#394 How Bioregulator Peptides HALVE Mortality: Telomere Reversal, Organs REGENERATED & the 8-Year Experiment With Dr. Bill Lawrence

Welcome to Longevity. I'm your host, Natalie Knidham. I'm a nutritionist, a human potential and epigenetic coach, and I created this podcast to bring you the latest ways to take control of your health and longevity. We cover it all, from new technology and ancestral health practices to personalized interventions and a very special interest of mine, peptides and bioregulators. Enjoy the show. Today, I'm joined once again by Dr. Bill Lawrence, a longevity researcher whose past episodes are still some of the most downloaded on this show. And for good reason, it has to do with my favorite topic, bioregulators. Now, Bill trained directly with Professor Cavanson, the scientist who discovered and researched bioregulator peptides and ran incredible human-russian studies where certain peptides actually cut mortality almost in half. Now, in this episode, Bill finally shares the long-awaited data from his eight-year telomere study and five-year epigenetic age study. We talk about what actually happened to real people's biological age, organ-level aging, and why the pineal and thymus peptides seem to punch so far above their weight. Now, I want to tell you about something pretty new just for listeners, and I'll thank a sponsor and then we're off. I've created an amazing holiday gift guide for you listeners so that you can get the best holiday deals on biohacking tools, supplements, and so much more. There are gifts in different price ranges and once a year price drops on your dream biohacks, and we are continually updating it. So if you've looked at it before, you're going to want to look at it again because we keep adding new sales. And hey, nobody said you can't shop for yourself. Now, to get your hands on it and to see the latest edition of it, all you got to do is head over to natnitim.com forward slash gift guide for my list of holiday deals and gift ideas. 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Go to beam minerals.com, use code Nat 20 and get 20% off your first order. Start with the basics, your body will do the rest. Dr. Bill Lawrence, we are finally back again. This is an interview that I've been looking forward to for a very long time. Thank you so much for taking time out of your schedule for this. It's my pleasure always, Natalie. Well, we have we have a bit of a history together. Guys in the show notes, you will find links to the first three episodes that we recorded together. I think those first two episodes we recorded together to this day are probably the most downloaded episodes that I've ever recorded on this podcast. So you get to you hold the prize for the episodes that blew people's minds the most. And there's a lot of mind blowing stuff on this podcast. I just want to say. So thank you for the work that you do. I mean, obviously, what we're talking about today is bio regulator peptides. And so much of what gets discussed and bioregulators is, you know, there's a lot of theory out there too often. And I find this even in the medical field, people disregard a lot of the foundational research that was done on the bioregulators. And so, you know, maybe maybe just to set the stage for what we're going to present today, which is really for people who've been following bioregulators, this is the moment we've kind of all been waiting for, right? This is the culmination of eight years of kind of field clinical research that you've been conducting in this space. Can we just set the stage a little bit for people in terms of the bioregulators and your interactions with Dr. Cavanson, who really is the man that kind of started this whole thing, like he is the he's the papa in the world of bioregulator peptides, who we all look up to or did. Yeah, I think I can give you a real quick summary of both the history of it, and then my involvement and my relationship with Professor Cavanson. Where this all started was during the Cold War. The Russians became aware that the American military was developing certain weapons that would have the ability to damage vision, hearing, and so forth. And I'm sure the Soviet Union was working on similar kinds of things. And the other thing that was happening was that the Soviet Union Navy was noticing that sending out these submarines with young submariners, I guess the column, sitting in a submarine that was built in the late 50s and early 60s with a nuclear reactor that was primitive, didn't have top-rate radiation protections over. They would come back after being on these voyages with all sorts of medical issues, primarily thymus destruction issues and so forth. Mune system was just a mess, and so they realized that they couldn't have this situation developing. They took a group of military doctors and scientists, of which Professor Cavanson was both, has an MD and a PhD, and said, you've got to solve this problem. We've got to have protection on the battlefield if these lasers that the Americans are working on come to be. And we've got to have the submarines come back with healthy sailors and so forth. And we're also concerned about our cosmonaut program, what's going to happen when they come back. Cosmonaut program is their term for the astronaut program. So according to Professor Cavanson, the Soviet Union just threw enormous amounts of money. It was basically a blank check, which in the world of science is just a wonderful situation to be in. And they went back and did research for starting with Ivan Pavlov back in the early 1900s. And they realized that when food breaks down into amino acids, it passes through the digestive system and so forth. But if you can break down into what we call peptides, rather than the proteins that most of it ends up being, that you found you could find yourself in a whole different world using peptides as substances that had dramatic regeneration properties. And what they discovered was that if you create very short little amino acids, peptides, little strings of two, three and four and so forth primarily, that the amino acids or the peptides passed through membranes, arterial system, even the blood-brain barrier and so forth. And what was mostly interesting is that where you sourced the peptides from, which in this case were animals, they were pigs and cows, that when you took a portion of that animal and you selected a specific organ like you selected the heart or the liver, kidney and so forth, and you broke it down into these short chain amino acids, that when a human being had that introduced into that the body, the liver peptides or the kidney peptides, they didn't just float around generally, they went to the liver, to the kidney, to the brain and so forth. And they were organ specific, there were receptors on those organs that recognized these short chain amino acids. And so when they started using them very quickly, the submarine issues went away, they administered the peptides to the submarine people before they were going out on these trainings and so forth. They gave them to the cat and they gave them to them also when they came back, they gave them to the cosmonauts and so forth. And so that's where this started and they only had two peptides to start with, they had a pineal gland peptide and they had a thymus peptide, but just using those two, they were able to get protective by, through regeneration, they were able to get into a protective situation with the sailors and so forth, the cosmonauts. And then they used them for the Olympic teams for recovery and so forth. And then as they realized how potent those two peptides were, they started to expand and they took different organs out of these animals and they ended up with basically 21 or 22 depending on how you count one of the peptides, they now have 21 or 22 of these, what we call natural extract peptides, all of them organ specific. So they have, you know, peptide, peptide for the pancreas, peptide for restoration of cartilage and so forth and so forth. And so what Professor Cavanson did was he started doing longevity studies or at least mortality reduction studies in the late 1990s. And we're going to show some of those in the slides here in a moment and I'll talk more specifically about them. But what they found was that not only could they do organ regeneration, but they could actually reduce mortality by huge, huge percentages and I'll go into the slides. So that's sort of the background. And Professor Cavanson has extremely well known in Europe, everybody in Europe knows him and he's been the head of this and that, you know, society and institutes and so forth. His biography is crazy. Yeah, yeah. I think the last count that I was aware of, he had over 700 articles in clinical studies published. Anyway, I got involved because at some point in my life, I decided to stop making money so much and focus on staying alive. Without going into the history, my family just doesn't, for the men, doesn't have a very long, good longevity history and my father had died early. And I thought I better do something, take a different direction. And so much school got the PhD, I had a law degree and a master's and a bunch of other stuff, got the PhD and decided to focus on longevity for obvious, very selfish reasons. And I ran across when Google translator became available, I started running, you know, at looking at studies that came from all over the world, because up to that time, you could only really look at studies from United States, Britain, Israel and so forth, very restrictive, but now the whole world opened up. And I came across a published study that I'm going to show you the results of in a few moments, where Professor Cavanson was able to reduce mortality over periods of six, eight, 10, 12 years by 60, 70%. I mean, it was just astounding. It was so astounding that I thought this can't be for real, but I dug into the data and so forth and realized it was for real. And unlike America, where you have to be very careful when you're looking at a pharmaceutical clinical study, there's a lot of manipulation of the data. In fact, when I got my PhD, the first five years, I basically was a consultant to medical clinics to analyze the pharmaceutical clinical studies and tell them the reality of those studies rather than the pharmaceutical sort of advertising that they do. Anyway, so I read these studies and contacted the Institute in St. Petersburg and said, I want to come over there and see what you guys are doing. And to my surprise, they said, yes, you know, we'd be happy to have you. And so Vess and I, this is like 12 years ago or something like that. We went to Russia, to St. Petersburg. And I think that Professor Cavanson and the staff there, I mean, they were gracious as could be. I think they were so surprised and literally stunned. I think you got on a plane. You know, I wouldn't consider