Health Longevity Secrets
A podcast to transform your health and longevity with evidence-based lifestyle modifications and other tools to prevent and even reverse the most disruptive diseases. We feature topics including longevity, fasting, ketosis, biohacking, Alzheimer’s disease, heart disease, stroke, cancer, consciousness, and much more so that you can find out the latest proven methods to optimize your life. It’s a mix of interviews, special co-hosts, and solo shows that you’re not going to want to miss. Hit subscribe and get ready to change your life. HLS is hosted by Robert Lufkin MD, a physician/medical school professor and New York Times Bestselling author focusing on the applied science of health and longevity through lifestyle and other tools in order to cultivate consciousness, and live life to the fullest .
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Health Longevity Secrets
Does Mitochondrial Transplantation Work?
What if we could reset our cellular batteries? In this fascinating deep dive into cutting-edge longevity science, Tom Benson from Mitrix Bio reveals how mitochondrial transplantation could revolutionize how we treat age-related diseases and potentially add decades of healthy living to our lives.
The conversation begins by exploring the extraordinary nature of mitochondria – those tiny power plants within our cells that generate 95% of our body's energy through molecular rotors functioning like miniature jet turbines. With approximately a quadrillion mitochondria comprising 10% of our body weight, these ancient organelles trace back to a symbiotic merger with our cellular ancestors over a billion years ago.
Unlike the nuclear DNA we inherit from both parents, our mitochondrial DNA comes almost exclusively from our mothers, creating fascinating maternal lineage patterns where thousands of family members share identical mitochondrial DNA. As we age, this mitochondrial DNA gradually accumulates damage, with factors like stress, smoking, and medical treatments accelerating deterioration. By our 90s, this decline reaches a critical threshold that appears to drive much of the aging process.
The most exciting revelation comes in learning that mitochondria naturally move between cells in our bodies – and scientists are now leveraging this phenomenon through transplantation techniques. By harvesting mitochondria from stem cells grown in bioreactors and reinjecting them, researchers are seeing remarkable improvements in cognition, strength, and immune function in aged mice, essentially restoring youthful cellular energy levels. Human trials are already underway, though still at small scale.
For anyone fascinated by the frontiers of longevity science and the quest to not just add years to life, but life to those years, this conversation offers a glimpse into one of the most promising approaches emerging today.
https://mitrix.bio/
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Hey.
Speaker 2:Tom, welcome to the program. Hey, Rob, nice to see you.
Speaker 1:Likewise, I am so excited about this topic today. Mitochondria, but not just mitochondria, but mitochondrial transplantation. Yes, yes, yes, so cool. But before we do that, let's just take a moment. This is the first time you've been on the show. Can you take a moment? Just tell us a little bit about your background and how you came to be involved in this space.
Speaker 2:How did I get into this crazy idea? Well, I have been starting high-tech businesses for maybe 40 years now. I am kind of a Silicon Valley person. 40 years now I am kind of a Silicon Valley person. I started a software company way back when and actually I was one of those people I was in Stanford in the physics master's in physics and decided to quit and start a software company because that was the hot thing back then, right.
Speaker 2:And then I did that for a while and then got moved back into science and did some different startups and including a fusion startup back before fusion was hot. And then I ended up working at Stanford Linear Accelerator, which is the big, two mile long, giant linear accelerator up above Stanford, and we were imaging mitochondria as part of our work that we were doing, taking these tiny little photographs of mitochondria, and I just got really interested in the field. So I started reading about it and I saw that there was all this amazing new research that was popping up that nobody was talking about. That was just completely changing our understanding of mitochondria and I just felt like I should do something with it.
Speaker 1:So and you guys were taking pictures of mitochondria with the accelerator, or yeah, well, no, it was it was actually it was a.
Speaker 2:I always tell people I worked at a giant underground laser beam. It really was. It was, uh, it's called the LCLS. It's a. It's a, a light source, what they call an x-ray light source, and you do x-ray crystallography, which is how you take pictures of tiny little molecules. So they were looking at mitochondria and chlorophyll and all these interesting molecules and, um, I just saw some interesting stuff that I didn't ever realize was true about mitochondria, and we're about to find out some of those.
Speaker 1:It's like, I'm embarrassed to say, as long as this podcast is going on, we haven't had that many episodes focused on mitochondria, and that is despite. The more information comes out, the more we know how fundamental they are to metabolic health and so many of the chronic diseases that we talk about on the show and that we're all facing. It's the 21st century epidemic of biblical proportions.
Speaker 2:Yeah, just about.
Speaker 1:So let's go back to ground zero 101. What are mitochondria and why are they important?
