The Tim Ferriss Show Transcripts: Dr. Peter Attia — The Science and Art of Longevity, Optimizing Protein, Alcohol Rules, Lessons from Glucose Monitoring with CGMs, Boosting Your VO2 Max, Preventing Alzheimer’s Disease, Early Cancer Detection, How to Use DEXA Scans, Nature’s Longevity Drug, and More (#661)

Please enjoy this transcript of my interview with Dr. Peter Attia (@PeterAttiaMD), the founder of Early Medical, a medical practice that applies the principles of Medicine 3.0 to patients with the goal of lengthening their lifespan and simultaneously improving their healthspan. He is also host of The Drive, one of the most popular podcasts covering the topics of health and medicine. 

Dr. Attia received his medical degree from the Stanford University School of Medicine and trained for five years at the Johns Hopkins Hospital in general surgery, where he was the recipient of several prestigious awards, including Resident of the Year. He spent two years at the National Institutes of Health as a surgical oncology fellow at the National Cancer Institute, where his research focused on immune-based therapies for melanoma.

His new book is Outlive: The Science and Art of Longevity (3/28).

Transcripts may contain a few typos. With many episodes lasting 2+ hours, it can be difficult to catch minor errors. Enjoy!

Listen to the episode on Apple Podcasts, Spotify, Overcast, Podcast Addict, Pocket Casts, Castbox, Google Podcasts, Stitcher, Amazon Musicor on your favorite podcast platform. Watch the interview on YouTube here.

#661: Dr. Peter Attia — The Science and Art of Longevity, Optimizing Protein, Alcohol Rules, Lessons from Glucose Monitoring with CGMs, Boosting Your VO2 Max, Preventing Alzheimer's Disease, Early Cancer Detection, How to Use DEXA Scans, Nature’s Longevity Drug, and More


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Tim Ferriss: Dr. Attia, Peter, nice to see you.

Dr. Peter Attia: Good to see you, man.

Tim Ferriss: I wanted to start with the personal, we’re going to get into all sorts of topics, many different aspects of your practice, lessons learned, et cetera but I went to your house recently. We had some Topo Chico and a bite to eat and a few other things. And I commented on how much larger you were and not larger as in obese, but muscularly larger. So I thought we would begin with the question of how and why, not necessarily in that order, you added so much muscle mass.

Dr. Peter Attia: In the fall of 2021, I had sort of hit a relative low in weight that wasn’t quite as low as where I was as a cyclist, which was probably about 165 pounds, but was still pretty low for me in the maybe mid-low to mid 170s. And I did a DEXA scan, which I do periodically, probably a couple times a year, but I hadn’t done one in a few years. And when I get my DEXA scan, I always plot the data. So I’m not just interested in body fat, but also bone mineral content and many other metrics. But one of them that’s really important is something called Appendicular Lean Mass Index or ALMI. Another one is called FFMI, Fat-Free Mass Index. And it’s probably worth explaining a little bit about what these are, but the ALMI takes what the DEXA scan imputes as the lean tissue in your arms and legs in kilograms divides that by your height in meters squared.

So it spits out a number like eight kilograms per meter squared. This is a pretty accurate representation of how much muscle you have in your arms and legs because the DEXA scan can really only identify three things, bone fat and other. And since things in your arms that are not bone and fat tend to be muscle, it’s pretty good at identifying muscle, whereas the Fat-Free Mass Index looks at the entire body and just subtracts out fat. That’s also a good proxy for lean mass, but there are many other things like organs that are taking up some residents there. Anyway, when I looked at these metrics, I was shocked. I was shocked at how much less muscle I had than 10 years earlier, almost exactly 10 years sooner.

And I attribute it to several things, but I really thought that chief among them was just how much fasting I had been doing over the previous three years. I had really kind of taken fasting to a pretty extreme place doing up to 10 days of water only, and routinely just busting out seven-day water-only fasts, certainly doing three days every month would be something I would do without hesitation.

Tim Ferriss: When you say 10 days of water only, over what period of time is that?

Dr. Peter Attia: Meaning how frequently would I do that?

Tim Ferriss: Yeah, I’m just wondering what the cadence was if we take it as a minimal — 

Dr. Peter Attia: Probably quarterly.

Tim Ferriss: Got it.

Dr. Peter Attia: Yeah, probably every quarter. And while I certainly think there are some benefits from doing that, I think what I was sort of confronting was, wow, there’s actually a pretty big cost as well. And I would go out of my way while fasting to still exercise. I was lifting weights every single day, which was difficult sometimes, but doing everything I could to try to stimulate muscle protein synthesis. But at the end of the day, if you’re not providing any nutrients, including amino acids, you’re basically just tearing down muscle to try to rebuild with that muscle. But your net effect is a loss. So I kind of just said, “I’ve got to fix this. I’ve got to do something about this, and I want to have my ALMI be in at least the 90th percentile, if not above the 97th percentile as I age.”

The data are pretty unambiguous that people live longer, better lives with an ALMI north of the 75th percentile. So not one to just clear the bar, I want to be considerably above the bar. So basically I just changed things around and said, “Nutrition and exercise are going to change a little bit,” so we can talk about those changes, but basically I’ve made big changes with exercise and nutrition to make those corrections.

Tim Ferriss: How much lean mass did you gain over what period of time would you say once making these changes?

Dr. Peter Attia: So in a span of, oh, God, I’d have to go back and look at the exact data, I believe it was 13 or 14 pounds of lean mass in about 12 months.

Tim Ferriss: Mm-hmm. And what were — 

Dr. Peter Attia: Which is, again, that’s not Herculean, right? These are not insane numbers, not taking anabolic steroids, this is relatively doable for someone who is making it a high priority to eat the right amount of protein, the right kind of protein, and spacing it and consuming it at the right times, and then also focusing, training on a little more hypertrophy.

Tim Ferriss: So for people listening, I’m asking these questions not simply because I’m interested in lean mass, but also the implications for longevity. So I’m guessing you did not put all of that lean muscle on your biceps and that there were other movements that were incorporated for very particular reasons if I’m getting my read on Dr. Peter Attia, right as I think I am. So perhaps you could just describe some of those changes and also protein and how you suggest people think about protein, how you began thinking about protein.

Dr. Peter Attia: Yeah, I’ll start with that and then we can talk about the training. So the protein basically went to a very conscious and concerted effort to increase protein to one gram per pound of body weight. People are going to ask, “Is that one pound of actual body weight? Is that one pound of lean body weight? Is that one pound of target body weight?” The answer is for someone my size and weight and my body fat percentage, I think at the time I was about 15 percent body fat, it really doesn’t matter. It could be basically, call it one pound of current body weight, one gram per pound of current body weight is sufficient. So that’s what I did. The next question that becomes timing. And this is something that right until a couple years ago, I wasn’t really paying enough attention to. So it wasn’t enough to just say, “Well, Peter, you’ve got to have 180 grams of protein in a day,” because for example, 290 gram bolus of protein doesn’t accomplish nearly the same thing as 445 gram servings spread out over the course of a day.

So there is kind of a sweet spot with protein where you really need to be north of about 20 to 25 grams to ensure that those amino acids aren’t just going into what’s called a gluconeogenic pathway. So we can turn protein into glucose, but we don’t really want to, protein should be thought of as a structural nutrient, whereas we want to really think of carbohydrates and fats as energy nutrients. So you have to have enough protein in a given serving that you don’t just have the liver take it and use its bit for gluconeogenesis. At the same time you don’t want to have too much and too much is a bit of an unclear limit, but my best reading of the literature is that you’re starting to hit too much at about 50 grams in a serving.

Tim Ferriss: And what type of protein are we talking about just in terms of, I’m thinking of bioavailability and so on, and kind of protein efficiency ratio. What type of protein, how should people think about quality or type of protein?

Dr. Peter Attia: So the first decision I think everybody wants to make is, am I getting this from plant or animal? And again, unfortunately, this has become sort of a contentious topic and it’s got its sort of political religious overtones to it. But if you don’t concern yourself with any of those things and you just think about biochemistry, there’s really no ambiguity here. Protein derived from animal sources are more bioavailable. So you can overcome some of that by cooking the plant. So once you start to cook the plant and free it up from the fiber, you can liberate more of the plant protein, but you’re still always going to be struggling with a bit of a bioavailability problem. That can be anywhere from a 20 percent to 30 percent haircut, you’re taking just on the net consumption of the amino acid. The second issue comes down to amino acid quality.

And if you’re really concerning yourself with hypertrophy, I think the three most important amino acids would be leucine, lysine, and methionine. And these are amino acids that also you don’t tend to have as high a quantity in plant protein. Now you can get them, and it gets especially hard if you can’t have dairy or eggs. So if someone says, “Look, I’m a vegetarian, I’m not going to eat beef or chicken, but I’m willing to have eggs and dairy,” it gets a lot easier. Eggs, for example, are a very high source of methionine. So what we typically will tell patients is rather than just fixating on the total number of grams of protein you need to eat, which you may have a hard time hitting, if you focus on the number of grams of leucine, lycine, and methionine you’re getting in a given meal or a given day, that will almost assuredly get your total protein quantity to the right place.

So for me, that really meant, I just wanted to make sure I was getting, gosh, probably six to eight grams of leucine a day, comparable amount of lysine, at least two grams of methionine a day. And I use an app to track what I’m eating just so that I can see where my protein is coming from and how much I’m getting and when and where and that tended to work out pretty well.

Tim Ferriss: What is the name of the app if you’re willing to mention it?

Dr. Peter Attia: Yeah, it’s called Carbon. I have no affiliation with it, but a friend of mine, it’s his app and I like it.

Tim Ferriss: Okay.

Dr. Peter Attia: I guess my affiliation is that it’s my friend’s app.

Tim Ferriss: I’m glad you brought up the leucine, lysine, and methionine, because I was going to ask earlier if while you were fasting, but losing lean muscle mass over time, you were supplementing with say, branch chain amino acids in any fashion.

Dr. Peter Attia: I was. I used to always drink BCAAs during workouts and for folks listening, there were three branch chain amino acids. And leucine is hands down the most relevant of them and we know from work that our mutual friend David Sabatini has done in his lab that leucine is a very, very potent mTOR stimulator. In fact, it might be the single most potent stimulator of mTOR, mTOR, of course, acutely, you want that thing stimulated. It’s promoting growth. You don’t want it chronically stimulated, but you want it acutely stimulated. The problem with branch chain amino acids, and I’ve got to tell you, Tim, I think it’s largely fallen out of favor. So I don’t even consume branch chain amino acids anymore. When I’m during a workout, I’m literally just consuming like an electrolyte drink. That’s it.

The problem is, one, they don’t stick around long enough and they’re free form, and two, you’re just not getting enough of them. The third thing is the temporal nature of when you take them in being in the workout or couple hours after the workout doesn’t really seem to matter, our window in which we can synthesize new muscle is sufficiently broad that even for an untrained individual who has a narrower window, it’s totally reasonable to say, look, just make sure a couple hours after that workout, you get in your big protein meal. So instead, today I just use high-quality whey protein post-workout, and I don’t trouble myself with consuming any protein in workout.

