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Transcript of the Interview with Nobel Prize Winning Anti-Aging Scientist Dr Bill Andrew on Reversing Aging and The Latest Breakthroughs in Telomere Science

Dr Bill Henry Andrews, Ph.D. is an American molecular biologist and gerontologist whose career has centered on searching for a cure for human aging. Andrews is the founder and president of the biotechnology company Sierra Sciences.

Aging is a complex and difficult topic that has been the centre of attention of many scientists for centuries. That's also what Bill Andrews, Ph.D. has made his challenge to solve.
Aging isn't an accident. We age because our telomeres get shorter and our cells age. Every time our cells divide, our telomeres get shorter and our cells age. Aging is also the cause of a lot of diseases. Research suggests that control of the telomere length has the potential to treat many diseases linked to aging.

This is what SIERRA SCIENCES group of scientists led by Dr Andrews has been working on for the last two decades and is close to finding cures that will change the way we live
our life forever. A number of products using their breakthrough techology are already on the market and more powerful ones are in clinical trials. In the lab they have already made immortal cells that never age or die at Harvard university has already reversed aging in rats and now the human trials are about to get underway. You won't want to miss this cutting edge research. If you want to live a long and healthy life then you will want to hear what Dr Bill, Nobel prize winning scientist has to say. 
Dr Andrews was also one of two scientists featured in a netflix documentary called "The Immortalists" which follows their pursuit of the fountain of youth. Click this link to watch the trailer: The Immortalists

We would also like to thank the sponsors of this show. 

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Transcript of the Interview

Speaker 1: (00:04)
Welcome to pushing the limits, the show that gets deep into the psyche of those who have achieved the extraordinary from sports people to business people to social change innovators, cutting to the chase to unlock the secrets of their success brought to you by running hot coaching, the platform that helps you achieve all your health and fitness goals.

Speaker 3: (00:34)
Well, hi everybody. It's Lisa Tamati here at pushing the limits and welcome back to the show and if you're a returning listener and if you're new to the show, welcome and your info an absolute treat today. I have some exciting guests on the show, but the man I have with me now could change your life, your future. He is what? He is the world's leading expert on anti-aging, on telomere shortening. And I have the amazing privilege that I am very close friends with his wife. So I've managed to get dr bill Andrews on the show. He's also an extreme ultra marathon runner and we're going to talk a little bit about that as well, has as his groundbreaking research in anti-aging. So welcome to the show, dr bill Andrews all the way from Reno. How are you?

Speaker 4: (01:19)
Thank you. Thank you. Thank you very much.

Speaker 3: (01:22)
It's a real privilege to have you on today. Now before we get into the science stuff, before we get into, you know, all the complicated sort of stuff that you, you're involved with, with the incredible research that you and your team at Sierra sciences do. I want to know a little bit, and I know a bit of your background, so, but I want to talk about your running career. You know, because I know everyone knows you as this amazing scientist, but you're an overachiever, not only in the science world, but also an ultra marathoning world. How long have you been doing ultras for bill?

Speaker 4: (01:56)
21 years now. I ran my first ultra marathon 21 years ago.

Speaker 3: (02:00)
21 years ago. So may I give away how old you are?

Speaker 4: (02:04)
Yeah, please.

Speaker 3: (02:05)
It's a 66 so that makes what, 40 45 you started?

Speaker 4: (02:09)
Yes, but I, I've been running since I was 10 years old. I ran my first endurance race when I was 10 and then I ran cross country and track all through high school and college started running marathons in graduate school. And so I ran, you know, did a lot of marathons between 1981 and 1998 when 1998 was my, ran my first ultra marathon. Maybe it was 19, I'm sorry, it was 1996. I ran my first ultra marathon.

Speaker 3: (02:38)
Amazing. And you've been doing it ever since. And I know like we, we've both done, you know, the likes of death Valley. How many times have you run through the bed water ultra marathon?

Speaker 4: (02:49)
Twice. Twice. And that's probably going to be the, the most that I would never do it again. I both times, both times I thought the race actually wasn't that, but my feet got so blistered that the second, so I ran two years in a row and when I ran out the second year, my feet still hadn't recovered from the first year. And so after the second year, my feet were beyond recognition. They were so badly burned and blistered the bottom and it took so long to heal. I said, I am never doing that race again, just to,

Speaker 3: (03:24)
I found that my feet were actually great. I didn't even get many blisters, but I've got Mary faith, you see good native face. But I was taught, you know, like I found those extremely tough, extremely tough races, both of them.

