LIFTS Episode 105 - Why Humans Age: Telomeres, Longevity, and the Limits of Lifespan with Dr. Bill Andrews

4 Jan 2026 · 1 h 4 min · 31 chapters

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In short

Dr. Bill Andrews argues aging is driven by telomere shortening (the “hard stop” to lifespan) that progressively limits cell division (Hayflick limit). He claims inflammation/oxidative stress accelerate wear-and-tear, which increases telomere loss until reserve cells (stem/progenitor) can’t replace damaged frontline cells. He addresses telomere vs cancer, telomerase, and skepticism toward products claiming telomere lengthening.

Guest background

Dr. Bill Andrews is a molecular geneticist/inventor and key scientist behind discovery of human telomerase. Founder/CEO of Sierra Sciences; holds 50+ patents; led telomerase discovery at Geron Corporation; has cancer research credentials and immunology leadership (Burlex Biosciences). Ultra-marathon runner with 100+ ultra races.

Key claims

Only telomerase expression can truly lengthen telomeres; ask whether a product induces telomerase. Many “telomere lengthening” claims are blood-cell population shifts, not true lengthening. Long telomeres are said to reduce cancer risk by lowering mutation rates; cancer cells become immortal via telomerase or ALT.

Notable examples

Rytelo (telomerase inhibitor) approved by FDA; ALT pathway after telomerase inhibition; hyperbaric/red-light claims criticized; “ride tickets” analogy for telomere attrition.

Written by AI. May contain mistakes. Listen to the episode to check what was said.

Chapters

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The Quest to Cure Aging Begins

0:00 to 0:34

Dr. Bill Andrews shares his lifelong ambition to cure aging inspired by his father.

“I decided because of my father's suggestion when I was 10 years old that I was going to cure aging.”

Understanding Telomeres and Aging

0:34 to 1:44

The hosts discuss the impact of genetics and lifestyle on telomere shortening and aging.

“Welcome to this week's episode of LIFTs.”

Historical Context of Human Lifespan

2:45 to 3:40

The hosts provide historical life expectancy data and discuss factors affecting longevity.

“And today, global life expectancy sits around 73 years, with many developed nations reaching into the late 70s and low 80s.”

Introducing Dr. Bill Andrews

3:40 to 4:53

The hosts introduce Dr. Bill Andrews and his significant contributions to aging research.

“If we've already doubled our average lifespan once, are we about to do it again, this time by intervening in biology itself?”

Pursuing the Impossible

4:53 to 6:14

Dr. Andrews shares his journey and philosophy regarding aging and scientific breakthroughs.

“and help uncover the mechanisms that tells ourselves when to stop dividing.”

Theories and Facts About Aging

6:14 to 7:20

Dr. Andrews discusses his views on existing theories of aging and his focus on telomeres.

“the things you said during the introduction.”

Aging and Telomere Shortening Explained

7:20 to 8:20

A detailed explanation of telomeres and their role in cellular aging and lifespan limits.

“And, you know, even in graduate school, I challenged all the theorists on theories of aging.”

Insights on Animal Studies and Aging

8:20 to 9:38

A discussion on the relevance of telomeres in different species and the implications for human aging.

“But after everything I've looked at, I've realized that the one and most important thing that we have to do to solve the aging process is find a way to prevent telomeres from shortening.”

Dr. Andrews' Perspective on Aging Mechanisms

9:38 to 14:00

Dr. Andrews shares his unique viewpoint on the causes of aging and challenges conventional wisdom.

“They're the very tips of our chromosomes.”

Telomere Shortening in Animals

14:00 to 15:00

Explore the uniqueness of telomere shortening in select animal species.

“Mice, you know, it's still debatable on what causes aging on mice, and I don't really care what causes aging in mice.”
Show all 31 chapters

The Mechanisms of Aging

15:00 to 17:00

Discuss various mechanisms causing aging, focusing on telomeres and oxidative stress.

“And so what I try to do is I try to look at the fact that there's multiple types of aging that are going on in all of us.”

Cancer and Telomeres Relationship

17:00 to 18:20

Understanding how telomeres influence cancer risk and cell immortality.

“I was National Inventor of the Year for my cancer research in the United States.”

Gene Expression and Telomeres

18:20 to 21:40

Learn about the role of telomeres in regulating gene expression and aging.

“because cancer cells do produce telomerase to become immortal.”

The Hayflick Limit Explained

21:40 to 24:10

Delve into the Hayflick Limit and its implications for human aging.

“that actually confirmed that telomeres are enhancer sequences.”

Inflammation's Role in Aging

24:10 to 27:40

Investigate how inflammation ties back to the aging process and cellular division.

“But we had a pretty powerful group of people.”

Understanding Aging and Inflammation

28:00 to 29:14

Explores the relationship between inflammation and aging, including cellular repair mechanisms.

“There's no question about inflammation is the number one cause of aging.”

The Role of Telomeres in Aging

29:14 to 31:41

Discusses telomere shortening and its implications for cellular regeneration and aging.

“about what aging is and why we age and how we age.”

The Connection Between Diseases and Aging

31:41 to 33:44

Analyzes how various diseases are linked to telomere length and the aging process.

“Believe me, alcoholism is one of those diseases that I really want to cure.”

Caloric Restriction and Longevity

33:44 to 36:14

Explores the impact of caloric restriction and GLP-1s on lifespan and health.

“Well, you know, GLP-1 is just one of the many things that we can do to improve our health.”

Exercise, Inflammation, and Longevity

36:14 to 41:22

Examines how different exercise regimens affect wear and tear, telomere health, and overall longevity.

“and just trying to understand everything I can because I want to live forever.”

Recovery Techniques in Fitness

41:22 to 42:00

Discusses various recovery methods and their role in enhancing longevity and fitness.

“Look, we should definitely go running, Dr.”

Exploring Longevity and Recovery Trends

42:00 to 43:36

Discuss the evolving landscape of recovery methods in fitness and wellness.

“But my running buddies used to be like Ann Trayson and Dean Karnasas and things like that.”

Understanding Telomeres and Misconceptions

43:36 to 45:40

Learn about telomeres and common misconceptions in the anti-aging industry.

“From where you sit inside the mechanisms, is this really accelerating progress or is it oversimplifying extremely complex systems?”

The Role of Telomerase in Aging

45:40 to 47:55

Discover the importance of the telomerase enzyme in the aging process.

“the average IQ of your company increases without anybody getting any smarter.”

Funding Research and Product Development

49:18 to 52:12

Understand how research funding works and the relationship with products.

“that actually can slow down the aging process, and that's a good thing.”

Evaluating Scientific Research Critically

52:12 to 54:40

Learn about the importance of critical analysis in scientific studies.

