154: Is Telomere Length Shortening the Master Switch of Aging?

In this episode, Dr. Bill Andrews joins Dr. Buck Joffrey to discuss the critical role of telomeres and telomerase in aging and cellular health.

He explains how telomeres shorten with each cell division, leading to aging and cellular senescence.

Dr. Andrews emphasizes the importance of inducing telomerase to potentially reverse aging and shares insights from his research on telomerase inducers.

He also addresses the challenges in longevity research, the relationship between telomeres and the hallmarks of aging, and the potential of gene therapy.

The conversation concludes with a discussion on lifestyle factors that can influence aging and the future of aging research.

Learn more about Dr. Bill Andrews:

https://sierrasci.com/dr-bill-andrews/

Get your first bottle of Telo-Vital for 55% off with free shipping to the US, UK, Canada, Mexico, Australia, New Zealand, and over 20 European Countries:

https://longevityroadmap.thegoodinside.com/special-offer-telo-vital-lp

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Transcript

Disclaimer: This transcript was generated by AI and may not be 100% accurate. If you notice any errors or corrections, please email us at phil@longevityroadmap.com.

   In order for the cells in your bone marrow to infiltrate the blood to add cells with long TLOs, they have to divide. Okay? And so whenever a human cell divides, the telomeres get a little shorter.

Welcome everybody. This is Buck Joffrey with the Longevity Roadmap. Uh, today we have a very, really, really interesting conversation with Dr. Bill Andrews. He is, um, guy who, uh, actually, uh, was the guy who discovered the telomerase gene. Uh, telomeres are a, a major part of the, uh, biological aging process. The shortening of, of telomeres.

Basically telomeres are, I mean, he'll describe 'em, uh, another way, uh, the way I've always thought of, um, as they're sort of the. Now the ends of your shoelaces, they're the little plastic things that, that over time they wear out. And, um, the shorter they get, the bigger problems you have in terms of, you know, your, um, your cells dividing.

And, um, over time they get shorter and shorter. And then eventually if they get too short, your cells become senescent. Uh, there was a lot of, uh, talk of telomeres. Um. Early on in the longevity space before, I think a lot of these other discoveries, and I, I think this is a really interesting conversation because I think it, it refocuses the importance of telomere length and the role of telomerase, which is the gene that actually can, uh, restore the length of the telomeres.

This guy, Dr. Andrews, is obviously very smart. He is, um, you know, he is known as, again. Uh, discovering the human telomerase gene. He's a inventor of the year. I mean, all sorts of stuff. And he is convinced, he's convinced that, you know, the key to the aging process or probably the biggest key to the aging process and one that all of these other hallmarks of aging, for the most part kind of go downstream, is the shortening of telomere.

We're gonna get into that, and we're also gonna talk about, you know, some potential ways of, um, reversing, uh, telomere, shortening, uh, or at least slowing it down. Uh, anyway, for those of you who love longevity science. This is gonna be a really good one. Enjoy it. Uh, and we'll have this interview right after these messages.

Hey, longevity enthusiast. It's time to take it to the next level. I've been fine tuning my longevity regimen for years, and I look better and feel better than I did a decade ago. In fact, my blood work is even better than it was back then, and it's all because of my data-driven regimen. And it's inspired me to create a course and community just for you.

It's called the Longevity Roadmap, and I urge you to check it out. If you're tired of your belly fat, tired of being tired, or just wanna optimize yourself for the next 50 years, visit longevity roadmap.com. That's longevity roadmap.com. Welcome back to the show, everyone. Today my guest on Longevity Roadmap is Dr.

Bill Andrews. He's a molecular biologist and CEO of Sierra Sciences. Known worldwide for discovering the human telomerase gene. He was recognized as National Inventor of the Year, holds over 50 biotech patents, and has published extensively in the field of aging and cellular biology. But his pioneering work focuses on reversing age by restoring telomere length.

A key factor in cellular health and longevity. Welcome to the show, Dr. Andrews. All right, thank you for having me on. Okay, well, uh, yeah, this is an interesting topic. Um, you know, a lot of people, uh, you know, you're best known for discovering the, uh, human, uh, telomerase gene. For listeners who aren't scientists or were, you know, they just, maybe just, uh, physicians even who heard about it in medical school, but, you know, maybe just a little bit of a reminder.

On, uh, a little bit in terms of what telomeres are and, and, and why they matter so much when it comes to aging. Well, first of all, they're, they're at the tips of our chromosomes and, um, I like to compare them to ride tickets at an amusement park, they're, every time a human cell divides, it loses a ticket.

Okay? And then when, uh, the cells lose the last ticket, they can no longer divide. They go into a phase called, called senescence, and then die shortly afterwards. And it's actually the, you know, there's several clocks of, of aging, but it's the clock that makes the most sense in terms of we know how it functions, we know what causes it to shorten, uh, we know we will to lose ride tickets.

It's the same as telomere. Shortening telomeres are DNA sequences. Uh, our cells lose a little bit of that sequence every time a cell device, just like it's as if it was right tickets. But we know how it happens. We know why it happens. We know how it affects, uh, epigenetics, which is the turning on and off of genes and our chromosomes that make it so that our cells and our body look older, feel older, and behave older, older.