Speaker 2:Yeah, well, yeah, and I agree with you. I think that the thing that attracted me to this work was that it looked to me like there was this whole area of medicine that was just a mitochondrially driven. So the mitochondria are tiny, little, what they call organelles, but they're like these little, almost like tiny little bacteria that are inside the cells and you typically a typical cell might have a hundred or 500 of them. They're really really really small and they float around and they're where the cell generates all of its energy. Okay, so 95% of the energy in your body comes from these little mitochondria. They literally are. They call them the power plants of the cell. That's what you saw in your high school textbook, right, and they literally are power plants. They have tiny little spinning molecular rotors on them, almost like I tell my kids I said you are powered by tiny little jet turbines.
Speaker 2:Okay, Every mitochondria has about 7,000 of these tiny little jet turbines that are spinning away and they're combusting glucose and oxygen and creating hot gas and using that to spin a rotor. It's just like a power plant that we have in our world, except a zillion times smaller. And you have about a quadrillion mitochondria in your body. We are 10 by body weight, composed of mitochondria generally, so it's a lot okay. And they uh, they were in. They, they merged with mitochondria, they merged with our dna. About a billion years ago there was a mitochondrial ancestor and some DNA and they came together and created this new type of cell. It's the basis of all life on Earth today really is mitochondrially powered cells, okay. So whatever they're doing, they've been perfecting it for a billion years, so it's pretty well perfected.
Speaker 1:So so these, uh, let me just interrupt you for a second, just that that point is such a such a fascinating thing. So the, the understanding, the accepted understanding, is that a primitive organism was a mitochondria. It existed by itself and then merged with another cell to make modern, these modern cells, in somewhere in the distant past, and but they're actually, they actually were for and now they're part of us in sort of an ultimate symbiotic relationship today and and over hundreds of millions of years they've been optimizing that relationship.
Speaker 2:So the mitochondria used to be much more self-sufficient and of course it's given away, like a lot of its stuff has been put into the nuclear DNA. Now Each mitochondria has its own tiny little ring of DNA which is completely different from our regular DNA. So I mean we have our nuclear DNA, which is the chromosomes that are the mother and the father. The chromosomes come together. That's our regular DNA. It's about 8 billion base pairs, I think. The mitochondrial DNA is a tiny little ring and it's only 16.5 kilobits. So if you think of a motherboard on a computer, it's the equivalent of that teeny, weeny little chip over there that just like manages the battery or something. It's really, really small, okay, but if they get screwed up it stops. The power plant stops working. They're absolutely critical to the operation of the power plant. Okay, these little mitochondrial DNA.
Speaker 1:And the DNA. Just to emphasize that again, what you said was our main cell in the nucleus. We get DNA from our mom and dad, and it's a mixture. Each kid, each child is a mixture of the parents, and that's really important.
Speaker 2:The mitochondrial DNA, though, we just get largely almost 100% from the mother, right? Yeah, basically 99.99% comes straight from the mother, came straight from grandmother, great-grandmother, great-great-grandmother, and it gets passed down via all the maternal channels. And so if you have a big family, there could be thousands of people in your family who all have exactly exactly the same mitochondrial DNA as you do. So it's not an individual DNA, it's a family DNA. It's very interesting, okay, yeah, and in fact it's also regional. There's there's, like you know, groups of mitochondrial DNA have migrated throughout the world from Africa 200,000 years ago, and if you go to Nordic or Eskimo mitochondrial are slightly different from tropical mitochondria, for example. They're modified in little ways, but they're all completely interchangeable, and so whatever you get when you're born is what you get.
Speaker 1:And so this maternal transmission of mitochondrial DNA has to do with the fact that sperm largely don't carry mitochondria from the male, and so it's just in the egg from the female. But, as you say, it creates some fascinating genetics and family tree things that you know. A few years ago there was the mitochondrial mother hypothesis that you know people were talking about.
Speaker 2:That's right. Mitochondrial Eve Mitochondrial.
Speaker 1:Eve Right, yeah, yeah. And tracking back mutations back to a common mitochondrial mother origin, you know.
Speaker 2:Right, and the thing that's been interesting in the last few years, I said, there's been all this new research. What we found out is that it used to be that a lot of people thought, oh well, you know, whenever the cells needs pneumo, pneumo, mitochondria just makes them, and so we don't really have to think about that. But what we're finding out is that that mitochondrial DNA you get a giant hunk of it from your mother. Every egg cell has 500,000 copies of the mitochondrial DNA, but they're really tiny, so it's like you. Really, actually, in a typical egg, you have two completely separate sets of DNA and we never talk about that one. You know it's just as much and we don't talk about it.
