Mitochondrial health is not one supplement or one pathway, but a living response to light, nutrients, repair, and cellular cleanup. In this conversation from Apple Finch Pudding, the strongest thread is not novelty for its own sake. It is the disciplined question underneath the trend: what actually helps the body become more resilient?
If you want to optimize your mitochondrial health, this is the episode for you. In this episode, we have three amazing guest segments. In our first segment, we will talk with Professor Roger Sevelt, also the creator of Metacram, on how we can activate and optimize our mitochondria. In our second segment, we will talk with Professor Michael Snyder on rejuvenation and how we can actually exchange our mitochondria and optimize our health for longevity, also by using supplements. In our third segment, we will talk with Professor Matt Kaeberlein on autophagy, on how actually broken-down mitochondria can be repurposed and torn down to rebuild some good, new, healthy cells. I hope you enjoy. She was able to show that that type of light that's penetrating through the human body is really able to touch every single cell in the body, even though it's not illuminating that particularly in its path. This is how we did it. The the tissue in the human body that has the highest concentration of mitochondria is the retina, and that's what he studies. He's been studying this for decades. And uh obviously, he's in the Department of Ophthalmology. So, he has a a surrogate way of measuring how well the mitochondria is working in the retina because the cones in the retina, which can uh detect different colors, red, green, and blue, are highly
red, green, and blue, are highly dependent on energy production by the mitochondria in those cones. And if the mitochondria in those cones are not working very well, there is a problem with color discrimination. It's a very sensitive test that he can use to test color differentiation. And what will happen is as we get older, the amount of ATP that's produced by those mitochondria can drop anywhere from 40 to 70%. So, as as those mitochondria start to come back online and produce more energy, the reduction in color discrimination that we get as we get older is reversed, and we actually are better able to detect the differences in colors very subtly. So, what he did was he he actually had three different groups in this trial. He had a LED bank of lights that were illuminating at 850 nanometers, which was sort of that area there that was the highest to being able to go through the body. And he had three groups. One where the light was turned off, so that was the standard, that was the control group. The second one was someone who was illuminated both in the on the head and the body, so everywhere. And then another one where it was just the body. He He actually put an aluminum container over the head to absolutely make sure that no light could reach the retina directly. And what he showed in the data was that there was a statistically significant improvement in color discrimination in the group that had both the head and the body
had both the head and the body illuminated, so clearly showing that this type of light was able to upregulate and increase energy production. That wasn't that new because they'd actually demonstrated this in in previous studies. But what was interesting about this was that when they put the container over the head, they were able to still see even though the light was not directly hitting the mitochondria through some sort of a remote uh way of communicating called the abscopal effect, that's well actually documented. He was able to show that upregulating mitochondria in the path of the light in one part of the body was actually able to improve the mitochondria output of ATP in other parts of the body that were not directly connected to this light. To make sure that I get it, we are talking now about infrared light, and it passes through the body. My first question would be what is the use if it passes through? But you said it activates the mitochondria. And it activates the mitochondria and that way that if it activates those in your abdomen, it also activates those in your eyes, your retina, right? Yeah. Okay. Now the first question I would say like we are upregulating our mitochondrial activity. Yes. What Why do we need to do that? Why do we need to upregulate that activity and why do we need those mitochondria? Yeah, so mitochondria are the powerhouses of the cell. You probably heard that expression before. They're like the batteries. And as we get older,
