Can a Transplant Cure Aging? | Catherine Baucom MD PhD

Imagine treating chronic disease by restoring the cell's energy engines rather than chasing symptoms. That's the bet behind mitochondrial organelle transplantation — delivering healthy donor mitochondria to failing tissues.

CHAPTERS:
0:00 - Introduction
2:02 - Mitochondrial Transplantation Explained
4:02 - Mitochondrial Dysfunction: Alzheimer's, Diabetes and Stroke
8:03 - Stroke Recovery via Mitochondrial Transplant Therapy
10:03 - Reversing Skin Aging with Mitochondria
14:04 - Military Medicine and TBI: Battlefield to Civilian Health
18:05 - Clinical Trials: Path to Widespread Patient Access
22:08 - NASA Zero Gravity Study and Mitochondrial Function
28:10 - Immune Rejection and Safety of Donor Mitochondria
30:13 - Blood-Brain Barrier Crossing in Animal Models
34:15 - Mitosense: From Research to Clinical Translation
40:17 - The Future of Mitochondrial Medicine

Mitosense: mitosenseinc.com

GUESTS: Catherine Baucom, MD PhD and Van Hipp
HOST: Dr. Robert Lufkin MD

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Transcript

A New Kind Of Transplant

SPEAKER_00 0:00

When you think about transplantation, a lot of times we transplant organs like the heart, the lungs, the kidneys, the pancreas, and all those people have to get on medication because they're from other people and our bodies reject them. It's not like that with mitochondria. They there's really no rejection. And so you can take mitochondria from some individual, a young, healthy individual, screen them just like um stem cell transplants, and inject them into um other people, and they will go to the areas that um are necessary for repair.

SPEAKER_03 0:59

What if aging, trauma, neurodegeneration, even ALS, and Parkinson's all shared a single upstream cause? And what if the solution wasn't a drug or gene therapy or even a stem cell, but a brand new type of transplant? Today you'll hear how scientists are injecting young, healthy mitochondria into patients and watching limbs recover, neurons regrow, and devastating diseases slow down. This is mitochondrial organelle transplantation, and it may just be the biggest medical breakthrough you've never heard of until now.

SPEAKER_01 1:40

And now, please enjoy this week's episode.

SPEAKER_03 1:44

Catherine Van, welcome to the program. Great to be with you, Dr. Lefton. Well, thanks for having us. Oh, of course. I'm so excited to talk today about mitochondria and and really the the groundbreaking work that your team is doing on mitochondrial transplantation. I mean, Catherine, you're chief medical officer at Midosense, uh, which is the uh a clinical stage biotech company that's really advancing mitochondrial organelle transplantation, and we'll we'll definitely dive into that. And you also direct the Elliott Mitochondrial Research Center, uh, where you oversee translational studies uh with mitochondria and trauma, aging, neurodegeneration, super stuff. And and Van, you're the former deputy assistant secretary to the US Army, and where you you were involved and and still are with uh medical and health-related issues for the U.S. troops. And this this is this is gonna be a lot of fun. So maybe I'll do I'll I'll throw a question out just to start. Most people think that mitochondria just make energy, and I know that that was what I was taught in medical school, and it's still kind of a common sense uh impression, but you're saying you that mitochondria can actually be transplanted like an organ. So so how does mitochondrial organelle transplation translation transplantation work? And why is it a game changer compared to anything else in medicine today?

SPEAKER_00 3:24

So, like you said, the mitochondria, it it has a whole bunch of functions for every cell, and different cells had different numbers of mitochondria in it, depending on their function. Like heart cell, heart muscle cells have a lot more than um there's certain cells in the skin called fibroblasts, and they have mitochondria. The brain uses mitochondria, everything uses mitochondria. But you can see a lot of diseases, um, particularly like ALS, or like if you look at the neurodegenerative ALS, Parkinson's Alzheimer's, but it even spans metabolic problems like diabetes, um, and even trauma like stroke, so or even heart attacks, things like that, all those have mitochondrial dysfunction. So a mitochondria inside the cell is damaged. Um, so are there are other ways to transplant mitochondria, but mitochondria started, they're very similar to bacteria, and so they can kind of inner cells. Um, there's really when you think about transplantation, a lot of times we transplant organs like the heart, the lungs, the kidneys, the pancreas, and all those people have to get on medication because they're from other people and our bodies reject them. It's not like that with mitochondria. They there's really no rejection, and so you can take mitochondria from some individual, a young, healthy individual, screen them just like um stem cell transplants, and inject them into um other people, and they will go to the areas that um are necessary for repair.

