Peter Attia, longevity physician and endurance athlete, recounts his 2004 Catalina Channel swim—7 hours, 90 strokes/minute—while debunking myths about fasting’s lifespan benefits, noting human metabolic adaptations differ from mice. He explores rapamycin’s potential (2–6 mg every 5–7 days) for improving heart function and immunity but warns of side effects like mouth sores. Elite athletes face longevity paradoxes, such as atrial fibrillation risk 10x higher than non-athletes, yet Attia’s "medicine 3.0" approach blends centenarian data, animal studies, and molecular insights to refine interventions. His Iowa farm, designed for hunting large deer with food plots, mirrors his obsession with precision—whether in archery, cycling, or health optimization—where technique trumps brute force, proving longevity isn’t just about genetics but disciplined, incremental mastery. [Automatically generated summary]
So I got into, I decided in, this is going to sound silly.
I read a book in January of 2004 about this woman named Penny Dean, who still to this day holds the record for the fastest crossing of the Catalina Channel.
So swimming from Catalina Island to San Pedro to not, you typically swim to Point Vicente.
And she had done it in like seven hours and 20 minutes.
Penny Dean had a stroke rate of 90 strokes per minute, which, I mean, that might not mean anything to someone who doesn't swim, but like to turn, to have a hand hit the water every, you know, third of a two-thirds of a second is a remarkable thing.
Yeah, I can't hold a cadence of that for 100 yards.
I mean, those of us that I'm not a member of this community anymore, but when I was, it was one of our favorite topics of discussion.
I think opportunities or ideas that were put forth were higher pain tolerance, something about being, you know, evolving to be able to give birth, just means they can tolerate pain a lot higher.
I think another thing I've heard is buoyancy.
You know, women are naturally going to have more body fat, which provides insulation.
When you do these swims, you're not allowed any wetsuits or aids of any sort.
No shorts.
You're in a speedo and a single latex cap, and that's it.
And so if you can have a little, and so I think women's hips, because they're going to have more fat on their hips, it corrects one of the big buoyancy issues that we have in swimming.
We didn't evolve to swim.
We're horrible at it naturally because we swim like this.
We drag our hips through the water.
And if you think about the importance of aerodynamics in most of the things that we think about, whether it be archery or race car driving or cycling, in water, it's that much more important because the density of water is thousands of times greater than air.
I just have been fascinated forever with people that are capable of pushing their brain to do things that other people just don't think are possible, like a Bigfoot 200 race or any of those things.
But the swim one is particularly crazy because you can't stop.
I read this book and I was like, I really want to do this.
At the time, I was actually in my residency in Baltimore.
And I was like, you know, I really want to do this.
And I'm going to have to learn how to swim to do it.
So I started taking swimming lessons.
And then, I mean, to make a very long story short, basically by about the summer of 2005, I entered my first swim race, which was a two-mile swim race in Lake Reston, Virginia.
And I did it.
And I was like, oh, my God, I just swam two miles in the open water.
You know, it was hard, but I was like, okay, that's the proof of concept.
Now you just got to figure out how to make it 20, 25 miles.
And so I just, you know, went completely psycho and ratcheted up the training.
And then in October of 2005, I did my first Catalina swim.
That's got to be a pretty good feeling, though, when you're done, that you are capable of pushing yourself to what most people think is an impossible distance.
I mean, I've never experienced that, but I was explaining the other day to a friend of mine about this camping trip that we went on in Montana when it was like nine degrees outside.
It was freezing cold.
We stayed out there for five, six days.
And then when we finally got to a hotel room, I took a shower and it was the most amazing shower I've ever experienced in my life.
The Maui Channel is a 10-mile channel, so round trip is 20.
The bigger question is time in the water because you rarely get to swim these in a straight line.
So the Maui Lanai one, I wanted to go Maui, Lanai, Molokai, Maui to do the triangle.
And that would have been 30 miles as a crow flies.
But we just, you know, boat captain wasn't willing to do it at night because of the tiger sharks.
And during the daytime, we couldn't physiologically figure out how one could suffer against the wind because the wind gets so brutal in the middle of the day.
So even the one that I did, which was just the there and back, I ended up swimming for 12 hours because the first way crossing where there was no wind took me four hours.
And then it took eight hours to get back because I was swimming like the hypotenuse of a triangle, right?
Like the current's going this way.
So I had to swim this way just to go in a straight line.
I mean, it was certainly, it was an amazing season of my life, but I think once my daughter was born, which was 10 years ago this summer, that's when I only probably did two of these after she was born because then the training just got so I just you got to live in the water if you want to do this sport like you got to including the winter you know like you know even in San Diego where I live it's still you know 55 degrees in the water and
You're going to spend three, four hours a day in the water freezing.
You know, it's just so I was like, you know, I just don't have the drive to spend 25 hours a week swimming.
And this is actually just before I swam the Maui thing.
Now that I think about it, that was 10 years ago.
I swam the Maui thing in June of 06, June of 08.
So I'm doing all my training in a swimming pool up in San Francisco because I don't want to acclimate to very cold water.
I actually want to be in warm water.
But I needed one long ocean swim of like 14 or 15 miles as my like last training swim.
So I came down to San Diego to do it.
And just by bad luck, I came down a few days after that guy was killed.
Now, this was a guy.
I didn't know him, but he was a triathlete training with a triathlon group that they would go out and swim every morning.
And I know the beach exactly where it happened in Solana Beach.
And unfortunately, like most people who get attacked by great whites, they have a very – they always attack the same way, which is below and behind, stealth bite, up and – and then they retreat.
So they're trying to basically injure the prey so their prey exsanguinates and then they take off and then they wait until you bleed out.
So they never saw the shark, but you could tell from the bite marks it was.
I actually had a friend who was on the beach and saw him when he came out.
And he was basically dead when he got to shore.
He had bled to death.
The problem is – so in this case, the shark had bit him and cut through his femoral arteries and veins.
And the salt water prevents you from having any hemostasis.
So it exacerbates the blood loss.
So that's generally how folks perish when they're bit by great whites.
How did they get him out of the water?
A bunch of other swimmers came to his rescue.
And luckily, that commotion prevents the sharks from wanting to come back.
So three days later, I go out and I'm swimming at that beach because I swam from – my training swim was La Jolla up to Solana Beach and back.
And I got to tell you, like three days after a guy dies where you're swimming, it is – it was about one of the most mentally challenging training swims to be like.
Because you can't see.
Like the water at that part of the beach is so murky.
You know, and you're only a couple hundred yards offshore that – like you can barely see your hands when you're swimming.
You know, when it's all said and done, all of the close encounters I've had, probably the scariest moment I've ever had in the water was doing a swim from Santa Rosa to Santa Barbara.
So Santa Rosa Island, which is the second furthest north channel island.
You've got San Miguel, Santa Rosa, Santa Cruz, and Anacapa represent the top four channel islands.
So we did this November swim.
It was a nighttime thing again, swimming from Santa Rosa Island to Santa Barbara.
And at about five in the morning, maybe six in the morning, you're just starting to get enough light where you can see and you're out there.
So you really have amazing visibility.
And I look down probably 40 feet and I see this enormous thing swimming like this, which is how sharks swim.
And I see the dorsal fin and the position that freaks me out and the tails this way.
And I like, you know, like lift up out of the water, kind of hyperventilate for a second.
And I'm thinking to myself, all right, you got to make a judgment call here.
If that's really a great white, you probably ought to get out of the water.
But if you, the moment you're out of the water, that's it.
The swim is over.
Like you just spent like months doing this.
Like it's done.
So then I convinced myself and I think I'm right.
I think it was a dolphin on its side because a dolphin on its side would, its fin would, its tail fin would be the same way and it could swim that way.
I became obsessed with this thing called the, uh, oh, what was it called?
Christ.
You, you, you'd put the thing on your ankle.
Like you had like a little Velcro thing.
You'd wrap it on your ankle and had a tail, like this long, you know, like four foot long thing.
And it was charged and it sends out an electrical impulse that, um, disturbs the shit out of the sharks.
The shark's nose is an organ that senses electricity.
So when a shark, like it could be pitch black, it could be soot water and they can still scope you, you know, from hundreds of yards away based on the electrical activity of your heart.
And that organ is their nose.
So this little thing, I forget what it was called, like the shark taser or some shit.
It puts out a signal that like tases them and they don't want to get within like.
Off of Catalina, I know it's one of the best shark fishing places in the world.
I have a friend of mine who told me that if you think about like wild places on earth that are just overrun with predators and terrifying like predator prey activity, Catalina Island is one of the top spots in the world.
I was like, what are you talking about?
He's like, I'm telling you, man, the shark fishing off Catalina Island is fucking insane.
And then I watched a television show, just, you know, synchronicity a couple days later.
And it was these guys shark fishing off of Catalina.
So biologists look at it in terms of the entire ecosystem, right?
They look at it in terms of the plants, the amount of waste, fecal waste that these animals are leaving behind, the fact that they're literally eating everything that they can on this island.
They're not supposed to be there.
And then they're competing with whatever things are native to that island.
And probably, I mean, if you've got a thousand-pound elk, it's not supposed to be on a fucking island.
And this thing is just eating everything it can.
And they don't have a winter either.
So it's just like the whole, like, they're just not supposed to be there.
I think Boulder is right up there, but there's less people.
And everyone's real healthy and active and hiking and stuff like that.
They don't allow hunting for mountain goats on the weekends because there's so many people hiking and going, they don't want people killing these mountain goats in front of them because people freak out.
Even though they have decided that they have to control the population and kill a certain number of them to keep the.
But so many people go out there that these things aren't scared of people.
So it's created this really weird situation where if you are hunting them, you're almost hunting something that's domesticated.
People feed them Cheetos.
So much so that a friend of mine was talking about it that he was up there with his daughter.
His daughter opened up a bag of Cheetos and the goat walked right to a wild goat, lives out in the fucking woods, walked right up to his daughter and they were laughing.
