#276 ‒ Special episode: Peter answers questions on longevity, supplements, protein, fasting, apoB, statins, and more
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Hey everyone, welcome to The Drive Podcast. I'm your host, Peter Attia. This podcast, my website, and my weekly newsletter all focus on the goal of translating the science of longevity into something accessible for everyone. Our goal is to provide the best content in health and wellness, and we've established a great team of analysts to make this happen.

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If you want to learn more about the benefits of our premium membership, head over to peteratiamd.com forward slash subscribe. Welcome to a special episode of The Drive. This is an episode that is set up like an AMA where Nick is asking me questions. However, this will be an episode that is available to everyone.

Where this differs from most AMAs is that in this episode, I haven't seen the questions beforehand, and I come in kind of blind. As such, whereas most AMAs go an inch wide and a mile deep, here we go, I would say, a mile wide and a foot deep.

For this conversation, the team pulled some of the most common questions that we are asked, including some that I traditionally can't stand answering. Of course, I have no choice here, and therefore we go through those in today's podcast. We end up talking about why I don't think people are currently going to be able to live to 120, 150, or 180, some of the claims you see out there all the time. We talk about what supplements I take and why you shouldn't just blindly follow me by taking the same thing.

We talk about how to lower your ApoB with and without medications. We talk about how I think about taking statins over a long period of time and what we know about other ASCVD-modulating drugs today or in the pipeline. We talk about why there's no such thing as good or bad cholesterol, why nutrition research is so hard, how I think about the question of, quote, what is the best diet,

how I hit my protein targets throughout the day, what my current favorite wearable is, and what the role for CGM is in non-diabetics, and much more. If you're not a subscriber, this episode will hopefully give you some insight into our AMAs, although as mentioned earlier, the format here is a little different. Without further delay, please enjoy this special episode of The Drive.

Peter, welcome to a special podcast. How are you doing? Doing pretty good. Good. So today's episode, we're going to do something a little different. It's going to be kind of like an AMA style where you're the one answering questions, but it's going to be an episode that's available to everyone. We've done this a few times in the past. Usually our Strong Convictions loosely held episodes celebrating the 100, 200 episodes. Those are just

Received really good feedback. And so what we decided to do was do another type of those episodes, but instead pull some of the most frequently asked questions that have come through the site and

And so we organized them a little bit by various topics, but this is going to be an episode that's kind of more old school style where it's just question answer. A lot of these questions you haven't seen before, which is probably good because some of them you've always refused to talk about on AMA, such as what supplements do you take?

I know it's not your favorite subject to go into those details, so we're going to get into them today, which I think will be good. And I think it should just be a fun conversation where you're coming into this blind and it should be really interesting, I think, for the listener and viewer. So with that said, anything you want to add before we get started? Why do people care what supplements I take? We can save that for the question. We will get to it and I think people will find it enjoyable.

The other thing I should say is, do you know why I'm also excited to have this conversation today of all days with you? No. As our friend Kyler Brown would say, based on some emails we've exchanged earlier, you kind of seem like you're in a spicy mood today. So I think it's going to be kind of fun to go through these questions. What do you think? I think I am in a very spicy mood. So for the listener and viewer, this should be a fun one all around.

With that said, first question, when people think of longevity, a lot of times in the space, they think of living to 120, 150, 200 years old.

I think anyone who's listened to your podcast, read the book, listened to interviews you've done, you're not really in that camp of very confident that we're going to live to 120, 150 years old. One of the common questions we get is just, why is that? Why do you think that's maybe not possible? And the follow-up would be, based on that, why do you think it's important to act and live like we might only get to 90 years old?

This is a bit of a complicated question. So why do I not have confidence in the biohacking your way to 120, 150, 180? I've heard all of these sorts of numbers because I don't think we have the tools to address the

underlying aspects of the aging of biology that are relentlessly pushing us towards the end of our lives. Again, that's not a depressing statement. I think it's just an obvious reality, right? So there are things about us as we age that we have the capacity to reduce the rate of change on. We can slow them down, but I've seen no real evidence that we can reverse them in a meaningful way.

Now, it's true that there are some people out there claiming they've got their aging clock and it shows that even though their birth certificate says they're 60, they're really 35. We could put some time into explaining why that's not correct. So the long and short of it is we don't have any evidence that we can take the diseases of aging and erase them or that we can take the underlying processes of everything from

defects in mitochondrial function, defects in protein folding and misfolding, changes in DNA breaking and repair, breakdown in nutrient sensing, all of these pathways. I haven't seen any evidence that we can undo that. So then what would you have to believe? So if you're going to believe someone my age, i.e. someone who's 50, is going to be around in 70 years, you have to believe that in the next

dozen years or so, someone is going to come up with a way to completely halt aging and or reverse it. In other words, it's not going to do me any good if this happens 50 years from now, because in 50 years, I probably won't be here. And I spend a lot of time looking at this type of literature. I really do spend a lot of time looking at this technology. I haven't seen many examples of

Where there's a bigger mismatch between what is actually happening scientifically and what is being talked about in the press, on social media, on podcasts. And that chasm is enormous. In other words, what's really happening is like nowhere near the sci-fi that's being portrayed.

So, because of that and because I have confidence that what's actually happening is more a representation of reality, I know that these things are not a decade away. That's why I take that point of view. Now, why does all of this matter? I think this matters because if you knew that this was as good as it was going to get, and I don't think it is, by the way. I do think there are incremental things that are going to make a difference even in the

But if you thought that, look, this is directionally as good as it were going to get, I think it would motivate you to be more serious about using the tools that we have today for primary and secondary prevention of disease, for optimizing and maximizing lifespan and healthspan. If for no other reason, you would do that as a hedge fund.

against the enormously long odds that something dramatic and miraculous is going to happen in the next decade or two.

To double click on a few things there, when you were talking early on about diseases, were those diseases what you call the four horsemen from your book? Is that what you're referring to? Yes. You still have to have a strategy that says, how are you not going to die of ASCVD, cancer, neurodegeneration, dementia? And of all of those diseases, the only one where I can see a pretty clear path

to delay it significantly would be ASCVD if you take really dramatic steps early in life. Instead of talking about what we think of as primary prevention, think of ultra-primary prevention, treating people in their 30s, making sure a person never, ever walks around with an ApoB over 30 or 40 milligrams per deciliter, making sure a person

Doesn't even spend one year with mild hypertension, making sure a person is always metabolically healthy. If you do that, I agree, you would not get atherosclerosis in a normal lifespan.

But we don't have that degree of certainty for pushing off cancer indefinitely, for pushing off neurodegeneration indefinitely, for pushing off dementia indefinitely. Nor do we have it, by the way, for pushing off, I think, sarcopenia indefinitely, or pushing off RPC.

arthritis indefinitely. I mean, there's these other conditions that are not as interesting to think about because they don't rise to the level of the horseman, but they matter a lot. So physical frailty is a really, really, really big one. If you manage to not die of heart disease, cancer, neurodegeneration, dementia, and you're willing to train really hard, like I really do think there's a path to be physically robust as a centenarian.