Uh, and, uh, so it's, um, it's, it's something that. I learned a long time ago is something we need to focus on first. Even though I do believe there's other causes of aging, uh, which I think of all as multiple sticks of dynamite that are burning inside of our cells, but the one with the shortest fuse in humans is the length of our telomeres.

And also we know now that the length of the telomere controls all the other clocks too. So like the DNA methylation clock, the IgG glycosylation clock, uh, which are, um, some of the more recent tools for measuring, uh, biological age. They appear to be very likely controlled by the telomeres, and if not, nobody has figured out what controls those ones.

So, okay. So they are correlated with agent, but they don't have any me understood mechanism as to why they correlate with agent. Telomere explains it better than anything. Where does, uh, telomerase come into this and, and you know how, uh, your discovery there? Yeah. Well, so every time our cells divide, it loses a ride ticket or our telomeres get shorter.

But if that was true in our reproductive cells, then our children, we'd be born with shorter telomeres than we have. Their children will be born with shorter telomeres than they have, so we knew back in the early 1990s. That our reproductive cells must have some way of not losing the ride tickets. Well, or, or when it loses a ride ticket, it's given a ride ticket back.

And so in my research at Geron Corporation, I led a team that ended up discovering this enzyme, human telomerase that is found only in our reproductive cells. No other cell of our body has it. And every time our reproductive cells divide. It does lose a little bit of telomere, but then telomerase adds it back.

So I think it like a tug of war. You've got shortening and then you've got lengthening two sides of a tug of war, and, uh, it's a tie. So it's back and forth, back and forth. But in all, every other cell of our body that telomerase isn't there. And it's because the gene that produces telomerase is shut off and therefore.

We only have a one-sided tug of war. We have just shortening. Every time a cell divides, it gets shorter and shorter. How does that telomerase activity vary over time? I guess as we, you know, when we're young, when we're children versus when we're, you know, middle age and older? Well, thous doesn't vary whatsoever.

It is just completely shut off is there's absolutely zero MOUs activity in all the cells of our body. From, from day one after, after we're born af. When we're conceived, even before we're conceived. Okay. The one machine appears to be shut off during the, even the per formation of the sperm and eggs that are fused and fertilized to to create the first single cell embryo.

So it's somewhere around the eighth cell stage of the embryo that at least one cell turns the telomerase gene back on. And then that cell becomes our primordial germ cell line, which is what produces our sperm and or ace. So, but it's, it's completely shut off. Correct me if I'm wrong, I mean, I'm not an expert on this, but the, there's sort of a non-linear relationship, um, where the telomere length doesn't necessarily shorten at a steady state, right?

I mean, it can lengthen or shorten in response environment, stress, lifestyle. Is, is that true? No lifestyle thing lengthens it. No therapies lengthen it. Um, uh, there's no diets lengthen it. Uh, the only way to lengthen, uh, telomeres is to induce the production of telomerase inside of all the cells of our body, not just our reproductive cells.

And none of the things that, uh, you hear about actually do it. Um, but you know, it's. Nobody's lying to anybody. I, I think a lot of people just don't understand telomere biology. Yeah. I mean, one, one study comes to mind with the, I'm, I'm sure you've, you're aware of this, the, there was the one with the Israeli studies in the hyperbaric or, uh, yeah, uh, there was Oxygen.

Big article about that in Scientific American. Um, okay, so here's the thing. And, and I, there's YouTube videos that people can watch and, and I can send you those YouTube videos where I explain what's going on here. Okay. So what they're measuring is before, and a, they're measuring telomere lengths before and after, and they're finding that telomeres are longer after, after hyperbaric oxygen.

Just for, just so people understand what we're talking about here, I actually don't wanna promote any products or anything like that. Sure, sure, sure. So, so, um, I, uh. You can say Sure, sure. There's this, basically this Israeli study that I'm referring to, and I don't have it in front of me, but broadly it's, it's, well, it's, it's pretty, I mean, it's often.

Referenced in this longevity space. Basically the idea is that over this, uh, period of time, this, uh, very, you know, rigid and lengthy hyperbaric oxygen, uh, schedule, uh, resulted in, in tel telomere lengthening. So that's what we're talking about. But, sorry to interrupt. Just wanted to give context. Yeah. But it is not actually telomere lengthening.

It's actually the telomeres are longer, but they didn't get lengthened. That's, you know, I understand telomere biology extremely well. I'm an inventor or co-inventor of every assay, or it's for measuring telomere length and measuring lumous activity. Uh, but what's happening here is that if you do anything to your body that causes, that is toxic, let's say, um, that can preferentially kill off the cells that have.

Short telomere and in inside of our blood we have cells with telomere of all different lengths, okay? Some cells have long telomere, some have short tel, so anything that's toxic is gonna kill off the cells that have short tel. And as a result, your average telomere length's gonna be longer. Okay? Just as if you had a company and you fired your dumbest employees.

