PhD at MIT: The Longevity Molecule That Reverses Aging (250 Studies) : 1316
19 Aug 2025 · 71 min
Dave Asprey talks with Leonard Guarente, an MIT scientist who studies aging, about NAD and sirtuins, molecules that may slow aging. They cover biological clocks, mitochondrial health, diet, and supplements backed by 250 studies on extending lifespan.
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Different plants work differently for different people. Different proteins, different fats. But at the end of the day, adequate NAD levels mean your mitochondria can handle with your diet.
If you could activate the sirtuins without the calorie restriction, that would be the best thing. And I think that's what you would do by boosting nad.
Leonard Guarente is a world renowned scientist and pioneer in the biology of aging whose groundbreaking discoveries on sirtuins and longevity pathways have reshaped how we understand healthspan and the future of human life. He's not just studying aging, he's redefining it.
If NAD levels decline, if they don't stay high enough, sirtuin activity will fall and you will lose this repressor of aging.
We must keep our NAD levels at youthful levels in order to be healthy over time. When's the right time to start enhancing nad? You're listening to the human upgrade with Dave Asprey. When I first learned about biological clocks and that we could measure aspects of aging to see whether we're doing a good job or not, I was so excited because before that it was, well, did the mouse die or not? Let's hope that I'm a mouse kind of a thing. What's your take on how good biological clocks are now?
I'm a fan. I'm a pretty big fan. It's in the context of what are called biomarkers of agents. So those of us who have studied aging in the lab use model systems. Okay. So over the years we've studied aging in yeast and in the roundworm and in mice. And in those three systems you can use as the readout for aging. How long does an animal live? Longevity, lifespan. And for yeast, that will be an experiment that takes weeks. For worms it might take a month, and for mice it would take two to three years. But still doable, right? In humans, that kind of study is extremely difficult to impossible. So you really need something else. You need a biomarker that is really reliable. That is a readout of biological age. So chronological age is easy. That's how old you are. But biological age is tougher. So biological age is sort of reflected in your appearance. People look younger than their chronological age or older your activity, people who are biologically younger or more active and so on and so forth. So what, when needed, is. And scientists like sort of quantitative measures. Okay, so you do this particular measurement and you've learned biological age. And there really hasn't been anything until about 10 years ago or so when these biological clocks came out that are based on something called DNA methylation, which is. Wasn't really strongly studied in the aging field before that. And I was extremely skeptical when it was first claimed. But what they showed is that. And it was all done by basically machine learning and AI it was done by having a lot of data and having biological samples of people of all different ages and measuring DNA methylation. And they of. And in our genome, we have maybe 1 to 10 million sites methylated. Okay, that's a lot. And they use. So you really can't analyze it by eye and decide what methyls would tell you something about aging. Let's say it's, you know, a tiny fraction of the million. You know, let's say it's a thousand or 100.
Never see that.
You can't see it. So they let the computer find them. And like then from. And that's called the, the. The data set that provided the algorithm. And the algorithm is you look at the quantity, quantify how much methylation is in these particular G residues sprinkled across the genome. Okay, so then you have to go to an experimental set now, a new, totally new set of data and use that algorithm and predict what the biological age is of this, that or the other thing. And biological age and chronological age, of course, are correlated. Right. So most of the early studies were done with chronological age, which is easy, right? Right. And they could do it. They could predict chronological age based on measuring methylation. Initial at a small number of sites, a few hundred. So from that it evolved and I started to Believe it at that point into using that data in studies that had been done for a long period of time. There was one of them is called, I think in Chianti. And to use data that was taken from people at a certain age, let's say 60, and the study followed these people for let's say 30 years. So by then you knew what the mortality looked like in this population. And then apply the algorithm to those 60 year old blood samples and predict how long they would live. And now you have the actual data, actuarial data, how long they lived, and you could do it, you can make accurate predictions. So that's when I really started believing it. Now the most recent breakthroughs, so that's kind of the phase one, phase two clocks use that algorithm, but they incorporate other measurements to get an idea of physiology. Okay, so your health, if you go for a good physical, they'll measure a lot of things, analytes in your blood, okay, Glucose, it's a good example, but others as well, fats, cholesterol and so on. And that will also affect the doctors outlook on your health. So these were incorporated into an algorithm. So for a person, if you had that kind of blood data plus the methylation data, and you put it together and get a composite prediction, you were getting closer to the biological age of that person because all the measurements, blood measurements and so on, would give you some idea of how healthy that person is that would go in in addition to the methylation test. And so we got closer and closer to being able to measure biological age. So these days the tests that are out there, including the test that Elysium, the company I helped get going, has, and the test will measure methylation, okay. But it has all these inputs into the algorithm and so it will give an output of your biological age and pretty accurately.
I've seen a few people say, look, you can't extend human life. There's no evidence. Biological clocks are not scientific. All you can do is have a good health span. What do you think about that perspective in 2025?
I don't think it's accurate. But a good way to look at it is say, okay, we've done a lot of these experiments already in animals. Yeah, it works. So what happens? And what happens? The most salient thing that you can measure in these animals, if they're treated in the experiments we've done with sirtuins, was genetic intervention primarily. But you can also intervene to raise NAD levels in the animals. And what you see most saliently is that they're healthier so they move around more at an advanced age and so on and so forth. And it would be the same with people. What you would see is they would be healthier, longer, they would be less inclined to getting this disease, that disease, the other disease. And longevity data is harder to come by because you have to wait till they die. Right, Right. So most of animals, we have both sets of data. Okay. And you get both. You get healthier and longer lived. And it makes sense. If you're healthier at the last. In the last decile of life, it's not surprising that you're going to live longer. Yeah. And an animal that doesn't get the treatment in humans, we have mainly the beginning to have. Because human data is harder to come by, but we're beginning to get data which is good. And then we have to rely on the methylation clock as a biomarker at this point, because there have been no prospective studies. But there are studies like the Incianti study that I mentioned that were done long enough that you can look at data that occurred earlier in the life of this person, like blood samples and embolism, and make projections that actually align with the real data of what happened to these people going forward.
What is a sirtuin?
Well, sirtuins are something we got into when we were studying aging. So we started studying aging in 1991, and we wanted to ask what genes control aging? Okay. So the system we worked with then was yeast, because yeast was simple enough that we could do what's called forward genetics and look for mutants that live longer. What we did. So we did this forward genetics, and we got a strain that lived longer, and we analyzed it. And let's bring it in. We're good. Thank you, Eric. Beautiful. And what it led to is this gene called SIR2 in yeast.