But I don't see a path to doing that at 120 or 150 unless there is a significant technologic breakthrough that would basically allow us to rewind

Maybe this is a different discussion, and maybe it's a longer discussion, Nick, and I don't know if we want to go into it because it's taking us a little off topic, but it really gets into what does it mean to age at a cellular level? What is the role of the epigenome in regulating our genetic code? I don't know if there are other questions about that topic, but we could certainly defer to that.

On that topic, I know that's talked a little bit about in the episode with David Sabatini, Matt Cabral, and so maybe we'll pull questions from there into a future AMA, kind of diving into that a little deeper. Kind of what I'm hearing you say is you still think that we will succumb to the same diseases that will kill us.

Your goal with medicine 3.0 and prevention is still to put that off as far as possible, but that doesn't mean you're going to put it off until you're 120 years old. The goal is to really live as robustly as possible and avoid those as long as you can, but still more in the traditional lifespan opposed to the 150-year-old lifespan. I think that taking all of the steps that I talk about in the book and

could seriously add a decade to life. I don't doubt that you can live a decade, a decade and a half, maybe two decades longer. I don't doubt that. But I don't think we're talking about adding 30 years or 50 years to lifespan. What I think is more important is that whether you're adding five years, seven years, or 10 years to your lifespan, what I think is much more interesting and much more important

is reducing or compressing the period of morbidity late in life. What I think people should fixate on is how do I not be really, really frail both physically and cognitively in the last decade of my life, what I call the marginal decade. I don't know if I'm going to live till I'm 85 or 90 or 80 or whatever. I mean, I don't feel like I have as much control over that. I think there are some elements of bad luck that factor into that.

What I feel like I have much more control over is when I'm in my marginal decade, can I still go for a ruck? Will I carry 80 pounds on said ruck? No way. But I might be able to carry 10 or 20.

Will I be able to swim half a mile in a pool? Yeah. Will I be able to swim it as fast as I can now? No chance, but I could still swim half a mile and get out of the pool under my own power. Could I sit on the floor? It's all those things that I talk about in the centenary in decathlon. Those are the things I think that we really want to relentlessly fixate on because I think most people would rather live to 90 and die of a heart attack while swimming in the ocean, but being...

otherwise in remarkable shape, then live to 120 and spend the last 30 years of that unable to do much. Earlier, you also mentioned there's incremental things you think that could happen that will help someone even your age at 50 live longer. Do you want to just lightly touch on what a few of those things are that you were talking about there?

One of the most interesting, and I talked about this on a recent podcast with David Sabatini and Matt Caberlin, is I still think we are really in early days of understanding what pharmacologic inhibition of mTOR can do. There's really a lot of promise with this approach in virtually every other model species outside of humans.

And that doesn't mean it will work in humans, but it's very interesting. And I think if we had better biomarkers, again, I think that's something that can happen in our lifetime. I think that's a very promising strategy. And it's especially promising when you consider that the animal models show that pharmacologic inhibition of mTOR using rapamycin or its analogs, even applied late in life, still provided lifespan and healthspan improvement.

And why that's interesting is very few other interventions that have shown to be Giro protective work when applied that late in life. So that to me is very promising. Last question on this aging topic would be, let's take someone who's listening, maybe your age, but they have a son or a daughter who is 10 years old.

How do you think that 40-year timescale differs as you look at a 10-year-old's potential lifespan today compared to your 50-year-old lifespan today?

That's a good question. I don't know. Look, I'm that guy, right? I mean, I have a six-year-old, a nine-year-old, a 15-year-old, and I often think about what's the difference between me and them in terms of their runway versus mine vis-a-vis the types of technologic breakthroughs that we're interested in. And again, the one that I'm most interested in is probably on selective

high fidelity, high precision modulation of the epigenome? I don't know the answer, truthfully. I simply don't have a way to predict the pace of that type of innovation. And of course, not to be a doomsdayer, but even though they have a longer horizon for good things to happen, they also have a long horizon for bad things to happen.

And when I think about bad things that can happen to our kids, of course, you can't help but think about nuclear war. By the way, in order, how would I rank them? I don't know. Probably I would say biological terrorism would be the single greatest threat to our species.

simply based on the low barriers to entry and the ease with which there's proliferation. But again, you could sit here and debate what's the greater threat to our species. Is it nuclear war? Is it climate change? Is it biological warfare? The point being here, they have just as much time to be exposed to really bad things that could obliterate our species as good things that could extend the life of our species. So I just don't know how to handicap the pros and cons on that.

That could be our next book. We could call it The Fifth Horseman, and it could be all about that. That's a good intro into this next section, which gets into drugs and supplements and the most common questions we get asked there. But I think you mentioned one thing in the aging section that I think would be worth touching on real quick. I think it will affect what we talk about here, which is we really don't have biomarkers for aging.

And you've been open about frustrations with that because when you look at geo-protective molecules and you look at if these things are working or not, we really don't know because we don't have those biomarkers. So do you maybe want to talk about that for just a minute to kind of set the stage so when people hear your framing for everything else, I think it will make a little more sense?

I think one of the most important things to understand when you're using some sort of intervention is do you have a biomarker to know if you're doing it correctly? So think of like really basic things that most people don't even consider as interventions like nutrition. How would you know if you're eating too much? Do you have a biomarker for it? Sure, there are lots. One biomarker might be your weight.

Another biomarker might be your waist circumference. Another biomarker might be your insulin level, your glucose level, your average glucose. I mean, you get deeper and deeper down this and you start to realize that how much you eat, you have a way of getting feedback from the system that tells you, do you need to correct this?

The same is true for exercise. The same is true for sleep. So there might not be a lab value that is specific to sleep, but there are clearly ways to get feedback to know if you're sleeping too much or not sleeping enough. If you think about it through the lens of taking exogenous molecules, you take a drug like lisinopril.

an ACE inhibitor for lowering blood pressure. How do you know if you're taking the right amount? You measure your blood pressure. Let's say you get started on a dose of lisinopril when your starting blood pressure was 135 over 85, and all of a sudden it's 115 over 75. That says the drug is working. Are you symptomatic? By the way, that's another biomarker in a sense. No, you're not lightheaded. Great. Everybody wins the game.

