we might be able to crack the the problem within ten years.

So if we don't really concentrate, if we take our time, it may be more like forty and if we're really not interested in it might take one hundred. Uh. Now, personally, I think a lot of his concerns are going to be taken care of just from other disciplines that are also working on similar problems, right, I mean, you have the whole field of oncology that's working on the cancer problem, and it may be that the solution is very similar to the one that degree proposes, or it may be

something totally different. But uh, I think that if you're looking as a unified discipline, yes, it's going to be one of those things that you know might be a tough sell just because it sounds a little outlandish when you first think about it, like I want to to stop to halt the process of aging or or the symptoms of aging, if you prefer. But I do think there are plenty of different disciplines out there that are working on these individual pieces and that's going to continue.

And absolutely, and there's there's already, I mean there's there's a bunch of examples from nature of animals that don't quite behave the way that that aging says that they should. Oh yeah, I mean well, i'd say one fact that is in de grace favor is that, um, that senescence is or that you know, normal rate, the kind of senescence that humans experience is not a guarantee across the

entire animal kingdom. Um, like you could. Uh. Well, for so for a while you may have seen this, there were these claims going around the internet that lobsters are immortal. Have you heard this? Yeah, I I remember hearing that phrase somewhere, and I never looked into it because I just got jealous. I also kept on imagining and they're just a lobster immortals battling it out until one of them's lives. Yeah, there can be only one lobster. That's

another highlander joke. I think I made one in the last podcast to several Uh no, well, it turns out this isn't exactly true. Um, so it's not. We don't have any evidence. As far as I can tell just from my research, we don't have any evidence that lobsters can live forever. Um, but we do have but we keep eating them. They're so delicious. That's the trouble. Every time we try to study them, the scientists end up getting some butter. They should just have made do it

because I'm allergic to lobsters. Oh wow, so you could get a grant. Yeah yeah, um, but no. So okay, here's what is interesting about lobsters. So um, they we we don't have any evidence that they would live forever if they weren't killed by you know, some fish eating

them or something like that. But we do have evidence that they have much slower sin essence than we see in lots of other creatures and um, and basically it's worth a lot more research into looking at the ways that lobsters age or don't age and and seeing what actually happens. So we don't know enough about that. One thing I was reading that it's apparently just kind of

difficult to track lobsters and dint move that fast. Um but uh and I mean i'd have to imagine that you interfere with their life processes when you remove them from the ocean and stuff like that. But also, um, but they do, like say, they continue to grow. That so a really old lobster the way we we grow until a certain age I don't know, you know, in the twenties or something like that, and then we start shrinking. Well, we might grow horizontally, but we we overall, we don't.

We don't continue to get stronger. I mean a lobster might, and and some other uh decapods that live in the water. Uh, they do the same thing as they get older. They just get bigger and bigger and more powerful, and they don't lose function the way we do when we age. Um. I saw one study that suggested a link. They said, so the the slow sinescence of lobsters might be UM linked to high telomeraise activity that you can detect all

throughout their body tissues at any age. And telomeraise UM essentially it's a it's a protein created by telomeres, which are those those end caps two DNA strands, right, that get a little shorter every time a cell divides, And so once that cap goes down to nothing, that's pretty much that's that's like the end for that cell, right right,

That's that's what triggers that cell death supposedly. Yeah, so they have a high telomerase activity all throughout the body UM and maybe that that prevents some of that that yeah effecture UM. But not just lobsters. Actually, there are some things that come closer to that that immortality claim, like, for example, the polyps called hydras. You heard about these tiny little things and apparently they can live as far as we know, they can seem to live forever for

all we can tell. Yeah, they just keep going. Uh. There's also the immortal jellyfish. I've heard about that one. To Autopsis Dorney, I'm glad that you said it, because I wasn't willing to to attempt to that one. UM. It seems to uh to reverse its life cycle back to the polyp stage and then grow again, and they think that it does this through um. During that rejuvenation, it undergoes cellular trans differentiation, which is what happens in

stem cells. Interesting. So so, yeah, that's exactly right. The the jellyfish, as far as we can tell, can do this indefinitely. We don't know of any point at which it has to stop. And yeah, and it's apparently kind of an issue. It can take over large segments of the ocean, and it can apparently grow in any ocean that it wants to. And it's immortal, so I mean, you know, it's running around with swords and just killing everything. I wonder if that what you just said has any

application to the idea of humans being able to live forever. Well, I mean, there's definitely been a lot of scientific inquiry into the matter, but it's bioethical. What I was referring to was the fact that you said that they can expand population wise if they're not dying off. Yeah, well that was kind of what our whole discussion was in

our last podcast too. Well, he had the whole section on that and de Gray for his his he pretty much doesn't acknowledge, or doesn't acknowledge is probably the wrong word. He doesn't focus on the questions of things like population or any of those other or political matters. He's looking specifically at an engineering problem. Yeah, I've I've read him make make comments that are kind of like, well, like, clearly people will just stop having kids and that'll be great,