SPEAKER_03 5:14

Wow, so so if if mitochondria are are truly the the master regulators of you know things like immunity, inflammation, and and aging itself, what does that mean for how we view these chronic diseases that now you know take up 80% of our healthcare resources? Have we been chasing the wrong targets all along?

SPEAKER_00 5:39

Uh I think that I guess yes and no. Chasing the targets in that we don't do a good job of trying to prevent problems. And then when problems do arise, we just go ahead and treat them with medication. Um I think you know, sometimes people are are gonna develop problems, and then other times these problems can be prevented. But uh if we and a lot of them are like going back to some things mentioned in in books, like you know, you if you exercise and you try to decrease how much sugar you're taking in, I think sugar is probably one of the worst things we can do. Our inactivity, all those things damage our own mitochondria. Antibiotics damage mitochondria. So I think trying to enhance our own mitochondria may help prevent some of these damaging effects. Um, but for those people who maybe don't know what caused these problems, having transplantation of mitochondria, I think, can help in the future.

Trauma Care And Saving Tissue

SPEAKER_03 6:47

Now you you folks are running uh studies and the traumatic brain injury with the with the VA and in neurodegeneration as well. So what what is why is mitochondrial recovery the missing link in trauma and brain health? And why hasn't medicine focused on this before?

SPEAKER_00 7:07

Uh I don't know why medicine hasn't focused on it before, but I think everything is shifting toward that. Um, like traumatic brain injury or any traumatic injury. Um, one, you lose blood supply to that organ, and then there's so the cell is damaged, and inside that cell is mitochondria, which is damaged. And we have some animal models from Dr. Kendi in Florida that show if you have an injury and then you inject mitochondria into even the a vein of a mouse, then that mitochondria can go repair that. And so once the blood flow is restored, the injury is less. Um, and and it can be applied to the brain too. Uh, we have all these, like for stroke, you have where a part of the brain didn't get the blood flow. Well, if you can give some mitochondria so that the effects after that stroke are lessened, that would be incredible. I mean, a game changer.

SPEAKER_03 8:13

Yeah, and we're used to treating symptoms, you know, fatigue, brain fog, even neurodegeneration or stroke. But if the if the mitochondria are upstream to all of this, what happens when we finally target the root cause like this?

SPEAKER_00 8:30

Well, I think that it can lessen the after effects. Um, like in different types of trauma, gunshot wounds, well, for military shrapnels, gunshot wounds, things like that, injury to the limb. Um, once the blood flow gets back there, if we could in the field give some type of intranasal or a patch or intramuscular injection of mitochondria, maybe we can save some of those limbs from having to be amputated, um, whatever or other organ is damaged, trying to decrease the severity of injury in the aftermath. I think that it absolutely could be a game changer for that.

SPEAKER_03 9:10

Yeah, and talking about sort of longevity and anti-aging, there have been a number of theories for that. Nobody really agrees on which one, you know, there's the there's the DNA damage, accumulated damage, there's another one with hyperfunction and turning on mTOR too much. And and now there's a new theory of aging, which is based on mitochondria being the root cause. What's your take on that?

SPEAKER_00 9:35

I I think that it does contribute. I mean, with aging, just the your your appearance, you get wrinkles, the skin, the different layers thin, so you can get sun damage. And a lot of that, we're we are actually trying to start getting into having repair if you have mitochondrial injections. There's some studies out there, it does show that it helps decrease um the wrinkles, it increases elastin and the connective tissues, the collagen, all those things can help um with some of the aging process of the skin. So yeah.

SPEAKER_03 10:13

Yeah, and and we're, I mean, we're in a revolution in the in the longevity space right now, you know, with uh companies now, you know, in Boston starting clinical trials for partial epigenetic reprogramming using Yamanaka factors, where you know the the uh cells are rewound to an earlier, uh more youthful state um using these transcription factors. Um and I mean we know it works because every generation we rewind our own epigenome when when human beings reproduce, you know, 40-year-old parents have kids that start from zero again. So it works. So but but that's for epigenetic changes in the nuclear DNA. Now, the mitochondria, as we know, has its own DNA and no no real epigenome. So what rewinds the mitochondria? What's the analogous uh action every generation that rewinds the mitochondrial DNA damage? Because that's that's a big factor, right? Accumulated mitochondrial DNA damage with aging, which you know occurs 20 times the rate of nuclear damage. So arguably it's it's you know really important. Do we know what the what the analogous um mechanism for mitochondrial DNA is to partial epigenetic reprogramming for nuclear DNA? Sorry for the long, it's long-winded question there.

