https://www.listennotes.com/e/7ca1698d838e49138bed88dd35e2ac9d

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One of the people on our board of directors is a former astronaut. We've got a whole idea of what's going to be needed for people going to Mars and people going to the moon.

There's a couple studies showing that You get a mismatch of mitochondrial DNA with nuclear DNA equals animals that don't thrive.

The way nature keeps us from aging too quickly in our mitochondria is just by giving us a ton of them in the beginning. We have 500,000 copies of the mitochondrial DNA in each egg cell. We're going to try to fix their mitochondria, grow a bunch of those, and then flush out their bad ones and replace them with good ones.

Wow. When you fix them, are you CRISPRing them, or how do you do that?

This is Tom Benson, a molecular biologist who's been asking one bold question for over for a decade. What if we could take out your tired old mitochondria, give them an upgrade, and put them back in better than before? From reversing disease to enhancing human potential, he's working at the edge of what's possible for science to ever accomplish.

If you want to be a good skier, you want the Eskimo mitochondria. If you want to be a really good long-distance runner in the Olympics, then you want the Ethiopian mitochondria.

If it's okay to fix mitochondria that have some problems and reintroduce them, can I take my perfectly good mitochondria, give them some superpowers, and then introduce them back in? You're listening to The Human Upgrade with Dave Asprey. This is an episode that I am so excited to do for you, and the reason is that I have fantasized about upgrading my mitochondria for 25 years. It's been just a thing, right? I understand I have unusual biochemistry in my cells, and I understand how mitochondrial networks work. I'm a network engineer by training. And Tom Benson, who's our guest today, was— you're a scientist and inventor, tech entrepreneur, and you've only started 3 high-tech Silicon Valley companies. And now you're working on a company called Mitrix. Am I saying it right? Mitrix? Mitrix?

I've just read about it.

Mitrix. Mitrix.

Yeah. Yeah. All right.

And you're looking at, oh my gosh, can we take mitochondria, harvest them, restore them, and transfuse them? And the answer is yes, we can. And I want to do it. How do I sign up?

So I always tell people, I say, my goal is to pump as many younger versions of your mitochondria back into you as we can get in there. I'm not trying to be too— like, I'm not like saying, oh, I'm going to put, you know, I could send them, maybe I can send them to specific organs, but we're not going to try to be too tricky in the beginning. We're just trying to do the basics. And the basics is, you know, for people who haven't seen any of this data before, What aging scientists have really come to grips with is that aging is caused by the accumulation— we think it's caused by the accumulation of damage to the genetic structure of mitochondria and the nucleus. Okay, so they're both declining as you get older and older and older. And of course, the nucleus is better protected. And it's more careful, it's got better quality control, so maybe it ages slower. The mitochondria is simpler and you start out with zillions of copies of it. The nature, the way nature keeps us from aging too quickly in our mitochondria is just by giving us a ton of them in the beginning. We have 500,000 copies of the mitochondrial DNA in each egg cell, 300,000 to 500,000. And it's just sheer numbers. That's just the way, like, you know, the nucleus has got this whole different system of quality control. For mitochondria, it's just sheer numbers, okay? And the other thing I always tell people is to remember that you are 10% mitochondria. 10% of your body is mitochondria, okay? So you're, and they're all running like crazy generating energy and they're like little jets, They're little jet turbines buzzing away. And so you, when Yoda says we are energy beings, it's really true. We are energy beings.

Luminous beings are we, not this crude matter.

If it wasn't for all that energy, we'd all just collapse into a pile of a puddle of goo. Right. So those mitochondria are there. Yeah. I mean, your Buddhist friends are right. All these things are gonna come together and the science supports it. The other thing I always like to mention is that, but the mitochondria are a billion years old. And for the first 500 million years, it was just single-cell animals or maybe 2 or whatever it is, 400 million years. So they had 400 million years to perfect themselves. And then we came along, they built us. Like we were built by the mitochondria, okay?

Yes.

And so, yeah, these are the things to remember.

It's funny, back when mitochondria first kind of became a thing around 1990, really, we started talking about it, right? I had chronic fatigue syndrome and my career was taking off in Silicon Valley. I'm like, I think I have a power plant problem here. So I just became obsessed with mitochondria and all the things you can do. And we have a very similar view now from what you just said. One of the things that, that came across my awareness is that you can look at mitochondria as the, the wiring diagram, right? And then you also have the physical infrastructure, like the walls and the building, which is nuclear DNA, right? And there's a couple studies showing that a mismatch of mitochondrial DNA with nuclear DNA equals animals that don't thrive. And that's right, it was done in sparrows, right?

Right.

So you're growing mitochondria, large numbers of them, in a vat.

Right, right.

Now, are you growing my mitochondria?

Yeah.

Or are you growing someone else's?

No, no, your mitochondria.

So I want like— whose mitochondria would I want? Like, I want—

hmm. Well, all right, let me tell you. Here's my— I'm going to tell you something that's very speculative. I actually have one of our volunteers for our group actually went out and did a mitochondrial study. You can get these for $140. You can get your mitochondrial haplotype, right? And this person did a mitochondrial haplotype and they found out that they had Inuit Eskimo mitochondria, literally. Okay. They had the same type as the Eskimos. And so I said, do you get like overheated really easy? And she said, yeah. Because I have this theory that mitochondria have very subtle little changes that they've evolved as the human race migrated around the world. If you take a mitochondria from an Ethiopian and a mitochondria from an Eskimo, they have different energy production levels. And they keep— though, so if you want to run, they— the— so the point is, if you want to be a good skier, you want the Eskimo mitochondria. If you want to be a really good long-distance runner in the Olympics, then you want the Ethiopian mitochondria. Okay. Because they're going to produce different amounts of waste heat.

