How Long will Humans Live? Immortal Reproductive Cells Future of Anti-Aging w/ Dr. Bill Andrews

➡ Nutraceuticals, which are generally considered safe by the FDA, are a safer alternative to pharmaceuticals for many people. However, out of millions of plant extracts available, only a small fraction has been tested due to high costs. The article also mentions a coffee company offering a blend that includes an anti-aging compound, which has shown promising results in increasing lifespan in mice and humans. Lastly, the article discusses the concept of telomeres, the tips of our chromosomes that shorten each time a cell divides, and the ongoing research to find ways to lengthen them, potentially slowing down the aging process.
➡ Aging can’t be cured unless we solve the problem of telomere shortening, a process that limits human lifespan to about 125 years. Telomeres, found at the tips of our chromosomes, shorten each time a cell divides, but they don’t shorten in our reproductive cells, which led to the discovery of an enzyme called telomerase that can lengthen telomeres. The tug of war between telomere shortening and lengthening is a key factor in aging, and understanding this could potentially lead to ways to reverse aging. However, progress in this field has been slow due to lack of funding.
➡ The text discusses the role of telomeres in aging and diseases like Alzheimer’s. Telomeres, the protective ends of our chromosomes, shorten over time, which can lead to diseases. However, lengthening these telomeres could potentially reverse aging and improve cognitive abilities. Despite promising research, funding for such studies is lacking, leaving potential treatments unexplored.
➡ A product that boosts athletic performance and aids weight loss is gaining popularity, especially among athletes and bodybuilders. It’s affordable and can be taken daily. Gene therapy is also being explored to improve health and longevity, with a focus on telomere lengthening. However, there are challenges in making gene therapy effective and safe, and there’s debate about whether aging can be tackled by addressing multiple factors or just by lengthening telomeres.
➡ Life is about the continuation of reproductive cells, which are essentially immortal. However, these cells need a human host to survive and pass on. Humans and a few other animals have evolved to age by shutting off telomerase, a process that helps cells live longer. Some animals, like lobsters and clams, don’t age in the same way and can live for hundreds of years unless killed by predators or disease. The goal of anti-aging research is to find ways to keep humans healthy and feeling good as they age, but this is currently expensive and not accessible to everyone. Nutraceuticals, which are natural plant extracts, are being explored as a safer and more affordable way to induce the production of telomerase and potentially slow down the aging process.
➡ The text discusses the concept of telomeres and telomerase in relation to aging. It explains that while some treatments claim to lengthen telomeres, they may actually be causing harm by killing off cells with shorter telomeres, forcing other cells to reproduce and shorten their telomeres. The text suggests that companies need to prove their products induce telomerase expression, which lengthens telomeres, rather than just showing longer telomeres after treatment. It also mentions a product called Telovital, which reportedly does induce telomerase expression and has other benefits like improving mitochondrial function.
➡ The discussion revolves around the comparison of two anti-aging products, Telovital and Defy Time. Telovital is more affordable and accessible, while Defy Time is more potent but expensive. Both aim to slow down the aging process, with the ultimate goal of extending not just lifespan, but also healthspan. The conversation also touches on the potential societal implications of extended lifespans, such as overpopulation and job scarcity for younger generations, but emphasizes that humans are adaptable and can find solutions to these issues.
➡ This text is about someone expressing their love for a particular podcast, stating it’s their favorite. They also appreciate the podcast’s star and wish them a good day.

SAM SA the advantage to nutraceuticals, besides them being safer than pharmaceuticals in a lot of people’s opinion, is that they’re generally regarded as safe by the fda. And so it’s, you can put these ingredients into a product and be able to market it without having to go through FDA approval since they’re already considered safe. So but the trick is there’s, there’s about 3 million different plant extracts that are available and we’ve only tested like 20,000 but we, we, I’d love to get more funding so we can continue to test it. But the testing costs us $2 million a month.

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I support them because they support me. Go to 1775 Coffee.com Sarah and reserve your kit. Give it a try. Drink longevity blend and reduce your aging every time you drink coffee. Welcome to business Game changers. I’m Sarah Westall. I have the great scientist Bill Andrews coming back to the program. He is world renowned scientist. He was on the front page of Scientific America back in what the early 90s. And that’s when people started realizing that we had these telomeres that every time your cell divides it gets shorter. He’s going to explain what telomeres are and why they’re getting shorter.

The most, the coolest part of this interview is my realization that reproductive cells are immortal and that we have reproductive cells in our bodies and they just continue. It’s like we have this strand of reproductive cells that go from person to person and those cells just last forever in our human species. That concept, I never really thought about it. Maybe to you it was just so obvious and to me it’s like my first time thinking about it. That is the living organism that passes on forever. And it just gave me a different perspective on that concept.

And we talk about that and how reproductive cells are immortal and what you can learn from those cells. We talk about all of things. But I got to tell you from my own perspective, the anti aging is more about feeling good as we age, not about living forever. That’s just how I feel when I live to 100 because we talk a lot about this at the end. How people, a lot of people for the last few decades of their life feel miserable. Not only do they feel awful, they’re isolated, they no longer participate in society. They.

It’s just an awful existence. Can you, you know, for those of us who are still living in vibrant and have community, it’s, you know, we’re living life. But when you start feeling awful, you can be younger and start feeling awful too. And then there’s other health issues which peptides and some of these other things I’m working on can help people with their health issues. But when you start to age, you start being disconnected from community, from society. And you know, for the last few decades of your life, you are misera and I sure would like to see that change.

Right? And so that’s a lot of what this conversation is. He’s been on a mission over the years to bring something that is accessible to people. And this is televital and it is something that’s available now through Touchstone, which is one of my. I love these guys. I sell the greens. The greens are amazing because it, it’s one of the best products I think there is on the market because it has the probiotics, the prebiotics, the digestive enzyme greens and vitamin D. Just nails a bunch of things all in one product, which I love. You can find that on my website.

But they also are doing this, which is the televital, which is only $39 that you can try it and then it goes to $49. This is incredible because it lengthens your telomeres. It works 200 times better than other nutraceuticals. And he’s going to explain what a nutraceutical is and how it works to, you know, increase your tailorman length. So if you are Interested in trying it 39 to try it you can go to the link below. I’ll go to sarah wessel.com under shop and you will find the link. You can only try it once at 39 but you can at least try it and see if it works for you and then it goes to a higher price.