And I'm like, well, I'm not sure. Okay, that's one. Okay, if you want to stick up in his defense for a second, it might be worth saying that, um, even if there could be negative implications to this, we at least want to have the option right now. His his point is that he says, look, why are you if you're sitting there saying that that young that children are at our disadvantage, or that that this is harming children

in some way by by telling people not to have kids. Uh. He turns that around and saying, well, why are you saying that old people need to die? That's that's kind of his the way he turns that around, like, that's agi you're saying that old people need to die so that we can make room for young people. And it's also certainly true that there are a lot of biological limits that if you go back to certain points in history, I mean, people would just have to accept as, yeah,

this is just what life is. You. You know, you die, most half of babies die before their five or something like that. Yeah, yeah, you know, just a couple of cent centuries ago, the human lifespan was only what like forty years. Yeah, but then that was because including infant mortal that if you if you live past the age of twenty one, there was a good chance you're going to see the right But but you had to live

to one first. The point I'm making is that just because something is basically the way things are, doesn't mean that we'll always see it that way. I mean, that's true. It could be in the future people would look back and be like, oh my god, what was wrong with these people? They just accepted that aging was inevitable. I mean, what a horrible way to live. And that's another thing

that he points out. And really, ultimately my view is that even if you were to disprove the sense approach, even if you were to even not maybe not disprove it, but at least say that it's unrealistic or it's too narrowly focused or or the solutions that have been proposed

are far more complicated than what we expect. And I would keep in mind, you know, his approach right now is looking at mice and that once, even if we do figure out how to make it work for mice, we may never figure out how to make it work for people. But let's say that, uh that all of that,

you know, you can just put that aside. The interesting thing to me is that if we do tackle this problem, even if we don't ultimately figure out how to completely eliminate the symptoms of aging, we will very likely learn other ways that can help us improve quality of life. It may not mean that you will be like a twenty five year old when you hit age seventy, but you might have, you know, a greater resistance to certain types of diseases that otherwise you might be vulnerable to.

So I think that that it's a very valuable line of inquiry, no matter what, what do we always say around here, Yeah, you know, it may not work, but still learn something along the way. Yeah, exactly. I mean that's I know, we we bring that point up and just about every podcast, but I really do believe that's true. I would much rather that people seriously look into this, because best case scenario, it works. The worst case scenario we learn stuff. Our worst case scenario is a cure

for cancer. That's that's still pretty good. Yeah yeah, now, now, truly, the worst case scenario is not looking into it at all and just accepting that what we've got is what we've got and that's it. But uh, I don't Fortunately, the human history is filled with people who refused to take that position, and I suspect that will continue. Uh. I mean, I I just know some people that's all yeah, one or two, and they tend to be no, no, These these are the people who are like, no, I'm

not accepting this. So anyway, I'm sure everyone else there knows someone like that. If you guys have suggestions for future topics that we should cover in Forward Thinking, I invite you to share the information with us, because otherwise we're just gonna have to keep on guessing until we finally cover how how telepathy is going to work in the future. Yeah, well that's probably you know, off of always I can't see it just yet. There are seven

steps to telepathy. Yeah, yeah, I'll tell you about them after the show. I think it's years off and an excellent and excellent guest there, Lauren, that's a number I'd print that all right. Anyway, The important thing is that I need you to send email or get in touch with us in some other way because I have not developed telepathy yet. So if you want to say as an email, that address is FW Thinking at Discovery dot

com or go to f W thinking dot com. We have links there to our social media, so you can get in touch with us on Facebook, on Twitter, on Google Plus. Let's know what you think, Let's know what you want to hear. Uh. You can also read up on our blogs. You can watch the videos. You can listen to other episodes of the podcast. There Everything you would ever want right there after thinking everything absolutely is right there after What you Thinking dot Com. I'm just

saying everything. Stop giving more examples, guys. That's we look forward to talking to you again, really say. For more on this topic and the future of technology, visit forward thinking dot com brought to you by Toyota. Let's Go Places