like the batteries. And as we get older, the mitochondria are really central to not only aging but chronic disease. So if there's well-documented studies that have been looked at, mitochondria is the epicenter of heart disease. It has been shown to be at the center of neurodegenerative diseases like Parkinson's and Alzheimer's disease. It's been shown to be the causative agent in kidney disease in a whole host of chronic diseases, the mitochondria and its inability to produce energy over time is one of those things. And think about the mitochondria as like an engine in your car. The engine in your car makes locomotion. It makes your car drive, right? But one of the intrinsic properties of a internal combustion engine is that it makes heat. And if you don't deal with that heat, it can make the engine more inefficient and it actually can shut it down. So you need to have a cooling system for that engine and that's very similar to what we believe is going on in the mitochondria. For people who understand the electron transport chain, at the very end of the electron transport chain, there are four electrons and four protons that need to be handed off to oxygen, which is my favorite molecule as a pulmonologist. It's the reason why we breathe is because those oxygen molecules are there to accept the four electrons. And when they do that, you get a water molecule. It's great, it's safe, it's water which you can use everywhere in the body. And the most important is is that there's no spare electrons floating around. The
spare electrons floating around. The problem happens is if you only transfer three electrons or two or one. In that case, you'll get a hydroxy radical, hydrogen peroxide, or superoxide molecule which are very very reactive and will damage anything that is next to it. Of course, if these are being produced in the mitochondria, what's going to be damaged? It's the mitochondria. Same thing with the engine in the car. If the engine is making heat, it's that very heat that is being produced by the engine that can shut down that engine. And so, we have cooling systems in the mitochondria that soak up that oxidative stress. Things like melatonin, which is actually produced in orders of magnitude higher concentration in the mitochondria than it is actually in the pineal gland that we all think about and hear about when we're talking about sleep medicine. A whole host of enzymes like superoxide dismutase, catalase. There's other ones like glutathione. These are all chemicals that are scrubbers of oxidative stress to make sure that oxidative stress doesn't damage the mitochondria. The problem is is that when we have chronic disease like diabetes, like high blood pressure, heart disease, these are not only the result of oxidative damage to the mitochondria, they also perpetuate more and more oxidative damage. And that one of the biggest ones that we've had a big hit on recently in the last 5 years, of course, we just talked about this in terms of why I got involved, is COVID-19. This is the reason why people who succumbed to COVID-19,
people who succumbed to COVID-19, SARS-CoV - 2, were people with oxidative stress, right? So, who are the people that were most at risk for for dying in the hospital? I I know this well because I saw it with my own eyes. People who are obese, people with diabetes, people with high blood pressure, people with kidney disease, they already had a certain level of oxidative stress, and now COVID was coming and making it worse. How was it doing that? Because when the virus hits the cell, it knocks out the SARS the sorry, the ACE2. So, if you want to picture this, you're asking about Your original question is, why is the mitochondria so important? It's extremely important. If you want to picture this in terms of a car engine again, imagine that we're all vehicles traveling on a road. And some of us are healthy and fit, and our engines are running nice and cool. The temperature gauge is way down, nice and low. Some of us are a little overweight or a little bit older. Uh maybe we've got diabetes or some other chronic disease. And as a result of that, our engines are not running as cool as they should be, and they're running a little bit hot. That that temperature gauge is a little bit higher up. It's not in the red, but it's getting close. And then all of us as we're going down the road, we hit this hill called COVID-19. Now, who's going to make it up that road? Who's going to make it up that hill? It's people who have nice cool engines. The ones that don't are the ones that are going to overheat on the way up over that hill. And that's that's exactly what we saw. And so, why this became important to me is if truly if infrared light is doing