Speaker 4: (03:40)
I acclimated by being in a sauna every day for an hour. You get into these hundred and 80 degrees saunas. And I forget if it's Fahrenheit or centigrade, but I think it's Fahrenheit. And the the first time you get in you, you can't even stay in for 15 minutes. But after like a month or two of doing that, every single day, you're running inside the sauna for like an hour, you know? And so it's really easy to get acclimated to the heat. And that made bad water easy for me. It's just that it wasn't no acclimation for the bottoms of my feet. That was the problem.

Speaker 3: (04:18)
Oh. And you've also done LA ultra, the high, another race that we have in common and now that incredibly tough race and very dangerous and exciting venture. And the first time, tell us a little bit your journey the first time, cause you did it the year before. I went and had a few dramas up there the first time around.

Speaker 4: (04:38)
Well, it was really exciting because I did it the very first year it ever existed and only three of us did it. Mark Cobain, Molly, my wife who wasn't my wife at the time and myself, nobody else that a lot of other people signed up, but they all dropped out only because they heard these stories from the Indian government saying it's impossible. A human cannot run at those altitudes for that distance. And so we were, you know, entering the unknown venturing into the unknown, trying to see what would happen. And now unfortunately on farm, I actually acclimated to the altitude really well with a device called Alto lab alt lab. And I know that Ray Sanchez later did it and I was the one that told Ray Sanchez about it. But I found out that the very first day I got there, I was able to go up to 18,000 feet and run with no problem at all.

Speaker 4: (05:32)
And so, so in that sense, I don't know if I might've been cheating or not, but that, that I didn't have to suffer like a lot of other people did. I actually ran over the first 18,000 foot peak. But the problem was, is that when I got to the lowest altitude, I suddenly started getting a really sharp pain and you know, just above my stomach and that area. And I asked, I thought it was because there was a lot of Smaug in downtown LA. And so I thought maybe something was happening there. So I had, I got into a car and asked him to drive me out so I could breathe some fresh air, but it just got worse. Now all of a sudden I said, get me to the hospital fast. And it turned out I had a gallbladder attack. And everybody says it was completely unrelated to the running.

Speaker 4: (06:23)
It just was really bad timing. So that year I only made it 50 miles. And then Molly, who was a ahead of me at the time, she ended up finding out that I was in the hospital when she had already done over a hundred miles. And when she heard, she started running and then all of a sudden she just realized that she'd lost enthusiasm, turned around and ran back and told the race director, take me to bill. So neither one of us finished that year, but fortunately Mark Cobain finished and proved it was possible. And so Molly went back next year and she finished it. I went back two years later and finished it. And then surprisingly, even though when I went back, I again at the lowest altitude, the race started, I started, I suddenly went to a walk when I was running down Hill and I thought, Hey, something's wrong. And I told the race director, you know, I need to see a doctor. Something's wrong here. A doctor came and checked me out and said, I'm perfectly fine. So I got up and started walking again. And as soon as I got out of this little village where I was, I started feeling good again and ran up the next mountain. And so I think it was, I was just having some allergic reaction to something in the air

Speaker 3: (07:38)
Actually. Cause we both, you know, I did it that second year and I really had big trouble with felt like someone had a fist right under my lungs right up in the, in the, in. I dunno, it felt like a sort of a stitch thing. So I had that trouble too. Going through lay from halfway down the down through lay and then out the other side for a long time. It felt like someone had a first of my stomach.

Speaker 4: (08:06)
Well, I felt like a nice, mine felt like a knife stabbing me. Wow. That's okay.

Speaker 3: (08:10)
No, if it's something to do with you know, going up and down and in the smoke was incredibly bad.

Speaker 4: (08:18)
The pollution in the air, because lay, even though it's way up in the Himalayas, there's no small control of everything. Every vehicle that goes by you is pushing out black smoke. Yeah. The second year when I ran it, the light, I wore a mask the whole way and I got a mask from LTL lab again. So it was a kind of a weird looking max. They had this thing where it covered my mouth, but it worked really well. And I never suffered any problems, but I still have the problems. Later on when I got out of lay and you know, like 40 miles later entered another little village and I forget the name of it, but it was a pretty much near the before just going up to the second Hill.

Speaker 3: (08:58)
Yeah, yeah. It was, it was a credibly brutal race. But you know, you guys were pioneers doing it the first year. And all I can remember is, you know, Molly didn't manage it that year because of the dramas, et cetera. And I thought, Oh, I'm going to be the first woman. I'm going to go, I've got to go, you know? And then when I got over there and there were four of us, four women and two guys, and I was going off for crying out loud and I thought it would be the only one that's quite peeved off at that.