She opened up the bag of Cheetos and put it, and he stuffed his head in the bag of Cheetos.
He knew what to do.
And this guy who was talking about this is a hunter.
And he's like, this fucking goat has like Cheeto dust all over its face.
Like it's the craziest thing.
Its face is all red with Cheeto dust and it's sitting there chewing these cheetos.
I think, I mean, I was talking to a friend of mine about this the other day, actually, and he was saying that there's probably only, like, in our neighborhood, there's probably only like two mountain lions left.
And the coyotes just, they've exploded.
There's so many of them around.
And it doesn't really bother me that much.
I mean, I actually kind of like listening to them howl.
But, you know, if they get into your chicken coop.
Yeah, I had one kill chickens just a few weeks ago.
Yeah, yeah.
I have got video of a dead chicken.
It was such a bummer, man.
We chased it away.
It was on the roof of the chicken coop.
The way they jump is so stunning.
Like, they're so graceful.
Like, I've never seen anything that moves like that in the wild the way a coyote does.
There's a six-foot fence.
It's on the ground.
It jumps to the top of the six-foot fence almost like it's under different gravity rules than us and touches the top of the fence and then boom, it's on the top of the chicken coop.
And the reason why they extended their range is because we went after them.
We hunted them down.
You know, they were able to eradicate wolves.
And the way they were able to eradicate wolves is they would kill the alpha.
And then they would take an animal like a horse, they would shoot it, and then they would fill it up with strychnine.
And so then they would rub the alpha, the body of the alpha, all over this carcass of the horse.
And then the other wolves would come and smell that the alpha had been there, and then they would eat the wolf or eat the horse rather and die.
And so they were able to do this and essentially use this method plus shooting them and things like that to eradicate them from the West because of ranchers and cattle farmers.
They've never been able to do that with coyotes.
When you shoot a coyote, if they do roll call, like when you hear them howling, if one of them is missing, it sends the females, it sends some sort of a signal where their bodies produce more pups.
So if one's missing, instead of having like three pups, you'll have six.
So you make more coyotes when you kill them, and they extend their range.
When you persecute them, they just extend their range.
They're a fucking crazy animal.
They are wicked smart, man.
They've been chewing at the roof of my chicken coop, trying to get in.
I came outside the other night.
My dog, I have three dogs, but one of them is a golden retriever.
He's just, well, he's only a year old, too, but he's just curious.
It's very weird living in proximity with all these things because where I live, we have a lot of hawks, a lot of owls, a lot of coyotes, and occasionally a mountain lion.
And I've seen, I saw a bobcat once, which is pretty interesting.
I'm like, that's one of the best podcasts I've ever heard in my life.
And I made a post about it.
Jocko responded to the post.
And then I got Jocko on.
And then I and Tim convinced Jocko to do his own podcast.
And now it's huge.
I mean, his podcast, I get text messages all the time from people thanking me for telling them to listen to it.
And then I get tweets from people thanking me for talking Jocko into doing it because it's just, there's outliers in this world, you know, in everything.
There's outliers in athletics.
But when it comes to discipline and motivation and just when you look at someone who's just undeniable, like Jocko's one of those guys.
Yeah, I'll tell you, I'll tell you a funny Jocko story.
I don't think I, I guess I can tell this story in public.
It's pretty funny.
So Jocko is in New York just after his book came out.
And, you know, and I was like, look, I want to introduce you to some of my buddies who run hedge funds here because a lot of what Jocko does is they, you know, he and his partner, like, they consult with guys like this doing leadership stuff.
And so we went up to the offices of one of my friends who has this very famous hedge fund.
And his office is like on the 50th floor on park.
And it's looking, it's like a beautiful view down park.
And we're just sitting there in his office just shooting this shit.
And I forget how it came up, but somehow we were just talking about like, how good is a sniper?
Like, what does it actually take?
And then, of course, we're talking very specifically about, I can't believe I'm blanking on his name.
But in fact, I think Jocko said, he goes, you know, yeah, Chris was a part of my team for more of his kills than any of his other kills.
And so then we were like, like, what sets him apart?
I mean, obviously, any Navy SEAL sniper has got to be amazing.
But Chris took it to another level.
What was it?
And he said, okay, let me show you what it was.
So he said, so he walked us over to the window and he goes, okay, you see that guy in that hat over there, like about a mile down the, you know, you could basically see it because it was like a pink hat or something.
I said, yeah.
He goes, okay.
If you're a sniper, you got to be able to lay down, not move, and put your eye up against this thing and like look out at him.
And you can't, if you ever take your eye off that, you're going to lose the sight.
So you've got to be able to stay in that position and not move and do it.
He goes, and I forget what the number was, but Jocko said, the average Navy SEAL sniper can stay in that position without moving, eye glued to the sight for X number of minutes.
And I forget what the number was.
Maybe it was like 15 minutes.
He's like, Chris could do that for two hours.
He could lay in that position, not moving and not taking his eye off that thing with one eye shut for hours.
And he just had a different gear.
And it was just an amazing, I mean, those are some of my favorite moments with Jocko is when he can tell you something that is like, there are like maybe three people in the world that would understand why that matters.
You're either on a bench or you're prone or whatever it is.
You're lying down most of the time.
This is all it is.
It's this with your finger.
Pull, pull, pull, pull, pull, boom.
Some people are way better at that.
Just think of that.
Coordinating your vision, getting the reticle set on the target, pulling that and without movement.
The outliers are the people who can do that.
And you got to think, like, when you break down physical movements, right?
Like you watch a gymnastics routine of the Olympics, like, holy shit, and it flips and land and they stick.
And it's incredible.
But now break it down to just the movement of your trigger finger.
Pull, pull, pull, pull, pull, bang.
No movement.
You know, I mean, it's, I'm sure you've shot guns, but it's hard to, like, if you shoot pistols and you have dummy rounds, you know, like a lot of people, they mix in dummy rounds so that they find out they're jerking the trigger.
And when you see, like, I was watching a video with Tim Kennedy, and Tim Kennedy was shooting at the range, and he's pulling, bang, bang, bang.
And it goes click, and he goes, woo, look at that trigger control.
Like, because it was, he, the way he pulled it, it didn't go off target.
It didn't move.
It was, there was no punch to it.
You know, but you, you got to fucking practice forever just to be able to do that, just to not anticipate the recoil of the gun and yank and move and twitch and just controlling the mind.
I mean, it's a fascinating thing to me that just pulling this one finger.
You would think fucking anybody could do that.
I could show you how to do that.
You know, like, like I've had friends that say they want to go hunting.
You know, I want to go hunting.
You know, what do I do?
Where do I get a bow?
I'm like, slow down.
Let's get your rifle because I could teach you how to shoot a rifle.
We could get someone, we could sight in your rifle, we'll go to the range, we'll sight it in at 100 yards, get you a good, accurate rifle, and then all you have to do is kind of keep it together.
A rifle, we get into 100 yards of a wild pig, you're going to be able to kill this thing 100%.
You got years before you're going to be able to shoot that thing with a bow.
And the bow is like, my wife said this to me a while ago.
She said, of all the things you do, she's like, archery seems to be the only one where even if you don't have a good day, you're still happy.
Like, if I'm on the racetrack and I'm driving a race car or if I'm, you know, swimming or whatever, and I just have a bad day, like, I don't, I'm just not firing on all cylinders.
Like, it, you know, it just kind of pisses me off.
There's something about archery where even if I'm not having a good day, like, maybe it's an extension of what you're talking about with the trigger finger.
So for me, I got into archery because of Tim.
And the story that the thing that he told me, which obviously for anyone who told me that immediately made me be like, I want to do this, was just anything that requires that much perfection just seems great.
And he was like, yeah, you don't take a shot unless you can kill the animal.
Like, you know, and so like you might take one shot in two days.
Like it's got to be a kill shot and the kill shot's got to look like X, Y, and Z. And I was like, oh, that's like, you've got to be dialed in.
So it was this idea of back tension.
You know, it was sort of like, wow, if you're taking a perfect shot, like it's all in the rhomboids.
You know, it's all back here.
And you've got to be able to do, as you said, you've got to completely be able to eliminate any anticipation, any of this business.
And so I think that I think of archery for me as almost like a meditation.
Like I'm talking in the way like Sam Harris would talk about sort of consciousness and the way you are so hyper-aware of what you're doing that yes, you can daydream and your mind can wander, but if you actually start to imagine the sensations of every part of archery, in many ways it feels like meditating.
So I think that's why I'm just like, you know, and I never really thought about it with shooting a rifle because I don't have much experience with guns, but I'm guessing it's very similar.
But as you said, like the difference between the good and the great in that is less obvious, you know, at a distance.
Yeah, I think offhand, shooting a rifle and shooting a bow, I bet I'm just as accurate at 60 yards as the average person is, not a sniper, but the average person with a rifle.
You can be pretty fucking accurate.
You can't off a bench.
So there's some similarities.
There's a similarity to having the, you have to have perfect technique, you have to have the right stance, you have to make sure that everything's locked in and your structure is correct.
But I agree with you that I think it's some sort of a meditation.
I also think there's something to hitting a target that is in our DNA that's connected to hunting, that's connected to survival, that's connected to the thousands of years that people threw arrows and fucking, what is that thing called?
So that whole experience of like the perfect release, you know, even when you surprise yourself, like I've been, I switched over to this Carter Evolution release about back tension release.
It's the most pure back tension.
It's better than the honey because the honey, you could still cheat a little bit.
You know, if you were getting lazy, you could twist.
That's in fact what got me into it because about two years ago, he was getting ready to go to a trip, do a five-day trip in Colorado, and he called me and said, hey, I want to talk with you about some training and some nutrition to get ready for this because it's going to be kind of an extreme whole deal.
You're at altitude, you're running around like crazy.
You've got to be able to sprint and then be totally relaxed.
And so he's like, can you help me think about how to train and what the nutrition would be?
And I said, okay, tell me more about what the demands are.