If your blood pressure goes too low and or you're symptomatic, which is probably the bigger issue, then you're taking too much. You have to dial the drug back. If you're taking the drug and your blood pressure comes down but doesn't come down enough, that's more feedback. Dial the drug up. So you have this sort of input-output ability with every drug that we like to think of. Again, the same is true with drugs for diabetes, with drugs for lipids, with

Cancer drugs that you take you would be able to look and study is the tumor shrinking is the tumor growing? So you have some are getting feedback Well the problem when it comes to Giro protection this broad category where we are not targeting diseases specifically But instead we're targeting the underlying Mechanisms of aging is we can't measure it. We don't have a way to measure it. So we take a drug and

We take a supplement that we believe is Giro protective and we don't know if it's working. Are we taking enough? Are we taking too much? Maybe if you're really lucky, you might find a side effect that tells you you're taking too much. But do we really want to be in the game of pushing things to the point of seeing overt side effects?

That's why I believe as unsexy as the world of diagnostics and biomarkers are, and it is a very, very unsexy world. This is not a place where people like investing money. This is not a place where there's an enormous amount of capital being thrown at the problem. It is a very important problem, and it's going to be very important in humans if we're interested in studying geroprotection.

Probably the very first time I went on kind of a long diatribe on this was back when I was really, really obsessed with trying to understand the perfect routine for fasting. I'm sure you can recall this circa 2018, 2019, 2020. I was very frustrated that as much as I was trying to study this in myself and doing every sort of blood analysis under the sun, I had no way of knowing if my fasting protocol of

Seven to 10 days of water only once a quarter, three days once a month. Was that too much? Was that too little? Was that doing anything? No idea. To this day, I have no idea if that provided any benefit at all. I could certainly point to some negative things it did, right? It cost me probably 20 pounds of muscle over six years.

But maybe that was a worthwhile trade-off given some other benefits, but how would I know? Don't know what the benefits are. Don't know how to measure it. It's a very important problem, and it's one that I hope more and more resources will be poured into because otherwise it's going to be very difficult for us to move further in understanding what works in humans.

On that, I do actually have another framework question, which before we get to the list of supplements, which I know people are anxious to get to, you've often talked about your analogy of, are you picking up a gold coin or a penny? Are you picking up in front of a train or a tricycle? And oftentimes when I've heard you use this, it's a lot of times as it relates to interventions, specifically drugs and supplements. Do you maybe want to quickly give people what that framework is? Because I think it is really important.

Based on everything you said, which is a lot of this is kind of a guessing game and we don't really know. So we kind of need to anchor it to another framework to try and figure out what are the risks and what are the potential rewards as we try and figure out within ourselves, what are we willing to do and not do?

It's nothing more than a very simple matrix of risk and reward, which I'm sure anybody would easily be able to walk themselves through. All I do is just to make it easy to remember, I just put very obvious concrete examples in the corners of the matrix. So it doesn't matter which axis is horizontal or vertical, but if you just say that the horizontal axis represents risk going from low to high,

and the vertical axis represents reward going from low to high, you would say, okay, at a very extreme level, low risk is bending down in front of an oncoming tricycle.

And as you move from left to right on that horizontal axis, it goes to jumping in front of a train track and grabbing something and then getting off the train track. So that's going from low risk to high risk. And in terms of reward, you would think of a penny being pretty low reward. And you'd think of a big, fat, juicy gold coin being very high reward.

So as you go from higher risk, you would expect and demand higher reward. So I'll tell you a story. I'm embarrassed to say this because it speaks to just how stupid teenage boys are and how much of a miracle it is that our species still exists with the utter lack of judgment that exists in the presence of young boys. So when I was in high school, one of our favorite games to play was

was when we would get off the train, we would immediately jump under the train and see who could lay the most coins on the train track and then get out as quickly as possible so that once the train started rolling you could see how many coins got flattened. Just think about the abject stupidity of this game. Another game that was tragically very popular when I was young

was playing chicken in front of the subway in Toronto. Who could be the last guy out? And very sadly, the younger brother of one of my friends in high school did not make it out. He was killed by a subway playing a stupid game of chicken. Talk about incredibly high risk for no reward. So how do we apply that to interventions? I guess we're talking about this through the lens of supplements. Well,

I think we have to acknowledge that there's a great uncertainty with many of these things, and therefore we should ask ourselves, how can we handicap the risk based on human data, animal data, safety data, efficacy data, as far as reward, and where on that matrix do we place this intervention? So if you're going to take, I don't know, fill in the blank,

some fancy supplement that some internet guru is telling you, like he's making with his own proprietary blend of crushed bird feathers and testicular juice. Okay. I mean, do you want to take that risk? Because it's hard for me to imagine the reward is really there. So one of the things I will push my patients on is when they show me their laundry list of supplements, I walk them through a framework about thinking through it and

And one of them is, where are you on the risk reward matrix? So with that said, let's get into Peter Atiyah's list of supplements that he takes. You can pick whichever one you want to start with. For some reason, I hate talking about this only because I noticed that it tends to show up online and it somehow becomes like,

well, if Peter does this, you should do this or something like that. And there's no context to it. And therefore, nobody understands the rationale. Nobody understands the clinical history and all of those things. So with that caveat, which I don't think matters because I just, at the end of the day, don't think people care. I think a lot of people just are sort of searching. But I take

EPA and DHA. So I take fish oil. Again, I'm happy to even state the brands that I take of these things because I don't have any affiliation with any of these companies. And frankly, I like to give a shout out to companies that I think sell good products. So I use Carlson's EPA and DHA.

I can't remember exactly which one I take. I can never remember their names. They're so convoluted. It's like super EPA or something, but it is the highest EPA version that they have. So by taking four of these capsules a day, I'm taking roughly two grams of EPA a day and probably a gram and a half of DHA.

The reason I take that much is I'm treating to a dose. I'm treating to a red blood cell membrane concentration of EPA and DHA of about 12%. So that's a blood test you would do. You have a biomarker that I can use to say I'm taking too much, I'm taking too little. Here you go. I take vitamin D. I'm sorry that I'm blanking on the brand. I can see the bottle, but I'm blanking on the brand. I take 5,000 IU of vitamin D. Why?

And largely because this is one of those things where I think the risk is insanely low. I think this is really a tricycle and I'm not sure what I'm picking up. I think it's more than a penny. I definitely think it's less than a gold coin. It might be a $5 bill, but I'd pick up a five. If I was walking down the street and there was a kid riding a tricycle towards me and I saw a $5 bill, I would pick it up.

I think that most of the studies on vitamin D have been very poorly done. And we do need to do a podcast on this. Maybe this is something we could deep dive onto in an AMA. So I won't get into it more now. But having looked very critically at the vitamin D literature, which is insanely underwhelming, I think it is almost assuredly the result of very lousy studies that add no value to our understanding of the problems.

So the dosing has been wrong, the duration has been wrong, the compliance has been wrong, and the targeting has been wrong. Everything has been blown, and so I would say we truly have no idea. I take Slow Mag, that is a brand, and I take two or three of those every day. So that is a slowly and completely absorbed form of magnesium product.

All in all, I'm trying to get up to about a gram of total magnesium or elemental magnesium in my system a day. And I get that through, again, through slow mag, through magnesium L3 and eight and through magnesium oxide. So I take all of those things. I take methyl folate and methyl B12. I use Gero as a brand.