SPEAKER_00 11:47

Uh I mean it's a good question. I think um have it definitely starting with healthier, younger mitochondria. I mean, the mitochondria are interesting in that they don't necessarily have to have a whole bunch of signaling or anything like they can get into cells that are damaged by themselves. The exact mechanism is unknown, but um, you know, given older people some younger mitochondria, I absolutely think can help the damaged mitochondria and the younger one can replace it. And especially if you do more of like serial or routine injections, I think that can absolutely help.

SPEAKER_03 12:30

So, so if somebody, I mean, this is not medical advice, but if someone wanted to get new mitochondria, they could get um a maternal relative, perhaps, to donate platelets. And uh, from the platelets, uh, assuming the haplotypes were matched, uh, would they get a benefit? Or do we need literally pounds of mitochondria based on the numbers in our body?

SPEAKER_00 12:58

Uh you don't have to match them.

SPEAKER_03 13:01

Oh, really?

SPEAKER_00 13:02

Yeah. You they because they don't have any of the antigens that you need, you can actually uh give different people uh mitochondria to you take a young, healthy mitochondria and give it to somebody else. You don't have to match them, there are different ways to get mitochondria. Um, plasma platelets is one. Um skin, there's fibroblasts in the skin that carry mitochondria, those can be used as well. I mean, there are different ways to almost any cell beside the red blood cells have mitochondria, and you can extract that. Um, and you don't have to give any, you don't have to match them, like I guess when you think of normal transplantation.

Why Veterans Became The Focus

SPEAKER_03 13:51

Yeah, yeah. Van, you you've spent decades uh bridging military medicine and biotech. So I I wonder what what lessons have you learned from the battlefield that are now shaping how we think about mitochondria in civilian health?

SPEAKER_05 14:08

Well, a couple of things. One of the great things, uh Rob, about military medicine, it's more about applied science and saving lives today, uh, versus the you know the historic model of the NH. So I that's why I've always been attracted uh uh to military medicine because so many of the great uh advancements are coming out of the military. And the reason we went to the veterans of the military first was there was a study out, I want to think it was back in 2017, that said if you're a veteran, you're 60% more likely to get ALS than the general population. And the VA had gone back and looked at data back to 1910. People asked, why is that? The number of theories that have come out recently, and I think we're we're we're we're we're closing in on a couple of them, but we made a conscious decision when we saw that that's who we want to work with, because the veteran's population is disproportionately affected by a number of these neurodegenerative diseases. And Dr. Elliott, our founder, wrote some of the first papers on mitochondrial dysfunction, he saw mitochondria dysfunction as uh really a common denominator in ALS and Parkinson's and Alzheimer's. So we so we made a conscious decision, that's who we wanted to work with. And quite candidly, it was physicians in Congress who looked at our data, the patient use data, put us in touch with the VA, and it was the chief medical officer of the VA who hooked us up with the Tampa VA Medical Center, where they treat more ALS patients than anywhere in the entire VA system. And we entered into a cooperative research and development agreement with the VA on ALS. And I got to tell you, VA's done a great job really in animal models validating our capacity use data, but also looking at Parkinson's, they've now looked at Alzheimer's, and then what was very interesting, they looked at traumatic brain injury. And they took the results and the data they had on that to the Department of Defense, or we call it the Department of War. They took it to the Army, the Walter Reed Army Institute of Research, which has studied mitochondria and has studied TBI. And what is significant about that is, to my knowledge, this is the first time where the Department of Veterans Affairs and our Defense Department have come together in a joint agreement to work with industry to try to come up with a therapeutic treatment for TBI. And we're we're honored to be part of that.

Compassionate Use ALS Results

SPEAKER_03 16:24

And and talk a little bit about uh mitochondrial organal transplantation used in the compassionate use case. We hear about compassionate use more and more for all sorts of cutting-edge therapy. So so what happened? What did you learn about it? And what's what's possible for patients who have no other options?