And the more he told me, the more I was like, why am I not doing this?
It was a huge bird, and I can't even remember what it was.
Yeah.
Yeah.
It was like a bird on the ground, like some huge ass bird.
But it wasn't a turkey.
It was like, I don't remember what it was.
But the shot, he was like, you know, it was one of those things where it was like, because, you know, like all my practice is on stationary targets, right?
So it's a totally new dimension when it's like the thing's doing this.
Yeah, I was reading something about the goose problem about how the goose population has exploded because of farmlands and that they literally don't know what to do with the certain population of different kinds of geese that are flying into this country from Canada.
So when I'm in, I split my time between New York and California.
When I'm in New York, it's absolutely one meal a day, no ifs, ands, or buts, because it's just the schedule is such that I'm seeing patients in the morning and afternoon, and I don't want to do, I don't want to waste time to eat.
So what are you doctoring?
That's a good question.
I mean, I trained as a surgeon and did cancer surgery, but my practice is based on longevity.
So it's sort of how do you apply nutrition, exercise, sleep, stress management, endocrinology, lipidology, supplements, hormones, all that stuff.
Like, how do you engineer how to make somebody live longer is my clinical interest.
So, yeah, so in New York, I eat one meal a day.
So it's basically like a 22-hour fasting window, and then I'm feeding within a two-hour window.
Well, I mean, if we're going to get really technical, we have to be clear that I think a lot of the benefits are overstated.
And a lot of the benefits are things that we've only studied in animals.
So there's a guy named Sachin Panda at the Salk Institute in San Diego who's, I think, one of the world's experts on time-restricted feeding.
But, you know, for example, a 16-hour fast in a mouse produces unbelievable results.
If you take a group of, you know, certain types of mice or strains of rats or other rodents and you, in a 24-hour period, deprive them of any nutrient for 16 hours, but then for eight hours let them eat whatever the hell they want, they can't gain weight.
So the reason we think is that once you give a long enough period of time when the animal can ramp up its enzymes in the liver that are responsible for fat oxidation, I mean, they just basically become fat-burned.
I hate that term fat-burning machine.
It's so overused.
But they basically just become unbelievably efficient at metabolizing fat.
So we have to be careful, though, when we extrapolate that, because you and I have a very different metabolism than a mouse.
Like a 16-hour fast to a mouse is much longer than it is to us.
So I don't know if those benefits would extend.
Also, it's not entirely clear that time-restricted feeding will produce the longevity benefit that we see in other sort of fasting or fasting-mimicking types of diets.
So for me, what it comes down to is, I mean, honestly, it's just an easier way.
It gives me much more liberty with what I eat during my feeding window.
I don't have to be nearly as restrictive when I'm feeding if I have that period off.
It just, just in terms of like my physiologic response.
Secondly, there's a convenience thing.
Like I kind of hate being tethered to eat.
Like knowing that, hey, if I get into a pinch, like I don't have to eat right now.
If I'm sitting on the airplane and they're serving dog shit, I don't have to eat.
I can wait another five hours until I eat.
I also just feel much more steady in my energy levels.
I kind of vaguely remember like 10 years ago when I was kind of like eating a normal diet, how I always had this lull in energy after lunch.
Like there was the post-lunch pre-dinner, I just don't feel good.
Like, not that I feel bad, but like, I'm not sharp.
I'm not in my A game.
And I don't even remember what that feels like anymore, which is not to say I feel great all the time, but I definitely don't have that vacillating energy level.
And people that it's, it's crazy that there's so many folks out there that are living their life that don't even understand that this is a process they're going through.
They just think this is eating and exercise.
This is what happens.
But it's not.
Your body, if you shut, cut that off, push it away, enter into a completely different food source.
Just change the way you eat, your body will change.
And just that concept, the people, that sounds like horseshit.
It sounds like, what are you saying?
What are you offering some miracle cure?
No, I'm saying you will change the dimension of life that you operate in.
It will change because you won't be the same person.
You won't be like who you are is dependent upon a lot of things.
But one of them is how much energy you have, how you feel, whether you're crashing.
If you change the way you eat, you change the energy you have.
But there's an interesting question, which I spend some time thinking about, and I've sort of accepted the fact that we might not know the answer, which is when I was growing up, I was exercising like crazy.
Not as much as I was when I was swimming, but I mean, I'm sorry, more than I was when I was swimming.
But I ate, like I had the world's worst diet growing up.
So I would eat, breakfast was a bowl of like a box of cereal.
So I'd take like one of these Tupperware bowls that was this big and fill it with a full box.
So each day I would have just a box of cocoa puffs or whatever I would start the day with.
And then lunch was a full loaf of bread, which would seven sandwiches, plus a plate of fries, plus a big tub of like, like a two liter jug of orange juice.
But I was training six hours a day, right?
So I would, you know, run 10 miles in the morning in the gym, you know, boxing.
Like it was, you know, you know what that shit's like.
I mean, it's ridiculously energy expending.
But the point is, I had a hard time holding my weight.
I mean, I was a middleweight, 160, walked around at 158.
Who walks around below their fight weight?
So, you know, my waist was 28 inches.
I was probably 4.5% body fat.
And I was eating anything and everything you could put in front of me.
And then something happened in medical school where that shit just stopped.
And I wasn't even eating as badly at the time.
But all of a sudden, the metabolic adaptation just vanished.
And, you know, I mean, I wish someone could study this, meaning you would have to take a group of individuals and do muscle and fat biopsies over the course of their life, or at least during this window when we think this is happening.
And I think for many of my patients or just even friends, like it seems that this happens kind of in your 30s if you're a guy.
For women, it's harder for me to tell because I think pregnancy can interfere with this.
So sometimes we get a bit of a skewed answer.
But if I had to hypothesize, I think that we go from having a lot of lipoprotein lipase on muscle cells and not much on fat cells to the reverse.
So when I was 16 and invincible, my muscles had a lot of this enzyme, LPL, on it, that could just absolutely take whatever I was throwing at them and churn it into energy for the muscle.
Whereas when that LPL exists on a fat cell, you're basically just going to store more fat.
And now why that would happen over time, I mean, we could guess reasons, but I'd love to know if that's the case.
Because I still can't really figure out, like, why is it today I am so carbohydrate sensitive when there was a day when I could eat, you know, I was probably eating 7,000 or 8,000 calories a day, of which 80% were probably carbohydrates when I was growing up and was lean and mean.
Back then, I don't think I did that much back in the day, which would also speak to the idea of better fuel partitioning.
Fuel partitioning meaning this sort of technical term for where your body knows to go to excess energy.
You know, are you going to glycogen?
Are you going to the fat?
And then where are you storing energy?
So I suspect I was just better at fuel partitioning as a kid, which I'm sure most of us were.
Anyway, it's kind of, of course, the real question, the reason we care about this is like, what could you do about it, right?
Like what, you know, for example, like that's probably one of the reasons why testosterone, as testosterone goes down, you're going to get fatter, all things equal.
And part of the reason is testosterone upregulates LPL and hormone-sensitive lipase and all of these other enzymes in the direction of making you leaner versus fatter.
So, but I just don't think that that's enough of it, you know.
I think there's something else that's going on that's triggering that decline.
So for you with this 22-hour window of not eating, what do you think the benefits are other than your energy and slight spikes in norepinephrine and some other hormones?
Oh, I mean, I think the claim would be that fasting mimicry, which could be, you know, like what, say, Walter Longo talks about, where you do a five-day hypocaloric diet of 750 to 1,000 calories a day for five days, followed by 25 days of ad libidum feeding, meaning eat whatever the hell you want in terms of total caloric content.
You know, the claim is, well, that's going to enhance longevity.
And or, you know, doing a 16-8 or 18-6 is going to enhance lifespan.
So just to take a step back, I am only aware of three things that have universally extended lifespan across all model organisms.
So if you think of like all eukaryotes, right, if you go from yeast to worms to flies to mammals, the only things that uniformly extend life or almost uniformly is caloric restriction and or dietary restriction.
So total reduction in calories during the lifetime and or reduction of certain subsets of those calories.
So there's a super famous experiment that was done.
Actually, if anyone's interested, I wrote about it.
It's on my blog somewhere.
But it's basically this, the best experiment ever done in caloric restriction was between monkeys.
And there was a group at the NIH and a group at the University of Wisconsin.
And it was like a 19-year experiment or something like that.
So you could really study the impact of caloric restriction over these things.
And that experiment showed us that caloric restriction extended lifespan if you had a really shitty diet and it did not extend lifespan if you had a really good diet.
Counterintuitive, but it also spoke to the idea that dietary restriction probably mattered.
So, in other words, if you're eating a regular diet of McDonald's every day, and then we put your counterpart eating 70% of McDonald's every day, that's going to move the needle.
But in the Wisconsin and in the NIH experiment, when you took the monkeys that were eating kind of, it wasn't their natural food, but it was less horrible food, the caloric restriction did not extend lifespan.
So, that threw a wrench in everyone's understanding of caloric restriction.
And there are certain strains of mice that also don't seem to be enhanced in terms of lifespan, meaning just time on Earth.
But for the most part, nutrient deprivation pretty ubiquitously extends life.
The second thing that uniformly extends life across this is a drug called rapamycin, which is kind of like my favorite drug in the whole world.
I mean, meaning it's like, I think it's the most important drug in terms of this space.
Not necessarily because it's a drug that we'll all be taking, though I do believe that is the case, but more importantly, because of what it's taught us about the nutrient sensing pathway and its target, which is this protein called TOR, the target of rapamycin, or mTOR, as you probably heard of it, is mechanistic target of rapamycin.
And rapamycin inhibits that.
Now, it's a bit complicated because there's two variants of it.
There's something called mTOR complex 1 and mTOR complex 2.
And if you take rapamycin day in and day out every day, which, for example, transplant patients do, it's an immune suppressant, that doesn't seem to really extend lifespan.
