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Let's get into telomeres, right?
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So one, how'd you end up starting to study telomeres?
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Like how did they come onto your radar, right?
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Because you are on a boy, now man on a mission to solve aging and this lands in your lap or you seek it out.
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And then, you know, what are, like, let's dig into what are telomeres and, you know, more.
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Yeah.
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When I was still in college and I had my anti-aging clubs, we would discuss what's causing aging.
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And,
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Nothing made sense.
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I always say all the twos and twos have to add up.
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The environmental kind of things wouldn't explain why dogs and cats age at a different rate than humans or why people at the North Pole and South Pole age at the same rate as people who live on the equator.
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There's just too many things that didn't make sense.
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The Hayflick limit was announced in 1961 that human cells can only divide a certain number of times.
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And most people,
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Boo-ha-ha'd it.
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Didn't believe it.
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But we actually decided, boy, this actually makes a lot of sense.
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And it was the only thing that ever came along that explained all the twos and twos about aging.
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But here's the thing.
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How could a cell know how many times it has divided?
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How many times it has left to divide?
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When cells don't have brains, they can't count, stuff like that.
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So we concluded when I was still in college that,
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that there had to be something like ride tickets at an amusement park.
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Okay, that every time a cell divided, it lost a ticket.
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Just like when you go to a ride, you go to an amusement park, your parents give you tickets.
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You can look at, you can,
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count the number of tickets you have, things like that.
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But the most important thing is when you lose your last ticket, you can't go on any more rides.
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So we thought something in cells was like that.
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But what was that?
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We couldn't think of any biochemical mechanism that was those ride tickets at an amusement park.
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But we also couldn't think of any other biochemical mechanism besides ride tickets at an amusement park.
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It had to be that way.
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So when I got to graduate school, when I got my PhD and I applied to every anti-aging lab in the world and got accepted to them all and to do my postdoc work, and I went and interviewed them to see if I wanted to go there, none of them made any sense.
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And so I just decided they didn't believe in this ride tickets and amusement park idea.
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And so I went into biotech instead.
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But then I want to say,
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12 years later, my father and I were at this conference, and I heard somebody talk about the fact that telomeres shorten every single time a cell divides.
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And that guy was Dr. Calvin Harley, and he had just been hired as the chief scientific officer at Geron Corporation.
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And I went up to him before he even got off the podium, and I said,
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has somebody figured out how to add more ride tickets back?
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Because that would be, from my scientific training and stuff like that, to prove something, you've got to reverse it.
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Then you've got to do a process called extinction where you unreverse it, things like that.
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And so I thought if somebody could figure out a way to re-lengthen the telomeres or add ride tickets back, that would provide proof that telomeres had something to do with aging.
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And he said, no, we've been working on it for years, have had zero success at all.
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We've been collaborating with labs all over the world and haven't had any success at figuring that out at all.
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And I just said,
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Let me come and work with you and I'll have it figured out in three months.
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And shortest job interview, he let me do it because I'd already had a very successful career in biotech, being an inventor of a lot of the big blockbusters in cancer, heart disease, inflammation, all kinds of different things.
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Dwarfism, multiple sclerosis.
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So I had a pretty successful career.
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So he offered me the job and three months later, my team discovered human telomerase.
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And we then right away did the experiments that everybody always dreamed of doing.
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And that was we put it into human cells in a Petri dish and showed that they not only stopped aging, but their aging was reversed by every method of measurement imaginable.
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And it totally abolished the Hayflick limit, which is the limited number of life times the cells can divide, which proves that telomeric shortening is the cause of the limit on our lifespans.
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We then grew skin on the back of a mouse, human skin on the back of a mouse, and showed that telomerase reversed aging in every way imaginable there too.
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And then Dr. Ron DePinnell, using our technology,
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created, he had already created engineered mice that I mentioned mice don't age by telomer shortening, but he created a mouse strain that did.
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And these mice would get old just like humans get old, and you could see all the changes.
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But he was able to introduce telomerase and show that they had what he called a remarkable reversal of the aging process.
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And that's a quote from an interview that Diane Sawyer did with him that anybody can Google and find.
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Diane Sawyer and Dr. Ron DePinnell, telomere biology, and they can find the study where he actually shows these mice having real age reversal.
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How was he introducing telomerase?
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So you've got an animal model, potentially easy in a petri dish, you could correct me.
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But now you're actually trying to introduce it into the animal to ostensibly have some systemic availability and impact.
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The way that Dr. Rhonda Pennell did this was...
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Okay, so I've been an expert in gene therapy since the 1970s, mid-1970s.