Again, here we do have biomarkers. You can measure B12 levels, but more than anything, I'm measuring homocysteine levels. That's why I'm taking methylated versions of those.

Basically, I take these to keep homocysteine below nine. That for me just means just taking one a day, so I take the standard dose of that. They do make it in two strengths, and I take the lower of the two, in part because my MTHFR gene, most of us have variants of MTHFR. The variants I have are reasonable at methylation. This is actually an interesting change.

I used to take 50 milligrams of B6 daily. I've now lowered that to three times a week. We have seen some people who, when they take too much B6, can actually develop a sort of neuropathy as a result of it. Though I've never experienced any symptoms from it, a little further digging has led me to realize we don't need nearly as much B6 as I thought we did. So I've lowered that to 50 milligrams three times a week.

And it helps with the homocysteine. You just have to be careful that you're not overdoing it. I take a baby aspirin a day. I think the evidence for the use of baby aspirin in cardio protection is pretty weak. This is kind of a soft call. I don't think there's an evidence-based reason why I should take a baby aspirin. And there's even some evidence to suggest that once you get

significantly older, unless your risk of cardiovascular disease is significantly high, the benefits of it, which are clear, there's no doubt there are benefits of a baby aspirin, but they're outweighed by the bleeding risks that are associated with aspirin use. In particular, if you fall and hit your head, that becomes a bigger liability.

Baby aspirin use falls in and out of favor over time. Given that I am very young, relatively speaking, to these study populations and not really at risk for a bleeding injury, I think of this as picking up like a dollar or two dollars in front of a tricycle at this point. But again, I'm always happy to reevaluate the use of this and any supplement for that matter in the presence of new data. That might be it for daytime supplements. In

In the night, I take ashwagandha. I take 600 milligrams of ashwagandha. I recently switched to the Solgar brand. I take two grams of glycine. I use the Thorne brand. I take magnesium L3 and 8, which I just mentioned. I use the Magteen brand.

By the way, anytime you're buying magnesium L3 and A, just make sure it has magteen in it. So you could buy it from any different company, but they have to have the magteen proprietary combination because they're the only people that have the license to make L3 and A. Occasionally for travel, I will take Gero's phosphatidylserine. It comes in 100 milligram capsules or gel caps.

For some reason, I like the gel caps better. No idea if they're just more quickly absorbed. I truly have no idea. And I'll take, if I'm really going to the trouble of taking it, I'm presumably on a long flight where I'm trying to overcome a significant time zone. So I'll usually take about 400 milligrams. That's a compound that's been tested readily up to 600 milligrams. It's possible I'm forgetting something else, but I think those are my supplements.

Sorry, there's two others I take, but they're not in the cabinet and that's why. So I take Athletic Greens in the morning. Disclosure, I am an investor in that company. I'm also an advisor to that company. So I take AG1 as a green drink in the morning and I take a probiotic called glucose. I think it's called glucose control by a company called Pendulum. So I take two of those in the morning with my AG. That's kind of like the first thing I consume in the morning.

With those, just on the whole, just because you take them, not everyone should take them and you're looking at your medical history. What percent of that, let's say the same drugs, the same supplements and the same doses were you taking a year ago? How is this changing? Yeah. Yeah. So that way, if someone listening to this down the road hears it, they don't automatically just go do the same thing.

Yeah. So a year ago, I was not taking the pendulum probiotic. That's something I've only been taking for a couple of months. And I'm doing an experiment there, which is looking at average blood glucose. So the reason I'm taking this particular probiotic is I believe having looked at all of these probiotics, I think this is the most rigorously tested and validated probiotic out there.

And in a small but double-blinded randomized clinical trial, it demonstrated a 0.6%, meaning 0.6 absolute percentage point reduction in hemoglobin A1C in people with type 2 diabetes. And that was only in 90 days, which is pretty interesting. It also was associated with, I would say more than associated with, it demonstrated and caused about a 30% reduction in postprandial

glucose AUC, area under the curve. So meaning when you gave people a glucose challenge and then measured and plotted a graph of their glucose response and looked at the area under that curve, the people who had been taking this pendulum glucose control probiotic had a 30% reduction in that, meaning they had become more insulin sensitive. And I'm

I'm a couple of weeks away from doing a blood test on myself to see if I've had any improvement in glycemic markers in response to that. Was not taking that a year ago. I was not taking ashwagandha a year ago.

I had taken it a long time earlier, but just came back to it, probably found a slightly more potent version of it. I was taking a different brand of fish oil before. I had used Carlson's in the past, had switched to Nordic Naturals. Now I've switched back to this. I find it to be just a slightly more robust product. The Nordic Naturals ones, for some reason, every third bottle had a broken capsule in it. And once a capsule breaks in the bottle, it just totally destroys the...

remaining of the capsules. It was just happening too frequently. I was kind of aggravated by it. I don't think I was taking a baby aspirin a year ago. I think, again, that's something I've kind of done on and off over periods of time and probably the same with vitamin D. It's possible I wasn't taking vitamin D a year ago. Yeah. So it's not only the drugs have changed, but even like the B6 you mentioned, the dosing has also changed. Right. So then if we look at outside of supplements and we kind of look at drugs,

The most common drug we get asked about would be rapamycin followed by metformin. And we won't get into those too much here because of that podcast with David and Matt. And then also we won't get into too much on metformin because you and Andrew did a journal club and you kind of focused on metformin. And so just for time's sake, we'll kind of punt those to those other resources. But outside of that, the question around metformin

drugs that we get an SMOS is kind of within the ASCVD. And you mentioned early, that's a disease that you think we have some chance to really stop it and to really delay the onset of it if we take early interventions.

And one of the most common questions we get is, how do you lower your ApoB and what's realistic with and without pharmacology? Without pharmacology, so first of all, exercise has no meaningful impact on ASCVD risk factors through lipoproteins. It does in other ways. But if you're just talking about managing lipoprotein risk, it really comes down to pharmacology, hands down the most potent way to do it, and then nutrition, a far less potent but not insignificant way to do it.

On the nutrition front, you basically have two levers to pull. You can dramatically reduce carbohydrates, which will lower triglycerides, and all things equal, the lower triglycerides, the lower the ApoB burden because you have to traffic fewer triglycerides with the cholesterol. The other way to do it is dramatically cut saturated fat. In a high saturated fat diet, what typically happens in addition to an increase in cholesterol synthesis is the liver, through something called the sterile regulatory binding protein,

says, I don't need any more fat brought in. I don't need any more cholesterol brought in. So it down-regulates LDL receptors. So it pulls fewer LDL out of circulation and LDL will skyrocket. So the reverse is true. If you cut saturated fat, the liver is going to want more LDL coming in. It will up-regulate LDL receptors and pull more LDL out of circulation.