Speaker 4: (09:23)
Well, let's see, I have the privilege of, I have the privilege of being the oldest person has ever finished and I think Molly is the oldest woman damaged and she's also the first American woman to ever finish. Yeah.

Speaker 3: (09:36)
Yeah. That was the first Kiwi woman and the second woman ever. So that was pretty cold behind Sharon Gabriel, who was an amazing athlete. But that was a, yeah, so bill, you, you've also done the backline marathons. Like there's something I like, who the hell takes on that craziness? Cause I wouldn't even it,

Speaker 4: (09:54)
That's the most exciting race on the planet. I know. Okay. You, you, you, the name of the show is pushing the limits, right? Well I believe in pushing the limits and doing it for fun. And the way that makes it fun is that, you know, I set my the highest goals possible, but I always adjust accordingly. You can't reach those goals. So whenever I finish a race, I've always accomplished something great. Even though I didn't come anywhere close to beating my original goal, I beat the latest goal that I probably said at 99 miles when I was in a hundred mile race. But that's the Barkley marathons. I like that you always go thinking I'm going to finish. And then then, Oh, let's see if I can, now I'm going to try to see if I can make one lap, which is 20 miles. And it's, I've done that race three times now.

Speaker 3: (10:50)
What was the furthest that you got?

Speaker 4: (10:52)
20 miles and that was, I could have gone further, but okay, so, well let me say the first two times only made it eight miles and he said is if you don't do the first eight miles in four hours, how could you not do eight miles? And if you don't do it in four hours, you'd have to disqualify yourself and go cross country back down to the Hill to the start, finish line. So that happened the first two times. And the third time I had it, I went early and practice on the course and learn the course. And cause a lot of the problem is hard to find your way. And a lot of times it's like, how do you get out of certain jams? There's one thing called son of a bitch ditch. Okay. And it's like you go down into this ditch and you can't get out of it.

Speaker 4: (11:36)
And so the third year I ran, I, I wore I took a grappling hook with me. I took a put on your shoes that let you walk on ice and I had Ninja claws and those work like beautiful. I jumped into that ditch and climbed right up the side, no problem. But and about 15 miles into the race, I encountered another runner lying on the ground, having some kind of heart attack or something like that. And so the, so all of a sudden my whole goal changed. And so we had to go over to mountain ranges to get to and help. So I carry, so I'd ran up to the top of one mountain, went, ran back down and got his pack here at his backup. Well, he called and then we did the same thing on the second mountain. And as a result, I didn't make the 20 hour cutoff in time in time, but it's the saying that he was going to talk to the race director about letting me go on. Anyway, I explained, I said, no, no, cause I didn't want, I didn't want the race direction. I know what happened to that guy. You know, it's like that would have made too much bad press for him. He, unfortunately, that guy recently passed away right after running a different race. That was also a cold.

Speaker 3: (12:54)
Obviously some, probably some heartless shoe or something going on. Yeah. But the Barclay marathons people are you can see it on Netflix and a few other places that it is the most craziest, stupidest, amazing race steerers. And there's only like, I think, is it seven or eight people in the history have ever completed it?

Speaker 4: (13:12)
Something like that. And it's been 30 years, 30 years. Yeah.

Speaker 3: (13:16)
Yeah. So when you say he got to the 20 mile Mark, that means something even, you know what I mean? Like it's not, I've seen people do North burn a hundred milers, really, really tough race here. I race over here and go to Barclay and not finished the first round. You know, it's that tough. But yeah,

Speaker 4: (13:33)
You are my number one goal to finish that race though.

Speaker 3: (13:36)
Really still. Oh my God. Oh well they were actually, that's a good segue because to do that you're gonna have to turn you know, keep yourself from aging. Cause and this has been the focus now of your your academic and science career for the last, what's basically your whole entire adult life has, has it not,

Speaker 4: (13:56)
Well, since I was 50, 55 years, 56 years, cause it was, I was 10 years old when my father first put the idea in my head and I just

Speaker 3: (14:06)
They, you know that you've been on this anti aging machine mission for 55 years.