is if truly if infrared light is doing something to upregulate mitochondrial production, which it absolutely has been shown to do with multiple studies, not just in humans but also in animals. And all of this is conserved by the way across species. Uh the mitochondria all behave the same way. If this has actually been shown to be true, what is it doing? Why is it doing it? And can it be used not only as a help for COVID-19, but also for chronic diseases well. I began to look at actually not only studies on individuals and clinical trials, but also epidemiologically. And the data is there, and it's actually quite astounding. This was the first segment with Roger Swelt. My main takeaway is that we should actually get outside. Well, we should get more infrared light both for our health and for our personal mood. Let me know what your key takeaways of this segment are in the comments below. Our second segment with Michael will be about what therapies exist to improve our mitochondria and what supplements we can take to improve their function. I think you need to do three things. The first one's easy, swap out your mitochondria. Pick up mitochondrial damage. Your mitochondria just say the way they work, they make a lot of electrons that damage um cells and the mitochondrial DNA in particular. Um and what we want to what happens then is your they become damaged as you get older and older. And it it's likely responsible for your fatigue
it's likely responsible for your fatigue as you get older. And cells will naturally swap mitochondria, believe it or not. So, I think we'll be in a world where you could get fresh mitochondria injections. You'll need billions of them, but it's not that hard to make billions of mitochondria. So, I believe mitochondria transfer will be one where you get injections and they'll naturally swap for some of the you know, into your cells and some of the bad mitochondria get selected away and the good ones will get selected for there. So, that's one. The second is that these what are called senescent cells. These are cells that um that some people call them zombie cells. They're they're basically they're not quite dead. They're sort of hanging out there. They make all kinds of bad inflammatory markers, things like this and they kind of screw up the cells around them. And there are several companies working on what are called senolytics, compounds that will kill these senescent cells. And there's some evidence to show that if you can get rid of senescent cells, you will also live better. Uh the third area is swapping out your stem cells. That's a hard one cuz you have to do it throughout your body including your brain. So, that's not so easy but believe it not people are working on ways of rejuvenating stem cells. We have stem cells in every organ in our body. Uh they're not many and some organs have very very few but we should be able to either you know, get stem cell generate stem cells from you or reintroduce them back.
cells from you or reintroduce them back. You have to do it in a way that doesn't cause cancer and you want to do it in a back way that's functional. And people are doing stem cell therapies for Parkinson's and other things actually now. So, that we're kind of on the cusp of some of this. They're not doing it for longevity just although some people do get stem cell treatments. It's that's controversial. It's not so clear how well they work. Uh a friend of mine thinks, well, it's not even the stem cells that's doing it. It's the mitochondria that's swapping from those stem cells. I don't know the answer to that. But the bottom line now this is that with some engineering uh I think we should be able to engineer people to live forever. But again, you'd only want to do that if people stay healthy because who wants to keep people alive versus just yeah, we want people if they're going to live a long time to be healthy. Uh it's funny if you ask people, do you want to live forever? Surprisingly, most people say no but even in aging class uh longevity classes, most people still say no but a subset say yes. My own belief is as long as people are healthy and you may have seen it in your parents or grandparents. As long as they're healthy, they're they want to keep going. Why not? They should. Um but once their health declines, it's well, then they're kind of ready to go and I do think that's true. Yeah, and there's some basic things you can do for healthy living. We're happy to talk about that, too. You keep making me curious. So, [laughter] okay. Maybe how far away are those treatments and what can we do that you just mentioned?
just mentioned? Oh, the the live forever treatments? Well, the mitochondrial transfer ones are happening now. Meaning there's some trials actually running. They're just starting. The anti-senolytic trials are running now. And the stem cell ones are happening on skin. Uh, people do start with skin first in the longevity field because you can put toxins on your skins like Botox. And that actually it's it's nasty, but your skin rejuvenates itself. So, people will run trials on their skin first to see if the thing's safe. And some of that is happening now actually in the field. And then I it'll move from there. I think it um into, you know, then maybe do something more systemic. There's a little bit going on that's a little wild west like, but in general there are not serious trials out there for the stem cell regeneration that are systemic, I would argue. And I would proceed cautiously there because you don't want to give people cancer, things like that. So, I I think it's fine to be careful about that. In the meantime, I think we can do other things like you may have heard the GLPs, the Ozempics and the Monjaros and things that are now out there. Those are being touted as longevity drugs and there's a lot of evidence that they they're having incredibly beneficial effects. I'm on them myself for my diabetes somehow beta cell defect actually. And and uh, I was on something