So if you were on a really low carbohydrate, really low saturated fat diet, you would indeed lower your ApoB. Would you lower it to the levels that I think are necessary to make ASCVD irrelevant? Most people probably not. And then would that be a diet that for most people is sustainable long-term? That's probably a very individual decision. So for someone like me,

who has very low triglycerides. I don't go out of my way to eat saturated fat, but I'm also not restricting it either. I'd say I probably am in line with where the average person is. My ApoB at a baseline would still be, I don't know, 90 to 100 milligrams per deciliter, which puts me at about the 50th percentile of the population. So that's my normal ApoB. That

That's far, far too high for someone who, A, has a genetic predisposition to ASCVD, and B, just somebody who wants to take the one horseman that can be taken off the table and take it off the table. My target for ApoB is 30 to 40 milligrams per deciliter. Therefore, that would require pharmacology. I take three drugs to do that. I take a PCSK9 inhibitor,

called Brapatha, and I take a combo drug called Nexlazet, which is bampidoic acid and ezetimibe combined into a single pill. And the mechanism of action of ezetimibe is that, well, not to get too technical, but it blocks the Neiman-Pixie 1-Liquan transporter in both hepatocytes and enterocytes of the gut. It prevents non-esterified cholesterol from

coming back into the gut after you've recirculated it through your liver and into bile. So it prevents you from reabsorbing your cholesterol. Of the three drugs I'm taking, that's far and away the least potent.

Bempandoic acid is a pro-drug. What that means is by itself it is inactive, so when you ingest it, it goes to the liver, it gets activated, and there it is a cholesterol synthesis inhibitor. It acts on a different enzyme from statins, and what makes bempandoic acid special, for lack of a better word, is that it only inhibits cholesterol synthesis in the liver, whereas statins, which are very potent inhibitors of cholesterol synthesis, they do so throughout the body.

because they don't have this pro-drug trick. When the liver senses less cholesterol,

it increases LDL receptor expression on its surface and pulls more LDL out of circulation. So that's how both statins and bepidoic acid work. They work indirectly. The difference is bepidoic acid is less potent than a statin and more selective in that way. So the combination of those three drugs will keep my ApoB negligible. And equally importantly, there are no side effects associated with that for me personally.

And again, when it comes to lipid management, it's certainly one of my favorite topics. I always tell patients we have tools today that we couldn't even fathom 20 years ago. 20 years ago, if you needed to have your ApoB slammed,

There was only one way to do it, which was mega dose of statins. I don't believe any patient needs to be on a mega dose of a statin today. We just have too many other tools. And I do have some concern about mega dose of statins because one, the efficacy curves show that statins hit their maximum efficacy at about quarter dose. The curve for the efficacy of a statin looks like this. For example, if you look at Rezuva statin, you're getting...

85% of its maximum ApoB reduction at 5 milligrams. Roughly 85%, you hit the maximum. And by the way, it's a drug that is typically dosed up to 40 milligrams. So once you hit 10 milligrams, there's no need to go any higher because all you're really doing is buying side effects and you're getting very little in the way of increased efficacy. So we're very quick to pivot patients off

statins if we can't get great efficacy with no side effects at low dose. On those drugs, including statins, let's say, if you can get the efficacy at the low dose, oftentimes while people who are younger in their 30s, 40s, even 50s kind of reach out and say, do you have any concerns about taking those drugs for such a long period of time? Yes and no. I think it depends on the alternative. So I think that

There are some people who kind of poo-poo the side effects of statins and say they're non-existent. Well, I think that's a ridiculous thing to say. There are well-documented side effects of statins, at least three, that shouldn't be ignored. One is muscle aches. The two is elevations of transaminases or liver function tests. And the third is insulin resistance. All of these are relatively small, but they're not zero. Two of the three are objectively measurable statins.

Why would we ignore that? So I really like when you have objectively measurable side effects. So I would say that if a young person is in a situation where perhaps they can't afford Bempadoic acid, Nexlazet, PCSK9 inhibitors, because to be clear, those drugs are expensive at this time and statins are not. Yeah, your alternative might be, I'm going to be on a statin, at least go through the trouble of trying to find the right one that produces the fewest side effects.

Again, we think that probably pitavastatin or livelo, rezuvastatin or Crestor are probably the best places to go, but it's also so highly individualized that I think you just have to try a couple until you find the ones that are doing the best without any collateral damage. You've talked about PCSK9s before, but

Do you think we're any closer to those being more widely available? And by widely available, just meaning at a potential lower cost to individuals? I think so, because we now have, through a different mechanism, you have a shot that can be administered once every six months. So I think that the twice monthly shot that I take for a PCSK9 inhibitor, which has already come down in price by more than 50% since that drug came out eight years ago, I think

I think there will just be continued price pressure on these drugs as more and more other drugs become available.

Speaking of drugs, you mentioned before you think for the future of LP little a, that there's a drug in the pipeline that you're pretty optimistic about being available for people who have a high LP little a, which could be anywhere from eight to 12 up to 20% of people. And we've had podcasts on that before. And so just with the amount of people that have a high LP little a, often they'll reach out because they're

Up until now, there's not really a drug that can lower that. So do you just maybe want to talk a little bit more about

what's on the future for LP little a medications? Truthfully, I haven't been following anything for the last few months. So I don't have anything new to say on this since I probably last spoke about it, but there is a drug being made by a company, I think in San Diego, that is an antisense oligonucleotide. So the drug disrupts the process of DNA making RNA to make APO little a.

It interrupts the synthesis of the protein that turns an LDL into an LP little a. The drug worked very well in phase two. So in phase two studies, which don't have clinical hard outcomes, the outcome is just, is the biomarker improving?

There was a complete obliteration of LP little a, and there were no side effects over the short haul. So what matters now is the phase three trial, which is ongoing, and that's testing the more important question, which is does eliminating LP little a via this mechanism reduce clinical events? Does it reduce major adverse cardiac events?

So the answer to that question will determine whether or not this drug is approved and therefore becomes available. But I will say this, it is unlikely for me to imagine that that drug will be approved to treat patients with primary prevention because the manner in which it's being tested, understandably, is for secondary prevention. This is very common in drug development where you first test the drug. The clinical indication is in the highest risk patient. So you get the answer relatively quickly.

So this is a trial that is looking at people who have already had major adverse cardiac events, and it's basically seeing, can we prevent subsequent events? And if the answer is yes, I believe the drug gets approved. It gets approved for that use case. It would still be able to be used by anybody for primary prevention, but it's not likely that an insurance company would pay for that yet. Very interesting.