The average IQ of the company goes up. Without anybody getting any smarter, and very few people understand that principle. Okay. And but the other thing is that if the product that, or therapy or whatever is, is immunogenic at all, inducing an immune response, uh, that's gonna drive cells that are in the bone marrow that have already long chalmers, even if you're 90 years old, you have cells in your bone marrow that have long kilometers, it's gonna cause those cells to start dividing and infiltrate the blood.

That again, is gonna cause the average length of your telomeres to be longer without any lengthening. Just as if you, your company hired a bunch of geniuses, the average IQ of your company increases without anybody getting smarter. Now, the only way to actually show that you actually had lengthening is to show induction that you are actually producing polymerase in the cells.

'cause as I said before, that's the only way to lengthen Telaris. And I'm not aware of any of these companies ever showing that kind of data. And I'm suspicious. And, and by the way, we, we test everything here and we, we haven't been able to demonstrate, uh, uh, polymerase activity any with the, any of the methods that are available.

But we think they probably did try to measure, 'cause that's an obvious thing to do. And, and the assays are easy if, if you, if you're lengthening TERs. Show that you're producing Telomers, and if you haven't, then why not? Okay. And that's what people should ask when they're, when somebody tells 'em they have a product that can lengthen their telomeres, they should ask, does your product induce telomere?

And if they say no, then their product does not lengthen telomeres. And the next question is, why not? You know, since it's easy. And, uh, but I would, I would not believe it. Not that they're lying, I'm just saying that they misunderstand it themselves. Your product isn't lengthening, but lengthening children.

But the big problem is that when you do kill off the cells with short telomeres or add new cells with long telomeres, that requires additional cell division in the body. And so even though the telomeres in your blood are longer, the average telomere length of your whole body is shorter. Okay? So it's actually accelerating aging.

So a lot of these. Products are accelerated aging the only, the only product. Explain that. A if you would just explain that part again, because in my mind, I mean, I'm, I'm following, like all of a sudden I, I totally understand your, your metaphor there. You're essentially knocking out, you know, these shorter TM or cells, and so the average of cells there becomes longer telomeres.

You're recruiting from bone marrow, you have cells there with longer telomeres. So explain to me how that accelerates aging. In order for the cells in your bone marrow to infiltrate the blood, to add cells with long telium, they have to divide. Okay? And so whenever a human cell divides, the telomeres get a little shorter.

So even though they're already longer than the telomere length in your blood, when they divide and produce a lot of cells that then infiltrate the blood, the those cells are have longer telomeres. Now the cells in your bone marrow are shorter as a result of that cell division. So the average of your whole body is actually shorter and anything you ever do that induces cell division in in your body is gonna cause thr shorten.

Got it. Got it. Let's talk a little bit about the, um. The, the, I guess the, the potential ways that you can attack this problem from a, you know, from, from the standpoint of what you're doing in your lab. If we know that, you know, telomerase is just not there. Af once, once conception basically what, what, what can we do to attack this problem?

There's, there you can do things to slow down the rate of accelerated kilo, more shortening. Okay, so. Before when you, about 10 minutes ago, you mentioned something that lifestyle and stuff like that can affect TEL or length. It can't lengthen it, but it can Sure. Accelerate the shortening. And that's like anything that's like smoking, obesity, psychological stress, oxidative stress, inflammation, all those things will accelerate tel or shortening.

Uh, and if we do the math on the rate of. Tel shorting without doing anything with, with having the perfect lifestyle and the perfect genetics, our lifespans are limited to 125 years, uh, as the only, uh, hard, uh, brick wall that anybody can run into in terms of, uh, extending their lifespan. You, you cannot exceed 125 years because of tel er shortening, but nobody ever lives to be 125 because we all accelerate our tel er shortening, uh, one way or another.

But in our research, what we are doing is we are trying to find anything that will cause ourselves to produce telomerase now, and let me say in a really short term, and there's YouTube videos of people want to hear more about this, but the reason why we shut off the gene in every cell of our body is because there's a benefit to our species.

Not the individuals. There's a benefit to our species to eliminate the longer lived people. Anybody who's lived long enough to raise their young, they do not contribute to the success of the species anymore because their best way of contributing to the success of the species is to shuffle their genes through sexual reproduction, to create offspring that have new diversity variations.

That didn't exist before. And the more diversity that exists in a species, the more likely a species will survive rapidly changing environments, or at least some members of the species will survive rapidly changing environments. So any species that evolved in aging process, uh, and will, any species that had sexual reproduction and then evolved in an aging process, was more likely to survive rapidly changing environments than a species that didn't.

That's, people understood what I just said, that's great. But if they didn't, their YouTube videos where I, I spent an hour at least on explaining that specifically. Sure, sure. When we talk about, I mean, the one thing I think about is, okay, well, I mean, I presume this issue with telomerase is across species.

Right? So even in Wales and, no, actually not. Uh, okay. It's, um, aging is a relatively recent evolutionary bent. And so many species have evolved different ways of eliminating the longer lived, okay? Humans, dogs, cats, horses, sheep, pig, and deer are the only animals that have ever been shown to eliminate the longer lived by er, shortening, uh, rodents, mice, rabbits, uh, things like that.

They do not age by tel shortening. They use other mechanisms most likely. Oxidative stress and mitochondria dysfunction to eliminate the longer lip. But, but some animals, like you'd mentioned, whales, humpback whales, lobsters, uh, tortoises, clams, uh, they don't have any aging process, any detectable aging process at all.

