DAILY HACKS To Stay Healthy Until You're 100+ YEARS OLD! | Peter Attia & Mark Hyman

That's where you want to put your energy, is change your environment. Change your environment so that you don't have to constantly rely on willpower, so that when there is friction, I make the easy choice. Make the easy choice the easier choice. Yeah.

Welcome to the doctor's pharmacy. I'm Dr. Mark Hyman, and that's pharmacy with an F, F, A, R, M, A, C, Y. A place for conversations that matter. If you care about your health, if you care about longevity, if you care about understanding how to optimize your performance, this is the conversation for you because it's with Dr. Peter Att, who is one of the physicians in the world that I respect and admire most. I met him first after a screening of Fed up, and I heard him speak at TEDMED in 2013. I encourage you everybody, to watch that talk on TEDMED because he told his story. Pretty remarkable story of being a physician who, whether most physicians like to admit it or not, or people like to admit or not, have a bias against people who are overweight because we kind of blame the victim. We say, well, you got diabetic and overweight because you ate too much and you didn't exercise enough. Turns out that is a bunch of horse. You know what? And Peter explains why and how he actually came to understand this through his own biology. So we're going to get into that story in a minute. He has a medical practice called Atea Medical in New York and San Diego. He focuses on the science of longevity. What is the science of longevity and how do we increase not only lifespan but also increase health span or quality of life? Uh, so he applies nutritional biochemistry, which one of my favorite topics, exercise physiology, sleep physiology, techniques to address.

How we can be more resilient in the form of stress and something called lipidology, which is a study of lipids and cholesterol. We're gonna get into that drugs and hormones. So Peter is quite a guy. He's trained at Johns Hopkins in general surgery. He won many awards, including resin the ear, and he wrote a whole book on general surgery. He spent two years at the National Institute of Health and Surgical Oncology and was a fellow at the National Cancer Institute, where he focused on immune support for melanoma and has been mentored by some of the most experienced innovated lipidologists, endocrinologists, gynecologists, sleep physiologists, and longevity sciences in the United States and Canada. He went to Stanford to get his medical degree and holds a bachelor's in science in mechanical engineering and applied Mathematics. Amazing. So welcome, Peter.

Thanks, Mark. God, that's. That's hard to sit through, man.

I know, right? You're squirming. Because it's. I know, but the truth is you have been on quite a journey. And. And one of the things that struck me was your story of how used to be this elite athlete, or you still are, I guess. And you were. You were swimming from Los Angeles to Catalina Island. And for those people who don't know how far that is, it's fricking far. It's. I don't know how many miles, but it's very far. You can barely see the island from land. And he would swim there, and he discovered that you discovered that you were pre diabetic. So tell us about that story, because that doesn't make any sense. Right?

Yeah. I mean, I think I was. I'd always been training my whole life, but. But definitely things changed when I was in residency. Something caught up to me, and. And in retrospect, I really think it was a combination of just absolutely debilitating sleep. Lack of sleep. Yeah. So probably sleeping an average of 28 hours a week. So even though that didn't mean exactly four hours every night, it worked out to that.

So I remember when I was in training and I rotated with surgery, they were like, lunch is a weakness and so is sleep.

Yeah. It was definitely a part of the culture and unfortunately, just a part of the way that the structure of residency at the time. I don't think it's nearly that bad today. But anyway, I think total sleep deprivation coupled with a not so great diet, coupled with just the inevitability of age sort of catching up to you. I mean, when I was in.

You were all 30.

Yeah, exactly. And something, you know, a switch sort of flips. Right. Between about 28 and 30 in me when you. Because when I was growing up, I ate poorly. I mean, breakfast was a box of cereal, not a bowl. So we had these large Tupperware bowls, and I would put the entire box in and that would just.

Was it like Froot Loops or was it like Cheerios?

No, it was total crap. It was Froot Loops or Lucky Charms or Cocoa Puffs.

But American Heart association says Froot Loops and Lucky Charms are healthy.

Right. It had no cholesterol in it. So that's the key thing.

No fat.

That's right. So I'd have, like, 27 dyes and lots of sugar. I mean, seven sandwiches for lunch every day. A whole loaf of bread, 14 pieces, you know, French fries. So I was eating non stop growing up. But, you know, when you're 16, 17, 18 years old, and you're exercising six hours a day, I don't think that matters. Yeah, you can, you can certainly skirt that. But. But it basically just caught up with me in my late 20s, and certainly by the time I was 30, I mean, I was way.

Way bigger than I should have been given all the things I thought were going on, you know, And I don't think I really internalized it probably until I was. I had and I didn't really probably. It wasn't until my early 30s, 32, 33, that I was sort of like, wait a minute, something's wrong here. And this is not a great trajectory.

You had a minute to look in the mirror.

Yeah. And it's funny, when these things happen slowly, you're not. It's easy to sort of miss it and sort of rationalize it or something like that. But at some point I just became like, this is. There's a funny story I tell when my wife, at the end of one of those Catalina swims or one of those marathon swims, she. She made some smart comment to me, which again, she to this day swears a. She swears she didn't say it, but she did say it. And two, she claims that if she said it, it was only in the most loving way, which I believe. But she said, you know, you got to work on being a little less not thin.

After I finished getting. After I got out of the water because there's this picture of me with a towel around my waist and my belly's like hanging out over the towel and stuff like that. So.

That day was kind of the day when I was like, all right, I got to sort of figure this out.

So you can't exercise your way out of a bad diet.

I don't think you can. With a certain other set of parameters in place. If your sleep is also problematic, if your cortisol levels are also problematic. Yeah, I think it becomes very difficult to exercise your way out of a bad diet and those other bad factors. And also.

One shouldn't aspire to do that. Right. Like, I mean, I was swimming at least four hours a day in training, you know, plus lifting weights and other things like that. So at some point you have to, like, have a life too. Like, you know. In other words, if someone had said, the answer, Peter, is you just need another two hours a day of exercise, I'm not sure that would have been a practical solution.

Four hours a day of exercise and you were still overweight.

Yeah.

Okay, so that is because you were eating.

I believe it's a combination of a lot of things. I believe it's a diet that was incredibly high in.

Both. You know, what we would consider, you know, reasonable carbohydrates, but also a lot of crappy carbohydrates. And I actually think one of the more sinister things was, especially when I go back and kind of look at my food journals, my training logs and stuff, is I was probably drinking like four 1 liter bottles of Gatorade Powerade a day.

Yeah.

And I think that's healthy.

Right.

So I, I think blue juice.

That's.

Yeah, I think a lot of that stuff coupled with.

Just constantly. That also there's belief that you had to sort of constantly be glycogen loaded. So. Yeah, like a lot of my big, big training swims, as you sort of got closer and closer to doing the long swims, you'd be doing these swims of six hours and stuff in training. And I remember the eating routine around that. You know, this, like, it never occurred to me that I could probably do that with minimal nutrition if I were more fat adapted. So instead it was I'd wake up and eat. You know, imagine taking a measuring cup and putting two cups of dry steel cut oats in that and think of how much that, how much oatmeal that actually makes when it's cooked right. It's like six cups of oatmeal or something. So I'd, you know, you know, I was always sort of glycogen loading.

But you can only load 2,500 calories of glycogen in your muscles, so you run out of that pretty quick if you're swimming for six hours.

Yeah. So then you're drinking your Gatorade and Powerade and you know, hammer perpetuum and all the sport drinks of the time. Yeah.

And that, and that led to this pre diabetes state. And then you kind of figured out that this carb loading and even though it was healthy, carbs still wasn't the solution. And you sort of discovered that if you actually cut out all that starch and sugar and started eating a lot of fat, it changed everything and you actually became a ketogenic for a while.

Yeah, I actually spent, you know, the journey started and for about two years I was really tinkering with carbs and, you know, which ones could be reduced, which ones could be maintained, et cetera. But, you know, it's sort of, in the end, I got to a point where the last thing I could try was this sort of at the time, really out there idea of nutritional ketosis. There weren't really a lot of people talking about it. There was not.

Like every bestseller book was keto, right?

Yeah. Nowadays, it's funny, it was. That was only eight years ago. And to think how much has happened since then. But at the time, you know, you had a guy named Steve Finney, who I still in many ways think of as arguably the most knowledgeable person around today when it comes to understanding the ins and outs of nutritional ketosis. A colleague of his named Jeff Volek, and they were Basically the only two. There was a guy named Lyle McDonald who had written a book on the topic, but he was just a hard guy to get a hold of. He wasn't someone that I just couldn't get a hold of him.

And those guys wrote a book called the Art of Low Carbohydrates.

They hadn't written it yet, but there was a book that they were in the process of writing called the Art and Science of Low Carbohydrate Living. And so I got an early pre release copy of that, plus just their mentorship and constant emails and phone calls as I started sort of tinkering through it.

Again. I haven't read a single book on keto, so I can't, certainly not in a very long time. But I still think that that first book they wrote, the Art and Science of Low Carbohydrate Living, is one of the best resources on this. If someone said, hey, I just want to read one book on how to do this, what's the book? I actually always sort of send them that way, although I'm sure they've written something much better since.

But yeah, I actually studied that book a lot when I wrote my book, Eat Fat, Get Thin, because I was really interested.

Yeah, no, it's. I mean, Steve's devoted his whole life to understanding the physiology of this. And also as I began trying to do something a little bit different, which was how could I compete athletically on a diet that seems very counter to the prevailing wisdom of how we need to do this and that in that sense, I looked back at some of the work that Steve had done when he was doing his PhD at MIT, a very small study he had done in cyclists that I found quite interesting. And from there it just became sort of more of a. An interesting thing to tinker in. And I think I learned, at least for me, where those limitations were. Where was the ketogenic diet going to be in its sweet spot. And then where was it frankly to not serve you well?

And what was your experience with it?

Well, I think the ketogenic diet is a great diet for steady state activity below threshold. And I think.