Speaker 4: (14:12)
He knew that he, he observed that I was very interested in medicine and science. My science teacher at my elementary school was telling my parents, his kids just unbelievably interested in it's kind of stuff. Then one day I was out in the front lawn of our house looking through a telescope and my father came out to the lawn and just said, Hey, you know, bill, since you're so interested in medicine and science, when you grow up, you should become a doctor and find a cure for aging. And he said, he said, I don't know why nobody's done that yet. And it was like, I thought, well, that sounds like a great idea. I'd love to do. And so I, I became interested in that from, from that moment. And I just spent years and years actually following everything I could all through high school, college just trying to figure out what was the secrets to aging. And it wasn't until the early 1990s I really found what I thought solved everything. And that was the tips of our chromosomes are actually a clock of aging.

Speaker 3: (15:15)
So this is the, the telomeres, the famous. So this discovery that this was actually discovered a, I believe in the 1950s while the Russians telomeres themselves, is that correct?

Speaker 4: (15:25)
Actually, telomeres, telomeres were discovered in 1940s by all, I'm going blank on her name, Ruth. I remember her first name is Ruth, but I can't remember her last name, but a scientist, she discovered Tila Merz and then Elizabeth Blackburn and Carol Greider and Jack SOSTAC discovered that they don't short. Everybody was saying, Sheila, mirrors need to shorten. Okay. Because everyone, whenever cell divides and the chromosomes are duplicated, there was no mechanism known inside of a cell to actually duplicate the very ends of the chromosomes. So every new chromosome is going to be shorter than the old chromosome. And, but it was Blackburn Greider instill stack that observed that they didn't shorten in a pond scum organism called Tetrahymena. And so, so they, they speculated there had to be some enzyme, which they called telomere terminal transfers, and they discovered some aspects of it and more specifically what's called the RNA component.

Speaker 4: (16:39)
But they never connected the dots to anything related to aging or cancer. They just, they were just studying this mechanism. It was later on when a guy named Calvin Harley wrote a paper speculating that maybe this is the clock of aging and, you know, so I met Kel Harley because he was like minded with me. He didn't believe in all the theories. They didn't make sense about agent. We both believed that there had to be some kind of clock chicken inside of ourselves. And this was the only thing that ever was discovered there could be that clock. And so when I talked to Cal, I, I asked him if anybody has figured out a way to lengthen them, because if it is the clock of aging, the way to prove it is to lengthen them and see if cells get younger.

Speaker 4: (17:26)
And he said, no, nobody's been able to figure out how to lengthen them. They've, they've been working on it, including Blackburn and Greider who had been with the ponds, gum organism, but nobody had been able to figure it out. So he hired me. I had a background already in a lot of big blockbusters in biotech. And so he hired me to work on it and I ended up discovering this enzyme called telomerase, which is, which is to Amir terminal transfers, but we didn't call it that. We call it Walmart's instead after only three months.

Speaker 3: (18:01)
Here was this boat, cause this is,

Speaker 4: (18:03)
That was, that was, well let's say first writer and still stacking Blackburn first discover the tumors don't shorten in the mid 1980s but Nope, they didn't put any significance to it. And then I ended up discovering human telomerase in 1992 I think was maybe 1993. Then showed that when, and it turned out to long races, only produced in our reproductive cells. And that's why our children are born with Tila mirrors just as long as ours.

Speaker 3: (18:40)
So let's, let's take a step back and, and just walk through the science so that because you know, like this is for you second, you know, second nature. And for most people it's like, what the hell? What are they going to tell him? Yeah. so I'll try and put it in layman's terms and you correct me where I'm wrong. So all of our cells, every cell in our body replicates itself. And before it dies, it, well, every cell knows it has to replicate itself before it dies. When it goes to replicate itself each time, it's like a poor photo copy. There's a slight difference from the original. And the difference is the telomeres. Now the telomeres are, you use the analogy of the sh the plastic at the end of shoelaces. And if the shoelace replicated itself each time, that little bit of plastic at the end that holds it all together gets shorter and shorter and shorter till it gets to the point where it's so short that the shoelace unravels basically.

Speaker 3: (19:38)
And so that shoelace on reveling represents the helix within the chromosome with our DNA then starts to unravel. And this is when we die. So from what I understand, we are born with telomeres length of 10,000 bases. Correct. At the end of our chromosomes, which are around hundred thousand bases, is it a hundred million? So it's very, very tips of these. So, so what people need to understand is that these telomeres replicated each time, but they get shorter and shorter as we age. And that's what's causing, so it's like a poor photocopy every time we were replicating ourselves, we're replicating Alyssa. But that doesn't happen in our reproductive, is that, is that clear?

Speaker 4: (20:24)
Yes. No, that was, that was really good. I, I sometimes explain it that way too, but clearly you've done your homework but you understand it very well. Yeah. And yeah, that just doesn't happen in our reproductive cells and it's just, it, it makes sense that it shouldn't, it couldn't that cause we would not be, we'd be extinct cause our chromosomes would be so short.