SPEAKER_00 16:46

So it was Dr. Robert Elliott and a patient that had been diagnosed with ALS. Uh, and you know, most times once you get the diagnosis, it's about two to five years uh before you succumb to your illness. So uh she requested, they signed all the appropriate paperwork, understood the liability and the risk of having experimental treatment. She got mitochondria intravenously, intramuscularly, um, and had a profound effect. Uh she was able to roll over in the bed, she was able to stand up on her own, so her upper and lower motor strength, um probably for about four weeks after the injections um were significantly improved. Um after between four and six weeks, I think they somewhat diminished. So I think routine injections did would have helped. Um, there were just limitations in that, but she did, she had a profound effect from from that, and she had no other alternatives at that time.

SPEAKER_03 17:54

Where are you in the pathway for for patients like this to uh either through the FDA uh you know Byzantine system or or through the VA and through clinical trials, where are you in the process and how close are we to uh seeing this uh having a much more widespread application?

SPEAKER_00 18:15

Well, I think we're we are getting ready to start the phase one clinical trial in Tampa um with the VA system down there. Um I think we're probably within a few months of starting that.

SPEAKER_03 18:27

That's and that will be primarily with neurodegeneration involving the VA also, and uh with that as well. Um and uh I wonder, uh Van, maybe be behind closed doors with a VA and Walter Reed, where you have tremendous experience, what's it really look like when you try and integrate a radical new therapy like this into the military or trauma care systems? Are they are they receptive to that? Very receptive.

SPEAKER_05 18:56

And I gotta tell you, I think they've been at the forefront. Many of the uh the military docs and the and the and the neuroscientists at the VA have really been at the forefront of this. I think I think largely because uh the veterans are disproportionately affected. Uh so uh in fact, it was last year at the World Mitochondria Society in Berlin, Germany, uh both the VA's uh top neuroscientists and uh Walter Reid's top neuroscientists both presented uh their work on mitochondrial dysfunction and and uh and tackling it uh and and working with us. So it's good to see, you know, the government can get so stovepiped and so so bureaucratic. But to see these two departments working together on something like this that has a uh unfortunately a profound uh impact uh on on both our our our warfighters and veterans uh is good.

Partnerships From VA To NASA

SPEAKER_03 19:42

Yeah, I mean you're you're a master networker over your career, and and and uh you your all of your group is collaborating with Walter Reed, with Uppsala University, and Greenwood Genetic Center. What's the significance of building this global mitochondrial network? And how does how do you see it accelerating the path to patients?

SPEAKER_05 20:05

Well, what we're trying to do is have key partnerships with people who are really the experts with that particular patient population. So, for example, the Greenwood Genetic Center, they've been around for 50 years. They are world-class leaders on tackling so many of these rare pediatric mitochondrial disorders. So working with people like that, working with the VA on ALS or Parkinson's, like I said, the uh the the Tampa VA that treats more ALS patients than anywhere in the VA system and maybe even in the in the entire United States. Walter Reed on traumatic brain injury. I gotta tell you, I got a call not that long ago from a physician who asked me, he said, Van, have you seen what is in cell? I said, no, Doc, I don't get up in the morning to go check what's in cell. What it was, Rob, NASA did a study published in Incel. It's on NASA's website today. They did a study of 59 astronauts. They found mitochondria dysfunction because of that continued exposure to low levels of radiation and microgravity. It is on NASA's website today that go the future of space travel may well uh depend on solving this mitochondria dysfunction uh problem. As a result of all this, NASA has had discussions with the VA and now us. So hopefully we're gonna be coming together uh uh to hopefully help tackle that as well. The key is working with the people who are the in the who are truly the experts in that particular patient population and that application of mitochondrial transplantation.

SPEAKER_03 21:39

Wow, that's a fascinating observation. And it certainly makes sense that the mitochondria uh, unlike the nuclear DNA, the mitochondrial DNA has fewer repair mechanisms for for repair of DNA. For example, deletions, it has you know trouble with and other things. Plus, it's surrounded by reactive oxygen species, so it's a real hot. Hostile environment to begin with, and you add added radiation from space. I wonder what the zero gravity effect was. What was that all about?

SPEAKER_05 22:09

Well, it was the combination. According to the study, this was done out of Ames, NASA. It was the combination of the microgravity combined with the low levels of radiation.

SPEAKER_03 22:19

Oh, I see. I see. Well, now there it sounds like if it this mitochondrial therapy works at a fundamental level for mitochondrial energy production. And if it if it works across you mentioned pediatric diseases, you mentioned neurodegeneration, and really truly all the chronic diseases, the literal tsunami of chronic diseases that we're facing, one could arguably make uh make an argument for mitochondrial uh effects there. So this this therapy uh arguably could could be used for so many different so many different things. Just no argument there, right?