“Up One, because I take things up a notch in terms of evaluating scientifically peer-reviewed studies.”

Quickfire Questions on Longevity Therapies

54:40 to 56:00

Get quick insights on various therapies and their effectiveness for longevity.

“People are publishing just so they can add more publications to their list because that's how they get grants.”

Understanding Health Metrics

56:00 to 57:00

Learn about health indicators like HRV and their impact on longevity.

“But they all, if I say all, then I blame the product, but a lot of them will make claims that aren't actually accurate.”

Pillars of Longevity

57:00 to 59:40

Discover key lifestyle changes to support longer life and health.

“But what would you say are some real basics in terms of whether that's exercise, diet, sleep, and we even talked about alcohol?”

The Impact of Mindset and Exercise

59:40 to 1:02:00

Explore how mindset and physical activity influence aging and health.

“Okay, I have nothing to do with this test, but I'm a big believer in it.”

Closing Insights and Future Discussions

1:02:00 to 1:02:52

Reflect on the discussions and potential future topics with Dr. Andrews.

“There's so much that we're going to unpack here.”
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Transcript

Automatic transcript. May contain errors.

0:00I decided because of my father's suggestion when I was 10 years old that I was going to cure aging. Some people have different genetics, some people have different lifestyles, and you can accelerate that telomere shortening by poor lifestyles and poor genetics. The question to ask when anybody claims to lengthen telomeres is, does the product induce telomerase expression? Pessimistic people have shorter telomeres than people their same age that are optimistic. So if you don't think you'll live to be 100, you probably won't.

0:34Matthew Januszek:Okay, we are live. Welcome to this week's episode of LIFTs. I'm Matthew Januszek. I'm feeling excited about what we're going to talk about today. I'm here with my co-host Mohamed Iqbal. Mo, how are you doing today? I'm doing great. Just like you're really excited about our conversation today. It's a topic that we tend to touch on a lot, but we don't really spend time exactly anchoring in on it. So really excited to get started. And I want to start today by zooming out. I mean, let's go way out before we go all the way in, because when we talk about longevity, I think that context really matters.

1:12Most of us typically grow up believing that aging is just where it's here. In fact, Matthew, I'm actually nursing a knee injury right now from some overtraining with running. I aggressively increased my mileage, and I know our guest here is a pretty avid runner. So they typically believe that it's something random, something that is inevitable, the slow accumulation of damage that eventually catches up to all of us. But modern science is telling us a very different story. Over the last few decades, researchers have identified predictable biological pathways of aging that involve inflammation, cellular replication limits, metabolic dysfunction, and genetic regulation.

1:57In other words, aging isn't just random, it's actually structured. And here's the thing, once something is structured, it can be studied. Once it's studied, it potentially can be influenced. To understand why today's conversation matters, for most of human history, tens of thousands of years, our average life expectancy hovered between 20 and 30 years, not because humans couldn't live longer, but because infant mortality, infectious disease, famine, and injury were constant. By the year 1800, global life expectancy was still around 30 years. Then, in a remarkably short period of time, everything changed.

2:41By 1900, life expectancy rose to the mid-40s. By 1950, it reached roughly 48 years. And today, global life expectancy sits around 73 years, with many developed nations reaching into the late 70s and low 80s. That's more than a doubling of our average lifespan in just 200 years. And it wasn't genetics. It was things like sanitation, clean water, vaccines, antibiotics, safer childbirth, and public health. In other words, humanity has already intervened in longevity once at the population level. What's more important, though, is how we did it. Nearly all of these gains came from reducing death, not from extending maximum human lifespan.

3:31The longest verified human lifespan still top out around 120 to 122 years. And that number hasn't actually changed in many decades, which raises a powerful question. If we've already doubled our average lifespan once, are we about to do it again, this time by intervening in biology itself? And that brings us to today's guest. Today's guest is one of the scientists closest to biological mechanisms behind that ceiling. Dr. Bill Andrews is a molecular geneticist, an inventor, and one of the key scientists behind the discovery of the human telomerase, which is something that I want to get into here shortly.

4:13That is the enzyme that protects the ends of chromosomes and plays a central role in cellular aging. He's a founder and CEO of Sierra Sciences, holds more than 50 patents in genetics and anti-aging research, and and has spent decades studying what he believes is a true hard stop to human lifespan, telemoral shortening. But Bill's story doesn't begin in the lab. When he was a kid, his father challenged him with a question that most people would laugh off, why don't you cure aging? That question never left him. Over the course of his career, Bill has worked at some of the most influential biotech companies in the world, contributed to breakthroughs in cancer research and regenerative medicine, and help uncover the mechanisms that tells ourselves when to stop dividing.

5:02And interestingly, he doesn't just study it. He actually lives longevity. Bill and I share a passion for running, but he definitely puts me to shame. Bill is an ultra marathon runner with more than 100 ultra endurance races under his belt. And he believes that consistent and durable endurance exercise is one of the most powerful tools that we have today to slow our biological aging, something that we talk about a lot on this podcast. Bill, we are so excited to have you on list today. I'm glad to be on board. I can tell you, I've, you know, one of the things, my running, for instance, and lots of other things, I've always been somebody that's been pursuing what everybody says is the impossible.

5:48My whole life, not only have I broken world records and the most like 100 mile races run in a year. I also used to hold the world speed record for barefoot water skiing. I've done a lot of things that nobody else would ever think of doing. But one of those impossible things was I decided because of my father's suggestion when I was 10 years old that I was going to cure aging. And I've been working on that my entire life. And, you know, let me just say responding to some of the things you said during the introduction. I do believe aging does begin with wear and tear. And I've been spending a lifetime of deep thinking on the subject of aging, and not just thinking, but actually hands-on lab bench research, trying to put all the pieces together.

6:41And I've logically destroyed all the theories that exist on aging, because I always say all the twos and twos have to add up and they don't. They don't explain everything. And so I've been trying to put together a model of what aging is, why we age, how we age, and therefore how not to age. And I've been all through schools and even beginning in high school and onward, I've been building an arsenal of tools that I need to really figure it all out. And I think I've made some very, very good progress on the understanding. What you hear is different from what anybody else has ever said. And, you know, even in graduate school, I challenged all the theorists on theories of aging.