Um, and, uh, at least nobody has found any yet. Uh, people didn't start looking until time of Darwin, and the only way to know is to, is to have 'em be there when they're born. Then watch 'em as they age, and almost none of 'em have the equivalent of rings on a tree that you can count to figure out how old they are.

So you don't know how old an organism is unless you can, you're there when it's born and you wash it entire life. And then 200 years later, they're still, animals are showing no signs of aging. Now the exception is clamps. Clams do have stripes on their shelves. They get a new stripe every year. And so a lot of people have started counting the number of stripes on the clamps.

Clams over 500 years old. Okay? People didn't know that lived that long. And these clams they have, and all these animals I just mentioned, lobsters were the first one that identified. But they all have telomers produced in all the cells of their body. Unlike humans, they don't have any tel shortening at all, and they never get cancer or any kind of diseases are extremely rare.

They have no agent, no detectable aging whatsoever. So that you're talking about not just clams here, but for example, that whale example I gave. So you do have telomerase. Yeah. You, so you do have, you do have telomerase activity after, uh, while the organism's living in, in, in those humpback whales. Yes.

Interesting. You polymerase producing every cell of their body. And, and it's interesting because, yeah, so, so I guess that idea then. If you're thinking about approaching this for humans is, as you said, trying to figure out if there's anything that can trigger telomerase activity. Is there anything promising right now?

Yes, there is. Actually, we, we've been doing this for 20 years and we've had a lot of success. We haven't come up with anything potent enough to actually produce enough polymerase to reverse agent. We are producing, we have things that will, will stimulate the production of, of, uh, significant amount of kilometers.

Just not enough to like win that tug of war that I was talking about or even tie thatt of war. Now see, the problem is that as I was mentioning before, there was an evolutionary advantage to eliminate in the longer lived after we raised our young. We do that by, there's a protein. It binds to what I call the dimmer switch.

Every gene has a dimmer switch and they're called promoters that turn genes on and off. And this protein binds to the dimmer switch for the TH gene and shuts it off. So we are looking for nutraceuticals, plant extracts, fractions, fractions of plant extracts. We, we've tested over 20,000 different, or close to 20,000 different plant extracts now, and we're looking for anything that will actually dislodge.

Repressor protein that's shutting that dimmer switch off to actually turn that dimmer switch back on. And so we have like high throughput robots here, uh, but that do a assay that's called the high throughput robotic mRNA, R-T-P-C-R assay. And, uh, it's, uh, a way of detecting, uh, production of telomerase in cells in a high throughput way.

So these robots are. They don't look human. They're, they're actually in the room, right? Be directly behind me right now. They take up a whole room, but these things can test up to like 4,000 different plant extracts a day. Our part is actually preparing that many plant extracts a day. So we have found, uh, close to 40, no, actually close to 60 different fractions of plant extracts that do induce telomerase and, um.

In humans. In humans? Yes. In humans. Okay. We, we've actually only tested it in humans so far, but I'm hoping it works on d dogs, cats, and horses too. We, um, licensed the top five to a company called Touchstone Essentials that created a product called Telo Vital. Um, I'm not, I'm not into marketing, but I wanna explain that the science there is, that there is in that product, there are our top five, uh, telomerase, inducers.

Mixed together. And, uh, so by taking that product, you are inducing the production of telomerase, but not enough to win the tug of war. But it's still anything that slows down the rate of tel shorting slows down the rate of aging. And so, even though I said that we have this theoretical maximum of 125 years, if we have perfect lifestyle, lead a perfect lifestyle, and have perfect genetics, this product has the chance.

Only product that can, that has the, the chance of extending this beyond that 125 and delaying, not just extending the lifespan and healthspan, uh, because the, we know from, uh, studies of gene expression and stuff in the role of things called enhancer sequences and stuff like that, the telomeres actually play a role in expressing all the genes that are involved in aging.

You know, wrinkled skin, hair color, things like that. All these things are. Can be slowed down by, uh, doing anything that induces polymerase enough to lengthen ERs, uh, a bit, but not enough, as I said, to win the tug of war. Let me, before you go to anything else, let me say qualify that we do know, and this is well published by other scientists that we do know, that when telomeres get critically short, they become a lot easier to blanken, so the tug of war can be won.

Telomeres by the, by the lengthen, when the telomeres are really short. So we, we suspect that, that people that do have critically short telomeres in either their, their whole body or some tissues of their body, they are gonna see some age reversal because of the lengthening of the critically short telomeres.

And I'm, I'm gonna be honest with you, I, and meeting with a lot of people that have been taking, uh, products that lengthen, uh, telomeres. The people that are showing the best results are the ones that are in their nineties and stuff like that, which I'm just blown away with. How much change I see them week after and see in them week after week, after week.

Uh, so I, I believe that we are lengthening their shorter steel. Um, what, what kind of, you know, I'm sure you're probably referencing some small clinical studies. Can, can you talk about those since these are plant extracts? Uh. And all the ingredients are things that people already eat anyway, that were just, they're fractions.