And what does that mean for the average person?

Yeah, so your threshold, you know, we talk about that in cycling or running as the maximum pace you can sustain for an hour. So if you're a lay person, you might think, well, that can't be that fast because if it's an hour, but if you're an athlete, your all out one hour pace is still pretty brisk. I mean, that's like, for example, I don't train in those sports anymore. Like the amount of power I used to be able to put out for an hour, I couldn't put out today for six minutes. Not a chance. So whatever that number is, when you're fit, anything that's above that, I mean, the ketogenic diet is really not the optimal diet. You need the glycogen and in states of ketosis, you're simply not optimizing around that. You're really optimizing around what the mitochondria are doing. And.

So, for example, if you were going to try to win the Tour de France, I think there's huge benefits to eating less carbs than you probably think you need. But I just need some. You absolutely do. And by the way, some is relative. You probably need like 3 to 400 grams a day, which by the way.

Is not a lot.

It's, it's not. And again, those guys are just different animals. You know, they just have a different level of physiology. But, but I think that sort of, the pendulum has swung a little bit too far. And now I hear too many people, I think, making bold claims like, you know, carbohydrates are bad for any athlete and you know, everyone should be able to do everything perfectly on a ketogenic diet. And I think that's equally sort of flawed and sort of misleading.

I find if I, if I just eat way too.

Little carbohydrates and, and more fat, I'll start to lose weight. Yeah, too much weight.

And yeah, some people have that issue, some people don't. I mean, I'm, I'm similarly very responsive to carbohydrate restriction. Even just a, a week of going back into ketosis, which I always do before my week of fasting. You know, it's amazed at how much weight I lose. And it's not just water weight initially, it's obviously quite a bit of water Weight, you know, as you start to deplete glycogen, every gram of glycogen that you. You lose, you're gonna lose about 3 to 4 grams of water. Initially, it gets displaced into the plasma, but then ultimately you're gonna secrete it. So. So you're losing that water weight. But. But, I mean, I'm definitely mobilizing fat very quickly on that diet. But, you know, I've been humbled by the number of patients I've seen who you put them on a ketogenic diet and nothing budges. Yeah, they gain weight. So that's the other thing that I think just, you know, people have to sort of temper their enthusiasm for all of these things, otherwise you run the risk of making the same sort of.

Not one verse fits all. Not at all.

And if other things aren't working right, you know, if your sleep is not correct, if you're. If you have hypercorticolemia, if you have these other factors, in my experience, it's just really difficult to fix metabolic syndrome or metabolic dysregulation with just a nutritional hammer.

Yeah. And there's other factors. Right. That we know of. We know that your microbiome plays a role, that environmental toxins play a role, and things that are less obvious, not so dependent on what you eat or how much you exercise.

Yeah.

Which is striking. I mean, you know, there's animal studies literally can take a skinny mouse and give them bacteria from a fat mouse, and that skinny mouse becomes fat without eating any different amount.

Yeah, yeah.

And vice versa. They can lose weight by simply doing the reverse. So, you know, this sort of brings me to the whole issue of fat and cholesterol and heart disease and lipids and blood tests around cholesterol statins. It's a very messy field. And, you know, one of the challenges is that, you know, we hear, and I think we've sort of gotten over this, that fat makes you fat and that fat causes heart disease. I think that's mostly been debunked, except for there's still a pretty hefty group of scientists who are saying that we should not eat saturated fat.

And.

And that, you know, if your cholesterol is high, you need statins. And it's. It's pretty LDL focused, which is LDL cholesterol, which is basically the test you get at your regular doctor's test. But you've gone into this in a really robust way. And for people who are interested, there's nine.

Articles on Peter's website. Peteratti md.com, which go into this.

So if you're in truth, I think those are so dated right now. Mark. I wrote that series in.

2012, 2013, and in terms of our understanding of this space.

I almost would be embarrassed to go back and read those when I contrast it with how much more is understood today. So if people are really interested, what I'd actually direct them towards is a few podcasts that I've done with the world's experts. The thing is, I'm not a world's experts.

Podcast is the drive.

That's right, yeah. So you can. Which you can find through there.

Great podcast.

And so there's an interview I did with Ron Kraus, which is one interview. And then there's a five part series I did with Tom Dayspring, who, you know, these would be two of the five most knowledgeable people on the planet, not in the country, on the planet when it comes to this topic. And you know, so, so that's the. Those would, to me be the best references on the nuances of this topic. And you know, the nice thing about Ron and Tom is they're both super interested in the nutritional side of this as well. In other words, they don't just come at this through the lens of, of the pharmacologic hammer is the only approach. And I think they also just bring with them sort of the humility that says, look, we don't know everything. In fact, we clearly don't. Because, you know, as the saying goes, the further you get from the shore, the deeper the water gets. So, you know, for example, like, here's something we don't know at all today that I think we thought we knew seven years ago. We thought we sort of understood HDL biology before. You know, everybody talks about HDL as the quote, unquote, good cholesterol, a term that makes me want to kill kittens.

Oh, no, our cats are hiding.

And we sort of thought we had a sense of what mattered, like a high HDL cholesterol was good. And we now know that that's, that's an association that's along for the ride. But any efforts to raise the cholesterol of HDL have either backfired and become harmful or at best, not helpful.

And there's no such thing as hdl. There are many varieties of it. Right?

Sure. And it turns out that it's the function of the HDL that matters. And yet we don't have a test to measure HDL functionality. So I'm almost at the point where I don't I think it's safe to say I almost don't even pay attention to HDL anymore.

Really? Someone's got an HDL 39, you don't worry.

I mean, a. There's nothing I can do about it other than if I believe that it is a consequence of metabolic dysregulation, which we're going to try to correct anyway. But whether I know the cholesterol content of the HDL particle, the number of HDL particles, or the size of the HDL particles, none of these seems to be good enough proxies for the function of hdl, the ability to delipidate, which.

Is, it's like the vacuum cleaner that cleans up the cholesterol in your system.

And in fact, we see the opposite, right? There are lots of case studies and I've seen clinical examples of patients with very, very high HDL cholesterol. And you think, oh, this is fantastic. And they have devastating cardiovascular disease because their high HDL is the result of their HDL being so backed up that they can't actually function. So they aren't able to go in there, delipidate. They're these totally backed up full. So we call, these patients have something called hyper alpha, like health, hyper alpha lipoproteinemias, very, you know, rare nerdy disorders. But, you know, these, these people will show up with HDL cholesterols of 100 milligrams per deciliter and higher. So, you know, I think we know a few things, and I think those few things are at least enough for us to make a decision today. Because every time you make a decision.

I mean, what, how do you figure this out? Because when people go to the doctor, they don't really get the state of the art cholesterol test today. Right. And we're still practicing 20th century medicine in the 21st century, right. And you talk about testing particle size, particle number, looking at it quite differently than most doctors. That's the first step, right? So figuring out what, what.

Yeah, the first step is hopefully finding a doctor who can do some advanced testing. And, and so the most important part of the advanced test for me is really twofold. I mean, there's, there's. So the first thing I do before I do any of this stuff, I sort of explain to patients what are we doing? We're using a blood test to try to approximate your risk of heart disease. So the first thing I want to do is understand what are the drivers of heart disease, how many of these things can be measured in the blood, because you always have blind spots when you do a test. You can't do a test and say, well, now I know everything about this patient. And so what I always do with patients is I. And it takes about 30 or 40 minutes. The very first time we review labs is I go through atherosclerosis, cancer, Alzheimer's disease, every single thing that one might ever care about. And I talk about what we believe today, the drivers are of those diseases, how we can measure each of these things. And then by the end, you have this huge map of everything that we believe is known and what we don't know. So at the very least from a sort of Rumsfeld like perspective, we have our known knowns and our known unknowns. We still have blind spots we can't see. But when it comes to cardiovascular, you say, look, basically four big drivers of this disease outside of smoking and hypertension. So those are huge drivers of this disease. But they're a. We don't really look for huge markers of them in the bloodstream. And secondly, we sort of, we look at the behavior and we look to fix that. But when it comes to, at the cellular level, we think of the lipoprotein, we think of the underlying state of metabolism, we think of inflammation, we think about endothelial function, and then we double click on each of those. So what does that mean? So the lipoprotein, which is the little particle that's going to carry the sterol into the subendothelial space provided.

In English means. You mean the, the carrier for the cholesterol particle that gets into your arteries.

That's right. And so, so let maybe start at the beginning. You've got this endothelium, which is this thin single cell layer that lines the artery. Okay.

So that's your barrier, like your Teflon barrier inside your.

That's right. So, so the first thing I say is, why is smoking at high blood pressure? Why are they bad? Well, they're bad because they, they, they reduce the efficacy of that barrier. So anything that's going to make it easier. Yeah. For something to cross them, that's going to be a bad start. So the, the first thing that we realize is lots of particles cross that barrier and most of them come right back out. So it's not the crossing of the barrier that isn't of itself problematic. It's the retention of a particle. It's getting stuck in there. And then it's this chemical reaction called oxidation.

It's rusting.

Yeah, yeah, effectively. I mean, it's a bit of an oversimplification, but I think for the purposes.

That goes rancid, that sort of oxidation.

Right, yeah, that's a nice way to think about it. And it's that oxidation that creates an.

Inflammatory response, which is what causes heart disease, Alzheimer's, cancer.

Well, I mean, I think it's hard for me to just say that. I mean, I would say that inflammation plays a role probably in most diseases, but of course, mostly inflammation does good stuff for us. I mean, if we didn't have an immune system and we couldn't mount an inflammatory response, we wouldn't be sitting here right now. We would have died in utero or shortly thereafter. So our immune system's doing its best, but on some level, when it comes to these lipoproteins depositing their cholesterol in the wall, a chemical signal gets kicked off. And the chemical signal is a warning. And that's something that we can measure both specifically and non specifically in the blood. So an example of that that I would hope every doctor measures is C reactive protein.