7:28Part of my PhD is in the evolution, is on the how and why of evolution, as opposed to the what and when. And so, you know, I was asking the question, how and why do we age? and uh it it i challenged in theses written in graduate school every expert every theorist on why we age that ever published anything uh and i i have my own uh proposals but i don't call them theories because i've i've made everything i've built it all out of facts things that we know happen and it turns out there's no need for theories because everything i'm going to discuss today explains aging all by itself without needing anything else to explain it that's a good place to

8:18Matthew Januszek:start bill or dr bill as um as as i'll uh as i'll call you respectfully um so so why don't we start there like what what causes aging you referred to the fact that um aging part part aging is partially caused by wear and tear on the body and on the organs that's that's one part of it but watching some of your really interesting videos on YouTube last night you there's another theory that you've got which is what causes causes us to age and also gives us some sort of predictable maximum end point on what that is so maybe you could just give us a very and let's say a dumbed version of what what what are some of the factors that causes aging and also that that determines that almost like a an end point to to life first of all i wouldn't call it a theory okay because what i what i have the my my perspective on what aging is and why we age is based totally on how we age is based totally on facts that we know and so so i look at after everything i've looked at And I understand all the theories on aging.

9:33But after everything I've looked at, I've realized that the one and most important thing that we have to do to solve the aging process is find a way to prevent telomeres from shortening. They're the very tips of our chromosomes. And as somebody said here already, they protect our chromosomes, but they do a lot more than that. They actually regulate, they control the regulation of all the genes throughout our chromosomes. And they change when the telomeres length decreases, it changes the expression of all the genes on our chromosomes, which is the explanation of why we see all the changes that we see in all of us as we age.

10:16And it also limits our lifespan. okay um it like so telomeres are found at the very tips of our chromosomes they're like ride tickets at an amusement park and every time our cells divide they get a little bit shorter and they get a little bit shorter by a very specific unit and essentially what we have is like we're conceived at with 250 ride tickets there's so much cell division going from a single cell embryo to a newborn baby that by the time we're born, we've already lost half those tickets. We've used up half those tickets. And so we only have 125 tickets left when we're born. And then we still have cell division.

11:01We're growing up. We're fighting wounds, infections, things like that. And just natural bodily functions use up, have wear and tear that we really can't control. It's just, we can't, we can't slow it down below a basal level rate of wear and tear just to perform basic bodily functions. And as a result, our telomeres shorten and shorten. And when they get down to, when we use up our last ticket, our cells lose the ability to divide anymore, lose the ability to function, and we shut down and die. And that's not a theory, okay? It's Anybody, anybody who works with human cells in a, in the scientific lab, and they order cells from any vendor who sells human cells.

11:51When you go to that catalog, you look at the age of the donor and the number of times that those cells have divided since those were obtained from that donor. And then you calculate how many more times can those cells divide before you can't do any more experiments on them. Okay. So everybody knows that these are facts. And that's an absolute limit on our lifespan. If we had the perfect genetics and led the perfect lifestyle, we cannot use up tickets slower than a rate that limits our lifespan to 125 years.

12:26Matthew Januszek:When I went down the rabbit hole of looking into telomere, there was a couple of things that came up, which I was just curious to get your view on it. One of the things I was listening to was that mice have longer telomeres than humans and yet only live two to three years. And birds have shorter telomeres than mammals, but live far longer. And I was just wondering, as a lot of experiments in particular are tested on mice, what do you think is the relevance to that? And then just following on from that, that also there are some age-related declines that occur before these telomeres become critically short.

13:11Matthew Januszek:So as I said, I'm no expert and I'm trying to avoid making myself look stupid. But I was just curious because there is definitely, it seems to be a debate online, you know, around this sort of like telomere, I won't call it theory, but proposal. And I wanted to get your thoughts on that. Yeah, you're going to find I'm totally, I have a different viewpoint than everybody. And I do not debate anybody on these kind of things. Because I'm out to cure aging. And as far as I'm concerned, as long as I know that I know, okay, that's all that matters. And it just wastes the time to try to debate people.

13:51But mice do not age by telomere shortening. And most animals do not. and it's anybody who's studying aging can go and read the relevant publications and show that there's only a few animals in the planet that age by telomere shortening where they even have telomere shortening and those are you know other non-human primates except for lemurs dogs cats horses sheep pig and deer those are the only animals that have ever been discovered to have telomere shorting. Mice, you know, it's still debatable on what causes aging on mice, and I don't really care what causes aging in mice. I just think they don't age by telomere shorting, and therefore a terrible animal model to be used in the study in aging.

14:37But I believe that the best guess on what is causing aging in mice is oxidative stress and mitochondria dysfunction. And humans have 100 times more natural antioxidants in our cells than mice do. And so we don't have as much of an oxidative stress or mitochondria dysfunction problem as mice do, but we do still have it, okay? And so what I try to do is I try to look at the fact that there's multiple types of aging that are going on in all of us. But I think of each one as a stick of dynamite that's burning inside of our cells. And the real question, which is different for every species, the real question is, which stick of dynamite has the shortest fuse?

15:31And right now, in humans, it's clear to me, beyond anything, that telomere shortening is the stick of dynamite with the shortest fuse. And when we put it out, when I put it out, you know, figure out a way to put it out. I'm going to put out another 30, 40 years to my life to figure out how to put out the next fuse on the next stick of dynamite. And I don't know what that is, but it could be oxidative stress, mitochondria dysfunction, which will give us a lot of time because I think that's a minor problem unless we really lead a very terrible lifestyle or have poor genetics or you know if we smoke or do things like that that's going to really accelerate our oxidative stress and damage to our uh dna and telomeres and things like that but the other thing okay so so let me so the next part of your question was um uh what was it um so the next part was why are there changes yeah go ahead yeah so other so um other um

16:36Matthew Januszek:that for example like like as i was looking into this for example that there are other age-related declines that occur before the telomeres become short and and in particular there seems to be a debate around cancer as well which i know you've spoke about in in one of the talks I was listening to so again just just to sort of help I suppose us understand from what's out there and and what you've discovered it just just curious to to understand like what if any are some of the some of the more sort of uh relationships between either shorter or longer telomeres with some of the some of the other um sort of lifestyle related issues that shorten life First, okay, the cancer situation.

17:24I was National Inventor of the Year for my cancer research in the United States. I do know a lot about cancer. And most people in the anti-aging field do not understand cancer that well. And so there's a lot of rumors going around that long telomeres and the enzyme telomerase, which we haven't really discussed yet, cause cancer. But it's because they don't, the people who are saying that stuff don't really understand cancer. And the main people saying that really didn't become cancer researchers until after my team at Geron Corporation discovered telomerase. And then, you know, we did some experiments.

18:01And, you know, I have, I've got one drug that just got approved by the FDA called Rytelo, R-Y-T-E-L-O, that I'm pretty much the only inventor on, even though other scientists got themselves included on the patent. It's an inhibitor of telomerase. because cancer cells do produce telomerase to become immortal. But they had to become cancer first. They became cancer first. Then their telomerase got really critically short because of all the cell division. They used up all their ride tickets. And when the ride tickets get really short, mutation rates skyrocket. And as a result, some of those cancer cells mutate to a form that survives whatever you're treating them with, and they actually come up with alternate ways of keeping telomeres long, even though telomerase is being inhibited.