So they, we had to, uh, eliminate some of the molecules in the plants because there's also things that will inhibit telomerase activity. So you could be, so if you were to take the whole plant, you might find that maybe you are inducing an expression of telomerase. But something else in that same plan is inhibiting the activity of telomers.

So we've had to do fractions. Like fractionate separate molecules in a plant by size or charge or something like that to, to separate inhibitors from the activators. And, uh, so those are in there now. It, it seems like the, this is kind of be because of the nature of, of omes in, or telomere specifically in, in, in, uh, different species.

It seems like a very challenging. Area to do longevity research. I mean, I'm just, you know, just thinking about like, you know, the interventions testing program, for example, as I'm sure you know, I'm sure you're aware, I, I, I can't remember if you said that rats have this issue with. Telomerase or not, but rats.

Rats have telomerase produced in all their cells. They have no tel or shortening. Yeah. So I mean, in that regard, I mean, you're never gonna see any potential benefits in animals. And can you talk a little bit about those challenges in this space? Well, first of all, yeah, it's really challenging. But yeah, my mission isn't to create a product that's gonna make me a lot of money.

My mission is to cure aging. My own aging, especially. Yeah, I, I get that. But I guess I'm just trying to figure out how do you, how do you measure it? I mean, so I wouldn't, I would never use mice or rats or even, uh, uh, what, what are, there's, there's another animal that's often used a rodent that's used for studies.

Rabbits either, but that's not the one I'm thinking of. Naked Mole rats is the other one I was thinking of. Um, but uh, if we were gonna do animal studies, we would, we would use pygmy marmosets. Okay. Uh, which are primates. Nonhuman primates very close to humans, and at least they've been shown to age the same way humans do.

Uh, and they're the size of mice, so, so it would make it easier to do clinical studies. But I, our preclinical studies in this case, which are animal studies, my company, my company, I, I, I run the company. I don't wanna spend a lot of time doing animal studies on intermediate products. Our goal is to find something that's gonna actually reverse aging.

When we find something that can reverse aging, at least in human cells in a Petri dish, then I want to spend all, because it's a lot of money and a lot of time to do the animal studies, and we are, we're discovering things new, all at the same. So frequently that before any study gets done, we're already gonna have a better ingredient.

So, so I'm waiting for something when we find something that's potent enough to win that tug of war. And then we want to do, uh, preclinical studies with pygmy marmosets. Uh, and then, then treat humans. And if it turns out that the product that we discover is a plant extract because of the FDA's ruling on plant extracts, having, being generally regarded as safe, we don't need to do the animal studies.

But because of the fact that I'm more interested in curing my own aging than anything else, I, I do want to do these animal studies and get as much knowledge about what, what's going on as possible. In the, uh, the big picture of how we think of, or I guess the paradigm that a lot of scientists use, the hallmarks of aging, like mitochondrial dysfunction, cellular senescence.

Obviously senescence can be downstream, epigenetic drift. Do you think that telomere shortening is upstream of all of these? Yes, absolutely. I think telomere shortening controls all the hallmarks of aging. Um, because even with all these hallmarks of aging, nobody's explained. The mechanism that these things happen, except for telomeres, telomere shorting is the only thing that has a well-defined mechanism to explain everything about aging.

Um, the, uh, you know, I'm trying to think if there's any, any particular hallmark of aging that I wanted to address specifically, but it's pretty much, maybe epigenetic drift is Well, ev curious. Yeah. Epigenetics is completely controlled by telomeres. I mean, there's other things that control epigenetics too, but.

The genes that are specifically involved in the aging process, those are very likely controlled by the length of telomere. Okay, so let me quickly define what an enhancer sequence is. Enhancers are well-known things in our DNA molecules that they can be like 10,000, a hundred thousand bases away from a dimmer switch.

A promoter and the DNA can fold over and bring these enhancers in contact with that dimmer switch and turn it on and off. Telomeres have all the hallmarks of enhancer es, and so they can fold over and affect the dimmer switch of genes on your chromosomes. But the difference between telomeres and regular enhancers is that telomere shorten.

And so when they shorten, they can't reach as far, and therefore we see changes in the gene expression with age, well with telomere shortness. So the shorter the telomere gets, the more changes you see. That are, uh, consistent with becoming older or longer lived. Um, and you know, lots of studies have been done now where we can show that re lengthening.

The telomere actually reverses these epigenetics in every way imaginable. Um, we've shown this in human cells, grown in Petri dishes. We've shown this in human skin, grown on the back of mice. Uh, and we have. Shown this shown. And, and a lot of this is done in other labs 'cause my company does not work with mice at all.

But we've provided the technology to other labs to do this. Next one is people have engineered mice to make them. So they do age by tel shortening. Uh, and these mice are incredibly because they, they have all the same human related aging, uh, uh, characteristics. When the kilometers are lengthened in these mice, age reversal occurs in every way imaginable, including this is a big surprise memory coming back.

So mice that had forgotten how to go through a maze and have symptoms similar to Alzheimer's or other forms of dementia. When the tumors got lengthened, their memories came back. And now when I go, when I speak at conferences, all in medical conferences all over the world and on all, all subjects, not just aging, but.