It makes so much sense. And the difficulty is that if you have, say, the Ethiopian-sourced mitochondrial DNA, but you have a hardware package that's Northern European, you're probably not going to perform as well as if there's a better match.

I think, I think that when the, when the, when conception happens, there's this magic where the nuclear DNA builds itself from the two, from the two, you know, male and female, the chromosomes rearrange, and then it's got to negotiate with the mitochondria. And of course, the mitochondria comes straight from the mother. There's no male or female mitochondria. It's all maternal. And so it's like two different worlds. They're alien species because the mitochondrial DNA is a bacterial DNA and our nuclear DNA is a chromosomal DNA, and they're completely different chemistry even. Okay, so I think there must be some sort of negotiation process and And maybe mixing a Northern European nuclear DNA with a mitochondrial, an Ethiopian mitochondrial DNA, maybe it might be a great combination, you know.

It can be both. And, and since there is no really, it's very rare to find, oh, I only have Northern European or, you know, South American DNA. Our DNA has been mixed pretty effectively. So we all have like random building diagrams and then we just want a wiring diagram that matches it.

Right.

And my theory, and this is very speculative, but it was in my fertility book. The only cells that have 100,000 up to 600,000 mitochondria are ovarian tissue. So I think those mitochondria have all that power and all that compute because they're trying to decide which egg to drop based on the environment around. So like, this is the egg that will thrive at this latitude with this kind of sunshine, this kind of nutrient, this kind of temperature. And then that egg selects the right sperm, which is a source of half the nuclear DNA. And like, that's how it has to work, at least in my engineering view of things.

Well, that's, that's very speculative. So of course, yeah, I won't go there. I have, I have so much speculation already that people nail me for. I'm going to let you enjoy that one.

And oh yeah, I get nailed all the time. It makes me laugh. And then I just make fun of their mitochondria.

Exactly. Your mitochondria are weak. But yeah. So back to your question. Our goal is to build an external bioreactor and to take somebody who's 85, 90 years old and take their mitochondria. And actually what we're doing is we're taking their stem cells. We take them from their body, but they've got— so they have damaged old mitochondria. Okay. Also, we could take people— there are kids who are born with mutated mitochondria from birth, and it's horrible. They don't, they don't live. I mean, it's a fatal disease and it's completely incurable. And it runs in families. And so from my perspective, curing a kid with damaged mitochondria from birth and curing an adult with damaged mitochondria from just living long enough to accumulate all that damage, that's for me really the same job. Okay.

It really looks the same. Here's a question, though. If the child has a genetic problem, if you culture mitochondria with a damaged problem, aren't you just making more damaged mitochondria?

Okay, so we, we take their stem cells, we put them in our gadget, our, our BioRector. Step one is we have to fix the mitochondria. Okay, so I don't want to grow a bunch of 90-year-old mitochondria and just pump them back in. That's not doing any good. I have to find a way to reverse the age of the mitochondria to make them 20 or 30 or something. And then you try to push as many of those as you can into the 90-year-old body, and then you end up with maybe 60 on average. You know, you're kind of— it's like mixing black paint, white paint. You're never going to get perfectly white again, but you can get it to gray. Okay. And so we're trying to, trying to flush out all the old mitochondria. In the case of the children, it's exactly the same thing. We're going to try to fix their mitochondria, grow a bunch of those, and then flush out their bad ones and replace them with good ones.

Wow. When you fix them, are you CRISPRing them or how do you do that?

That's— I can't talk about that. That's okay.

Got it. That's the secret sauce.

That's the secret sauce. And it's so— I mean, we're talking way on the edge of, edge of science right now.

It's the coolest stuff though.

Okay.

Yeah, I got it. Because if it's okay to fix mitochondria that have some problems and reintroduce them, can I take my perfectly good mitochondria, give them some superpowers, and then introduce them back in?

Maybe 50 years from now. I, you know, we have to— right now, that's why I always tell people, I'm focused on one thing at a time.

Okay. I respect that.

Just doing what's in front of us is plenty. Okay. And the other thing people always ask is they say, well, if you're doing it the autogolus approach, autogolus means that you're growing someone's own mitochondria. And people always say, well, that's going to be very expensive. And it is because there's just a lot of work involved. What about just mass producing mitochondria, which means you would have to find a generic version of the mitochondrial DNA that would not hurt people. And I mean, if someone's in the emergency room and they've had a heart attack, you know, you're not going to care. You're going to give them whatever you have on hand, right? And by the way, emergency room doctors are starting to look at this for all kinds of emergency situations.

It would make sense. And you look at blood sepsis, you know, when someone goes into septic shock, it's mitochondrial network shutdown. Put in some young fresh ones in there and watch what happens, right?

Well, I wrote a whole paper about that, about curing sepsis in mice with mitochondria. We did that. Wow. 2.5 years ago. So look on our website, you'll find the paper.

Paul Allen would still be here today if this was further advanced.

Paul Allen would still be here today, maybe. And I always feel sad when I say that because, yeah, I mean, you know, oh gee, if we just had this, but I mean, you just, you can't think about that too much. You just have to go on. So the allogeneic question is, I think eventually in order to scale this up really on a global basis, I mean, I think everybody over the age of 55 at minimum should get mitochondrial supplements. I think it's like a vitamin. I think everybody should just get it.