myself a scientist at that point, but certainly I was a researcher, would be so interested in their work. And so they literally took us in. And that was 10 or 12 years ago. And after I'd worked with them for a couple of years and understood the peptides and so forth, Cavanson and I talked about, let's do an American study. You know, we have all these studies here in Russia. Let's do a study in America and duplicate some, I call it a confirming study, duplicate what you've done here in Russia. And let's do it as a longevity study, because I'm not a doctor. So I can't be, you know, repairing kidneys and livers and so forth, even though the peptides would actually do that. And indirectly, we actually sort of do that. So we decided to put together this clinical study. And what I'm going to talk about today and show in the slides is the results of eight years of that study for a telomere and about five years epigenetics. Those two biomarkers are primary biological age markers. And so people sometimes, I think, they get confused. It's not possible to have an accurate biological age for a human being. It's the systems too complex. I mean, human systems are so complex that you cannot have one number that represents. What's interesting is that we've gone, and I'll talk about this with some of the slides, we've gone from having just a one number where we're now able to break down different systems and organs and determine a, and I don't like the term biological age, but it's something people can understand. We can determine the biological age of about 19 different organs, as well as the overall system. So we started our study using telomeres, which I'll explain briefly when we get to a slide. And then after that, epigenetics, which is about gene modification. And we've gotten outstanding results. And I'm going to share with everybody those results today. Yeah, that's exciting. That's a beautiful summary of really what those first couple of episodes were about. So if people are interested in getting into the details on some of that stuff, then definitely go back to those episodes and come back to, you know, if you don't want to read the end of the book before the beginning of the book, go back to the beginning of the book. Because this is, this isn't the end of the book, but this is definitely the next level, right? We've all been, we've all been waiting for these results with bated breath. And as you mentioned, like this is building on a lot of the clinical studies that Professor Khavenson did run in Russia. There was, there's the, you know, I always laugh when I use these terms, because these are straight off the paper, the old people study, the elderly people study, there's the Gazprom study, which is, was, was conducted in a factory in Siberia. And what's notable about all of those studies, which you've replicated in your work, is that people were not asked to change anything else. They were not asked to change their diet, they were not asked to change their lifestyle, whether they did on their own, or they didn't. Is it is, is not even the point. The point really was to identify what impact could these tiny proteins called bioregulator peptides have on a person's mortality rate. And, and it was, you know, I think you made this point also earlier was that people live too long to do a longevity study. So we do a, can we prevent people from dying sooner? Bottom line is kind of what it boils down to. I think one of the things that, that I found really interesting when I was reading a lot of the earlier work was when he was talking about food, and please correct me if I'm wrong here, but I think one of the things he described is that these sequences of peptides, these little bioregulator peptides, they kind of, they're embedded in the proteins in food, and they have, they have cleavage sites that are very specific that allow them to be, to remain intact so that when they get transported out of the gut into the body, you have this little peptide that's kind of going to find its way to the target organ. Is that, is that about right? Because that's, that was one of the things that was so fascinating to me is that they exist in food. Yeah, that is absolutely correct. I sometimes will use the metaphor of the, because I lived in Alaska for a long time, the salmon, you know, the salmon will depart from, you know, where they were basically hatched and so forth, and they'll go out and spend, you know, four or five years in, you know, in the oceans and so forth. And then there were thousands of creeks and rivers and so forth to choose from. They all go back to where they were originally born or, or you can see if you might say and so forth. We call them cleavage sites, we sometimes refer to them as docking sites. That is, the amino acids will swim through the arterial system, pass through the membranes, and they're looking for the liver, and they're looking for the receptacles on the liver. And that's what allows these peptide bioregulators, literally at the cellular level. People talk about cellular reprogramming. There's a lot of information thrown around, unfortunately, not very much proof yet. But that's the concept is that these amino acids are cellular reprogramming substances that then result in tissue rejuvenation and then finally organ regeneration. Yeah, you've got it down. And I think I got this from you. I will refer to bioregulators often as the ultimate epigenetic switches because they have, they are actually able to influence the way that our DNA expresses. And you had said in our last interview together that your hypothesis, which may still be a hypothesis or you may have proved it since then, is that what they're actually doing is correcting the expression of the DNA or resetting it back to a more youthful setting so that, you know, just as we used to heal on the go as young children, as we age, we lose that capacity. And maybe it's restoring at least some of that capacity back without going into the weeds and so forth. What's going on is that the peptide bioregulators are the only substance that I'm aware of that can fix what we call the DNA repair system. And the DNA repair system is built into our cells. It's sort of like you might have an assembly line, you know, where they're putting together some highly technical kinds of things. And on the assembly line, there are checkpoints to make sure that all the parts are being put in. You'd see this on an automobile line and so forth. And what happens is that when we were first conceived, this DNA repair system is operating at an optimal level. And that's why, you know, 99.999% of cell regulation occurs and cell duplication, replication occurs and everything, you know, runs smoothly. As we age, though, this DNA repair system basically starts to kind of deteriorate just for a lot of reasons. Part of it is the mutations that occur, you know, from the environment, from poor food choices and so forth, that they damage the assembly line or the DNA repair system. So what the peptides do, and there's a couple of clinical studies that Cavanson did publish that prove this, is they go in and they fix the DNA repair system. They return the DNA repair system back to something close to what it was when you were conceived and when you were born. And as a result, when you have a DNA repair system that's functioning as it should, there's a huge cleanup that takes place at the cellular level. So we could spend an hour just talking about that. But that's sort of what we've discovered. So I have another question for you. For the pineal gland bioregulator, which just for the audience, the pineal gland bioregulator has several different names depending on which form you're more talking about. So as a whole, the pineal gland bioregulator has an impact on, seems to have a positive impact on the immune system. It, you know, of its laundry list of benefits that are often cited is that it may upregulate the activity of telomerase, which is the enzyme that preserves telomeres, which we're going to talk about, you're going to talk about in a little while. It also helps to restore melatonin and it restores melatonin to optimal levels rather than boosting it or depressing it. It's looking to normalize. It has a positive impact on the circadian rhythm. There are some studies that Professor Kavinsen did that shows that it may have some benefits in the case of cancer, which, you know, the one I'm the study I'm most familiar with is a mouse study, but there may be others that I don't know as well. And then also talks about being beneficial for cellular oxidative stress. When we talk about the bioregulator going like kind of homing in on its home tissue, being the pineal gland, are all of those impacts being to your knowledge? And I don't know if you know the answer to this question, but this is one of those burning questions I've always had in my head. Is all of this happening from the pineal gland acting on those systems? Oh, and also it helps to balance the endocrine system. It has a balancing effect on hormones. Or do you think that there's receptors for that pineal gland bioregulator in other systems? Like, you know, I always think of it as kind of the master bioregulator. But do you have any insight in that? Or is that still a little bit of one of those things that still need some clarification and elucidation? The latter, it needs clarification. We don't really know. But it's interesting when I put together a protocol. And when we're focused on the two tests that we use as biome, in fact, let me step back from it. Since it's difficult to make an assessment of overall biological age, what we have to use is biomarkers. And the biomarkers that there are many biomarkers for reflection of biological age, but the two that are pretty much predominant are telomeres and epigenetically or DNA methylation. We know those are very much reflective of a person's biological status. But there's many other things as well. But these are the two that are primary. And most importantly, these are the two that we can actually do testing on, or four, you might say. Going back to the question about the pineal gland and so forth, we don't know, into any depth, we don't know how on multiple levels, things like the pineal gland peptide, how it does what it does, how it knows where to go in terms of docking or claving and so forth. But what we do know based on Professor Cavanson's studies, extensive studies, is, and I'll have to kind of preface this, while we're focused on telomeres and DNA methylation or epigenetics, if a person in the clinical study has some other organ related issues, they've got some heart history, they've got arterial problems, they've got kidney, even some of them, stage three kidney. And by the way, when we first set up the studies, we would accept anyone into the studies pretty much unless they had active cancer. But then several years ago, as the