Yeah.

So the problem is those aren't very specific. Yeah.

You can blood test for inflammation. You could have an infection, a sore throat, or you could have heart disease.

That's right. And you know, the extremes are good. When someone has a C reactive protein of 0.3 or 30, you're, you're, you're, you know, you feel better. Because the 30 is not heart disease. The 30 is that person's sick.

Right.

Like, you know, then they usually know they're sick. And then, but then we look at very specific markers of inflammation that may be more unique to this case. So something like LpPLA2, which is an endothelial enzyme or oxidized LDL specifically. And then we look at these other metabolisms.

And by the way, those are tests that are available at a regular lab. Most doctors don't.

That's right, yeah. So our cardiovascular panel is not just looking at the lipoproteins, of which there are four. We pay close attention to really three, if I'm really going to be pushed to it. And we like to do things in threes. It's lp, which is, you know, to me, the worst atrocity in modern medicine today when you consider that cardiovascular disease is the leading cause of death in this country. And when you combine it with cerebrovascular disease, I think of this as atherosclerotic disease.

Right.

These are far ahead of cancer. Even though people say, well, cancer is going to surpass heart disease in 20 years or maybe less. But atherosclerosis is the only inevitable disease of our species.

It's hardening of the arteries.

Yeah, it's this inflammatory process of the arteries that ultimately leads to heart attack, stroke, things like that. So atherosclerosis is inevitable. And somewhere between 8 and 12% of people are walking around with a genetic predisposition to it in the form of this special type of LDL called lp. So it's just like an LDL particle, but it has a little extra apolipoprotein attached to it. And unfortunately, the nomenclature of lipidology doesn't serve it well when it comes to communicating it.

Confusing.

Yeah, yeah, yeah.

So it's genetic, though. We don't.

It's genetic test for it.

But you can change it.

You can't change it yet. I mean, you can, using one drug.

Go up and down. Yeah.

It'S.

It's. It's an acute phase reactant, so it can move a little bit, but. But as a general rule, it doesn't. As a general rul, what we do is we treat residual risk with the ldl. There is a drug right now called an antisense oligonucleotide that's in phase three to lower it, so it attacks the DNA.

Cycle of making the apo little A. So the. So when that drug works, which it seems to work very well, you basically take an injection twice a year and it wipes out apo little A, which means you have no lp. So one, you got to know that you have to know a person's LDL particle number. So you alluded to cart cholesterol. That's the one that most people get. So when someone says, I went to the doctor and my LDL is 100, what they're saying is my LDL cholesterol is 100 milligrams per deciliter or 6 millimolar or whatever, depending on what units you're using. And that's just saying what's the concentration of all the cholesterol contained within the LDL particles?

It's the weight of it in your blood, basically.

Yes. Well, it's the density, right? So mass per unit volume of the cholesterol in the particle. Now, that has some predictive capacity, but it's not actually great. And if you look at the really good data, both in the largest cohorts that have ever been studied, in both the Framingham population and the MESA population, the number of particles turns out to be much more predictive. And in fact, anytime and every time particle number so how many of those LDL particles do you have, which you can do either directly through some techniques in chemistry or indirectly by measuring something called apob? Because every LDL particle has one of these little APOB things sitting on it. If you count those, you count the particles every time you put these head to head, it's no comparison.

Yeah.

Knowing the number of particles always beats the cholesterol concentration in terms of predicting risk.

So to break it down, if you have a cholesterol LDL of 100, you could have 3,000 particles, or you could have 300 particles, and you get the same number when you go to the doctor, with totally different implications for your risk of heart disease.

Right. And more commonly, it wouldn't be that much of a spread. But to give you a real example, you could have an LDL cholesterol of 100 milligrams per deciliter, which places you at about the 20th percentile of the population. And I think most people would say if your goal is primary prevention, there's nothing wrong with that. But that person could have 700 nanomole per liter of particles, which would be very low. That's the fifth percentile. So they're discordant in the right direction.

Yeah.

Or they could have 1500 particles placing them at closer to the 70th or 75th percentile. And they're discordant in the wrong direction.

Yeah.

And then on top of that, everything I've said tells you nothing about their LP.

Right.

So that person could have an LP, which normal would be less than 50 nanomole per liter in terms of the particle number. And if that person is walking around at 150, even if their LDL particle number is normal, they're still at greater risk of not just atherosclerosis, but aortic stenosis as well.

Yeah. I tell my patients, I said, make sure you tell your doctor to get an nmr, which is basically a MRI of your cholesterol. Look at the number particles sometimes. There's another test called Cardio IQ, which is quest, but NMR is through LabCorp. Cardio IQ is request they measure those things, and they're valid and they're not that expensive, and they're available.

The good news is now there's an even more accurate test than NMR called electrophoresis. So centrifugation electrophoresis are ways that actually insurance companies are now reimbursing for. So. So we've actually switched over in the past few months to using electrophoresis to measure LDL particle number as opposed to nmr.

Some people say that we should focus on not only the particle number, but also on how many small particles there are, because you can have.

Yeah. This is an interesting discussion I get into with Ron Kraus in that podcast, because Ron is in the camp that says the size of the particles independent of the number of particles also matters. So if you had somebody that had a thousand particles, but their distribution was mostly small, they're in worse situations.

Six or seven hundred.

That's right. Then the reverse.

And.

And I. I think that is probably the case, but I. The. The reason I don't fixate on that number is I don't have a direct treatment for it. In other words, I can indirectly try to address that because that seems to run as a proxy to metabolic health. In other words, nobody would deny that patients with smaller particles, all things equal when compared to patients with large particles, are metabolically less healthy. So I tend to focus on things where I feel like I can more directly impact it, such as their insulin level, their average glucose level, things where their triglyceride level.

Double clicking on the metabolic.

That's right.

Tab. So when you click on that tab, what do you. What do you see? And how does it relate to the cholesterol? Because you just hinted at it, that insulin, blood sugar, that may be the driver of these abnormal.

We know glucose and insulin play a really intimate relationship when it comes to vascular disease, and we learned this by the studies that have been done in patients with type 2 diabetes. So most people know that type 2 diabetes is a condition of. Well, I shouldn't say most people. I would say most people would not define it the way I'm about to define it, which is. Type 2 diabetes is a disorder of carbohydrate intolerance.

Yeah.

So, again, that's not a. That would be sort of a controversial definition in some circles, but I think between guys like us, that's. To me, it's the most logical explanation possible. So if you have a disorder of carbohydrate metabolism, you are not able to metabolize whatever carbohydrate load you have, your glucose levels are going to be higher and higher and higher. And so the diagnosis of diabetes is made, in my opinion, poorly by using this proxy, or of average blood glucose called the hemoglobin A1C. And once a patient's level reaches a 6.5%, which corresponds to an approximate average of something like 130 to 140 milligrams per deciliter, we Say that's the threshold. I could talk for hours on why I disagree with that approach, but directionally, it yields a reasonable answer. Right. Someone with a hemoglobin A1C of 5% versus 7.5%. There's a clear difference in those people. Now, studies to lower glucose have found interesting things. The first is if you lower glucose with insulin, so you take those patients. Well, it makes some things worse and some things better.

Blood sugar better, but makes blood sugar better.

Yeah. So why is that? Because there's more to the story. Right. When you give those patients more insulin and you lower their blood sugar, you actually do fix something. You fix their microvascular disease. They do need less amputations. They have less kidney destruction. Their erections are better. Right.

Blindness.

Blindness is better. Exactly. So you do fix the microvascular stuff. The really, really, really tiny blood vessels that you can't see with your eye, Those get better in response to aggressive glucose lowering using insulin. But the point you made a second ago can't be forgotten, which is their mortality doesn't improve. Yeah.

Their heart disease goes up, their strokes.

And heart disease go up as there's their aortic disease. And that offers us an insight into the role that insulin and glucose play, which is that insulin is probably damaging to the macrovascular disease. So the reason their microvascular disease is probably getting better is they have less of that glycosylated hemoglobin that is actually creating this mechanical obstruction in those tiny, tiny, tiny blood vessels. The best tool is a tool that can lower glucose and lower insulin. And while there's, you know, drugs like metformin that can do that, there's really nothing that beats nutritional biochemistry as the strategy for that.

Yeah, no. I shared a story the other day on the podcast. There's this woman at Cleveland Clinic who came in with, you know, BMI of 43. She was. That's very overweight. Normal is less than 25. She had diabetes for 10 years on lots of insulin. Heart failure, ejection fraction 35%, renal insufficiency. You know, kidneys weren't working. Liver was trashed. High blood pressure. And within three days of putting her on a very low carbohydrate, higher fat diet, not keto, but, you know, some version in the middle. She got off insulin within three months. Her blood sugar was normal. She was awful. Her meds, she lost 43 pounds. Her ejection fraction was 54%, which is normal. And her kidney functions got better. And every year, she lost 116 pounds. And it was all through food. So food is. When you think about a drug, if there was a drug that could cure high blood pressure, cure diabetes, cure heart failure, cure kidney failure, cure liver failure. Oh, my God, it buys stock right away. But there is. It's called food, except it's not patentable.

Yeah. And look, it's harder, Right. I mean, the reason we, I think, are. The reason we like drugs is they're. The effectiveness is higher. So food, I think, has more efficacy for the most part. It depends on the situation. But as a general rule for metabolic health, food by far has the most efficacy or absence of food. I would argue fasting is the single most important tool we have in our nutritional toolkit.