Right.
And SIR2 was known as a gene. The SIR stands for silent information regulator. And. Yeah, maybe I will take one of yours.
All right.
This one is old enough that the paper is sticking to the.
Yeah, it's not a good sign. So you want to let this melt up here, the xylitol go down. Don't just suck on it. You'll get a pretty good hit. I'm going to break it in half. Unless you're a regular nicotine user. Okay. 3 milligrams. I just use it for the mitochondrial effects and neuroprotective effects at lower doses and. Yeah, just let it sit up there.
Yeah. This reminds me of Elon Musk smoking pot with Joe Rogan.
There's Tobacco and marijuana in there.
That's all it is.
I'm coughing.
Although this is. Presumably what you gave me is legal.
It is absolutely legal. And it's. It's not smoking. It's not tobacco. And having been on the Joe Rogan show, man, you go right before the cameras roll, he's like, exhaling, and you want some. And if I'm high on your show, I'm gonna be an idiot. So I. I declined.
Great. I don't think it did Musk much good either.
I probably wasn't good for him. This is going to do good stuff for your brain, though. I think you're going to like it.
Yeah, I do already. Okay, so we got this gene, Sirtu.
Yep.
And the key experiment was if we added an extra copy of that gene to regular yeast cells, they live longer. That says this gene is a longevity gene.
Right.
Slows down aging somehow. Okay. And it turns out it does the same thing in other organisms.
So could I just do some gene therapy to add some extra sirtuin genes to myself?
Gene therapy is almost impossible in humans.
But, I mean, didn't I do it with the Follistatin gene? It cost me 25 grand. You don't think I was only good for two years?
No. I mean, it's possible.
We'll have Liz Paris, and you will do a fade here.
Yeah.
Kidding. Okay. It is hard to do and expensive. Yeah.
And there are better ways.
Okay.
To get to the same.
Well, then. All right, so I want more sirtuin activity of my cells.
So these sirtuin genes are really important, slowing down aging. You might be like this fact. Let me give you a fun fact about sirtuins. So, as I said, we have seven sirtuin proteins encoded by seven sirtuin genes.
Right.
All in the nucleus of the cell. Okay. Three out of those seven genes encode proteins that, like, all proteins, are made in the cytoplasm of cells. But three of them then go to the mitochondria and live there. So the.
You take nad. Almost half you take nad, or sirtuins increase, and you take some other stuff, too, and then half that goes into the mitochondria.
The effect will be felt in the mitochondria. Doesn't that say the mitochondria must be important in aging? Right.
Yeah, that's a good case.
Yeah. Okay. Yeah. So that's the fun fact. We can come back to that later. But that was really what first pulled me into the mitochondrial world. A lot of people thought that mitochondria with no Evidence mitochondria were important in aging, but this, this was quite startling.
Okay, so that was a really strong piece of evidence for that.
I think so. All right. I think so.
Make sure that it's just melting up here. If you suck on that thing, you're going to get a rapid dose of nicotine. You're going to get pretty happy.
Well, you know, the early philosophers and ethicists. Yeah. Thought that life should be aimed at human happiness.
I think they're right, don't you?
I do. And, and, and, you know, in the Age of Enlightenment, in the, you know, 1700s, this was the dominant view. And that's why people like Jefferson and, and so on were of, of that school. That's why the Declaration of Independence says the goal, one of the goals is pursuit of happiness. Wow.
You know, I've studied the Enlightenment because that's kind of how this quest to understand nature with science came together. And one of the features of the Enlightenment that we don't talk about very much is the rise of the coffee house. So during the Enlightenment, coffee first made its way from Africa to Europe.
Turkey. Right. That was important.
Yeah. And they, they actually tried to ban coffee houses because people were having intellectual discuss and they're becoming rabble rousers. So coffee equals freedom, which is why there's my caffeine tattoo on the arm. But it, it seems to play an important role in mitochondrial biology. Caffeine's involved, right?
Yeah, it's in the mix for things. Yeah. Good for your health.
So enlightenment equals coffee. In my mind.
Yeah. Yeah. So anyway, so, so I think these sirtuins really set the stage.
Okay.
For an important gene family that affects aging. The second finding we made in the 1990s, the very end of the 1990s, papers published right at the turn of the decade in February 2000, is that they require a compound that cells make, otherwise they're dead as a doornail. And that compound happens to be nad. And that was the link between NAD and aging. And what that says is if NAD levels decline, if they don't stay high enough, sirtuin activity will fall and you will lose this, this break, this repressor of aging, and it will go faster.
So we must keep our NAD levels at youthful levels in order to be healthy over time.
Well, at least to benefit from this class of proteins, sirtuins. Okay, okay. And also, NAD helps cells make energy, mitochondria make energy. So NAD is really important. But this finding to me said NAD is going to be very, very important in the aging process.
There's another ingredient that you use with elysium, and it's related to resveratrol. So I started using resveratrol when I was about 23 years old. This is in the mid-90s. But I switched about 1999 to Pitero Stillbean. And if you're listening to this, you're going, what? What? It's P T E R O is how that's spelled. And I always thought of it as resveratrol on steroids. So what's the difference between resveratrol and terrastilibine?
Well, you, you were prescient and got me excited about. So tarot is extremely similar to resveratrol. So resveratrol has these two phenyl rings that are connected by a short carbon chain with a double bond trans. Double bond for the chemists out there. And it has three hydroxyls. That's the all in resveratrol. Tarot is exactly the same thing, except three of those, oh, hydroxyl groups are O methyl. And that means instead of the hydrogen on the oxygen, there's a CH3, one carbon and three hydrogens on it. So it's a subtle difference, but it tends to make a big difference because it was shown in studies in cells that you could get the same effects of resveratrol on the cells, a good effect on the cells with a much lower dose. And the reason is it gets into cells better. So it's more having that carbon, the methyl group instead of a hydrogen makes it better able to get through hydrophobic surfaces. And that can be, you know, in cells or membranes and going through your gut and getting, getting absorbed into your blood.
It's like a delivery system.
Delivery system. It's more, it's what they say is it's more bioavailable. Got it. Okay. Okay. That's why we included it. And it's the second ingredient along with nicotinamide riboside, which is the NAD booster in our first product basis. And the idea was you're going to give this double whammy pill that will hit sirtuins in two different ways and that will be more effective than either one of them alone.