SPEAKER_05 23:04

Yeah, well you I'm gonna let Dr. Balcom uh answer that, but but before she does, uh this actually came up at a recent congressional HHS uh hearing with Secretary Kennedy, and they asked him about mitochondrial dysfunction, and they particularly asked him about what the Haney VA Medical Center has done uh uh in their work. And he said that uh uh mitochondria dysfunction is the heart and soul of a current uh chronic disease epidemic. I agree with him.

Competing Approaches And Delivery

SPEAKER_03 23:33

Wow, what a what an amazing time. I mean, this this is not a political channel. I love my Republican friends, I love my Democratic friends. I wish they could just get along better, but it's truly amazing to think in the last few months I'm hearing words spoken on a national stage from politicians and you know, and other people that I've never heard before, like metabolic disease, like seed oils, like you know, mitochondrial function. You know, who knew? It seems like we're really we're really entering a new era where people, you know, hopefully both sides of the aisle are paying, you know, so much more attention to this space. And, you know, hopefully it will follow with you know your support for metabolic for mitochondrial health as well. The there are several there are several companies working in literally the mitochondrial transplantation idea, which you know, which is a testament to the fact that this is so important and it's happening really fast. How how do the approaches differ with these companies? Or is everybody doing really the same thing with just you know slight variations, or are people taking radically different approaches?

SPEAKER_00 24:53

I think um most of them are different. I think ours is probably the most simplistic. A lot of them put them in different vesicles, like extracellular vesicles, um, or they'll use um stem cells or different types of cells that contain mitochondria, but then you that's when you don't really know is it getting where it needs to go. This is just are they some of our injections are contain like a hundred million mitochondria. Um, and so you're just getting straight mitochondria to to go and to the the places that need it. So I do think it's up and coming. A lot of there's a group out of Boston, they uh Dr. McCullough, and he's a cardiothoracic surgeon, he will take mitochondria from uh the heart muscle, and so it's the same patient, then go and take it to the lab and and then go back and inject it into that same patient. Um that is that is one way, but not everybody has access to that. Um, so I think all of us are trying to get the same thing, mitochondria into the body, and how we're going about it is all different. I think my dissent, ours is probably the simplistic and probably the most effective in that you are just giving what exactly you need and really nothing else. Um, we are looking into other ways just for the longevity so and and shelf life of having mitochondria, which are alive essentially, um, and being able to ship it out. So you want something that is accessible and gonna be potent and viable for at least 48, 72 hours or longer, really, for weeks on end. So I think ultimately we're all going to we're we're trying to get to the same goal.

Donors Manufacturing And No Matching

SPEAKER_03 26:43

Yeah, and there are obvious advantages of using your own uh autologous uh heart cells uh to get your mitochondria and concentrating them um and then reinjecting them. Um what and maybe just remind us your your process, uh like if I'm a patient, you know, with uh with one of these neurodegenerative conditions, what would what would I go through in the process to uh undergo this?

SPEAKER_00 27:14

So we have uh a donor and they were screened for all the susceptible viruses, bacteria, infections. Um it's a young healthy donor that we actually acquired the mitochondria from fibroblast from skin. Um and then that is uh used or was is used for the injections.

SPEAKER_03 27:38

And how important is youth? You mentioned a young donor. Uh what what are your windows for aging and how how much of a role does that play? Because the gentleman in in Boston, they're injecting presumably an older patient with a heart, heart myocardial problem. You take his own or her own cells eject it back in. There's no age differential, but you're you're introducing younger mitochondria. How what is your thinking around that?

SPEAKER_00 28:10

Well, uh, you know, as we age, we kind of talked about before, the cells don't work quite as well. I mean, chronologically, they age all the cells age to a certain point. So just the younger, healthier mitochondria, or or you know, some people um don't have healthy mitochondria. They they have just uh diseases whether they're acquired or they were born with. Um so healthy just kind of refers to a it's not just a specific age, um, but but they exercise and eat healthy um as opposed to somebody who doesn't do those activities.

SPEAKER_03 28:54

So you specifically look for younger people who who have a good lifestyle, and probably not smoking and drinking, and you know, but yeah, sort of healthy no drinking, no medications, you know, work out, eat healthy. And you mentioned before that as far as the immunologic risk, uh, you know, when we transplant blood and stuff, we look at you know, blood groups and haplotypes and everything. And is that necessary with mitochondria? And if so, what do you do or why or why not?