Speaker 5: (20:48)
We couldn't exist.

Speaker 3: (20:50)
So our babies are born with a full length telomere on each cell. So I answer a question for me that I've been thinking about the last few days. You know, Dolly, the sheep that was cloned, that was cloned and, but it was the same age as its mother when it was born. Correct. Because it wasn't, didn't have this, this telomerased actually doing its job. So reproductive cells. So answer me one more question and this is a very personal question for me right now because I've been, we've been trying to have a child and the problem that I've got is I'm an old, I'm very old, I'm 49 and the doctor's going, your eggs are old. If our reproductive system doesn't age, why am I eggs too old?

Speaker 5: (21:43)
Because of damage from environment. So and, and it's not, you know, it's, it's actually kind of incorrect to say that the eggs are old. It's the eggs are, are more depleted. Okay. It's you know, when you, when you, you're, every woman is born with a 450. Eggs are cells that are destined to become egg cells and reaches puberty. She starts to lose one, one a month and a 450 months later she loses her last one. And that's when she enters menopause. Okay.

Speaker 3: (22:20)
Thousands of eggs or millions of eggs in there.

Speaker 5: (22:23)
Well there, there's, there's a lot of cells in there, but most of them are actually there to just nourish the other, the other cells that are actually destined to become excels. And, and so, so that's, that's really a problem. I, I've never considered menopause, an aging related thing. It's just correlated with aging, but it's more of a counting mechanism. And, but you know, the solution is, is actually very near and that's, that's companies like by all time B I, O. T. I, M, E they're working on making it so that they can turn your skin cells into egg cells using what's called induced plural potency. And that way, even when you're 70 years old, you could probably have a child that's right around the corner. Yeah, that's right around the corner.

Speaker 3: (23:16)
Oh, can I get myself on the list? I'll be the first one to experiment.

Speaker 5: (23:20)
Yeah. Well, it's, it's, I forget their exact website, but if you do a Google search for bile time and they're located in Alameda, California, in case there's more than one bile time in the world. And the, the main guy who runs, who's the president of the company is Michael West who just happens to be the guy that hired me at Geron corporation. He used to be the founder who was a founder and president of Geron corporation

Speaker 4: (23:46)
Where I discovered telomerase.

Speaker 3: (23:48)
You'll have to introduce me, see if he can recharge my eggs in some way, shape or form. But open all jokes aside, you know, is, I, I've, I've, I've heard you speaking you know, you, you've, you've worldwide media attention for the breakthroughs that you and your company, Sierra sciences has had. I know that you have gone through over, well back a while ago, it was 300 and something thousand compounds to try for LinkedIn to find the enzyme that turns on the telomere res or

Speaker 4: (24:23)
It was not an enzyme to find a molecule that will get into our cells and induce ourselves to produce the enzyme telomerase. Right?

Speaker 3: (24:32)
Right. So this is like a switch that we obviously have with our reproductive cells that is, Oh, it's in the cell, but it's not turned on, on the rest of our somatic cells. Only in our reproductive cells. So in our reproductive cells, our it is turned on. And so when a reproductive cell duplicates itself, so when the baby's developing inside the womb, it is making a complete and proper copy of each cell without the shortening. Is that correct?

Speaker 4: (25:04)
Yes, that's exactly correct and reality and more accurate, but probably overdoing it here. When when a reproductive cell divides, the telomeres do get a little shorter, but then the long race really lengthens them. Okay. So divides again, it gets shorter and then telomerase, Sri Lankans them. So I often compare it to like a tug of war. You've got things shortening and LinkedIn going on at the same time and your reproductive cells.

Speaker 3: (25:29)
One of the questions that I've been thinking about in the research is if you can lengthen telomeres, okay, you found the breakthrough, you're, you're lengthening the telomeres. How can that actually reverse the damage already done to the genetic the actual helix, the way they are with the DNA and the chromosome? How can I it

Speaker 4: (25:50)
It can't, but cells that have damage are eliminated from the body when there are other healthy cells that can replace them. And that's something, you know, a lot of people overlook when they talk about how, you know, you've got to solve the damage problems, but, but if the damage has no negative effects on the cells, so what, but if it does have negative effects on the cells, that it probably makes them grow slower and unhealthier and less able to compete with other cells. And so you can eliminate them. But if you, if you view the other cells in your body have short telomeres, they lose the ability to replace those damaged cells. But yeah, when we do experiments in the vitriol and the Patriot dish, and we have a mixture of damage cells and undamaged cells, after, you know, a few months of culturing that damaged cells are gone. You know, the healthy cells take them off,

Speaker 3: (26:40)
They take over. So you get enough, it takes a for them to get through this process because in the laboratory, you've, in the Petri dish, you've turned a skin cells, oldest skin cells into infant skin cells. Correct. And you can hold, you can, you can keep human cells alive and definitely they don't age within the Petri dish environment. That's my motto. Hence the title of your, your documentary, which has worldwide famous documentary. The Immortalists. So you've also, I know that you gave some compounds to Harvard university, correct. That they did some Bret studies while back.