But the effectiveness, which means the ease with which one can implement it, tends to be higher. So pills have less efficacy, meaning when taken perfectly, they don't work as well, but they're much easier to take if all you have to do is take a pill a day or a shot a day. Not that the compliance is perfect there, but it tends to be easier. So, again, my view is I just want to be agnostic to all of this stuff. And I tend to sort of, I don't know, shy away from the debate about medicine versus food the way I sort of. Because I do have patients that come in and say things like, well, I don't want to take any pills or I don't want to take any drugs. I'm willing to take supplements, but I'm not. And I just sort of look at them and I say, if I was your general contractor and you brought me in to build your house, and I said to you, listen, I don't use skill saws and I don't use hammers, and I only use Robertson screwdrivers. How would you feel? I mean, wouldn't that sight strike you as odd? Yeah, it's like.

How about a contractor who says, I have every tool there is and I'm quite facile at using them. And we'll spend all of our time trying to understand what's the best tool for the particular job. So. So I think there are five broad baskets of tools of which nutrition is one. Yeah. And drugs are one.

Yeah.

And I think we're solving a very hard problem.

And what are the other.

Everything that has to do with sleep, everything that has to do with exercise physiology, and everything that has to do with managing distress.

So stress. So stress.

I don't. I hate the word stress, Mark.

Distress.

Yeah. I think distress is much more. It's sort of Distress tolerance is really what it comes down to stress, I.

Mean, stress resiliency or it's, it's, it's.

Broader than that, but it's everything that fits around how you manage the endocrine response, physiologic response to distress, how you.

Manage your life, basically in your response to it.

Yeah. And it's, you know, this is something that I think up until, you know, four years ago, I dismissed as sort of outside of the purview of trying to live longer. I just didn't think that, that ma. I thought that was 100% sort of a function of your disposition as a person and it didn't matter that much. And, you know, and I interviewed Robert Sapolsky who wrote the why Zebras Get Ulcers recently, and it was just a wonderful discussion to really get into kind of the physiology of stress. And why is hypercorticolemia problematic? And this is when you get stressed.

Whether it's a real or imagined stress, it creates a response in your body that raises cortisol, which is the stress hormone and adrenaline. And that cortisol is great in the short term for running from a tiger, but it destroys your body over the long term.

Right. And because we didn't evolve around the long term stuff, it served us very well in the short term. Obviously, as you said, if you're in a situation of danger or, you know, you needed to get something done, evolutionary pressure was very good at driving that. But I mean, one, I think I would like to believe that we had more acute stress and less chronic stress as our ancestors, that is. And today it's probably flipped. We have less acute stress other than social media and more chronic stress. And so we're now sort of dealing with the long tail effect of hypercorticinemia in addition to some of the other hormones beside the glucocorticoids that do this. And I mean, cortisol to me is just such an interesting hormone. You know, one hormone that can do the same thing to the, can do two different things to the same cell, that there's not a lot of hormones that do that. So if you look at insulin, for example, insulin is always going to do the same thing to a fat cell. It is always promoting lipolysis.

So it is production of more fat cells, more fat.

It's making this, I'm sorry, not like doing the opposite. It's producing lipogenesis. So, so insulin is always making a fat CE matter. So on the, on the inside, on the door into the fat cell, it's Promoting esterification, taking these triglycerides, lumping them together and making them into their storage form and on the way.

High insulin prevents your fat cells from releasing them.

Well, that's the other point I was gonna make on the outdoor. It's doing the same thing. It's inhibiting the lipolysis. That's allowing these things to get out.

Well, that's important. Just pause there.

Very important.

Because. Because what, what, what Peter's saying is that when you eat a diet that raises your insulin, which is usually a diet that's high in starch and sugar, it puts the fat in the fat cells and it's a one way door. You can't get out. And so as long as your insulin's high, it's very tough to lose weight. Which is why low carbohydrate diets often work so well for weight loss.

Yeah, I mean, actually might be worth coming back to this. I think there are sort of, broadly speaking, like three macro phenotypes of obesity, and one of them is this hyperinsulinemic phenotype, which responds really well to carbohydrate restriction. But the point I wanted to make about cortisol is cortisol can do both. Cortisol can liberate fat from the fat cell. Because if you think about it, you're being attacked by a tiger. You want to burn through your creatine phosphate, your glycogen, but you also want a lot of fatty acids around. It's an all hands on deck, give me all the energy I have. So that actually requires lipolysis, or breaking fat out of the fat cell. So in that sense, it is catabolic to a fat cell, breaks it down. But cortisol also is anabolic to a fat cell. It can also put fat in. So if you think about this clinically, we see this all the time. Patients that are taking corticosteroids, prednisone, things like that, or even in disease states like Cushing's disease and things like that, these patients accumulate preternatural amounts of fat. I mean, it's enormous. But in the short run, cortisol can stimulate hormone sensitive lipase and actually break down fat. So I always found cortisol to be a misunderstood hormone, including by myself, and one that I'm just, you know, really excited to learn about because it also feeds into this other phenotype, which is I've seen patients with completely normal insulin levels who cannot lose an ounce.

Yeah.

And you put those patients on carbohydrate restricted Diets, nothing happens now. They'll gain weight. It doesn't, it doesn't mean anything. They're going to eat all the fat in the world and they'll get fat matter. And in these patients, you have to be looking at the other endocrine systems. And I sort of think of them as four big systems. The thyroid, adrenal, sex hormones, and then this fuel partitioning system of which insulin and glucagon are a big part of them. So I don't know, I would just.

Say you just said a lot in that sentence. And that is what Peter just said is some of the most important thinking in medicine, which is that what is the cocktail of hormones in your body? What are they doing at any one time? And how are they affecting your risk of disease, of diabetes, heart disease, death, you know, affecting longevity, affecting your mood? I mean, it's, it's so powerful. And they're modulated by all those things you talked about. They're modulated by diet, by exercise, by sleep.

Yep.

By how we interact with stress, by. And then medication sometimes.

And that's another great example. I mean, I've seen the phenotype of normal insulin levels.

I mean, just how to.

Yeah, so I've seen the, the sort of. I have normal insulin levels, I have seemingly normal cortisol levels, but that person's not sleeping. You know, that person sleeps four hours a night.

That person's gonna have a brutal time losing weight. It is really hard to get the body to, especially if they're eating, even if they're not eating horribly. But if they're just sort of grazing all day, if they're sort of feeding, if they're constantly being exposed to nutrients, which again, is more likely if you're, if you're awake 20 hours as opposed to being awake, say 16 hours, you've got four extra hours to feed. But also a lot of that feeding comes at a time of day when I think there's evidence emerging that the later you're consuming food, the worse all things equal. In fact, there's a study that just came out.

We had dinner before the podcast. Instead of.

We absolutely should. No, if it were, I mean, if I could be czar of the world for a day and change, one thing.

On that list would be completely changing the social structure around meals and making breakfast the dominant meal and totally inverting the way we do things. So in other words, if we could.

Eat from so intermittent fast on the back end, not on the front end.

Yeah, it would be if we could eat from 6am to 2pm and then, you know, go to bed at 8pm or something like that. Like if, you know, you would. I really believe that would have a profound impact on people's health. And there's experimental data to support this, including studies of patients. You know, Satchin Panda and colleagues just published something two weeks ago, I believe, looking at a study that took patients with type 2 diabetes and randomizing them. Well, they actually did a crossover, but there were two groups that you. So you were your own control and you crossed over into early versus late time restricted feeding. So meaning you were either eating from 8am to 4pm or noon to 8pm so same feeding window, same amount of food. Both groups had an enormous reduction in average glucose relative to their non crossed over self. But the early feeding window had lower average glucose than the late feeding window.

Interesting.

And, and again, I think that's consistent with the animal literature that says we are more insulin sensitive in the morning.

Okay, so backing up a little bit.

When you talk about phenotypes, you talk about there are different types of obesity. It's not uniform.

Right.

And there are different types of profiles of your cholesterol and it's not all uniform and they don't respond uniformly. I have, I have patient, just two interesting patients. One had the worst lipid profile with, you know, a total cholesterol of 300, triglycerides of 300, an HDL of like 30. This is terrible numbers. And her particle numbers were really high, over 2000 for LDL. And really struggled to lose weight, tried to do the right things. So I put her in a ketogenic diet, cross my fingers, she dropped 20 pounds like that. Her numbers plummeted. Her cholesterol went to 200, her triglycerides went to under 100, her HDL popped up 40 points. And I was like, this is impressive. So another guy, but he wasn't overweight, similar profile, it actually didn't change. And he was a biker, he exercised, and he's probably what we call the lean mass hyper responders. And I think I'm probably in that category because if I tend to eat more saturated fat, I'll see my lipids get worse, whereas others get better. So we say saturated fat is a good or bad. The answer is sort of it depends. Right.

That's my take, Mark. I mean this is a controversial topic and I'm probably at the limits to which I'm interested in talking about it because I've spent so much time talking about it. My view on this is.

So it Comes down to the belief, which is, are lipoproteins necessary but not sufficient for atherosclerosis? That's a very important question in biology. We always have to ask that question about anything we're trying to figure out. Right. Is an APOE gene necessary but not sufficient? Necessary and sufficient. Neither necessary nor sufficient for someone to get Alzheimer's disease. And we have to be able to unpack everything that way. I think the evidence with atherosclerosis and lipoproteins is as close to unambiguous as you can get in medicine and biology, which is to say the lipoprotein, the LDL thing that we talk about is a necessary but not sufficient condition for atherosclerosis. In other words, you can't get atherosclerosis if you don't have the lipoprotein. But just because you have the lipoprotein or a lot of them, doesn't mean you're going to get atherosclerosis.

It was not a one to one correlation.

No. And the debate, which makes it really confusing. It absolutely does. And unfortunately that's biology. But look, that's most things. Smoking is neither necessary nor sufficient to get heart disease, but it's still causal.

Yeah.

This is very important. Let me repeat it. You don't have to smoke to get heart disease and just because you smoke, you're not going to get heart disease. So it's neither necessary nor sufficient. But would anybody dispute the causal relationship between smoking and atherosclerosis? No. What about hypertension? It's neither necessary nor sufficient. You can get tons of heart disease with normal blood pressure and you can have raging high blood pressure and not get heart disease. Would anybody at this point dispute the causal relationship between hypertension and atherosclerosis? No. Yet somehow when we come to lipids, people get all phosphorylated over the fact that, that you can have high ldl.