Tim Ferriss: So I just want to mention a few things for folks. So number one, there’s a huge difference between no animal products and lacto-ovo vegetarian. And one example of that would be Bill Pearl, who became Mr. Universe as a lacto-ovo vegetarian. So it does make a huge difference. The second I’ll just mention, we may come back to this and discuss keto at some point, we have discussed it at length in previous conversations, but the gluconeogenesis is one of, well, is I suppose the pathway by which you can knock yourself out of keto if you consume too much protein and not enough fat. Liver just loves to convert that into glucose and then bada bing, bada boom, you’re out of ketosis, or at least out of sort of the range that one would be aiming for.

So let’s come to the book. So you and I have had many offline conversations about the book. We’ll probably not repeat some of them. Why did it take so long? And I believe there were three iterations over six years, and the first iteration had a zero translation into the final version. Something along those lines, maybe you could correct me if I’m getting that wrong, but why have you taken so much time to work on this book?

Dr. Peter Attia: Yeah, it’s a really good question, Tim. I think there are probably several factors, some of which are related, some of which are not. I think on one level, my appetite for how “good” I needed this book to be was very high. And I say that with no — 

Tim Ferriss: So unlike like you, Peter.

Dr. Peter Attia: Yeah, yeah, yeah. Look, I think there are some people out there who can churn out a book a year, and more power to them. But the way I viewed this book was that this is sort of the one and only book I ever want to write. Will I ever write another book? It’s hard for me to ever imagine the answer to that question is yes, but again, maybe at the end of my life I’ll have something else to say. As I’m 50 years old now and I’m at the midpoint of my life or slightly past the midpoint of my life, I feel like everything I ever want to say on this particular topic is in this book. And therefore, it was just a very long book. I mean, the final version is probably 140,000 words. The version I ultimately submitted was 200,000 words.

This has been chopped way down by 30 percent into what is still obviously a book that is quite long. So that’s part of it. I also think part of it is, and maybe you can relate to this, Tim, I don’t know, we’ve never actually talked about this, but I think there’s just a vulnerability that comes with writing in this manner that is unlike all the writing I’ve done in the past. So I’ve been blogging insanely for 12 years, that’s different. You’re not really putting yourself out there when you write a blog post. You don’t have to read the comments that people write. You don’t have to pay attention to any of that stuff. I think when you write a book, you are really saying to people like, “Here I am, tear me down.” And I just think there’s, on some level, maybe it’s embarrassing to say this, there’s just been a little bit of a reluctance to be that again, for lack of a better word, vulnerable, just to sort of say, “Okay, I’m willing to say everything I have to say on a subject matter and now let the arrows come flying.”

And that’s, again, I don’t know that that makes sense, but I’m sure that anyone who does something very public feels that way. But it’s different with podcasting, which I don’t have a problem doing, and it’s different with blogging, which I don’t have a problem doing. But this strikes me as maybe what an actor feels like when they make a big film or a director, or again, like an author like you. So I think there was a little bit of subconscious dragging my feet and hey, maybe I can just keep working on this book forever, but it’ll never actually come out.

Tim Ferriss: So I do identify, and I would say for me at least, part of that is when you put out a book, it might be one of the 20 books the publisher’s working on that season, but especially if it’s a book of this depth and also I will second vulnerability, not just on the personal side when discussing physical health, but also in the chapter or as a dissection really on mental health, psychoemotional health, and so on, I mean, you really show sides of yourself that are uncommonly shown, I think in some of your other formats. And unlike a blog post, it’s very hard to just delete a book from the world once it is published. So I, number one, think it was right to take it seriously. And however long it takes to do a book of this quality is the time that it takes. And I think that’s the way it should be.

And I will say, just as a side note, and I mentioned this to you and you know this, that my dad, who has struggled in various ways with health for decades now, picked up your book, which I had at home when he was visiting me in Austin and could not put it down. I won’t get into all the details of why this is the case, but if that isn’t a testimonial, I cannot imagine what is to the extent that I ended up giving him my copy so he could take it home. So that should tell everybody.

Dr. Peter Attia: I didn’t know that, Tim, thank you. Because when you guys came over, he mentioned how much he was liking it. He had just picked it up, but I didn’t realize he’d finished it and he enjoyed it, so thank you. That means a lot.

Tim Ferriss: Yeah, definitely. And with that, let’s talk about perhaps this is a good place to start, objective, strategy, tactics. Why are these three pillars important, and why all three?

Dr. Peter Attia: I learned about this stuff about a decade ago when I was working on a problem that is irrelevant now, but I think the message was important, which was, I think I had a vague sense of what the objective was, and my immediate tendency, which I think is normal, and I think we all do, because I don’t think anyone’s hardwired to go through the middle step, was to go from objective to tactics. In fact, I think most people just kind of go to tactics without even thinking about objective. And certainly not having that strategy piece in the middle makes life really complicated. So the first thing, I think, is to understand what’s the difference. So objective is pretty straightforward. It needs to be stated. It should be very clear, though. So for example, my objective might be to live longer.

If you said, “Well, what are the tactics now? What should I eat? How should I exercise? Do I need to take this supplement or that supplement?” The probability that you are going to come up with the right set of instructions is vanishingly small. It’s somewhere between zero.

Tim Ferriss: Even if provided this list, this laundry list of tactics.

Dr. Peter Attia: Well, I guess the question is how do you come up with the list? Are you filtering on that list? Right? So there’s no shortage of tactics that one could think about because the world is rife with everybody offering their tactics. But it’s not like I’m not suggesting tactics, but what I really want people to do is say, “Look, let’s anchor to a strategy.” So for example, if one of your objectives is, “Okay, I’m going to live longer,” it’s like, no, let’s deconstruct that. What does living longer mean? Well, to understand what it means to live longer, you have to understand what ends life. Well, what ends life is a very clear and easy-to-understand dataset so let’s look at it and let’s look at it in great detail. We call this the death bars analysis. So what are the death bars? Well, it turns out if you’re over 40, you don’t smoke, we can really clearly tell you that there’s about an 80 percent chance you’re going to die from atherosclerotic cardiovascular disease, cancer, neurodegenerative disease, or metabolic diseases such as type two diabetes and things like that.

Probably I would include accidental death in there, so falling or automotive accidents. So that’s an important insight because now you start to work backwards from there. So wait a minute. You think, oh, if I want to live longer, I have to avoid those things. Okay, how do I avoid those things? Well, let’s start with the chronic disease bucket. There’s two ways to think about that, right? I love when things turn into somewhat binary decisions, is one way to live longer, to live longer with a chronic disease or live longer without a chronic disease. So might not be entirely obvious which of those is true, but if we look at the data, it’s pretty clear. The data unambiguously make it clear that you will live longer if you can extend the period of time that you live without a chronic disease, rather than extend the period of time you have the chronic disease.

So in other words, it’s better to get cancer later in life than to live longer with cancer as one example. It’s better to have your first heart attack very late in life than have it early in life, and then be right on the verge of having another one as time goes on. Well, just by going through those very simple questions, all of a sudden you start to formulate a much clearer strategy for living longer that points you much more clearly towards this idea I talked about in the book called Medicine 3.0 rather than Medicine 2.0. And once you iron all that out, then you start to get into the tactics. Oh, all right. Okay. So how does nutrition layer onto this? How does pharmacology layer onto this? How does exercise layer onto this, et cetera.

Tim Ferriss: I want to just share an anecdote, which will not surprise you, but when I published The 4-Hour Body, and no doubt you’re going to get a lot of these types of requests if you haven’t already, I had a number of, not morbidly obese, but out-of-shape CEO friends say, “Look, I just want the index card. Just give me the index card with the seven things I should do, and I’ll do those seven things.” Can you guess what the compliance rate was with that, Peter? What’s your guess?

Dr. Peter Attia: Very close to the success rate of skipping the strategy step.

Tim Ferriss: Zero percent. Not a single one of them actually implemented any of it. And just as a quick side note, which you might entertaining, I had an amazing mega-successful investor named Ed Thorpe on the podcast, if not over 90, 90 right now, he’s in excellent shape and he plans his travel around minimizing time in automobiles. And he’s sort of run through the numbers just as an anecdote.

Dr. Peter Attia: Very underappreciated, very underappreciated cause of morbidity and mortality. Yeah, I think about it a lot.

Tim Ferriss: Yeah. We might come back to as I think about a different seat belts that you can use in life, which initially, I don’t want to turn this into a Tim Ferriss TED Talk, but initially thought about with respect to COVID early, which was like what minimally inconvenient, easy-to-do things can you do to dramatically mitigate risk. So even though you’ve never had a head-on collision, the downside of having a head-on collision is so high that most of us will wear a seatbelt when driving on the highway. Most of us will have a fire extinguisher in the kitchen even though there’s never been a fire in your kitchen, et cetera. So where else can we take very small steps that are easy, low cost, that prevent dramatic downside risk?

But so we may come back to that, but I want to bring up a graph that you have in your book, page 28 for those who want to find it, where if you remove the top eight contagious/infectious diseases, meaning we’re accounting for the advent of antibiotics, at least as I understand it. We haven’t really seen a material or at least large change in mortality rates since what, 1900 if you sort of account for some of these variables. Why do you think that is? Because certainly most people don’t want to die.

Dr. Peter Attia: Yeah. So you’re absolutely right. So life expectancy since 1900 to today, has increased by twofold. It’s remarkable. It’s gone from about 40 to about 80 plus or minus, but that’s directionally the change we’ve seen in, call it 120 years. And I do think that understandably, it’s tempting to tout that as the marvels of modern medicine. And you’re thinking, well, oh, my God, we went from 40 to 80 in 120 years, the next 40 just based on Moore’s Law, that’s got to get us to like 160, right? Okay, maybe. But let’s take a closer look at the data. So you do this very simple analysis, which is, okay, let’s go back to 1900 and march forward. But when we go through the mortality tables, just strip out the top eight leading infectious disease causes of death.

And what you see is exactly what you describe. There is now no change in mortality from then until now effectively. There’s a little bit, it’s been a little bit better. And I think what it speaks to is two things. One is the remarkable success of Medicine 2.0 in solving acute care and infectious diseases, and the remarkable failure of Medicine 2.0 in addressing the chronic diseases that sat under the surface of the water waiting for the tide to go down.

Tim Ferriss: And those would be presumably the four or five likely causes that you mentioned earlier. Perhaps this is a good place for you just to define or describe briefly, not Web 2.0, try that again, for you to describe medicine — I’m not going to be the only interviewer who fucks that up, Medicine 2.0 and Medicine 3.0.

Dr. Peter Attia: It’s probably easiest to just for the take completeness, start with Medicine 1.0. Medicine 1.0 was basically everything that occurred prior to the transition period of the late 17th century into the late 19th century. So that 200-year period marks a transition from when medicine had absolutely no basis in science whatsoever. So I mean, we can mock it now, but truthfully, they didn’t have a scientific method or a scientific tool, so all they could do was sort of think about the gods, think about bad humours come up with the best rationalization they had for what was going on.

In fact, arguably the most insightful thought that occurred in Medicine 1.0 was thousands of years ago on the part of Hippocrates, who was the first to believe that diseases were somehow caused by nature and not the gods. That was truly a remarkable insight now, beyond that, he had no clue what was going on, but that was a remarkable insight, and that was probably the apex of Medicine 1.0. With Francis Bacon in the 17th century, we had basically the first push towards the scientific method. This became really important, and no one has done a better job explaining this than our mutual hero, Richard Feynman. 