Speaker 2:But it turns out that there are enormous implications for health, for chronic disease and also for lifespan. So what we have found and this is, by the way, everything I'm saying I just want to do the, I'm gonna do the, the disclaimer here everything I'm saying is very, very new. It's very, a lot of it is unproven. These are my theories and our company's theories, but don't you know, this has not been tested to human beings, so don, so, don't take this as being fact. Okay, this is very new, but anyway, what we're finding is that as people age their mitochondria, as the years go by, your mitochondrial DNA starts to kind of fray. It gets broken up and damaged and it's steady. And when you reach a certain point if you make it to, say, 90, 95 years old you reach a certain point where it seems to really fall off a cliff. And so we believe that that is at least 50% of what's driving aging in our bodies. Is that decline of that mitochondrial DNA Okay?
Speaker 1:in our bodies is that decline of that mitochondrial DNA Okay. So so the mitochondrial DNA ages? Um, not, unlike there's. There's other aging factors and genetic mutations may may not be the primary driver of of regular DNA aging, but it certainly is, it's foundational and I mean it is. And so but we know, we know about, like telomeres. Are there telomeres in mitochondrial DNA?
Speaker 2:No, no, because it's a ring, it doesn't need telomeres. In fact, there's a lot of data that implies that telomeres may be, in fact, a type of clock that the cell is using to track the decline of the mitochondrial DNA in order so that the nuclear DNA and the mitochondrial DNA can kind of keep balanced as to where they think they are in your lifespan. Okay, so the dna is making changes to our bodies as we age in order to allow for the fact that it knows that there's going to be this reduction in energy production by the mitochondria. And, um, that's very, very new, uh, conceptually, but that's what we think is that the telomeres and also there's this thing called epigenetic reprogramming, which is the epigenome on the nuclear DNA. It gets modified as you get older and we think a lot of those modifications are helping us kind of manage this mitochondrial decline Well so, before we get into epigenetic reprogramming, before we leave telomeres, is there a hayflick limit for mitochondrial DNA?
Speaker 2:No See, mitochondrial DNA or bacterial DNA. They're a completely different system. They don't have sexes. There's no male and female. It's what's called clonal inheritance. That's just. It's just. It's just.
Speaker 2:That's why there's no, there's no contribution from the father. There's no changes over the years. It just clones itself over and over and over again for a billion years now. But what happens is, as you age if you get this let's say you're when you're a baby your mother has basically given you an ideal inventory of mitochondrial DNA. You start with a whole bunch of them and they're really perfect, and then, as you get older and older and older, they just degenerate and what you call replication errors. Every time the mitochondrial DNA is reproduced, which happens constantly there's always the odds of some little bit of noise getting in there, just by accident, okay, and if you're under a lot of stress, a lot more noise gets in there, because it replicates very quickly and it's very messy. It doesn't do a very good job. That's why we found that things like stress and smoking they tend to cause a lot more mitochondrial damage and so by the time you're 75, you've already burned them out.
Speaker 1:So the same factors, if I understand you correctly, then the same drivers of mutations that damage our main DNA also damage our mitochondrial DNA. Although it's a different type of DNA, it's still susceptible to smoking stress, reactive oxygen species, all these kinds of things.
Speaker 2:Right, and you also can be born with prematurely aged mitochondria. There are children that are born. There are tens of thousands of children in the world who were born with prematurely aged, broken mitochondria, and they've often it's really a horrible thing, I mean, there's no cure for it and they frequently they just die by the time they're before they even are babies. They just die within a couple years. Sometimes they make it into teenager to be teenagers, but their bodies never work properly there. They go blind, they lose their hearing, they can't move because they only have 20% healthy mitochondria out of all of all of their mitochondria. They might only have 20%, okay, and so mitochondrial dysfunction can actually hit you at different ages, but it's pretty much automatic as we age. That's the natural way of your mitochondria going downhill. Is is just from being around long enough. If you're 90 years old, you've had time to get a lot of um, a lot of errors in the mitochondrial code. Okay, yeah.
Speaker 1:When I just emphasizing what you were saying, when I went to medical school, which was a long time ago, we studied, we were, you know, we learned about mitochondrial disease, but it was a short list of devastating congenital abnormalities that the children you know sadly did not do well and survive long. No, but now. But it's interesting that today that there's increasing evidence that mitochondrial dysfunction is at the root of all these chronic diseases that everybody gets you know, practically all of us are going to die of one of these chronic diseases and mitochondria appear to be at the root cause of that also Right.
Speaker 2:And, and, by the way, you can, you can. There are some cases where we suspect that you can acquire mitochondrial damage. For example, if you take a fluoroquinolone, which is known as Cipro, which is an antibiotic. If you take too much Cipro, Cipro damages mitochondrial DNA. That's what it does, that's what it's designed to do, because the bacteria that it's attacking all have that same little ring of DNA. See, so you're killing off the bacteria, but you're also killing off the mitochondria in your body, and there are people who have gotten overdoses of that, where they have acquired mitochondrial mutation disease when they're in their 20s and 30s and they have the same symptoms.