I couldn't agree more. And I've, I've had my stem cells taken out, my bone marrow and my fat cells. I've had them culture expanded, reintroduced, and I've had my NK cells taken out, culture expanded and introduced to give me a young, a young immune system. And why wouldn't we do it with mitochondria?

The mitochondria literally are just a variation of what you just told me. I mean, the techniques we're using are the same as what you just described. Okay. Except we're just doing it optimized for mitochondria, which means when you got a stem cell treatment, you probably got, you know, maybe 150 million stem cells, right?

Yep.

We figured that that's about 3 days worth of youth. Okay. It's unfortunately most stem cell treatments, they're great, but they're just not enough. Okay. And so what we're trying to do is say we're going to do trillions, trillions of mitochondria, which is the equivalent of 5,000 stem cell treatments. That's the goal. But that's, you know, a challenge, of course, to pull that off. But if we can pull it off, then instead of 3 days of youth, maybe we can get years, right? Or I say youth, I mean health, you could say health. Same thing, right? Yeah.

So they kind of go together.

Healthspan.

I'm one of the few people I think really is our goal actually just healthspan. I would like to live twice as long with my health. So healthspan to me is like it's a weak goal. Come on.

It's, it's a little bit of a wishy-washy term that somebody invented in order to be politically correct.

Okay, exactly.

I use it all the time and my, my people are like, oh, Tom, you got to be more careful. You don't sound like you're being too extreme, but People in the know know when you say healthspan, what are you really talking about?

We're talking about life extension and everyone's— Yeah.

Or at the very least, you know, we're going to be 60 up until we're 100. And then, you know, I don't know who— nobody knows what's going to happen. But like when we do the tests in animals, we don't actually spend a lot of time worrying about lifespan. What we do is focus on can we reverse their their physical age in the moment. So can I take a mouse and give it— and we do this all the time— give them a whole bunch of mitochondria and maybe exosomes too. And then can I look a month later and see that that mouse has became 30% stronger and 30% better cognition and can knock out sepsis? And we've done all 3 of those things. We've done strength, we've done cognition, and we've done immune system function, and they all work.

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How much does it cost with the research levels you're doing now to do this for a human? Is this like a half a million dollar thing? We don't, we don't We don't even know.

I mean, there's no way to say right now. So that's like saying, how much is it going to cost to go and rebuild some old castle in Scotland somewhere? Well, nobody knows. You got to go look. You know, it's like nobody's tried it before.

So this is so cool.

It's right now it's about getting the funding to do the research and get the first— I mean, we want to do 5 people and just to do the first 5 people, I mean, that, you know, that's expensive. But that's true of any— I mean, people are out blowing billions of dollars on all kinds of longevity ideas. So this is—

oh yeah, yeah, this is a very well-founded idea that's worthy of funding if anything ever was.

Uh, that's my argument.

Yeah, I've done consulting work for multiple longevity venture funds and have invested in some things in the space, and this is the kind of thing that's worth backing.

You know what's very interesting? I'll just say one thing about funding, having now been through it. Of course, I wasn't in biotech, so I don't know. I didn't know what I was getting into when I started the biotech thing. You know, we've, we've raised about $4 million, which is very little, and we've kept it very small, very tight, you know, fast-moving, small team, the whole bit. My experience is that there's this huge difference, and maybe you've noticed this, there's a huge difference between people, it's kind of about 55, 60 years old. There's a cutoff. And the people who are younger are focused on other kinds of longevity, which is appropriate for them, which is things like, you know, extending what I already have, which is very inexpensive. And so I'm a big believer in that, right? Like, take care of the mitochondria you have now, okay? Because that's the cheapest way to get longer healthspan. Just take care of what you have. Like, if you smoke, you're taking 10 years off your life right there, okay? Whether you get lung cancer or not, you're, you're, You're just nuking your mitochondria when you smoke. If you're stressed, like stress destroys mitochondria. And we all know it instinctively 'cause we can see it in day-to-day life. You know, people who have stressful jobs and the people who live to be 105 are usually some guy who's like, you know, a hardware store owner in some little town somewhere that's just kind of has an easygoing life or he's a farmer or something. Doesn't worry about things, okay? So before 55, 60, that's where most of the investment goes. And then to get the, what we're doing is really for people who are elderly, okay?

Yeah, to reverse it, right?

Reversing is much harder and it's much more complicated. And so we're focused on people who are 75, 80, 85 years old. That's our volunteer crowd. And those are mostly the people who, who invest is people who want it for themselves.

You know, it seems like a lot of the, the most disruptive and biggest swing for the fence longevity things are go through that same path. And I've also done gene therapy, you know, that's not cheap, but I'm willing to overpay for it because I want the— I want it to work now versus later because I, I feel like any longevity thing you can do earlier in life the better off you are, because it's very cheap when you're 16 to keep your healthy mitochondria, and it's very expensive when you're 65 to get them to be 16 again. So the highest ROI comes earlier in life.

That's right. Yeah, going backwards is really expensive. We're going to get there. I think— I'm convinced we're going to do it, and it will— I think it's going to give us much longer lifespans, and I think it's worth it because obviously the cost of, of healthcare is so expensive, and the cost of all these diseases The good thing about mitochondria is that there's thousands of uses for them in traditional medicine anyway. Like I'm working with people who don't have anything to do with longevity. They're just trying to cure Parkinson's.

Oh yeah.

Okay, and Parkinson's is a very good, and ALS, and you know, we've looked at retinal diseases, even glaucoma. It turns out glaucoma may be very much a mitochondrial disease. And so there's all these opportunities that are not related to longevity. They're just traditional medicine. And so, but you still need a bioreactor because you need— there's no real sources of mitochondria for all these great cures. So we need the bioreactor one way or the other.