But if you take it in a pulsatile way, you selectively get this mTORC 1 inhibition without the MTORQ2 inhibition, that seems to produce longevity big time.
Well, this is sort of one of my main clinical interests because I obviously am waiting for the day when I can start taking it and ultimately, you know, feel that it's safe enough that I could give it to patients.
If I'm extrapolating from all of the best data out there, so that's looking at the work that's come out of a guy named David Sabatini's lab.
David's a guy at MIT.
He's a professor.
He's actually the guy that when he was a medical student doing his PhD in 1994, actually discovered how rapamycin works in mammals.
He's actually the guy that coined mechanistic target of rapamycin, M-Torque, as a name.
And so now, whatever we are, almost 25 years later, you know, he's still running the powerhouse lab that understands it.
So if you look at all of the literature that's coming out of their lab, coupled with a guy named Matt Caberlin at the University of Washington who's doing rapamycin studies in dogs, along with the work done by someone named Joan Manick, who was at the time at Novartis, is now at a company called Restore Bio, and a few other people.
My intuition is that somewhere between two to six milligrams every five to seven days is probably the sweet spot.
But, you know, am I confident enough in that to say that we should all be taking it?
Not yet.
There's a couple things that like I want to be able to measure before we do that.
But in the animal data, this stuff's remarkable.
If you look at Matt Caberlin's dog data, it's remarkable.
Well, so for, so you own a dog, you know this, right?
I mean, if you look at outside of euthanasia or accidents, how do dogs die?
They basically die of cancer and heart, and they get dilated cardiopathy.
So it's a different type of heart disease than humans get.
They don't get atherosclerotic disease.
They get heart failure.
Their hearts just get too, too, too big, and their ejection fraction, which is the amount of blood, the percentage of blood that leaves the ventricular chamber with every contraction, as that number goes down, bad things happen.
Now, to put that in perspective, you and I sitting here, a couple of normal fit dudes, we probably have a resting ejection fraction of 60%.
And if we went out there and like killed it and worked out as hard as we could at peak, we might get that up to 80, 85% ejection fraction.
So once the ejection fraction gets below 30%, you know, a person starts to become very symptomatic.
Well, Matt took these dogs that had low ejection fractions to begin with, and I forget what the exact number was, but it might have been like below 40% or below 30%, put them on rapamycin for 12 weeks, and in just 12 weeks saw an absolute 10% improvement.
So that means that's not going from 30 to 33, that's going from 30 to 40 percent EF improvement.
In other words, it's hard to measure an effect in 12 weeks of a drug.
And certainly you're not going to be able to measure a longevity impact over that.
So much of the study that's being done with this is looking at surrogate markers that we assume would portend longevity.
So Matt's work focusing on the ejection fraction.
Manic's work was focused on immune response, which again was, so this was the turning point for me.
This was like December of 2014 was like when everything in my professional world shifted in terms of my interest towards like rapamycin as the thing I want to know everything about.
Because when I was a surgical resident, you know, we used to give rapamycin out like it was cotton candy to all the transplant patients.
It was an amazing drug that revolutionized transplant physiology because it had far fewer side effects than massive doses of prednisone and things that we used to have to give patients.
Now you could give them much less prednisone and you could give them rapamycin or cousins of rapamycin like FK506.
And so I think in two, so in a moment, I'll tell you the story of how rapamycin came to be because I think it's the most interesting story in biology, certainly in the last 25, 30 years.
But when it was approved in 1999 by the FDA, it was for this indication.
It was an immune suppressant.
It was 10 years before anybody figured out that, oh, wait, this could also extend life.
And therein you had this paradox, which was, wait a minute, how can an immune suppressant extend life?
I mean, everybody acknowledges that immunity is a core element of health.
And so in December of 2014, I feel like it was like almost Christmas Day.
I remember thinking this is like the best present I've ever got.
Manic's group published this paper, which they did in a group of about 320 65-year-olds-ish.
So they put them into four groups.
There's a placebo group.
There was a group that got, and it wasn't actually rapamycin, it was Evrolimus, which is an analog of rapamycincin.
It's basically the same drug.
So there's a group that got one milligram every single day, five milligrams once a week, 20 milligrams once a week.
They did this for something like eight to 12 weeks, and then they washed out, meaning they got nothing for eight to 12 weeks, and then they were hit with a flu vaccine, and then the scientists measured the immune response, doing these really complicated assays where you look at T cell function.
So relative to the placebo, paradoxically, all groups, and I say paradoxically because even the group that got one milligram once a day all saw an increase in immunity, which is a good thing.
But the 5 and 20 group saw an even bigger response.
The people who just got 5 once a week or 20 once a week saw an even bigger response.
But the group that took 20 once a week had more side effects.
And the biggest side effect of rapamycin acutely is these awful, awful mouth sores called apthos ulcers.
They're nasty.
They're brutal.
I used to get them all the time just from, I think, sleep deprivation or any, you know, something that was weakening my immune system.
So once I had one so bad that I was like, this is when I was in residency and I was like, it was just driving me nuts.
So I went to the OR and I got a bunch of lidocaine, which is a local anesthetic, and I went into the call room and I just grabbed my tongue and just injected like lidocaine in it.
And just when I did that, somebody walked in and I've got like blood dripping down from my mouth and I've got a needle in my mouth.
And they're like, and I'm like, no, no, no, it's not what you think.
It's a guy named William Stewart Halstead, who was so near and dear to my heart because he was the original, he was the founding surgeon at Johns Hopkins and one of the original four horsemen.
So the four main physicians that basically have shaped medicine in this country all started out at Hopkins.
Osler in medicine, Hopkins in surgery, and two other guys, Walsh and I'm blank and Kelly was the third one.
And he basically figured out, because you got to remember, like there was a day when surgery was staggeringly barbaric.
Like prior to ether, surgery was like, all right, can you hold them down?
Like gag them, get them drunk, gag them, and like we're going to do our thing.
I don't remember any of the exact dates anymore, but it was like kind of like mid-1800s to late 1800s when up at Massachusetts General Hospital, I forget the name of who it was, but someone basically came up with ether.
So ether became the first form of anesthetic.
But you were sort of knocking people out.
Well, it was, you know, fast forward probably 20, 30 years when Halstead figured out that this thing called cocaine could provide local anesthetic.
So he began experimenting with like crazy and of course in the process became like patently addicted to it.
So you have this entire generation of surgeons at Hopkins from that early era that were completely coke addicted.
So Halstead and all of his first generation of residents.
And then of course from that we got lidocaine, bupivacaine, all of these things that don't have the same properties.
But to this day, cocaine is still used and most people don't realize it, but cocaine's a Schedule II drug, meaning it actually has a medical application, unlike heroin, which is Schedule I in the DEA.
But cocaine is Schedule II and it is still used in some ENT surgery because it has some favorable properties over even lidocaine and bupivacaine for nasal surgery.
So that study, I remember reading that and thinking, okay, so if you looked at that study, you realized if you're going to be in the placebo, the one a day, the five once a week, or the 20 once a week, the five once a week was the way to go.
Now, my shtick is, so right now, rapamycin's off patent, right?
So the drug was approved in 99 by the FDA, but this is after an unbelievable, amazing story of like how, you know, this drug almost got lost forever.
Like, you know, so there's no economic incentive for a company to, you know, figure out how to do this thing with rapamycin.
And even Everolimus, I think ultimately Novartis.
And I'm saying this with no actual knowledge other than just my own speculation, but I suspect Novartis was like, well, you know, we're not going to play this game just with Everolimus.
And that's, I think, why it probably spun into this other company, RestoreBio, to sort of combine it with other agents.
But at an N of one level, what I'm kind of interested in doing is, You know, using myself as a guinea pig to start to measure the benefits of it, because my hypothesis is three things have to be true if rapamycin is working.
Now, I could be wrong, but this is my hypothesis, and this is what I test with other scientists: if you were taking rapamycin at the right dose, so assume you're not getting all the nasty side effects, you're not getting the mouth sores and stuff like that.
Three things have to get better.
One, your glucose metabolism should at least get no worse, but potentially better.
I suspect it's a function of where you start.
So, there is one doctor in New York who has like a rapamycin practice.
I think he's in the Bronx, actually.
And I've talked to him a bunch, and when he started it himself, he said like the improvements were remarkable just in terms of glucose metabolism.
But I think he was starting at a pretty bad spot.
But if you or I took it, we might not notice much getting better, but we definitely should not get worse.
So, that's easy to measure clinically.
You do an oral glucose tolerance test would give you that answer.
But two things should get significantly better.
The first is immune function should get better, not worse.
There's no clinical way to measure that, but we do know how to measure it.
I mean, when I was doing my postdoc, it was in an immunology lab.
Like, I know how to do that assay.
I just don't have like a million dollars worth of equipment to measure it.
It is, and it's different on two levels because when you're giving it every day at a lower dose, you still end up producing tissue levels that might even be comparable to where that person was getting with the spike of 20.
And in general, this isn't always true, but in general, in pharmacology, side effects are the result of certain side effects, are the result of the nadir dose, and certain side effects are the result of the peak dose.
So, with every drug, you kind of have to understand this a little bit.
But going back to this rapamycin thing, the third thing that has to be true, in my opinion, I could be full of shit, but I think the third thing that has to be true if you're taking the right dose is you need to see an uptick in autophagy.
And so, just as if you autophagy is this process where the body cells start eating themselves, so it's kind of like a programmed cell death, although technically we reserve that term for something called apoptosis.
But when you're fasting, why would fasting produce a benefit?
I mean, I think the most logical explanation is enhanced autophagy.
So, the body basically has to prioritize in the absence of nutrients.
The underperforming cells are basically told, eat yourself.
And, you know, we can recycle some of your components.
Maybe this mitochondria is worth saving.
This Golgi apparatus is worth saving.
And then we selectively, when we refeed, repopulate the better cells.
And in many ways, I think rapamycin can do that in a pill.
So, the problem is we don't have a blood test to measure autophagy.