SPEAKER_00 29:30

So all the different organs, blood, you know, kidneys, pancreas, all that, you have to look at all the different like the HLA, the human leukocyte, all the antigens that people have in their own bodies and organs, and mitochondria do not have that. Um, so that's why you don't necessarily have to have um matching like you do for a kidney or a pancreas transplant. You have to have all that match. Mitochondria don't have that, and they don't um provoke an immune response either, because they they're kind of like bacteria. When you get a bacterial infection, um, you don't have all that your immune response is basically from the infection, not from the foreign body coming in.

SPEAKER_03 30:17

Yeah, yeah. So, okay, so I'm I'm a patient, and then you identify a donor that's young and healthy. That donor gives uh skin cells. Is that through like a punch biopsy or how invasive is the procedure for the donor?

SPEAKER_00 30:36

Uh just a just a skin biopsy.

SPEAKER_03 30:39

Oh, okay. And so relatively simple, simple procedure for them. And then the mitochondria are somehow isolated from from their cells. So we just we just have mitochondria, is that right? In in a solution, I assume. Yeah. And do you amplify them or get certain numbers? I mean, some of the some people talk about you know massive mitochondrial transplantation, like large amounts are necessary. Uh, do you do you amplify them as well to increase the numbers?

SPEAKER_00 31:15

Uh yeah, like uh probably most injections have about a hundred to three hundred uh billion mitochondria in them. Um I guess in reference, the liver cell, each liver cell has probably between five and eight thousand mitochondria per cell. And the hard cell has maybe three to five thousand roughly. So yeah, you amplify it up significantly for the injection.

Crossing The Blood Brain Barrier

SPEAKER_03 31:45

So it's yeah, those those numbers are hard to comprehend. It's like the national debt. Just you know, just more zeros. But so it's a it's a large number. Then the question is um, obviously, in the the the procedure with the heart we mentioned uh in the Boston group, they're injecting it into heart muscle. So we know we get delivery there. Um with your protocol, or they inject it in the cerebrospinal fluid or in the bloodstream. How do we how do we know we're delivering it? And what is the bioavailability of mitochondria?

SPEAKER_00 32:20

Well, so our animal studies show you they injected it in the vein of the mouse, and then they did serial injections and they they varied the dose. Uh, and then they sacrificed the animals with all the correct protocols. Uh, and they showed, and this is Dr. Kendi in Florida, that the mitochondria injected were in the brain. So they looked at like an ALS model, um, uh and uh Parkinson's model, and they actually and Alzheimer's and they show that there was an increase in the neurons in the brain. So they would take their experimental with nothing, uh, compared it, and so they were, they had the mitochondria and they attacked them. They so it showed that those mitochondria crossed the blood brain barrier and they were in the area that they needed to go to improve whatever symptom there was. Um anytime you deal with humans, we we obviously can't do that, but we can see based on some of the clinical sides and symptoms of improvement. Um so if the animal studies show that it actually is there clinically, you see the symptoms pretty drastically improve.

SPEAKER_03 33:37

Yeah, that's such an important point. That's huge. And I I think it's something that wasn't appreciated, you know, many years ago. In fact, there was a another cell paper that just came out about intercellular mitochondrial migration. And it's been known for a while, but it it it's it's certainly a lot of people aren't familiar with it, the idea that mitochondria migrate between cells, and you know, and like you say, in some in some patterns in in the body as well. So, so basically it's just a matter of of ejecting them into the into the veins, and it's not necessarily to put them into a brain cell or anything like that, but they will just in the bloodstream, they will naturally accumulate in the areas that need it. Is that is that the way of thinking of it?

SPEAKER_00 34:25

Yeah, because these injections done in the rodents, they were not injected intracerebrally, they were injected in the vein, the tail vein. So they it just showed that they went to exactly the location. I think they looked at like the hippocampus for Alzheimer's, so that part of the brain that's really affected with the memory. So in the mouse, it you know was pretty clear the data showing this is what happens if you have no intervention and all the loss of neurons. And this is the one with intervention, is that you you have this upgrowth and um more neurons and better connectivity, and you know, the little mice, they did all the mazes, and the ones that had the injections did far superior than the mice that did not have the treatment.

Dosing Cadence And Scalability

SPEAKER_03 35:17

So and and I realize this is very, very early, and I'm asking you guys to speculate. Uh, but I mean, just uh from your your experience so far, do you how do you how do you anticipate the implementation of this? In other words, will somebody have to get these every week or every month or every year? Or uh how often do you need to replenish them? Once you once you give them some of these these fibroblasts mitochondria from a young donor, how long do they last? And do you have any sense of that?