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I think you might have been the first in our supplement out there. I remember talking about you guys maybe in the second year of the show. It was, yeah, I've used it quite a bit. Okay. Question about delivery systems. So it seems like you can take most compounds that will accept a methyl group and that usually increases their bioavailability. Sometimes it makes them stick around longer in the liver and all that. But you can also add a phenyl group to things, which makes it really powerful. Things like phenyl gaba and whatnot. What's the resveratrol with the phenol group thing called? And has anyone tested it?
I don't know. I don't know.
I want to try it.
Yeah, the tricky thing there is a phenol is pretty big. Okay, okay. So, you know, you can do something negative, you can do something bad by really changing the molecule radically. So it's not the same molecule.
So we should give it to a yeast first. Yeah, okay, we'll do that.
Yeah. They don't complain.
And I'm sure by the end of the episode your mind will have like done all the 3D folding and that and you'll know the answer, right?
I don't think so, but.
Ah, after 40 years, come on, man.
Never know. All right, But I can't think of exactly a molecule like that in nature.
Yeah, sometimes they aren't. I don't think phenyl gaba is out there in nature, but man, you take that for sleep, it will knock you out in a way that GABA won't. So somehow it's getting past the blood brain barrier. But just.
And there are a lot of compounds where fennel will do something. There are things called chemical chaperones, and what they do is they help misfolded proteins to fold better. And a good example is a butyric acid with a fennel on it.
Okay.
Phenyl butyrate.
Oh, yeah, I'd take that stuff too. Yeah.
And. And that is. It will help misfolded proteins fold better. And misfolded proteins can be normal proteins. But if you have a mutation in a protein, this could be a heritable mutation.
Oh, wow.
Could be a heritable disease mutation. Okay. There's some evidence that a compound like that can actually help that protein to fold.
Is it ethical to give a drug like that to people?
Well, it is if it works and it passes through FDA tests. So that's a drug. So it would have to go all the rig through all the rigorous testing FDA requires and be safe. So if it's safe and you do a human trial and it works, then yes. And in fact, the compound I mentioned, phenylbutyrate, has been given in people, and it's effective in a metabolic disease.
I'm sort of asking in jest because of course it's ethical. In fact, I would say it's ethical even if the FDA doesn't approve it. It's probably ethical because their hit rate isn't so good lately. But I would like to take that and put it into just aging in general. It feels like it's ethical to give people pharmaceuticals or nutraceuticals or, you know, special lights, whatever it takes that makes us live longer. And that to not do that is unethical. But you teach an ethics course at MIT on medical ethics. What's your take on the ethics of extending human life?
So I'll give you both sides.
Yeah.
And I'll tell you right away that I'm on the side that says it is ethical. Okay.
Yeah.
And I think it is ethical because of this close connection between slowing down aging and warding off diseases. Okay. And all of medicine.
Yeah.
Or most of it is based on preventing or mitigating human diseases. Okay. And so if you have a compound that will do that, then a side effect is it makes you live longer. Oops. How can that not be ethical? So that would be my argument with you 100%.
What's the counterargument?
Counterargument is that you look at the species as a whole. Numerous ones. But one of them, one of the prominent ones, is, you know, what matters most for the sake of the species is that we continue to reproduce, because otherwise we go away. And what's important for reproduction is what happens early in life, the first half of our lives. Okay. And if you have an intervention that will make you live longer, it's kind of irrelevant for the propagation of the species. So we shouldn't waste any time on our energy or any money on that. We should be focusing on diseases that kill people, like cancer and that can kill people early in life.
That seems from that mindset, that seems unethical too, because you would want Darwinian evolution to keep our us really strong. So if you're opposed to longevity therapies, you should also be opposed to public sanitation. So we could breed only the strongest next generation. And that would make you an asshole. Or am I missing a point here?
Yeah. So Darwin would say that, you know, what's. Again, what's important is the species. Yeah. And so, you know, as long as you have reproduced, have succeeded. Wow. In terms of the speech.
So it's like an Elon kind of thing.
What comes after. Yeah, it doesn't matter so much. Okay. And yeah, that's the other argument against these kind of interventions, is it? It, it goes in the direction of eugenics.
Okay, I know eugenics.
I don't, I don't buy into that. I buy into the notion that it's a part of medicine.
Got it. If we were to take NAD supplements and give them to children, they wouldn't do very much because their levels are already high. Right.
Yeah.
When's the right time to start enhancing nad?
It's a good question. I mean, and I think I would say the right time is when it starts to decline. And, you know, I don't think we know that with precision, but somewhere in the middle of life, because by the time you're sort of middle age, you know, and you're like age 50, Nad is down. Okay.
So you should probably do it at 40 or something.
Maybe. Maybe 40, maybe even earlier.
35.
Ish.
30.
I can't. Again, we don't have precise data on that. But. And you know, if it's really. There are no bad side effects. Yeah. You know, why not? And if it's making you even a tiny bit healthier. See, what I think is the way to ask the question is when does aging begin conception? Well, I think, I think aging. You can't just say that aging is happening during development. I think, I mean, it could be, but maybe that wouldn't be a good start.
But it would be one of those very flat asymptotic curves where there's, it's, you know, 0.1% in the first five years. It doesn't matter.
Yeah. Yeah. So I think when aging, it's going to accelerate is post reproduction, post normal.
Age of reproduction, which is late teens. If we didn't have education and all the stuff we do. Right.
Yeah. Okay. Something like that. Yeah. So at that point, if aging is starting to go up, that should be the best time to intervene, really, because if you don't, then you will sustain aging during whatever period you haven't intervened.
Yeah.
And so, yeah, intervening later is still going to work, but it's not going to work as well as if, if you started earlier.
And prevention is cheaper than reversing by orders of magnitude from what I've experienced in the longevity field.
But, you know, I started late by necessity.
We didn't know.
And, you know, I'm still, I still feel lucky.
I started quite early in life because I had many of the diseases of aging before I was 30, had arthritis. I had right on the edge of diabetes. I had the Chronic fatigue, the brain fog, and just this whole host of things. Very high risk of stroke and heart attack because my blood was too thick. And just all the bad things. And so I said the stuff that's making these old people young is making me as a young person way more powerful. I got my health back thanks to the first generation of longevity researchers, even like Derek Pearson and Sandy Shaw and all the stuff they were teaching. And so I'm just profoundly grateful because I got to learn from guys who'd been studying like you had been.
Even I remember reading a few years ago, the obituary of Jack LaLanne. Yeah, Jack LaLanne.
Yeah, absolutely.