Speaker 1:Well, before we get into that, let me back up one last thing and emphasize that. Um, so we we talked about our main dna and aging, we talked about mitochondrial dna and aging, and mutations occur in both of them. Recently there's a revolution our knowledge about. Like you, you mentioned the epigenome, the, the way expression is controlled of our main dna, our nuclear DNA, right, is there a similar? What is the analog of the epigenome for mitochondrial DNA?
Speaker 2:Hmm, Well, what we just discussed is the analog, and the epigenome is adjusting the nuclear DNA, it's adjusting the gene expression to allow for the fact that it kind of evolution knows you're getting older and so it changes the genes so that instead of being a 25-year-old you're now a 70-year-old, and that means you're reducing skeletal muscle and you're letting the skin go slack and there's all these things that the body does. I think it's pre-programmed to do it, to allow us to live longer with what we have. You know, if you look at an antelope, for example, that's 150 pounds versus a human, that's 150 pounds. The antelope will live maybe 30 years. That's its max lifespan. We live to be 90. So why don't we live three times longer? That's a really fundamental question. I think it's because nature has programmed us to use our resources slowly, to ration the resources so that we live to be older, because for our particular species, species, being older is better, because then we can pass knowledge on to the young people. And there's all these evolutionary theories why we have such long lives.
Speaker 2:Okay, but that's all something that's done at the, at the nuclear level, allowing for the fact that the mitochondria will burn out. If they'll burn out in 30 years, they'll burn out in 90 years. It depends on how they're used, and so that's the new theory behind mitochondrial aging, and the implication would be and this is part of the longevity field I mean, of course, there's now all these people throwing, you know, resources into developing longevity tools. There's a whole bunch of companies in Silicon Valley, for example, that have been pouring funds into epigenetic reprogramming, which is where you go in and you reset the nuclear DNA and convince it that it's 40 years younger.
Speaker 2:Okay, you just basically reset the programming. But what we say is well, the other half of the issue there is you've got the mitochondrial DNA, which is also old. You can't. You got to reset that too, or they're going to be out of balance and that will be bad. That would be a very unhealthy okay. So that's what we're working on. That's our half of the of's, our half of this new idea of age of health. Span extension is what they call it.
Speaker 1:Let me summarize that, if I can, you can go on. This is so important.
Speaker 2:I know this is deep. This is complicated stuff so it takes a while.
Speaker 1:I want to make sure everybody follows it, because this is so good, it's so important. So the epigenome in the nuclear DNA, it's histones and methylation and everything Is it a similar mechanism for the mitochondrial epigenome that controls expression? Is it?
Speaker 2:similar, it's, it's. It's a completely different mechanism. We're trying to do the same thing, but it's, they're just completely different. The mitochondria and the nuclear DNA are like whole different worlds.
Speaker 1:Okay, so the the tools that are so effective in reprogramming nuclear DNA, yamanaka factors and other epigenetic reprogramming techniques? So the mitochondrial DNA doesn't respond to the usual partial epigenetic reprogramming.
Speaker 2:Yamanaka factors and other things Not at all right.
Speaker 1:Except through nuclear effects, but specifically on the mitochondrial DNA. It doesn't reprogram it right.
Speaker 2:Yeah, because there is no real reprogramming, there's no epigenome, there's not a real, it's not the same as the nuclear DNA. The nuclear DNA is very, very well protected and very, very well, has tremendous quality control, and so it stays pretty pristine, and then the epigenome is what changes it over time. The mitochondrial DNA is just a completely different thing. Think of a giant factory with smoke and flames billowing everywhere. Those mitochondrial DNA are just getting burned up. It's a factory, okay, and so you don't have the frou-frou niceties of the nuclear DNA. You know, it's really so. It's a completely different approach to fixing it, but it's the same idea. We need to fix both at the same time, okay, in order to extend health span, in order to reverse age, for example.
Speaker 1:So before we get into how to fix it, a couple other just clarifications, kind of to set the framework. You mentioned that certain things burn out mitochondria at a faster rate or exhaust them. What kinds of things are those?
Speaker 2:You know, it's the things that we all know, right, and now we're seeing all these, these papers are coming out. There was a whole series of papers brilliant papers from Columbia, uh, from some researchers that showed how stress hormones in the bloodstream cause the mitochondria to replicate more quickly, but they also then they're replicating sloppily and so then the mitochondrial DNA, very quickly it gets completely trashed. Okay, so stress? Well, what a surprise, right? Smoking? Of course, smoking is enormously damaging because it's hitting all the mitochondria in your lungs and it's damaging them. Is that from?
Speaker 1:the tobacco, or from the combustion products, or do we know? No idea, okay, no idea.