18:58And those alternate ways are called the ALT pathway for alternate lengthening of telomeres. And it's a big problem. But the point is that if you keep telomeres long, you decrease the risk of cancer because you decrease the skyrocketing mutation rates that short telomeres cause, and you also increased the ability of your immune system to fight cancer. I used to also be head of immunology, the molecular biology division of immunology at a large biotech company called Burlex Biosciences. And it's another thing that I understand extremely well. When I talked before about the arsenal of all the tools I put together, those are some of them.

19:39So gene expression is also one of my arsenals, or tools in my arsenal. And that's, I really understand that better than most people you ever talk about. But there's things in our DNA called enhancer sequences. They are things that are found like, so genes, like DNA is like a long string of beads. There's four different types of beads, A, G, C, and T. And it's the sequence of those beads that tell us what our eye color, hair color, et cetera are. Okay, now all these genes that are made up of these beads, they're all regulated by things that I call dimmer switches. Their name is really promoters.

20:21But the promoters are things you can turn on and off and on and off to whatever you want. But in fact, we can't. It's hard for us to turn it on, but our cells do this. And one of those enhancer sequences are things that control those things. So you have this DNA molecule, you'll have an enhancer sequence at like 100 ,000 beads or bases, they're called away. And then you'll have a gene over here, and proteins will bind to the enhancer and proteins will bind to the promoter. And then the DNA actually folds over and comes in contact. And when it comes in contact, it turns the gene on, and suddenly the gene gets transcribed and then translated to produce the protein or whatever the cell is producing.

21:08Now, telomeres have all the hallmarks of enhancer sequences. And I learned this 30-plus years ago. um and it's like because of my knowledge of enhancers i could look at a telomere sequence and i say wow that's got all the hallmarks of enhancers it's got the repeated sequences it's got it's got proteins that are equivalent to transcription factors that bind to them it's got histones that bind to telomeres that are the same histones that bind to enhancer sequences and so as a result and then now just last year somebody actually published a paper that actually confirmed that telomeres are enhancer sequences.

21:50The telomeres actually fold over, just like I talked about, they fold over, come in contact with dimmer switches, promoters on the chromosomes, turning them on and off. But here's the difference between a telomere and enhancer. The telomeres get shorter. And when they get shorter, they change the gene expression, which is called the epigenetics, the turning on and off of genes. not how they get turned on and off, but to the level that they're turned on and off is called the epigenetics. And the epigenetics changes as the telomeres get shorter because the telomeres can't regulate the genes as well as they could when they were longer.

22:33Okay, so that change in the gene regulation is what explains all of the changes that we see, that all of us see in all of as we age. Okay. And that's why, because of the consistency in this, that's why you can look at anybody, you can observe anybody and you can estimate their age pretty accurately without any other biomarkers of aging or anything like that, just by observing their appearance and behavior and everything like that. That's because the genes are all being regulated by the telomeres as they shorten, and we all have relatively same rate of telomere shortening. And we see differences because some people have different genetics, some people have different lifestyles, and you can accelerate that telomere shortening by poor lifestyles and poor genetics.

23:26I just want to take one step back. So just for the audience who might not be thinking about telomeres as you are, Really, this goes back to almost like the 1960s when Leonard Hayflick showed that human cells divide roughly 50 to 70 times before they permanently stop. And that discovery fundamentally changed biology because it showed that aging wasn't infinite. You said before that telomere shortening is not the only universal heart stop to lifespan. Why does everything else, like inflammation, disease, and lifestyle, eventually funnel back to this? Well, so you said a lot of things. And let me just first say that when Leonard Hayflick first published his paper in 1961, people did not believe it.

24:17It did not change the world. okay but some people like me when i was in the 1970s when when i was in college and i was running anti-aging clubs and we were having discussions about aging and stuff like that and trying to put it all together and destroying all the theories and things like that you know and one of the members of this anti-aging club when i was in college was dr bruce boiler who wasn't a doctor at the time but he he ended up winning the nobel prize in medicine in 2011 i think it was, or maybe it's 2010. I can't remember. But we had a pretty powerful group of people. And we concluded that the only thing that ever made any sense whatsoever about the aging process in humans was Leonard Hayflick's Hayflick Limit.

25:04Okay. And so that was what led us to the conclusion that there had to be something like ride tickets in an amusement park inside of ourselves, because the Hayflick limit, the limit on our lifespan explained all the twos and twos. It explained why dogs and cats age at different rates when they're in the same environment as we are. And it explains why people who live in the North Pole and South Pole age at the same rates that people on the equator when they're in different environments. It explained just about everything. And so we started thinking, okay, now brains, cells don't have brains. So how do they know how many times they can divide.

25:41And the only thing we could come up with was there had to be something like ride tickets at an amusement park. And after that, it took me 20 years before I actually figured out that it was telomeres. And between that time, I went into biotech and used all my arsenal of tools on a whole bunch of other things. So I got a lot done during that time. But I spent those 20 years just deep thinking, really trying to figure out what those ride tickets could be and things like that. And it wasn't until 1993 that I actually heard somebody at an anti-aging conference talk about the fact that telomeres shorten.

26:25And you can measure them. You can determine a person's lifespan by measuring the length. And you can also figure out how long they'll be before they die of old age from the length of their telomeres. But most important is that even that speaker said, this explains the Hayflick limit. Okay. Now, it took several people. Hayflick, Leonard Hayflick was pretty much ignored for a long time before we came along and essentially proved him right. Because when we first discovered this enzyme telomerase, which I led the team doing so at Geron Corporation in the early to mid-1990s, we showed that when we put telomerase into a normal, the gene for telomerase, into a normal human cell, it completely obliterated the Hayflick limit.

27:20It did not happen anymore. We proved the Hayflick limit occurs. We showed why it occurs, and it's all because of telomere biology. And so Leonard Hayflick and I clearly became good friends after that. But it was like for a long time, people refused to believe that actually human cells had a limited number of cell divisions they could undergo. They thought, why would a human cell be any different than a bacteria cell grown in a Petri dish, which grows indefinitely? Okay, so I wanted to finish that first point. Now I can't remember where you went after that. But what's the next thing you wanted me to address?

27:58Well, I think, you know, why does everything else like inflammation, disease and lifestyle eventually funnel back to this? There's no question about inflammation is the number one cause of aging. I think every single person in the anti-aging field would say so. But inflammation and oxidative stress cause all kinds of things. Now, here's the real question. we have the ability to repair our wear and tear we aren't old trucks sitting in a field that are exposed to sun and wind and rain we can repair our wear and tear so why do we age okay and so it's an inflammation inflammation is dividing of cells really and that's uh and it attacks and damages cells, and so does oxidative stress, but we can have other cells divide to replace those cells.