studies were growing larger and larger, we restricted the admission pretty much to physicians. And so at that point, we could start using the peptides, or I should say the physicians would use the peptides to deal with various health issues, etc., like a kidney problem, heart problems, or so. When I would put together a protocol focused primarily on longevity, I would look at the telomere situation, we test people for their telomere length, then the epigenetics, we test them for DNA methylation status. But then we would profile what health issues are they concerned about. And we would then add appropriate peptides, because we have say 21 of those. So we would add relevant peptides. But back to your pineal gland, there is never ever a protocol that we've created that does not include emphasis on the pineal gland. And again, we don't understand exactly how it does all these amazing things, you know, in the endocrine system and so forth. But it is at the prime, I would say it's the single most important of the peptides followed only by the thymus peptide. Yeah, I call those my desert island peptides. Although you could argue that if you were on the desert island, maybe you wouldn't even need peptides, because you wouldn't have all the horrible things that we're exposed to in the modern world. But a little help never, never hurts. Before we launch into the presentation, people are going to want to know, what are you using to test? I know that you've kind of changed testing companies, we don't need to name names necessarily, but people would love to know probably which tester you currently using to assess people's telomere length and biological age. DNA methylation, sorry. Yeah, the tests are the same. It's just that like anything in the technology world, they are enhanced over a period of time. And some labs are more enhanced than others. There are some labs that doing telomere testing that don't kind of move along with the science as it has progressed. And so for telomeres, we use a couple of labs that measure the telomeres on the end of our chromosomes and now show some slides that demonstrate that. We've been using a lab since 2012. But we're now looking at, we're doing beta testing with another lab because we see that their results seem to be much more accurate. Again, it's, you know, you start, some of the businesses are labs, they start doing things in a certain way, and it's very difficult for them to change to something else. So, that's the telomeres. For the DNA methylation, we've used, and by the way, for the telomeres seven, eight years ago, longer than that, I beta tested probably six or seven different telomere testing labs, including those in Europe and so forth. And when I say beta testing, I would have the blood samples from the same person sent in over a period of two or three weeks. So there'd be two or three samples for the same person. And I would then look at the results to make sure that they were consistent and the ones had a large variance, of course, were dismissed and so forth. Anyway, so for the DNA methylation, same kind of story with the DNA methylation, when it first became commercially available about 2020, 2019, there were a couple labs that were doing the testing. But the state of the science at that point was that they could only give you a what we call a DNA age, they can measure the DNA methylation and figure out which genes that related to longevity were turned on and turned off, and give you that one number. Then about a year later or so, one of the labs, again, very progressive people, they were able to divide that up and give us a separate DNA methylation age, you might say, or gene related status of the immune system separately from an overall biological age. And then a couple of years later, about a year later or so, that particular lab partnered with Harvard and Yale and so forth. And they started using very large data banks of information and using algorithms. And they then moved on to where they could give us their predictions of 11 different organ systems and so forth. So we could get an overall age, biological age, you could call it epigenetic age, and then we could get a predicted age of things like the brain, the pancreas, the heart, the liver, and so forth and so forth. So as is true with all technology, it develops, it gets better and better. And right now we're beta testing a new company that's giving us the biological age or epigenetic age of 19 of the systems and organs. And what we are very interested in is that prior to this, they were pretty much just giving us predictions. That is, the lab that was doing this before was able to use the large data banks and the algorithms used to predict what people's epigenetic age might be for the heart, the liver, and so forth. This new lab actually doesn't do predictions, it actually does actual measurements, which is phenomenal. And so I can get a very accurate, within probably about a two-year time span, I can get an accurate age for someone's heart. In addition, I can, the information also gives me the pace of aging of that heart. In other words, is that heart aging faster than the overall body or slower? And so when we create the protocols for these people, we look at all these, and wherever we see accelerated aging pace, then we use more. So if it's, say that's a heart that's got accelerated aging, it's aging say 10% of your faster than your calendar age, then we use more heart peptides. Yeah, no, that makes total sense. That's really fascinating. So the new lab, are they doing telomere testing as well, or you use a different methodology for that? I'll say that again, Natalie. The new lab, are they doing telomere testing as well, or are you using a different lab for that? We're just literally in the process, when I say beta testing. Whenever I engage a new lab, then it takes months to get the test kits, get them out to various people, where we're sending multiple kits to the same person, as I mentioned earlier, as well as on myself and so forth. So it's a process of several months, and we are in the midst of doing beta testing with a new telomere lab. I'm liking what I'm seeing, and we've moved on to this company. I can use the name Generation Labs, which is certainly the leader in the world for epigenetic assessment of the overall system, as well as those 19 different ... Okay, so DNA methylation is Generation Labs, and you're not ready to share the telomere test yet, just because you're still assessing it? Yeah, until I'm convinced that it is more accurate. But also, let me put this in some perspective. When we get into the slides, we're going to show some slides pertaining to reflecting clinical studies, where there's significant, in fact, just amazing reductions in mortality, and I'll be showing you what those numbers are and so forth. And what we're trying to do overall with people is basically a makeover, you could call it, of the most significant systems, the epigenetic system, the telomere system in the body. And while I pay attention to these tests, they're not the most important thing. The most important thing is what we're doing is matching what Professor Cavanson was able to do in his multiple-year clinical studies. And so even if we didn't do any testing, I'll explain that in a moment, if someone just took these peptides for a period of three or four years, Professor Cavanson's research, my experience is they're going to get all of these benefits. We primarily use the testing because people like to see results. They like the results that they can actually see on a lab report to show progress. And so I have to caution people oftentimes that, yes, the lab results are significant. We establish baselines and then we also establish goals for the telomeres and so forth. But really, the program here is to get 21 peptide bioregulators out of the boxes and into your body for the next three or four years. And we know the answer is that based on Cavanson's work, we know that that's going to extend your lifespan really significantly. And it's going to regenerate organs, and I have a couple slides that show that. It's going to regenerate organs. So sometimes I'll say it's like an automobile. You've got this 57 Chevy that I had when I was a kid. And it's got tires that have to be renewed periodically. The engine and the transmission and all that stuff will run a long time. But at some point, it all wears out. And what the bioregulators do is with the telomeres, it's like putting on a new set of tires. And I'll explain that with a slide. What the rest of the bioregulators do is they go through and they restore everything in the automobile, the engine, the transmission, the computer system and so forth, so that you can drive that car another 50 to 100,000 miles. And it's difficult to test each of those stages in terms of where the automobile is in terms of its assessment, call it age. So I don't want to spend a lot of time on it, but the tests are helpful. But really, the goal is get a bunch of these peptides into your system over the next three or four years and go live a long life. In Professor Cavanson's reports, in those two studies I mentioned earlier, the elderly people study and the old people study, you know, some of the metrics he reports on is better quality of life, better immune system. Like they just were healthier in general. They slept better. Their bone density was better. He wasn't looking at, is your pineal gland healthier? It was like, what are the downstream effects? How is this expressing in the person's health? And I know that certainly, you know, in my communities where I've sometimes worked with people with bioregulators, we sometimes see liver enzymes improve where they were out of balance or how people feel and how they're sometimes we see better blood sugar regulation. They're still doing all the other things, but the bioregulators seems to add another piece to the puzzle, as it were. And the last thing I would just want to, I wanted to invite you to talk about a little bit before we get into the slides is this idea that of a bioregulator modulating, like normalizing function versus boosting function or suppressing function. And this, which is part of the reason I think why they're so incredible. And it speaks to what they're actually doing, because if you're restoring the body's tissues and organs ability to function properly, you're not boosting the immune system. You're not boosting the thyroid. You're not suppressing anything. You're basically laying the work so that the thyroid goes back to working the way it was supposed to, or the immune system is working the way it was supposed to. I should be interviewing you. No, I'm, this is all stuff I learned from you. Are you kidding? Well, but you just answered the question that you were sort of getting, getting close to asking. Yes. Well, but I'm, but you're the guy, but you're the guy who worked