When I'm at a conference on something like Alzheimer's, I hear people now saying that Alzheimer's isn't necessarily the loss of memory, it's loss of access to the memory, and lengthening telomeres is restoring that access. So the memory is still there. We, I actually have a clinical study in clinical trials.gov ready to start testing.

Um. To see if, if we can bring the memories back in Alzheimer's patients and actually save them, save their lives. Uh, the unfortunate thing is that we are using the only thing that really does lengthen telomere, and that's a technique we've been using for 30 years to, um, study telomere and telomeres.

That's gene therapy. So gene therapy is something that we wanna do, but it's not the kind of thing anybody wants to be doing yet because it's still in clinical studies. Super, super expensive. At least it can provide us with proof of concept by seeing if we can save some of these people that have Alzheimer's.

So, um, you know, I know we, we were talking earlier about nutraceuticals, um, but could you talk a little bit about the idea of gene therapy and like what, in that situation, uh, I mean, would you be using, you know, various CRISPR technologies or whatever and delivering telomerase or how would that work? Well, CRISPR only edits genes.

Okay. And, uh, uh, there, there's also other methods for editing genes such as zinc fingers and talons that existed even before crispr. But, um, what we wanna do is we wanna deliver, and we, we do crispr and talons and zinc fingers, but what we think is the most likely to work is delivering a new gene to the cells that has that dimmer switch.

Permanently on the full strength on position. Okay. So, so we're delivering a new gene, but you know, gene therapy is risky. It's, it's doing clinical studies. It's great for animal studies in our clinical studies. We are only gonna be treating people that have like less than a year to live because of like Alzheimer's or something like that.

And we're hoping that, that we save them and the side effect will be seeing that they get younger in every way imaginable. Sure, sure. Um, you know, in, in terms of just, just thinking about some of the, the dangers of gene therapy, I guess one of the, I I mean, there's critics who talk about, you know, when you upregulate the potential of upregulating, telomerase, ac, you know, activity, or, you know, just creating telomerase activity, I guess is the potential link to cancer.

What do you, what do you say to that? Well, I was National Inventor of the year in 1997 for my cancer research. I do understand cancer a lot, and I've invented like at least five different treatments, therapies, drugs that are been through clinical studies and are now available for use. Uh, and some of those are actually dealing with inhibiting telomerase.

But here's the thing is that there's a. A rumor going around, and it's only hearsay and rumor. There's absolutely no data whatsoever saying that telomerase can increase the risk of cancer. But there's an incredible amount of data showing that it decreases the risk of cancer and it's, it's actually short telomeres that cause mutation rates to skyrocket that cause cancer.

'cause all cancers come from mutations and then it's the short telomeres that actually. Allow cancers to sometimes survive the treatment and then come back. Okay? So if you're being treated with a, a drug to kill the cancer, you can see the cancer disappear. But if the tel are short, the mutation rates are gonna skyrocket still, and it's gonna, the cancer's gonna mutate to a form that can come back and be resistant to the treatment.

Uh, and so, so one of the like examples is. Drug called Ry, R-Y-T-E-L-O, that just got approved by, uh, uh, in clinical studies just a few months ago. Uh, I'm, uh, the inventor of that and I argued all the time that that's, you know, gonna give short term survival, that the cancers are always gonna come back, and that's why it took so long to get that drug approved because that turned out to be right.

So, but, uh, I'm very interested in coming up with ways of. Treating cancer by, uh, poisoning cells that are producing telomerase. Um, while you're not taking a telomerase inducer that is, uh, but bottom line is telomerase decreases the risk of cancer, not increases it, it actually boosts the immune system. And the immune system is our best defense against cancer, boost immune system by lengthening kilometers in our immune cells.

The way that ERs gets produced is by cancer. So it still has to become cancer first, and then because of all the cell division, the telomere get critically short, and then the mutations induce the production of ERs. Okay? So cancers are, they wanna live longer just like we do. Okay? But if you can produce erris before the cell becomes cancer, it actually decreases the chance that it'll ever become cancer.

Uh, and so there's. There's actually another video, uh, where, 'cause this is, people used to, a lot of people used to be saying that TE causes cancer, but you don't find anybody saying that anymore. Uh, in 2017, I gave a presentation in Tokyo. I mean, it was a really big presentation. Only doctors were invited to be in the audience, but there was like 500 doctors.

When I got off the plane, I saw my picture on billboards and stuff like that. It was a really big thing. But there was, on the news, uh, somebody claiming that, you know, telomerase causes cancer. So I had, I actually added something like 45 minutes to my presentation just to review all the data and all the facts about why some people believe telomere causes cancer when it doesn't.

And then. All the studies that have shown that it doesn't cause cancer. I went through all that and, uh, um, now I never ever hear that that was such a successful presentation and it's available. I, that was such a successful presentation. I've never heard anybody say that tolerance causes cancer again, unless there's somebody who's so far removed from the field that they just remember the old rumors that existed, uh, eight, nine years ago.

How optimistic are you about, you know, with the things that you're doing, that we can, you know, with gene therapies, advancements in AI and, and all this, that, that we can come to some kind of a solution or find some sort of method, um, you know, to to, to solve this problem of aging? Well, lemme say first. No matter what else we do to cure aging, um, aging will never be cured unless we also solve the telomere shortening problem.