There’s a great video, which I’m sure you guys can find for the show notes, where it’s an old grainy black and white where Feynman is talking about the scientific method. And he’s saying, “Look, you make a guess, right? You design an experiment. The guess is called a hypothesis, by the way, it’s just a fancy word for a guess. You design an experiment to test that hypothesis. You do the experiment. You compare the results of the experiment to your guess. And then you decide to either discard or update your hypothesis.” This was such a profound concept that it basically propelled us into Medicine 2.0. And the place where that shone greatest was unquestionably in the world of microbacteria, of microscopic organisms, so viruses and bacteria. And so, again, it’s a brutal, bloody slog to go from Semmelweis to Koch to Lister. But that transition effectively brought us into the modern era where, hey, all of a sudden doctors were washing their hands and not operating on people with dirty hands.

And of course, eventually we had antibiotics and eventually we had vaccines. And taking smallpox and polio off the table and reducing the mortality of influenza and having antibiotics, all of that stuff had such a profound impact on human health that it cut mortality rate down by a half and doubled our life expectancy in the process. So now we’re into the maturation of Medicine 2.0. We saw these other amazing success stories. I think the two most notable by far would be Hepatitis C and HIV. I mean, to think that we’re at a point now where a virus that is as tricky as HIV can basically be rendered a chronic disease on the back of highly active antiretroviral therapy is nothing short of amazing. 

When I was in medical school, Tim, we’re not talking a long time ago, this is 25 years ago, we were told Hep C will never be cured and it will break the back of the US and global transplant infrastructure, meaning we’re going to need so many livers to put into all these people with Hep C that, by 2030, the system will break. And lo and behold, we have a drug that within a matter of weeks will eradicate this thing. So again, huge successes. Now, counter that with what we’ve done against cancer. When Richard Nixon declared the War on Cancer, before you and I were born, it was more than 50 years ago, the goal was to eradicate this disease by the bicentennial in 1976. Well, not only did that not happen, but here we are more than 50 years later, and survival for cancer is barely five percent greater than it was in 1970. I could go on and on, but let’s just look at neurodegenerative disease. So you were talking about six million people with Alzheimer’s disease in this country. If you add up those with Lewy body dementia and Parkinson’s disease, we’re talking about, gosh, another four and a half million.

So we’re looking at more than 10 million people in this country with very, very significant neurodegenerative diseases. And that says nothing about ALS and Huntington’s and things like that. We don’t have a single thing, like a single thing that we can do to cure these people. We have barely a few things that can slow the progression of their diseases. But we’ve made paltry steps against chronic diseases. When you and I were born, the prevalence of type two diabetes was less than one percent. Today it’s 10 percent, effectively. So we’ve seen a log fold increase in type two diabetes. 100 to 120 million people in the United States are metabolically sick, meaning have metabolic syndrome or pre-diabetes, or type two diabetes outright.

So something’s not working. And the current system of Medicine 2.0 doesn’t really seem equipped to address it. It intervenes late, and by the time it’s intervening, it’s not really fixing. So this thing I’m proposing, this idea that of course I’m not the first person to suggest, maybe I’m the first person to talk about it this way, is we want to pivot to this newer way of thinking about things which deviates from Medicine 2.0 in a couple of really important areas. The first is in its timeline. So Medicine 2.0 is largely focused on treating disease. And it’s really interesting when I think about it, because it’s so obvious that I can’t believe I didn’t notice it earlier. But when you’re in medicine, when you’re in medical school, when you’re in residency, when you’re in practice, you sort of need a code for a disease.

You need a code for a disease that you bill for and you treat. And prevention doesn’t really fit into that. So when I went to medical school, I didn’t learn a single thing about nutrition or exercise or sleep or stress management or emotional health. I learned a lot about pharmacology. And it’s tempting at this point to say, well, pharmacology is either good or bad. No, it’s both, right? Pharmacology is good and it’s really valuable, but over-indexing it is bad. And ignoring all those other things is problematic. Those other things turned out to be far more efficient tools of prevention. But if no doctor learned about them, then why are we surprised that Medicine 2.0 is unable to cope with that? So one, we have to understand prevention, and we have to understand the timeline for prevention must start much sooner. You have to start doing these things long before diseases are ravaging the system.

The other big difference is that, as I talked about it, the scientific method was such an important part of Medicine 2.0, and with it came something that I’m sure you’ve talked about many times, which is the randomized controlled experiment. This is the tool that allowed us to do that thing that Feynman described. The randomized controlled experiment is really wonderful. It is insufficient by itself to solve the problem. So Medicine 3.0 needs to go from what we call evidence-based medicine, you only do what the randomized control trial says, to evidence-informed medicine, which is, you take the insights from the randomized control trials, but you have to then modify them and specify them to a given patient. So those are really the huge leaps that we have to take to now make this next transition.

Tim Ferriss: Could you say a bit more, expand a bit, or give an example, hypothetical or otherwise, of moving from the — I don’t want to say sole, but extremely strong focus on only making decisions for patients based on RCT data to what you’re describing?

Dr. Peter Attia: Exercise is a great example. So exercise would say, okay, the recommendations would be to — I’m going to give you two examples, by the way. So this one’s kind of a simpler one, and then a more nuanced, sort of nerdier one. But the nameplate recommendation around exercise is something to the effect of two and a half, three hours a week of moderately vigorous activity. But no one is parsing these data down and actually looking at what metrics matter. Like how much strength do you need to have the absolute lowest risk in mortality? How much cardiorespiratory performance do you need to absolutely lower your risk, literally fourfold, relative to someone in the bottom quartile? So do I have a randomized controlled experiment that tells us that? I don’t. No one’s going to do that experiment, which is, I’m going to take a group of 10,000 people, randomize them to different levels of training, increase each of their fitnesses to relative levels, and follow them prospectively for the remainder of their lives.

That experiment can’t be done. So instead, we have to be able to triangulate between these other sources of data. Another example, maybe a bit more glitchy, might be the way we might use different forms of lipid-lowering medication. So this is kind of a whole other tangent we could potentially dive into, which is if you’re really interested in preventing heart disease, which by the way, number one cause of death in men and women in the United States and in the world, so it’s the four-for-four champion of death. It’s such the champion of death that for every woman who dies of breast cancer, there’s like eight to 12 women who are dying of heart disease. So pink ribbons matter; red ribbons matter more. This disease would be largely preventable if people didn’t smoke, controlled their blood pressure, and had apoB levels that were equivalent to the levels they had as children.

No one will do the clinical trial that will get us there, yet we have all the Mendelian randomization, we have all the mechanistic data. And so an evidence-based approach says, look, we’re going to target LDL cholesterol to 100 milligrams per deciliter. This approach is going to say, actually, that’s probably insufficient for this individual because their risks are higher, and by the way, their appetite for reducing the risk of this disease is higher. So we’re going to take a more aggressive posture, even though the recommendation in the literature is going to be far less aggressive.

Tim Ferriss: So Medicine 3.0 seems to comprise a number of different elements, one of which is early intervention or certainly much earlier intervention, hence, early medical, I can only imagine. And another is medical literacy and a more, perhaps, proactive approach to education and intervention on the part of the patient. So it’s not a passive experience of being shepherded through a system by a doctor or a team of doctors. You take a much more active role. And I wanted to chat about medical literacy because what I’ve noticed, just to give a personal example, I long ago wanted to potentially become a doctor and certainly became fascinated by competitive sports and performance enhancement. And that led to doing my best to read studies and dig into the science and understand as much as possible. I was unsure of the value of that once I shifted courses and decided to do other things.

But in the last, I would say, decade, as my parents have gotten older, as more and more of my friends have run into issues, it is astonishing how valuable this minimum effective dose of medical and scientific literacy has become. I mean, it’s astonishing how much it helps you to navigate things and make decisions and parse signal from noise. So I’d love for you to speak to medical literacy and how one can become more medically/scientifically literate. And certainly, I would highly, highly recommend, I’ll just double down on this, that everybody read this book because I think that your book does a good job of this, a very, very good job. And I’ll just add maybe a sidebar note so I can hear myself talk a little more.

Which is that there’s, I think, a very common trend among people who are well-educated in some areas, but not in medicine or science, to succumb to Scientism with a capital S where they’ll know the term randomized controlled trial, and they will insist that if you say anything outside of the purview of that, that it is unsubstantiated nonsense. And there are other examples of this. Or they’ll over-index on one thing, as you mentioned. So pharmacology, it’ll be either good or bad. But the fact is, anything totally over-indexed, sort of the Paracelsus “The dose makes the poison” type of problem. But could you speak to medical literacy? Somebody’s listening, they say, “You know what? I recognize that I don’t know much about this. I would like to go about it in a really effective way. How do I do it?”

Dr. Peter Attia: I think you and I have even talked about this once before, Tim, and I don’t think I had a great answer for you then, and I don’t know that I have a great answer for you now. It’s really not a simple thing to do. Let’s just start with the nomenclature. My first day of medical school, I still remember one of the professors saying — and I don’t remember the numbers, so the story is not as cool because I don’t remember the actual numbers. But I’m making the numbers up, but not the point, okay? He said, “Well, all of you are smart hotshots that just graduated the first of your class in college. You have an average vocabulary of X words.” And X was like, whatever number. I honestly don’t remember what it was. Call it 20,000 words. He said, “In the next two years, i.e., just in the preclinical phase of medical school, we are going to add Y words to your vocabulary.”

And Y was bigger than X by like 20 percent. And those were mostly going to be Latin and Greek words, by the way. And he was right. I mean, it was like learning a new language. So part of it is just the semantic problem. Now, do you have to know all of that? Of course not. But what’s proximal? What’s distal? All of these things kind of factor into this stuff. By far the biggest issue, though, and this is the one that we try to solve the most for on a weekly basis, there’s a reason that we go to great lengths to write a newsletter every single Sunday. It’s basically a class. A lot of times it’s like such-and-such a study is published, and the news picks it up and writes a take on it that we think is demonstrably wrong. Or a paper gets published that gets a lot of attention that says this, and we think it’s an important paper and we want to highlight it.

So we try to use those things as case studies, and I honestly think that’s the most efficient way to go about learning this. Now, we did write a series six years ago, I think, called Studying Studies, which is I think a five-part blog series that Bob Kaplan and I wrote. And I think it’s probably a great foundation to just get the basics. What is a case cohort study? What is observational epidemiology? What types of bias exist, and how do you look for them? Consider that sort of your basic foundational knowledge set, but thereafter it becomes reps. I think Layne Norton also has a course that he just launched, and I think it’s actually called REPS, but I can’t remember what REPS stands for. But it’s basically a scientific literacy course in how to read studies about nutrition.

In his case, it’s about exercise and nutrition. Again, we try to cover everything in our newsletter. We’ll talk about a drug study, we’ll talk about a supplement study, an exercise study, all those sorts of things. So those to me are the ways you go about doing this. You just have to dive into it and a little bit overcome the fear of it. I suspect it’s not unlike what you would say if I was asking you, “Tim, I really want to learn Japanese. Is there a particular app that I should look at?” I think at the end of the day, you’d say, “Look, man, you’ve got to learn it. Here’s the way to get the foundational skills, and then go and find people to speak Japanese with.”

Tim Ferriss: Well, let’s actually use that example. So learning Japanese. Because I do think there are parallels here. I think it comes back to objectives, strategy, and tactics. And I just wanted to share a quote that’s one of my favorite quotes that also might help folks, which is from Ralph Waldo Emerson. And the quote is, “The man who grasps,” this is, of course, people, but “The man who grasps principles can successfully select his own methods. The man who tries methods, ignoring principles, is sure to have trouble.” This applies as much in medicine, developing scientific literacy or learning Japanese. It applies in all of these places. And so what I would say, and please feel free to pick this apart, is that to learn Japanese is a very broad objective.