with Professor Kavenson. You're the guy who's done the eight year study. I'm just dabbling and I'm compared to you. I'm just dabbling. So what I'm looking for is, is this what you've observed as well? Oh, absolutely. Yeah. And we can, we can measure, you know, a good amount of that, particularly now with the new DNA methylation stuff. What the myoregallias are doing, unlike, let's say the synthetic peptides, which I think are wonderful actually, the synthetic peptides are giving a quick boost to whatever the system is or whatever the organ issue is and so forth. And so they go in and it's like the fire department showing up, you know, and they're putting out the fire and so on. Okay. The peptides act differently. They're not going to do anything quickly to start with. Okay. What we know is with exception of some things like kidney restoration and thyroid restoration. So you're not going to see any feel any or even lab test any real significant changes for about a year. It's a slow process, of course, to rebuild at the cellular level, you know, these organs in these systems. So for instance, with the telomere testing, I tell people don't expect to see anything of significance for at least 12 months with the DNA methylation. I tell them two years. And that's why we ask people to stay in the clinical studies. We, you know, it's not a contract, but we give them some information and ask them to sign that they've read the information. We tell people stay in this thing for three to four years. Because that's how long it takes to sort of do this regeneration. It's not a fast process. So should we go to the slides? Let's do it. So for those of you who are listening to this podcast, this would be the part where you might want to hit pause, head on over to your computer, turn on YouTube and go to somewhere around minute 38 or so, maybe minute 42. And that's where you're going to see this slide presentation. We'll do our best to explain it to you if you don't have the option to do that. But this is going to get visual. What if your coffee had a smarter sidekick, wired and tired, task switching and a crash that shows up right when you need your brain most? Who needs that? So to avoid it, I pair my morning brew with this brain support stack. My focus stays sharp. My mood stays steady. And I don't bargain with my to-do list at 3 p.m. It's built for synergy. New PEPT and J147 support BDNF and healthy energy signaling. Alpha GPC fuels acetylcholine. Hooperzine A helps maintain it. L-tyrazine and urodine show up for motivation and synaptic repair. Synapses is where your neurons connect. Theocrine gives long lasting lift without the tolerance curve and altheanine helps to keep things calm and clear. Phosphatidylserine supports memory and stress resilience so you can think, not overthink. This is quite the stack. Boost your brain and productivity with Neutropept at leveluphealth.com. That's leveluplvluphealth.com. And make sure to use code NAT at checkout to get 20% off your purchase. Okay, so here we are. We have the infamous slide presentation up. Let's fire away. This is one of the reasons I went to Russia. I read this study that was published about roughly about 2000 and so forth. And of course, the title caught my attention, you know, the mechanisms of peptide regulation of aging. Those words regulation of aging just jumped out at me. And I started reading everything that I could get my hands on or everything that I could translate and so forth. And I realized that this was for real. I mean, this had, at that point, this had 40 years or more of science behind it. And, you know, I, of course, did background on Cavinson and learned that he's just, you know, as bona fide as you can possibly be, as I said earlier, well known in Europe, well known in pretty much the rest of the world, but not here in the US, so forth. So this is what got me over there. And so what Cavinson and I did was, this would be about 2000, I don't know, 10 or 12 or something in there was I said to him, you know, you've done this amazing work, all of it's science based and so forth. Everybody knows who you are in Europe and so forth. You're unknown in America. And unfortunately, in America, they only pay attention primarily to studies that are based in America or maybe Britain sometimes Israel and so forth. Let's basically do what I call confirming studies in America. Let's use your published studies where you've shown tremendous mortality reduction, where you've proven organ regeneration. Let's add to that biological age reversal because Cavinson wasn't interested in, you know, called anti aging at this point. He wasn't focused on it at all. What he was passionate about was developing new peptides that could be used for mortality reduction and organ regeneration. In fact, he told me he thought that it was kind of odd the focus that Americans have on anti aging. He says, because you can't have anti aging. He says, you can improve, you know, at the cellular level, you know, he would give me the scientific part of it. Yeah, he's getting, he's kind of getting into semantics, like you cannot de-age, you can, you can age well, but you can't de-age. But he, you know, we had several discussions, you don't convince people like Cavinson of anything, you give them data, you give them information and they'll let them decide. I have said several times that he's the most brilliant person, scientist I've ever encountered. I put him literally in categories with Einstein and some of the other greats. I mean, when you see the results that he has produced and so forth, it is mind boggling. Anyway, so, you know, gradually he came around to and he said to me, you know, Bill, if you, if you want to do a confirming study in terms of biological age interventions, so we're then sure, let's go ahead and do that. And then we'll publish those studies in America and also here in Europe. So that's sort of how this got started in 2017. And we had to figure out, you know, how do we measure biological age and changes in biological age and as I talked about earlier, the two most trackable interventions would be telomeres activation or telomere lengthening and DNA methylation. And so we use that as our framework to prove that the peptide bioregulators could have a positive impact on biological age. And so this study was the one that I ran across that was just incredible because what we have going here is in an elderly groups of people, we have a significant reduction over a period of years in longevity. And as you mentioned earlier when we were talking, it's hard to have to do longevity trials and so forth because people have to live a long time for where you can determine if the intervention has been helpful and so forth. But what Cavinson did was over a period of two to six years and then the test or the process continued on for as long as 12 years, he was able to show very significant reduction in mortality. And that's what this, this is what the abstract is showing us. So I took the abstract and I basically then created some graphs that would make it easier to understand. And so what we have is there's two groups of people here, the elderly people as they were called in the study and they were that people from 60 to 74 years of age. And then the older people down below, Russians are not the most diplomatic calling them old people. That's now the group I'm in, I'm 78, I'll be 79 in two months, I guess. So in the group of 60 to 74 year old, the control where it says polyvitam is there in the yellow are the people not on the peptides. And if we look at mortality rate in different time frames and mortality rate in eight years and then dropped down where it says 12 years, we'll focus on the 12 years. So it was a 12 year study. The control group 44% of those people died. Okay. And that would be normal for that age group over that period of time. Using a new you and I were just talking about the pineal gland and how extensive the impact of the pineal gland and the peptides have on the whole body. Notice that in the peptide group using just that one peptide, the mortality rate over 12 years dropped in half. It went from 44% to 22%. I mean, that's unheard of. I mean, that's just, there's nothing else out there that I've come across. Now I've been at this 30 years now that will do that. And then with just one peptide. Okay. So we then moved on to the older group, 75 to 89. And in the control group, the non peptide group, the mortality rate was basically 82%. You know, that for that age group, that part of the world, this by the way was Russia and Ukraine. But using again, the pep, the pineal gland peptide, it dropped the mortality rate down to 46%, 45.8. But look what happens when a second peptide, the thymus peptide was added, it drops to the mortality rate from 82% mortality to 33. Yeah. I mean, that's just mind-woggling. Yeah. And the interesting thing about this, and I know you know enough of the history and so forth, and you read enough of the studies in this, the old people one, they only use the peptides for three years. Yeah. That's, you know, that's shocking on the one hand. And on the other hand, it makes total sense. Yes, it does. Right. But I think one thing that I would like to point out to the audience is that the form of the peptides that they were using here is different than the form that we currently can access in North America. So the pineal gland peptide was epithalamin and the thymus was thymiline. And these are actual extracts of those organs of animals that have been prepared for an intramuscular injection, which is why the polyvitamins is relevant to here, because everybody was getting an injection of something, but nobody knew what they were getting as an injection. Yes, that is correct. But in the clinical study, we weren't, we're not using intramuscular. Oh, I get it. But I'm just saying in these studies, that's what they were using. And I just think these studies sometimes get misquoted quite often because, you know, I think what's interesting about the work that you've done now is you've shown that the oral bioregulators, the natural bioregulators can very effectively, in many ways, reproduce, at least get us in there. You know, you haven't done the 12 year study, the same study that he did. But at the same time, what you're showing is that those oral bioregulators, the natural bioregulators very much produce very powerful results. Yes, they are, they are the natural extracts in capsule form. And that concerned me a long time ago when we were in Cavinson, we were talking about this. And so what Cavinson did was gave me some telomere studies that he had run using the injectables, using, you know, the natural extracts and, or I'm sorry, using the synthetics because he had synthetics for Pytalon and for the thymus, and then using the oral capsules, the extracts that I'm using. And so over a period of time, looking at the