That's why I'm focused on that, even though I don't believe it's the only cause of aging. Uh, but, so I'm about 80% certain. Let's say you're asking how optimistic. I've 80% certain that when we have something that can lengthen telomeres, we will show. A reversal of aging and life extension and health span extension in humans.

Now, when that happens, we might not find it is perfect. We might find that there's other things going on, but that's why I'm also working on mitochondria dysfunction, oxidative stress, things like that. Because if there's, if, if telomeres, lengthening, telomeres don't work to cure aging all by themselves. We have to combine it with something else.

I want to make certain that we're ready for that. And I would say mitochondria dysfunction is the most likely thing. And uh, and, and it turns out that, you know, you can, you can do things like, there's mitochondria turnover when, when the cells can dispose of dysfunctional mitochondria, uh, by uh, uh, what's called mit.

Some people pronounce it mitophagy, but that's, I've been. Saying auto autophagy instead of autophagy for 40 years. So I, I can't, I'm not switching, but the words are different. But in order for the cells to produce more mitochondria, telomere have to be long because 90% of the genes that 90% of the proteins of the mitochondria are encoded by the nuclear chromosome.

And we have shown, or others have shown that key proteins such as PGC one alpha. And two, they are regulated by tel length. So tel, so the tel length reaches over, turns that dimmer switch on and off, uh, our nuclear chromosomes. And so when telomere get really short, we can't produce PGC one alpha anymore.

And so we can't make new mitochondria and tel are short. So whatever we do to dispose of dysfunctional mitochondria, that's not gonna be a benefit unless we can also produce. New mitochondria called mitochondria biogenesis. When those mitochondria, the new mitochondria come in, are those typically with, you know, with normal, not shortened, uh, mitochondrial DNA or, well, mitochondria, DNA is circular, so it doesn't have ends, so, but uh, yeah, but they're, they're just as healthy as any mitochondria ever.

Uh, unless, unless you have mutations. Even if you had a mutation to the mitochondria, that would be a, a reason to actually dispose of that mitochondria. But, uh, yeah, so it's, yeah, it most likely is the answer. Got it. Um, tell us about the, where, where people can find those videos that you were talking about.

You know, I'm just a medical researcher. I, my company is 10,500 square feet of lab space. I'm in the only office right now that exists here. Uh, so we don't really. Work on keeping our website up to date, but I can send you a list of like all the key videos that include what aging is, why we age, how we age, how not to age, and, and like all the stuff about cancer.

And we're also, since we're not a academic lab, uh, we're not controlled by the publisher parish rule. So a lot of the data we have. Is not published, but we presented it. It is all public. We present it publicly and stuff like that, and it mostly by the videos. So the videos are the best place, in my opinion, to really learn what the, what, why, how, and how not of aging there is.

Got it. Uh, there's a product called Telo Vital. Is that, can you, can you tell us a little bit about that? Well, that's the product that Touchstone Essentials is now marketing that contains, uh, our top five. Uh, telomerase, inducers. When we add each of these to cells, uh, human cells, it causes those cells to produce telomerase.

And so, in my opinion, there is nothing on the planet that's better for somebody to be doing to slow down their aging. Uh, and, uh, there's other things they could be doing in addition, such as, uh. Uh, you know, antioxidants, anti-inflammatories to decrease accelerated tel or shorten. And then there's things that they can do like taking nicotinamide, riboside, uh, or, um, MIT pu uli a, um, things that really benefit their mitochondria and energy production.

Uh, because until we get something potent enough to actually win the tug of war. You're still gonna benefit from the other things that cause aging and mitochondrial dysfunction is the key. And oxidative stress, which is very associated with mitochondrial dysfunction. And then anti-inflammatories.

Anti-inflammatories are really important, but there's also lifestyle. Whatever I I, we wanna switch to that we can. Okay. So there's a lot of things that people can do to slow down their aging. They just can't slow it enough to, uh. Overcome this theoretical maximum of 125 years. Um, and unless you take something like Telo Vital, uh, and, uh, uh, but those include like, let's say one of my favorites is exercise, endurance exercise, or there's running kayaking, bicycling, whatever, skiing, um, endurance exercise.

It's kind of like a weird thing because it's got a like a Goldilocks effect. There's such a thing as too much and too little, and in the middle there's a way of actually decreasing inflammation a lot. Okay? Now when I say too much, I don't mean how many hours a day you exercise. I'm talking about how hard you exercise, how hard you push it.

So I always say consistent endurance exercise is very important. You, so you should do it every day, but quit when it quits being fun. When it quits being fun, stop, save it for another day because if you keep pushing it, that's gonna cause inflammation and it's gonna cause accelerated aging. So, you know, the examples I use, uh, there are a lot of really great runners that, you know, win marathons and things like that, that typically run every.

Two weeks. They, they don't train at all hardly. They just have good genetics and so they, they don't need to train as hard as some people, but they run, they, they run every two weeks and then they do well in the marathons. They'll oftentimes cross the finish line on their hands and knees throwing up, but even worse, they'll be stiff as a board for two weeks.