Okay, let’s get into this. Really interesting. I love talking to Bill. I think he’s, he’s just, he’s a giant. Okay. I’ve had a lot of giants on my show. I had Reggie Middleton this week. If you haven’t seen that. He’s a giant in the crypto space. Most patents, most relevant patents in the world. And then I had Bill Benny. He’s the NSA whistleblower. He is the, you know, he developed thin thread when it comes to digital surveillance and what’s going on in the intelligence agencies. He’s a giant in that area. Now I got Bill Andrews this week who’s a giant.

I mean he’s the forefront scientist in longevity and telomere lengthening. And you know, people who know me, that’s what I love to do. I like to be. That’s what my show started out being is the edge of change. Then I started realizing that threatens people. I don’t want to threaten people. I just want to expose people to where things are going and where the world’s at. And let’s try to. If you don’t know where the world’s going, you don’t have any control. You’re just mindlessly, aimlessly involved. But if you do, you can get involved and you can maybe can gear this in a way that’s pro human, that’s better for everybody.

So that’s what I love to do. That’s my background. I’m a scientist by trade. That’s what I’ve been. So I love the edge of change. So this is my really Fun interview with Dr. Bill Andrews. Hi Bill. Welcome back to the program. Hi, glad to be back. It’s. It’s been a while. I think is. It has. But I’ve had you on so many times over the years. You were the first one when, when you announced the, the defy time ingredient back in the day. It was, I even think it was before defy time. It was back when you found the first significant increase in telomeres or telomere lengthening.

We. You announced it to the whole western world on my show. Well, okay, yeah, that that would have been C057684, which was the 57854. 5, 7, 6 8, 84th compound that we had tested. It was the first one that we had ever, ever discovered in the world that actually induced telomerase when applied to human cells. Yeah. And you were, you were testing, you’re saying thousands of you just kept testing and testing and testing, and now you found more. Can you talk about. It’s just incredible what you’re doing, what you’ve been doing. Can you talk about what telomeres are so people can understand what that is? And then your process of figuring out how to lengthen them.

Okay, so telomeres are at the tips of our chromosomes. My favorite analogy is they’re like ride tickets at an amusement park. So every time one of our cells divide, it loses a ticket, just as if you were on an amusement park and going on a ride, you’d lose a ticket. Now, the cell doesn’t really keep track of how many tickets it has because it doesn’t have a brain. But when it starts loot, when it gets down to its last ticket, it can’t divide anymore. And that was discovered in 1961 by Leonard Hayflick. That’s called the Hayflick Limit.

It’s found in humans and a few other animals, not in rodents, contrary to popular belief. And, but it’s. That’s one of the reasons why rodents make a bad animal, to be able to be testing for aging related stuff. They die of, they die of oxidative stress, mitochondria dysfunction. Yeah. Other reasons. And they do. We die too, of that. Right. I mean, there’s all these reasons we die, and this is one of them. Yes. And we, we can’t just solve the telomere shortening problem. We have to solve all the problems. And so. And, and that’s what we work on.

But, but let me just go on a tangent here and say that no matter what else we do to cure or try to cure aging, aging will never get cured unless we also solve the telomere shortening problem. And we can’t say that about anything else, like oxidative stress and inflammation and things like that. Telomere shorting is the only hard, fast block to our longevity. There’s. Mathematically, we can calculate that a human can’t possibly live longer than 125 years because of telomer short. We know how, how often human cells divide just performing, just from the wear and tear from performing bodily functions.

Okay. There’s a minimum rate that they can survive. So essentially, a cell divides about once a year, okay. And then as a result, every time the cell divides, it loses a ticket. And we know how many tickets it has, and we know that it can only divide about 100 times. And so it puts us at a theoretical maximum of 125 years. And that’s why nobody’s in recorded history is lived to be 125 years. Some people like Noah and Methuselah and things like that live to be 900 plus years. But it’s now well accepted that they probably were measuring a year by full moons.

So that’s 900 and plus full moons, not years, actually. But so that’s what the telomere is. And so. So it’s like, right, they’re found at the tips of our chromosomes. They don’t shorten in our reproductive cells. Okay? And that’s important. And that’s what. One of the things that. One of the logic, I guess, to say is that led us to discover this enzyme telomerase that lengthens telomeres, because that’s. Hold on a second. The fact that it doesn’t shorten in the reproductive cells is pretty profound in the way that. And that’s why you found the Taylor, Maurice, because then you could figure out, well, how those cells essentially are immortal.

Right? Yeah, they’re. They’re. That cell line called the immortal germline has been going on since the existence of life on this planet. It’s just been passing through it. So we can think of this cell line as. As like just one cell line is passing from one person to another and. Oh, that’s cool. So basically, because. Yeah, because those reproductive cells become the baby, and then the baby, you know, is born and it’s the same cell passed down from. I never passes that on. Yeah. And so. So we. So our bodies are just a kind of like tangent off of this line.

Okay, so we could get this. There’s some videos where I’ve done where, where I show this immortal germline and then all of a sudden the cells are dividing. Then I show this tangent where suddenly a human gets created, but a human’s mortal or the germline is immortal, okay? And the reason why the germline has to be immortal is because. And why it can’t have telomere shortening is because our children would be born with shorter telomeres than we have if there was telomere shortening in our reproductive cells, and their children would have been born with shorter telomeres than they have and we would have been extinct as a species millions and millions of years ago.

So, so why. So at the time we didn’t really know that telomeres didn’t shorten, but we, we assumed they can’t. So we went started right away to find out why not. And that’s how we discovered this enzyme called telomerase. And it turns out that because every time you lose a ticket, tolomeras adds a ticket back. So it’s like a tug of war between shortening and lengthening. And it’s a tie in our reproductive cells. It ties at a certain length of about what I call 15000 bases or a hundred ride tickets. And where was I going with that? Well, is it, is it theoretically possible then? And because the reproductive cells is almost the key aging in the sense that why do they not have mitochondrial damage and all these other damage? You know, could our cells technically, you know, reproduce without the damage? Well, okay, so cells do have damage, but when, if a damage is neutral, so what if it’s, if it’s harmful, then that germline cell never survives or has a lesser chance of surviving, so disappears.

So there’s a lot of talk about accumulation of mutations and things like that. And I tend not to be that convinced that that’s a serious problem because we, you know, if you have a mutation to a cell and that mutation causes harm to that cell, that cell is less likely to survive and another cell is going to divide to replace that cell. And so I believe that if we, if a 90 year old person is got mutations all through his, his or her body and then we come up with a way to prevent telomere shortening or even lengthen telomeres to allow that person to the cells in that person to be able to divide again.