So, in the lab, when you measure autophagy, you need muscle biopsies, or they typically even just sacrifice the animals.
This has become a very hot area.
So, the Nobel Prize in Medicine and Physiology was awarded for the genetic, basically the elucidation of the genetic regulation of autophagy in actually, it was 2016, so it's very recent, about a year and a half ago.
This is what the Nobel Prize was awarded for.
But what I'm hoping is that we can develop a signature for autophagy with a blood test.
So, I believe that you should be able to look at someone's blood and look at all of the metabolomics, all of the small molecules, all of the proteome, and there should be a signature.
It should look different from the way we look when we're fasted or sorry, fully fed.
Yeah, and I'm willing to do it all, and I probably will.
We're just trying to get what's called an IRB, an institutional review board.
So, to do these kinds of studies in humans, even if I'm the only subject and it's just like, I don't care what you do to me kind of thing, we still have to get an IRB.
So, we're working on getting an N of one IRB so that we can take muscle biopsies, fat biopsies from me, blood tests, and then start to actually look for that signature.
I probably have to talk to people who have a lot of experience doing this with animals.
But it actually wouldn't surprise me.
Like, if I were going to do it, I would just start in the legs because the muscles in the legs tend to be the harbinger of what's going on in the body.
So, for example, one of the first signs of diabetes, like a decade before you get diabetes, one thing that if you're actually doing this kind of testing in people, you'll notice glucose, like insulin resistance in the muscles of the legs.
So once the legs start to get insulin resistant, you're on a glide path to bad things happening.
First of all, from years of martial arts, but also because over the last year or so, I've been doing a lot of running, and it's one of the only muscle groups that I can work out every day.
I can run hills every day, and I'm not sore.
Like, that's not even possible for any other group.
I mean, I can kind of do that with boxing.
You can hit the bag.
But as far as like running hills is essentially like plyometrics.
Like you're pushing your entire weight up and then you're catching it with the other leg and pushing it up.
You can't do that.
You can't bench press every day.
Your fucking arms will fall off.
I mean, there's probably someone out there doing it that's proven me wrong, but there's nothing like the amount of endurance that you have in your legs.
Like you can, you know, especially if you really have good proprioception.
For example, like if you're deadlifting, you know, I actually think if you so you know how you have like the positive and negative motion, concentric, eccentric motion of a weight?
If you're willing to do away with the negative, you can lift heavy every single day.
And it was all put together by this guy named Ryan Flaherty, who actually introduced, that was another one of my sight unseen introductions to Tim for a podcast.
It's a great podcast with Ryan Flaherty on.
And he's, I call him the guru of speed.
This is a guy who like single-handedly, I shouldn't say single-handedly, I mean, he's on the shoulders of many other people who have done great work, but has really done an amazing job of figuring out how to make people run fast.
And it's a very long story, and I mean, he does such a great job on the podcast, I won't go into it.
But for the purpose of this discussion, one of our interests was, hey, could we translate everything you've learned about sprinting into cycling?
And his biggest observation was the following.
If he took 100 runners and lined them up and knew, like before they ran, knew how hard they could hit a force plate treadmill, he could predict the order in which they'd finish the race.
So a force plate treadmill, as its name suggests, a treadmill, but it's a special treadmill where it measures the force that you hit.
And the higher that number divided by your body weight, that became what he described as mass-specific force.
That number, if you rank order it, is the order in which people would finish the run.
So it kind of makes sense if you think about it, right?
The harder you can hit the ground relative to your own weight, the higher you go.
And the higher you go, the longer you travel with each stride.
So Usain Bolt has the highest ever force plate measurement calculation.
And it's, I forget what his ratio is.
I want to say he's like 6.9 or 7 times more force than his body weight every time he hits.
So you're never getting the actin-myosin filament to tear past, because that's what's happening in the negative, is the actin and the actin is coming off the myosin, and that is creating a micro tear in the muscle, and that's what the muscle rebuilds.
That's why we get larger when we lift weights.
But when you drop it, you unload the muscle when you're relaxing it.
So the muscle's not going to get bigger.
So you're getting all the benefits, all the strength, which is primarily around the type 2B muscle fiber and without the size.
So anyway, when I asked Ryan, hey, could we do this in cycling?
We did this experiment, which was he kind of came up, this was for me and two other guys who were very good cyclists.
Like I was like, I'm a popper, but these guys were like cat one, cat two, collegiate cyclers, but cyclists, but they were like my training partners.
So we did this thing where we did the same routine that he had the sprinters doing.
And it's a bit more complicated than I've described because you're also juxtaposing the positive only with something called a post-activation potentiation, which you may have already experienced this, but I don't know if you've ever tried to do plyometrics after deadlifting, but it seems counterintuitive that you'd be able to do more, but you can.
Well, we were talking about like, you really got to be able to get the lats fired, but how do you get the lats to fire at such a weight and then without having to do the negative as well?
So we just couldn't really kind of figure out how to do it.
So we adapted part of his technique to swimming, which was the actual training routine.
Meaning, so one of the big misconceptions if you're trying to go fast is that you need to still train slow.
But the reality of it is like, you know, if you're trying to run a marathon at, you know, call it a pace of 215, you know, world-class marathon runner, there's not a lot of benefit to spending much time running at a pace slower than that.
If anything, you want to be running slightly faster than that.
You know who Meb is, the American marathoner who won the Boston Marathon three years ago?
I think he's the only person to have won the New York Marathon, the Boston Marathon, and to have won an Olympic medal in marathon.
He won a silver medal in the 2004 Athens Games.
But when he won the Boston Marathon, he was like 38 years old, which in marathon parlance is like, you might as well be 100.
And he had not really had a great race in the previous few years.
So he had been effectively written off in the sport.
And Ryan actually helped train him.
And all they did was apply this principle of sprinting into marathon running, which was, all right, Meb, if you want to win the Boston Marathon, you need to be able to travel like four inches further with every step you take, taking the same number of steps at the same cadence that you currently run.
And they, you know, Ryan did the math and said, That means your force number has to go from where it is now, which I think was 1.7, meaning he could only deadlift 1.7 times his body weight.
You have to get that up to like 2.6 or something.
And so when Meb trained for the Boston Marathon, he was focusing heavily on these deadlifts and doing much shorter, faster runs.
And, you know, I mean, if you watch the video of his Boston Marathon win, it's incredible.
Like, you know, he just takes off and like leaves everybody behind him.
And they're like, yeah, there's no way he'll be able to keep that up.
I don't think people understand like what a I mean, I was never a great runner.
I was about a 250 marathon, 255 marathon when I was a boxer, but never trained as a runner.
Like it was just, I just ran so much and I was pretty fast.
But like when I think about how hard I would have to run to bust out a 250 to 255 and to think like, was there any chance I could have ever got that down to a 230?
I can't speak to what the other guys do, but I think a lot of those guys are frankly in the state of where I was when they were younger.
Meaning like they can probably get away with a lot more.
If you look at the physiques of most of these guys, they're perfectly built.
Like I'm talking elite level.
I'm not talking about like anyone who go runs a marathon, but if you're talking about like the people who are going to win the marathons, they are basically all engine and then chassis in the right place.
That's basically all they come down to, right?
I mean, they are enormous cardiovascular system, very strong quads, hams, glutes, and then everything else is very tiny.
I mean, you never know cause and effect sometimes.
You could argue, like, maybe these guys were, maybe the people who are drawn to those sports are the ones that are, you know, or drawn to be elite in those sports, already had a genetic predisposition.
That's sort of my feeling is it's a bit of a case with Lance Armstrong.
I think what Lance had that was pretty unique, even amongst the world's best, which is what he competed with, of course, I think his lactate threshold was a lot higher than most people.
And then, of course, and again, you know, I mean, I know it's such a controversial topic, although my view is I think that every single cyclist, at least from 1991 till 2011, was on highly, highly, you know, augmented programs.
So, you know, that Lance won seven of those years in that context just tells me that he was, you know, training harder and being more specific to the race.
I mean, what people don't understand is like, I mean, Lance only peaked for one race a year.
Like everything that that team, U.S. Postal, did, was geared for that one race.
And also, when you really look at how much doping they did, it actually wasn't that much.
Like, you know, when they were blood transfusing, it might have been two units over the course of a race.
And I'm not saying that that wouldn't help.
It would help a lot.
But that's nothing compared to what people were doing just a few years before Lance came along.
So Lance won, I think, his first one in 99.
The guy who won before that in 98 was Marco Pantani.
Before that was a game of Jan Ulrich in 97.
And before that was a guy named Bjorn Rees.
Bjorn Rees' nickname was Mr. 60 because his hematocrit was always over 60.
That's freaking staged.
Like how that guy didn't die of a stroke, I don't know.
They would basically always titrate with Epo and or hemoglobin up to 50, which was the trigger.
So, you know, but I think, and again, I've never, I don't know Lance at all, so I certainly don't know anything about him beyond like the little bits that I have read over time, but I do think his lactate tolerance was remarkable.
Meaning, you know, we measure lactate in athletes, swimmers, and cyclists when they're, you know, trying to figure out what their performance is.
And as far as I can tell, there seem to be these two phenotypes.
There's the one phenotype where people can tolerate staggeringly high amounts of lactate.
And again, it's not lactate per se that is causing the pain that you're experiencing.
It's the hydrogen ion that accompanies the lactate.
So lactic acid, the acid part of that is the hydrogen ion.
And that's actually what's poisoning the muscle and preventing the muscle from having this effortless actin myosin act, you know, contract, release, et cetera.
But we use lactate as a proxy because where lactate is high, the hydrogen ion is high.
And there are some people who can just tolerate like incredible doses.
I used to work with Olympic swimmers.
And I mean, there were just a couple of these guys.
Like they could actually be standing with a lactate of 24.
I mean, when I was competing, if I had a lactate above 16 or 17, I couldn't be standing.
Like, that was just too much pain.
Like, I was on the floor.
If I was over 17, I was puking.