Speaker 5: (27:26)
Yeah. We didn't actually give them any compounds. What they did is they, they licensed the telomerase gene from Geron corporation where I was working and, and with the idea that they were actually thinking that telomerase would cause cancer. So they were, they put them in, put the, they did off a gene therapy way of introducing plumbers to the mouse cells, all the cells of the body. And we're were shocked when the, when the mice didn't get cancer, actually, the rate of cancer decreased. Which is something I, I'd always been saying that keeping two of them as long as the best way to prevent and fight cancer. But to his surprise, after three weeks, he saw what he calls a remarkable reversal of the aging process. He saw all the mice get younger in every way imaginable, which nothing else on the planet has ever done.

Speaker 5: (28:21)
That everything you hear about resveratrol and NAD and all those other things, they, they, they may make improve the energy of an animal, but they never reversed everything about Asia. And that's what, 200 then that's the best I call support of concept that we've ever seen for the idea that telomeres are the clock of aging. But, but he was really blown away. And Diane Sawyer did it. She's a newscaster. I don't know if you know her. Zeeland is very good. She did an interview of him, which is really remarkable. And a lot of times in my presentations I show that interview because I was so excited about the fact that somebody proved what I was 99.9% certain to be the case. And now we just gotta get in humans,

Speaker 3: (29:07)
These pumps, these old mice turned into younger mice in every way imaginable. Parameters even disappear. The dummies, the brain size returned to normal herding heated. They had a gray here. They're all the things that are associated with aging and mice. They are basically everything reversed.

Speaker 5: (29:29)
Yeah. But th not just their brain size, their brain cognitive functions came back, which has really gotten a lot of people now when I attend medical conferences, I find everybody's saying like dementia and, and things like that isn't a loss of memory. It's a loss of access to the memory and memories somewhere stored in your brain. And when you get Alzheimer's, you lose the connections that get access, that memory. So by lengthening the telomeres, it appears that it is very likely that that length and sealant marriage restores access to that memory. So I, I believe that we actually have a clinical study underway right now to test Alzheimer's patients to prevent, see if we can prevent Alzheimer's.

Speaker 3: (30:13)
Oh my gosh. So, so this is not just for anti aging as an, you know, we were going to live longer, but we're going to be living healthier in the future. So all these degenerative diseases, these horrible,

Speaker 5: (30:25)
Every, every person in the world that's working on trying to cure aging is not just trying to make us live longer without us being healthier. The goal of everybody is there's no point in living longer if you're not living healthier. So we've got to live healthy longer. That's, that's the goal. And reverse declining health as well as aging.

Speaker 3: (30:44)
So how far away, I mean you have gone through over, I don't know how many hundreds of thousands of compounds now that help turn the human Telemark raise a hundred dollars. 500,000. Nowadays. My gosh. So every day you've got a robot robot in your laboratory that's testing all these compounds, these compounds that you're putting together. These are synthetic compounds or chemicals.

Speaker 5: (31:06)
Yeah, maybe for the first, like 200,000 and we were doing chemicals or random. Yep. We ended up discovering something like 900 different chemicals and we were able to, that actually did induce telomerase in like we testing fiberblast cells, which is a cell inside the skin. Yep. So these 900, we looked at the structures of all these 900, and we're able to divide them up into 37 different families. Okay. Cause there were some, a lot of them look very similar to each other so we could build them into 37 families and know since then we've been doing what's called medicinal chemistry instead of just taking chemicals, a random, we've been designing our own chemicals based on the structures that we learned to, to increase, decrease toxicity, some of them. So you know, some of the ones we discovered at random had severe toxic side effects. But then we were able to get rid of that toxicity by doing medicinal chemistry. And our, our best chemical to date is something called Tam eight one eight. Yep.