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In fact, I wrote a thesis when I was still an undergraduate on how to cure Tay-Sachs disease using gene therapy.
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And almost, you know, went to work in a gene therapy lab at UC San Francisco with Mike Bishop.
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So when we first discovered telomerase, the very first thing I did was to create telomerase.
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gene therapies, gene therapies for delivering the gene.
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So when I say that we added telomerase to cells in a petri dish, we infected the cells with a virus that carried the telomerase gene in, and the gene was turbocharged.
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This is one from my molecular biology.
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I learned how to really turn on genes to the maximum.
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insert the turbocharged telomerase genes into the cell, so they produced a lot of telomerase.
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That's why we saw the reverse ovation.
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So that's what Dr. Rana Pennell did first too, but he first had to engineer mice to make it so that they did have telomer shortening, because mice, rabbits, rodents, and most, and a lot of animals have telomerase already produced in all their cells, okay?
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They don't have telomer shortening,
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And so he had to first create a mouse that didn't have telomerase produced, so he shut off the telomerase gene.
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Telomerase got really short, and then he started seeing these mice start aging just like humans, male pattern baldness, all kinds of things similars.
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Then he used the gene therapy to reintroduce telomerase to the cells and saw what this remarkable reversal of the aging process, hair color, hair coming back,
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The biggest surprise was mice being able to remember how to go through a maze again, the mice that were suffering from dementia, maybe something similar to Alzheimer's.
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Now when I go to medical conferences, especially brain disorders and things like that, I hear everybody saying that Alzheimer's and other forms of dementia are most likely not the loss of memory.
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They're a loss of access to the memory.
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and telomeres, lengthening telomeres might restore that access.
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So I actually have a clinical study in clinicaltrials.gov where I'm trying to get a clinical study started to actually look at lengthening telomeres as a way of curing Alzheimer's.
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Unfortunately, gene therapy is very expensive.
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It may cost a million dollars, it cost me a million dollars to treat one person once.
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And it's also risky.
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Okay, so we would only do it on people that had no other choice.
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But so that's what Dr. Rondopeno did.
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He used gene therapy, delivered the thalarmus gene to the mice and saw that remarkable reversal of the aging process.
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Okay.
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So before he's genetically modified these mice so that their telomeres shrink, I mean, mice do age, right?
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Like they don't age via telomere shortening, right?
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They age.
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Do we understand the mechanisms that they tend to age in?
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I don't think we totally understand it, but we do know that they have extremely high oxidative stress and high mitochondria dysfunction.
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And so those are probably playing a role, but they're way, way higher than humans.
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And so I think the only people that actually...
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So that's, I'm sorry, that supports your idea that if we solve this telemorphic shortening, we may just be pushing out to the next problem, right, which might be this oxidative stress, which is the thing that ultimately takes out a lot of other animals.
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Yes, and it does take out a lot of humans that lead poor lifestyles.
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Okay?
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Yeah.
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So if you take your antioxidants and you live an antioxidant lifestyle, same with anti-inflammatory lifestyle, telomere shortening is the thing that's going to get rid of you, not oxidative stress and mitochondrial dysfunction or inflammation.
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But yeah, that's how a lot of it happened.
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Now, my company,
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Since gene therapy is risky, there's been a lot of clinical studies done on gene therapy where half the people in the study died because of the gene therapy causing cancer.
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Most gene therapies integrate into the chromosomes randomly.
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And if they integrate into a gene that is like a tumor suppressor or oncogene, they will give that person cancer.
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And that's what happened.
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In fact, it's one of the reasons why I really frown on the FDA, the fact that they even allowed such studies to happen, because anybody with a molecular biology 101 background will know that gene therapy with a virus that integrates into the chromosome is going to give, and integrates randomly.
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is going to give that person cancer almost for sure.
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And that's exactly what happened.
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And the fact that the FDA approved it, it makes me very disapproving of the FDA on that kind of stuff.
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I often will say at conferences that I don't,
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think the FDA is qualified to be overseeing safety.
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I think that falls under the shoulders of the principal investigators, things like that.
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But and then you can't even trust all of them.
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Yeah, as it turns out in some cases.
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Yeah.
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I hope you enjoyed this episode of the Live Beyond the Norms podcast.
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Make sure to subscribe and follow.
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Also, make sure not to be that guy, the guy sharing this podcast with people who are not interested in living beyond the norms.
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If you would like to learn more about the ESS60 molecule, the molecule responsible for the single longest longevity experimental result on mammals in history, a full 90% extension of life, visit myvitalsea.com.
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That's myvitalsea as in carbon.com.