They're foaming at the mouth.

Yeah, they're just, they're just.

That's a fancy metaphor.

They're foaming at the mouth. Yeah, yeah. And so, so, so people will say one of the arguments is, well look, you know, so and so is on a great diet, he's on a ketogenic diet, his LDL is through the roof. But look, his insulin is low, his hemoglobin A1C is low, he's metabolically healthy, he can't get heart disease.

Yeah.

To which I would argue, by what logic? Like what is the evidence to suggest that I would Argue that certainly someone with high LDL who's metabolically healthy is in a much better shape than somebody who has a high LDL who's metabolically unhealthy. Of course, there is benefit in being metabolically healthy, but given that we don't really have the data, which I think is the argument of, do we have a cohort of 10,000 people on ketogenic diets who are in the phenotype you've described, which means they have. They're metabolically healthy, but they have sky high LDL, and we have followed them for 40 years.

Yeah.

Do we have that cohort? Because if we do, we could get the answer to the question. In the absence of that, my rational brain, whatever says, look, we have to abide by the precautionary principle, which is, in my mind, those patients should be treated. So with a statin, it depends. Again, there are four ways that LDL gets driven. LDL particle is driven by four things. The first is by the burden of triglyceride you have to carry. So the more triglycerides you have, the more of those particles you need, because those particles are carrying not just cholesterol, but triglyceride. So the first thing I'm always asking is, what is the burden of triglyceride? And if the LDL particle is high and the triglyceride is high, those patients will often respond very well to nutritional therapy. But if they don't, they're the normal.

Triglyceride, then it's not as easy.

Or if they don't respond. So.

I just actually saw a patient for the first time last week, and his trigs were a thousand.

Well, that's a genetic thing.

Exactly. But, you know, the funny thing is the doctors he was seeing before didn't seem that concerned about it because he had normal LDL cholesterol. So he had an LDL cholesterol of 130, which is about the 50th percentile. He's young. He's 38. But his trigs have historically varied between 300 and 1,000.

And again, that's just an example of. I don't want to say bad medicine, but it is. It's just bad medicine. Right. One, when you count his particles, they're through the roof, because his particles aren't just having to carry around all of the cholesterol that you measure in the LDL cholesterol, but also the triglycerides. And secondly, he has. He does have a con. He has a type 3 lipoproteinemia. 3B. And so he's at risk not just from his LDL. Even if you drive his LDL down to zero with all the drugs in the world, his risk is still sky high because his VLDL remnants are going to stick around forever. Yeah, so these are patients that need to be on another class of drug called fenofibrates to lower the triglycerides. You have to lower the triglyceride specifically. So then the next way, the next trick we have up our sleeve is we lower cholesterol synthesis. And that's the drug of choice. There is a statin. Statins inhibit an enzyme that is in the early part of the pathway for making cholesterol. And so by giving that enzyme, we reduce cholesterol synthesis. Now, most of the efficacy of statins probably doesn't come from the reduced cholesterol synthesis. It's that it plays a little trick on the liver. And the liver upregulates LDL receptors and it pulls more LDL out of circulation.

It's also an anti inflammatory and an antioxidant.

It almost assuredly has benefits from both of those things as well. So these sort of so called pleiotrophic benefits that come from its benefits beyond lipid lowering. And I don't think it's an accident, by the way that statins occur in nature. I have this shtick that I think.

It'S on Chinese red roast pork. That's all red. That's. What's that?

Yeah, I mean, I, I don't think it's an accident that the three most, in my opinion, impressive drugs in the toolkit of longevity are all naturally occurring. Because.

Okay. Which are.

Well, I think rapamycin, metformin and statins. And, and they're. And the reason, which is not to say everybody should be on any or all of these drugs, but I just think these are drugs that do something. Each of them attacks or targets a very important piece of our biology that if, if you didn't know any better, and I just said, hey Mark, I got a great idea for you. Let's, let's come up with a drug that stops mtor. You'd be like, that's a crazy idea. Like MTOR is so central to your existence. Well, okay, fine. Or with, you know, but. Or I said, let's go after a drug that targets complex one of the mitochondria. I mean, that sounds crazy. It shouldn't work. It should have profound toxicity. And yet the toxicity of statins, of metformin, of rapamycin is so low. And my totally unscientific rationale for that is all of these things occurred in nature, and nature's super smart. And for example, the bacteria that secreted rapamycin, which is how rapamycin was discovered on Easter island, they had a billion years to work out the kinks of having something that was toxic enough to kill off the yeast that it was fighting, but not so toxic to kill itself.

A natural antibiotic.

Yeah, I sort of think of that again. Antibiotics are another great example. Right. Naturally occurring compounds that do remarkable things but have surprisingly low toxicity. So. So anyway, so that's the second category. The third category is cholesterol absorption. So you. And you can measure how much a person synthesizes or absorbs by looking at proxies. So you can look at intermediaries of the cholesterol synthetic pathway and measure their synthesis.

You can.

Absolutely. Nothing I'm talking to that, nothing I'm talking about here is hard to find.

You're going to get. When you go to your doctor, he's not going to say, well, you're a high cholesterol absorber, you're more of a synthesizer, or you're both, or you're neither.

That's right.

You're not going to get that information, but it's available through commercially available tests.

I mean, I guess I take for granted that I have these tests and that every time I get to make a decision about this thing, I get to look at those tests. But I feel bad for docs that are trying to make these decisions without.

Those decisions, looking through goggles that are completely fogged up and trying to make a decision to do. I'm in shock. I mean, I've been testing these things for 20 years when no one was testing them and people thought I was crazy. Crp. Why would you ever check that? That's a waste of money. Lipid particles. It wasn't even. It was a small little lab, I think, somewhere in the Southeast that was doing this. And I used to work with them. Now it's. It's more out there. But, you know, Ron Kraus you're talking about, he figured this out like 40 years ago.

Yeah, I mean, you know, Ron's. Ron's been a very steadfast and yet sort of modest, quiet champion of this stuff. Alan Snyderman basically, you know, figured out the importance of this thing called APOB and how these number of APOB particles mattered. I mean, Alan is in Canada. He's at McGill University also. Just an incredibly close mentor, actually, someone I really hope to have on the podcast, because, I mean, between, you know, Ron and Tom and Alan, I mean, he's, as you noted in the introduction, I mean, that's how I've been able to learn this stuff. It's that I've got people like that in every subspecialty and every little nook and cranny and whole of medicine that have just been so generous with sort of sharing this knowledge with me. And then, so, so then cholesterol absorption, as you said, we can measure this. We look at phytosterols, we look at stanols, they tell us how much they're absorbing. And, you know, just today I saw a patient with, you know, her LDLP is. Her LDLP particle number is actually reasonable, but her family history is pretty bad. She actually has some calcifications in her coronary arter, so we're not at goal yet. She's already on a statin, not a high dose. But when you see her sterols, you realize the wrong answer is to just hammer her with more statin when I have this totally other target of these, you know, profound high absorption. So we give her a different type of drug that actually blocks the absorption of her sterol.

A bile acid block.

No, I gave her a Zetia azetamide. Yeah. The bile acid sequestrants are. They work, but they're not that well tolerated. Yeah. And then the last thing is, if you have patients who have normal triglycerides, normal synthesis, normal absorption, or even hypo, you know, they're hypoactive on those things and they still have sky high levels. You know, these patients usually fit into a category called familial hypercholesterolemia, where they have a defective. They have defective LDL receptors. And even though there are literally thousands of SNPs that make up this very heterogeneous variation. That's right. That make up this genetic sort of heterogeneous population, there are lots of people that don't rise to the level of having familial hypercholesterolemia, but they still have the same issue, which is defective LDL receptors. And so you can treat them indirectly with a statin, although I like to be very careful of that. If they don't synthesize too much cholesterol. I don't like giving statins to patients that don't have a high degree of cholesterol synthesis. And we have a new drug now that's been around for four, maybe close to five years now called PCSK9 inhibitors. And of course, there's issues with these drugs. They're not cheap. Right. And they're not going to be approved for most patients unless they have very advanced disease, they've already had a heart attack, or they in fact have familial hypercholesterolemia. But, you know, I probably have a dozen patients taking PCSK9 inhibitors as well. And they're remarkable drugs. Which, bringing it back to something you asked about earlier, also lower L.P. in most patients by about a third.

But, you know, it's interesting. You write that, you know, cholesterol is essential for life.

Absolutely.

It's not something that's bad. It's part of every cell membrane. It's what your sex hormones are made from. You know, it's essential.

And yet you hear some cardiologists going, let's get it down to zero. Like, let's just use these, these new drugs, these p, C, K, S9, well, inhibitors, and get them.