SPEAKER_00 35:51

Uh I think it's probably about four to six weeks. So, like some of the other chronic diseases, um like rheumatoid arthritis, Crohn's disease, they will get routine injections every four to six weeks. Um, so it'd be similar to that, that it would have to be an ongoing treatment um and on to help replenish the mitochondria. So probably for every four to six weeks.

SPEAKER_03 36:18

And the and the the mitochondrial injections for rheumatoid arthritis, let's say, is still intra intravascular, it's not into the joint or something, right? It's not necessary to do that.

SPEAKER_00 36:28

Correct.

SPEAKER_03 36:30

I mean, and and it sounds like this, you know, potentially could be very affordable for people um that it it would scale and be deliverable, really cost-effective results to people. Is am I is that your take on it, or I'm am I missing some steps here? I mean, this it sounds like you know it it could work in a cost-effective way.

SPEAKER_05 36:53

I think scalability is one of the key differentiators of us. That's what we have focused on. That's why we're uh we've got the kind of partnerships that we do. You take Uppsala University in in Sweden, we've got a great study out with them that really we think is a breakthrough in mitochondrial preservation. Uh, where we we actually showed they took extra extracellular vesicles from MSCs and were able to enhance the cold preservation of isolated of isolated mitochondria. So we're working with uh a great team uh all about scalability because what we want to do at the end of the day, we want to be able to get these treatments, these therapeutic treatments out to as many people as possible and help uh uh as many people um uh fight these chronic diseases. So scalability uh really is the key.

SPEAKER_03 37:40

And um if if um if we're treating somebody, uh I'm a I'm a patient, like we said, I go through the process, I get the young donor, the healthy donor, fibroblasts, go into my bloodstream. Well, how do you assess when I'm ready for another dose or whether you've assess effectiveness? Is it mainly based on clinical uh markers or lab markers? And although also, are there any specific mitochondrial markers that you follow in following these patients?

SPEAKER_00 38:13

There are markers to follow. Uh, we have not implemented them. Um I think probably we would do that with the clinical trial. Um, but a lot of it's based on clinical symptoms as well.

SPEAKER_03 38:30

And it it's interesting that I mean the way you're describing it, it's such a powerful technology. And um obviously, you know, the devil is in the details, and you know, it's everything's a lot simpler than it seems when you talk about it. But but you know, you you can imagine the way that offshore stem cell therapy clinics have spun up and you know, exosome therapy, and you know, with the with the you know, unbridled interest in longevity and chronic disease, do you see, I mean, do you I mean it sounds like is it we'll probably be seeing clinics that are harvesting mitochondria from from young donors and injecting them into people willing to pay the cost? I mean, is that I I guess the laws would be against it in the US as far as uh it wouldn't be a yeah, there were there's certain guardrails on that, although um, you know, depending on the situation, compassionate use or some of the new states like Montana and Utah are you know really changing things, but do you see that as happening or is it happening already?

SPEAKER_00 39:42

I don't think it's happening already. Um, but you know, I'm sure people can do knockoff of anything, any treatment. Um, so I'm sure that it there's a possibility that it could happen.

AI For Early Detection

SPEAKER_03 39:55

Yeah, yeah. I mean, it's uh just just an exciting time. Um sort of rounding out a real uh popular thing is AI, and you're using AI and and the NVIDIA inception program, I think, to monitor patient outcomes. And how do how do these predictive analytics and digital biomarkers transform you know mitochondrial medicine from science fiction into clinical reality? What what what helps you there?

SPEAKER_05 40:26

Well, number one, being in the NVIDIA, you know, we have been accepted into NVIDIA's inception program, which really gives us access to a number of very outstanding uh AI tools. But one of the agreements we have with the VA is is they are sharing with us data, uh patient data that we are then be able or going to be able to take and put into the framework that our folks have developed. Uh, and and also with those NVIDIA tools, we are going, we hope to have an algorithm uh working with the VA that would really provide for the early detection of so many of these neurodegenerative diseases, which of course would be great for the docs if you get that early diagnosis of patients could begin treatment much, much earlier.

SPEAKER_03 41:09

Yeah, I mean that's the thing that that that I'm constantly struck with uh that these chronic diseases, including the neurodegenerative diseases, begin years to decades before the doctor makes the diagnosis. And when we wait for the doctor to diagnose them, we miss a huge opportunity for prevention and lifestyle changes and other things. And and and um so the markers you're looking at, are you looking at uh specific disease markers, or is it something even more basic, a root cause like mitochondrial function?