Because when I was a kid, he would always be on TV exercising, right? And he had just, he, he, he just cut a perfect figure in perfect shape. And when he was young, he was sick all the time, he was overweight, and he had a miserable life. So what he did was, you know, he, he decided that he was going to embrace extra extreme exercise.
Right.
And, and you know, I think in his 80s, he was still swimming and pulling boats.
Wow. It's funny that you bring that up. What I observed as a young man trying to figure out my own health is that there was this incredible body of knowledge from bodybuilders. There's some of the best biohackers out there. Well, what are all the variables I can do? I, I have a goal and I'm gonna manipulate everything. And then I'd go to my longevity nonprofit group and they didn't look like bodybuilders. Like some of them were on that low calorie forever like I.
Restriction.
Yeah, not, not a happy place to be. But there was almost no crosstalk. And then you talk to the neuro guys and they didn't talk to the other guys either. And, and then the meditation crowd, they were weird. That's a different conference. But there was some sort of common element. And all of those seem like they're aspects of aging. How much? If you were to weight this on your, this is your personal beliefs, but you're just a believable guy. I mean, look what you've done. So you can put, if you have a hundred dollars, right, and you got to spend it all, some goes in a meditation stress management bucket, some goes in a nutrition bucket, some goes in an exercise bucket. And we'll say some goes in, you know, supplements and pharmaceutical stuff. Where do you allocate those resources?
Well, I think it's more subtle than that even.
Okay.
I think the first is you have to identify the buckets. Okay. Which you just did now in your comparison of calorie restriction on the one hand and bodybuilders.
Right.
Okay. And you say. Okay. It's kind of similar, isn't it? Except what happens is for the people doing calorie restriction, so in animals it works great. They live longer, but they're in a very protected environment. And people who do it. Okay. They're really energy starved. Yeah.
It's not a good place.
And so they have low muscle mass and they're somewhat frail and cold. But they also don't have as good an immune system. Yeah. Which requires energy. Energy. So they're vulnerable to infectious diseases. So they're kind of, you know, doing it in a way that is exposing other weaknesses. For the way bodybuilders, they're taking anabolic steroids. Yep. Right. Which I think probably has an optimum. It's kind of a bell shaped curve.
Yes.
And I'm sure they're overshooting.
Oh, especially the older ones. Yeah.
They're optimum.
Crazy stuff.
And, and, and that's going to get them in trouble with cardiovascular disease. And so, so, you know, they're both in the right buckets, but they're shooting themselves in the foot in a way.
That'S the degree of magnitude. Okay.
Because it's, it's the, it's getting the balance just right of how much to do it with what intensity. Okay. And the calorie restriction. So that's why when we were first studying sirtuins, one of the first things we link them to is calorie restriction. Because what we found is in, in yeast, if you just lowered the glucose source, which is their food. Okay. That's what you feed them to grow. You can make them live longer. And you could also activate, you can make sure too more active. Okay. So that led us to think that if you could activate sir2, which is.
One of the seven.
Right. Which is one of the seven sirtuin. But in yeast, it's the anti aging gene. It's simpler. Okay. If you could activate it, is there a way you can activate it without lowering the glucose? And of course, that's what we did when we added an extra copy of the gene. Okay. So in people, if you could activate the sirtuins, I felt without the calorie restriction, that would be the best thing. And I think that's what you would do by boosting nad.
It makes so much sense.
You're eating normally. Okay. And again, if you eat to excess, you'll also undo a lot of good things.
Right.
That You've done otherwise. So I think the best thing would be to have the right interventions that hit on the right pathways in the cells, like sirtuins. Okay. And avoid, you know, like extreme lifestyle choices.
So maybe ultra endurance athletics and CrossFit might be too much athletic stimulation. What about carnivore versus vegan? Those are both pretty extreme.
Yeah. Again, I would say there it's. I would lean towards the vegans.
Really?
Okay. I would certainly lean away from red meat.
Why?
Because there's lots of evidence that red meat has a lot of fat and leads to cardiovascular disease.
Interesting.
And I would, I would just stay away from it and whatever else they feed the animals. That's not good for you, you're taking in. Yeah. So. So I really believe that. Now as far as other meat sources of protein or fish, I eat a lot of chicken and fish and even pork. That's lean pork. It's easy to get rid of the fat.
You're not doing the saturated fat side of things. Is. Is the red meat thing because of like the rare sugars that are in red meat the way Dr. Gundry talks about.
I. I don't know. I'm not going to say. I'll play agnostic to that. I know that the, the fat and the saturated fat in red meat is not doing you any good.
Interesting. And is that like a mitochondrial biology perspective or is it because it's escorting loop of polysaccharides across the gut membrane? Like, look, do we know a mechanism there? Because I, I ended up in a different camp on that front and I'm not one of those takedown debate guys. I'm genuinely curious about how you arrive at the conclusion.
So they. The fats have been linked to the development of plaques and your blood vessels, which are one of the culprits in cardiovascular disease. Because plaques are, you know, and can become an obstruction to blood flow.
Causal or correlational.
You find a lot of fat, in fact, the first thing you see in blood vessels as a young adult, even if you're healthy, called fatty streaks. So the fat tends to deposit in the inner linings of your blood vessels and those form a nexus for the development of a plaque with cholesterol and LDL and so on that will eventually lead to cardiovascular disease. So, you know, again, I suppose if you ate the right amount of red meat, which might be very little, but some, it would be okay. But I think that in the past it's changed somewhat in time. But when I was young, people ate a lot of red meat and people Died of heart attacks very frequently.
Don't they die more of heart attacks now than they did 20 years ago?
Well, 20, I'm thinking 50 years ago.
I don't know if I don't know the data from 50 years ago.
50 years ago. You know I remember my neighborhood and there were middle aged men just, just disappearing.
Interesting.
With heart attacks, fatal heart attacks.
I was a vegan, I was a low fat guy and I, I ended up after I saw a couple studies showing that all the plaque when they did like isotope studies was coming from gut bacteria where it was actually a fermentation derived plaque. So for the past 15 years I eat almost all saturated fat, butter, cheese, grass fed meat. And I just did a clearly scan and we're looking for diffuse plaque. I don't have any diffuse plaque in the body. I have two spots where there is small amount of plaque and the interpretation on that is it's probably from when I had Covid that there was actually like some scarring there that's in the process of healing. But everywhere else there's nothing.
I think you're blessed and which means you probably have a good gene or two.
It could be my supplements too, I.
Mean other supplements and you're blessed. But for many people, perhaps most, I think they're not going to have that outcome. They're going to have the opposite outcome.