telomere results using those different methodologies, the difference between the oral natural extracts that we're using, and the injectables or the synthetics over a period of several years, a 10% difference. In other words, the oral capsules were 90% as effective in lengthening telomeres as the injectables or the synthetics. That's amazing. So the synthetics matched up with the oral, or did the synthetics match up with the injectable natural? As I recall, about halfway between. Somewhere in between. So then the most the ones that move the needle the most are the natural injectable. Yes. Form, which is the epithalamin and the thymalin. The next in line is the oral natural. That is the endolutin. No, the next in line is the oral synthetic. Oral synthetic. Yeah, there's about six or eight. Cavinsen has about six or eight of the peptide regulate regulators as synthetics. We don't use them. They're not used outside of Russia. But the synthetic group in the middle was less effective than the endomuscular, but more effective than the natural extracts. Okay. And what about the synthetic like epithalon that the synthetic ones that are available outside of Russia? Have those been studied at all or not so much? Slightly. They're faster acting. Yeah. As any synthetic will be. That's why the synthetic peptides that are used like BPC and all the rest of those are very quickly used. But if you're looking at long term, which is what the longevity studies are focused on, if you're looking at long term, you don't want the endomuscular. You don't want the six or eight different synthetic bioregulators. They're good. What you want is to run the race to the end of three or four years. You want the oral capsules in natural extracts. Okay. Great. All right. Okay. Moving on. So yeah, what this was showing was that previous slide where Cavinsen, I showed that what his work has been all about is mortality reduction. The next part of this is going to be a short one on organ regeneration. And then we're going to get to the biological age part. Perfect. Here's the organ regeneration. In other slideshows, I have many of these kinds of things, but no pun intended. But if we're using vision and retina issues, you can kind of see the difference between before and after treatment. And so in all of these retinal conditions, diabetic retinopathy, age-related macular degeneration, and my favorite, retinitis pigmentosa, when we're looking at these field of vision on the left, where I know that the people listening can't see, but there's a definite amount of what we call yellow and black occlusions, in other words, where people don't have almost any eyesight where it's shown as red and black and so forth, where it's shown as green as the vision they have remaining. And so in each of these, there is a significant amount of red, black, and yellow, which is impairing people's vision. On several of these on the retinitis pigmentosa, it's almost all black. Yeah, it's incredible. Yeah. And what people tell me is that if you're going to have any of these retina diseases, you don't want retinitis pigmentosa. It just closes down. There's nothing that can be done about it. Actually, it's truthful. There's really nothing in the Western world that can be done about any of these retinal conditions. There's some drops that the ophthalmologist used, but basically it's non-reversible in the US, progressive and so forth. So when we look at the screen, the screening field of vision on the right hand side in each of these categories, the amount of green, which is vision restoration, is dramatic. I mean, if we look at the diabetic retinopathy, I would say there's been a 70 to 80% increase in the green and a huge decrease in each one of these situations, the macular degeneration, the red and red pigmentosa, there's enough improvement that a person, I would say on the whole, it's a generalization, but on the whole, a person can have a pretty natural life. I mean, if you look at the diabetic retinopathy, that person probably cannot drive safely a car. On the other hand, after treatment, and the treatment usually lasted two or three years, on the other hand, after two or three years of treatment, they're whizzing around in their car. Yeah, 100%. And also with the macular degeneration, not only are you seeing a reversal of the loss of vision, but that means it's a double win because you stop the degeneration and you've reversed back to a better state of vision. Absolutely. I mean, it would be enough of an achievement if you could just stop the progression of the diseases, because now with the testing, being able to identify these conditions early on, if you could stop the progression, I mean, that's amazing. But this situation, it isn't just stopping the progression, it's reversing it. Yeah, it's incredible. And then the retinitis pigmentosa, I mean, that is a sentenced to blindness. And here we have, I mean, you know, this person still has impaired vision, but the increase in the green area is dramatic. So, yeah. And the problem, the issue with retinitis pigmentosa is that it tends to manifest itself in much younger people. It's an inheritable disease, typically kind of skips a generation and so forth. But many, many people are diagnosed in their 20s and 30s. I mentioned before, and I'll do it just real quickly, I had two brothers, you know, in a family where there was a history of retinitis pigmentosa who were diagnosed in the same year in their teens. I think the younger boy was 13 and the older boy was 16. Both of them were diagnosed with the retinitis pigmentosa. And that's very, very common that it's diagnosed at an early age. Typically, it depends, you know, on each individual case, but as an example, over about a 10-year period of time from diagnosis, they go completely blind. Everything is black. Well, through a friend who, you know, had new me and knew the family and so forth, long and short is that we put these boys, this would be 2012, we put these boys on the vision peptides and a couple others. We always use a multiple of peptides and never just one. We put them on the peptides within six months, their night vision, which is impaired first before other things started improving. 10 years, 12 years later, they have perfect vision. They have families, they drive cars, they have careers. Whereas 10 years later without the peptides, they probably would be in utter blackness. Yeah. So are you able to share the peptides that, you know, the family of peptides that are used in these, because it's not just the retina peptides. There's a couple of, if I'm, you know, I think that the blood vessel peptide usually plays a role here and our infamous pineal peptide also seems to play a role in this stack. Am I right about that? For a condition, now let's go back to what I was saying earlier that the goal is longevity, okay, organ regeneration and so forth. But we don't ignore conditions that people have. And if the individual, primarily about 80% of the people in the clinical study, I think there's about 140 people in the clinical studies, 80% of them are doctors. So I have a kind of a free hand to be able to create protocols for different medical conditions. And where a person in the clinical study is not a doctor, we then work through their doctor in putting these together. And the norm would be for a condition, a minimum of three different peptides, typically oftentimes five different peptides. So someone with retinitis pigmentosa or any retinal disease would have the vision peptide, the arterial peptide, the thymus peptide, the pineal gland peptide, always in those. And those would be probably the four that we would use for vision issues, thymus, pineal, vision, arterial. Yeah, those would be the four that we would have. But because we're doing longevity for these people, the average person on a monthly basis is taking, I would say five or six, a few people are taking seven different peptides during the course of a month, because we're, you know, focused on telomeres and epigenetics. But they're only taking, except in a rare case, well, go back to retinitis pigmentosa, we would put someone on a high dose protocol for probably about three months. And a high dose protocol would be maybe two capsules a day of each one of those peptides, sometimes three capsules a day for two or three months. And then we'd start graduating down to a lesser program. For the people who are just looking at longevity, telomeres DNA, the norm that's used in almost 90% of the cases is, say they're on five different peptides, two capsules a day for 10 days only. So a total of 10, you know, say 10, 10 days only, and then off for 20 days. That's the normal process. They're not unlike American pharmaceutical drugs and so forth, where once you go on a drug, you're probably on it for the rest of your life. And then the whole period is basically about a three to four year timeframe. And then we're done at that point. Back off. Yeah. Do you think you might, at overtime, do you think you might revisit like a maintenance protocol? Well, that's the problem. After a two years break, like, what do you think about that? That's the problem. That sounds, theoretically, that sounds like a smart thing. And that's what Cavins and I thought would happen. We figured that at about the three or four year period, when we get real close to the goals that we set for these people, that we would say goodbye to them from his nobody wants to leave. Yeah, literally. So we had to develop a maintenance program. I think one person maybe in all these years left, I can't remember why, but not disgruntled, but oh, no, yeah, he said he checked back in five years. So we put them on a maintenance program, maybe two different peptides a month rotating through all of those peptides during the year, and then we change it for the next year. Yeah, cool. Okay, so let's move on from this is the organ regeneration. So this is just a summary here. We had 124 participants in this leg or track of the clinical study on different dosages, low, medium, high. And as you noted, I think earlier, there were no other lifestyle changes or interventions. We didn't tell people to change anything else. We never inquired basically about other things that they were doing, other treatments, lifestyle changes, diet, none of that. We just wanted to the only thing we wanted to do is add the peptides. And this is just a listing of the ones that we use the most of. And they're in capsule form, as I say, the normal dosage is two caps a day for 10 days out of the month. So we get to biological reversal, which is the goal that I was focused in in terms of doing these studies. And we started with telomeres because there was testing for telomeres easily available as blood tests 10 or 12 years ago when we started. And I won't spend much time on the science of telomeres, but they basically telomeres are little in caps on the