1
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Let's get into telomeres, right?
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So one, how'd you end up starting to study telomeres?
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Like how did they come onto your radar, right?
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Because you are on a boy, now man on a mission to solve aging and this lands in your lap or you seek it out.
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And then, you know, what are, like, let's dig into what are telomeres and, you know, more.
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Yeah.
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When I was still in college and I had my anti-aging clubs, we would discuss what's causing aging.
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And,
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Nothing made sense.
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I always say all the twos and twos have to add up.
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The environmental kind of things wouldn't explain why dogs and cats age at a different rate than humans or why people at the North Pole and South Pole age at the same rate as people who live on the equator.
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There's just too many things that didn't make sense.
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The Hayflick limit was announced in 1961 that human cells can only divide a certain number of times.
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And most people,
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Boo-ha-ha'd it.
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Didn't believe it.
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But we actually decided, boy, this actually makes a lot of sense.
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And it was the only thing that ever came along that explained all the twos and twos about aging.
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But here's the thing.
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How could a cell know how many times it has divided?
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How many times it has left to divide?
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When cells don't have brains, they can't count, stuff like that.
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So we concluded when I was still in college that,
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that there had to be something like ride tickets at an amusement park.
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Okay, that every time a cell divided, it lost a ticket.
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Just like when you go to a ride, you go to an amusement park, your parents give you tickets.
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You can look at, you can,
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count the number of tickets you have, things like that.
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But the most important thing is when you lose your last ticket, you can't go on any more rides.
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So we thought something in cells was like that.
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But what was that?
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We couldn't think of any biochemical mechanism that was those ride tickets at an amusement park.
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But we also couldn't think of any other biochemical mechanism besides ride tickets at an amusement park.
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It had to be that way.
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So when I got to graduate school, when I got my PhD and I applied to every anti-aging lab in the world and got accepted to them all and to do my postdoc work, and I went and interviewed them to see if I wanted to go there, none of them made any sense.
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And so I just decided they didn't believe in this ride tickets and amusement park idea.
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And so I went into biotech instead.
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But then I want to say,
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12 years later, my father and I were at this conference, and I heard somebody talk about the fact that telomeres shorten every single time a cell divides.
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And that guy was Dr. Calvin Harley, and he had just been hired as the chief scientific officer at Geron Corporation.
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And I went up to him before he even got off the podium, and I said,
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has somebody figured out how to add more ride tickets back?
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Because that would be, from my scientific training and stuff like that, to prove something, you've got to reverse it.
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Then you've got to do a process called extinction where you unreverse it, things like that.
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And so I thought if somebody could figure out a way to re-lengthen the telomeres or add ride tickets back, that would provide proof that telomeres had something to do with aging.
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And he said, no, we've been working on it for years, have had zero success at all.
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We've been collaborating with labs all over the world and haven't had any success at figuring that out at all.
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And I just said,
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Let me come and work with you and I'll have it figured out in three months.
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And shortest job interview, he let me do it because I'd already had a very successful career in biotech, being an inventor of a lot of the big blockbusters in cancer, heart disease, inflammation, all kinds of different things.
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Dwarfism, multiple sclerosis.
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So I had a pretty successful career.
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So he offered me the job and three months later, my team discovered human telomerase.
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And we then right away did the experiments that everybody always dreamed of doing.
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And that was we put it into human cells in a Petri dish and showed that they not only stopped aging, but their aging was reversed by every method of measurement imaginable.
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And it totally abolished the Hayflick limit, which is the limited number of life times the cells can divide, which proves that telomeric shortening is the cause of the limit on our lifespans.
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We then grew skin on the back of a mouse, human skin on the back of a mouse, and showed that telomerase reversed aging in every way imaginable there too.
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And then Dr. Ron DePinnell, using our technology,
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created, he had already created engineered mice that I mentioned mice don't age by telomer shortening, but he created a mouse strain that did.
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And these mice would get old just like humans get old, and you could see all the changes.
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But he was able to introduce telomerase and show that they had what he called a remarkable reversal of the aging process.
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And that's a quote from an interview that Diane Sawyer did with him that anybody can Google and find.
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Diane Sawyer and Dr. Ron DePinnell, telomere biology, and they can find the study where he actually shows these mice having real age reversal.
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How was he introducing telomerase?
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So you've got an animal model, potentially easy in a petri dish, you could correct me.
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But now you're actually trying to introduce it into the animal to ostensibly have some systemic availability and impact.
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The way that Dr. Rhonda Pennell did this was...
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Okay, so I've been an expert in gene therapy since the 1970s, mid-1970s.