What's a traditional timeline for drug development to go from that first use case, which is the most urgent, to that primary prevention? Is that usually years, over a decade? The rule of thumb is one decade and $1 billion for a drug to go from IND to FDA approval. And again, once a drug is approved by the FDA, anything can be done with it. It

They were very quickly employed for primary prevention, probably even before primary prevention trials were published because the drugs weren't that expensive. The only reason I think this is an issue here is I do not expect this drug to be cheap. Got it. Anything else you want to say on the drug supplement category before we move on? Only that I can't believe we wasted how many ever minutes we wasted talking about that. As a reward, you get to talk about nutrition. We go from one positive to another.

The first question is, what set of words trigger you more when you are asked, which diet is best or what is good cholesterol and bad cholesterol? I don't know. Those are pretty upsetting questions.

Let's start with the second, considering we just hit ASCVD. You made a YouTube video about this, but I do think it's an important subject because not only is there a misunderstanding of this with patients, but also the amount of doctors out there who I think still use good, bad cholesterol. Do you just want to give a rundown why there is no such thing as good and bad cholesterol?

The term originates from the differentiation between low-density lipoprotein, LDL, and high-density lipoprotein, HDL. So let's start with where there's a grain of truth here. So LDL, or low-density lipoprotein, which is not cholesterol. LDL is the carrier molecule. It's the low-density lipoprotein. It's the boat or the submarine that carries cholesterol. LDLs are bad.

And HDLs, high-density lipoproteins, are good. But HDL and LDL are not laboratory measurements. There's no such thing as an LDL or an HDL that you can check at a lab. You can measure the content of cholesterol within the LDL. That's called LDL-C. And similarly, you can measure the content of cholesterol within the HDL. That's called HDL-C. So when you have a basic lipid panel,

And it says your HDL is 50. Well, if you read the fine print, what it's actually saying is your HDL cholesterol concentration is 50 milligrams per deciliter. So don't say that your LDL is 120. Say that your LDL cholesterol is 120 milligrams per deciliter. It's very important, I think, to be accurate in our nomenclature.

So the reason that saying there's good cholesterol and bad cholesterol is nonsensical is because cholesterol is cholesterol is cholesterol. The same molecule of cholesterol inside the HDL is present inside the LDL. What's bad about the LDL is that the LDL traffics that cholesterol into the artery wall where it will get retained and oxidized and lead to the process of atherosclerosis, whereas the HDL will not do that.

That's the fundamental difference. We should really never say good cholesterol and bad cholesterol because it's highly inaccurate and it only reflects a lack of understanding of what one is talking about, which is why it certainly would be a red flag if a doctor ever said that. And then moving to the nutrition side, do you maybe want to take a minute to talk about why nutrition research is so flawed and so hard to do?

And then how, because that's true, that kind of affects everything you look at within nutritional epidemiology and trying to understand that question of which diet is quote unquote best. Well, I mean, we could spend an hour on that question, which I don't have the appetite for. I think it comes down to the complexity of the organism at question, which is us and the complexity of the intervention, which is eating.

So it's really the worst of both worlds. We can study something as complicated as nutrition in a simple organism that can be put in a cage where you can control everything and where lifespan is short enough that you can actually measure how inputs affect outputs on a reasonable timescale. But to be clear, even studying the effects of nutrition in a confined environment using more complicated mechanisms

organisms such as rhesus monkeys, as was the case in the NIA Wisconsin experiments from the 1980s, which again began in the late 80s, I believe, that's an experiment that could never be replicated. I mean, it took north of 20 years to do an experiment in rhesus monkeys where you could still have perfect control over what they ate. And it's not entirely clear what the answer was. That was an experiment that sought to test the question, does caloric restriction extend life?

And the answer turned out to be, it depends if your monkey lives in Wisconsin or Bethesda, Maryland.

Of course, I'm being tongue in cheek. I think that study did answer the question if you knew how to read the study. I won't get into that because I think I have a whole chapter devoted to that in the book. That's basically the long and short of why it's so difficult to study. So when you study it in humans, you can do controlled experiments in a research setting. But by definition, they can't tell you anything about health in the long term sense because it would be almost impossible to confine humans for more than a month or so and control everything they ate.

So one can do those types of experiments to understand very precise mechanisms of action, but those rarely translate to a clear understanding of health. If you want to understand

what happens over the course of a year, three years, five years, 10 years, by definition, you have to do that outside of a hospital and you have to do it with patients being able to eat what they want. There are some historical exceptions to this rule. So for example, the Minnesota coronary study was a seven-year study that was, well, I shouldn't say that. I think the actual intervention was probably closer to three or four years. I could be wrong on that, but it was done on patients in a nursing home.

And there you had the interesting situation where you had patients who were relatively old, therefore at high risk for ASCVD, but the investigators had complete control over what those patients ate because every meal was being provided to them. That experiment was rather interesting in that it did not yield what the hypothesis suggested. I think there's lots that could be learned from that potentially. But net-net, this is why nutrition in humans tends to rely heavily on epidemiology where you...

You are looking for patterns without doing an experiment, without randomization. So with your patients then, are you still continuing to try and manage their nutrition, manage their diet, not to you put everyone on the same diet, but more so what is that patient doing and how do you get the best metabolic health for that patient?

Yeah, I mean, we think that the most important parameter for determining metabolic health is energy balance. So even the quote unquote best diet

if it's in excess of energy balance, will produce poor metabolic health. So regardless of what you think the best diet is, if you think it's a keto diet or a paleo diet or a low-carb diet or a Mediterranean diet or a vegan diet, take any version of those and consume them to excess to the point where you are no longer in energy balance and you are accumulating

adipose tissue that leaks out of the subcutaneous space and gets into the liver, gets into the viscera, you're going to be unhealthy. So I always think people are majoring in the minor and minoring in the major on nutrition when they start to fight in dietary tribes on this stuff.

There are some general principles. Look, I do still think that clinically, in my experience, patients with profound insulin resistance tend to respond better to carbohydrate restriction as the best tool to reduce total intake. You have to create a caloric deficit in those patients. And in my experience, they respond better to carbohydrate restriction than they do straight caloric restriction or fat restriction.

Ultimately, it matters most that you can find something that is manageable and sustainable over the long haul. None of this matters if you can adhere to the perfect diet for three months and then you can't. It's better to have a 7 out of 10 diet in terms of quality and perfection that you can sustain indefinitely than a 10 out of 10 diet that you can only sustain for three or six months.

Some other questions we see come through are questions where people are kind of confused on why should we not just look to populations with longer lifespan and attribute their longevity to their diet? So there's different populations around the world who will traditionally live longer. And so do you associate their longevity with their diet? Is that a mistake for people to do?

It's a complicated question because there are probably too many factors that factor into why these populations live a long time.