Speaker 3: (32:14)
So it was explained the name there. Cause you explained it to me before and I thought that was just like,

Speaker 5: (32:19)
But the name, the name of it was Caesar three one four eight one eight because that was our 314818th chemical. We tested and we licensed that to a company called defy time and they didn't like that name. So they changed it to Tam, which stands for telomerase activating molecule eight one eight

Speaker 3: (32:42)
And this is a proven actual compound that is available on the market today that will influence the aging. How potent is that compound?

Speaker 5: (32:54)
It's not potent enough to make an 80 year old become a 24 year old. Okay. And we are working on developing things that are potent enough to do that right now. In fact, we have one in clinical studies right now. But Tammy, when we estimate is about six foot lower in potency than it takes to turn an old person into a young person.

Speaker 3: (33:20)
Why there?

Speaker 5: (33:21)
Yeah. So I mean that's, that's one sixth of the way there is way close. Okay. Cause we, when like years before we discovered Tam, eight one, eight, we had other chemicals that were maybe a hundred fold less and then a 20 fold less and tenfold less. And then we got to six. And but we, we kind of shifted gears because some new technology was developed. The technology of gene therapy wasn't new, but there was a new type of gene therapy that was discovered that had absolutely zero side effects. And so we employed that gene therapy to start delivering the gene to cells in the body. And we have in the laboratory just been able to reverse aging in every way imaginable and human cells. And so that, that gene therapy has been our approach right now because that is, when I say that family one eight is six fold less than the potency needed to reverse aging.

Speaker 5: (34:27)
This gene therapy is 30 fold higher than what we need to reverse aging. And so unfortunately, it's super, super expensive. I mean really millions of dollars to produce enough to treat one person once, but a company called Livella, L I V E L L A Livellla gene therapeutics licensed this from us and they got approval to do a clinical study and they are clinical study is underway right now. So I'm really excited. I'm a spectator just like everybody else. But I'm real excited because for the first time ever we will actually get to see if, if all my ideas for the last 25 years are real or not are true

Speaker 3: (35:15)
By then take this to market. Why? Why did you get another company? So your Sierra sciences does just the research also thing and then you pass the ball to someone who can actually bring it to market or get the clinical trials. In this case going, and this is what clinical trials on actual humans, not human cells in a Petri dish. This is, yeah. Yeah.

Speaker 5: (35:36)
So, so

Speaker 3: (35:38)
The reason why we didn't do this ourselves is because from day one, when we first started, when I first started this company in 1999, my business model was we would never become a marketing company because every company like mine, as soon as they get a product on the market, they suddenly quit doing science and an afternoon. So they hire all these business people and the top scientists suddenly lose control. And next thing you know, all the scientists are fired and the company is just becoming a marketing company. So I just, I want to keep us doing research, I want to complete our goals, and we are licensing every discovery that we make to other companies that then market them and they pay us a royalty and that the royalty is a hundred percent of that protein goes into the research. So that's how we get our money. Yeah. And whittling away at this problem. So this, this compound that is now being tested, that is 34 fold stronger than Tam, eight one or actually 34 fold stronger than actual reversal of aging.

Speaker 5: (36:41)
Yeah. So it'd be 30 times six, so 180 200 times more potent than Germany when it, but it's not a compound, not a compound. It's a gene therapy, which is a very different, it's, it's, I compare it to like a soap bubble and inside the soap bubble is the gene for telomerase. And when that soap bubble comes in contact with a cell, which you think of the big cell as another cell bubble. But when they come in contact, they fuse and become one. Just like any kids ever seen blowing soap bubbles in the air. They, when they bump into one show, they become one. And so that's so it delivers the gene to the cells and the gene is on, it's, it's switch is turned on so that as soon as it gets in cells, it starts producing telomerase.

Speaker 3: (37:29)
How did, how do they get the delivery to every, and we're getting technical here, but how do you get the delivery to every single cell in the whole of our billions of cells?

Speaker 5: (37:38)
But that's the beauty of our bodies is that every single cell of our body has to get nutrition from our blood. So any, so you put anything in the blood, it gets to every cell of the body. Now there's some like brain cells where there's some blood brain barrier where they don't get there, but it turns out this gene therapy, it gets there too. Oh my gosh.

Speaker 3: (38:00)
Yeah. Yeah. I mean the blood brain barrier. I've been fighting with mum, mum and her case with the aneurysm and using hyperbaric oxygen therapy to get through that rod brain barrier. But so what do you think, do you think it isn't within your grasp or within the grasp of these other companies? Never now licensing that we will within our lifetimes or within the next 10 years, have products there can stop us from aging and if we can, as they're only going to be available to the super, super rich, or is the products available now that have this term eight one eight that we can, the general public can get access to?