And I saw dudes that could stand there at 24.
In fact, one of my good friends, he won a gold and a silver medal in the Sydney Olympics and retired from swimming in 2004, then came back to swim masters.
He actually was trying to make a comeback to make the 2012 Olympic team.
And when he was training for that, I would poke him between races.
And I saw him get out of a 400 individual medley race, which is the hardest swim race of them all.
The 400 IM is, I mean, you might as well just shoot yourself.
It's so painful.
He got out of that, had a lactate of 18.
Two minutes later, not two minutes later, maybe seven minutes later, jumped on the blocks and won 100 breast race, came out with a lactate of 21, that kind of thing.
So there are those guys.
And then I think at the other end of the spectrum, the word on the street is guys like Michael Phelps are at the opposite end of that, where they are so efficient at shuttling lactic acid out of the cell back to the liver, where this thing called the Cori cycle actually turns lactate back into glucose that they never have high levels of lactate.
Now, again, all of this is sort of speculation because I think they were very hush-hush about Phelps' numbers.
But I heard from reliable and reasonable sources that he would rarely have a lactate above 8.0, including when he's breaking world records.
But for, you know, he was so efficient at getting rid of it that, yeah, he could, you know, set the world record in the 400 IM and have a lactate of eight.
Again, I don't know if this is true, but I've there's certainly a plausible mechanism by which it could be.
Well, it's fascinating that this could potentially all be engineered, right?
That like through use of CRISPR or something else, you could take all these various facets of performance-enhancing modalities, extend a person's ability in so many different ways and create a superperson.
Well, does it if you have someone like Phelps who has this genetic predisposition to getting rid of lactose, lactate, and you take someone like me who probably has none of that and you juice me up to his level?
I mean, this is why people like Daniel Coyle, who are so critical of Lance Armstrong, say, because on the one hand, you'll have camps that say, look, it's the great equalizer.
But I have a different reason for arguing that way, which is I think having done these sports and nowhere near at the high level that those guys do it, I just know how destructive they are.
Like, the Tour de France is the most unhealthy thing on the face of the earth.
When those guys finish the Tour de France, they are osteopenic.
I mean, their bone density has eroded.
They have lost so much muscle mass.
I mean, it is a devastating, grueling event.
Now, nothing's going to completely ameliorate that.
But like, if we think that watching these guys kill themselves riding six hours a day, hitting peak thresholds of, you know, six watts per kilogram, if we think there's anything physiologically reasonable about that, we're out to fucking lunch.
I mean, isn't that the point is that you can push your mind to do something your body absolutely doesn't want to do, so you should be rewarded for that.
But I also think like the testing on this stuff is so, like, it's so JV.
Now, there's this idea called the biological passport that was introduced many years ago, which basically said, look, we're going to develop a signature for every person.
And now, if you deviate much from your signature, that'll be the trigger.
And the argument, again, by certain people, and I think Daniel Coyle argued this a lot in one of his books that he wrote, Ripping Apart Lance, was the reason doping is unfair, because the everybody does it argument doesn't hold water, is because if you're a person who naturally lives at a hematocrit of 47, you're only getting a slight improvement going from 47 to 50.
If you're a person who naturally lives at 43, you going from 43 to 50, you get a much bigger advantage.
To which I say, yeah, but that's true on a relative basis, but at an absolute level, if everybody's walking around with a hematocrit of 48 to 50, they still have the same oxygen-carrying capacity.
And it's also worth putting in mind that, and this is sort of my pet peeve with this whole drug and sport thing is like, I mean, personally, I don't really give a shit.
I mean, I just have bigger things I care about than like how many steroids Barry Bonds took to hit all those home runs.
But what really does chap my ass is when people don't actually understand how steroids work, right?
Like it bugs the shit out of me when people assume that if you take steroids, you will have, you know, you will hit that many, you know, home runs or you will run this fast or lift this much.
The only thing that steroid is doing is enabling you to recover faster from the brutal work that it takes to actually do those things.
So, you know, if I shot myself full of EPO, I mean, you've probably seen Icarus, right?
I mean, I thought that was, I thought he did it.
I thought Brian.
Yeah, I thought Brian Fogel did a really good job of showing, like, I mean, and he was a pretty good responder to the EPO.
I think he did growth hormone, testosterone, and EPO.
I mean, you saw in the end of the day, he finished worse the second year round.
I mean, I mean, I, you know, when I stopped cycling competitively, I think a big part of it was I just realized that performance and longevity stopped being collinear.
They started to become somewhat orthogonal.
They started to deviate.
In other words, the things that I was doing that were enhancing my performance.
And I'm not even talking about drugs.
I'm just talking training-wise.
It seemed to come at the expense of what I believed was going to make me live longer.
So specifically, the thing I cared most about was cardiovascular health.
Now, the incidence of atrial fibrillation in highly trained athletes is 10 times higher than that of non-athletes.
So like that's a little counterintuitive, right?
Like why would people who have such amazingly fit cardiovascular systems have 10 times the risk of this horrible condition called atrial fibrillation, which yeah, many people have it, but not young.
You're not supposed to have that when you're 40.
And it's usually associated with cardiovascular disease.
And yet people are, you know, showing up with these.
I mean, I have four patients who have had to get ablations for atrial fibrillation.
An ablation is a procedure where they stick a catheter up through the femoral artery or in the vein and then they burn pieces of the heart, specifically around the pulmonary veins.
And they basically are trying to burn away and create or remove the ability of the electrical system to move in this way.
So what's basically happening with this type of athlete's heart is when your heart is constantly being exposed to that high stretch, high ejection fraction load, you're basically stretching out the electrical system because the electrical system of the heart runs within its muscles.
So as you stretch it out, a certain group of people, and we don't know why certain people are susceptible and certain or not, but they just develop this dysrhythmia.
Someone said once, and I don't know if this is true, maybe you would be able to have some insight, that there's a concept that your entire life you have a certain amount of heartbeats.
Yeah, I don't tend to agree with that because you can't compare one beat to the other.
I mean, you can't, you know, it's hard for me to say that, you know, an 80 to 90% ejection fraction beat under incredible load is the same as the beat that I'm, you know, like is beat per beat the same as the beat I experience when I'm sleeping and my heart's rating, you know, my heart's beating at 40 beats per minute.
I think maybe there's a directional truth to that, but I feel like when you're talking about human longevity, it's a game of inches.
And that is like something that's probably directionally true within a mile.
Now, when you're talking about human longevity and you're thinking about all these different things that you could do to extend, how much of that is supplementation?
And do you supplement?
Like, are you a person who takes colloidal minerals?
Or are you a person that is interested in antioxidants?
So my view on longevity is it's the hardest problem there is.
And so you got to have every, like, I'm agnostic about what the approach is.
So I want to understand everything that you can do with respect to, you know, food, drugs, supplements, hormones.
And to be clear, the only difference between a drug and a supplement is one's regulated and one is not.
But, you know, I have patients that will say things like, oh, you know, doctor, I don't want to take that drug.
I'd rather do it naturally.
Can I do it?
And it's sort of like, well, okay, you don't want to take a statin, but you do want to take red yeast rice.
Well, they both inhibit HMG-CoA reductase, the enzyme that catalyzes the first step of cholesterol synthesis.
You're willing to take one that you buy in a drugstore that's totally unregulated and you're not willing to buy the one that comes from a drug company where the FDA has their foot up the ass of the company making it to make sure it's perfect.
That just strikes me as a false equivalent.
So I only say that to just say like, I think everything should be on the table.
And then the question should be, how do you decide what to do?
So there are absolutely a bunch of supplements that I take, but I don't have kind of a one-size-fits-all approach to it because I think you've got to be able to kind of measure what's going on in a person, get a baseline and figure it out.
So, you know, I mean, my guess is you've had a million people on the show that can talk your ears off about, you know, which people should take methylated vitamins versus which shouldn't.
And if you have this MTHFR mutation versus this one, should you be taking this versus that?
I think all those things are valid.
Some of the stuff that I find even more interesting is actually a lot less sexy, and I don't have a good answer for it.
But, you know, looking at, for example, vitamin D levels.
So, you know, you see a huge disparity in the vitamin D levels people have.
And it begs the question, do all people run effectively at the same vitamin D level?
And is that a function of not just their own individual, like how much sun they're getting, but more importantly, like potentially genetically where they're from.
So I'm starting to feel like people who have northern European blood might actually run better at a lower vitamin D level than people like me who, you know, come from places near the equator where maybe I just evolved to see more sunlight and have more vitamin D. What's your ancestry?
My parents are both from Egypt.
Oh, interesting.
So, and the range, like when you look at a laboratory test, when you check somebody's vitamin D, like the range that's offered is 30 to 100 is optimal.
So I personally think the range is probably 40 to 60, but I also measure something called parathyroid hormone that allows me to further titrate that range and stuff like that.
Well, when you're talking about this, it's really obvious, really clear, that there's so much data to go through.
We're learning this.
I don't want to say it's at its infancy, but if we look back a thousand years from now, we will most certainly say that your understanding of this science is at its infancy.
I mean, the issue is how do you make sense of a problem or how do you try to solve a problem which is unsolvable?
And the reason I say that is the following.
You know, you have what I call kind of the medicine 1.0 world, which was, I define that as everything that took place before Francis Bacon.
You can probably tell me when that was.
I'm going to guess Francis Bacon is like 1650 to 1670 or something like that.
But that was basically the first person to come along and codify the scientific method.
So anything that came along before the scientific method may have been correct, meaning there were things that were certainly done back then that proved helpful, but they weren't grounded in a principle of science.
In other words, even a blind squirrel is going to find nuts sometimes.
And then we basically, through, following the codify, you know, the elucidation of a scientific method, the development of statistics to actually make sense of data, we then got into the sweet spot where I think we are now, which is medicine 2.0.
And to me, medicine 2.0 is really good at solving problems that are amenable to relatively short, simple clinical trials.