Those, the new dividing cells will replace the mutant cells and there’d be a rejuvenation in terms not just from telomere lengthening, the rejuvenation effects that longer telomeres have, but also from the displacing the, the bad cells, the mutant cells. And you know, we know that in a petri dish, when we have cells in a petri dish, that happens when you have, when you mix unhealthy cells with healthy cells and let the culture grow, after a while the healthy cells are gone, the unhealthy cells are gone. The healthy cells have taken over that, that could happen in the body.

And nobody’s proven that that doesn’t happen. So we don’t, we don’t really know. But I Think that even in the case of the mitochondria mutations and things like that, that same thing could be happening in our germline cells. The mitochondria mutations might make those cells less likely to be involved in reproduction. Now, of course, some. Some do get through, and that’s why we have a lot of children that are born with terrible genetic diseases and stuff like that. But unfortunately, you know, they don’t live long enough usually to reproduce or their ability to reproduce is less likely.

And so that mutation disappears from our species. But it’s. You know, I. A lot of people have these ideas that this is absolutely certain and that’s absolutely certain, but we don’t really know, okay? There’s. There’s a lot of stuff that we don’t know about aging and getting old that we’re not gonna know and have no way of knowing until we find a way to reverse aging and see what happens. So scientists. That’s what I’m trying to do. Find out the answer to the questions. Do you think we’re closer now? I mean, because right now, I always tell people, because I’m into regenerative medicine, right? I’m into peptides, I’m into this.

I mean, to anything that helps me feel better as I age. And that’s my goal. When I’m 85, I want to feel good. And I don’t know if I want to live to be 200, but I sure the heck want to feel good the longest, you know, while I’m here. But do you think we’re close or getting closer to being able to live past 120 or even live good to 120? I feel like we’ve been in a stalemate for over 10 years. Okay. And I would say that the real big problem is not the science, it’s the funding.

And it’s like, I. I know I’ve got a whole plan of how I want to continue my research way beyond anything that we’ve come up with before. Because even, like you mentioned, defy times. Well, that. That particular telomerase inducer produces only about 16 as much telomerase as is needed to reverse aging. Or. So if it was 16, it was, what is it, one over 16, about eight times more potent, it would stop aging, and then more potency would. Would reverse it. So it slows it down, makes you feel better because I’m. I know my dad, his cognitive abilities increased significantly when he started doing that.

And you said that it. Back then, you said that it has this weird ability to go to the shortest telomeres first. That’s exactly where I was going to go to next, now that you mentioned it. So in my book, my book called Telomere lengthening, I described this tug of war in detail and in. So in both cases, shortening. When you, when the telomeres are shortening and the shortener, the people pulling on the tug of war to shorten as they get. As the telomeres get shorter and shorter, the back, the people in the back of the line pulling start falling off a cliff.

Okay. So when the telomere gets shorter and shorter and shorter, it gets easier to lengthen and lengthen and lengthen. Oh. And so when you have critically short telomeres, you can lengthen those a little bit until, because when, when the people that fall off the cliff, when the telomeres start getting a little longer, they start coming back off the cliff and they start joining in. So, so there’s a, like a, you find a stalemate. Okay, where, where the telomeres stay, where the tug of war is a tie. But it depends on how much telomeras there is and how many people are pulling.

So that is changing all the time. The shorter the telomere gets, the fewer number of people pulling to shorten, the longer the telomere gets, the fewer number of people to are pulling to lengthen, at least in cells that do produce telomeres. Huh. So it does kind of keep it at a steady pace. So it’s almost. For the shorter ones. It can be really effective for keeping it at a steady pace, but it might not reverse. That’s exactly. Well, it could. So if you are somebody that’s suffering from some type of like telomere related disease, which almost all diseases are, and you have a lot of critically short telomeres, there’s a really good chance you will see age reversal.

Okay. Now in all the products, like some of them that been discontinued now mostly because of profit margins weren’t high enough, but by some companies, but not because they didn’t work, but people, people would see some age reversal. And the only way to explain it was that they had critically short telomeres that got lengthened. And I believe that that’s one of the reasons why people need to take these telomerase inducers all the time, because the critically short telomeres will get lengthened a little bit. That’s, that’s exactly why my dad has seen a significant improvement in his cognitive abilities.

But as you age your, you, that’s the most critical, I think to most people is Your ability to think. I mean, if you feel like crap, maybe you don’t want to know what’s going on, but in general, people want to keep their cognitive ability intact. Yeah, I know. I always call Alzheimer’s the disease worse than death. Okay. It’s. It, you know it’s coming. You know you’re going to lose your ability to know who your family members are, things like that. I, I’ve been studying Alzheimer’s for 40 years, and this is long before I ever knew that I had the gene in my family.

Okay. The APOE4 gene. And so both my father and my younger brother developed Alzheimer’s and passed away from it. I fortunately did not inherit that gene from my father, so I don’t have it. But I’ve been so. So I’ve been motivated to treat that disease long before I knew it was in my family. Yeah, but it’s, it’s something that, like, really important. And I do have clinical studies enlisted in clinical trials.gov to treat Alzheimer’s by lengthening telomeres through a process of, called gene therapy. Now, did that work because I had Liz Parish on and I’ve had you, and I’ve had the clinic on that was trying to do a targeted brain test, a trial.

How did you, how did that end up coming out? Where. Because it was so expensive to do the full body. So you just focused on the brain. How. What were the results? I know this is such expensive, expensive area and getting the funding is really difficult, but you were trying to do some, you know, limited, just full brain kind of work. We never, we never got the funding to do it. That’s, that’s. It’s been sitting in clinicaltrials.gov now for 10 years. Why do you think that the funding isn’t coming? Because that’s an interesting thing. Because this is something that could significantly reverse Alzheimer’s.

Alzheimer’s. It could significantly reverse. I mean, is it the population they’re trying to depopulate and they’re worried that this will increase population? I mean, what do you think is the reason? I’m a scientist. I don’t really understand. I just, I think that there’s, there’s misinformation being circulated. I get, I try to talk all the time. There’s a really good talk I gave in, in 2019 where I explained all the details and I even explained that, that in mice, engineered mice that were, you know, I said that mice don’t age like humans do, but there’s engineered mice that do age like humans.