Speaker 2:So stress, tobacco, drinking alcohol, of course, anything that is any kind of disease Like, let's say, you get cancer and you go through chemotherapy. Well, we're doing that. We have a thing called mitoclock that we created where we can actually look at the number of these damaged sectors in the mitochondria. It's almost like a hard disk. You can count the number of damaged sectors, and so we go in and we analyze the mitochondrial DNA and some mitochondria that we get from urine. We could do a urine sample and you can see it's this decline as people age, and our feeling is that when you hit something like chemotherapy it's going to go boop, it's going to drop 10%, boom, right there, because chemotherapy is specifically designed to destroy mitochondria. Okay, um, bone marrow transplants, tremendously damaging to mitochondria. Cipro I already talked about that maybe some viral infections there's a series of paper that have come out that have shown that covid specifically damages mitochondria. So so.
Speaker 1:So now we know some of the things that can damage the mitochondria and we know that aging is associated with decreased mitochondrial function, increased damage. What are some of the symptoms of mitochondrial damage? Putting aside those childhood diseases, but just like what should we? When should we suspect mitochondria? Are there any specific symptoms or is it more generalized?
Speaker 2:Yeah, I mean Parkinson's, alzheimer's, als, you know AMD, which is macular degeneration, you know sarcopenia, which is muscle weakness, basically all age-related diseases. Every time somebody says, oh, is mitochondria involved in this age-related disease? And the answer is always yes, because as the mitochondria decline, what happens is all these diseases kind of pop up. All right, arthritis. Or I'll give you an even simpler example when people who are in their 80s get, let's say, pneumonia or COVID, they end up in the hospital. Right, and we all know this. I mean, who ends up in the hospital with COVID? The old people. Well, why Well? Doctors say well, because their immune system isn't strong enough to fight it off. Well, why Well? The doctors say, well, because their immune system isn't strong enough to fight it off. Well, why is their immune system not strong anymore? Let's just ask the dumb question why, well, because they're old? Well, what does that mean? I mean, you know you could keep asking this question. At the end of the day, what we found is the mitochondria in their immune system cells in their white blood cells are very weak. In their immune system, cells in their white blood cells are very weak. They're equivalent of a battery that's been discharged 75%. You know the little rechargeable cars that you drive around or the rechargeable drills that you use at your house. You know, maybe you've used up half the battery and so it just doesn't go as fast as it used to. So that's all these white blood cells. They don't have very strong mitochondria and so they can't fight back, and so you can't fight off an infection.
Speaker 2:We've done experiments in mice where we've taken a whole bunch of young mitochondria from young mice. We just get it from their platelets in their blood and we inject them into old mice who've gotten this. We give them a disease and give them these mitochondria and they just brush off the disease as if they were 30 years younger, or the equivalent of 30 human years younger. Okay, so we can re-energize the immune system. We've been doing that for years. And what if we could just do that with all the old people in the in all the hospitals? I mean, just think what a change that would be, and it's not even that complicated to do it. And what if we could just do that with all the old people in all the hospitals? I mean, just think what a change that would be.
Speaker 1:And it's not even that complicated to do it. Yeah, yeah. So we sort of set the stage here. Mitochondria how important they are in aging, how they affect so many diseases.
Speaker 2:You founded a company that is working with an idea that may be a solution for this. So tell us about mitochondrial transplantation.
Speaker 1:What is that? How does?
Speaker 2:it work. Go for it. Definitely starts sounding like science fiction once we're getting to this I'm telling you. Everything I'm about to tell you is happening. It's real. Definitely starts sounding like like science fiction once we're getting to this. It's I'm telling you. Everything I'm about to tell you is happening. It's real. Um, so yes, we're doing what's called bioreactor grown mitochondrial transplantation. Okay, and when I said there was a whole bunch of new research coming out, that I got excited about what I what we found about.
Speaker 2:10 years ago, some researchers tried transplanting mitochondria from one part of the body to another and everybody said, oh, you're crazy, that'll never work. Well, it worked fine. It turns out that mitochondria don't just sit there in the cells. What we're finding out is that mitochondria are constantly moving around between cells. They just go right through the walls of the cell. There's a little mechanism that lets them through.
Speaker 2:They are transplanted, they are transported in the blood constantly. They're transplanted, transported between different types of brain cells. So, for example, the astrocytes in the brain, which are a type of brain cell. That's where it seems to be, that's where they're kind of manufactured, and then they're put into little tiny vesicles and they float over to the neurons and the neurons use them to run, and then when they get burned out, they send them back. So it's kind of like a little manufacturing site for the neurons. Your platelets in your bloodstream. You have about a trillion platelets in your blood. At any given time, every platelet has five mitochondria in it on average, and they uh, whenever they reach the end of their lifespan, they squirt those mitochondria out in these little vesicles, what we call extracellular vesicles, and they're absorbed by the rest of your body, and so the platelets are transplanting transplantation no-transcript so your body. There's been a billion mitochondria that have been transplanted through your bloodstream in the time that we've been talking.