And there has been no better example in this space than infectious diseases.
So if you think about the unbelievable improvement in human longevity that has come from antibiotics, antiviral therapy for HIV, I mean, remember, 30 years ago, HIV was a lethal, no questions asked lethal condition.
Today it's a chronic disease.
For virtually every patient with HIV, it's a chronic disease today, meaning you will die with HIV, not from HIV.
That is, that's almost hard to fathom when you consider how shitty we are at addressing other chronic diseases like heart disease, cancer, Alzheimer's disease.
So the problem is, if you want to know the answer, should I eat this way or that way?
Should I exercise this way or that way?
Should I take this drug or that drug or this supplement or that supplement to live longer?
We can never know the answer in humans because there is no clinical trial that can answer that question.
Now, we can do that experiment in everything that's not human, but we've already learned the hard way that what happens in not humans doesn't necessarily extrapolate to humans.
And we can do things to be slicker about it.
You know, when you study rhesus monkeys for 20 years, it's certainly more interesting than studying mice for one year.
But in the end, they're still animals in captivity.
They're still not in the same environment and all these things.
So my view on this topic is the only way to go to this kind of medicine 3.0 is you've got to have kind of a strategy around how you think about it.
And so in many ways, that's what I spend most of my time dealing with is what is a strategy for longevity that becomes a scaffolding upon which you anchor every new piece of data.
Because, I mean, I know things today from a data standpoint, I didn't know 10 years ago.
And to your point, even in five years, we'll look back at stuff we're doing today and think, God, we have more data.
Is that still the right thing to do?
And so that strategy to me is sort of fundamentally based on three bodies of literature.
And the first is like, what did we learn from centenarians?
So the people who naturally live to 100, they have the advantage, or that body of literature has the advantage of being based on humans.
It has the disadvantage of it not being experimental.
So we, you know, like, we don't know like what cause and effect was.
And then secondly, if you look at all of the animal literature or non-human literature where you can actually do the experiments, what's common there?
And then if you look at the underlying molecular mechanisms.
So I feel like if you tie those three together, you come up with a general scaffolding for what it means to live longer and live healthier, then we can try to look at one thing at a time and say, hey, vitamin D, yay or nay.
So when a paper comes out, if it is never cited again, meaning for the remainder of time, no one ever even goes back to reference that paper, you could probably make the case that that paper is not relevant.
And if you then further strip out auto citations, meaning the only time it's ever cited is when the author then goes back and cites his or her own paper, something like 70 or 80 percent of papers never get cited outside of an auto citation again.
I was like, literally, as I was driving here today, I was talking to a buddy of mine and I was like, dude, I'm the fucking bottleneck, and I hate it.
Like, I'm now the bottleneck because the analysts are now churning out stuff faster than I can even provide ancillary feedback.
Because my job is like, you know, you hire great people who are smarter than you and like you just guide them.
You just point them in the right direction.
So what we mostly do is create programs where we're going out and looking for new knowledge.
So for example, one of the questions that is tormenting me right now, because I still don't know the answer, is is there any benefit to taking human growth hormone from a longevity perspective?
There's clearly a performance benefit.
Growth hormone is probably the single most abused drug in all of sports.
There's no question about that.
But is there a way to take it where it makes you live longer?
I've never prescribed growth hormone to a patient because frankly, I'm not yet confident that I know the answer to that question.
But I feel like it's worth knowing, right?
Because I can certainly make a teleologic argument for why growth hormone could be helpful, but I can also make a teleologic argument for why it could be harmful.
And so, like many things, your knee-jerk reaction to something can often be wrong.
And my knee-jerk reaction to growth hormone has historically been causes cancer.
Because why?
Well, growth hormone tells your liver to make IGF, insulin-like growth factor, and two-thirds of tumors seem to thrive on IGF.
So ostensibly, you would think, well, growth hormone can't be right.
But then one of my analysts, Bob Kaplan, pointed out to me a year ago, he's like, you know, Peter, I've been thinking about this.
And he's like, given how ubiquitous growth hormone is in sports and how long it's been ubiquitous in sports, like, I mean, this was the drug that turned around U.S. Olympic athletes in the late 70s, early 80s.
He's like, where's the body count?
Like, where are all of these people dying of cancer from all these years of staggering growth hormone use?
We don't really see it.
When we went back and looked at literature, I mean, we found that the data on growth hormone and IGF are not nearly as straightforward as people have made it out to be.
In fact, there's, I mean, I could draw it actually for you.
Not that anyone will necessarily see this, but at least you'll see what I'm talking about.
If this is percentile, so higher, and this is IGF level, right?
Well, so what that means is, so for example, Alzheimer's disease and heart disease have an almost monotonic reduction in risk as IGF gets higher and higher and higher.
It's only cancer that seems to have that uptick where risk starts to actually rise once you cross past the, call it 70th percentile.
And so when you integrate all of these curves together, that's why you see this slight uptick.
Now, again, this is epidemiology, so one has to take this with a grain of salt.
But this is, to me, when I saw this graph, which Bob put together, I don't know, a while ago, I was like, wait a minute, this doesn't jive with my preconceived notion of like growth hormone is bad.
This warrants way further exploration.
And so what that basically turned into is now an enormous internal project that will take us probably a year to complete and will constantly be updated.
Like we did this already with testosterone two years ago.
We put together like a 40-page white paper on the topic.
And then at least once every two weeks, it gets updated every time a new paper comes out.
Basically asking the question, like, is testosterone replacement beneficial or harmful?
And under what situations should it be considered versus not?
And again, the goal is to do this unemotionally.
And that's hard to do because for reasons I'm not entirely clear on, basically everyone's kind of just emotional about this stuff.
You know, starting with Lister and going all the way to Fleming when we figured out, like, you know, if you if you cut open a cadaver and then go and deliver a baby, that's bad.
Um, because there are these microscopic things that none of us anticipate, right?
We haven't had a step function improvement in mortality in nearly 100 years.
So what's next?
Now, I think there are a couple of potentials for that.
But what I don't know is if like they're going to happen in my lifetime or in your lifetime.
But I want to buy the optionality to stick around for it by doing all this incremental little shit.
No, I think some people are just so insulin-resistant that it becomes really hard to fix them without doing draconian stuff.
I mean, I have one patient who is really now, I think, going to, in many ways, become the poster child for he's definitely the toughest case I've ever had.
And why he's such an amazing guy is he was actually able to do something that's really hard to do, which is stick to something with complete blind faith in me, even when it didn't feel good, even when I knew it would take a long time to see the results.
So, he's probably 5'8, weighs 235 at the start.
So, 5'8 ⁇ , 235, metabolic syndrome, huge amount of fatty liver disease.
Not the typical patient in my practice.
Most of my patients are kind of young, healthy people who want to like, you know, want this immortality thing.
But this is someone who doesn't fit that description, probably 70 years old, on like, you know, four drugs for blood pressure, 10 drugs.
His liver, this is, I mean, and that's interesting, but not nearly as interesting to me as the fact that his transaminases, which are the enzymes that the liver makes in response to how much fat is accumulating, you know, normal is like less than 40.
He was like in the hundreds, and the ultrasound showed it was just a bunch of fat, and he doesn't drink alcohol, so we knew it was fatty, non-alcoholic-fatty liver disease.
I've never tried to figure out whatever came of that patient.
I can't imagine he'd be alive now, though I know he was young at the time.
But the part that interested me was that he didn't regain all the weight seven years later.
And that suggested that there was a, like, it was a reprogram.
He got the blue screen of death on the computer.
He did the hard reset.
He got to be a new person again.
Because I'm not of the camp that thinks like that guy got to be 400 pounds just because he was a glutton and a sloth.
Like something fundamentally broke in that dude.
And what broke was he basically lost the ability to partition fuel correctly.
Now, could food play a role in that?
Absolutely.
Certainly if you eat enough shit, that can happen.
But I think it's more complicated than that.
I think it could be epigenetic, if not outright genetic, but probably more epigenetic.
And so I'm interested in this idea of how do you reset people?
And again, this is all kind of a long-winded way of saying, like, one of the advantages of practicing medicine is you get to, you say humble because every time you think you're smart and you're like, I got this shit figured out, like, you don't.
There's like some patient who's got a problem that you can't figure out and it just, you know, drives you nuts.
But you realize like, I mean, even just today I was talking to a friend of mine.
He's not a patient, but I mean, my God, he's just going through like this devastating health situation.
He's been, he has seen every doctor.
He's been to Mass General.
He's been to Stanford.
He's been to Hopkins.
He's been to the best hospitals in this country.
They can't fucking come close to figure out what's wrong with this guy.
And so as bad as that is for him, I think that level of humility is actually good for the profession.
He's having these horrible neurologic symptoms where he gets these fasciculations and muscle weakness.
And obviously the big concern about six months ago when this started was he was presenting like he had Lou Gehrig's disease, which, you know, obviously is about as bad a fate as you can have.
Luckily, that has been ruled out, and they've done a million muscle biopsies and all these other things, but they don't know what's going on.
Well, I told him today, I was like, look, I'm going to send you a kit.
We're going to do a certain blood test on you and a certain urine test on you.
And I want to just figure out what's going on with your four hormone systems.
There's basically four hormone systems that play a pretty big role in how we feel.
And adjusting those doesn't, I'm not convinced it necessarily makes you live longer, but it can certainly make you live better.
So I want to kind of understand, I suspect he's not firing on all cylinders on that dimension, whether it's a result of whatever is going on that nobody can figure out or not.
But I'd rather focus on something that I think we can fix.
And I got to tell you, I know we love to, we love to beat up on fat people.
We love to turn it into a character defect.
But I got to tell you, virtually every fat person that I know or that I've taken care of, they are not disproportionately eating more than their peers.
In some cases, yes, but not on balance.
The problem is that they simply do everything incorrectly metabolically.
Yeah, and it's, you know, I think there's a genetic component.
I think there are dietary exacerbations.
I think certainly not exercising makes things worse.