And when they got old and demented. They. Their brain sizes got smaller, they couldn’t remember how to go through a maze, things like that. And Dr. Rhonda Pennell did the work using our technology, because we don’t work with mice here at Sierra Sciences. But when he lengthened the telomeres, they got smarter, their memories came back, their brain sizes got bigger and they, and they look younger in every way imaginable. Well, that was my dad with his cognitive abilities. Yeah. And the I, I thought 10 years ago, that’s going to solve all our funding problems forever. And it didn’t.

And I’m not sure why. I mean, it’s like I, I do believe that lengthening telomeres is the cure for Alzheimer’s. Okay. I think, I think telomere shortening is the main cause because, I mean, people will argue with me, but there’s, you know, our neurons, the, the neurons are the problems. Okay, the neurons are failing. But neurons are actually very, very healthy cells. They can last longer than a human being can. But they have what are called caregiver cells and bodyguard cells like oligodendrocytes that wrap, that wrap myelin around the cells to protect the neurons. Those, those cells, they have, they divide, they have telomere shortening.

So when those telomeres and those cells get critically short, the neuron becomes unhealthy because it has no caregiver cells to take care of it. And then the neurons start failing. Same thing with the astrocytes, which are essentially our bodyguard cells, which are our immune cells like in our brains. And those also divide and have telomer short. And so length, so the neurons don’t divide, so they don’t have telomere shortening. Unless you, unless there’s some really terrible oxidative stress problem. But, or, you know, you get exposed to some high levels of radiation or something like that, then, then your neurons can have telo accelerated telomere shortening, but they don’t normally.

So if we could lengthen the telomeres in our oligodendrocytes and our astrocytes, I believe we’ll be seeing a reverse. Memories will come back. That’s one of the things that, from that mouse study with Dr. Rhonda Pinnell, it said that Alzheimer’s and maybe other forms of dementia are not the loss of memory, they’re loss of access to the memory. The memory is still there. And by lengthening the telomeres restores access to the memory. It’s like a database. What’s that? It’s like your brain is Like a database which they know how to store data on it now on bacteria and all sorts of things.

So it, it’s some kind of a data storage device. And then the processing power comes back. Yeah, it’s processing and retrieving of data. Yeah. And I, I, I, you know, I’m too, I, I don’t very, I’m trying my best not to become a businessman because there’s so much science that needs to be done and I’ve known so many scientists that are really good at what they do and they became business people and they never went back to being scientists. I don’t want to be that person. I want to cure aging. But I, I try to work with people that are business people that are helping and can’t, I can’t get.

All of them are surprised at how difficult it is. And yeah, the, I think it’s, you’re running up against a machine that is wanting to, they don’t want the population explosion. And I also think it’s the same reason why we can’t get free energy when there’s so many promising scientific breakthroughs in that area as well. And they’re seeing huge resistance. It’s really interesting how this is happening. I, I think possibly. But I don’t understand why there isn’t these families that have somebody who’s suffering. They’re billionaires. They have somebody in their family suffering from Alzheimer’s. Why aren’t they providing us the funding to cure their person? We, we’ve talked to people like that who have since died.

Well, that’s what I didn’t understand is because I, you had, we’re on my show. Liz Paris was on my show. You were doing some kind of study with them. And I’m like there’s, it’s not that at 50, 000 and you’re going to get a full. I remember that study for Alzheimer’s and they were going to do a full brain thing and there had to be many people with hundreds of millions of dollars in billionaires who would. You only need like six people at the time who would have just funded it. I mean I would have. If my, if I have somebody in my family that had Alzheimer’s and I was that wealthy, I would have been like this is a no brainer.

I didn’t want to, I don’t understand it. They didn’t want to be the first ones to do it. They wanted somebody else to go first. I used to say why don’t you pay for somebody else to go first then? And they Wouldn’t. It’s why though, because you’re gonna die. Anyways, quick break from the program to share with you something amazing. This is called sloop. It’s actually Slupp Dash 332 but it’s been shortened to Sloop. And this thing mimics exercise. It seems too good to be true. I first shared this on my sub stack and I had Dr.

Diane Kayser and we went through all the benefits of this and the whole thing sold out. You can’t get it anywhere really across the industry and the people who are using it the most are athletes and bodybuilders and people who want to see extra performance in athletics. Because this and pre clinical studies with mice increased their endurance by 70% and they’re distance by 45%. I mean it’s incredible. And it’s been shown to mimic exercise even when you’re at rest. In pre clinical studies with obese mice they lost upwards of 12% of their body weight in four weeks and it increased muscle.

So this is really taking the industry by storm. It’s actually not that expensive either. With my 10% coupon it’s about $80 or maybe a two month supply if you take one capsule a day. If you decide to up it to two capsules a day because your dosage depends on what you want, then it’s a one month supply. But Dr. Diane recommends doing one capsule a day until your body gets used to it. You might not see the same level of results right away that the mice did, but your body can get used to it and see if it’s something that you really want to do.

If you are, are interested in this, I will have a link below so you can try it yourself. We’ll go to sarah wessel.com under shop. Remember to use the code Sarah to save 10%. I, you know, someday maybe we’ll know. I wish some of these millionaires get on your show and tell us why not. Because there’s no, there’s nobody going out saying what Bill Andrews is saying won’t work. You won’t find anybody saying that. And we do have like, you know, my greatest ally is Liz Parrish who you mentioned before. Yeah. She, she’s doing everything she can to try to get this technology moving forward.

She’s treating people with, with the gene therapy through a company called ihs. But I don’t know, I don’t know if the dose is high enough. Okay. And also the, the vector we, the vector that everybody’s using nowadays for gene therapy is called aav. And for adeno associated virus. And what we have found in our studies is that its ability to infect cells because it is a virus, the virus carries the telomerase gene into the cell. Its ability to affect cells is extremely low. It takes 10 to 100,000 times as much of that virus to infect 50% of the cells as do most other gene therapies.

But the other gene therapies have problems of causing cancer causing immune responses, things like that. So we can’t use them. That’s why everybody’s so focused on aav, because it’s safe, but it’s also very ineffective. Okay. And so Liz Parish has actually come up with a new vector that we are working on now using the cytomegalovirus. And it’s unfortunate. Very difficult fires to work with in constructing the gene therapies, getting the genes into them. But once it’s constructed, it could be the best of all worlds. It doesn’t have the cancer or immunological problems. Plus it, its infectivity rate is like 10,000 to 100,000 times better than AAV.