28:55When I talk about this at conferences, and people can go to my videos. If they go to my website, I'm sure you put the link for that on it, and if they go to my website, there'll be a button you can push that is key videos and documentaries, and people can see me talking about what aging is and why we age and how we age. And that's what we're talking about right now is how we age and how not to age. And so the how to how we age is because even though we do have the ability to repair our wear and tear, we all organs and tissues have cells that are what I call frontline cells, where all the action is occurring, where all the natural bodily functions are occurring and there's therefore wear and tear that is unavoidable okay well our wear and tear causes these cells to be removed or they they die essentially they become inactive but we have other cells called reserve cells that's the least terminology i use reserve cells which are stem cells and progenitor cells these cells can divide and replace those cells okay so we can constantly be regenerating ourselves after the wear and tear.

30:12And this is something we discussed even when I was in college at these anti-aging classes. Why do we suddenly stop, have a decline and then stop repairing our wear and tear? And the Hayflick limit explained that. And so the problem is, so if we have inflammation, a lot of inflammation, we actually accelerate the wear and tear. and I'm going to use an analogy here that everybody seems to understand more than anything else okay drinking alcohol drinking alcohol kills liver cells that's something everybody knows we've all been hearing that okay that's okay when we're young okay because those killed liver cells are replaced by other cells from the reserve cells okay so our livers can constantly can for a while constantly replace the damaged liver cells that we're killing because of our drinking.

31:09But then when we get to be like 40 or 50 years old, because of the accelerated rate of telomere shortening above the normally bodily functional rate of telomere, or cell division, I mean, we suddenly, our telomeres get so short, our cells cannot replace those damaged cells anymore. And so we get an accumulation of damage. And that's what liver cirrhosis is.

Read the full transcript

31:32Matthew Januszek:Is that what you feel worse when you're older after you had a couple of drinks and what you did when you were younger? There's also the alcohol dehydrogenase gene and things like that. Believe me, alcoholism is one of those diseases that I really want to cure. And I believe that alcoholism has nothing to do with aging. It has to do with mutations or variations of the alcohol dehydrogenase gene. But it's like I want to cure aging first. And then that's one of the things, alcoholism and sickle cell anemia, and there's a whole bunch of other things that have nothing to do with aging that I want to focus on curing.

32:07So you took me on a tangent there for a second.

32:08Matthew Januszek:Sorry about that. Yeah, no, that's okay. But it's the feeling. When I'm not talking about the feeling, I'm talking about the damage to your liver that kills people, okay, from drinking excessive alcohol. Now, the same thing happens if you have a genetic situation like the dystrophin gene. okay if you have a variant of the dystrophin gene that causes muscles cells to divide faster from wear and tear you get muscular dystrophy muscular dystrophy is caused by a variant of a gene called dystrophin and so that accelerates telomeres shortening too but you don't you don't experience muscular dystrophy when you're young you only experience it later after you have had all those cells divide so much that the telomeres got so short that the damaged cells can't be replaced anymore.

33:00And same with AIDS, okay? Acquired immune deficiency syndrome. When people first get infected with the virus, they have no symptoms, but the virus is killing immune cells, and other immune cells are divided and replace those cells. But when you run out of telomeres, that's when AIDS starts showing its symptoms and you can't replace the damaged immune cells anymore. And that's why it's an immune deficiency syndrome. Okay. It's like there's everything aging and every, almost every disease you've ever heard of is connected to the length of our telomeres. And I always say bad things happen when telomeres get short and we have to solve that problem.

33:44And no matter what else we do to try to cure the aging process, nothing will ever cure Asian unless we also solve the telomere shortening problem because that is the one hard fast limit to our lifespan that is completely understood without any theories

34:00Matthew Januszek:sorry what about you know GL we've talked a lot about GLP ones and and if you look at some of the reports out there what what they seem to say is calorie caloric restriction is having a huge impact on people's lifespan um and a lot of these glp drugs because of some of the side effects or positive side effects that that people are not eating anymore they they these drugs are keeping people as well as losing weight they're keeping them um they're extending their lifespan so what what is your um sort of view on if any that the link with with a lot of the work that you're doing and some of these GLP-1s in relation to caloric restriction and that causing people to live longer?

34:48Well, you know, GLP-1 is just one of the many things that we can do to improve our health. And what happens as a result is that we reduce our wear and tear, okay, just with everything, okay? So everything we do that's healthy is actually reducing the wear and tear, which is preventing slowing down the rate of cell division that is needed to do to repair things. And that includes caloric restriction and stuff like that from producing less free radicals, which damage tissues and cells. There's also mitochondria dysfunction. Mitochondria dysfunction is a very important thing that correlates with aging, but it does so by not really causing aging.

35:31It causes a wear and tear that eventually will lead to teloneres being so short that we can't repair the wear and tear anymore. Okay, so, I mean, I can, if we had hours and hours to talk, I could talk forever on mitochondria health, how to maintain good mitochondria health, how to, you know, all the benefits of caloric restriction, senolytics, NAD. I mean, these things I understand fully. Better than most of the people that are even in the field studying these things. Because I spend every minute of every day just thinking about aging and figuring it all out and just trying to understand everything I can because I want to live forever.

36:19Matthew Januszek:So do you see, just for me, and dumbing this down then, Bill, is so you've got the wear and tear side and then you've got the extension or saving or preserving the telomeres. So some of the things that we've talked about such as GLP-1s, reducing alcohol, I guess things like exercise, even though I guess that does cause some inflammation. I'd be interested to get your thoughts on that as well. We'll skip back. But some of those things, what you're saying are helping to reduce the wear and tear on the organs, which are naturally going to assist. But then there's this other side which is the telomere, which also works to extend your lifespan.

36:58Matthew Januszek:Have I understood that correctly? Yes, but, you know, we're talking about a five-hour podcast here. I speak all the time at not just anti-aging medical conferences and cancer conferences and heart disease conferences, but also at sports conferences, okay, about athletics. okay so yes athletics if done wrong incorrectly especially endurance well endurance exercise and bodybuilding and things like that can accelerate your wear and tear and telomere shortening and things but there's also ways that exercise that don't do that now i used to hold the world's record for the most 100 mile races run in a year and people would think well isn't that a contradiction to everything that I think.