They also do substantial amounts of olive oil, but not all olive oil. So I always encourage people get your lab tests and try something for three months, look at LP PLA2 and if there's any damage to lining of your arteries, you're going to see it and then modulate your fat intake. Knowing stearic acid is different than palmitic acid and it gets complex just like you're saying.
For everything I would say to get back to vegan. Yeah, I mean I think that for me what works is, you know what would be considered the Mediterranean diet.
Got it. Very common.
And, and I, for me I would include the, the wine.
The wine. Interesting. So that that's kind of controversial.
It is controversial right now. It wasn't controversial 10, 20 years ago.
That's true.
That, yeah. So things that change over time, right. Like you know, butter versus margarine and so on and so forth. And when there's a new finding I tend to kind of be dubious about it.
I think the answer may be radically different for different people, which is why having access to your speed of aging is so foundational. So people could say all right fine, I'll be a vegan for six Months and see what, there's how you feel, but then there's what do your markers do? And if they're breathing, keep being vegan, but check them again in a year because you might not like it. I went about a little bit more than a year and I started shattering teeth because of mineral depletion, probably from excess oxalate because my biology doesn't handle oxalate well. And people are like oxa what? So bottom line is different plants work differently for different people. Different proteins, different fats. But at the end of the day, adequate NAD levels mean your mitochondria can handle if your diet's not perfect.
Well, the important thing about NAD though is NAD goes down in everybody. Okay.
As you age. Right.
That's kind of a universal.
So it's tied to resilience. Right.
If it's high, if you're just raising, just counteracting that effect of declining nad. And NAD at adequate levels is a positive, that's kind of a no brainer, isn't it?
You want the resilience to eat the french fries even though you know they're bad for you, because some, a lot of people are going to do that. That. So if your NAD levels are high, that spells resilience inside the cells and that then spells resilience for your whole biological system. Right?
Yeah. I would say with regard to the french fry question, I also like french fries. Yeah. For some people, a lot of french fries would be no problem at all.
Because there are people who handle it.
Yeah, lucky people have good genes for that.
Although the damaged canola oil might be an issue for even those people.
Right. Okay.
Yeah.
For others, if they get the amount of fries they eat just right, they're still okay. But many people are going to overshoot for their biology and then they get in trouble. So, you know, the general recommendation would be to kind of, you know, limit your intake of things like french fries and certainly red meat.
I've on record saying I'm looking at the math. If I was forced to eat french fries or smoke a cigarette, I've never smoked a cigarette in my life. But I'd smoke the cigarette because the inflammation from that is eight hours and the french fries is 48 hours. And they're kind of similar. And I know nicotine has neuroprotective effects and would at least probably be fun after I finish coughing. So I think I'm an extreme, though.
Well, you know, I smoked at one very short period of a few months my whole life.
Let's talk about survival and when you're young, my experience has been until you're about 28, you can do whatever you want. You stay up all night, eat the pizza, drink five nights a week, and you're gonna wake up around then and.
Go, you know what?
I'm actually noticing that that's slowing me down. So there's something that happens in your late 20s that's like the very first little tingles of aging and biological limitations. Is it that we're unaware of it before we're 28 and it's happening, or is it that our, you know, our HPA got weak, our ability to make adrenaline and cortisol went down? What's going on around that time?
I would. First of all, your premise I would agree with, but not. Not totally. Okay.
Yeah, explain.
Yeah. If you look at mortality function of age, okay? So let's say we start at birth here, okay. And, you know, it's going up ever so slowly, Right. And now you're enter your teens, and there's a blip, high mortality, that then comes back down. Right. And it's in males only. It goes up, it comes down, and then it goes back to. It's, you know, accelerating slowly. And what's happening is, you know, those are the years of, you know, young men dying in car crashes and shootings and so on and so forth. So there is a blip. Okay, okay. But otherwise, I agree with you. It's slow. Okay. And what's happening, I think, is, you know, aging is happening. That's what I think. And I think you're unusually perceptive to notice it at 28.
Oh, I was. I'm really good at pattern matching because I used to have Asperger's syndrome before I rehacked my brain.
You had conditions.
I had all those old people conditions, including arthritis. I was 25.
You were in a. In what's called a poised population. Okay. You were poised to see a biological effect of aging. Yeah. Okay. In fact, aging trials, just a little side thing here, if you do a try, if you want to measure, is something likely to make you live longer. Okay. One kind of trial you can do is in what's called a poised population. So, for example, obese people. Right, Right. They're poised.
Would have been me.
You don't want to give them. You don't want the trial to look at them dying or anything, but you can look at whether what you're giving them is going to ameliorate any aspects of their obesity, for example, inflammation that they experience. And that's a really Useful trial because those things that have happened in the obese people at a young age are going to happen in normal people. Or, you know, I shouldn't say normal. I should say people unafflicted with the condition when they get older and aging is causing it.
It's interesting. One of the metrics that I'm starting to work with at Upgrade Labs, right. AI Longevity, lifestyle franchise. We're calling it Fat age tm and we're looking at the distribution and amounts of fat correlated with aging. And it. No, it's not pheno age and it's certainly not what you're doing with Elysium, but it's a very easy to get metric. That's. Huh. Like there's a curve and where do you land on the curve? And it seems important to, to manage that along with everything else.
Yeah. So I, I should say, I think the very first intervention to come out of the Sirtuins work was resveratrol. Okay. And that was studied in mice. Right. In the lab. And the decisive experiment to see that it's a good thing was mice fed a high fat diet. Right. Okay. Mice fed a high fat diet live longer given resveratrol. So again, they were poised for you to see an effect and you saw it. Now, resveratrol should have worked really well in humans, but it didn't. And the reason why it didn't, it.
Yeah.
Well, it's sort of why your intuition led you to pterostilbene in 1999. And the reason is it's not so bioavailable in people and it's hard to get the dose high enough to do anything. So it did work in some trials and some conditions, but it was too spotty and too sporadic in its effect for people to take seriously.
Okay.
So I think that's why I think you were really ahead of the curve in turning to terrastilbene at such an early date.
I would like to say it was because I was really smart. It's cause I hung out with the leaders of longevity movement every month in Palo Alto doing community education. So I just learned from basically my elders and said, yeah, these guys are smart. I'm going to do what they're telling me to do.
It's kind of the reverse of me hanging out with a tough kid.