actually. And and uh, I was on something that helped with my beta cell. Now I'm on the GLPs. They work amazingly well. Uh, my case though they they I'm trying not to lose weight cuz I'm a pretty thin guy and they do cause all your fat just evaporate, which for a lot of people is good. But they have other beneficial effects besides just reducing fat and improving your glucose. They basically are improving cognition, cardiovascular disease, kidney There's like 12 areas now they've all been shown to have benefit. Some of them independent of the weight loss, meaning they're probably having benefit even in their own right. So, a lot of people think the GLP's may turn out to be a longevity drug. That's a lot of folks are doing what's called microdosing, little small amounts of it to with the goal of getting that benefit. We'll have to see if those studies pan out, but um they may. Yeah, a lot of people are also taking specific supplements like NMN for longevity. What's your opinion on that? Yeah, the jury's out on many supplements, but for some it's shown to be good like vitamin D3. It's pretty clear that's now been associated benefits many areas cardiovascular disease a number. A lot of people are are short on their vitamin B12, so actually keeping that up is good. Some of them there there may be a an appropriate range. Like some people say to This part's not clear yet either. Too much vitamin D3 may be bad for you. By the way, if you do the vitamin D3 you're supposed to do K2 as well because that helps
K2 as well because that helps absorption, but that that's a technical thing. In fact, we just launched a I don't know if you can throw this up on your podcast, but a new supplement website called My Supple Hub and we're doing it not [clears throat] because I I believe some supplements are good for you. I mentioned vitamin D3. I suspect a lot of others are good like I take those myself. See, some of these antioxidants they've been shown to be great with in the context of food. There are a lot of clearer studies like Mediterranean diet which is rich in polyphenols, which is antioxidants, are very very beneficial. So, it's very clear that's true, but then what hasn't shown is whether the you know, taking it as a supplement works. That's where the gap is. And so, many of us think it probably works, but it hasn't been shown. So, we need better studies out there. So, we're launching this website with the idea it's called My Supple Hub, uh where you can look it up on our website. And we want people to go First of all, I want to try and understand what people are really taking, what they self-report is. And And NMN NMN is one of these controversial ones. Some people say it works, some people say it doesn't. And maybe it depends on who you are. Maybe it does work well. It's thought to be beneficial because your mitochondria efficiency This part's clear. It does decline with age for the reasons I said earlier. And NMN helps provide an energy source.
And NMN helps provide an energy source. So, it really does make sense. It probably would help a lot of people, but have the proper studies been shown for that? I would say not there yet, but many people believe there's lots that they tend to have very small studies, things like that. So, you know, I did having said that, I you know, I'm 70. I take my antioxidants. I take some anti-inflammatories. I take not nitric oxide, beetroot extract, which makes nitric oxide, which is good for your endothelial cells, a basal dilator, uh which helps your blood flow. So, um I I figure it's not going to hurt me and it probably should help me. There's a lot of reasons for thinking keeping your vascular system up is a big deal. Have there been proper studies around that? I would say no, nothing 100% convincing, but they make sense to me. And as a scientist, I'm happy to try them. I certainly haven't noticed any bad effects from those things. And if anything, some of them do seem to give me a little more energy, like the NMN NMN one. So, yeah. So, I yeah, I have about um 10 supplements that are up on my website. And you're welcome to take a look at them. But I'm I'll be the first to say we need a lot more studies here. It's not clear. And then clear a lot of these things are snake oil, too. So you have to watch out for that. This was the second segment with Michael. I am looking forward to some of those therapies and I will keep my eyes open of what changes in this landscape.