I was just talking with a friend who has Parkinson's and is a billionaire, and I'm like, you don't have Parkinson's, you have a mitochondrial disorder, and Parkinson's is a symptom of mitochondrial weakness.

It's the expression of the— or premature mitochondrial weakness.

Exactly. And it just so happens the most energy-intense part of the brain that makes dopamine your mitochondria failed there first because you have a systemic mitochondria problem. Let's address mitochondria. So I think when your technology matures and becomes available, huge numbers of incurable diseases will magically become curable because mitochondria are foundational to so many things, right?

Right. I, I am careful not to say magically because, you know, I don't want— you know, this, it's complicated. We don't know yet, but the opportunity is huge and we should be chasing it. The other one is that I've been, I have some people in my group who, for example, have fluoroquinolone toxicity, which is Cipro. Okay. There's actually in statins, there's quite a few drugs that damage mitochondria and we're not paying attention to that. Okay. And there are people who have become absolutely damaged. Their lives are destroyed at age 25, age 35. I mean, I know some people and it's horrible. And so there's this whole world of pharmaceutical interaction with mitochondria that we have not been really carefully looking at in medicine. And we have to because we're leaving behind this trail of these disabled people.

It's funny, at the biohacking conference last year, the guys at Me Health launched their product, their mitochondrial health assay.

Oh yeah, no, we've got one of those big, Okay.

You have to be working with Hamil Patel, the PhD behind that, and he's been on the show as well because this really does feel like the future. And Sachin Panda's work around light and mitochondria. So almost every biohack that I'm, I'm teaching people are around signaling to the mitochondria what you want them to do so that they'll do it. And it's really changed my cognitive function, all my markers of aging. And I do all this stuff, but it seems like everything I do affects mitochondria. Like, oh, testosterone affects mitochondria. You know, everything.

Mitochondria make testosterone.

Exactly. And estrogen too, right? And melatonin. A lot of people don't, don't think about cellular melatonin. And that's a big deal, right? And they actually don't make glutathione, but they power glutathione production that they then use. And like, it's such an elegant system and it's— it just seems eminently hackable. From the perspective of someone's like, how do I increase performance and availability of distributed systems, which has been my entire career before I turned biohacker, right?

Right. And I'd also mention that like your friend with the Parkinson's, why does one person get Parkinson's and another person gets ALS and another person gets early onset Alzheimer's and somebody else might get early sarcopenia or whatever? You know, the thing is what they found out and actually that paper just came out 2 weeks ago. There was this great paper that said, that it's absolutely— you cannot predict the distribution of mitochondrial function in the body. Mitochondria kind of randomly scatter when we're embryos, and sometimes some bad ones get in there and they get replicated, and you end up with a bunch of bad ones in one organ, and you end up with good ones in another organ. Oh, wow. It's chaotic. And so we're going to be at the point where I think we need to— well, first of all, we need to do nationwide mitochondrial testing. And so your MiScreen, we have a test that we've been working on that is actually looks at the amount of deletions and damage in the nuclear, in the mitochondrial DNA.

Oh, wow.

And we have a whole like program where we've been doing that. We're gonna use that as one of our tools for our process. And, but even that, like even if you look at the DNA, let's say you look at the mitochondria from a blood sample, it's gonna be completely different from the mitochondria from a urine sample or from a skin sample or from, you know, a spit sample. The mitochondria in different parts of your body are all at different levels of health. And we think that they're actually being supplemented by the bone marrow. The bone marrow is kind of the source of truth in our model. The bone marrow stem cells are what are kind of creating all the mitochondria that it's using to supplement the rest of the body where they're getting burned out. And this is what most people don't understand. The mitochondria in your cell, they may not last more than 10, 20 years and they get burned out because they're under stress. You're running from, you know, predators, whatever you do when we're in the jungle, right? When you're an animal, you're under stress all the time and that causes your mitochondria to replicate too quickly to accommodate the emergency. But when they replicate really quickly, they get damaged really quickly. Their mitochondrial DNA gets, lossy. You get, you get a lot of errors and, and like transcription errors. It's like a hard disk with a lot of bad sectors, okay? And the bone marrow is the source of all the replacement mitochondria that the body is using to replace the ones that are going bad. And our theory is the reason human beings live to be 85, 90 years old, whereas an antelope the same size as us— antelopes only live to be about 30, okay, at best. I think the reason is because our bodies have been programmed to ration the mitochondria more carefully and to reduce the size of the skeletal muscles and do all these things because for humans, long life is a real survival advantage, okay? And so I think that evolution has been programming mitochondrial usage for all the different species. And Like, we're going to find all this stuff out. It's going to be amazing. I think the finding out, as you said, the network administration aspect of mitochondria in the body, right?

I've been doing a lot of work on signaling mechanisms and people who are not network engineers, you wouldn't, you wouldn't know that when you pick up a phone, there's an entirely separate network called SS7 that's setting up your call and it's invisible to you. Like, I don't know, there's a connection there. But all the switching, all the stuff that happens, mitochondria have a bunch of different ways of signaling. And we use light and photons and electricity and heat and vibration and exosomes.

Lots of exosomes.

Yeah, lots of exosomes. And just hormones. Chemical signaling is kind of a big thing too, right?

Right.

And so there's this beautiful— like Martin Picard, I think, writes about it the best— beautiful whole garden community It's like people who've made kombucha, you get that SCOBY, or you make sourdough and you have the perfect ferment. We're the same. We're a big SCOBY there. And there's all these variables that we can change. And are you familiar with Dr. Veech's work?