But remember, what we're measuring in the blood, which is what they're talking about, is largely irrelevant. I mean, the. So when you look at how PCSK9 inhibitors came about, they came about after a really interesting paper in the New England Journal of medicine circa 2004. It's a very recent discovery, which was this population of people that had mutations of PCSK9. So they, the first group that were found were people that had hyperactive PCSK9. So what is PCSK9, aside from being a mouthful? It is an enzyme, sort of an enzyme. You should really technically refer to it as a protein, but functionally it's an enzyme that degrades LDL receptors. So remember, and again, this, you can start to see why the layers of complexity make it such that it's just easier to take a black and white view of this stuff. Because if not, you then have to get into these details of your liver has LDL receptors, you got this protein, it can break them down. And if you have a hyperactive version of that enzyme, which a subset of people do, you are constantly breaking down the LDL receptors. Your LDL goes through the roof. These people are getting ravaged by heart disease. So that population was discovered first, but then more recently, a population of the opposite were discovered. These people had hypoactive PCSK9. So their enzyme was pretty pathetic. And therefore they were just growing LDL receptors all day long. They were staying there and their LDL was really low. Again, these numbers were measured in LDL cholesterol level, but they were typically 10 to 20 milligrams per deciliter. I mean, you would Incredibly low. Incredibly low. And guess what? They never got heart disease. And guess what? They also didn't seem to get any more cancer, Alzheimer's disease, or any other bad things as well. And I think for some people, that really stumps them because on the one hand, we're saying cholesterol is vital for life, which it is. But on the other hand, they're saying, but how can these people have such low cholesterol and be so functioning? And it basically comes down to realizing how narrow a window it is to look in the body at just the lipoproteins in the bloodstream. The lipoproteins in the bloodstream are just the things that are trafficking cholesterol between cells and back to the liver and unfortunately, sometimes over to the arteries of the heart, and fortunately, sometimes from the artery of the heart back to the liver and doing forward and reverse cholesterol transport. But it's, you know, you want to talk about how narrow a view that is, that's sort of like trying to look through, you know, a tiny, tiny crack in a door and actually see everything inside of a building. I mean, it's a. It's a grotesquely simplified view. The reality of it is every organ, every cell in the body makes cholesterol. Every single cell. There's some debate about whether there are certain cells that maybe can't do it as well. But the bottom line is every cell makes cholesterol. And we have to sort of also trust nature a little bit. I just, I think during the process of evolution, which was optimized around our early survival and reproduction, there is simply no way the body wouldn't have 150 redundant ways to make sure we had enough cholesterol. Because as you point out, essential for life, if you, if you don't have cholesterol in your cell, you're gone. Yeah, there are, there are rare genetic disorders of low cholesterol, like synthesis and function, and these babies die in utero. I mean, these are rare, rare, unheard of things. You know, anything that's going to prevent you from making sex hormones, forget about it. You would have figured that a long time ago. Yeah, so. So, look, I'm not suggesting that everybody needs to walk around with an LDL cholesterol of 10 or 20, and I don't manage any of my patients to that level. And nor do I feel that statins should be in the drinking water, which is the extreme opposite view.

You know, it's like the amount of promotion of prevention for statins seems to be out sort of pacing the science of it. I'm not against statins, but I think they're used excessively. And I think that I always have the question in my mind of, you know, if you're doing it in such a targeted, specific way that you are, it makes sense if you're just saying, like anybody with an LDL over 100, we need to get down to everybody. Everybody gets on statin. There's mitochondrial injury, which we'll get into the longevity conversation in a minute, affects longevity. It seems to be linked to increased risk of diabetes and then some resistance.

Yeah, I mean, that's the most quantifiable risk is there is clearly an increase in the risk of type 2 diabetes, but it's also important to quantify it. Right. It's in absolute risk. It's actually quite small.

But also the muscle effects are real.

Yeah, the muscle effects are real. And we talk about this with Ron. I talk about this at length with Ron Krause. So they reported the, in the literature, the incidence of myalgia is this muscle pain with statins is about 5%. I think most clinicians feel it's closer to 10%.

Yeah. Or more. I mean, I just, you know, an average doctor, I'm not a cardiologist, and I see, you know, lots of patients and it seems to be just the sniff test. A lot of patients have intolerance of statins with muscle pain and aching and even without their muscle enzymes going up.

Yeah, well, and you're, you're, you know, that's a good point. Right. It's not necessarily correlated with the ck and it's not correlated with the, with lfts. And it's challenging because I think a big part of it is the placebo effect as well. There's just no denying the power of the placebo effect. So it's really hard to study this. And that's why I think studies of self reported, you know, myalgias have reported as high as one third. Again, I said the literature says about 4.9%. I think it's probably in the 10% ballpark. But the other thing that I think most doctors aren't paying enough attention to is just how many statins are out there and how. I mean, I've had patients that absolutely, positively have to be on a statin. It's, you know, it's, you know, it's really in their best interest. And when you cycle through the really popular ones, Crestor and Lipitor, they really experience pain. And I believe the pain is real. Again, even if it's the placebo effect, it doesn't matter. If they're experiencing pain, they're experiencing pain. So. But a lot of doctors don't realize you've got things like Livalo out there which are far less potent, meaning they're not going to do as great a job at lowering ldl, but they are going to spare them a lot of those symptoms. I've been using Prevastatin a lot, which is a very old school statin. Yes.

It's less toxic.

Oh my God. It's way. Prevacol is basically pharma grade red yeast rice. It really is. It's really, you know, 80 milligrams of Prevacol is comparable to about 2,400 milligrams of red yeast rice.

Yeah. Which I found it worked really well in some patients.

Absolutely. It just comes with the advantage of being pharmaceutical grade. So.

No, I mean, I think.

Yes. Yes. Yeah. No, just meaning, like you could argue they're equivalent, but I sometimes, unless the patient is really adamant against not taking a drug for whatever reason, then I'll say, fine, but, but anyway. So you also have to partly just sort of be nuanced in your approach to these drugs. I mean, there's like, like, you know, a dozen statins out there. Not a dozen, but they're close enough. So it's, it's, it's. I think you just, you just have to take the time to sort of play with these things and figure out what the right cocktail is and then.

What'S the minimum effect responders, you know, with where they eat fat and they get high cholesterol. Right, right. More particles. Do those people need statins?

In my opinion, it's just a question. It's just, look, it's just a question of like, do you want to play with fire? So, so, you know, one argument is, well, you can get more information and I don't see any harm in doing that. So if you do something like calcium score. But again, it's important to understand these calcium scores are, you know, calcium scores give you a two by two of information. Right. So either the score is high or low and the patient is young or old. And I actually talk about this at length on a podcast with Ethan Weiss. And we, he's a preventive cardiologist at ucsf, really a bright guy. And what we talk about is, look, you've got.

You'Ve got two squares of that, two categories of that four square that are not particularly helpful. So an older patient with calcification, you sort of Expect that. So if a patient is, you know, 70 years old, not that that's even that old anymore, but you know, what we would say historically, you know, so someone who's 70 years old with a calcium score of 100, I've learned very little by the fact like that doesn't make me want to treat them any more or any less. Now an 80 year old with a calcium score of zero, all of a sudden, that's a different story. Maybe that's the person you don't need to treat if there's another contraindication to it. Similarly, when you talk about the young patient. So I had a patient yesterday, he's 48 years old.

His lipids are pretty wacky. And so I actually did a calcium score on him. I also did a CT angiogram on him for a different reason. And he was clean as a whistle. So I said, look, the good news is you're clean as a whistle. The bad news is I expect you to be clean as a whistle. You're 48 years old. I mean, people don't understand what calcium means, like how late a state that is the last and final stage of atherosclerosis. Yeah.

Instead of soft plaque, it's hard plaque.

It's the concrete on top of Chernobyl. So, you know, I'm all, I'm delighted that you don't have a calcium score at the age of 48. But that doesn't give you a clean bill of health. That just means that your 10 year risk is really low. I said, you know, the probability you're going to die of a heart attack by the time you're 58 is less than 2%. That's awesome. It's better than if it were more than 2%. But if you're playing the long game, and the long game is delaying atherosclerosis as long as possible, I'm just not sure on what planet you want to walk around with an LDL particle number through the roof. And again, I'm only interested in the long game because atherosclerosis is inevitable. Your risk of cancer and Alzheimer's disease starts to decline by your ninth decade. Not so with atherosclerosis. It's the only thing that rises monotonically.

Wow. Okay. So Speaking of being 100, let's pivot to longevity. This is a huge area of interest for you. You talked about the difference between your health span and your lifespan. And you talk about how do you get in the centenarian Olympics as opposed to just being alive when you're 100. And you've mapped out a number of things that, that are linked to more rapid aging and, and ways to address that. And the factors that seem to be coming up in the science are things like inflammation and mitochondrial issues, which is your energy factory, and the role of sugar and glucose, and some of these really interesting things that we can actually modify. So what's your view of the whole idea of how do we biohack our lifespan to get our health span to equal our lifespan? Meaning you.

Yeah, yeah.

Healthy till you die and then you just die, right?

Yep, I think.

But what are you going for? Because I'm curious.

Look, I mean, I. I just want to exceed what my genetic potential is. I mean, I think genetically I'm probably the guy who's wired to make it to his 80s.

So I use 100 as a mental model because I can picture how old my kids will be when I'm 100 and how old their kids will be and probably how old their kids kids will be. And I've mapped all this out not because I have any belief that I have some control over this or that somehow the world is predetermined in that way, but it allows me to think about how to reverse engineer this problem. So, you know, you talked about sort of the Centenarian Olympics, which is this idea that I developed about a year ago as a way to kind of communicate this to my patients, which says, you know, so back up for a second. Four years ago, I basically just stopped doing competitive sports. You know, I stopped, you know, doing like bike races where, you know, like you're trying to like win a little trophy or a medal or swim races or all these sorts of things. And, you know, I sort of felt a bit of a void in my life when I stopped in 2015, which was this is the first time in my life since I was 13. So that's almost 30 years where I don't have a goal. Like there's not a specific purpose that's taking me to the gym to do this thing, to train for this event.

Right.

And what I realized is actually I do. I have a much more important goal than I've ever thought of before. Because those other goals were quite arbitrary. Like how fast can you ride 40km.km on your bike or, you know, can you swim to Catalina Island? Those are interesting but quite arbitrary. But a much more interesting goal to me is how could I be the most kickass 100 year old to make sure that, you know, when my kids are in their 60s and their kids are in their 30s and their kids. Kids are the age of my kids today. What is the life that I imagine living? And I mapped out 18 things that I need to be able to do physically to feel fulfilled.

Wow.

Yeah. Very, very specific. Okay. I need to be able to carry four bags of groceries up a flight of stairs. Pardon me? Four bags of groceries up four flights.

Of stairs all at the same time.

Yeah, carry four. Because I could do that today. And I love the fact that I don't have to take an elevator to walk up to my apartment.