Exactly. I feel so lucky even that I went through all that health garbage because I met amazing people and I learned so much and it's been able to be shared. You put this combination that really comes from a wealth of experience. You call it NrPT, which is the Elysium formula of these two compounds in the right ratios. Yeah. Right. What do the trials show? Like, when you run real hardcore things on that.
So the first thing I felt we needed to show is that we really could raise NAD in a sustainable way in humans. Because if you don't raise NAD with this, you give up. Right. It doesn't work. And that's a trial you can do fairly easily because you can measure NAD levels. And so we did that trial. It was published in 2017. It was totally Elysium sponsored trial. And it was amazing because in one month you could see NAD levels rise about twofold. Wow. People were, I think between 60, 70 years old and that age group already suffered the decline in it. And it came back to just. It came back exactly to where it were, being young people.
And how do they feel when they, when they double their nad?
Well, feeling things like is tricky because of something called the placebo effect. So in that trial we didn't do surveys. Okay. You know, so without a placebo control trial, if you just, you know, give a few people something and say, does it make you feel better? Yeah, A lot of them will say yes, of course. So you have to do a placebo controlled trial. And you know, we have a tremendous amount of anecdotal data from customers now and customers report a lot of things. And so you can say, well, is that real or is it not real?
Yeah.
If you hear something enough, though, patterns emerge. You think it might be real, Especially if it's something unusual. Yeah. And so, you know, early in the early days, what we heard with basis is that people were saying it cleared up their rosacea.
Interesting. Increases in mitochondrial function can cause a reduction in autoimmunity in studies.
Yeah, yeah. But keep in mind, you know, sirtuins do more than that. So three of them are in the mitochondria, but the other four aren't.
Oh, let's talk about the other ones. Besides SIRT 2, what do those do?
So they're all sirtu related. So they're all SIRT 2.
We have SIRT 1 through 7, though.
Seven, yeah. We have humans. The reason we're so complicated, one reason is a gene that's present in one. Just one copy in yeast might be present in three, five or seven copies in humans. But the seven aren't identical. They're somewhat different. A little bit different. They all have the basic activity. But for example, with a mitochondrial sirtuin versus a nuclear sirtuin, they're different because they're in a different neighborhood in the cell, and so they have to have different functions. So we have all these sirtuins in different compartments. And the mitochondrial, I'm sure, are contributing to the health of the mitochondria. The nuclear ones are doing something really important. I alluded to it earlier. They affect silencing of DNA of the genome, and that's something called epigenetics.
Right.
And epigenetics is very important in aging. It's just. It doesn't get a lot of publicity because it's. It's. I think it's partly the word just. See, people think it's impossible to understand.
Yeah.
But it's not that hard to understand.
It's very easy.
Basic way to think about it is, let's say you compare your skin cells to your blood cells. They're pretty different from each other as cells, right? Yeah. Okay. They have the same genes, they have the same genome. Exactly. The human genome, identical. So why are their cells different? And the reason is the genes that are expressed that are turned on in a skin cell versus a blood cell are different sets of genes.
Right.
And so that means there has to be ways to keep some genes turned off. So if all the genes are turned on in a cell, you've got chaos. Correct. There's no cell like that. Okay. It's not compatible with life.
Yeah.
Right. So keeping that straight, genes that are on and genes that are off in a skin cell, in a blood cell, in a brain cell. Okay. Is very important. And if you lose that fine tuning and cell, that's gonna blur things. And that's a part of aging, and that's called epigenetics. And that's what sirtuins do. They control what genes are turned on and off, along with other genes in different cell types.
Can I let you in on a little secret?
Sure.
The definition of biohacking, when I launched it was the art and science of changing the environment around you and inside of you so you have full control of your biology. It's just epigenetics. But epigenetics is bad branding. Biohacking is good branding. But it's literally change this and then change this, and you have control you didn't think of. And that's why sirtuins, the stuff you're doing with pterostilbene, with nrpt with basis. It's a part of biohacking, is you're changing the environment inside your cells, which is epigenetics.
Exactly. So that's why I think sirtuins are poised to do this because they can affect epigenetics in the nucleus.
Okay.
Which is so important in aging and in. In everything, but especially aging. And you have the mitochondrial ones, right. That can affect the mitochondria. So, and the mitochondria are extremely vulnerable places because the way they make energy, okay. You know, we breathe in oxygen and we breathe out carbon dioxide, right?
Yep.
And as a result of that, we make the chemical energy in a cell, which is called ATP. Okay, but all. But that means the oxygen is going through a series of reactions that affects their amount of electrons they have attached to them. And there's something called reactive oxygen species, or ros, that are produced along the way. And they're very bad actors. Right. Okay. And they. They destroy proteins and cells, RNA and cells. They destroy molecules. We need to live. Okay. Now this is all done in mitochondria to produce ATP. So the mitochondria didn't take the biggest hit from the Ross, because that's where they're produced. Okay. And that's why they're very vulnerable.
And they also don't repair themselves genetically the way your nuclear cells do.
That's right. So one of the ways they do repair damage is through an enzyme called superoxide dismutase, which just reverses some of that damage. Okay. And one thing that controls the activity of superoxide dismutase is one of the Sirtuins, Sirt3.
Really? And when I take NRPT, does that help my Sirt3 levels?
Yeah, it will help your Sirt3 because of the NAD. And we have another product, but basis is really for all the cells in your body.
Okay.
And, you know, I think it's a really good product. But just to fine tune on mitochondria, a second product is called Signal. It's a newer product.
Okay. What's in it?
So Signal also has an NAD booster. Okay. Okay. This one's nmn, which is very similar to nr.
Right.
Okay. But we wanted to incorporate NMN into our portfolio because it's very similar to nr, but not identical.
I've recommended those both since the first set in nmn.
So with you there's.
I haven't tried Signal. No, because you guys didn't send me any. But I did buy a kilo of NMN from China when the first study came out.
But the important thing about Signal is that it has second components. What is it? So basis has a second component, which is tarot, still being, and it's called hinokiol.
Oh, I like this. I wrote about HINOKI in Superhuman, my aging book. This is really a powerful substance and most people never heard of it.
Yeah. Dug deep to find this, but there's.
You're gonna send me some of this.
Yeah. And there's a good literature that says that one of the things enochial does is it activates SIRT 3, which is exactly what you want to help mitochondria fight against oxidative damage due to ros. So that product was developed specifically to help cells via helping repair mitochondrial damage.
Fascinating. I'm going to predict something when people are taking. Taking signal, the new formula, if you can manipulate your sod levels. Gray hair, one of the three causes of it is from an excess of free radicals, and SOD is what quenches them. So do people see less graying or even a restoration of hair color when they're doing signal?