open of what changes in this landscape. It looks really promising. Let me know what your key takeaways of this segment are in the comments below. Now we'll go dive into the third segment, which is with Matt Kaeberlein. Michael talked more about autophagy, about how we can break down dysfunctional cells to rebuild new functional healthy cells with functioning mitochondria. There is evidence to to support the idea that autophagy can increase longevity in laboratory animals. Again, most of that comes from nematode worms and fruit flies and yeast, little bit in mice, but not a lot direct. So I And again, conceptually it makes sense, right? Autophagy is a People call it like the cellular recycling center, right? It's a way to degrade damage that has accumulated and we know damage accumulates with age, we already talked about that. So if you could selectively degrade the age-related damage, that would be expected to be beneficial, potentially increase lifespan and healthspan. Autophagy is a mechanism to do that. In very simple laboratory animals, turning up autophagy is necessary for lifespan extension from things like caloric restriction or rapamycin. We haven't talked about rapamycin yet. So rapamycin is a drug that increases autophagy and also increases lifespan in lots and lots of different animals. An interesting question is does rapamycin increase lifespan by increasing autophagy? Maybe. Probably that's part of the story. It's not going to be the whole story. But that is kind of where the data stops. And then that gets over-interpreted into
And then that gets over-interpreted into fasting is beneficial because it induces autophagy. So fasting, if you fast long enough, will in fact induce autophagy. How long you have to fast to get robust induction of autophagy is unclear in people. And in part it's unclear because we don't have great tools to measure what's called productive autophagy. We just can't really measure it right now. So, people who are saying you should fast for 16 hours cuz it will boost autophagy are doing a major extrapolation from what we actually know that may or may not be correct that you're boosting autophagy and even if you were, that may or may not be beneficial. I think it probably would be, but there's an if there. If you don't then eat twice as much the next day to make up for fasting the day before. Cuz if you do eat twice as much the next day, that's going to have a negative impact that might offset the benefit of the fast. So again, it's complicated and it really depends on the context and whether or not the fasting or time-restricted eating is also helping you to not over-consume a total number of calories that are suboptimal. So, I think the main goal is still actually caloric restriction. I mean, this is where I think it's we have to be a little bit careful not to extrapolate too much from the laboratory animals. Because in mice, you can go down to a caloric intake that would probably be about equivalent to, I don't know, 900 calories a day or 800 calories a day for typical person. Like really, really severe caloric restriction.
really severe caloric restriction. That's where you get the biggest impact on lifespan, at least in the genetic backgrounds that respond to caloric restriction well. I think we know, well, we do know mice in the laboratory live in a very well-controlled environment. They have It's They're not like it's not sterile, but they don't get exposed to a lot of the pathogens that you they would in the wild or the pathogens we experience. Temperature is really well-controlled. So, it's a low-stress environment, I think it's fair to say. I think we know if you took most people and you put them on an 8 or 900 calorie a day diet that that's going to be really challenging. There's going to be physical challenges, there's going to be emotional challenges, mental health challenges, social challenges, and I think there's a risk that because our environments are so complicated and we are exposed to a lot of pathogens, there's also going to be the likelihood of negative impact of being exposed to the pathogens because at that very low calorie level, you are your immune system is not going to be functioning as well as it would if you're getting optimal calories. Other thing that's really important to appreciate is mice in the laboratory and rats, while they do see declines in bone density, they are less likely to die from the consequences of low muscle mass and low bone density because they're in this protective environment, you know, they're in their cages 24 / 7. So, in people we know with age, loss of muscle mass, frailty, and low bone density is a much greater driver of disability and death than it is in mice.
disability and death than it is in mice. If you're on a very low calorie diet, you're much, much more likely to be under muscled and have low bone density. So, I would personally be concerned with recommending that type of calorie restriction. Even if it slows biological aging, it might have more than equal negative impacts on health span and life span for other reasons like low muscle mass and low bone density. So, I think it would be a mistake for most people to to try to take what seems to work in mice and apply it with respect to chloric restriction in humans. I would feel much more comfortable saying I mean, we kind of know what is too much body weight or at least been a body composition that is under muscled and over adipose, over fat, and we know what is too low. So, let's try to shoot somewhere in the middle and eat what you need to eat to get there and make it a high quality diet. Like I think that's a pretty solid recommendation that is going to be true is that optimal? Probably not because we don't know what optimal is yet, but it's a pretty good bet for the for for having a good quality of health span for longer than what most people are currently achieving. I also want to emphasize something that you said. Even if you do caloric restriction even as a small amount, we still need to have nutritious food. I think that's Yeah, that's absolutely really important and I think it's important to explicitly say. That's not just true for caloric restriction, it's true for the different sort of types of dietary approaches people may consider.