end of our chromosomes. And they're vital for allowing cell replication to occur. And we know from hundreds of the last time I checked there were 2500 PubMed studies and so forth related to telomeres. And what we know is that every time we have a cell replication, we lose just a little bit of that in cap. And while that in cap is intact, when we're young cells replicate, you know, as they should, you know, the replication goes smoothly and so forth. But as we age, and as those in caps deteriorate, then you start having problems with the quality of the replication and it leads to aging, acceleration, mortality increases as well as chronic disease. Bill Anders is a well known scientist here in America. And there's a quote here where he says, every time our cells divide, our telomeres get a little shorter and every time they shorten our cells age. Elizabeth Blackburn was one of three people, American scientists who received the Nobel in 2009. And she says in this quote that, telomere slows the rate at which telomeres degrade and research indicates people with longer telomeres have less risk of developing the common illnesses of aging. So that's what telomeres are all about. So the idea was, could we re-lengthen, could we slow the process of telomere loss and in fact, could we re-lengthen them? And so on the screen right now is a study from Professor Cavanson in 2003, where he shows that the pineal gland peptide induces telomorous activity, we won't go into the mechanics of that, basically resulting in telomere lengthening. And that was remarkable because slowing the loss of telomeres and lengthening them is one of the holy grails in all of science. And to my knowledge, while there are some claims out there, there is no one that can on a consistent basis lengthen telomeres except the Russians. And now of course, our clinical study. So what I'm showing next is my results over a period of time. I mean, a good scientist, I think experiments on himself, much like this parachute is famous for doing and so forth. And then you start testing on all of your loved ones and your friends and you hope that they continue to be your friends and so forth. So in 2014, this is before I met Professor Cavanson. It's before I knew anything about peptides. I was 68 at that time. And my first telomere test showed that my telomeres were equivalent to someone of a 75-year-old. In other words, when they measure the end of my chromosomes and look at the telomeres, they can sort of equate that to a biological or to a chronological age. So my telomere age, as we called it, was 75 or in other words, my telomeres had accelerated loss and I was seven years younger or might you might say older than my chronological age. Not a good situation for a 68-year-old that accelerated aging. No. Two years later, I was retested and at that point I had been on the peptides for about a year, had met Professor Cavanson, so forth. I'm now 70 and at this point my telomeres are equivalent to a 68-year-old. So I've gone from seven years older telomere-wise to two years younger. Two more years later, 2018, I'm 72. My telomere age is 44. I've been on the peptides for about three years plus. 2019, I'm 73 chronologically. My telomere age was down to 35. And then the most recent test, holy cow, look at you. No wonder you look younger. I was 76 at this point and my telomere age, as we call it, was equivalent to a 23-year-old male. Amazing. That's really impressive. Yeah. So I decided to decrease the attention on the telomeres because I was concerned that Vess, my wife who you know, was going to leave me for a mature older man. But you could always claim immaturity when you do something that the noise heard. Always say, look, I mean, I'm now 23, the equivalent of a 23-year-old. We know that the male really doesn't mature. So what, 26 is the current number? I thought it was forever. Well, possibly. No, Vess wouldn't buy that anyway. I know she wouldn't. She doesn't buy that nonsense. In any event, this is very impressive. So that was in 20. So have you tested since 2023 or are you just writing away? I'm actually in the process of retesting, beta testing with this new company right now. Oh, wow. Okay. Well, that'll be interesting. When do you expect to get results from that? Four weeks. All right. Well, we'll have to check in with you in September. Yeah. These lab tests are not like, you know, running down to the local lab and, you know, where they do a lipid test and so forth. And you get the results, you know, two days later. Yeah. They're much more complicated. There's some work to be done. It wasn't just me. Okay. Yeah. This is a photo of Tora Bright. Tora Bright was a three-time Olympic gold and silver competitor and was a Olympic gold and silver winner in snowboarding, skiing and so forth. And of course, the Olympic doctors, I guess, they do extensive testing. I was stunned to find out that they do telomere testing, but then I understood why because we won't spend the time on it today. But what we know is that the one, the number one situation that causes accelerated telomere loss is stress of all things. And of course, these athletes, Tora had been, you know, skiing since she was about five or six years of age and she was now chronologically 32. Her doctor, Olympic doctor tested it for telomeres and her telomeres were equivalent to a 56-year-old woman. Yeah. I think that you brought, I was going to ask you about the stress anyway because that came up earlier in our earlier interviews. And I just want to say to the audience, because we're going to go long on this podcast, that if you take nothing else away from this podcast episode, it's the massive impact, the chronic stress that is not dealt with properly will have on your ageing, really, on accelerating your ageing, at least from a telomere perspective. Yes. In fact, Lidlbeth Blacksburg, who I mentioned earlier, Nobel Prize and so forth, professor at UC San Francisco, she's done extensive studies on stress and telomeres. And what they've discovered is that if a woman is pregnant and she's not happy about being pregnant or there are financial issues, she's a single mother, there's a death of loved ones in the family, just a very difficult pregnancy, she will give birth to a newborn on average with 15 to 20% shorter telomeres at birth than a woman giving birth where she was happy about having the child. Money wasn't an issue, she's got a supporting spouse, all these kinds of things. It's that powerful that can be passed down to an unborn child. Yeah. Well, I mean, there's a lot of talk about generational stress being passed down to a child, and that may be part of it. So we put a tour on about a 18 month program of telomere bioregulators and two years later, we retested her now, she's two years older at this point, but her telomeres were equivalent to a 31 year old. Tora wins for the win again. Yeah. So we had about 120 some odd people, and I know that your viewers can't see this, but this is one of many, many pages of spreadsheets where we track all of this information on the 124 people. So with this spreadsheet is showing a baseline telomere test, both in terms of length and age equivalency, and then a couple of years later, after we've had the people on the peptide program for a while, we do our secondary testing, that's the yellow line here, and that shows on the whole significant telomere lengthening and improvement. And then over on the far right, the green actually shows the number of years of telomere age that we were able to reduce. And so we're looking at numbers of 31 years, 18 years, 19 years of reduction or lengthening, you might say of telomeres, 14, 11, 12. But it's interesting because of about 5% or so of the people only get one or two or three years worth of telomere lengthening over a multiple year protocol. And we believe, because I know knew a lot of these people in the beginning, it has to do with stress in their life. Typically, the busy business people and so forth or people with stressful lives ended up receiving less telomere lengthening. The interesting thing is that every year we lose a little bit of telomeres, but nobody lost a single year in the clinical study, even though they were two or three years older. Yeah, yeah, it's dramatic. I mean, it kind of makes, you know, what's interesting is one of the interventions, certainly before I heard of bioregulators, one of the few interventions that people believe could help to restore telomere length is meditation, like real meditation. Being a meditator and a skilled meditator would be one of those strategies that could help you to manage your stress levels. And I would think I've never really looked at the studies, I'm aware of them. I would think that it would be a significant, not only for telomeres, but for many things, everything. So the average decrease in what we call a cell year or biological age was over a three-year period of time, was basically almost 22 years, 21.62 years, or in other words, for every 12 months on the program, people were able to lengthen their telomeres and reduce their telomere age by about seven years. That's amazing. Per year. Beautiful. Okay, then we went on to the epigenetic methylation study. It became possible to measure using epigenetic technology and I'll explain in a moment briefly what epigenetics are all about, but it became possible commercially about 2020, so that's when we added this study. And while going into all the details, it's all about genes that are related to longevity being turned on or turned off. And what we find is that the gene status of genes that are turned on that are related to helpful with longevity reflects itself in a younger biological age for people. And we know that what affects the genetics of those genes are things like diet, stress, exercise, their sleeping pattern, climate, literally, nutraceuticals, peptides, etc. In other words, everything that we do affects the, what we call the epigenetics of gene expression. One person said to me, it's sort of like that the genes are like our computer hard drive and the epigenetics of this is the software and software can be changed. So that's sort of a short course in epigenetics. The key here is that if you have a younger epigenetic age, in other words, more genes that are related to longevity turned on than off, you basically that will translate into a younger biological age. This just shows, you know, how we do the measurement and so forth. We'll just kind of skip through this. It's based on DNA methylation patterns that we can actually measure at this point. And what's interesting here is that if you have a situation where you're, call it your biological epigenetics, if your epigenetic age is older than your chronological age, Dr. Stephen Horvath at UCLA and other scientists were able to figure out and report with numerous clinical studies that if your epigenetic age is older than