Okay.

Like, I like that. I need to be able to get up off the floor.

Which you have to do in New York, by the way. Like we have no elevator in our building. So you have to walk up the stairs with your groceries and your luggage.

Yeah, I need to be able to get up off the floor using a single point of support. And why do I realize that? Because I realized, like my boys who are two and five, we play on the floor a lot. Like we're playing with stuff. And I have to come to their world.

Yeah.

They're not going to come sit at the table and play with me. Right. I have to get on their floor and play with their toys there. And I love doing that. But you have to be able to get up after doing that. And it. I mean, how many hundred year olds do you see that can actually stand up on their own with a single point of support or even get up.

Out of a chair.

That's right. I have to be able to.

Which by the way, is why most people end up in a nursing home is not because of a disease, because they can't get up out of a chair anymore.

Yeah, this. This what I call. Well, there's a whole larger discussion, but I'll give you a few more. So I have to be able to put a 30 pound bag in an overhead compartment of an airplane. In other words, I want to be able to like travel through an airport and actually put my stuff away. And I noticed, I travel a lot and I noticed how many people can't actually put their bag up or take their bag down? And I just don't want to be that guy.

And not because they're short.

No, no. It's just like there's something wrong. Their shoulder, their back, something like that, their neck. I want to be able to pull myself out of a swimming pool without stairs. So you got to be able to like lift yourself up. So Anyway, I've got 18 of these things and look, they're subject to Change. I'm sure I'm going to think of other things, but they basically come down to a level of physical exertion that I want to be able to have. And by the way, there's a lot of things I'm not going to be able to do when I'm 100 that I can do now. You know, before we started this, I was showing you some pictures of places in Hawaii where we're hunting. And some of the terrain is the most complicated terrain in the history of the world. I mean, will I be able to hunt like that when I'm 100? Probably not. And I'm willing to accept certain things, but these 18 things became my bottom line. Like, I want these things. And now, even though I'm only 40, that gives me 54 years to train to do that. And each of these things then projects back into milestones. So if you want to be able to do those things I just described, when you're 100, you do what's called back casting. Well, what do you need to be able to do when you're 90? And then what do you need to be able to do when you're 70 and 60 and 50? So right now I'm very fixated on what the 50 year old version needs to be able to do to make sure I hit those 18 things when I'm a hunter. And so that becomes the Centenarian Olympics is this event that I'm training for. So I now do have an event in life and it requires a totally different way of training and it's totally foreign to me. Well, it's a much, much greater emphasis on stability, which gets virtually no attention. So mobility is the big buzzword. Everybody wants to talk about mobility this, mobility that, flexibility, balance, all of those things matter and they're all a subset of stability. But stability is the thing that most of us have lost generally by the time we're five. So if you look, I'm lucky. I have a two year old, so I get this beautiful firsthand view of what amazing movement is meant to look like. And when you look at the things that they can do, you realize that every inch of them is connected. So when they're moving their arm, when they are doing something on the floor, when they're rolling, when they're turning, everything is connected. They are transferring force across their body through the muscles and not the joints. And then something happens. I mean, there are a lot of things that happen that I won't get into just for the sake of time. But one of the Biggest insults is we start doing this sitting down. Yeah. Once we start sitting, we lose our connection to our pelvic floor. And it's this cylinder that sits within our body, from our diaphragm to our pelvic floor and around all of the muscles that line this tank. As we lose that connection, all of a sudden, we start to lose the ability to connect what's happening here to what's happening here and what's happening here to what's happening here, and all of these chronic injuries start to crop up. So both on a personal level, I've experienced, I mean, what. What I can only describe as the most remarkable transformations in terms of my own physical health, you know, without relying on surgery to fix injuries that I like.

What. What do you do?

Oh, I mean, I have torn labrums in both shoulders that at one point left me completely unable to do even one pushup.

My elbow was in such debilitating pain that I could barely. I mean, I could still function, but I was basically in pain 24 7. And of course, to learn that that was coming from the inability, I had to stabilize my scapula. So anytime I was doing anything that was pulling or pulling up or carrying anything, it was transmitting force all to this joint, as opposed to these huge muscles we have here that were designed to transmit that for us, you know, pain up. You know, I figured a different way.

Of training and figured out a totally.

Different way of training. Yeah. And so. And so, you know, now we're actually bringing this to our patients.

Is this stuff like Pilates or strength training?

It's. You know, I would take a broader step back and say, I don't. Do you know who Bruce Lee is? You remember Bruce Lee? Yeah.

So karate guy.

Yeah, yeah. So. So one of the things about Bruce Lee that I just always idolized was this system that he created called Jeet Kune do. So Jeet kune do, the way of no way or the way of the intercepting fist was this martial art that he created where he took, you know, something to the tune of 30 different martial arts, and he, in his own words, extracted what was useful from each of them and discarded what was useless. So to create sort of this.

Unbiased view of what he was trying to optimize for, which was self defense. And so this approach that we're taking is the same one, which is you take little pieces of yoga, Pilates, lots of pieces out of something called dynamic neuromuscular stabilization, all sorts of different training programs, and we're. We're Sort of building a protocol around how does one regain stability in the core, in the hips, in the scapula, in the neck, all of these areas. And so through that then you learn how to transmit force correctly. And now you do the strength training, you do these other types of training that are necessary. So, so basically the four pillars of preparing for the centenarian Olympics is the stability piece, the strength piece, the aerobic piece, which is the mitochondrial efficiency piece, and then the anaerobic piece. So there's lots of things that are missing from that.

Right.

You know, this threshold training is not a part of it because I actually.

Think going super fast interval training interval.

Yes, but so, so basically where I think most people are training incorrectly for longevity is, you know, you have like super high intensity interval training, like a tabata, something like that. And then you have this sort of what we call zone two, aerobic base training. A lot of people are spending too much time right in the middle and they're so they're not getting enough of the benefits here or here. And you know, I think that, I think there's a lot of emerging data. James o', Keefe, I'm sure, you know, Jim's work cardiologist, you know, looking at sort of athletes heart stuff, you know, higher, you know, we're seeing athletes that are seven to 10 times more likely to get atrial fibrillation.

Yeah.

And, and again I think that's largely the result of spending too much time at that sort of of sub threshold area, which is again, that's important if you're trying to win a race. Not saying that that type of training shouldn't be done, but you have to be clear on your objective. And if your objective is to win a race, then you have to train at that zone. But if your objective is to do all these things that I have on my list of 18, what's more, functional life, physical fitness. Right. Physical fitness is incredibly efficient. Mitochondria, incredibly fit. Aerobic base with the capacity to take very, you know, hard short term bursts.

Amazing. Okay, so back to the other aspects of the Centenary Olympics is not just the physical part, it's all the.

Right, so the physical piece is one part of it then. So that, so we talk about sort of physical or exoskeleton demise and then there's a cognitive piece and then there's an emotional piece. And so I think the, the three parts of healthspan than our physical, cognitive and emotional.

It doesn't the physical also depend on nutrition?

Oh yes, yes, yes. Remember, these aren't the, these are the objectives. So I'm talking about the outcomes. Right, yeah, so, so you have, you know, I sort of think of the five tactics that we have, right. The nutritional piece, the exercise piece, the sleep piece, the distress management piece, the drugs and supplements. Those are your tools to affect change. But ultimately what we're trying to do is enhanced longevity. That means delaying death by delaying the onset of chronic disease and then enhancing health span by enhancing that exoskeleton, cognition, emotional health.

So one is, one is not getting the bad stuff that's going to kill you and the other stuff is how do you supercharge your system to function optimally?

Yeah, because.

And they're kind of related, but they.

Are, but, but they do require very, each of those four axes require very deliberate attention. The, the not dying part requires attention and you know, basically you're gonna die. If you're a non smoker in the developed world, you're very likely to die from atherosclerosis, cancer or an accident. Those are, and again, you can dive into what those accidents look like. This is where you see an intersection with physical, the physical centenarian Olympics piece, right. Is you know, what's the leading cause of death? Overall, it's accidental death. But when you start, when you leave that to people who are in their ninth decade or eighth decade, it becomes accidental falls. So a fall becomes a more likely cause of demise when you get older. And you know, as you sort of alluded to earlier, it's not always that you just fall and die. It's usually that you fall and you break your hip and the broken hip results in immobility that very quickly begins to spiral your quality of life and you end up in the nursing and all these other things. So it's fighting all of these, you're sort of fighting all these fronts, which is why I think one should be paying attention to every possible tool they have to make this change.

So in terms of the food part of healthy aging and getting to 100, you talk about a lot of different techniques, whether it's intermittent fasting, calorie restriction, fasting itself, ketogenic diets, all of which seem to do really amazing things which are all similar, whether it's boosting your own stem cells, helping your mitochondria work better and clean them up, increase your antioxidant levels, reduce inflammation, boost your hormones that need to be boosted, reduce the ones that need to be reduced. It's pretty amazing when you start to look at these mechanisms, how do you parse what's the right approach for the long term? And you earlier mentioned that you fast. So you do a ramp up to fast with keto and then you fast.