Because of all the inflammation, the body thinks, oh my God, it's being attacked by some virus or something like that. And so it sends inflammatory cells throughout the bodies that accumulate, especially in your joints. And so you're stiff. But if you're somebody who does endurance exercise every day, always keeps it fun.

Even during races, if the race quits being fun, quit or slow down, you know, if you don't, because you're gonna start inducing a lot of inflammation. And, uh, uh, accelerate your aging. So that's number one. Exercise, I think is the key thing. And you know, like I I, I used to hold the world record for the most a hundred mile races run in a year.

I'm an ultra marathon runner, and I, I've, I've always checking my c reactor protein in other inflammatory markers, uh, before, during, and after some races. And, and I, because of the attitude that I took, just keeping it fun. I never had inflammatory reactions and I could run a hundred miles and the next day go out and run 50 miles 'cause I wasn't stiff.

Okay. So, um, the other things that you can do are yoga and meditation. I've been the keynote speaker at several yoga meditation conferences showing data, showing the people that meditate because yoga is really just a form of meditation. People that meditate actually have longer tels than people that don't because they decrease the psychological stress, which is causes oxidative of stress and inflammation.

Uh, so yoga, meditation is really important. Um, uh, losing weight, don't smoke, uh, drinking, uh, you know, drinking especially kills liver cells. And, uh, that's okay when you're young. Because you have other liver cells that can divide to replace the killed cells. But now since you're killing liver cells at a faster rate than normal, your other cells are dividing faster than normal and therefore telomere is going telomere.

Shortening is occurring faster than normal, and so you run outta cells to divide to replace the dead cells by the time you're in your forties or fifties, and you start experiencing liver cirrhosis, which can kill you. Liver sclerosis is really just the accumulation of dead cells because nothing's kicking those dead cells out of the way anymore.

Um, 'cause the tels is too short to do it. Uh, same with genetic, uh, variations such as osteo dystrophy. Uh, the dystrophin gene actually causes muscle cells to be to die sooner, and therefore other muscle cells divide to replace them. And that's why people don't. Experience the symptoms of muscular dystrophy when they're young.

This is when they get their forties, fifties, they suddenly start experiencing the symptoms of muscular dystrophy. And there there's these, along with all, a lot of other things are ways of eliminating the longer lived. So it's beneficial to our species to not evolve away, to not age, not have muscular dystrophy, not to have other things that cancers heart disease.

Uh, and uh, so because. Those typically, all those diseases occur and the longer lived after you've raised your young. And so it's a benefit to the species survival in rapidly changing environments to eliminate you, which we're smarter than evolution now. So I, I have no intention of letting evolution control my life and l spend.

Uh, just, just outta curiosity, when you started taking that TLO vital, did you notice anything? I mean, I know it's, it's at the cellular level, but, you know, just cur uh, pure curiosity, if you've noticed any, uh, changes. Yeah, no, I, I, I'm not a big fan of anecdotal data, but there is a lot of anecdote I like. I wish we had studies going on where we were measuring a lot of different things, but because these are plant extracts.

Because I'm more interested in spending my time finding even better, more potent planet extracts and trying to characterize the ones that exist. Now, we, we aren't doing those studies, but the FDA has already said they're generally regarded as safe so they can be marketed. But, um, I have seen my vision get better.

I have seen my endurance get better. Like, every week I meet with people that are taking the products to pr, you know, answer questions for them and stuff. And I am getting a lot of feedback, especially from like a 94-year-old and a 101 year old that's on the products. I just can't believe they don't have to say anything.

I just see the differences, uh, when I'm talking to 'em on these Zoom calls that I do. And that's because they must have critically short telomeres throughout their body. Critically short telomere are getting lengthened. Even though the product's not en doesn't produce enough telomers to lengthen all the telomere, it is lengthened the shortest ones.

Um, now I have heard people and seen it. I've seen people, some people, if their hair's coming back, their hair colors coming back, that can only be true if the reason they lost their hair or their hair color changed because of er shortening. And so there's a lot of other reasons why that could happen. So.

People aren't gonna see it if they're, they lost their hair or their hair color, lost their hair color because of something besides tel. Um, I'm trying to think of other things in, well, endurance, I think I mentioned that I, I've seen my endurance get better. Um, but, uh, can, it's anecdotal and I would love to do a study where I, it's really hard to do and I, the study would probably be better with pygmy marmosets because of the fact that it's hard to get humans.

To be completely controlled. You need to have identical twins where the twins were raised separately in different environments and they were very consistent in order to really do the study properly, that just doesn't exist. Well, thank you so much for being on the show today. And again, this product is Telo vital and, uh, we, we'll put, uh, put a link in the show notes to that.

Uh, but I do appreciate all your time and, uh, all this, uh, really, uh, great information for us. Okay? And I'll send you the videos in a few minutes. Fantastic. Thank you so much. Thank you. Thanks for listening. A quick reminder that while I am in fact a surgeon, nothing I say should be construed as medical advice.

Now, make sure to include your physician in any medical decisions you make, and also, if you're enjoying the show, please make sure to show your support with the like, share, or subscribe.