No, I'm familiar with Picard. He's great. I don't know about Veech.

Dr. Veech studied with Hans Krebs and spent 40 years studying mitochondria and ketones. And this show was the last, last interview he ever did in his 80s before he passed. And he talked about how ionizing radiation when you fly is so bad for your mitochondrial DNA, but that the presence of ketone bodies is protective against that. It's like we cannot go to space until we hack our mitochondria with ketones. And so it's connected to like all human flourishing is really mitochondrial flourishing.

Oh, by the way, I'll just I'll just mention one of the people on our board of directors is a former astronaut and he's a Stanford doctor, former astronaut who studies radiation, okay? We've got a whole idea of what's gonna be needed for people going to Mars and people going to the moon. We're gonna need mitochondrial supplements for them because that radiation damages mitochondria, yeah.

I once asked the president of SpaceX, I'm like, well, you guys have hardened all the electronics, going to space? What have you done to harden astronauts?

Yeah.

And she said, no one's ever asked me that in 17 years. I'm like, well, you know, there are people thinking about that. You're one of them, obviously. And so I want to harden myself just for life on planet Earth, you know, then I'll just live longer. But if I end up going to Mars, hey, I want to be hardened for that too.

That's right. I mean, the bottom line is I don't think the human body is quite up to the job as it is. We're too fragile and we need to not be so fragile, really. We need to be We always say more durable, more resistant to radiation, cancer, and infections, you know. And like, I don't think that we're going to be super beings. I think, you know, I think when you're 25, that's about as— you're about as strong as you're ever going to get. But certainly we can be more resistant as we get older. And that's what I'm aiming for.

Do you think we'll ever get to the point where we can add a USB charging port for ourselves. I mean, they're run on electricity. Why not, right?

Well, this is the next thing. This is the next closest thing. But, you know, one of the things that people don't realize, like, people talk about, you know, when as you get older, you know, I'm, I'm mature, right? Like, so I, I'm old enough that I know what's going on, right?

There you go. Got some wisdom in there.

I got some wisdom in there, unfortunately. And one of the things people always complain about is as you get older, it's harder and harder to keep off the fat, right? You're like, men get this tummy fat, women get the thighs. And for any mitochondrial person, it's like, oh, well, that's obvious because you're eating the same amount and your body is supplying all those nutrients in the bloodstream. But the last mile of energy conversion is the mitochondria. It's like, it's like if the, if the cell can't get those nutrients through the mitochondria, it can't take them in. And so what happens, there's not enough mitochondria to process all that fuel. That you had when you were 30. Now you're 60. You don't have the same number of mitochondria. You don't have enough furnaces to burn all the fuel. And so what happens? It all gets sent off to a dump pile, you know, which is white fat. And your body's like, oh, I'll keep it for later. And of course, there never is later because you always, you know, we're— yeah, I was like, so I think if we can improve the mitochondria, if nothing else, maybe we'll all just be a little slimmer.

You know, it appears that that's possible because I was the, you know, the, the computer hacker from Jurassic Park 1. I was 300 pounds when I was in Silicon Valley and I'm 52 and I'm not on—

I look at you now. All right.

Yeah. Right.

For you.

And, and I, I don't limit my calories at all. I, cause I've literally done everything that I can think of and some that I think are going to work, but I'm not sure yet to make my mitochondria really good at processing air and food. Right. I think by popularizing this as the next step beyond stem cells and exosomes and as a major part of longevity, as important as NAD even, this, this is, this is where it's at. And I have a couple questions. So I understand this. So I was blown away in 2001. There was a book called The Daughters of Eve or The Seven Daughters.

Oh, yeah, right.

My grandmother, who was a nuclear engineer, actually sent it to me, and she was so fascinated by this and saying, oh, there's 7 kinds of mitochondrial DNA. That's true just of Europe, right? Because we didn't have data back then for other cultures. But so there's what, 30 or 40?

26. There's 26.

26. Okay.

1, 1 per letter. So it's A through Z.

A through Z. Okay, cool.

Yeah.

What would happen if, say, someone has one of those 7 European haplotypes and they get some other haplotype infused, are these mitochondria going to form a new network, become friends? Are they going to go to war? Has anyone ever experimented with this?

We don't know yet. And that's why—

Do it in a mouse and tell me what happens. I got to know.

We've— no, no, we've done— there have been studies like someone took mouse egg cells and they took out half the mitochondria and they put in a completely different type and the mice lived, but they weren't— it wasn't great. Okay, they didn't, they weren't, they were runty. Okay, they didn't do well. On the other hand, there have been, I mean, we've injected mice with vast, we're up to the point where in our animal injections, we're up to doing now 1% of the animal's mitochondria per injection. Okay, that's how far we've gotten. And it's getting to the limit of what the animals can handle. And so, but we wanted to know how much we could do. So, you know, in a human being, that's like an unbelievable amount of mitochondria. Okay, that's 1% of your body weight per injection. And we— I think this would be something where you do like these, you would do these every few weeks over the course of a year or maybe once a month or whatever, and you slowly build your stock back up. But the reason I want to use your mitochondria is because we don't know yet what happens if we use someone else's. And it's just another variable we don't want to deal with. Maybe there's—

I totally respect that.

Yeah, maybe there's a type. Maybe there's a type O mitochondria. See, maybe after we go through all this, we'll find out that, you know, type L mitochondria actually work fine for everybody and then we could just mass produce those. Okay. We just— that's going to take research.