So if you look at, for example, the Okinawa, right, everybody loves to talk about the Okinawa in Japan, unquestionably a very long-lived people, although I've read recently not as long-lived. As the current generation of Okinawan adopt a more Western lifestyle, inclusive of diet, by the way, a lot of those things seem to go away. So it suggests that it might not just be the diet that is responsible for the benefits that these cultures bring.

are bestowed with. So what are some of the other things that could factor into that? Well, we could certainly look at activity level, exercise level, sleep, stress, social connections, lack of other toxic elements in the environment. I think the same exercise is true when you look across all of these populations. The other reason that I think it's very difficult to say there's any one perfect diet is when you look at these different

populations and pockets over the past hundred years that have popped up and have been studied who seem to outlive others, even in relative proximity to them, their diets are actually quite diverse. So what does that tell us, right? So if you have people in Japan and people in Switzerland and people in this part of Africa,

and people in this part of the Arctic or whatever, where you see reasonable pockets of longevity, but their diets are relatively diverse. It might be interesting to look at what's missing from all of the diets, or what do they have in common in their absence, or what do they have in common in their presence. But to me, at least, it suggests that there's probably...

pretty robust nature within the human to manage a variety of different dietary conditions. Again, it comes down to provided energy balance is met, and I think provided that a person stays metabolically healthy, so they're active, they're sleeping well, cortisol levels are not through the roof. All of this is to say, I think our diets are problematic in this country, but

I don't think that changing the way people eat alone will turn us into quote unquote a blue zone. You hinted at this earlier question we get asked a lot, which is, are you still doing your longer fasts? And if not, why is that?

I'm not. And I think there were several reasons I'm not, but truthfully, perhaps one of the most logistically relevant ones is just, I don't travel anymore. I used to only do my long fasts when I was traveling, when I was away from home. And it was just so much easier to be fasting when I was in New York than being at the time in San Diego. But now I never travel. So it would mean that if I wanted to do long fasts, I'd be doing them at home

and I just don't feel like doing it. And I don't have a better answer than that. I think it also speaks to the fact that I don't have a clear sense of what the benefit is. This is one of those things where I'm going to reserve the right to completely change my mind. If I had some biomarker that could convince me that a seven-day fast, even once a year, had a meaningful rewrite on some negative processes in my body, I mean, I would happily make that sacrifice again. But in the absence of knowing that, the cost is a bit high right now.

Another thing on the nutrition side that you talk about a lot is the importance of protein. We just did a premium email that kind of looked at the pros and cons of protein because when you look at protein and aging, it does seem like it's a bit controversial in sense of what people will recommend. And so the question that came through and comes through often is if someone's under 50, so let's say you're 30 or 40,

Do you think it's important that they err on the side of caution and eat less protein based on the research? Or do you still think no matter what age you are, protein is so important and that everyone should be getting as much as possible of it? I think it depends on how much muscle mass that person has. So if you have an individual who's overnourished and adequately muscled,

So they're overweight, but they actually have a sufficient amount of muscle mass and they need to go into a caloric deficit. We would certainly tolerate also a little bit of a protein deficit in that individual, not because I think it's necessary, but because I think it's easier to hit caloric targets.

If you are able to relax your protein targets. In other words, if you say you need to be in a caloric deficit and hold one gram of protein per pound of body weight, that becomes really challenging. If you say, look, you could be at 0.6 to 0.7 grams of protein per pound of body weight and create a caloric deficit is much easier.

Conversely, if a person is overnourished and under-muscled, I think we do have to toe that fine line of keeping protein high because that person needs to be putting on muscle as they're losing fat. The truth of it is, I don't find the data for people below 50 having an increase in mortality with high protein being at all convincing. I think that is easily attributed to caloric excess as opposed to protein excess.

And I think that there are enough other confounders there that it's really a proxy for poor health than it is a proxy for high protein. Furthermore, the absolute mortality in people below 50 is so low in terms of absolute amounts that even a slight increase in the relative amount is trivial. Finally, it's very important when people are still able to put on muscle that they put on as much as possible.

Because once you're in the over 50 category, you're kind of clawing on for dear life and trying to keep as much of that muscle as possible. So I don't really want people entering middle age with a muscle deficit. This kind of goes back to our original question, like,

Even if someone comes up with the solution for cancer and Alzheimer's disease and all of these other things, you still have to ward against frailty. You still have to make sure that you enter that marginal decade physically robust. And most people don't come close to it. They're really, really under-muscled late in life.

Another question we get asked a lot is how do you eat so much protein in a day? As we're kind of going through Peter protocols, why don't you just run us through your protein per day and what that looks like?

Again, I have the luxury of being at home, so I have more control over what I eat than if I was back on the road, but I get a lot of it through venison. Maui Nui, again, disclosure, I'm an investor in that company. They make a really, really good venison jerky stick, and I love it because it has no garbage in it. It's literally just got some natural flavors in it. I absolutely love the taste of it, so that makes life easy. Each stick, I eat the peppered ones

It has like 9.9 grams of protein in it. It's funny, the USDA makes you, or I don't know if it's the USDA or whichever governing body determines food labeling, you have to round down. So it says nine grams of protein on the stick.

But it's actually 9.9 grams is what it measures. So I actually think of each stick as having 10 grams of protein. So I will easily throw down 5 to 10 of those sticks a day. And that would represent one versus two high-protein snacks. And then the rest of it, I'm kind of getting in my food, basically.

Lately, I haven't really been doing much on the protein shake front because the jerky sticks are just quicker and easier for me than making a shake. But I would also use a high quality whey protein shake if necessary. So it's not that hard for me to kind of hit my goals throughout the course of a day. And by the way, what am I targeting? Somewhere between 150 and 180 grams of protein per day. And how often does that spread out between? Typically like four hits.

Yeah, I've been in plenty of meetings with you where you'll walk in with just a handful of jerky sticks, drop them on the table. You'll be like, anyone else want one? And then within 15 minutes, they're all gone and all the wrappers are right in front of you. So I can attest that I've seen you do that protocol for sure. Anything else on the nutrition front you want to talk about before we move on? No. All right.

Next section, wearables. What is your current favorite wearable or just a device that tracks things for you? So maybe it doesn't have to be something that is like on your body at all times, but just what's your favorite device for tracking? And it can be tracking anything.

I've been using something called Morpheus lately. It's got two heart rate monitors. It's got a chest strap and a wrist strap, not a wrist, a forearm strap. It's got an app that in the morning you lay down and put the heart rate monitor on and you answer four questions. How long did you sleep last night? So I checked my eight sleep for how long I slept and then how well did you sleep? So I look at my eight sleep score and get a sense of the quality of my sleep and then I enter that and

And then how do I feel and how sore am I? So it asks these four questions. And then I do a two minute lay down with the heart rate monitor on and it measures my heart rate and my respiratory rate and my heart rate variability. And then it spits out a readiness score and it provides training zones via heart rate for the day.

So for the past six months, I've been doing an experiment where every time I do a Zone 2 workout, I'm using the heart rate that it predicts. I'm riding to my RPE, and then I compare the lactate at the end of that ride to the predicted heart rate from Morpheus to the RPE heart rate.