37:45But no, because it turns out that when you exercise consistently, like I run every single day, I haven't missed a day now in six years. If I run every single day, I train, but I keep it fun. Okay. And the rule is if it ever stops being fun, quit and save it for another day. Because when you are one of those runners, let's say, It's not just running. It's kayaking, bicycling, hiking, everything you can imagine in endurance sports. If you are an occasional endurance exerciser, let's say you run every two weeks, and then you go and run a marathon, you'll do okay. But you'll be on your hands and knees throwing up afterwards, and you'll be stiff as a board from inflammation for two weeks.

38:38and that's all because your body isn't conditioned to know what all this means okay your body doesn't have brains but the systems send the pain on your joints are sending signals to your brain and everything like that causing an immune response inflammation is going to the joints to fight whatever is there but if you run every single day your body doesn't do that because it it gets conditioned, okay, or acclimated, okay, is probably the better word. And so I've done, I've gone to ultra marathons, even when I was running on myself, I've taken blood from runners beforehand, during and after the races.

39:20And I've looked at all kinds of things from electrolytes to inflammation markers to oxidative stress, looked at correlated with their electrolytes and their lifestyle and things like that and i think it's very very clear that those people that exercise mostly for the fun of it okay and like when the runners who go out running for the adventure more than the the strain are actually decreasing their inflammation and oxidative stress not increasing okay so so i think there's so running is is a goldilocks effect kind of system where there's such a thing as too little running, too little exercise or endurance exercise that actually increases oxidative stress and inflammation.

40:07And then there's too much. By too much, I don't mean quantity. I mean intensity. Okay. So don't be one of those people that push so hard that you are on your hands and knees throwing up after an event. Be somebody that, you know, 90 miles into 100 mile race, you're saying, Oh, my God, I'm having the time of my life, I wish it would never end. Okay, that is, that's the way I am when I'm running a hundred mile race. Okay, I just can't get over the adventure that being out in nature and things like that. And it's like, I really don't want it to end. Sometimes I even fall asleep while I'm running.

40:43I'm so running so long. And I suffer from something I call can't turnaround disorder. Okay, it's like, I just what if I say, tell somebody I'm going out for a two mile run and I get on a trail, I just can't turn around because I'm just, what's around the next turn? What's over the next hill? I'm not saying to myself, oh, I need to train harder, get more exercise. I just know it's just the running is just by exploring and having fun is actually really good for me. And it's, but yeah, I just probably spent most of our time just on that short description. No, it's all good. Look, we should definitely go running, Dr.

41:24Bill. I run almost every day. I've not done an ultra marathon, but I've done numerous marathons. I don't think on mile 22 I'm thinking about I can go for another 22 miles. I'm thinking about how can I finish the last 4.2 miles of a marathon. So I still need to get there. But ultra marathon running is completely different from a running one. And by the way, Michael Wardian, who I think you probably know, lives a mile away from me. So I see him on the trails. We run together all the time. And I'm going to look you up on Strava next. We can be Strava friends. If you know him, I'll tell him that you said hi and that we had him on this podcast.

42:01I know of him. I don't know him personally. But my running buddies used to be like Ann Trayson and Dean Karnasas and things like that. It's a different time. Um, I, let's see, there was something I want to add. I want to, just quickly ask for years. One of the things that we talk a lot about on this podcast is longevity and recovery. And you've kind of touched on both. So we, our industry, the industry that we're in, which is predominantly, most of the people listening are in the fitness or wellness industries. And over the last five years, they've really incorporated all forms of recovery into their facilities, into the training.

42:43We're talking about things like Norma Tech boots, compression boots, red light therapy, cold plunges, just hyperbaric chambers, which actually that's kind of shown to increase the length of telomeres. I'm just curious, when you look at influencers, founders, consumers asking about what comes next, then you've got people like Brian Johnson and Dave Asprey that are pretty much running public experiments. certainly not with the science pedigree that you have, but they're tracking biomarkers, tracking a ton of things and sharing everything in real time. On one hand, the good thing is that it's unprecedented engagement that we've ever seen with science, if you can call it that.

43:27But on the other hand, biology does not really move at social media speed. So they're trying to really accelerate things. And as you said, you want to live forever. Brian Johnson says, it doesn't want to die. From where you sit inside the mechanisms, is this really accelerating progress or is it oversimplifying extremely complex systems? Because here's the thing, telomeres is not something I've ever heard a Gary Brecka or a Brian Johnson or Dave Asprey actually talk about. 99 % of the anti-aging field is looking for ways to make a buck out of anti-aging products, whether they work or not, okay?

44:07And they don't really try to understand everything like I do, because my mission is to cure my own aging. I want to be around when we find life on other planets, okay? It's like a lot of great things are going to happen in the future. I don't want to miss out. So I'm focused on really what's going on with aging. But, you know, you'd mentioned things like hyperbaric chambers make telomeres longer. Okay, well, that's a total misunderstanding. And I've talked to a lot of, when I see them at conferences and expos selling, making these claims, I'll say, okay, so where's the data showing that telomeres are being lengthened?

44:48Okay, because there are ways of making telomeres longer in your blood without them being lengthened. Okay. And it's actually not making them longer. You're just actually causing a change in the cell population in your blood to either bring in cells that have longer telomeres. So cells from your bone marrow. So if you have an inflammatory response, cells in your bone marrow, which have long telomeres, even when you're really long lived, they have long telomeres. They're going to divide and infiltrate your blood And as a result, the average length of your telomeres are going to be longer. Same is true with toxins and stuff like that, which are going to preferentially kill off cells that have short telomeres.

45:36As a result, the average telomere length in your blood is going to increase. And the analogy that explains that best is if you have a company and you fire your dumbest employees, the average IQ of your company increases without anybody getting any smarter. Same as if your company hired a bunch of geniuses, the average IQ of your company increases without anybody getting smarter. These things are happening in our blood. And so what I try to say is that when somebody tells you that they have some kind of product, whether it's a lifestyle, diet, therapy, et cetera, supplement, ask them, does your product induce the expression of telomerase?

46:18because that's really the only way to know if your telomeres got lengthened. The only thing that can lengthen telomeres is this enzyme telomerase, which we haven't even talked about yet. It's like in the 1990s, when I first learned about telomere shorting, I was essentially recruited by this company called Geron Corporation to lead an effort to discover a way to lengthen telomeres. And I discovered this enzyme telomerase by the fact that our reproductive cells couldn't possibly have short telomeres shortening. If they did, our children would be born with shorter telomeres than we have. So in our reproductive cells, I and my team discovered this enzyme called telomerase.

47:01And we then put it into other cells and showed that we could totally stop the aging and process in those two and stop the hayflick limit, as I mentioned before. But you have to show, so if there's a product out there that somebody's claiming lengthens telomerase, they have to show that it induces the expression of telomerase. And so I encourage people to ask that question. And I'm going to right now tell you, because I know we're running out of time. That's what my main research is doing, is trying to find anything that can get inside of our cells, turn on the gene for telomerase, which exists in all of our cells, because for reproductive cells produce telomerase, we have the gene for all of it, in all of our cells.