I don't know.
I would predict that based on pathways.
Yeah. We could find out. When you make predictions like that in biology, it's always tricky. Biology is always more complicated than what you know. But we can look into that.
It makes sense.
What I would say is that certainly tissues that really need a lot of energy, like muscle, brain.
Right.
Okay. It would really behoove them to have mitochondria that are robust and clearing up damage as it occurs. Okay. Okay.
Fast.
And.
Okay. So that signal. And there's something else that it's almost boring at this point. It's methylation. And my very first book was on fertility. And I'm recommending a folinic acid, which is a methyl donor that doesn't overshoot. And there's all kinds of technical stuff. In later years. You've seen Gary Brca talk a lot about MTHFR and homocysteine. And I just tell people, look, there's a lot of stuff you can measure, but if you can get your C reactive protein, which is. I have an infection somewhere. And you get your homocysteine, which I have a problem epigenetically with my B vitamins. And you can get some marker of vascular inflammation. I like lp PLA too. Do those things and you've probably got the big guns for inflammation, which is a sign of mitochondrial things.
Yeah.
So what do you do with homocysteine and aging?
Yeah, homocysteine is a big. A big player. And it's not well appreciated. I think out there it needs to be. It really needs to be. So homocysteine is produced in our cells as a byproduct of metabolism and specifically methionine biology. Methionine can get degraded to produce homocysteine. And so the B vitamins are useful because they can both slow production. One B vitamin can slow the production of homocysteine from methionine, and two others can promote the degradation of homocysteine. So in both cases, you're diminishing homocysteine in one case because you're making less, and the other case because you're degrading it faster when it does get made. So we got into this homocysteine from a study that was done at Oxford University about 12 years ago. Oh, wow. It was a human study on aging adults. And the hypothesis of the professor at Oxford who was doing the study was that homocysteine was a bad actor, and if you lowered it, you would have beneficial effects on the brain.
So it's not just a signal that you have a problem, it's actually a cause of the problem.
Oh, it's a culprit. Beautiful.
Okay, that's interesting.
It's a cpr. So they spent time showing that a particular concoction of three B vitamins at the appropriate concentration, and it's much higher than you would get in a normal multivitamin.
Methylated B vitamins or just regular B vitamins?
Regular B vitamins. Okay. Folic acid is one. Okay. I think paradoxal is another one.
And paradoxine, you mean B6. Aparoxal. Okay, yeah. Okay, got it.
B6 and B12. Okay. Is the other one. No, B3. B6 and B12. So B3 is just niacin.
Yeah.
And so what they showed is that first of all, it definitely. So, you know, people have different amounts of homocysteine, and if it gets above a certain level, it's very bad.
What's the bad level?
Yeah, it's the measurement. They measure it in total homocysteine in the blood. And I think once you're at something like 10, I think it's migs per deciliter.
Yeah, I forget the units in the.
U.S. but I think. I think it's migs per deciliter. About 20%, 10 to 20% of Americans have dangerous levels, and about 30% of people in China have dangerous levels, and that leads to cognitive impairment. So what they did in the study that I was about to tell you. Yeah, it's interesting is the lean on the study is they measured brain volume in these people over a two year period. So it was a two year trial. And the control. And it was placebo. Controlled the placebo group. Placebo. The intervention Group got the three B vitamins at the appropriate dose and that what they were doing is imaging. This became possible only recently because imaging got so good that they could measure precisely the volume of the brain. So with normal aging, the brain shrinks and that's bad. And they measured the rate of shrinkage. And in some of the people it was much faster than in others. And it turns out that it was the group that it was faster in is the people who started with high homocysteine. Okay. So what happened in the trial is people who took the B vitamins who had the higher homocysteine, okay. Which was about, I think almost 50% of the people showed a massive reduction in the shrinkage of the brain and their cognitive function was preserved. So homocysteine is affecting other things besides the brain.
I'm sure, I'm sure, like systemically.
But this was easy to measure because you could measure brain volume. With the great imaging that we can now do with mri, something like a.
Third of people have genetics where they just aren't going to be able to process folic acid. Right. So maybe those people in the study didn't have MTHFR genes, they just had homocysteine.
I don't know. Okay. Folic acid alone is going to have some benefit, right? But it's the really the three vitamins that are going to have three in combination, much more potent agent. And so we developed a product based.
On that, interesting, for the brain called Matter Matter.
Okay. It's so simple.
It's just got a ratio of those.
Three of those three B vitamins and that will clear up homocysteine problems.
I've been managing my homocysteine for a long time because my longevity practice and I keep it around 7 or 8. It is a good number. And if it's too low, it's apparently not very good either. Like you don't feel good when it's really low. So over suppressed homocysteine probably isn't good. I don't know that anyone's done the science on the right amount. And we know that over 10 is bad. And just maybe six months ago I ran one of the Axo panels. Axo is the lab testing part of upgrade labs. And my homocysteine was like 16.8. I'm like, that is not good. What just happened? This is abnormal. So I looked and I'd run out of one of the cell phones that I take, so oops, shame on me. So I started taking it and it's back down right to where it should be. What was it, the supplement? It was trimethylglycine, which is a big. It has three methyl groups that you can do. And I also added in vitamin B12.
By the way, works on single carbon metabolism. That's what it does. So you might have been benefiting by that mechanism.
Oh, it could have been. I also added folinic back in which I've taken. And what I found was if I took methyl folate, which a lot of people like to do, that causes muscle cramping throughout the body. Over methylating is a really nasty sensation. Like you want to really mess with someone, give them like 10 methyl folates and they'll like be the horrible, horrible earlier.
A lot of these things that have an option. So the dose matters.
Yeah.
And you can't do things willy nilly. And that's a question I have. You know, and I'm not saying putting you in this group you can.
Yeah.
But the biohackers do is they get a little bit of information about something and then they apply it in the wrong way.
Yeah.
And it's a problem and the consequences may not be good. So it's really important to take the information but be able to process it in the right way. So you get a product and a dose that's going to work, but then you have to test it. You can't assume it's going to work.
You have to test it. The other mistake a lot of humans will make this, including biohackers, is we have about 25 different ways of making a decision in our brain and they're based on energy metabolism. Like a really good decision. I spent all day pondering, I did notes, I did research. Took a lot of energy. And so you wouldn't do that to decide if you're going to have eggs or not have eggs for breakfast. Right. So you make a snap decision. But every decision, whether it was a good one or not, they feel correct. Because we're humans and it's just an energy saving. Yeah, well there's placebo and there's also just. The basic algorithm is if something is good, more is better. If something is bad, don't have any like homocysteine.