So I would encourage someone to refine that substantially. And they might refine it to, I would like to be conversationally fluent, which means I understand and can convey maybe 80 percent of what I hear or want to say, in a conversation that does not include specialist terminology that is abstract, like economics or art, fill in the blank. So you’re discussing what happened to whom, when. I was born here, I went to school there, I have two brothers, whatever it might be. And with that goal, then I would say for the vast majority of people, if, and this is big if, they were willing to make it a part-time job, let’s just say with three or four hours per week spread across four consecutive days.

That if they layered things properly, within three to six months, if they then added in a couple of larger sessions for bulk memorization, and you can use space repetition tools, but the tools don’t matter as much as being really clear on the objective, that you could become functionally fluent, conversationally fluent as I described it, which omits reading and writing completely in Japanese scripts, probably within three to six months if you took it super seriously. And there are some adjuncts I would add to that. So to give people maybe a glimmer of hope on the medical literacy side, I would say if people started with your AMA number 30, this is episode 188, “How to Read and Understand Scientific Studies.” If people listen to that first, and assume, folks, before you listen to it that you’re not going to understand at least 30 percent. Let’s just make that an expectation so you don’t get frustrated.

And if they further maybe read some of the case studies from your newsletter, made that one of the hours that they spend per week, just like the Japanese. If they maybe read a book like Bad Science by Ben Goldacre, who’s an MD. British, so some of the cultural context and examples may not resonate for US readers, but he runs through some of the basics. And they read Outlive, that making this literacy your part-time job, a very light part-time job, for three months is one of the best investments you’ll ever make in your life. I mean, I really feel like the payoff is so tremendous that it seems almost crazy to not learn. And you don’t have to learn a hundred thousand words, but you need to be familiar with, let’s just call it a few dozen concepts, that you’ll be able to look at databases of studies, or at least abstracts, not going into all the supplemental stuff, and make some sense of A, B, or C.

Are there any suggestions you would have for just becoming familiar for with what the scientific method actually entails? So I could think, read the Wikipedia entry as a starting point. But for instance, where a lot of smart people or seemingly smart people screw up with the scientific method, is your guess, although it is a guess, aka the hypothesis, needs to be falsifiable. And a lot of people start with completely impossible-to-falsify guesses. And it’s just you’re painting yourself up shit’s creek with without a paddle. Any suggestions for how people could at least become familiar with the scientific method and what that means as far as structured thought and process?

Dr. Peter Attia: I don’t off the top of my head have a resource that I can point to. I agree with you that there’s so much more nuance to it than just understanding the caricatured version that I explained earlier. For example, how you design an experiment is essential. So even if you have a hypothesis that can be falsified, if you design the wrong experiment to test it, you can miss out. This becomes very important, by the way, as you start to look at studies. If a study is “negative,” how do you know if it’s negative because it was too small in size and what we would describe as underpowered, versus it was adequately powered, but there was no effect. At the other end of that spectrum, sometimes a study will find a statistical significance, but it was overpowered, and that difference, while statistically significant is clinically irrelevant.

Now, that kind of stuff we do cover in the Studying Studies stuff. But I think what you’re describing are these more important heuristics that truthfully, maybe there is a great book out there, and I’m just ignorant of what that book is that goes through this, but that’s the kind of stuff that I think you learn with practice. And unfortunately, if you’re not doing experiments — I mean, again, I think I learned most of this stuff not in medicine, but in the two years that I spent at the NIH where I was a fellow, but doing research. So I was a research fellow, not a clinician. That’s probably where I learned more than anything about how to do science. And so I think anybody who’s been in a lab is just learning that. But it’s very informal. At least for me, it wasn’t a structured thing.

Tim Ferriss: But in terms of priorities, I would say, folks, man, I’ve seen so many people lost in the medical system, especially when they suddenly have a serious diagnosis with some form of cancer or otherwise. And they are absolutely helpless because they do not have a handful of concepts that they’ve become comfortable with and just a basic set of terminology. So at the very least, look up Sir Francis Bacon. I’m sure there’s a biography, an excellent biography out there somewhere. And it will no doubt track the development of the, I guess, Baconian approach.

Dr. Peter Attia: One thing I’ll add to this, Tim, before we leave this topic, is also for folks to look up Austin Bradford Hill. So Austin Bradford Hill, scientist of the middle part of the 20th century. To him, we owe the Bradford Hill criteria. So there are, I believe, nine Bradford Hill criteria, which are the criteria that we use to scrutinize observational data. So when you have epidemiologic data, how can you scrutinize them to understand and change your confidence in the likelihood that these data are causal? I mean, causality is one of the most important concepts in science.

Tim Ferriss: Could you also just define observational study versus randomized control trial so that people have that?

Dr. Peter Attia: Yeah. So an observational study, it doesn’t have an intervention. So you can observe things, either looking backwards, so things that already happened, you can go back and look at what happened. You can even observe things prospectively, but without intervening. So saying, hey, we noticed that there are a group of redheads over here and there are a group of brunettes over here, and we’re just going to follow them for the next 10 years and see if the color of their hair predicts their life satisfaction, making this up, of course. And so you might get an answer from that and say, oh, my God, the people with red hair were so much more likely to get melanoma. I mean, this is devastating, and it must be that something about red hair is causing skin cancer. And it must be that brown hair must be reflecting the sun and those people aren’t getting skin cancer.

So there’s a correlation. So another question is, do we know if there’s a cause there? Do we know if the red hair is causing those people to get more skin cancer than the people with brown hair? And the answer is probably not, right? The answer is probably that red hair is associated with fairer skin and that that’s the issue. Because if you really wanted to know if red hair was causal, you would randomize people to different groups and you would actually dye the hair in one group one color, and dye the hair in the other group another color, and then you would follow them. You see? So what Bradford Hill’s criteria allow us to do is look at nine factors, such as the strength of the observation. So what’s the actual magnitude of the observation? What’s the reproducibility of it? What’s the biological plausibility of it?

Is there an analogy to it? Is there a dose effect to it? And as you go through these nine criteria, which I think I actually do this a couple of times in the book, because so much of the data we look at around nutrition and exercise are unfortunately epidemiological. We can’t do the controlled experiments. But it’s what allows us to say, when I read a study that says 12 hazelnuts will reduce your risk of death, 12 hazelnuts a day in consumption reduces risk of death by 10 percent, I can look at that and say, total nonsense. That’s just epidemiologic nonsense. Conversely, when I look at epidemiologic data that say, people who are really, really strong live longer than people who are really, really weak, by going through those nine criteria, I can be much more confident that that is actually causal.

Tim Ferriss: I’ll mention two things. The first is if you’re going to get — because we’re mentioning a number of different books, and this is not just to blows smoke up Peter’s ass, which by the way was a real thing. I found a menu from the wild west, and it was all these various things you could have done to you, and blowing smoke up your ass was like $50. It was the most expensive. So that’s a real thing. So it’s not just that I’m doing that, but if you’re going to buy one book on this stuff, get Outlive because it covers a broad spectrum. And I want to also mention, because I think this is really critical, and we’ll probably come back to this, but it isn’t just about extending lifespan, but extending healthspan and having full optionality physically, or trying to preserve that to the greatest extent possible for the longest period of time possible.

I will add, though, that people will see, for instance, and a lot of this medical or scientific literacy is so you don’t get fooled by misinterpretation or sensationalism in media. Because you’ll see a headline that’s something like “Bananas increase your risk of colorectal cancer by a hundred percent.” And what that means, though, if you dig into the data is like, all right, your risk goes from one in five billion to two in five billion. So it’s just like, from a behavioral standpoint, it just does not matter at all. There’s a book called How to Lie With Statistics by Darrell Huff, which I think is a very fast read. And that will also complement everything that we’re talking about. So let’s look a little more closely at some of the content and interventions and tools in the book.

And I’m not sure this is a great way to kick it off, but there’s an expression I’ve heard at least applied to medicine quite a few times, which is 50 percent of what we know is wrong, we just don’t know which 50 percent. And so I’m curious to know what you have seen, peeking behind the veil at what is not working, and what you have then designed to address that misfire, in your practice and by extension in the book. You mentioned a few things, like apoB levels. You mentioned being very specific with exercise prescription, being extremely specific, and the possibility of lowering certain types of risks fourfold. So I’ll let you tackle that however you want. We can start wherever makes sense.

Dr. Peter Attia: Well, I mean, we could probably talk about different things within different buckets. So starting with sleep, I think that with sleep, I like to simplify things a little bit sometimes. So one thing that I think is happening a lot right now is people are getting, probably at least some people overly anxious about what their sleep trackers are telling them. So we’ve got a problem where the pendulum has swung a little too far to the other side, where maybe 10 years ago, nobody thought at all about sleep. 

Now you’ve got a class of people, me among them, who maybe think too much about sleep. All of a sudden, it becomes a little bit counterproductive. We see this in a subset of our patients. The first and most important prescription for those people is stop tracking. Take the tracker off. Let’s just focus on the fundamentals. What time are you getting into bed, and what time are you getting out of bed? If we can, within 15 to 30 minutes on either one of those, completely fix that and completely toggle on the basic blocking and tackling aspects of sleep hygiene, which have to do with food, alcohol, light, temperature, noise, et cetera, I mean, you’re going to be okay. I don’t really need to know what your sleep score is and how many minutes of this sleep versus that sleep you had.

I personally go through this myself. I’ll go through phases of time where I’m not looking at any sleep-tracking device. If I know I’m going to be in an environment where sleep is compromised, which is basically a lot of the time if I’m traveling, I don’t even take a sleep tracker with me because why do I need something to remind me of what’s probably happening? How about I just do the best job I can and be a little less data focused? That’s an example of where I feel like, a couple years ago, I would’ve just said, “More data is always the answer.” Now I think I’m a bit more measured, and I say, “Look, sometimes more data is not always the answer.”

Now, the flip side of that is there’s nothing that will demonstrate to a person how much late night food and alcohol are ruining their sleep than a sleep tracker. I do think it’s really valuable to see that. For many of my patients, that has been the most decisive thing that has reduced their alcohol intake.

Tim Ferriss: Oh, for sure. Yes.

Dr. Peter Attia: Despite what a lot of the epidemiology will tell people, alcohol is not good for you in any dose. It doesn’t mean we shouldn’t drink it at all, but let’s not delude ourselves into thinking it’s actually healthy at some low dose. It’s not. Understanding that it’s a toxin can, I think, help you have a more measured response. My response to alcohol, while we’re on that topic, is if I drink something that doesn’t taste incredible, I pour it out. I’m never going to tolerate a bad glass of wine, ever. It’s just not worth it.

Tim Ferriss: Since we’re on it, well, I’m going to pull us back to this question of data, probably through the lens of continuous glucose monitors and the best uses and maybe the most common misuses for people who do not have type two or type one diabetes. But let’s just sit with the alcohol for a second. What are your personal rules for alcohol consumption, outside of if it tastes mediocre or shitty, it gets poured out, which is a great rule, but what are your favorite types of alcohol? How do you personally navigate that?