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In fact, I wrote a thesis when I was still an undergraduate on how to cure Tay-Sachs disease using gene therapy.
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And almost, you know, went to work in a gene therapy lab at UC San Francisco with Mike Bishop.
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So when we first discovered telomerase, the very first thing I did was to create telomerase.
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gene therapies, gene therapies for delivering the gene.
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So when I say that we added telomerase to cells in a petri dish, we infected the cells with a virus that carried the telomerase gene in, and the gene was turbocharged.
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This is one from my molecular biology.
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I learned how to really turn on genes to the maximum.
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insert the turbocharged telomerase genes into the cell, so they produced a lot of telomerase.
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That's why we saw the reverse ovation.
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So that's what Dr. Rana Pennell did first too, but he first had to engineer mice to make it so that they did have telomer shortening, because mice, rabbits, rodents, and most, and a lot of animals have telomerase already produced in all their cells, okay?
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They don't have telomer shortening,
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And so he had to first create a mouse that didn't have telomerase produced, so he shut off the telomerase gene.
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Telomerase got really short, and then he started seeing these mice start aging just like humans, male pattern baldness, all kinds of things similars.
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Then he used the gene therapy to reintroduce telomerase to the cells and saw what this remarkable reversal of the aging process, hair color, hair coming back,
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The biggest surprise was mice being able to remember how to go through a maze again, the mice that were suffering from dementia, maybe something similar to Alzheimer's.
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Now when I go to medical conferences, especially brain disorders and things like that, I hear everybody saying that Alzheimer's and other forms of dementia are most likely not the loss of memory.
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They're a loss of access to the memory.
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and telomeres, lengthening telomeres might restore that access.
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So I actually have a clinical study in clinicaltrials.gov where I'm trying to get a clinical study started to actually look at lengthening telomeres as a way of curing Alzheimer's.
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Unfortunately, gene therapy is very expensive.
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It may cost a million dollars, it cost me a million dollars to treat one person once.
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And it's also risky.
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Okay, so we would only do it on people that had no other choice.
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But so that's what Dr. Rondopeno did.
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He used gene therapy, delivered the thalarmus gene to the mice and saw that remarkable reversal of the aging process.
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Okay.
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So before he's genetically modified these mice so that their telomeres shrink, I mean, mice do age, right?
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Like they don't age via telomere shortening, right?
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They age.
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Do we understand the mechanisms that they tend to age in?
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I don't think we totally understand it, but we do know that they have extremely high oxidative stress and high mitochondria dysfunction.
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And so those are probably playing a role, but they're way, way higher than humans.
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And so I think the only people that actually...
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So that's, I'm sorry, that supports your idea that if we solve this telemorphic shortening, we may just be pushing out to the next problem, right, which might be this oxidative stress, which is the thing that ultimately takes out a lot of other animals.
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Yes, and it does take out a lot of humans that lead poor lifestyles.
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Okay?
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Yeah.
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So if you take your antioxidants and you live an antioxidant lifestyle, same with anti-inflammatory lifestyle, telomere shortening is the thing that's going to get rid of you, not oxidative stress and mitochondrial dysfunction or inflammation.
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But yeah, that's how a lot of it happened.
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Now, my company,
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Since gene therapy is risky, there's been a lot of clinical studies done on gene therapy where half the people in the study died because of the gene therapy causing cancer.
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Most gene therapies integrate into the chromosomes randomly.
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And if they integrate into a gene that is like a tumor suppressor or oncogene, they will give that person cancer.
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And that's what happened.
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In fact, it's one of the reasons why I really frown on the FDA, the fact that they even allowed such studies to happen, because anybody with a molecular biology 101 background will know that gene therapy with a virus that integrates into the chromosome is going to give, and integrates randomly.
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is going to give that person cancer almost for sure.
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And that's exactly what happened.
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And the fact that the FDA approved it, it makes me very disapproving of the FDA on that kind of stuff.
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I often will say at conferences that I don't,
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think the FDA is qualified to be overseeing safety.
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I think that falls under the shoulders of the principal investigators, things like that.
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But and then you can't even trust all of them.
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Yeah, as it turns out in some cases.
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Yeah.
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I hope you enjoyed this episode of the Live Beyond the Norms podcast.
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Make sure to subscribe and follow.
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Also, make sure not to be that guy, the guy sharing this podcast with people who are not interested in living beyond the norms.
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If you would like to learn more about the ESS60 molecule, the molecule responsible for the single longest longevity experimental result on mammals in history, a full 90% extension of life, visit myvitalsea.com.
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That's myvitalsea as in carbon.com.