Okay.
High homocysteine bad. Make it zero. Not good either. So what a lot of biohackers, especially when they start, well, if this is good, I'm only gonna do that. And most curves are U shaped or J shaped. Like they're not what you think they are. It's not just a linear thing.
Almost always case yeah, that's the case.
And so the only answer is decide.
What goal you want to test it. It has to be tested. And. And you have to know the right dose.
If you had unlimited resources to run one longevity trial, what would it be?
I think the trials that I'm in, so I really believe in nad. And so then the question boils down to, well, NAD for what? Okay, so for longevity. Okay. But we're getting indications that NAD may have a lot of other benefits and other pathways, ones we haven't discovered yet. Yeah. Or ones we have hints about. But it requires a really proper, rigorous human trial that might cost, you know, in the millions of dollars.
What's one of those things that you have a hint about a hypothesis you would make and want to test about nad?
So, you know, we have a pilot study, not published yet.
Elysium is doing this. Okay.
On menopause.
Oh, this is a big thing. And there's mitochondria tied in with menopause. Right. Tell me more.
It shows that, you know, basis on a small number of people seems to reduce the symptoms of menopause.
Wow. So you just had a lot of guys buy this.
Flashes, for example. So what do you do in that case? And the limits of the trial are it's not a standard placebo controlled trial. It's what's called an open label trial in which you give people the pill, they take it, and they report what happens. Now, that's a trial, as a scientist, I don't find as rigorous as a placebo controlled trial.
It's still data, though.
It's data, but the people don't know. In a placebo controlled trial, they don't know what they're getting. And so if you see a difference between the placebo group and experimental group, that really cannot be due to the placebo effect because they don't know what they're getting.
So don't we know the placebo effect is like 32% or something like that?
Significant. Right.
So if you have an Open label and 90% of people are getting results which is way in excess of what you expect from placebo, that's pretty good, useful data.
Or no, it's okay. It's not. But still, you want to do the gold standard trial all once and you want a number of people that is going to pass statistical muster. Okay. So I would want to do the trial with a large number of people. Okay, okay. And have it be, you know, blinded. No one knows what they're getting. People doing the trial, you know, they, they who are administering the drugs don't know what the. Whether it's a placebo or the drug. It's blinded all around and the data is locked. So the data no one has access to can see the data while the trial is going on. And at the end of the trial, the data is then unlocked and the statisticians analyze it to see if is there a difference between a placebo group and experimental group trial done. So data cannot be altered at that point. And that's how drugs hit the marketplace in big pharma. And I would like to see it done here because that would be a significant improvement in people's lives. Wow.
I. It really would. Menopause people, people don't talk about, especially perimenopause, the economic impact of it. I mean, there's the suffering for the women going through it and also, like, their whole families around them. Like, it's a really meaningful stressor. A study from the UK said that every year it was costing something like 10 billion pounds of lost productivity, even, not even accounting for suffering. So if you can make a dent in menopause with this trial, that's.
That's a big game changer.
W. Yeah, it's impressive.
So that's one thing. And, you know, there are other things like that, that some things we are moving down the road, like als. And trials from a pilot study.
Wow.
Showed promising data to a bigger trial where you'd be able to see, you know, is this thing really likely to work? And ALS is something where there have been just so many trials that failed that anything that. That produces, you know, would be extremely helpful.
I tend to look at ALS, MS, Parkinson's, even some weird sleep disorder things they can be around failure of mitochondria in certain parts of the brain.
And mitochondria really in play for the brain. Yeah, for sure.
So something that helps one of those quite often helps others if it's via a mitochondrial pathway, but if it's via some other pathway, then it's not going to do it. So I would almost want to see a trial where you're like, let's try it on all these. These neurodegenerative diseases.
Yeah.
Because it's going to help most people.
Right now that's being tried on als, as I mentioned, but also Parkinson's. Beautiful.
Yeah.
And because those dopamine. There's a published paper on Parkinson's from a group in Norway.
Oh, interesting. Yeah, that's because that part of the brain where the dopamine neurons are densest is one of the most mitochondrially demanding parts of the brain. So it's like a little bit of a power fluctuation there. It could be contributing to it.
It's called a phase one trial, which means the initial trial, smallish people. But the data looks really promising, so we'll see.
Okay. All right. You're a scientist, I'm a scientist. How much of aging is just in our head, the psychological aspects of it?
Some of it. So this is something I always like to say. So my mom, when she got older and got more isolated, and she used to say to me, loneliness is a killer. This is maybe 30 years ago. Loneliness is a killer. And I said, probably. Now there's real data that says that loneliness really does, you know, make end of life sooner.
Wow.
So there are things that are, you know, part of it is structural, the way our society is that older people get isolated. But you know, for older people, or, you know, not even people old old, but people getting older to the extent you can stay engaged and that can be family, you know, try to extend an olive branch to relatives, grudges, volunteer work, community groups, anything that keeps you engaged with people or is likely to be of benefit. So I. And I think that's. And that's, you know, I guess psychological. Although it's going to impact physiological pathways, it certainly does.
In fact, Dr. Murthy, former surgeon General, before he became Surgeon General, was on the show. The only book he ever wrote was about the epidemic of disconnection. Yes, he should have. Just for Brandon, he should call it the pandemic of disconnection. They would have given him $10 billion to fix it.
But, you know, branding, if you're young, that's going to make you more prone for drug abuse. Yeah. And if you're old, it's going to push you off the cliff.
Very, very well said. Well, Lenny, 40 years of research in this at one time little known and just rapidly becoming cool field of mitochondrial research. Thanks for this curiosity, the 250 papers and for making supplements with really good science. And I always ask people come on the show, you got to help out listeners here. And you guys came through Elysiumhealth.com code upgrade 25 to save 25 off your first month. And if you listen to the show, order the test to see what your age is and get the supplements because you're getting 25 off. Right. Thanks for making the trip to Austin and I appreciate your patience with my lack of air conditioning in Texas in summer. But, hey, that's how it is.
That's how it is. You know, they say a little bit of stress.
Ah, there you go.
You know, if it doesn't kill you.
This is the sauna episode with hormetic stressors. There we go. And guys, it's upgrade25elysiumhealth.com this is longevity 101 stuff. You want to do it? See you next time on the Human Upgrade Podcast.
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