Dr. Peter Attia: Well, I’ll start with quantity. Yeah. I would personally just say there’s got to be an insane reason to have more than two drinks in a day. It’s somewhere between zero and two. And it’s got to be a really good reason to drink on more than three days a week. In the back of my mind, I’m keeping a tally, which is I really shouldn’t be having more than about seven drinks in a week. Again, seven drinks in one day is very different than one drink a day for seven days. It’s the frequency and dose that defines the poison.

The second thing is I really have to make sure that drinking is a good three hours away from sleep. Again, when I say these things, people say, “Peter, you must be a robot.” No, I’m just saying these are general principles. There are going to be times when I violate that. I think I posted something on Instagram a little while ago, which was the most rancid night of sleep, when my sleep data were comically bad. The reason was we had friends over. It was very late. We drank. We ate. I basically went to bed. By the time they left at 10:30, I went to bed, and we had just finished eating. Not surprisingly, my sleep sucked. The point I made in the post was I’d do it again. It was a fantastic night with our friends. The four of us hadn’t had dinner together in a long time. You just have to be very thoughtful and deliberate about the choices and trade-offs that you make.

As far as the type of alcohol, this is, again, an example of something I think we tend to over-index to. It’s “I drink a lot, but let me tell you, it’s just vodka and tequila. It’s got to be good for me, right?” It’s like, “No. Alcohol’s alcohol.” I love tequila. I love mezcal. I love really good wine. I love really dark Belgian beer. I’m not deluded to think that any of those are healthy. I know that there are some people who have a horrible reaction to certain types of alcohol. Well, I would put that in the same category as people who have a horrible reaction to certain types of foods. Don’t consume them. I think mostly where I focus, Tim, is on how much am I going to drink, how close is it going to be to bed, and what’s the total tally per week, and never exceed a certain tally in a given day.

Tim Ferriss: I was waiting for the right time to bring this up, Peter I know that people say cookies are bad for you, but I’ve only been eating Nutter Butters. I’m kidding. I feel like that’s the equivalent although it’s less of a neurotoxin. Let’s hop to continuous — 

Dr. Peter Attia: I do love Nutter Butters, by the way.

Tim Ferriss: They are good. They’re so good.

Dr. Peter Attia: I don’t know the last time I had one, but oh, my God, now that you reminded me of that. That’s horrible of you to do that.

Tim Ferriss: Well, that’ll combine nicely with all the GBs and the CGMs. Inside joke. Could you speak to continuous glucose monitors? For a long time, I mean, even still now, these are broadly thought of as something that one might only use if they have some form of diabetes. However, there are people who do not fit in those categories who use them. I would love for you to just perhaps give us a bit of an overview on CGMs and what you have seen as the best uses and how you use them in your practice.

Dr. Peter Attia: A continuous glucose monitor is a device. There are really two big ones on the market right now. One is made by a company called Dexcom, and one is made by a company called Abbott. The latter is called the Freestyle Libre. I think it’s a company that Abbott acquired many years ago. These are devices that are worn usually on the tricep. They can also be on the abdomen. They have a little, tiny filament that is quickly shot in with a needle into the subcutaneous space. The filament remains after the needle comes out, and the filament sits in a part of the body where it can sample something called interstitial fluid. This is basically the fluid between cells. To be clear, it’s not sampling the blood. It samples the interstitial fluid, and it measures glucose level there. It’s basically calibrated to know, based on what the reading is there, what the glucose level is in the blood. A continuous glucose monitor, as its name suggests, is a way to give you real-time information about what your blood glucose is.

As you said, for people with type one diabetes, which was the first use case, it was a very important innovation because people with type one diabetes are by definition dependent on insulin. They are using insulin exogenously to do the job of their pancreas, which is no longer working. The pancreas, of course, is this brilliant organ, where it’s the one that’s auto regulating glucose and insulin, or glucose via insulin. When that goes away, they have to be the one to do it. So now they have this device that is at least giving them real-time glucose information, and they can adjust insulin injections as needed.

It obviously didn’t take long for that to expand into a much, much larger market, i.e., 10 times the size, which is people with type two diabetes, some of whom do require exogenous insulin, some of whom do not, but all of whom by definition have a carbohydrate and glucose tolerance disorder. The very definition of type two diabetes is based around unregulated peripheral glucose. This tool is therefore helpful. It’s helpful in, first and foremost, I think, knowing what to eat. I think, historically, we have given people with type two diabetes abjectly horrible news and insight with regard to what to eat. I mean, we just haven’t really helped them think through this problem. The CGM makes it pretty clear that not all foods are created equal when it comes to managing glucose homeostasis.

Everything I’ve said so far is relatively straightforward. This is a great example, by the way, of Medicine 3.0 versus Medicine 2.0. Everything I’ve said so far more or less makes sense if you’re in Medicine 2.0. In fact, I think we’re finally at the point where even Medicine 2.0 is starting to accept the fact that carbohydrate restriction is a really good idea for people with type two diabetes. It’s not the only way, by the way. Caloric restriction in general will work to improve insulin sensitivity, which therefore improves glucose regulation. But it does seem that carbohydrate restriction, as a form or a gateway to caloric restriction, has greater efficacy than other methods.

Once we now talk about people without diabetes, Medicine 2.0 would argue a CGM plays no role. Okay. Is there a randomized control trial demonstrating the efficacy of CGM in anything outside of patients with diabetes? There is not. But now we have to get into the leap of faith that one takes when you start triangulating between other pieces of data. We want to start with one, which is, in a population of non-diabetics, is there any evidence that glucose levels matter? Type two diabetes is defined as having a hemoglobin A1C above 6.5 percent. Hemoglobin A1C is just a way to measure how much glucose is stuck to hemoglobin. By knowing what that number is, you can impute what the average blood glucose is in that individual over the preceding three months. So 6.5, which is the cutoff, translates to an average blood glucose of 140 milligrams per deciliter.

The question, then, would be if you take two people who don’t have diabetes, one of whom has a hemoglobin A1C of 5.0, and one of whom has a hemoglobin A1C of 6.0, neither of them are diabetic, is there any difference in their outcomes? To put that in perspective, the guy at 5.0 has an average blood glucose of about 100 milligrams per deciliter. The person at 6.0 has an average blood glucose of about 130 milligrams per deciliter. Pardon me. 120 milligrams per deciliter. They’re both outside that diabetes range. Well, the answer here is actually pretty clear. It is that there is a difference. In fact, for a non-diabetic population, the lower the average blood glucose, as estimated by hemoglobin a1c, the lower the all-cause mortality.

What’s the implication now? Well, if the implication is, if you take a group of people who don’t have diabetes but want to live longer, i.e., they want to lower their risk of cancer, they want to lower their risk of cardiovascular disease, they want to lower their risk of neurodegenerative disease, I think we can make a pretty reasonable leap of faith that having a lower average blood glucose is better than having a higher average blood glucose, even if that higher average does not put you in the range of a diabetic.

So now the question becomes, are there tools to help us manage that? One tool would just be the A1C. You could say, “Well, I’m just going to get my hemoglobin A1C measured every six months.” The problem with that, as we know, is that hemoglobin A1C is very easy to mislead. It’s very dependent on red blood cell turnover. The more rapidly red blood cells turnover, the more artificially low the hemoglobin A1C will be. Conversely, the longer the red blood cell sticks around, the higher, artificially, the hemoglobin A1C will be. It’s for that reason that we like to use CGM to actually get true measurements of average blood glucose.

When a patient who doesn’t have diabetes puts on a CGM for the first time, they’re invariably surprised. There’s this real learning phase that comes. You’ve done this, Tim. I know you were doing this. Probably 10 years ago, you wore your first one. Everybody goes through this. I remember for me, it’s been about eight years since I started. At first, you simply cannot believe the things that drive your blood glucose up. It’s so simple — 

Tim Ferriss: Can you give some examples?

Dr. Peter Attia: — it sounds dumb. Yeah. Yeah. I remember the first time I had Raisinets. It’s not like I didn’t expect it to go up. I didn’t expect it to go up like that. Exercise. Certain forms of exercise. By the way, I’m not saying this is pathologic. There’s nothing wrong when you’re exercising for your glucose to skyrocket if you’re doing tabatas or you’re doing HIIT workouts. Again, it’s not pathological, but it’s super interesting. Other things that I think are pathological is how much your blood glucose goes up if you had a poor night of sleep.

Tim Ferriss: Yeah, for sure.

Dr. Peter Attia: If you have a horrible night of sleep, your insulin sensitivity gets crushed the next day, and your glucose levels go up. Well, that’s actually very interesting. Again, maybe you could argue that adds too much stress to the fire, but it’s an insight, nevertheless, that can help drive a behavior change. I think in the book, I cover my 10 best insights from years of CGM in myself and patients. It’s about different foods. Foods high in fiber are going to have one effect. Lean sources of protein versus fatty sources of protein, all those sorts of things.

Ultimately, I think CGM becomes a really helpful tool for compliance. It becomes a behavioral tool. We tend to gamify it a little bit. I know that when I’m wearing CGM, which, I just happen to be right now, by the way, I’m going to think twice before eating something stupid. Again, it’s purely just because my personality likes to gamify things. It’s like, “Yeah, I’m tempted to go and eat all the leftover waffles on my kid’s plate, but I just know.” It’s like, “Eh, it’s going to shoot my blood glucose up, and I like not doing that.

Where I think people get into trouble and where the counter-argument is, which is a fair argument, is, look, if you only index on blood glucose, you could still end up doing a bunch of things that aren’t healthy. If you ate bacon for every meal every day, your blood glucose would not go that high, but it’s probably not the healthiest choice. I would agree with that. But by that logic, we shouldn’t look at body weight, either, because by smoking cigarettes, your body weight will go down. Does that mean body weight is a lousy measurement? No. It just means that any measurement in isolation can be ridiculous and can be gamed. We shouldn’t ignore blood glucose any more than we should ignore body weight or body fat or body composition. We just have to understand that it’s one of many tools that we can look at. The CGM, again, do I think this is necessary to live a longer, healthier life? Of course not. It’s simply one tool that we have to help us understand how to regulate one of the four macronutrients.

Tim Ferriss: I’d like to just add two things to that. The first is people listening who have not experienced a CGM may hear puncture filaments and imagine something out of Hostel 2 or something like that. I will say that 2008 was the first time I used a Dexcom, which was the size of the cell phone used by — 

Dr. Peter Attia: It’s like a baseball.

Tim Ferriss: — Gordon Gekko in Wall Street. It was huge. The experience of putting what felt like, to me, subjectively barbecue tongs into my abdomen was very unpleasant at the time. I have, however, tried the latest generations, and you basically feel nothing. I mean, it’s so easy in my experience. I don’t know how many of your patients report a lot of pain with that, but I was shocked by how completely innocuous the whole procedure was. It was very, very mild, very quick, very easy. So I just wanted to mention that. Secondly, this probably applies more to your patients than to you, but in the book, you mentioned the Hawthorne effect, which I think was first coined in manufacturing, and looking at worker effectiveness or output. That is the phenomenon whereby people modify their behavior when they’re being watched. I think that is another selling point for some form of accountability. Is there anything you’d like to add to that?

Dr. Peter Attia: No. I mean, I think there are some patients of ours who actually want to utilize the Hawthorne effect. If we agree mutually to do so, we can see all their data. They can just say, “Look, I want you to be looking at my CGM data every day. You’re an accountability partner for me, so I’m going to eat less junk food.”