So we’re working on that right now. And that could be a solution that will make not only genes therapy safer and more effective, but also a lot, lot cheaper because we’ll have to use like 10 to 100,000 less of the virus. Wow. Okay. Well, one thing that Liz Parrish told me is that she was a little frustrated that, and, and this was a while ago, but Google is investing and some of these big corporations are investing in gene therapy, but they’re suppressing everybody who talks about gene therapy, which is really interesting. I don’t understand. Nobody’s suppressing me from talking about it.

She was, she was talking about it. Yeah. So I, I don’t, I’m just bringing that up, but. Okay. That’s the first I’ve heard that she hasn’t mentioned that to me. And I talk to her once a week. She mentioned it to me back in the day. So maybe it’s changed, I don’t know. But it’s basic business. You don’t like business and I respect that. It’s not that you don’t like it. You’re focused on the science. I totally respect that because I could see how that could happen. And then you don’t get anywhere. You never, You. Society doesn’t and humans don’t progress.

One thing about aging is, you know, I have a systems background, systems back degree and computer science and all that stuff. And I look at everything from a systems perspective and the aging problem has really been. This is what Liz Parrish talked about, is the looking at the entire aging as a system. We, you know, of telomeres being one, a foundational element. It’s almost like a foundational element, and then it’s a system around or other elements around it. And some say there’s seven, some say there’s nine different things that affect aging that you have to solve in order to tackle that entire problem.

What do you think about that? Everybody’s trying to get their word, their words in and stuff like that and come up with explanations for aging. But when I look at all the hallmarks of aging, I think all of them might be solved by just lengthening telomeres. That’s why I say aging will never be cured unless we also solve the telomere shortening problem. It’s the only thing. Telomere shortening is the only one that has a full explanation of its entire process. We understand why the telomeres shorten. We understand how they affect aging. We affect everything. We know everything about it.

We just know that lengthening telomeres will do good things. Now, hold on a second. Because we were talking about the immortal cells, and they don’t. They don’t have shorter. And because the cell can then reproduce as a young cell. So that’s why I asked you earlier, in theory, can’t the cell just reproduce as a young. As a young cell? And we’re good to go if we produce telomeras, okay? But the reproductive cells do produce telomerase. But as soon as our cells start becoming a human, like even at the eight cell embryo stage, the telomerase gene gets shut off, okay? And that’s why we suddenly start having telomere shortening.

And so, so what? My PhD is in molecular and population genetics. Population. The molecular genetics is understanding the gene expressions and engineering genes and things like that. But the population genetics is all about the how, how, and why of evolution. Not the what and when, like you normally hear about evolution, but the how and why. So, so the question comes up all the time is why have we never evolved a way not to age? Why did we evolve an aging process to begin with these kind of questions? And I think the answer is very clear, and that’s that in order for a species, any species, to survive rapidly changing environments, it has to have a lot of diversity within its species.

And so ever since, especially since sexual reproduction occurred, and then we could start shuffling our genes, that. That increased the rate of developing diversity in our species a lot. Okay, so now. So now that now that sexual reproduction is the best way to shuffle our genes and create diversity. It turned out the only way to improve on that was to eliminate the longer lived. Okay. Because when you allow the longer lived to keep reproducing, you don’t get as much diversity as if you let the offspring interbreed. So a successful species, every successful species that has still hasn’t gone extinct yet has evolved a way to eliminate the longer lived.

And by longer lived, I mean any, any member of the species that has already raised its young. After you’ve raised your young, there’s no evolutionary advantage to living any longer. In fact, you’re in the way, you’re interfering with the production of diversity. If, if that’s the only reason to live. But yes, yeah, I mean that’s their sole purpose is reproduction. Well, in for, let’s, let’s see. We’ve got to think beyond just humans, okay, so yes, in the humans that’s true. But, but prior to humans, okay, and the rest of the animal kingdom and stuff like that, there was really no purpose for species except to reproduce.

That was the only purpose. And so if so a species ability to reproduce was, was key towards its ability to survive rapidly changing environments because of creating diversity within. Well, it’s a, Keep the immortal cells going. Yeah, that’s, well, that’s the key is to keep the, the living, the, the living, the immortal cells are the only thing that they want to keep living. And to keep those immortal cells living, you have to do everything you’re talking about. So life is really all those immortal cells passing through. Whatever. So how do you keep these immortal cells alive? Well, first of all, you got to get rid of the word want because the cells don’t have intelligence and stuff like that.

It’s just that the cells that don’t, that don’t evolve a way to get, get, eliminate the longer live. They end up dying from rapidly changing environments. So the ones that remain are the ones that did accidentally evolve a way to eliminate the longer live. Well, but if you look at everything I, I, it’s just so fascinating if you start to take the whole perspective that life is really about these reproductive cells continuing these reproductive cells and those are the only ones that matter. Everything would go around that, that is, that is exactly what’s happening. Okay, so the, but the reproductive cells are immortal and they continue on and on and on.

But in order for the reproductive cells to pass on, they have to go through a human being. And the human being needs to survive in order to do that. But, but Only survive long enough to raise its young. And then it’s better to let the young pass the genes on than let the longer lived person pass the genes on again. It’s. But, but that’s why, that’s why humans evolved a way to shut off the telomeration. Okay. Because that’s how we, that’s how humans eliminate the longer live. That’s the key way to do. Turns out that only, only a few animals evolved that mechanism of aging and that includes humans.

Non human primates except for lemurs, dogs, cats, horses, sheep, pig and deer. All the. Those are the only animals that we’ve ever discovered that actually age by having telomerase shut off and telomere shortening. Really? What do the other ones do? Oxidative stress, mitochondria dysfunction. Some of them have no aging process at all. Like lobsters, things like that. Lobsters. I’m guessing, and there’s support for this in the literature, that the only reason why lobsters don’t live forever is because every time they change, they get a new shell. They get bigger and bigger and get less able to protect hide from octopus.

They get killed. Yeah. And they get eaten. Yeah. Same thing with a lot like tortoises. They have no detectable aging process. A lot of whales don’t have any detectable aging process. Lobsters is the best example. Clams. Clams are the only animal that actually have wings on a tree. You know, you can count rings on a tree to figure out how old a tree is. Clams have stripes on their shells. They get a new stripe every year. And so they can live forever. They’re immortal too. So they just die in other ways. Yeah. And, and there people have discovered clams now with counting the stripes that are over 500 years old.