Speaker 5: (38:44)
Well, I believe that the very first person's actually going to get treated crawly in may. Let's say we were shooting for March, but there's been some things delaying us, but I would say that, you know, when we get through our delays, Labella will then treat the first patient by probably may of 2018 and I expect that we will see age reversal before the end of this year, if not in less than three months afterwards. So, well, well within our lifetime, but as you said, unfortunately this is something only the super, super wealthy can afford and that's what Labella is a business model is the clinical study is so expensive that no company in the planet could actually afford to do it. But if, if there are people that are really suffering from what I call okay. So some type of disease or something like that that's going to kill them because of tumor shortening.

Speaker 5: (39:49)
Yup. And then if they're super wealthy, it's really to their advantage to pay whatever it costs, even if it's five, $10 million because it'll save their life. Okay. Now, if I was, if I was a multi multimillionaire and I was told that I was gonna die within like a, a year because of something due to short telomeres, I would sign up for this in a minute. Now, I'm not super wealthy and one of the reasons why I haven't done this on myself is I can't afford to make enough to do the treatment. But believe me, as soon as we get some of the patients signed up and we start getting Labella starts putting on the market and we start getting royalties you believe I can, I'm going to get this done on myself as soon as possible. Like I'm already solve most of the problems, but I, I'm, I'm just excited about the idea.

Speaker 3: (40:47)
Yeah. Yeah. It actually, for you and for your family and for your friends and for everybody that's listening, you know, you're like, this is the hope. This is the hope that we're going to be able to.

Speaker 5: (40:57)
This is the only reason. My whole goal in life right now is to do this. And so I'm, I, I'm just excited as, as I said before, I'm a spectator, like everybody else, but I am just, I can't wait to see what happens with the first patients.

Speaker 3: (41:10)
Yeah. Oh, this is, this is, this is going to be really, and we'll have to do a, another interview in a, in a year's time to see where that exactly is at and what's happening with it and how it's gone. Is there any downside to this lengthening of you? See it, it's, you were, I remember an interview you talking about cancer and there was some discussion is, is this gonna actually make cancer worse? And you said in your belief it wasn't as he rather any other downside to this human telomeres. Why hasn't the universe tuned this arm? Why hasn't nature made this available to us so that we don't age? What's your point?

Speaker 5: (41:48)
Well, there are several questions there, but first, first, let me say that the cancer, there are people saying that this is going to get everybody cancer. But that's all hearsay. There's no data supported. And there's for every study that's ever been done that even suggest possibly that there might be a cancer issue. There's over a hundred other papers showing that telomerase actually prevents cancer and fights cancer. So, so people not taking this therapy are going to be at a higher risk of cancer than people that do take the therapy. And then so the other question was why did nature not give this to us? This is something that, it's common sense, but a lot of people never think this way until it's actually explained in order for, from an evolutionary perspective, in order for any kind of species to survive, it needs to be able to shuffle its genes.

Speaker 5: (42:44)
Okay. And that's why we always have to a male and a female bridge to produce an offspring because that creates a randomness of jeans. This never existed every time anybody's born an animal or humans born. Yep. Okay. So in order for the shuffling to occur, it's important that the offspring interbreed with each other. Okay. And if, if the old never die, then the offspring would never be able to survive. I mean the, the offspring could never compete with the old people, so, or the old animals. So every species, and it turns out there's a multitude of ways that different species have done this. Every species has to figure out a way to knock off the old after the old have raise their young. Okay. So once, once the, once any animal has raised this young, it's only in the way it's better for the survival of the species that that person or animal is, is removed from the population by finding some way to kill it off.

Speaker 5: (43:51)
Okay. Now it turns out humans, dogs, cats, horses, sheep, pig and deer. All did that by Sheila or shortening. Okay, so we are, we and the other animals I just mentioned are designed so that our Amir has give to a critically short length, just about the same age as when we'd finished raising our young. Yep. Okay. Now other animals like rodents, mice and rabbits and things like that, they don't have chillum or shortening. They do it by what's called oxidative stress and mitochondria dysfunction. The experiment that was done as you, you're talking about at Harvard on mice that was actually done by on engineered mice that were engineered to age like humans with Tila machine, which was unheard of in most world. It's probably to great. Yeah. What about Aubrey degree?

Speaker 3: (44:46)
Was that his work? Is that his work? The my mitochondria dysfunction and yeah,

Speaker 5: (44:52)
So, so now I believe that mitochondria dysfunction and oxidative stress do impact humans


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