SPEAKER_05 41:45

Well, for uh the VA, we're beginning with ALS, but we think we're gonna be able to to use it for other neurodegenerative diseases. But as far as the biomarkers are concerned, and and go back to one of the earlier uh questions, we are actually in discussions right now with uh uh with someone who's a real expert all on mitochondrial biomarkers. We see a lot of synergy there because if they can if they can tell the person's got the mitochondria, mitochondria dysfunction and we've got a therapeutic treatment, uh, those are the kind of folks we want to work with.

SPEAKER_03 42:18

So, so I want to be sensitive to your time and everybody here, but looking ahead, let's let's get out the crystal ball and looking 10 years ahead, which you know some people are saying in the next 10 years we're gonna have as much medical progress as we as we've had in the last hundred years when you combine AI and all the breakthroughs that are happening. But looking 10 years ahead, do you see mitochondrial organelle transplantation as kind of a rare last line rescue therapy or something more mainstream, even even like uh you know a vitamin IV drip for your mitochondria?

SPEAKER_00 42:58

I think if you we try to look ahead, I mean, you want to treat the people that need it. Uh, there will always be some people that want um as just prevention for aging, for youth, for whatever, but you know, it it crosses and spans all kinds of different diseases and specialties. And like Ben was saying the NASA for the um astronauts, could they just have give themselves some injections of mitochondria when they're in space to help with their mitochondrial dysfunction? You have the aging, the metabolics, the neurodegenerative, all those things. I think that we would like to have accessibility um for multiple people or multiple scenarios.

SPEAKER_03 43:42

That's yeah, that's great. And we've we've covered so much here. There's so much, so much great information. I have to ask, is there anything we haven't covered that you would like to touch on? Any uh anything we've left out in the time we have remaining?

SPEAKER_00 43:58

Uh well, I guess it's people. And dietary changes and exercise and the supplements can help increase um some of the reactive oxygen species. I mean, all those can absolutely help, but I think we need to have some courage. Our bodies usually stop compensating for our bad habits, probably about the fourth or fifth decade. And that's when trouble arises. So if we can try and get before then, I think it would be better.

Where To Follow And Closing

SPEAKER_03 44:42

So it's a great, great point. Well, Catherine, Van, thank you so much for uh being with us today. Could you could you tell us uh we're gonna include include in the show notes uh your links, but maybe you could just tell us how people can follow you on social media and and get in touch with you.

SPEAKER_05 45:00

Our website is mitosense.com. We're on Facebook, X, LinkedIn, uh, and uh uh and on all those platforms we try to keep folks up to date with the news. And uh uh we're all about we're all about trying to restore mitochondrial health to fight chronic disease. And uh Rob, I want to but particularly thank you for what you've done to help bring awareness. These podcasts are great because at the end of the day, it's about the individual uh taking control of their own health. And and your book, uh uh, I mean, really, and I shared this earlier with uh with Dr. Balcom. I felt like I was listening to to the late Dr. Bob Elliott, our founder, because it was all about Otto Warburg, it was all about ketogenic diets when uh his patients were going through therapy, and he was always thinking outside the box how he could improve uh patients' lives. So, but it's it's education, it's awareness. I want to thank you for what you're doing.

Subscribe Ads And Medical Disclaimer

SPEAKER_03 45:53

Oh, thanks, Van. You're very kind. And uh again, Catherine Van, I I want to get you back again uh to talk about this some more. So many things are happening with your clinical trials. I can't wait to see, you know, to to watch this as we all will in the next few months to see what happens. So thanks, thanks so much for today. Thank you. If you're enjoying this program, please hit that subscribe button or even better, leave a review. Your support makes it possible for us to create the quality programming that we're continually striving for. Half of all heart attacks strike without warning. Your best early warning? A CT calcium scan. We've made it even better by adding arterial age and liver fat quantification, all from the same scan. Now available nationwide without a doctor's prescription. Use the code LUFKIN20 for 20% off. This episode is brought to you by El Neutra, maker of the Prolonged Fasting Mimicking Diet. Use the link in the show notes for 20% off.

SPEAKER_02 46:59

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SPEAKER_04 47:36

Can I start? Is it recording?

SPEAKER_02 47:38

It's already recorded.

SPEAKER_04 47:39

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