Tim Ferriss: What are some of the other perhaps under-emphasized or underutilized metrics that you think are important? This could be in the realm of metrics or tools. It could be forms of screening. It could be blood markers of different types. There are a few that come to mind that I imagine are on this list. It could be physical performance markers of some type. What are some that come to mind?

Dr. Peter Attia: If we’re going to just talk in magnitude, VO2 max and muscular strength stand in a league of their own. There’s really nothing that’s within the ZIP code of those two metrics. Having very, very high VO2 max for your age and sex, and being very strong, I mean, again, they have more of a positive impact than any single thing we can think of has a negative impact. That includes having end-stage renal disease, being on the wait list for a kidney while you get dialysis, being a smoker, having high blood pressure, having type two diabetes, being obese. The downside of those things is relatively small compared to the upside of having a high VO2 max and being very strong. We almost shouldn’t even talk about things until people are willing to accept that fact and take the steps necessary to address them.

Now, you might say, “Well, how many people can become very, very strong or have a very high VO2 max?” The answer is I don’t know. I don’t know, especially on the VO2 max side. To get into that top 2.5 percent of the population where you really start to see an enormous gap between you and everybody else in terms of lifespan, yeah, maybe only a quarter of the population has the potential to get there. But the point is everybody has the potential to be more fit than they are, outside of people who are already doing everything they can. So just going from being in the bottom 25 percent of the population to the 25th to 50th percentile of the population cuts your risk of all-cause mortality in half at any point in time. There’s nothing that compares to that. There’s no drug out there that’s going to do that. Again, I think we could talk about drugs all day long and how I think they’re really important and how we could think about controlling apoB and rapamycin and metformin, all these other things. All that stuff is pixie dust compared to what these things are.

On the strength side, the same thing. I mean, anyone who’s got older parents knows this. If you really want to watch somebody suffer when they’re aging, you watch them losing their cognition, and you watch them losing their physical body. You watch them lose the ability to move around with ease, to have balance, to be pain free, all of these things. Well, a big part of that is being strong. Strength is something we can actually hang onto as we age. We lose quickness long before we lose strength. That’s the good news. The bad news is you have to be very deliberate in how you train it. I’m sure on the podcast, you’ve discussed type one and type two muscle fibers. People are probably familiar with that.

Tim Ferriss: Well, why don’t you reiterate that?

Dr. Peter Attia: Our muscles are made up of these fibers. They’re very unique properties. Muscles are these multicellular things where the cells are these long fibers that contract past each other. That’s what creates the contraction of a muscle. But if you dig a little bit deeper, you have different types of fibers. You have type one fibers, which are fueled mostly, if not entirely, by an aerobic process. They can use fat. They can use glucose, but they do so in the presence of oxygen primarily. They’re very slow to fatigue, which is mostly where the name comes from, but they don’t generate that much force. These are the muscle fibers that are mostly on display when you’re walking or just carrying out activities of daily living. You can go for a walk for — 

Tim Ferriss: Commonly called slow twitch, as you alluded to. Slow twitch muscle fibers.

Dr. Peter Attia: Correct. Yeah. You can do things for a long period of time, and these things don’t fatigue. Conversely, another subset of these fibers are type two fibers. They’re called fast twitch muscle fibers. They’re fast to fatigue. Now, they’re much more powerful. When a type two fiber contracts, far more is happening. It’s generating far more force, but it’s doing so with a different metabolic strategy. It’s glycolytic. It’s just using glucose, broken down glycogen, and it’s going to fatigue quickly. It’s accumulating metabolic byproducts that are leading to fatigue. There’s a reason why, if I say, “Tim, jump up and down as high as you can, as many times as you can,” this is not going to be a long exercise. We don’t have to sit and wait two hours for you to finish that. You’re going to fatigue pretty quickly if you’re doing maximal jumps. Whereas, if I say, “Jump rope,” you could do that for 30 minutes easily if you’re relatively fit person. So you get the sense of the difference.

Now, as we age, we lose power and explosiveness more than anything else. We lose that the soonest. That’s due to the atrophy of the type two fiber. Again, this comes back down to strategy. That’s why, if you want to live a longer, better life, you have to have a strategy in place for maintaining type two fibers. You’re not going to get that without resistance. You can’t say, “Look, I play tennis every day. I walk every day.” Those things are great. They’re not doing something for your type two fibers.

Tim Ferriss: Yes. Let me hop in for a second. I want to get specific on that because I think some of the approaches or tools might be counterintuitive for folks. First, just some random trivia for folks who might be interested. If you’ve ever carved a chicken or a turkey, neither of those like to fly very much. The breast meat tends to be white, and then you have the dark meat. Well, there you have type two, type one fibers respectively. So just for the next time you’re cutting up the bird.

Dr. Peter Attia: Yeah. The reason the legs are dark is they have much more mitochondria. Those are their slow twitch muscles there that are heavily dependent on oxygen delivery and oxidative phosphorylation. Whereas, the white meat, the breast meat is very fast twitch. Quick, quick, quick flapping. Doesn’t have the mitochondria, has far less of it, and therefore that’s a less oxygen rich muscle.

Tim Ferriss: I think the quick, quick flap — 

Dr. Peter Attia: We, of course, look — yeah, we look all red.

Tim Ferriss: Go ahead. Go ahead.

Dr. Peter Attia: Yeah. When you dissect us, of course, you don’t see that difference. Our type one and type two fibers are less clearly separated.

Tim Ferriss: If someone wants to improve strength, correct me if I’m wrong, but you have a number of — maybe they’re not just heuristics. I mean, they’re direct indicators, but you have a number of things that you focus on. I’m sure there are many others. But in the strength category, I would love to know how you define very strong. Perhaps this would be a place to talk about, or at least include, hand strength, farmer’s carry, or anything else that you’d like to add that might not immediately show up on someone’s mental radar when they’re thinking of strength.

Dr. Peter Attia: Yeah. I mean, there are a handful of strength categories that we think really matter and just ideas that are important when you think about strength. One of them is the importance of understanding eccentric versus concentric strength and how both are very important. I actually put something up on Instagram the other day about this, where I just explained that the concentric phase is basically the go and the eccentric phase is the slow. You accelerate through concentric force, which is the force a muscle generates as it is shortening. That moves you forward. The eccentric phase, which is equally important but oft ignored, is the strength or the force that a muscle is exhibiting as it is lengthening. That’s what’s decelerating. That’s what’s slowing you down.

Andy Galpin, I think, recently talked about a great metric, and I agree, this is a fantastic metric. I’ll check mine constantly. How far a broad jump can you do? I want to make sure that I can do a standing broad jump that’s higher than my height laying down. If I’m five foot 10, I want to make sure I’m jumping at least six feet on a broad jump. A broad jump’s a really interesting test. It’s a profoundly extreme example of concentric and eccentric strength in the same movement. If you’re just standing there and you want to jump six feet in front of you, that requires an enormous explosion. That’s a very high concentric load. But guess what? If you want to not break your nose when you land and destroy your knees, you better be able to decelerate and slow yourself down. That’s an unbelievable eccentric ask.

While that’s a very extreme example, consider walking up and down stairs. Walking up the stairs is very taxing concentrically. But where do most people get hurt in life? It’s actually walking downstairs. If you watch, especially as people age, the difficulty they have in slowing themselves down when they’re coming downstairs or taking a step off a curb, this is where people are falling and breaking their hips. It’s far less that they’re falling due to concentric weakness and far more that they’re falling due to eccentric weakness. Therefore, principle number one in our strength training is always be doing both, not necessarily in the same movement, not necessarily focusing equally on a given day, but everything we want to do, we want to make sure that we are hitting the concentric and the eccentric phase, not just the more obvious, which is the concentric.

Tim Ferriss: Now, does that take the form of simply accentuating the lowering in the case of, say, a trap bar deadlift or something like that, where you have something like two seconds up, four seconds down? Or does it take other — 

Dr. Peter Attia: Yep.

Tim Ferriss: — specific forms?

Dr. Peter Attia: Exactly. I mean, there are other ways. They’re a very specific exercise that you’ll do. For example, a Nordic rollout, a Nordic fall for a hamstring exercise where you’re — you know what I’m talking about. When you’re kneeling on a mat and your feet are held in position and you sort of allow yourself to slowly come down? That’s just purely eccentric.

Tim Ferriss: Requires quite a bit of starting strength to do.

Dr. Peter Attia: Well, truthfully, we wouldn’t have people do that out of the gate. You’ll do that with assistance to start, because most people simply don’t have the hamstring strength to do that. Yes. It can be accomplished greatly by using slow, what we call negatives. So focusing just as much on the negative is the positive. So for example, one of my favorite exercises to do are step-ups because one, it’s a single leg exercise, it’s a beautiful hip hinge.

We can talk about it in some detail in a moment because hip hinging is another one of the big principles and it allows you to do a very nice isolation of the eccentric on the step-down. You really have to be able to control that. If you can’t control it, you’re using too much resistance, obviously. So hip hinging is another big important principle. Again, hip hinging, when people think about that, they think, does that have to be a squat or a deadlift? No, it doesn’t have to be. It can be a hip thruster, it can be a lunge, it can be a step-up. I think the step-up might be the single most important one for people to do because it doesn’t have any axial loading.

Tim Ferriss: Can you explain what you mean by that?

Dr. Peter Attia: Yeah. When you’re doing something like a squat or a deadlift, there’s weight that is basically pulling your spine down to your hips. The squat, it’s because the weight is actually sitting there and the deadlift, it’s because the weight is being — the force is being transferred through your arms there. But in either case, you are loading the axis of your spine and that’s fine if you know how to do it safely.

But as you know, having done these things, that’s not just something you can walk in off the street and do. You really have to be coached how to do that stuff safely. Stepping up onto a block is something that’s much safer to do. It’s also something that you can do with a single leg at a time, and therefore you get to see what your asymmetries are because we all have them. I am so deep down the rabbit hole of step-ups that I can’t even explain the nuances in oblique compression, pelvic angles in the difference between when my left and right leg do it.

But tinkering with that stuff allows me to work out so many kinks with how my body works. You mentioned another one earlier, which is being able to carry heavy things. This is just such an essential skill for our species. It’s something that we do better than anything. There is no animal that can carry with their hands what we can do. Certainly a strong male, but certainly even a strong female can carry their body weight in their hands. Half their body weight in each hand is not an insurmountable ask for us. So carrying got so much — 

Tim Ferriss: Would that be a hypothetical target for your patients?

Dr. Peter Attia: Yeah, we would like to see our patients carry half their body weight in each hand for a minute. Yeah.

Tim Ferriss: For a minute?

Dr. Peter Attia: So walk around with half your body weight in each hand for a minute and having strong hands, it’s one of the most correlated findings with longevity. So we talked earlier about what does it mean to be really, really strong? Well, unfortunately, the data on this are based on what the studies show and the studies are testing interesting things, but they’re not exhaustive. So they’re usually looking at grip strength, leg extension, bench press are the most commonly tested things, but grip strength comes up over and over and over again in studies as such a proxy for longevity, lower risk. I think there’s a figure in my book that talks about the unbelievable monotonic decline in both the risk of onset of dementia and death from dementia as grip strength increases. Again, you just kind of go back to the Bradford Hill criteria and you look at the strength of the associations, you look at the consistency of these associations, you look at the dose effect of these associations.