your chronological age, you're in trouble. You've got significant mortality risk over time. And so these are a couple of charts that show the increase in mortality risk based on having an older epigenetic age than a younger. The converse of that is that if your epigenetic age as measured is less than your chronological age, you have a decreased mortality risk. And without going into all the detail in these slides, I show if you're seven years above your chronological age, you have an 82% increase mortality risk compared to your same age peers. On the other hand, if you're seven years below your chronological age, you have a 50% decreased mortality risk. So the goal in the clinical study was to make an assessment of people's epigenetic age and then use the peptides at different dosages to reduce their epigenetic age. And I know that the people can't see the colors and so forth until they get to YouTube, but the chart that is sort of red, raspberry and so forth is the increased mortality risk. The other one that's kind of green and so forth is the decrease. Our goal is to get all the people out of the red into the green. So some test results. These are mine again. But I had been on the peptides for about four or five years before this testing became available. And it was September of 2020. I was 73 years of age at that point. But again, I had been on the peptides for four or five years. This lab called at true age, basically my epigenetic age was 69 or four years less than my chronological. That translates into about a 28 to 30% reduced risk of all cost mortality. Great place to be on baseline, but again, I'd been on the peptides. Most people, particularly Americans that we test as bait lines are three to five years older than their chronological age, which puts them in an increased mortality risk. So a couple years later, two years later, I retested and I was at that point 75. And my epigenetic age was 65. So I was now 10 years less with a significant reduced. And I think my last test, I don't think I have it in this set. I'm 21 years younger than my chronological age epigenetically. That is remarkable. And once again, I'm going to point you guys, the listeners back to one of the earlier episodes where you talk about one of the drivers to you doing this work right at the very beginning. And you mentioned it very briefly at the beginning of this podcast is that longevity was not a quality in your lineage, in your family lineage. And so people will then understand, never mind how impressive these, I mean, your results are impressive regardless, but they become even more impressive when we understand the backdrop of your family history. Yes, unfortunately, all the men going back a long, long time, because we have, we do a lot of research and so forth, genealogical research, they all died in their 50s and 60s, all of them. My father had his first heart attack and they all died from heart disease. He had his first heart attack at 57 and died of heart disease at 64. And I'm now coming up on 79. So you're doing all right. Yep. I wake, I am grateful every morning when I just wake up and I realize, ah, I'm breathing again, I get another day. Amazing. And now we have, we have someone here who saw some really impressive results. So yeah, what we have here is, this is Mark, one of the participants and just a sample. I mean, I didn't take the best and so forth, but on his baseline, he is chronological age was basically 63. And this is very typical his intrinsic age as this lab called it, which is his age epigenetically was basically 70. So he was seven years older, which translates to about an 80% increased risk. Two years later, after being on the program, he's age now is 64 and a half, basically. But his epigenetic age has been reduced to 48 years. Yeah. 16 years younger than his chronological age. Do you know Mark? Well, like, does he feel better? Like people will want to know like the test is all fine and dandy, but does he is this showing up at all in his life? Or do you know, or is that not data that you were necessarily collecting? I wouldn't have access. I mean, I talked to these people a lot, a lot of emails and text messages and so forth. It's such a subjective thing. I can say this is that people's labs, because again, they're mostly doctors and they share their labs and so their labs are enhanced significantly. And when I ask them how they are doing, you know, some of these people have now been on the study for seven, eight years, they say, I've never felt better. But again, it's subjective thing. But what I do here is that they don't have anywhere near, you know, most of these people are a great deal. They're 60 to 80 years old. I don't hear about any real medical problems. Once in a while, something will come up where, you know, kidney labs will have gotten deteriorated a little bit, but we get quickly in with the kidney peptides and fix that. But these people are the healthiest group of people that I've ever come across. Even they went through COVID and I think probably 5% of the people even just came down with COVID. Nobody died, nobody had any Assyrius. And there were even four or five of the individuals who, doctors who had to get vaccinations in order to be able to practice medicine and so forth. So everybody came through the whole COVID thing intact as far as I know. Amazing. Great. So this next slide here is, as I said earlier, the technology improves and we now contract, you know, we contract the immune system independently and overall epigenetic age, so forth. But we also can figure out now what we call a pace of aging. In other words, we can compare a person's biological aging to a standard calendar year aging. And so we can determine if you're in a situation where your epigenetic age is accelerating and you're aging biologically faster than your calendar aging. So this is my results. Again, people can't see this, but in 2020, again, I've been on the peptides for four or five years. My pace of aging was 0.92. In other words, I was aging each year 8% slower than my calendar aging. In 2021, it improved a little bit and I was aging 9% slower. 2022, I was aging 11% slower. And my last test, the latter part of this last year, 2024, I was aging at 0.79, which is 21% slower than my calendar aging. And that's because of the peptides. Yeah, exactly. I mean, that's notable. And this one is a kind of a before and after, again, like Mark, this is someone else in the program where at their baseline testing, he was aging 12% faster than his calendar age. And then about two years later, he was aging 10% slower. So a significant turnaround. And I won't go into this one, Natalie, it's a lot of detail that shows basically over a period of a year, huge improvement in this person's age. Yeah, huge, huge wins. Huge, huge wins here. I mean, this is a person who started off at a DNA methylation age nine years older than their chronological. And after one year, they had now, they were now only three years older than their chronological age. So it's not the right person, am I looking at the right thing? Yeah, no, you're looking at it correctly. Look at the, what we call the immune age. That's that secondary test. The DNA extrinsic. Yeah. He had a really good epigenetic immune age 10 years less than his C age. But then look a year later, he was now 18 years less. Wow. And his pace of aging went from 12% faster to 10% slower. Yeah, that's a massive delta. Yeah. And I would say this is pretty typical. I'm going to show you in a moment of slide that has the results for the whole 124. But this is, you know, not cherry picked. This is pretty much what we saw. This is what we call symphony age. The this particular lab, again, technology, you know, advances and so forth. So what this lab was doing was they were able to then take 11 of the organs and systems and determine an epigenetic age for each one of those 11 systems and chart them. And so the person's current age was 63. But they identified that there are one, two, three, four, six of the organs, including his lungs, musculoskeletal, inflammation, kidney, and hormone age, that were a number of years older than his chronological age. And he had a couple of them that were much younger, like his liver was four years younger than his current age. And so we're able to break it down at this point. And this is incredibly helpful to me, because when I'm putting together the protocol based on telomeres and epigenetics, I can target then for this individual, I would be using more of the lung peptide, musculoskeletal, inflammation, so forth, kidney and so on metabolic, even like the pancreas, the liver, yeah. So it gives me some tools that I can be very specific when I'm creating these protocols. Although just one thing that's really interesting to me is that his liver age is four years younger, but his metabolic age is six years higher. Magnificently, yeah. Yeah, interesting. So, but now what's again, technology advances. And so a lab called Generation Lab, where I'm actually doing the beta testing now, they have a 25 page clinical study, peer reviewed and so forth. And they've been doing this for a little while. But I don't take that by itself, I've got to do my own testing. Yeah, but they're giving you an aging rate, a pace of aging by system, that's pretty dramatic. It is very last test that was giving you a, you know, a global pace of aging, which is also very helpful. But, but in terms of targeting your, you know, your attention on different systems, this would definitely give you some insight. It does. And again, it gets incorporated into the protocols that I put together. And, you know, and outside of the peptides, of course, we have there, people having this information can, you know, do other interventions and be focused elsewhere in terms of what they can do, you know, in terms of those that are elevated or faster aging. So there are 19, I know that your audience can't see all this, but there are 19 different systems and organs that they've been able to determine an epigenetic age of and mark those that are aging at a faster speed than those that are younger. This person was 44, I think, as I recall, I think it was 44, it was his chronological age. Is that, is this a man? Yes, it's a man. So then why would they get a reproductive system age on ovaries and uterus? Let me take a look and make sure it's a man. Just a second. No, it's not. It has to be a woman. Because he's pretty remarkable guy. Yeah, he is. No, I just grabbed one of what we call the system age breakdown sheets. I just actually, we threw this in this morning. Yeah. Well, I'm, you know, I'd be curious. I definitely want to have a conversation with these guys because I'd be curious to know on the reproductive system what, what they would say on a post menopausal woman versus a pre menopausal woman because post menopause, I don't know how much attention, you know, I