It is going to take research. And I'm so happy you're doing it. Do you find that the mice who are receiving these high doses of their own mitochondria are living longer? Like, what do you see?

They are living longer. But again, I don't like— I don't really trust mouse life extension because anything you do with a mouse will make it live longer. So no, it's true. There's like 1,000 different things you could do with a mouse that'll make it live 25%. I mean, just take it out and give it and pet it once in a while. It's going to live longer. Okay. Mice, they're so variable. And so I don't— we just don't put it— we don't hang our hat on that. We're looking at can we make them stronger and better cognition and improve their immune system? Because those are real things that are right in front of us. Okay.

And they're, they're measurable. And I always laugh when you see these, these studies to your point about mice, especially from the pharmaceutical industry, they're saying, well, you know, we controlled for all variables and you go, oh, was it a man or a woman who fed the mouse?

Yeah, exactly right.

It turns out massive change in cortisol response because mice know that men kill them and women run away. So they're not afraid of women. And like, that's a big variable, guys, but they don't even know.

Right. And is it the nice technician who likes the mice or is it the technician that doesn't give a crap? The mice know that. All right.

They totally know.

They can bond and they're very emotional. Mice are very emotional little guys. Are they— do they have, you know, do they have a piece of fluff to make a nest out of? Do they have a wheel? Do they have friends? I mean, they're in solitary confinement, really. So, I mean, yeah, I— they made this— they made it now where, you know, the FDA is no longer requiring all these animal studies. And I'm a believer in than that. I don't think animal studies really are very good.

So they're better than nothing. But now that we can fully create a virtual cell for the first time, thanks to AI, and we can run experiments on that in a way that's pretty accurate, I think it does save a lot of messiness. And frankly, I have no problem with eating animals that are treated ethically, but I'd rather not have them suffer in labs unless it's the only way forward, in which case I'm willing to do that.

Well, and also mitochondria are so different in human beings compared to animals that we actually went through this whole process a year ago and we talked to our 85-year-old volunteers and they're like, yeah, there's no point. Just, just let's just try it. You know, they finally, the decision was by the group that going, trying to do this in animals just wasn't worth it. And we just do it in human beings, start slow, do it very, very slowly, you know, be very, very careful. And, and do lots of— and that's what our human trials are going to be, is just slow increases in dose.

Good for you. That is the future. And this idea that a government regulator says whether a human is allowed to take certain risks when they're at the end of their life or they have a life— sorry, that's not a government decision. That's a me decision. And so for someone who's 85 saying, you know, I'd like to learn something before I go and who knows, maybe I'll get some benefits. Like, I respect that greatly.

Like, well, I think that's— and again, there's children, there's children who have these diseases. And so a lot of my old folk are like, hey, let me be the guinea pig. I mean, they, they consider that to be absolutely an honorable thing to do. And in fact, they're, they're just, they're just dying to do it because they want to do something to help kids, right? And so look at that.

See, that's the innate goodness in humans. And, uh, after I send you the, the book, I actually make the case that kindness is wired into our mitochondria. Yeah, but only under certain conditions. And I think a lot of our human emotions are actually driven by a mitochondria network. That is speculative. It just makes sense.

The other thing I just want to mention, it's funny because getting back to the very beginning of our conversation, I said there was all this new research coming out. One of the things I didn't mention was that, you know, the textbook version of mitochondria is that they just sit in the cell and the cell just remakes them whenever they want. They're kind of stable, right? What we found out is that's not true at all. Mitochondria are completely true. You know this. They move everywhere in the body. They're flowing between cells. Cells are loaning them, okay, and then having them be returned. Stem cells are mitochondrial loaners, okay. They have pictures of stem cells where there's a cell that builds a little nanotube to the other cell, and you see that you actually see the mitochondria marching down this tube. It's really cool, right? The body is— those tissues, they're all about keeping everybody healthy, because if the cell next to you is dying, that's bad for you. And so you're going to loan your mitochondria to them to give them a jump start, okay, if they've been damaged. So it is about kindness, okay? At even at a biochemical level, our, our cells are taking care of each other. Because they're a society, right? It's like a— it's like a beehive. You know, the beehive is the same kind of thing. Bees are these, you know, they have to take care of each other to keep the hive going.

Is a single mitochondria sentient?

I will not speculate on that. You—

why not?

Because I already have too many. I already have too many speculative things out there.

Let's put it this way. You have $1 million and you have to bet on one or the other, and the proceeds go to charity. Which one would you bet?

I would depend on your definition of sentient. Okay. I just— did you see me just dodge? I just absolutely—

but now the charity didn't get the $2 million that was coming their way.

But I know I didn't— I know I didn't get the money. What can I say?

It's a fair question. And I think AI is making us really ask questions about what sentience really is and what consciousness is. And I am on the side of until proven otherwise that it's very likely that they— that an individual one is. And as a distributed network, they sure look like they are, right? And, you know, distributed systems, multicellular systems can exhibit really complex behaviors.

And if you said, does part of our— just part of our intelligence and our consciousness reside in the mitochondria? I'd say, yeah, hell yeah, because, you know, the mitochondria and the neurons are I mean, our thoughts are mitochondrial, okay? Because our brain is a bunch of energy gradients being maintained by those mitochondria and they're going, I mean, you know, the brain is the biggest user of energy in the whole body. It's got tremendous energy needs. And there's all these specialized components that the mitochondria are very special in the brain. So, and as you said, these things like Parkinson's and Alzheimer's that come on You know, when the mitochondria get prematurely aged, you know, you start getting these mental diseases. So, and by the way, there's a whole bunch of work going into looking at mental illnesses in relation to mitochondria. You probably know, you know about Chris Palmer, right? Dr. Chris Palmer and, you know, autism and schizophrenia and depression and are they related to mitochondrial weakness?