Very hard for me to believe that there isn’t causal relationships here. That being stronger training to be stronger will actually improve outcomes. Not just that strength is a marker of health, which is obviously correlated with living longer, if that makes sense. I mean there’s a distinction there, so. Yeah, we think that carrying things is very important and yeah, I’ll go through different phases. As you know, I love rucking. So that’s another thing that I think is just a great all round way to now combine two different types of exercise, something that’s part of strength and something that’s part of endurance. Also, rucking gives you — so just for people who don’t know, rucking is just basically carrying a really heavy weighted backpack. Probably one of the most important tools used in the training of special forces in the military. We have so many friends that have been through that and I’m amazed at how much they rucked. It’s like eight hours a day. They’re just walking around with 75 pounds on their back if not more.

Tim Ferriss: What does your protocol methodology look like for rucking?

Dr. Peter Attia: So I use 55 to 60 pounds, and I’ll typically do an hour ruck because of where I live. It’s really hilly, so I really like that. But going up the hills, I’m going hard. I’m really pushing my cardio up the hills and I’m trying to find the steepest hills possible to come down because that’s working that huge eccentric, that gear, it’s really forcing me to be able to decelerate on the way down those hills with a lot of weight. You’re not getting the pounding. I think that’s the beauty of — 

Tim Ferriss: Exactly.

Dr. Peter Attia: You’re not pounding your knee with the impact you would if you had to run to produce that effect.

Tim Ferriss: Yeah, that’s probably the most compelling reason that I started rucking a few years ago, especially in preparation for certain alpine hunts and so on, did a ton of rucking and the collateral benefits, they’re not really collateral. The direct benefits were this sort of holy shit effect that sometimes I’ve seen with kettlebell swings and other things where this translation that you wouldn’t expect pops up in all sorts of ways. I used to be a runner, but I ended up — you probably didn’t know this, but I used to be a cross country runner when I was, say, up to about age 15.

Then through poor choices, like doing lots of wrestling and other impact sports, developed knee issues and so stopped running. But I always missed the sensation of getting a good workout while walking or moving in some fashion on ground. Rucking solved that. So coming back to VO2 max, so VO2 max, I’ve always wondered to what degree someone can improve VO2 max, you already spoke to the benefits, even if you’re moving from say, 25th percentile, the 50th percentile, huge benefit, right? I mean half I think you said halving, halfing cutting in half certain mortality risks. What have you found to be the best approaches for improving VO2 max?

Dr. Peter Attia: Well, first off, it can actually be improved quite a bit. I think the research out there understates how much it can be approved because the research studies are relatively short. So it’s true that in a 12-week study, you might see an eight percent improvement or a 10 percent improvement. I would say that’s just the tip of the iceberg, we’re not talking about 12 weeks of training here. We’re talking about a lifetime of training and we’re talking about 25-50 percent improvement in VO2 max that anybody who’s been involved in serious training will see all day long.

So the, how is also very important, the analogy I like to use, which I’m borrowing from one of my old cycling coaches, is that think about building a pyramid. The VO2 max is the height of the pyramid. So if you want to build a really high pyramid, it also has to have a really wide base. So the key for building a high VO2 max is saying, “I’m going to spend about 80 percent of my aerobic training time in zone two.” This is counterintuitive. A lot of people think, “Oh, my god. If I want to build a high VO2 max, it has to be all intense training.” No, you have to first and foremost build that huge aerobic base. That is the pyramid.

Tim Ferriss: That foundation.

Dr. Peter Attia: That allows you to make the peak higher. So once you have that aerobic base, that other 20 percent of the time is used well above. So basically most people are training too hard to build the base, but not hard enough to build the peak. So I kind of think of as garbage training zone and not to rip on — 

Tim Ferriss: Not to get too technical.

Dr. Peter Attia: Yeah. But that’s sort of the problem with doing a lot of fun classes and stuff. Look, it’s absolutely better than sitting on the couch for sure, but it’s not specific enough to achieve this goal. So you really want to separate that zone two from that zone five. When it comes to VO2 max, you basically have to be in the three- to eight-minute range is the sweet spot. So it’s got to be intervals that are about three to eight minutes. So three minutes at the low end, meaning you’re doing something that is so hard, you can only do it for about three minutes and at the high end, eight minutes. So if you can do it for more than eight minutes, it’s not doing a lot for your VO2 max. If you can’t do it for three minutes, it’s also not doing the maximum amount for your VO2 max. 

Tim Ferriss: Just for clarity, that’s the zone five that you’re referring to, building the peak?

Dr. Peter Attia: Yeah. Yeah, exactly. Here you’re typically doing about a one-to-one work to rest recovery. That’s how hard these intervals are. So if you do three minutes at that, whatever that output is, you’re going to need about three minutes of recovery before you can do it again. So we typically say, “Look, a good starting point is four by four,” four on four off four times. That’s just a great workout to start just doing that workout once a week. So let’s say three days a week you’re going to do your cardio and it’s going to be kind of the low-end zone two cardio. One day a week, you pick an exertion level that you can barely get through four minutes of it, you can do it, but you’ve a little bit left in the tank, but not much. That you need four minutes to recover. Then you do that four times. Sandwich between a warmup and a cool down.

Tim Ferriss: If I’m understanding correctly, that would be the building of the peak. What does the zone two training look like?

Dr. Peter Attia: Long and slow.

Tim Ferriss: Yeah.

Dr. Peter Attia: Yeah.

Tim Ferriss: Aside from subjective perceived exertion, is there a heart rate range or anything else that you can use as sort of a proxy indicator? So people can have something to aim for?

Dr. Peter Attia: Once you get fit enough, lactate becomes really good. So measuring lactate with a point of care like a finger prick device is what I do. You’re looking for a lactate level of about 1.7 to two millimole for most people is the zone. For people who aren’t yet fit enough, their lactates are usually going to be way higher than that while they’re still training that energy system. Or if people just don’t want to do that. For those people RPE, rate of perceived exertion, is really the best way to do it and it’s far more accurate than heart rate. So the RPE is you should be able to talk, but you don’t want to. So today I did a zone two ride. I spent the entire — this is very unusual, but just because of the way it was today, I spent the entire zone two on a phone call. My entire workout was on a phone call.

There was absolutely no confusion on the guy on the other end of that line that I was on my bike and that I wanted him to talk more than me, like I was breathing like this. He was like, okay. So yeah, I mean, that’s kind of how I was going at it. I can nasally breathe when I’m doing zone two, but I’m right at the limits of what I can do. It’s very easy for me to nasally breathe. I don’t mouth breathe at night or anything like that. So that kind of gives you a sense of it. If you can talk pretty easily while you’re doing it. If you’re out on a walk and you’re talking to somebody, that’s too easy. If you can’t talk at all, that’s too hard. I think that, by far the best test.

Tim Ferriss: Just to give people some more specifics. So for the zone two, how long would a target session be? How many times per week? Then similarly for the four-by-four, let’s just say that you described for the zone five building the peak, how many times per week would you do that?

Dr. Peter Attia: I think if we can do that once a week is great.

Tim Ferriss: That’s zone five?

Dr. Peter Attia: Yeah, zone five. I think for zone two, we think minimum effective dose. So again, it depends on where you’re starting. If you’re starting with you’ve never exercised in your life, I mean, boy, we’d be happy to get you doing two 30-minute a week zone two sessions, but you very quickly will start to adapt to that. Then I think we start to get into three hours being the MED. That might be three 60-minute sessions or four 45-minute sessions.

Tim Ferriss: Have you ever tried, Peter, and I’m just going to bring this up because we’ve spent a good amount of time together, and this has been a bit of a revelation for me. Have you ever tried skinning on skis going uphill with skins on skis?

Dr. Peter Attia: Yeah, so Lance Armstrong’s a good buddy and he moved out of Austin to Aspen a few years ago, and I keep giving him crap for it. I’m like, “Dude, why did you leave? Why leave?” He’s like, “Yeah, it’s tough.” Especially in the winter because he’s a summer sport guy, but this is his form of winter exercise. Having him describe it to me, I’m like, “Yeah, I can see that. That sounds pretty awesome, actually.”

Tim Ferriss: So this, Peter, but people listening may not, I historically am about as far from an endurance athlete as you could possibly be in the sense that if you look at my sports career, such as it was, it’s all optimizing for trying to win very quickly within three to five minutes generally. Anything close to extended exercise has always been rightly and probably wrongly punishment in my view. I just have really disliked it, which means I’ve gravitated towards weight training, things like that. Skinning and rucking are the two things that have changed that. 

My body, including my low back pain and so on, feels so much better when I am doing skinning and rucking. I will say with the rucking, and I don’t know what your setup looks like, but I really benefit from having a waist strap. There are rucking backpacks out there that do not have a waist strap, and I find those can cause some back pain if I have either too much weight, use them for too long or both, but — 

Dr. Peter Attia: Well, can I make a shameless plug for my friend Jason McCarthy’s company? GORUCK?

Tim Ferriss: Please. Yeah, please.

Dr. Peter Attia: I have no affiliation, but I love Jason and I love the company. So yeah, the GORUCK is the way to go here. Again, you just need a backpack with weight, but if you want to invest in it, they make amazing packs. You can buy these bolt on waistbands that allow you to support because I’m like you, I like to have 80 percent of the weight on my hips and virtually none of it on my shoulders. I don’t even link up the little strap across my chest because I want to be able to breathe fully. So I’m very light on the shoulders, incredibly heavy on the hips and their packs and the weights that come with them. Just make this a very elegant solution. Yeah, totally agree.

Tim Ferriss: Yeah, Yeah. So GORUCK. I also use GORUCK, so I’ll give them a plug, I don’t know the founders, but ended up honing in on GORUCK. I will say also the breathing component, aside from the loading distribution that you just men mentioned, one of the benefits that I find of rucking versus, say, a weighted vest, which are quite popular in the CrossFit communities and so on, is where you are bearing the weight and also the ability to breathe. So those would be two advantages. 

I’m sure there’s a lot to be said for the weighted vests as well. Although funny, I’ll tell you, Peter, I don’t know if I’ve ever told you this. This was probably 2009, 2010, I decided I was going to try weighted vests and I was like, “This is going to be fantastic. I can’t wait.” So I bought this monster, which was loaded up, it looked like a suicide bomber vest, you just had all these — they looked like canisters full of weight. 

Dr. Peter Attia: How much did they weigh?

Tim Ferriss: Well, okay, I’ll get there. So I thought to myself, it’s just walking. At that point, I was very seriously, and I know this is not winning any records, but for me, it was a lot.

I was probably 180 and I was deadlifting 475 for reps, which is as high as I got. I thought to myself, I walk all the time, let me get — I think it was a hundred pound vest. So I get this hundred-pound vest and I put it on and I decide to go for a leisurely two or three-mile walk and I get a mile out and I’m like, “I can’t carry this thing, I’m just going to collapse into a puddle on the sidewalk.” So I had to leave the vest on the sidewalk, this is in The Mission in San Francisco and go back to my house to get a car to come get it. I thought to myself, if anybody steals this thing, they deserve to have it. Not surprisingly, the weight vest did not move. It stayed exactly where it was. So yeah, rucking, I suggest rucking and start later than — 

Dr. Peter Attia: Yeah, I recommend people start with a sixth to a quarter of their body weight.

Tim Ferriss: You’ll end up dropping. It’s a good chance you’ll end up dropping it somewhere.