Speaker 1:And one question I forgot to ask how do mitochondria reproduce, or do we just get one set that stays with us?
Speaker 2:No, the cell reproduces them. So when the cells need more of them, they divide them. Just like you know, it's called mitochondrial biogenesis. The cell can do it. The mitochondria can't divide by themselves. They don't have all the equipment anymore because they've handed off all the replication equipment to the nuclear DNA.
Speaker 2:So, you start as an egg with 500,000 copies of the mitochondria DNA and by the time you're an adult you have about a quadrillion, 10 quadrillion, whatever the number is mitochondrial DNA and then over the years those are constantly being rebuilt and rebuilt and refreshed.
Speaker 1:So within our body, then the mitochondria move all over and they do internal, internal transplantation sort of all the time. But that's not what you're talking about. You're talking about something completely different. What is that?
Speaker 2:We're taking advantage of that whole process where we say, ok, if the body is already doing this, maybe we could just supplement it minute. Okay, if you've already got a flow of mitochondria in your blood and as you age by the way, that internal amount goes down, just what you'd expect, okay. So what we're saying is well, gee, if we could supplement that and prevent that reduction in that internal flow by giving you an external source of mitochondria, maybe we could keep you healthier longer. And so what we do is we take your stem cells, we put them in an external bioreactor which is pretty common these days A lot of people who do this for other sorts of gene therapies we grow those cells in vast, vast quantities, we extract the mitochondria and then we inject them back into your body. And the idea is to, basically, if your mitochondria are declining 1% per year you know, until you're 90, we're going to try to boost you back up again and get you back to the where you have.
Speaker 1:You know you have maybe 10 or 20% more than you had before and so the the idea of using the stem, my stem cells, for my mitochondria. It eliminates any um, any transplantation, rejection or immune system factors and all. And let's come back to that and hold that thought in a minute. Are there any possibilities for, because of the simplified DNA in mitochondria, for using, say, not my own stem cells but from a female family member, or something like that? What?
Speaker 2:are the challenges. And, by the way, let me just say one thing this is not just us. There's a whole movement now around the world pushing this concept. There's several companies and different, several startups in different countries israel and and switzerland and other places. We just had the first annual mitochondrial transplantation conference about a month ago in.
Speaker 1:New York.
Speaker 2:Congratulations In New York yes, and some amazing people at Northwell Health, which is a hospital out there, did this. There's universities all over the country now are studying this and finding out. Oh, you know, we can help people who've had heart attacks and strokes and wound healing. They're finding all these uses for it and so it's growing very, very quickly. Our focus and, of course, these kids, as we talked about. We have this disease. There's actually human trials going on right now to try to help these kids by giving them healthy mitochondria. We're taking all of that and trying to apply it to old people. That's what our that's what Mitrix is focused on.
Speaker 2:Because the kids obviously wouldn't be able to use their stem cells because their stem cell mitochondria would be dysfunctional, presumably so in that case we might go to a sister who doesn't have the disease but has exactly the same mitochondria and we might use those mitochondria for these transplants. And since it's my genital, there's no reason that it shouldn't work just fine.
Speaker 1:And of all these at this conference, of all these different companies, they're all looking at different spaces and different kind of applications and approaches. So your company is looking at the longevity application of it for, essentially, not just living longer but these chronic diseases that determine our longevity really.
Speaker 2:Right, exactly All of us that do that.
Speaker 1:What are the? What are the challenges you're facing now, like where are we on this path? Should I you know? Should I schedule my transplant now or?
Speaker 2:book some time. It's funny because I tell people we've been around for four years and we're a tiny company. I mean, we've just been. We've been getting just angel investments from people who want this to happen. You know, and it's always nice when it happens we're at the point where I've got. I tell I joke with people, I, but we're at the point where I've got it. I tell I joke with people. I've got a big red start button on my table and as soon as we have enough funding we need to get enough funding I'm going to push that start button and we're going to do our first full human trials. We're ready to do that immediately. Okay, so it's, the biggest challenge is funding. It's just so new, you know, yeah, new things. The government, actually the some of the government groups, are very interested in this, but it just takes time for people to, you know, get there.
Speaker 1:So and and um what have there been any like uh, really exciting home runs or lab work or anything anything at this conference or that you're aware in this space that we can point to and say see, it does work, you know or yeah, like what?
Speaker 2:what would you like to highlight from that? Well, okay, so there's two things going on. First of all, we've been doing a lot of injections into mice and we've now gotten to the point where we've transplanted up to 1% of the total mitochondria in the mouse per injection. So we give that mouse one injection and then and as I just said, you're 10% mitochondria, so you can imagine how much that is. It's a huge amount. And well, oh well, will it kill the mouse? Mouse? You know, that was our first question.