Wow. There’s a famous clam named Ming M I N G because it was born during the Ming dynasty. It’s over 500 years old, but unfortunately it’s not a lot. They, they didn’t count the shells and the stripes until after they caught it and was it was killed. Oh, that was too bad. They’re like oh geez. But there. But living, living is, is tough. I mean it’s like passing your genes on and things like that. So is is tough with rapidly changing environments. And then by changing environments I don’t mean just temperature and things like that. I mean different species, different predators coming along, it can kill you.

Different infections that can occur in the nature, things like that. There’s all kinds of environmental changes that can eliminate the species. Okay. And so having more diversity increases the chances that at least one or two members of that species will survive whatever comes along. Well, let’s talk about the tug of war thing again. When the tug of war, when you take defy time or you take the new supplement we’re going to be talking about, it can go to the shortest healing reverse. So if you’re doing that constantly in theoretically you can at least keep yourself stable while you might get killed from other things, mitochondrial dysfunction, other things.

But you can theoretically keep yourself feeling pretty good as you age. Theoretically. And I’ll tell you, I’m looking forward to seeing if that’s true or not. But the only way to know if that’s true or not is to wait 50 years and see what happens. I mean, treating like maybe 100 year olds and stuff like that could give us that answer sooner and see what happens. But those studies are still underway and it’s like I, I’m not aware of any hundred year olds that are actually doing any of these treatments. I do know one person, a friend of mine, I won’t mention his name, but he’s 101 years old that has just decided to start finding out.

And me and Liz Parish are following him like a hawk. How is he doing? Well, he, he’s, he’s only just started. Okay, so we’ll have to see. But he’s, he’s, He’s a unique 101 year old because when, when he comes and visits my company, I never feel like he’s 101 years old. I feel like he’s intelligent like a hawk. Talks business. He gives me business advice left and right, which just blows me away. He, he does walk a little bit like he’s not normal, but, but very, you know, I know a lot of 30 year olds that walk worse than he does.

I mean, he still has a driver’s license. Wow, that’s great. So is he doing more than the telomere lengthening or is he also doing some gene therapy and some other things? He’s doing everything. Okay. He, me and Liz Parrish advise him all the time and he’s, he’s actually, I, I’ve connected him with what I consider to be the best doctors in the world. How much does it cost? Like how much is he spending to try to decrease his aging? Millions. Okay, so this guy has millions and so he’s, he’s spending millions every year doing this. And that’s the problem, right, is that that average person can’t, it’s not accessible to the Average person.

That is the problem. And that’s. That’s the problem that both Liz Parrish and I want to solve. I mean, I. I am talking to people that are trying to help me find funding that agree with the idea that when we do have a cure for aging, let’s just drop it from airplanes, okay? Not charge anything. Because, I mean, I’m not in it for the money. Liz Parish isn’t in it for the money. We’re in it because we want to make the world happier and healthier, period. You feel so much better. Like my dad’s cognitive abilities. Okay, but let’s talk about.

You have a new supplement that works. Divide Time is a pharmaceutical grade. And, you know, I. I offer it, but I also. I have. About 35% of my audience is international, so it’s available. International. It’s a pharmaceutical grade. What is the difference between. Between. You have. Televital is a new one, right? And Te. Vital. Yeah, yeah. Televital or telovital. Both pronunciations are correct, but it’s amazing. But it’s not. It’s a nutra. Nical. Right. Nutraceutical versus a pharmaceutical. Can you explain the difference and how. How do they compare? Well, nutraceuticals are. Are from plants. Okay. They’re plant extracts or they’re.

They’re ingredients. They’re purified from plants, and so they’re completely natural, and so they’re safe. People. People have been taking these things for thousands and thousands. Unless you’re. Unless you’re allergic to one of the ingredients, they’re safe. There isn’t a chemical on the planet that somebody’s not going to be sensitive to. That’s right. So. Yeah, so there’s. There’s going to be some people that are going to have trouble taking this product. Now, you froze. Are we still talking? No, we’re. We’re good. Okay. The. But. So. So the advantage to nutraceuticals, besides them being safer than pharmaceuticals, in a lot of people’s opinion, is that they’re generally regarded as safe by the fda.

And so it’s. You can put these ingredients into a product and be able to market it without having to go through FDA approval, since they’re already considered safe. So. But the trick is there’s. There’s about 3 million different plant extracts that are available, and we’ve only tested, like, 20,000. But we. We. And I’d love to get more funding so we can continue to test it. But the testing cost us $2 million a month in the. But. But in the process which has gone slower than expected. We, we have discovered out of the 20,000 different nutri or plant extracts that we’ve tested, we have found about 40 that do induce the production of telomerase.

And so telovito is a mixture of the five most potent telomerase inducers. And the reason why we just don’t put the number one most potent one is because of the possibility of synergy between the five. And it could be that like telomerase gene, as I mentioned before, when we become an embryo, is shut off. The gene is turned off, but it looks like it’s turned off by more than one mechanism. Them. It’s like evolution has gone to a lot of trouble to make certain that this gene is shut off. So it’s, so we, we, we’re, we just hope that, and we don’t know how it shut off.

Okay, so we just hope that mixing more, more than just one together will be shutting off more than one of the mechanisms to shut off the telomeres chain. So, so we got a mixture of five of them in there. And I mean there, there are other products on the market that claim, other nutraceuticals that claim to lengthen telomeres and induce telomerase. But the problem that I have with them is that none of them actually demonstrate the production of telomerase. They all claim that they produce telomerase because they see telomeres get longer. But what, what most of them fail to understand is that you can have, you can do it before and after.

You can measure telomere length in your blood before and then after treatment. It’s not just the supplements. There’s also like therapies you can do that they’re claiming like lifestyle changes, diets, you can get machines that will provide you different wavelengths and different temperatures and things like that. Or, and they claim to actually lengthen telomeres. And I believe they do. I do believe that the telomeres are longer afterwards than before. But what everybody fails to understand is that there’s other ways besides having telomeres be longer in the after samples than before than by lengthening telomeres. Okay. So the main things are, it’s well published that any kind of toxin is going to preferentially kill off telomeres that have the cells that have short telomeres.

And so if you are take, if your treatment is either is, is toxic, it’s going to kill off the cells in your blood that have the shortest telomeres. And as a result the average length of your telomeres is going to be longer. It’s because those cells are weaker. So you could be. Those cells are weaker. Yes. So you could be doing something destructive and lengthening your telomeres in a study. That’s exactly what I’m practical. But from a practical standpoint, you, you didn’t do anything but maybe harm yourself. So you have to be able to understand what the mechanism is and that this is actually lengthening your telomeres, not destroying.