There's some pretty strong evidence that mitochondria and autism are tightly linked. I had Asperger's syndrome that runs in my family, and I say had because I don't meet the diagnostic criteria anymore.

And you're on— you're doing a keto diet, right? You're on a—

not always. I popularized the keto diet, but I make sure there's ketones present most of the time. But I eat carbs frequently, but not excessively. But for a few years there, I didn't. And what I came to understand from talking with a lot of mitochondrial researchers and autism researchers is that A characteristic of autism is that mitochondrial energy production is artificially low. And so when you have that in a kid, that means that their brain is trying to make sense of a lot of signal processing without enough power. So it develops low-power algorithms in the brain, right?

Yeah, that's good.

And then you—

you're a techie. You're such a techie, you know.

Oh, it's super. Does it show?

Yeah.

All right. And so if you think about then, okay, let's reboot the mitochondria with maybe your technology, right? Or anything else that gets mitochondria working better. And now all of a sudden you have a brain that's good at low-power things, but now it has adequate power. So it's a more efficient brain. And then you have to fix all the signal processing that the brain never learned. And for me, that was like a 10-year journey of reprogramming my eyes and my ears and my tongue and all sorts of weird crap. But the idea that if we can get these kids, even when they're in the womb or when they're very young, and just get their mitochondria healthy, we should see a massive reduction in autism and some of the other childhood things like ADHD and all those.

They—

it just seems universally, you improve mitochondria with known things that in just in the short term improve mitochondrial function, symptoms go down for almost all of that stuff, right?

Well, and that's the thing. And of course, I just want to mention, we also don't know if those kids have mitochondrial dysfunction from birth. I mean, there are low-level mitochondrial mutations that are floating through the human gene pool that we don't know about because we're not testing. That's why I said earlier, I think we should do nationwide population-level tests of mitochondrial DNA to see what the mutation load is out there in the gene pool that we don't know about. We're only tracking the ones that get up to the big enough level that people die. When people, when kids start dying, then they look to see if they have mitochondrial mutations. Well, what about the kids that are just not prospering very well that might have a lesser a lesser level of mutations and nobody bothers to look. Okay. So, yeah. And it runs in families. It can run in families for dozens of generations. It could be passed down from 500 years ago and no one would know it.

And we always blame the nuclear DNA, but it may be the mitochondrial DNA or it may be the interaction of the two. So it skips a generation here because that— and now we can get the data. How many companies, or how hard is it to do a mitochondrial DNA test?

It's almost impossible.

I mean, yeah, I haven't seen it commercially available.

No, it's not commercially available at all. You have to go, like, to get one, even if you have a child that's dying, you have to almost pull your teeth out to get the mitochondrial analysis. And it's very hard to do. And there's like maybe 2 people in the, 3 people in the United States who can do it well. And, you know, no, it's so new and I just want to say again, there's no funding going into this.

Tom, you've got to start 26andMe.

No, no, no, we want to. We actually, we have a thing called MitoClock and we're thinking about spinning it off as a separate company. I'm not here to promote, but I mean, I'd love to turn that into a separate company or maybe this guy with this MeScreen thing, maybe he'll do something that'll give us the same information, right? So we need to all come together and come up with a really good mass-producible mitochondrial tool test, and we need to start using it.

This is music to my ears. And knowing that a 3-time successful tech entrepreneur is working on this gives me hope because you learn something after a couple companies growing them, just how to make stuff happen in large networks of humans. Like, it's hard to be a CEO in a, in a new field. So you're taking all that wisdom you accumulated and putting it towards what I would consider to be one of the most important longevity projects underway right now.

Well, I could tell you that if I just wanted to have a successful business and make money, I'd just do software. Software's a hell of a lot easier. So much easier. Biotech is hard. And, you know, it's, it's also been lately, it's just been really hard because it's just getting nailed from all directions.

So is this something you're going to be able to do in the US or are you going to have to go to somewhere like Abu Dhabi or Costa Rica where the laws are a little bit more flexible on this kind of stuff?

Abu Dhabi is— they're making a big play for this kind of stuff.

Yeah, they are.

We need to do— we have to do it in the United States because we have a lead right now and we can't lose that lead.

I just—

I mean, I'm just saying, you know, we need to stay in the game. And they are now talking about reducing the FDA. Of course, the FDA lag time has been horrible and especially for biologics. And the FDA has no conception of how to manage aging, as you already know. I don't have to talk about that. They don't know what to do about aging, and they're struggling trying to figure it out. So hopefully they're going to reduce the overhead. Also, at the same time, I don't know if you're aware of this, but individual states, they're— I mean, Montana just passed a law that is breakthrough, the Montana Right to Try law, right?

I mean, I, uh, I think I know the guy who was the funding behind that campaign. And yeah, so maybe the states will just reclaim some of their rights and they'll just, you know, they'll just say, no, we're going to just—

and doctors can make their own decisions. The FDA should be— a lot of people say the FDA should focus on small molecule drugs and let the biologics be regulated by the traditional, you know, state boards and state organizations. And also there's this question of What happens when you have individualized genetic treatments? Like you're building a genetic treatment for one person. You're going to go to the FDA with that? That makes no sense at all.

None at all.

So it's one way or another, we have to figure out how to make this work in the United States. And so right now, I think between Montana and Florida and Utah and some of these other states, I think we'll probably be able to do it here.