Speaker 2:No, the next day and these are in really old mice. These are 27 month old mice and that's about the equivalent about 90 years old by human years the next day, the mice are running around like crazy. They're so energetic it's like wow, it's like they really. It really. I think it gives them kind of a buzz because they get all this. You know it's pretty quick how quickly it affects them. So after doing that over the course of 10 weeks, what we're seeing is significant increases in cognition. We do all these maze tests and they are much, much faster. During the maze test. We're seeing significant increases in strength and endurance. So they run on their wheels, they can hang on to things. They have what's called grip strength, and then very significant increases in immune strength, where they just kind of shrug off infections like they were young again. So, and in the longevity world, those are the three things that you kind of use as your starting point cognition, muscle and immune strength. Okay, if you can get those, you're doing really well.
Speaker 1:Yeah, I mean I'm sure some of our listeners are probably thinking about, you know, many of them are interested in longevity, like we're talking about, and they've, you know, they've been hearing about stem cells, like you mentioned, and, uh, regenerative medicine and they go. Well, hey, I'm already going, you know, offshore to get my stem cells yeah, yeah, right will this accomplish the same thing, or how is it different?
Speaker 1:if I, if I get my stem cells and I don't grow them in a bioreactor for mitochondria or anything like that, but just my own stem cells, will I get the benefit of young mitochondria with that, or what?
Speaker 2:happens there? Yeah, a lot of people. They go to Panama, they go to Los Cabos or wherever, and you can get those kinds of treatments. What I always tell people is that mitochondria are I mean, we are in, in fact, a type of stem cell treatment. It's just that we're taking the stem cells and we're squeezing out kind of the magical ingredient in the stem cell. And the reason is that when I give you, when I say I'm giving you 1% of your mitochondria per injection, that's a thousand times larger dose than a typical stem cell treatment.
Speaker 2:Okay, so at the end of a full, at the end of one of our full treatments, we will have given you as much as 10,000 stem cell treatments. It's just what I will say is there's nothing wrong with stem cells. They work fine, but they're just not enough. You need big amounts. When you're 90 years old, I mean, you've lost so much by the time you're 90. We've got to pump you full of new materials and the mitochondria are kind of the rocket fuel component. So that's what we focus on. Okay, A lot of our volunteers for our trials are already getting stem cell treatments and they get a little benefit from it, but it doesn't last very long.
Speaker 1:And so again further comparison with stem cells. We hear about side effects with stem cells. You know they're not without risks, you know for cancer and other things. Are those risks the same with mitochondria? Are there additional risks or are they diminished? How does that risk profile look?
Speaker 2:with mitochondrial transplants. They're significantly less risky, and that's another reason why. That's why a lot of people are jumping onto mitochondria, because it seems to be a lot less risky than the stem cells. And the reason is that when you inject stem cells I mean stem cells are huge and they have their nuclear DNA in there and if something goes wrong, that nuclear DNA can get damaged and then you're putting damaged DNA into your body and that can cause cancers to grow, teratomas right, whereas if you do mitochondria, there is no DNA in the mitochondria, except for the little ones which don't have any. They don't have the ability to cause any kind of cancers, and so the mitochondria you're getting all the benefit without as much of the danger. That's what we've seen so far. Okay, I also do want to say there have been human trials on this. Human trials have been happening for the last couple of years, but they've just been very small scale. We're trying to.
Speaker 1:We're trying to scale it up to these very large trials yeah and um, and I can't remember if we, if we, if we answer this or not, or we discuss it with the, obviously yamanaka factors aren't going to work. Is there's no, there's no epigenome in the way that the nuclear DNA has an epigenome. Is there an analogous process for rewinding or we just get the stem cells which are already rewound? The mitochondria are already young. Is there, is there a way to take old mitochondria and rewind them without going to stem cells? Or do induced pluripotential mitochondria, you know, like stem cells?
Speaker 2:No, no, that's a very, very good question. So there are people who are trying to fix the mitochondria in the body without going to an external bioreactor. There's really two camps, okay, there's two approaches. There's those of us who say, oh, we're going to do this in a bioreactor. And then there's those who say, oh, no, no, we're going to figure out how to do it in the body. Of course, I'm a bioreactor person.
Speaker 2:I don't think that the in-body solution is going to work, and I'll tell you why the people who are going to be doing this are going to be 80, 90 years old. That's really who we're talking about, because people, younger people, they're probably not going to do something this powerful. So this is a very big treatment. So the elderly people, people who are 89 years old, are chronically energy depleted at a cellular level. I mean, their bodies are barely hanging on as it is. If you try to go in there and repair those mitochondria, I say it's like trying to fix the engine of your car when you're driving down the freeway at 60 miles an hour. I just don't think it's a good idea. I think it's risky.