For a while, a week, and then, and then come off it with a keto diet for a week. So it's like kfk, we call it KFK sandwich. So a week of keto. Yeah, I missed me some kfc. So yeah, a week of keto, a week of fasting, a week of keto. I do that quarterly. And so, you know, again, I think with nutrition, I like to take a big step back and say, what are we talking about here? So I sort of start at one side and I say, like, there's this thing called the Standard American Diet. And I think we can all agree, no matter what your dietary bent is, we can all agree the Standard American Diet is not a good diet. I don't, I don't think we need much more evidence of the futility of that. So then the question becomes, how would you escape the gravitational pull of this thing? And in my practice, I think there are two ways. There are two techniques to get people out of that pull. One of them is dietary restriction. And dietary restriction is anytime you restrict some element of the diet. So it's, it's taking away, yes, taking away some part of the what. So you're not really restricting the when and you're not restricting the how much, but you're restricting the what. So this has the largest number of things in its bucket, right? So this is a low carb diet, a low fat diet, a Mediterranean diet, a paleo diet, a vegetarian diet, a vegan diet, blah, blah, there's you. I, you know, you need scientific notation to count the number of things that fit in that bucket and they all get termed diet, which I sort of, sort of don't find typically appealing. The second major way to get people to escape the gravitational pull of the standard American diet is time restricted feeding. Where you don't restrict explicitly what they eat or how much they eat, you just restrict when they eat and you begin to compress that window of feeding and those two things are not necessarily done in isolation, you can then start to combine those things and say, well, if, because we're going to see, any form of dietary restriction, almost without exception, is an improvement over the standard American diet, which is why I sort of get a kick about these warring feuds that exist in these camps. My paleo diet's better than your vegan diet and blah, blah, blah. The answer is like they're both infinitely Better than what you were doing before. And by the way, they can both be infinitely idiotic. Right. So you know, the paleo brownie and the vegan cookie are equally bad, of course. So. So, but you can take the best of both worlds. You can take sort of the best of dietary restriction and combine it with time restricted feeding and then you get an even more potent tool and then you move from there into intermittent fasting where you take these periods, you know, in my opinion, sort of three days is the minimum effective dose. Five days is probably the sweet spot. Seven days is, you know, also with benefit and totally doable. And you either fast in a complete way, which is my preference personally, to just water only for those periods of time, or in a hypocaloric way.

The Prolon fast.

That's right. So Prolon is one example of that. It's a, it's something called a fast mimicking diet I think is their trademark name for a hypocaloric five day fast.

Yeah.

And obviously there's an infinite number of permutations and combinations to how you would go about doing intermittent fasting. And, and again we, we usually by the time a patient's been with us for about a year, we are really pushing them into that world where they're, they're going to be spending some time.

Doing that not all year long, but for periods of time.

Well, by definition not all year long. Of course. Yeah, it's intermittent and by the nature of its name, but it is a.

Fasting you, you can do every day.

Well no, I refer to that as time restricted feeding. And that's why I really like to be strict about the terminology so that, so time restricted feeding isn't really a fast, it's just not eating for certain periods of time. Fat. We, we reserve the term intermittent fasting for fasts of three days or longer. Yeah. Or, or if not outright fasts, hugely reduced caloric intake.

So do you think people should do time restricted eating every day?

I don't know. You know, this is tough, Mark, because I, I think one of the challenges. Remember how I said if I could be czar for a day, I would change dinner time? I haven't eaten yet today. What time is it? It's like almost 7 o'.

Clock.

So I know we gotta go.

And so this will be my only meal today. But the problem is. So I'm gonna eat a little more than I normally would cause it's the only thing I've eaten today. And I know that that's actually not great for My circadian rhythm. I'm gonna pay a little bit of a price when I sleep tonight, because let's say I eat dinner at seven tonight and I'm gonna eat, eat more than I normally would. And let's say I go to bed at 10. I just know that my body works best if I've got a much bigger gap between when I eat, especially a large meal, and when I sleep. So, no, I don't think everybody should do this every day. And in fact, I like to mix it up quite a little bit. And I actually, I really love to mix it up and reverse it and sort of do all of my eating early in the day, especially when I'm in New York, because I don't have my kids here.

Yeah.

And my family's not here. So I don't have this pressure to like, you know, having dinner with your family is a really important thing in America.

You know, most of breakfast is dessert.

Well, yeah, but I mean, we can work through that. Right? I mean, I'm confident that a committed individual can have a good breakfast. But the bigger issue is the social one. Right. Like, so much of our lives revolve around dinners and that, so. But I think time restricted feeding very likely has benefits. I think it's a bit soon to tout the magnitude of them because so much of that research has been done in mice or other animals, and especially in mice. And. And as you know, the metabolism of a mouse is so different from ours. So the benefits that you see by giving a mouse a 16 hour fast are unbelievable. But that's not the same as you or I going 16 hours without food. That's probably closer to you or I going two to three days without food.

Yeah. So for you, what does your day look like? How do you construct all the things you've learned about these five pillars of health and longevity? How do they integrate into your daily life? You're a busy guy. You have practices on two coasts, you have a family, you're schlepping around, you're doing podcasts. How does it work for you?

You know, I was just talking about this with my assistant this morning because I was sort of, or maybe it was yesterday, and I sort of said, you know, I haven't meditated in a few days. And I really feel the difference. Like, I'm really, really snippy and grouchy and, and just generally kind of a jerk. And she's like, you know, she's like, look, Peter, you just need to be more disciplined about this. You're so Disciplined about, like, you never miss a workout. You're really disciplined about, you know, all these things you do. You're very disciplined about your archery. You know, you're up there practicing twice a day every day when you're home and blah, blah, blah. And she's like, you know, we need to get back to a routine that we've done in the past, which is we used to put your meditations on the calendar. And it was. You treated it like you treated an appointment. And I was like, you know, you're right. I've been, you know, I've been a little bit out of my routine, which is. So for me, the right day is I wake up and I meditate before I do a single other thing, before I make a coffee, before certainly before I look at email or anything like that. And, you know, over the past few days, I think I was just, you know, something came up. And so there's a little bit of an issue going on in my life, and it sort of pulled me out of my routine a bit. But. But in many ways, I think the bottom line is these are all things that, whether it's exercise, nutrition, meditation, sleep, you have to prioritize them.

Yeah.

You know, you. And people don't want to do these things. And they, you know, one of the exercises I do with patients is I sit down and we look at the 168 hours in a week and look at where they're allocating time. And I say, look, you know, like, let's say you run a hedge fund or something. I say, your whole job is capital allocation. You're an. You're an asset allocator. You take money and your job is to decide where to put it into which companies to generate the right profile of return, liquidity, volatility, etc. So you are an asset allocator. Well, I said, well, everybody's an asset allocator when it comes to an even more precious commodity than money, which is time. And this is one where we're all the same. We all get 168 hours in a week, and you got to figure out how you're going to spend them. And, you know, I'm really committed to saying eight hours of those every single night are going to be for sleep. And that means I really want to get my 7 1/2 hours a night total at least of 8 hours in bed. And that's a. That's a sacrifice because there's a lot of times when I'd like to stay up and watch a movie or Screw around on Twitter or whatever. You know, you can pick a hundred things that you could do, but I'm really committed to allocating that time. And then you sort of go through this and say, well, you know, for example, using food, how much time do people really allocate to thinking about food choices? Because you have to be kind of deliberate about it.

Yeah.

You know, it requires for me at least surrounding myself with good food choices because I actually really struggle with food. Like, if left to my own devices, Mark, I could eat. I could just eat non stop junk food all day, every day. And so the reason I don't is not because I have some great discipline. It's because I surround myself with good food choices. It's like the worst thing I can possibly eat in a moment of weakness is like a piece of dark chocolate.

Right.

You know, you don't have in the.

House, like I don't have Ben and Jerry's Chunky Monkey in my freezer, because if it was there and I had a long day and I was tired, I would eat it.

Me too. And I think it's okay. I think people need to start accepting the fact that it's okay to say that, that like, we are humans and we're not perfect. And to me, this is why I love sort of behavioral economics and the work of Richard Thaler and others is you change the default environment and that's where you want to put your bandwidth, that's where you want to put your energy, is change your environment. Change your environment so that you don't have to constantly rely on willpower to do, you know, to eat a certain way or to do a certain thing. So, so basically my whole life is basically one big hack that tries to make eating, sleeping, meditating, doing all the things that matter to me as frictionless as possible, so that when there is friction, I'm make the easy choice. Make the easy choice, the easier choice.

Yeah, yeah. I think that's really important piece of advice because I think it really takes intention. We spend so much intention on so many things that matter far less in designing and figuring out what we want, but not about these things. And when you do, it's not that you're really training for this centenarian Olympics.

You're.

You're training for the quality of every single moment in your life, which dramatically enhances when you do these things. It's not about, oh, I'm going to do these things so I can get to 100 and be able to get.

Up off the floor. Yeah. The process itself is beautiful, right? I mean, I feel better. Yeah, exactly. I mean, it's a fair point, which is this isn't just about suffering until you get to be a hundred. So you can do all these feats when you're 100. I feel better. I feel infinitely better today than I did two years ago physically, because of the journey, because of the training.

It's so fantastic. Peter, you are a wealth of knowledge. And I. I know how much you think about these things. I know how deeply you think about these things. I think it's evident from the conversation. And I'd encourage everybody who's listening to this podcast or watching it to go to Peter's website, Peteratti md.com and sign up for his podcast. Because the Drive is one of the richest, deepest sources of medical health information. You're going to find out there that's more rigorous, more smart, and less promotional than anything out there, including me. So I really mean that. I really have tremendous respect for. For Peter and his critical thinking and understanding at the end of the day, that if we all want to have a quality of life and we want to actually live well and have a health span that equals our lifespan, that we have plenty of science, we're going to get more, but we have plenty of science and we can apply it. And that's the gap right now, is the application of what we know to what we do. And Peter helps us do that. So thank you, Peter, for being on the podcast.

Mark, thanks so much. Honor to be here. And I couldn't agree more with what you just said, by the way. I think that is people always say, gee, which drug do you think we need to be putting all of our efforts into in terms of development and stuff? And I say, I have thoughts on that, but that's missing the boat. It's really taking the stuff that we know now with respect to nutrition, sleep, et cetera, exercise, and actually figuring out the right way to apply them and helping people do it well.

Thank you, Peter. And you've been listening to the Doctors pharmacy. This is Dr. Mark Hyman. If you love this podcast, please share with your friends and family on social media. Leave a comment. We'd love to hear from you and subscribe wherever you get your podcasts. And we'll see you next time on the Doctor's Pharmacy.