Short length sells. That’s. Yeah, I’m, I’m impressed that you understood what I just explained so well. It’s the analogy that I usually use is if you have a company and you fire the dumbest people in your company, the average IQ of your company goes up. But that’s a smart business tactic without anybody getting smarter. That’s super smart. Because now your average intelligence level in your company is smarter and you’re going to perform better. But. Yes, but, but, and, but the point was that nobody got. I know. No, but the point from your body. But from a body standpoint, you might feel better though, right? You’re getting rid of your weaker cells, but you didn’t solve the, the aging at all.

Other cells have to come out of your bone marrow, stuff like that. That’s right. Divide. When they divide, their telomeres get shorter. And because the bone marrow, the memory cells and the naive cells in your bone marrow are have very long telomeres, even in a very old person, when they divide to replace those killed off cells, you have their, their, their telomeres become shorter. So your average telomere length in your whole body becomes shorter. So you could be. Even though the blood got long, you could be. So you summarizing this because you’re killing off the weaker cells, the shorter telomeres, your other cells have to reproduce and you could be to able actually creating instigating a shorter cell across your body.

If you don’t know what you’re doing because your cells now you’re promoting those cells to reproduce and which is shortening their length. Even though in the study it shows it is longer in the test. But you could be. Shows the overall length could be longer because you got rid of your shorter telomere cells, but you’re forcing them to reproduce and your entire cell length is shortening. Absolutely. Okay, I’m impressed you understand that so well the. Because I, I’m actually at a conference in Las Vegas in a few days and it’s been, I’ve been struggling on trying to how explain it so everybody understands it but at the other extreme, you did good.

Suppose, suppose the treatment, whether it’s a supplement or, or you’re getting in some type of chamber, that’s going to make some change to you. Suppose those cause immune reactions. Okay. Well again, the cells in your bone marrow are going to divide to flood your, your blood with new cells that have longer telomeres. And as a result, your average telomere length in your blood gets longer. So all you have to tell people is that if you’re forcing your cells to divide prematurely, you’re decreasing the length of telomeres. Even if the test shows you longer telomeres because you’re getting rid of all your really short ones, you cannot induce cell divide if you’re trying to lengthen your telomeres.

Exactly. And the, what I always say is that what these companies need to do that are selling these other products, they need to show that their product is inducing telomerase expression, is turning that gene back on. None of them do. Okay. And so I, I, I tell people that, you know, if somebody comes to you and says they have a product that lengthens your telomeres, ask them, do they have data showing that their product induces telomerase expression? And when they say because you become could be making it worse. Yeah. When they say no, ask them why not.

Because it’s easy to measure telomerase activity. I’m one of the inventors or co inventors of practically every test there is to measure telomere length and telomerase activity. Those are not that difficult to do. But the question comes up, well, it’s obvious. If they have a product that they’re claiming produces telomerase, why don’t they have data showing that it produces telomerase? That’s right. And my guess is they did try to get that data and it was, it failed. They didn’t understand why. But they say their telomeres got longer, so it must have worked even though their assay didn’t work.

And so they don’t know why they make it. But doesn’t it, isn’t that the, the pro. I have a problem whenever anybody, I mean sometimes we don’t have the source of the issue, but why have a problem when they something happens and they don’t know why? It’s like, well, if you don’t know why, it’s, it’s kind of the whole problem with the whole medical system in general is the not knowing the source, not knowing the why, and sometimes you won’t know the why. And we just, that’s the best we got. But in general, if you don’t know the why, then you’re just kind of fumbling around.

But here’s the thing. Telovital and we test everything, okay? We’re not trying to market anything. We’re just a research we test. Our Telovital contains the only nutraceutical supplements on the planet right now that actually do induce telomerase expression. So the only thing that telomerase does in a cell is lengthen telomeres. And the. The problem is, and no product is not potent enough to win the tug of war, okay? But that’s okay, because decreasing the rate of shortening in that type of war is a really good thing. It delays the aging process, it slows down the aging process.

And that’s what we want to do as much as possible, especially to increase our chances of still being alive when actually something does come along that actually does reverse aging. But it also helps with the mitochondria function and some other things. Absolutely. So this has another benefit to it because I know Anna, who is the one that was telling me about this project initially. You ended up working with them, which is really great because I’ve already sell some of their products. But she was saying that it helps with her mind. She feels so much more energy because it’s helping with their mitochondria.

Can you tell me why is it doing that? Well, most of the genes, most of the proteins, in a minute, most of a mitochondria is made up of things that were produced off the genes in the chromosomes. Okay. So like, this is going to get more scientific than necessary. But there’s we. We know about things called enhancer sequences that are found in our chromosomes. These are sequences that are like 10,000, 100,000 bases away from a gene. The DNA folds over this enhancer, comes in contact with the gene gene and turns it on and off. Okay. This is a really common method of gene regulation in the human body.

Well, telomeres have all the hallmarks of an enhancer sequence. The telomeres fold over and come in contact with genes on the chromosome. And some of those genes are mitochondria genes. Okay. And so it turns those genes on and off, depending on which is the right thing to do in each particular case. But when the telomere gets shorter and shorter, it can’t reach as far. Okay. So by re. Lengthening the telomeres allows it to reach again back to those, let’s say, mitochondria genes and the chromosomes start producing the mitochondrial proteins that Go to the mitochondria and rebuild that mitochondria.

Okay, well, it gets back to my. It gets back to the original thing where we said that theoretically just lengthening the telomere might solve the aging problem altogether. That’s what we. We’ve done so many studies with. Like, we have cell lines that we can turn telomerase on and off at will by other mechanisms. Okay, well, engineered mechanism. So we can let cells get really short telomeres and then re lengthen them again and then let them get short again and re lengthen them again. And we find a lot of like. Like things like search ones and methylation patterns and stuff like that.

DNA methylation patterns. They change proportionally with the telomere length, as if the telomeres are actually controlling. Interesting. The production of search ones or the. It’s a master methylase enzymes that methylate the DNA, things like that. Say it again. It’s a master switch. Essentially. That’s Dr. Rhonda Pinnell when he was interviewed by Diane Sawyer. He said it’s. It’s a. Oh, no blanket. What his exact words were. But he said it’s the. Something of. It’s like the master switch of aging, but he used another word. But essentially the same thing. So. Okay, so now what is the difference between the nutraceutical and the pharmaceutical? Because defy times a lot more expensive.