Speaker 2:A lot of the changes that we're making in the mitochondria, the body already can do it, but your body just doesn't have enough time and space and energy left to keep the mitochondria young. If it could have been doing this when you were 90, then we'd already be living to 200. If we'd already done it, we have to get outside our bodies. We're a closed system. We're pretty much optimized. We're going to go outside of that closed system and use a bioreactor where we have infinite space. I mean when I say a bioreactor it might be as big as a room, for all I know, for one person. We have a lot of space. We can use an infinite amount of energy. We can have all kinds of scientists watching it and quality control, and you don't inject those back into your body until you're really comfortable that they're really healthy. Okay, I just think that that's a more practical way to do it.
Speaker 1:Yeah, well, looking, looking forward to the future. If you can match it, wave a magic wand. Let's say 10 years. Well, no, let's say. Let's say five years. So let's push it. Let's say we're aggressive, and between five and 10 years. If we had, if this were more widely available, what would the use case or the scenario be? For you know XYZ, you and I are 90, we're ready for our stem cell. What would we experience? Not our stem cell, our mitochondrial transplant thing. What would we experience? Another?
Speaker 2:stem cell, our, our mitochondrial transplant. What?
Speaker 1:would we experience?
Speaker 2:what? What we'd experience is? We'd go in and it almost be like getting chemotherapy, except the reverse. You go in and you get this long infusion of mitochondria and that's really just like getting a blood transplant. Okay, there's a bag of mitochondria and they and they drip it into you and at the end of it you feel like a million bucks. Okay, because you're you know, all the mitochondria are just sizzling and they're going into your cells and your cells are oh I've got all this extra energy.
Speaker 2:The biggest danger actually is that you'll be, you'll be too energetic and you'll go out and overdo it. So it's going to have to counsel people to, to do physical therapy, to do slowly, okay. So I think you could do. Maybe, let's say you do that over a year you get one. Maybe you get one of these a month and by the end of that year I'm hoping. I mean, nobody knows, I hate to make predictions, but my hope is that you're more or less 20 years younger. Okay, does that mean you live longer? Nobody knows, but you certainly will be healthier. You'll be 90 years old. You won't be losing your ability to walk.
Speaker 2:I mean, I have a 96-year-old mother and she's losing her memory and she's losing her ability to walk and I'd like to prevent that. I'd like her to be able to take care of herself longer, right, and I have some of my volunteers in our volunteer group that are 80-year-old tennis pros, you know, and they want a mitochondria so they can play better. You know, that's what I think will happen in their first five, 10 years. It'll probably be very expensive at the beginning, but that's just true of everything. I mean, like computers were very expensive in the early years and then they got cheaper because we learned how to mass produce.
Speaker 2:The eventual goal that we have is we'd like to have factories all over the world just pumping mitochondria out by the ton and anybody who hits the age of 50 can just go in and get some and it's just an automatic thing, and that would reduce all these diseases so much. I mean just Alzheimer's. If you could just cut Alzheimer's by 50%, that would save unbelievable amounts of money and heartache for the world. So it is, it's kind of this, this mission, you know, to try to improve the health of the, the health of the world.
Speaker 1:So yeah, this is. This has been such a great conversation, thomas, or anything we didn't cover that you wanted to to mention or that we need to touch on.
Speaker 2:I just want to say people often say, well, okay, so when are you going to start human trials? I'm going to say it again we're doing it. I mean we're doing, they're doing trials in kids. I've got now I've got 20 some odd elderly volunteers, some of whom are you know. I've got scientists and physicists and doctors and VCs and Silicon.
Speaker 1:Valley.
Speaker 2:CEOs, I've got all these volunteers who are saying yeah.
Speaker 1:I'll do it.
Speaker 2:You know, everybody's like I'll be at the guinea pig, so we're looking for people to help us do this. So you know, that's what I would say is we're looking to build our network.
Speaker 1:Yeah Well, this has been such a great conversation and we're definitely going to do this again. I want to have you back again and get deeper and get the progress on this, but for today, I think how can people follow you on social media and the website for the company Could?
Speaker 2:you? Yeah, the website is mytricksbio, and if you look up mytricks bio or mytricks mitochondria on Google, you'll find us. We're all over the place. And then I post a lot of stuff on LinkedIn and so if you find us on LinkedIn, we have a lot of updates. So we try to spend a lot of time educating people because we're trying to spread the word.
Speaker 1:Yeah, and it'll be in the show notes as well. It's Mitrix, not Matrix. It's Mitrix with an. I, if you're listening to this, M-I-T-R-I-X.
Speaker 2:Sometimes people call it Matrix. That's fine too.
Speaker 1:Well, thanks again, tom. This is such exciting work and thanks for spending an hour with us. We really appreciate it. This has been great, my pleasure.
Speaker 2:Well, thank you for letting me talk I.