dietary approaches people may consider. You can have a very high-quality vegetarian diet and you can have a really really low-quality vegetarian diet and the impact on your health is going to be dramatically different if you're eating a low-quality vegetarian diet. So, that that quality of food is important, you know, independent of the sort of dietary strategy that you gravitate towards that you find works best for you. Yeah, sugar is vegetarian and so That's right. You already briefly mentioned rapamycin. I think we should talk a little bit about that at least. If I'm not mistaken, you have used rapamycin yourself against inflammation. I think it was frozen shoulder. Can you tell us a bit more about that? Sure. So, just to take a step back, I mentioned rapamycin in the context of it's a drug that has been shown to increase lifespan, improve healthspan in lots of different laboratory animals. It's a an inhibitor of a protein called mTOR. mTOR actually stands for mechanistic target of rapamycin. So, the protein named after the drug. Uh the reason why I'm bringing that up is mTOR is in the same sort of network as IGF-1 and growth hormone, which we already touched on. So, it is a central growth regulatory component that every cell in our bodies and every animal has. And it really helps the cell, the animal sense the environment and make the decision is it a good time to grow and reproduce or if not is it better to be stress resistant and shut down reproduction. One of the key pieces of information
One of the key pieces of information mTOR uses in that decision is nutrient levels. How much food is available? There's not much food in the environment so really really bad time to grow and reproduce and have babies because you don't have anything to feed them. This gets back to our evolutionary arguments for aging. So, calorie restriction for example turns down mTOR because there's not much food around and that turns down growth and promotes stress resistance and that's probably at least in part that stress resistance that accounts for a increased lifespan slower aging. Turning down mTOR also turns up autophagy which we talked about. Why does it turn up autophagy? If there's not much food in the environment, you need to break down the excess material within your own cells to have the building blocks to build the stuff you need. So, that's probably why calorie restriction turns down mTOR increases autophagy. Okay. So, rapamycin is a drug that tricks the cell into thinking that there isn't much food around. So, it turns down mTOR sort of independent of the nutrient level that's available in the environment. And when you do that, in laboratory animals and this works in every animal where this has ever been tested, you increase lifespan and you seem to delay the declines or the changes that go along with aging at every level, cellular, molecular, tissue level and in more complicated animals like mice and rats, you seem to delay many of the diseases of aging. This was a third segment with Matt. I hope you enjoyed it. So, my key takeaway is that we actually should eat healthy
is that we actually should eat healthy and reduce our caloric intake if possible. Let me know what your key takeaways are in the comments below. I hope you enjoyed and I will see you for the next episode of Apple Finch Pudding.
Transcript auto-generated by YouTube. Verbatim — duplicates intentionally preserved.
The episode begins with infrared and longer wavelengths of light, which may influence mitochondrial function in tissues such as the retina and skin. The deeper idea is simple: cells respond to environmental signals. Light is one of them.
Morning sunlight, outdoor time, and thoughtful light exposure are not decorative wellness habits. They are part of the body’s daily timing system.
Autophagy and mitophagy are the body’s recycling systems. Damaged cellular parts need to be cleared so function can be renewed. That process is tied to nutrient status, stress, fasting signals, exercise, and age-related change.
Longevity depends on maintenance. Energy is not only produced; it is protected by cleanup.
Mitochondrial transfer, senolytics, GLP-1 medicines, rapamycin, and supplementation all appear in the conversation. Some are early, some are established for specific uses, and some remain experimental.
The practical takeaway is not to chase every frontier. It is to understand that mitochondria sit at the center of resilience, then build the daily conditions that help them work.
Resilience is built when the signal is strong enough to adapt to, and measured enough to return from.
Prioritize outdoor light, movement, sleep, and nutrient sufficiency as mitochondrial basics.
View autophagy as maintenance, not a reason for extreme fasting.
Separate emerging therapies from daily practices that already have a strong risk-to-benefit profile.