And I will say that it tracks pretty darn well, better than I would have expected. And the reason I'm doing this is to see if this could be a good tool for our patients to use who might not be as clued in to their own RPE and who clearly don't want to check their lactate levels. And are you using Morpheus for anything else?

Do you use any of that data for anything outside of zone two? Are you using it for how hard you'll push that day lifting, anything like that? I don't. Certainly that's how they would suggest you use it. I don't wear it outside of my zone two or VO2 max training. So I don't wear it when I'm in the weight room. I don't wear it rucking in large part because I hate wearing heart rate monitors in general. I don't find them comfortable. I can sort of tolerate it when I'm on a bike, but I don't want to be rucking with one. I don't want to be lifting with one.

It's probably the case that it would be an even better predictor of my training if it could see me across the day. If it could see me train in every workout, it would probably be an even more effective tool.

Because it would understand where I am in terms of overload. Another wearable we get asked a lot, you've talked a lot about this and I believe you still use it with a lot of patients, is CGMs. Is that something you're still using a lot with your patients? We do, yeah. We use CGM a lot. It's a great tool. When we have questions...

It provides answers. We could sit here and look at a person's OGTT. And some cases, it's just a slam dunk, like this person isn't super metabolically dialed in. In other cases, it's a complete slam dunk. This person has type 2 diabetes by OGTT criteria, even if not by A1C criteria. But there are a lot of people in the middle. And this is a great way that we can glean more information and really dial in our treatment for them.

And so there was some controversy way back when on if CGMs were still valuable, still useful for people who are non-diabetics. Have you changed your opinion on that at all? Not one bit.

Do you maybe just kind of want to walk through people what you look for with CGMs and ultimately what people if someone's wearing one because it seems like it is more widely available for non-diabetics now and so you see a lot more of them around so if someone gets one what are some of the things you like to see within patients what are some of the things you look at how do you use it?

I mean, we still look for the same things. I think average blood glucose is still the most important metric we care about because that's the one for which we have the most data. In other words, we know all-cause mortality data as it relates to hemoglobin A1c. Hemoglobin A1c is a measurement that's used to impute average blood glucose.

So this is a very, very close proxy. When we can see average blood glucose on CGM, even though that's not the same as measuring A1C, it's very difficult to argue that knowing your average blood glucose on

and knowing your A1C aren't highly comparable, and therefore by proxy, the lower your average blood glucose on CGM, the lower your all-cause mortality. Because it is abundantly clear that the lower your hemoglobin A1C, even outside of the diabetic range, the lower your all-cause mortality. So first and foremost, that's the metric we care about. The other metrics we look at, of course, are what's the standard deviation. So all things equal, do you have less variability in your glucose than

then more. And then finally, and the least important, I think, is how big are the spikes you're seeing? Now, in truth, that becomes less important if the first two are reasonable. If a person's average blood glucose is 98 milligrams per deciliter with a standard deviation of 16 milligrams per deciliter, it doesn't really matter what kind of spikes they have because they're clearly not going to be too many unless they're using insulin. You could

obviously arrive at those numbers the wrong way. So I would say that fixating on average blood glucose and standard deviation are probably the most important thing. From when you would wear one, do you recall what caused the biggest spike you ever saw? No, I don't recall. A buddy of mine took me to this vegan restaurant in New York once. I think it was called like Candle 79 or something. It was really close to my apartment.

And it was great. It was amazing food. But obviously by definition, like it's just basically all carbs. And I remember the dessert was so incredible. And I remember looking at my CGM afternoon, it was like 180. And I feel like that's about the highest I'd ever seen. Funny. Do you think...

We're any closer to continuous blood pressure monitors. Absolutely. You do? Oh, yeah. How far out do you think that is? Because I know in the past with Ethan Weiss, the AMM blood pressure, you've talked about how important that is as a device. I think we have it. So I think the Actia device works. At least it works as well as an automated cuff works. So this is a device that is not yet FDA approved.

but it is approved by the similar governing bodies in Europe. So this is a device that's already on the market in Europe. It's a bracelet that you wear that optically measures a signal in your wrist and you calibrate it against an automated cuff. And every two hours, it gives you your average blood pressure. So over the course of a day, you'll get 12 blood pressure readings. I would say even though automated cuffs in general aren't nearly as good as manual cuffs,

For an automated cuff, I don't see any difference really between this and pick your favorite automated cuff. So I really hope that this device gets approved in the US because we'll certainly have every one of our patients wearing this and it would do away with ambulatory blood pressure cuffs, which are cumbersome and difficult to use and low compliance and artificial. Interesting. So any listener viewer who

in Europe would have access to this. That's right. And then what do you think the rough timeframe for people in the US? Is it years, a decade? How does that process typically work? It's entirely dependent on the FDA. It's possible it doesn't get approved at all if the FDA is difficult to work with on this, unfortunately. I hope that's not the case. So if anyone listening and watching works for the FDA, something to internally push on then. Yep.

Any other wearables that you're excited about, whether they're close to being here or even in the long term, like 10 plus years? I would always welcome continuous lactate monitoring during exercise. That would really, really make zone two training enjoyable for me. Just as opposed to having to do the finger pricks all the time or just knowing where it's at?

To me, it's the most accurate way to really understand what's happening. I mean, even heart rate and RPE are just approximations for what you're really interested in. So I think, yeah, just being able to monitor lactate levels while you're exercising, especially doing cardio training. I'd also love to be able to do my VO2 max workouts with a lactate meter, continuous lactate meter, so I could actually watch lactate rise and clearance on each subsequent set.

As I'm fatiguing, am I really just breaking down metabolically as much as anything else? So Peter, I think that was the majority of the questions we wanted to get through. As we kind of said at the outset, those are questions that come through often. So we compiled them here, but any closing words you want to tell people? No. What episode number are we at roughly? Well, at the time of this recording, 267.

So this will be in the 270s, creeping up on 300, but also at the time of this recording hit five years as a last month, which is crazy because...

That's what was fun to have David Sabantini and Matt Caberlin back on is because they were not only the first 10 episodes, but if I remember correctly, I think that was you and Bob interviewing them and recording it for the book that we then turned into a podcast, which one shows that we didn't even think about the podcast at that time. And two, it shows how freaking long you wrote that book for.

That's right. I remember those interviews. I went up to Boston with Bob in the summer of 2017 to interview David. And then Matt came to New York and I interviewed him a month later. And that's like a year before the podcast came out. So yes, that was literally just done for the book. Pretty funny. Yeah. It's kind of crazy to see how far things came along, not only with the podcast, but also now

seeing the book out and the reception from that, which is great because we've joked about it before, but I think we can both seriously say there was a lot of periods of time where we didn't think that book was ever going to get released. Yeah. Right up until a couple months before. Yeah. Yeah. All the way up until 2023. So awesome. Well, hopefully people enjoyed this kind of a little different of a style, but until next time, Peter, have a good one. You too, Nick. Thanks, man.

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