don't know how meaningful it would be that your system age is older. You would think that it would be just by virtue of the fact that it's pretty much, you know, out of its prime years. Yeah. Yeah. I'm going to connect you up. I think you're going to find this fascinating, but you know, this is just how, as we all know, this is how technology works. It just gets more specific and, you know, broader, more detailed, more accurate and so forth. So we're beta testing this one and I, if the beta tests turn out the way I think they will, then we're going to be switching our whole system over to them. So, okay. And so the epigenetic study, 124 participants, the average decrease for the whole group in epigenetic age was 4.67 years. Now, that doesn't sound very impressive when we're looking at telomeres, you know, where you get 20 and so forth and so forth and so forth. But if you're getting a 4.67, what would say, epigenetic age benefit based on horvus work and so forth, that can turn into a 50 or 60 percent. I think this one turns into a 56 percent decrease in all cause mortality risk. I'm not aware of anything out there that actually can match that. Yeah. No, that's pretty dramatic. I mean, and you know, obviously it depends if the person was showing up 10 years older and now they're only five years older, obviously you're going to be better off if you're below the line, if you're younger than your chronological age, but it still represents a massive decrease in risk and hopefully gives you the impetus to kind of keep moving so that you can get below that line. Yeah, absolutely. And notice, because this was a more recent clinical study, we did the cutoff at two years. If a person's on it for four years, what's their result going to be? Exactly. The people who are at risk are those who have an older epigenetic age than their chronological and to be able to reduce that by more than 50 percent is just really remarkable. So the review of both the telomere and the DNA methylation or the epigenetic age is that in the telomeres over a three-year period of time, we were able to lengthen people's telomeres by almost 22 years and in epigenetically over a two-year period of time, we were able to reduce their epigenetic age significantly, but more importantly reduce their all-cause mortality risk by 56 percent. It's pretty sweet. So this slide just shows the kind of what we call current aging expectations. This is how people view aging. They start off as an infinite young person, middle age, and then they start declining and they're frail and so forth. Cavincent and I don't believe that this is everyone's fate. We think that with the bioregulators and also when I say the bioregulators, you still have to do a lot of other things to be healthy as you and I have talked about. Thank you. You've got to clean up the diet and so forth. But this is how Professor Cavincent and I see things where a person hits middle age, they start getting older and then they clean up their life with bioregulators and diet and all the other technical things that are becoming available and they end up having extended life by 10 or 15 or 20 more years. And healthy years, right? Healthy years. Yeah, it's not just the number of years. Yeah, exactly. Exactly. So I'm going to stop the sharing here. And by the way, we haven't touched on it, but the bioregulators have no adverse side effects. They're natural extracts. 100%. I think that that's a very important point to make. And I think the other important point to make on the bioregulators is, and in a lot of the studies that Professor Cavincent did on humans, he was able to show that in the event that people did need medication, the bioregulators often helped to improve their outcomes even in combination with conventional medications. He was not one to throw away the baby with the bathwater. Like he was definitely, you know, as a researcher, as a scientist, as a medical doctor, and all of those things, he was still held allopathic medicine with some with respect. And because I just know that I've seen a number of his studies where I think there was a so in particular, there's a COPD one where they had a control group, they had the people getting just the medication and then people who got medication and bioregulators, and the people who got the medication and the bioregulators actually had a way better outcome than the people who just got the medication. Absolutely. As you said, he was first in, you know, at all an MD that was just training and so forth. Yet St. Petersburg at the clinic there, they have besides the research part of it, they have a clinic where they treat people for, you know, a variety of diseases. They do not exclude medicines, you know, mainline conventional medicines when appropriate. Yeah. So yeah. So that's the kind of the coming to the end of the clinical studies. It's been 19 years and so forth. And we're doing now maintenance for the people that are in the clinical studies. But our focus now is elsewhere. We're taking the peptide program, as we call it, versus the peptide clinical study, and taking it internationally. Recently in Bali, Indonesia, next month will be in Dubai. And there are individuals in medical clinics and so forth who want to embrace without the restrictions that we have in this country and other countries in terms of, you know, cutting edge things like stem cells and so forth. So we're going to be focusing in those markets mostly at the invitation of these clinics and things. Well, that's amazing. That's a beautiful outcome. Do you have now, but you know, you mentioned that the line share of the 124 people were physicians who took part in the clinical trial. Have any of those physicians or have all of those physicians essentially integrated the bioregulator peptides into their own protocols with their patients? Or are some of them offering it? Or do you think you'll ever, they'll be sharing that kind of information with people in case people want to have a physician's guidance in using bioregulator peptides? Yes, I kind of naively thought that many of them, if not most of them, would be using for the patients. The reality is that because there's a cost to the peptides, they're not excessively expensive, but there's a cost and so forth. The patients who have medical issues diagnosed by the physician are the ones that the doctors will of course put them on these peptide protocols because every day I write protocols for the doctors, you know, they'll say I've got a stage three kidney patient and so forth and so I'll write them a protocol. But where it didn't expand is that the average patient wants their medical problem taken care of, but they're not really interested in the longevity. I mean, if you asked them about it, they said, oh yeah, I want to live an old life. Do they want to invest money? You know, because you know, the cost of these mounts up over three or four years, very few of those people have said, oh my goodness, you know, I listen to Lawrence's things and I've listened to you and so forth and I want to live to 100. That happens very rarely. Once their medical issues are taken care of, they're done at that point. Yeah, I would say that the audience listening to this episode possibly falls outside of that group of people. What's wrong with that? I mean, if we have, if we've fixed, you know, if we've turned around their liver labs and heart labs and all that stuff, that's wonderful and that's maybe all that they're interested in at this point. What we are seeing though is older, wealthy people are getting very focused on and they've realized that they maybe have a lot more money than they have years left. And so those are the people that are seeking us out. And I, as you know, we don't do any marketing. I don't have a webpage. I try and make myself kind of difficult to find, partly because I'm trying to impersonate a hermit, but also partly because I really want to have balance in my life and I don't want to be overwhelmed. So I would say there's a tickling, you know, maybe one a week comes in, as we call it, concierge people. But then I've got this clinic that I mentioned to you in Dubai that's got 30 people lined up for the concierge program next month. So. All right. So the work continues. Yeah. Well, Natalie, it's been a pleasure to always as fun to talk to you. I had no idea that this was going to last this long though. I apologize. Well, we had a couple of, a couple of little interruptions along the way. So Dr. Lawrence, this is the part where I usually ask my guests how people can get in touch with them. And as you just explained, you're kind of not in that world right now. So we're just going to thank everybody for listening and keep your eyes and your ears open. There will be, I know that there will be doctors out there and practitioners who, and there already are who are leveraging the bioregulators to help their, their communities, you know, and certainly those who are interested just in longevity and others who are interested in moving the needle on certain health challenges that they have. It's already happening. And I just think I think it's just going to keep growing. I think that, you know, you're, you're really kind of part of a huge piece of the legacy that Professor Cavanson kind of left behind. And I'm sure he's smiling and very proud. Yeah, I'm proud to have known him all these years. But one last thing I will say is, I know you've got different, several different groups, you know, in terms of peptide bioregulators and various things and so forth with your, you know, because you're not a doctor and you don't need to be to suggest to people, you know, various peptides that will enhance their health, including their liver, their, you know, I know that you have enough knowledge and I think you can, you can provide peptides indirectly to people. Yeah, no, and I have been through my, through my membership community for sure. I run a program there. Sure. People should just contact you and let you give them some guidance. I mean, you know so much about this that you could do a wonderful job and very few will be interested in probably the longevity kind of part, but they want to be, you know, healthier. So you're the go-to person. Thank you. Well, thank you for that. Here we go. Yes, okay. Dr. Lawrence, thank you so much for being here and your time and generosity and why don't you come back into the frame for one more second? Okay, sorry. Here we go. Thank you so much and I'm looking for all, hopefully we'll bump into each other at some point in the not too distant future in real life. Thank you. Hey, folks, just a quick reminder that all of the information presented in this podcast is for information purposes only. No medical advice, no diagnosing, no treatments suggested here. Before you try anything that you hear about or learn about here, make sure that you check with your medical provider.