But it. It works a little bit better too. Right? Because it has. It induces more. But this. It works a little different. Right. The other stuff has synergetic, synergistic abilities, but this is a little bit stronger. Can you talk about that? The defy time. The pharmaceutical defy time does produce. Induce more telomerase than telovital. But it is a pharmaceutical. It has a lot of regulations. It’s a lot, lot more expensive. And it’s. It’s not gonna. It’s not gonna reverse aging too, just like Telovita will, but it will slow down the aging process. But it’s like the advantage.

The advantage of Telovital is that. And this is what’s important to me is it’s available to everybody. It’s accessible. Yeah, because one of the things you were saying when we were doing those studies on the Alzheimer’s, and it was. We were talking about a million dollars to get. You had those little lemurs and you were doing the full body stuff. It was over a million dollars for one treatment. And we said, God is so expensive. And you said, your goal. I remember this, your goal was to make it accessible. For the average person, the Tila Vital right now people can try it for only $39 and then ongoing it’s only $49.

That is a huge defy time for. And I take it every day. I take it every day. Defy time is 500amonth. So there’s a big difference in accessibility. It might be a little stronger, but this is accessible. Yeah, and, and by, by being a little stronger isn’t really going to make that much difference. It’s just gonna. Because it, you know, it’s going to lengthen your telomeres a little bit and get stabilize. But it’s going to be a way to allow people to stay around longer while we come up with stuff that is even a lot more potent than defy time.

We need to get more than eight times more potent and defy time before we’re going to reverse aging. Yeah, but I gotta push back a little bit. It’s not just to keep you around longer. It’s to make you feel better as you are around. Because even if you don’t live to be a hundred, you feel better when you’re on the journey. And the cognitive abilities. It’s important to understand that every anti aging researcher when they say be around longer, they mean be healthy longer too. There’s nobody on the planet that is trying to extend our lifespans without extending our health spans.

So. Yeah, so, so a lot of us, especially me, forget to say that. But believe me, I’m more interested in extending my health span than I am extending my health lifespan. Well, because I want to feel good. If I die at age 100, I, I just want to go at 100, but feel freaking great until 100. And if I go fine, but I want to go like fast. I want that to be a thousand. I want that to be a thousand or longer. But what do we do? And we had a conversation and I know you got to go quick here and this isn’t a five minute conversation, but I’m going to throw it out there, give you a chance to do it in five minutes.

What do we do if suddenly we can seriously live longer? What do we do about the population issue? You don’t think it’s an issue? Well, no, it is an issue. It’s a real. In fact especially how are the young going to get jobs when the old never retire? That’s a really big problem. But what we have to do is it’s, it’s a really big problem. But it’s not as big a problem as we have now. People, people People, young people, don’t understand how bad things are now because all the old people that can’t care for themselves are sitting in nursing homes, assisted living homes, hospices.

They are miserable. I mean, I would. I don’t know why, but when I was in high school, I would go. My. My high school had a program where they put everybody in a bus and take us to some of these homes to talk with these people. Partially, partially to give these people somebody to talk to because they’re isolated and plus also to help us get an education into what, what it’s like to be old. And so things are bad now, things are terrible now. No matter how bad things get in the future, they’re never going to be as bad as they are now.

Well, fix that problem. Well, the last 30 years of your life, for a lot of people are just misery. Who wants to live in misery for the whole. For decades before you die? And as soon as you go into that miserable life, you disappear from society and society. Society doesn’t know about you anymore. Okay? You don’t have. Society’s not a community anymore either. Yeah, yeah. And a lot of people, they’re alone. They’re all by themselves. That. But I always say that 100 years after we cure aging and we have all the problems like overpopulation, things like that, and somebody says, well, I’m.

I’m putting on the ballot that we should ban the cure for aging because of all these problems. Nobody’s going to vote in favor of that. Nobody’s going to want to go back to the way things are now. Okay. But also, humans are very good at adapting. Okay. And my favorite example of that is the World Wide Web. I. I don’t know. You’re too young to remember this, but when the World Wide Web first came along. I’m not too young for that, by the way. Go ahead. Well, it. When the World Wide Web came along, it was terrifying.

Everybody thought, oh, my God, this is so ridiculous. We can’t live with this. This is just too complicated. Nobody can handle this now. We can’t survive without it. Okay? Something. We adapted. We adapted. Now all of a sudden, all these terms like www and.com and things like that all mean something to us that are just natural, okay? So we can adapt. Humans adapt really well. We’re going to figure out ways of solving the overpopulation problem. Maybe another planet. That’s exactly. I think we’re going to be explorers. I think we’re going to. Things are going to change.

And I think knowing that we’re going to live long enough to see all those changes. It’s going to increase the chances that we do those explorations. Because I, in a lot of my talks, I start off by saying, you know, I show a scene from Star Trek, First Contact where James Cromwell meets God. I forget his real name, but that meets a Vulcan for the first time, they shake hands. It’s like First Contact with aliens from outer space. And I say when, when that happens, I want to be there. And so I, I have this, my picture shows up in that picture doing a three way handshake with, with James Cromwell and oh God, what’s the other guy’s name? Well, he’s not Spock, but he’s a Vulcan.

And I’ve become a Facebook friend with the actor. Oh. And I’m suddenly, I’m going blank on his name. But he, he, he and I communicate a lot because he’s important to me as he played that role. Oh, that’s awesome. But don’t you think that we almost need to not age, live longer just to solve some of these problems? Because I don’t think you even start thinking about some of these problems and some of these bigger challenges until you get a little bit older. I don’t, I don’t. That’s why I do everything possible to extend my lifespan and health span right now so, so that I can finish my work.

Okay. I believe I spend every single day thinking about don’t do this or don’t do that because it’s going to accelerate my aging. Do this or do that because it’s going to slow down my aging. Okay. And I’m, you know, I, I just, I’m constantly, every single day I’m focused on doing that well, we become explorers, then the whole aging problem goes away. The whole overpopulation problem goes away. I unfortunately have to go to my next meeting now, which is. Yes, you do. You gotta go. Well, thank you, thank you so much. Let’s do this again.

Follow up. Yeah, please, let’s do a follow up because I’ve got so much more to say and I, I so enjoy your podcast there. That, my favorite podcast, to be honest with you. I podcast, but this is, you’re, you’re the number one star in far podcast. Thank you. I appreciate that. Okay, have a great day. You too. Sa.
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