47:45It's just shut off, but it's repressed in all of our other cells. I've been looking for ways of de-repressing the telomerase gene to produce telomerase in all of our cells to lengthen our telomeres. And I've tested, I've got million dollar robots here that can test 4 ,000 different plant extracts a day or chemicals a day or molecules a day. And the best thing that we've ever, I'm going to do some marketing right now. This is a product called Televital. It's produced by a company called Touchstone Essentials. It's USDA organic. And what I really like about this product, one thing I like about it is it contains the top five most potent natural products, natural ingredients that we've ever discovered.

48:34Okay. And it mixes these things in here. When somebody takes this product, it induces telomerase inside of their cells. It doesn't, telomere shortening and lengthening is like a tug of war. They're shortening and lengthening. But in the absence of this product, there's only shortening. So this is adding some people to the lengthening side of the tug of war to lengthen telomeres, but it doesn't, it's not potent enough yet to win a tug of war. But in a few years, we're going to have something that wins that tug of war. Okay, but - Bill, just on that. Well, let me just say, this slows down the aging process.

49:10And a lot of people say, you mean it doesn't reverse aging like all the other products do? Nothing reverses aging, but this is the only product that I know of that actually can slow down the aging process, and that's a good thing. Sorry.

49:22Matthew Januszek:No, it's okay. So with this, obviously, we have a lot of people online. Mo gave a few examples of people like Gary Brecker, who I like a lot of what he says, but I'm always very skeptical when he comes out of it because I'm waiting for the product drop to happen at the end. And obviously, you've got a product, and I guess that's what funds it. I don't have a product. Oh, you don't have a product. I discovered the ingredients that this company put into their product. Okay. All right. So on that, just to be clear then, how are you, I guess, connected with the company or with this product? And I just want to get clear to see whether there's arguably any kind of influence or leaning towards a particular product that that supported or supporting any of your research in into this particular idea.

50:14Matthew Januszek:And maybe that's for the people that are listening as well, because, you know, you have to be quite skeptical with people that have an opinion and even some of the ways that research is funded, because it could lead you to a particular direction. And somebody's creating a huge pharmaceutical company or vitamin company behind the scenes. So just just curious if you can kind of, you know, give us a clear overview of that as well. So any like we do, like, bring in go to market partners, okay, but we don't actually go out and pursue go to market partners, we, when we when we make a discovery, we put it on the shelf, because we're too busy doing research to actually try to think about products, because our goal is to cure the eating process, we want to, we would have loved to have been able to turn like somebody like Betty White back into a 25-year-old.

51:02Look, feel, and behave 25. That's the goal of our research. But then we do get contacted by companies that ask if they can license, let's say, some of the discoveries that we've made and just put on the shelf. And we'll say, sure, but you have to provide my company with a royalty that will go 100 % towards the research. Okay, so it's a way of helping to fund our research. Our research here costs$2 million a month. Okay. Now that some product sale, like some of the other Televital or some of the other products, they will never, ever come close to covering that full expense. So, so it's a lot of, a lot of other sources of funding too, but, but we do get a royalty, but believe me, we don't go out of our way to try to find those royalties to try to make money because we're too busy doing our research.

51:55Our goal is to curate, and especially in my lifetime. Yeah, so I do understand. I see this all the time. I see a lot of people trying to market products that actually don't work. They're based on poor science, and I actually have my own podcast, which is called Up One, because I take things up a notch in terms of evaluating scientifically peer-reviewed studies. So I don't just do what is called critical meta-analysis of peer-reviewed studies. I don't just do meta-analysis. I do critical meta-analysis, which means I read all the papers. And with my arsenal of tools, I am good at looking at experimental design, data analysis, construct validity, statistical theory, all these different things that make a paper good or bad that most reviewers will actually miss.

52:46And that's why a lot of junk papers get published. But I will go through this in my podcast and really explain to people what really works and what doesn't really work. And so I will be honest with you, 90 plus percent of the products on the market do not work. And I don't actually say their names or go out and point fingers at them and stuff like that. I will tell people what questions to ask. and the question to ask when anybody claims to lengthen telomeres is does the product induce telomerase expression and this product does okay this product does induce telomerase expression and i'm not going to say if other products do or not but i'm going to say go and ask them and if somebody tells you that they do have a product or somebody tells somebody who's listening to this podcast somebody does have a product that they say they show data that lengthens telomeres or that induces telomerase expression and lengthens telomeres.

53:47Show me the data because I would like to look at, because I'm the inventor or co-inventor of every method there is for measuring telomere length, measuring telomerase activity. And I just swear to God, I see so much crap out there. Scientific publications where people actually on the very first page of their publication show a picture of what's called an electrophoresis gel showing that their product induces telomerase expression. And then me and my colleagues that really know all this stuff look at that paper and they say, that's not a telomerase assay. It's like they're showing some garbage data and telling everybody it's telomerase and it's not even telomerase.

54:31This is the kind of crap that occurs. And people, this whole, you're going to get me going on. There are actually videos of me talking about the problems with why cancer is not cured, why publish or perish is a rule that has destroyed the scientific industry. People are publishing just so they can add more publications to their list because that's how they get grants. Then there's – We tried to pause there. And by the way, there's also a lot coming from China as well on the research field. One thing you look – And it's good. And it's good. A lot of good stuff. Yeah. Yeah. And what we typically do, just because we're short in time here, we typically like to end with our final takeaways on this podcast.

55:15I think you've been a fantastic guest. We need to get you back on. I've got a couple of quickfire questions, just maybe one answer questions, Matthew. I'd love to give you a couple as well. So let me go through my list here, and I'd love to find out yes or no. So first question is, in the year that you set the record for running the most 100 mile races, how many races did you run? I ran 12. 12, okay. That was 1998. Incredible. And in terms of some of these therapies that we've seen, yes, would you say that they work or not? Red light therapy, effective or no for longevity? See, I don't do that, but I will tell you that they all have benefits, okay?

56:02But they all, if I say all, then I blame the product, but a lot of them will make claims that aren't actually accurate. I'm not saying that they intentionally do it, they just might unintentionally not understand what's really going on. Okay. Is HRV a North Star indicator for health or longevity? So many people use that. Well, no, it's health. Okay. It's a measure of health and poor health is going to decrease longevity. And it's important to separate the two. How about cold plunging? Is that a great recovery tool? You're putting me on the spot. I don't do it. Okay.