So there are lots of predisposing factors.
But at the end of the day, what's happening is when you and I eat, like let's take a meal that, like if you had pancakes, bacon, and scrambled eggs, that would be like a really good mix of, that'd be a third carbs, a third protein, a third fat.
So that's like a shit ton of nutrient, right?
If you or I ate that, yeah, it probably wouldn't be that good for us.
But like we, you know, let's say we just finished a workout or something, like we're going to partition such that that glycogen will first and foremost go to replace the muscle and liver stores of glycogen.
Because we have bigger muscles and our muscles are more insulin sensitive.
We can actually disproportionately put more glycogen into our muscles, into the leg muscles, because you'll have done that run up the hills, right?
And then furthermore, when we want to recruit energy again, we'll have the ability to actually go back and get fat.
In other words, break down fat at lower ATP demands than necessarily always going to glycogen.
So in other words, we partition fuel in a smarter way.
And these patients, I mean, you can measure this clinically using something called RER and of course doing other blood tests.
Like they just, they just, they can't break down their own fat.
It's a hard problem because the way I explain it to people is, and I'm, so clinically, I'm not interested in weight loss, right?
I mean, that's just not, I'm much more interested in longevity.
And yes, sometimes weight loss comes with that, but I, like, if I ever get stuck doing, you know, weight loss, like, I'm doing the wrong thing for my interest.
But the way I say to people when they want to lose weight is, look, you don't want to lose weight.
You want to lose fat.
Let's be very clear on our semantics.
Weight is irrelevant, right?
Unless you're a cyclist or some athlete for whom the actual scale means something.
But for people like us, you want to lose fat, not weight.
And then when you say you want to lose fat, what does that mean in English?
Well, do you want fewer fat cells or do you want each fat cell to be smaller?
Those are totally different questions.
If you want fewer fat cells, have liposuction.
But we know that that doesn't fix you metabolically.
So if you want fewer, if you want to be less fat, you have to have smaller fat cells.
Now, a fat cell, conceptually, has two inputs and one output.
So now I say, let's reframe the question.
You've got a room with 100 people in it.
You want fewer people in the room.
What has to happen?
More people have to leave the room than enter the room.
So similarly, if you have a fat cell and you want it to be less fat, you've got to get more fat out of it than enters it.
And the fat that exits the cell exits via a process called lipolysis.
And the inputs to a fat cell are something called de novolipogenesis, which is turning carbohydrates into fat, and reesterification, which is turning fat, like in a free fatty acid, into a triglyceride back into a fat cell.
Each of those three doors is controlled by hormones.
And so the purpose of nutrition or fasting or exercise or drugs or hormones or all these things is to manipulate those hormones in the direction of what I call negative fat flux or what would be referred to in the literature as fat balance, negative fat balance.
And the hormones that drive that are many.
Insulin, hormone-sensitive lipase, testosterone, estrogen, cortisol being the five most important, in my opinion.
Maybe someone will disagree with that, but I think those are the five that rule the roost.
And so, you know, how do you manipulate those?
Well, insulin seems to be the most important of the five.
And there's no better way to lower insulin than to not eat.
So the first thing that happened to that dude who went 382 days without anything but water and minerals is he basically had very low insulin levels.
In fact, once he got into raging ketosis, which he got into by about day seven, his insulin came up only to prevent him from going into ketoacidosis, which was what would happen if he had no insulin response.
In other words, if he was a type 1 diabetic, he would have died of ketoacidosis because he wouldn't have had the insulin to regulate the uptick of ketones.
But if you or I did this, because we have a normal pancreas, we would actually make just enough insulin to suppress ketogenesis and keep that beta-hydroxybutyrate level in the, you know, kind of in the neighborhood of probably seven or eight millimolar, as opposed to getting north of 12 to 15, which is when you get into trouble.
So, you know, how do you manipulate insulin?
Nutrition is the first way.
If you can't fast, the next best thing is to reduce carbohydrates.
Carbohydrates, obviously, are the most insulogenic of food.
Although protein can be quite insulogenic as well.
It has a different response.
And then that's when you start to think about these other things.
You know, I've seen patients where they just can't lose weight.
And I watch what they're doing, and they're doing everything right, but they just can't lose weight.
But then you notice their cortisol levels through the roof.
It's hard to get rid of fat when you have lots of cortisol.
Cortisol is a very anabolic hormone to fat and a very catabolic hormone to muscle, which is the exact opposite of what we want.
Testosterone, of course, is the exact opposite.
Testosterone is catabolic to fat, but anabolic to muscle.
And then, of course, women have a harder time because once women go through menopause, they lose all the estrogen and all the testosterone.
And so now they lose two hormones that play a very important role in regulating this.
I mean, I kind of lift three days a week and then I ride like a stationary bike, like a Peloton, or I prefer this thing called a Wahoo kicker where you actually put your bike on it.
So I'll do that three or four times a week.
I would guess when I sit down to throw down, it's probably 3,000 calories.
Yeah, no, no, it's totally, I mean, I completely understand what these people are going through, at least in as much as what the, as the physiologic desire for it.
I mean, obviously they will experience something even worse because there's the, like, I can, like, look, I don't have abs on, I don't have veins on my abs anymore.
I used to.
When I was in a ketogenic diet, you know, I was 7% body fat.
I was completely ripped.
I'm not ripped anymore, you know, relative to that.
That kind of bugs me, but like, nobody really knows that.
I mean, nobody really gives a shit.
So I can still look like a super healthy dude, a super lean dude, even if I'm not.
But oh my God, like when shit's going wrong, like I want to eat some of the worst foods that have ever been created.
So a lot of times we'll see when people either turn to sugar or salt in times of fatigue, a lot of times it can be, you know, they don't have the right level of free cortisol at that moment in time.
I'm just happy that I didn't eat a sandwich of my own as well as the crusts.
Because I probably could.
Once the fucking gates are open, once I'm out there making spaghetti and meatballs, like, all right, let's get some fucking ice cream in this mix, too.
You know, once I'm already fucking off.
So what do you, what do you eat?
Like when you sit down for these 3,000 calorie meals?
And he's way more jacked than me, so he can get away with eating way more naan than me.
But yeah, that night, I mean, also those sauces are like so fatty.
Like, I'm sure that was a 4,000-calorie throwdown.
The other thing I'm pretty good about is when I'm done, I'm done.
So that's the other thing about time-restricted feeding that I think I get away with more because like when I go back to my apartment, I will rarely have another bite.
And when I wake up in the morning, it's like black coffee.
You know, I'm not sneaking little shit in throughout the day.
Like, whereas if I'm not fasting, it's just too easy for me to just like sneak stuff in.
So anyway, that night, I knew we were going to go out for a killer dinner before in Brooklyn, before we went to the show.
And so normally I exercise in the morning, but that day I was like, look, I will, your muscles will be a little bit more insulin sensitive if you can exercise about 30 minutes before you eat.
That's probably about the sweet spot.
So if I were to ride at like 8 in the morning and then not eat until 7 at night, I mean, I would still eventually get the glycogen there, but it wouldn't be quite as easy.
It would require a little bit more insulin.
So in that case, I just modified my day and was like, you know, made my schedule such that I could ride at 5 p.m. in anticipation of that.
And I also rode a little longer and a little harder, just, you know, like, let's really crush this session so that, you know, I can go and enjoy dinner a little bit more.
I mean, I think, I think this longevity thing is the perfect culmination of all of my previous lives in terms of professional lives.
So, I mean, I used to be an engineer and then I went into surgery and then I left that and went into management consulting and had nothing to do with medicine for several years.
I just worked in credit risk modeling.
And so in many ways, like when you combine medicine with engineering, with risk management, that is what longevity is all about.
Like if you want to take the practitioner's, you know, the roll-up-your-sleeves approach, that's what it is.
So I think that scratches that itch.
But I think for me, like, I have to be sort of mastering something.
So that's where archery and race car driving today become just total obsessions.
And like when we were talking earlier, it's like, yeah, I mean, I don't know that I'll ever go hunt because I don't know that I want to spend three days, you know, taking 10 shots when I could be spending, you know, three days taking 300 shots in my backyard.
Like in the end, I think what I really just obsess over is trying to get better at something.
And the nice thing when you start things late in life, like I didn't get my racing license till three years ago, and I've only picked up archery two years ago or maybe a year ago.
Like when you suck so much, like the opportunity to get better is awesome.
So I think the bigger itch for me is not intellectual.
He moved to Iowa just so he can kill big giant deer because he literally bought a farm in Iowa, a giant chunk of land and raises it for, he has, he does do some farming, but essentially what he does is raises deer.
He doesn't raise them.
Like there's no fence, but he makes it very make it favorable for them to be there.
He has food plots that he grows.
And I mean, I hunted on this place a couple years ago.
No, he's literally the best in terms of like the average person who's interested in it.
He's got a great podcast about it, knock on podcast, but he gets so geeky and technical in his descriptions and his understanding of it.
I mean, he constantly obsesses about form and structure and, you know, archery.
To me, my history as a martial artist, it really jives with me.
It makes sense.
Because you could muscle things and do them wrong and develop bad habits and you'll never reach your full potential.
Or you could do things correctly and be very, very disciplined and focused and understand why you're doing something and then really actually reach your full potential.
There's really no other way.
And with archery specifically, it's so satisfying.
Like as we were saying before, when you do pull it off and you do execute that perfect shot with your rhomboids and the hand goes over the back shoulder and you watch that arrow shunk go right into that bullseye.
And I think that's an interesting point about certain things, right?
So to me, the other thing I like about archery and race car driving is you have to learn some emotional discipline.
So you can't get pissed off and work your way through either of those things.
You can sort of get pissed off on the bike and it can actually charge you, which is not to say that cycling doesn't have technique in it, but it plays a much smaller role.
And in the end, the Gur factor can out-trump it.
But you can't gir your way out of a shitty shot.
And you cannot, in a car, if you start getting pissed, you're done.