I certainly hope so, because there's no reason we should be moving that offshore. No, it's just that it's so slow and expensive, mostly because of overregulation. And, you know, there's all sorts of stuff we could talk about, the regulatory capture and all, but yeah, that's a whole other— yeah, we don't need to get into that. It's just what is the situation. And so I've seen, even when I worked with one of the— I think it was the first at-home cardiac monitor to replace a Holter monitor.

Oh nice.

They ended up having This was back as a Mayfield-backed company back in like 2001. And they, they ended up doing all of their trials in India and then coming back because there was another $100 million to do it here. So I feel like the U.S. is becoming a little bit more open and a little bit more focused on like, this is a national kind of economic survival thing.

Yeah, exactly. I mean, if you look at the level of chronic disease, it's going to swamp us. In fact, it is already swamping us. So we have to deal with chronic disease. And of course, that's a big initiative already. They're talking about it. But mitochondrial treatments are one really big, big, you know, thing in our toolkit to deal with chronic disease. So if we don't move— anyway, this is my— this is a CEO. This is my claim that mitochondrial transplantation is a big thing and we need to attack it. Aggressively, right, as a national initiative.

And you, you could be biased because you're running a company, and you're not biased because you chose to run this company and you didn't have to do anything because you could have retired, right?

I could have started another easy software company, you know, and just, yeah, and just, yeah, done what I'd already do. Yeah, but I mean, anyway, I'm not complaining. This is, you know, it's not often at this point in one's career that you get a whole nother exciting, you know, thing like this. It's very rare, actually.

So what a gift.

I'm the luckiest guy on the planet. I really am.

So that is, it's so profound. And I'm, I'm really happy to get to, to chat with you about this. And this is planting a seed. You know, millions of people listen to the show, and a lot of the innovations that have come out in the longevity field, this is a very early source of info and interest. And I, I know there's a lot of investors who listen to the show and I hope that just by shining a light on what you're doing, that it helps to move it forward. There are probably some researchers who may reach out. You know, there's, there's just a whole community who's just eager to support the kind of work you're doing. I want to know, you've got some wisdom, as you said earlier. So what does your longevity practice look like? I mean, are you doing little lines of mitochondria at parties? How does this work?

I've got my secret stash and I'm like, I'm like, I've got tracks up my arm. Well, you know, people always say, you know, Tom, are you going to use this on yourself? And I'm like, of course I'm going to use it on myself. I mean, you know, I'm patient zero. Okay. You know, I have my own little problems that I've accumulated over the years, just like everybody. I'm in my mid-60s and I intend to fix them. And I, yeah, I want to keep going. You know, it's funny because one of our, one of our, our kind of our number one volunteer is a guy named John Kramer, and I know he's okay with me saying his name. He's 90 years old. He's a former physics professor at University of Washington. He's written books on quantum physics. He's like worked at the big physics facilities like this, and he's written 3 science fiction books. Okay, just this incredible guy. And he's a biohacker. He follows, you know, I think he watches your show. He's our main volunteer because he's 90 years old. And, you know, we're like, okay, we're going to be the first two. So, you know, I've got 90-year-olds, I've got 85-year-olds, I've got doctors, I've got scientists, I've got VCs. I've got a lot of people who are kind of quietly volunteering to be, you know, the first. Yeah, yeah, you're in. You're right. If you want to try it, you're, you're in. Uh, we're not— as I said, it really isn't— I don't think this is going to do much for people under 55 or 60 years old. It's just your mitochondria, they're still in pretty good shape. So what we're saying is people over 55 or who have Parkinson's or Alzheimer's or some other chronic disease—

um, ALS is a problem, but you know, and there's any strong autoimmunity ought to improve with this. I I would imagine.

I don't know. I, I'm completely— I don't know about autoimmunity. We don't want to try to mess with cancer yet. I think there's a lot of people who think that cancer is going to be helped a lot.

I, I would bet a lot of money on that, knowing what I know about the Krebs cycle and all. And I know cancer treatment is just fraught with risk and all. I wouldn't, I wouldn't make any claims about that until you have a lot of data.

That's a toughie. But, you know, T-cells, like, killer T cells, if we can boost, I know how to boost the mitochondria and T cells, we can do it anytime. It's easy. And so like if we can boost the performance of the T cells and the killer cells in your body, then of course that's a cancer. That could be potentially a cancer thing.

You just inspired me. If you'd be up for it, ask John Kramer if he wants to come on the show, a physicist, science fiction author, and biohacker who's 90. I have something to learn from him.

So that's, that's That's right. We have, we have some great people in our group. It's just we have a lot of ringers.

Well, Tom, I, I deeply appreciate that you chose to do this, and just, I can sense your excitement about it. Like, this is the coolest stuff I can think of to work with, and you're right at ground zero of something that I am predicting, and I'm pretty good at predicting, this is going to be really, really big.

Yeah, I hope so. And, um, you know, I, uh, I'd be more than happy to see it get big. And that would, that would be a big, that would be a big win for the world.

So your website is Mitrix, M-I-T-R-I-X, dot bio.

Bio. And yes, and anybody who wants to just go to our contact page. So we get, we get inquiries all the time and just remember we're a tiny company. So if it takes a while to get back, just be patient.

That's reasonable. I imagine you're going to get some very interesting contacts after this interview and I hope so.

I hope so.

I am even more hopeful than I was at the start of the interview. So thank you.

Wonderful. Well, thank you very much.

See you next time on the Human Upgrade podcast.

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