56:46Matthew Januszek:Matthew. I've got one question. And it's, again, Bill, it's more to many of the people that are listening to this that are in the health and fitness and wellness space. Outside of the supplement that you recommended there, which I think we'll like to get the details and we'll share that with people that are listening. But what would you say are some real basics in terms of whether that's exercise, diet, sleep, and we even talked about alcohol? What would be three or four of your recommendations that you would say are solid pillars that we should do our best to follow that will help support some of the research that you've been able to find about essentially living longer?

57:39Well, decrease the rate of cell division and decrease the rate of telomere shortening. Okay, is really the most important things. And so antioxidants, anti-inflammatories are extremely important. Vitamin C, well, vitamin C is really important, but more important than that is vitamin D and omega-3 fatty acids. Those things are the most well-published and past muster in my critical meta-analysis of peer-reviewed studies on the ability of able to decrease their rate of telomere shortening. Okay, now they don't lengthen telomeres. Okay, so when I was talking about the tug of war between shortening and lengthening, we can add people to the lengthening side, but we can also remove people from the shortening side.

58:26Okay, and so those kind of things. So quit smoking will reduce the number of people on the shortening side. Quit drinking, same thing. Yoga, meditation. I speak at yoga and meditation conferences all the time, and I show data showing that people that do yoga and meditation have longer telomeres than their friends of the same age that don't. Exercise is fun. Lose weight. Obesity actually accelerates aging by accelerating wear and tear, therefore accelerating telomere shortening. And it does so by the induced inflammation and oxidative stress that burdens the body from all the excess weight. Then there's other things like even pessimism.

59:12And I don't really understand why, but there's two studies showing that pessimism, actually pessimistic people have shorter telomeres than people their same age that are optimistic. So if you don't think you'll live to be 100, you probably won't. And telomeres will tell you so. I'm trying to think of what else to tell you. I would, to reduce inflammation, I would take the ALCAT test, A-L-C-A-T. Okay, I have nothing to do with this test, but I'm a big believer in it. It's a test that measures what foods cause inflammation in you. Identify what those are. You can find it on Google by A-L-C-A-T. also read Dr.

59:57Sandra Kaufman's book called The Kaufman Protocol. She's written two books now. I think they're the best books ever written on the subjects of what supplements each person should take and every person is different. And this book tells you how to identify which ones you should take. And there's also like cardiovascular disease, okay, which I don't know if we didn't have time to talk about, but I've invented a lot of cardiovascular treatments and drugs and things like that, as well as cancer and other things. But there's books by Dr. Amy Donin and Dr. Caldwell Esselstyn. Her last name is D-O-N-E-E-N.

1:00:38His last name is E-S-S-E-L-S-T-Y-N. Those books are the best written. I'm also going to add Floyd Shilton, who's written inflammation nation. Dr. Caldo Esselstyn's book is Reducing and Reversing Heart Disease. Dr. Amy Donin's books are called The Heart Attack Gene, and she's got another book on brain health because brain health is very cardiovascular related. But those books, I mean, I have those books here. I've read everything. I've got them all marked up as which pages are important, really critical. I think they're really good, but I'm trying to think of what else to tell you. It's do endurance exercise, keep moving every single day.

1:01:26On the subject of marathons and stuff like that, I'm going to tell you, my wife is the most incredible person when it comes to marathons. I'm imaginable. She's just about to turn 69 years old. She just a few months ago ran seven marathons on seven continents and seven goals okay and then she after that she got on a boat my friends who did that she got she got on a boat and went to the north pole and ran a marathon right after that so she's she she's one of the handful of people because they had a leg of that in antarctica too yeah that was the first the first leg of the race uh to do seven marathons on seven continents in seven days was on antarctica that's right and they went to i think dubai and then south africa yeah south you're right south africa then dubai then perth i i've lost track after that it's just she's non-stop and she's she's the oldest person to ever do that okay and i don't like using the word old i just did it accidentally she's the longest lived person to ever do that because living is about, life's about living, not getting old.

1:02:42Okay, so. Well, this has been fascinating. We're going to have to get you on. There's so much that we're going to unpack here. I just want to thank you for coming on. Matthew, I will hand it off to you to close.

1:02:53Matthew Januszek:Yeah, thanks again, Bill. We always say this, there's always a lot more to talk about, but I think in this case, maybe what we can do is we can come up with a few specific areas that that you particularly focus on and maybe do a little bit more of a deep dive because we've, we have tried to cover a lot of things. And we've also tried to deal with some of the sort of skepticism of, of a lot of the information that's out there with, when it comes to the word longevity or the biohacking space. And, and you certainly have, you know, you've, you've certainly got a lot of information and research to, to back that up.

1:03:30Matthew Januszek:So thanks again for, for joining us, please uh we'll we'll put some information on how you can find more about bill how you can find out about his podcast and some of the research he's done we'll include that in the show notes and also on the email that we put out and um thank you very much for listening i hope you've enjoyed this episode as much as we have

1:04:05Thank you.

From the publisher

Welcome to the latest episode of L.I.F.T.S, your bite‑sized dose of the Latest Industry Fitness Trends and Stories.

In this episode of, hosts Matthew Januszek and Mohammed Iqbal sit down with Dr. Bill Andrews: molecular geneticist, inventor, and telomere pioneer to explore what actually causes human aging and whether it can be slowed, stopped, or even reversed.

Key topics covered:

  • What telomeres are and why they determine human lifespan.
  • Why aging isn't random, but biologically programmed.
  • The real relationship between telomeres and cancer.
  • How exercise, inflammation, and lifestyle impact cellular aging.
  • Why most anti-aging products fail scientific scrutiny.
  • The role of telomerase in extending cellular life.
  • What longevity influencers often get wrong.
  • Practical habits that may slow biological aging.

👉 To learn more about Dr. Bill Andrews' research, click here:

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

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00:00 Welcome to LIFTS

03:30 Introducing Dr. Bill Andrews

05:00 The Childhood Question That Sparked a Career

08:45 What Actually Causes Aging?

09:45 Telomeres Explained

14:30 Why Mice Are a Bad Aging Model

18:20 Telomeres, Cancer, and Mutation Rates

22:00 Gene Expression and Epigenetics

27:40 Inflammation, Wear & Tear, and Aging

33:45 Caloric Restriction and GLP-1s

36:30 Exercise, Endurance, and Longevity

42:10 Recovery Tech and Longevity Claims

47:30 Telomerase and Slowing Aging

55:00 Rapid-Fire Questions

56:30 Practical Longevity Habits

1:02:30 Final Thoughts

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LIFTS Episode 105 - Why Humans Age: Telomeres, Longevity, and the Limits of Lifespan with Dr. Bill AndrewsEscape Your Limits & LIFTS · 1 h 4 min
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