Dr. Peter Attia: Truthfully, I think Michael Easter, who’s written about this extensively in his book The Comfort Crisis, which if your listeners haven’t read that, not that we’re trying to give them more books to read, but The Comfort Crisis, I can’t recommend highly enough. I think he said that even the military right now thinks that you don’t really need to go above a third of your body weight. So let gravity help you more than that. But sort of anywhere from a sixth to a third, your body weight is probably the sweet spot.

Tim Ferriss: Where I’ve ended up, and this will make me sound weak maybe, but is right around 45. In some cases I’ve added a bit more weight, but I probably weigh 175 right now. 45, and then focusing on inclines, basically just going for the sort of geographical altitude, or not even necessarily altitude, but the incline challenge rather than slapping on a ton of weight and walking on flatter ground. 

What are some other for you, crux — we’ve spoken about strength, we’ve spoken about VO2 max, just so I can maybe explicitly explain why I’ve spent, and we have spent some time on this, it’s because these are not purely — the implications are not purely muscular. 

Maybe this is a place to talk about what you have learned about neurodegenerative disease, and specifically, perhaps, Alzheimer’s. Because I think this will all tie in and show people that the sort of Cartesian duality of body and mind is really illusory, could you speak to that?

Dr. Peter Attia: Yeah, I think that probably the first time I took a hard look at this would’ve been 2014, maybe 2015. At the time, I had one analyst, his name was Dan Palenchar, look at this in detail. God, it was probably a six to nine-month project. it was a really, really exhaustive look at the literature and the deepest dive we could do at the time of what do we know about the prevention of Alzheimer’s disease? So again, we started with a very bold hypothesis, which we were not alone in, but most people thought was crazy, which was that these diseases have some degree of prevention. There is a way to prevent these to some extent, maybe not completely, but luck is not the only thing, or bad luck is not the only thing that is driving these diseases. We have some control.

So to make a very long story short, after Dan kind of went through all of this analysis and after analysis after analysis, the thing that stood out above everything else was the benefit of exercise. I just sort of told Dan to go back to the drawing board. I was kind of like, “Dan, I think you screwed this analysis up, buddy. There’s zero chance that exercise is actually the best thing here. Are you going to now tell me that chicken soup is the best thing for colds? I wanted some insight here. I didn’t want some stupid platitude,” but it turned out Dan was right and I was wrong. So I think the data are pretty unambiguous. In fact, I’m doing a podcast on this. I don’t know, by the time this one’s out, it might be out.

I don’t know, I don’t know. But I’ve got a podcast coming out on brain health and here we are back again now with many more analysts and much more tools at our disposal to understand the literature and still exercise remains the most important modifiable behavior we have to reduce the risk of Alzheimer’s disease and probably Parkinson’s and Lewy body dementia, by the way. So I can’t say that for every single neurodegenerative disease, I don’t have any real insight into how you prevent Lou Gehrig’s disease, which is an absolutely horrific disease that is fortunately much more rare. But when it comes to the big three — Alzheimer’s, Parkinson’s, Lewy body dementia — exercise, exercise and exercise matter, and part of that has to do with movement reserve. So when you think about Lewy body and Parkinson’s, these are primarily movement disorders. So they’re kind of on a spectrum. So you’ve got Parkinson’s at one end, pure movement disorder, a little bit of cognitive. Lewy body kind of bit of both. Then Alzheimer’s, much more cognitive, having a higher movement reserve and having a higher cognitive reserve are protective. So people — 

Tim Ferriss: What do you mean by movement reserve? Just greater range of motion ability? So spectrum of movement patterns that they can sustain?

Dr. Peter Attia: Yeah. The greater physical capacity. So people who are really good dancers, who are really good at doing complicated, coordinated, problem-solving things with their body who have kinesthetic awareness, they’re going to have a much slower decline even when diagnosed with Parkinson’s disease, for example. So we want our cognitive reserve high, we want our movement reserve high. Then on the other side of that, you get the sort of hormonal vascular metabolic benefits that come from the actual exercise. So one is the benefits you get from being in the state, one is the benefits you get accruing the state.

Tim Ferriss: Could you expand a bit on the hormonal effects and otherwise, I mean, I think this is probably just because it has words in the acronym that I like, but brain-derived neurotrophic factor, et cetera? To what extent can you weight some of these factors?

Dr. Peter Attia: Yeah. BDNF is one of the most important. Yeah, I don’t know I that I could tell you a relative weighting, but certainly BDNF is a very important one. So it’s a very important growth factor for neurons. But also, of course, when you think about the metabolic effects and the hormonal effects that come from what is exercise doing to cortisol levels? What is exercise doing with glucose and insulin levels? I mean, we see an unbelievably strong association between type two diabetes and Alzheimer’s disease. Well, again, here’s an example of where Medicine 3.0 I think gives you a little bit more confidence to make the extension, which is, look, if type two diabetes is bad, having insulin resistance without type two diabetes is also probably bad. Therefore, we want to take all steps possible to maximize insulin sensitivity, glucose disposal, all of these things that fit under the bucket of metabolic health. Again, exercise is not unique in its ability to act on those things. Nutrition absolutely does as well, but boy, does exercise have a profound effect on those things.

Tim Ferriss: Yeah. Let’s talk about training the trainer, maybe. By that, I mean the vast majority of people listening to this will not be able to work with you or a practice like yours. What types of requests can they make of their physicians? What types of tests might they ask for? This may be a clumsily worded question, but how can they make their doctor and their health plan per se better? Are there any recommendations you have?

Dr. Peter Attia: Yeah, look, I think that it kind of comes back a little bit to your medical literacy question at the outset, which is, I think part of it is also just being a bit more clear about what your objectives are when you’re finding a doctor and understanding a little bit about what their style is. I mean, asking them what is their philosophy on something? How much time do you spend learning about things that you did not learn in medical school? I go back to something I said earlier, which was, there’s almost nothing I do today, Tim, that I learned in medical school. I can’t think of one thing. It’s not because what I learned in medical school wasn’t valuable. Maybe that’s the wrong example, by the way, let’s be a little more less glib.

If I look at the physicians in my practice who trained in internal medicine and ask the question, “What did you learn in residency that you’re using today?” The answer’s probably like 10 to 15 to maybe 20 percent, max. So where did that other 80 percent come from? I’m arguing that if you want to participate in Medicine 3.0, you have to be able to learn outside of your training. I think that’s a discussion that should be had very deliberately and not obliquely. So I think understanding where they sit on prevention, understand how they’re educating themselves, what are they reading, what are they learning? If the answer is, “Hey, it’s not a good fit, great. Better to find that out before you jump in.”

Tim Ferriss: Yeah. As we’re talking about this, two things came to mind, and please feel free to dismantle this, but the first is to be able to assess medical literacy, you have to have a certain base level of medical literacy yourself. So I would say kind of step number one is developing a working vocabulary and also frameworks, many of which you provide in Outlive, such that you can actually assess other people to some extent. That’s kind of step one. 

The second is that if we think about many Western-trained, or I shouldn’t say Western-trained. Physicians who are sort of schooled in a Western paradigm as those focused on the sort of addressing of disease rather than prevention of disease, broadly speaking.

May be unfair to paint so broadly, but let’s stick with that for a minute, that as you think of your healthcare, it goes beyond just your primary care physician and could very well and probably should include people like exercise physiologists or people who are trainers, given how much overlap and integration we’ve discussed in the course of our conversation. It just occurred to me that — this I think is quite true, that it’s a lot easier. Not that you shouldn’t look for concierge doctors if you have the means and that’s a possibility, by all means do that. But you can find excellent, excellent strength coaches, I would say, much more easily than you may be able to get yourself into a economic position where you can afford concierge medicine and the payoffs. I’m not saying they’re comparable, but the payoffs of having a good strength coach or an endurance coach go a long way. Those came to mind also.

Let’s just say they’re asking these questions of their doctors. They find a doctor. Are there any particular recommendations you would have? A couple of things come to mind that I have in my notes here related to tests to request. For instance, I don’t know where you stand now on GRAIL, which I guess would be considered a liquid biopsy, right?

Dr. Peter Attia: Yep.

Tim Ferriss: Scans like Prenuvo for instance, and perhaps more intelligent approach to family history is something that I know you cover in the book. Would you like to speak to anything that might fall in that category of things to consider requesting?

Dr. Peter Attia: Yeah, we think it’s really important to be testing, as I said, APOE is one thing for sure. We really do want to know that genotype. And again, if you believe that Alzheimer’s disease has some element of prevention baked into it, then knowing that you’re high risk should be a valuable thing to understand.

When it comes to understanding cardiovascular disease, we care deeply about apoB. apoB, again being a more important metric than LDL cholesterol, or non HDL cholesterol, or HDL cholesterol. This apoB is the concentration of all atherogenic particles, so includes all the HDLs, VLDLs, et cetera.

Also, knowing LPa, which is a genetically determined very high-risk particle that while it can’t be modified, will allow you to understand how much more you need to optimize, for example, apoB. So knowing LPa, knowing apoB, knowing APOE. I think there are other biomarkers obviously, that we care deeply about uric acid, homocysteine insulin, liver function tests.

Cystatin C is one that I think is largely underappreciated. So most doctors are using creatinine as the measure of kidney function. Creatinine is a joke, actually. I, actually, at some point, I wish I had the time, and maybe I’ll make the time to do a deep dive into how it became the defacto gold standard for measuring and estimating glomerular filtration rate. It’s an absolute atrocity.

For a person who’s very low in muscle mass, it really overestimates kidney function. For a person with high muscle mass or who’s just exercised, it really underestimates kidney function, but it virtually never correctly estimates kidney function. Whereas Cystatin C, which is another blood test, probably costs a few more dollars, but certainly not much. It might be the difference of $1 versus $7 or something, completely more accurate and unlinked to these issues of muscle mass.

Tim Ferriss: How do you spell Cystatin C?

Dr. Peter Attia: C-Y-S-T-A, Cystat, as it sounds phonetically, I couldn’t do the spelling bee. But it’s C-Y.

Tim Ferriss: People will find it on Google.

Dr. Peter Attia: C-Y-S. Yeah, exactly. Don’t ask me to spell anything longer than “ah.”

Tim Ferriss: All right. How about on the early cancer screening side?

Dr. Peter Attia: Well, again, I think that cancer chapter is probably a very long chapter for a reason, but I think one of the big takeaways on that chapter is the overwhelming evidence that treating cancers when they are detected early has significantly better outcomes than treating the exact same cancer later on down the line, even using the same cocktail of drugs.

I think the two examples in the book I use are that of colon cancer and breast cancer, and looking at, for example, using the FOLFOX regimen of chemotherapy to treat a patient with adjuvant treatment, meaning, so a person that had a stage two or stage three colon cancer that is resected and at least surgically, you don’t see any gross disease, they just have microscopic disease. You treat those people with the FOLFOX chemo regimen, which is a multi-drug regimen, and you compare that to people who have metastatic disease, the outcomes are vastly different.

In the latter group, nobody’s going to survive for 10 years and very few of them will make it five years. In the former group, 80 plus percent are going to survive 10 years. Go through the similar example of breast cancer. The point here is the fewer tumor cells you have, the fewer, the smaller the burden of cancer, the fewer the mutations, the fewer the escape mechanisms that are in place to evade the immune system, the more likely you are to survive treatment.

And therefore, until we figure out ways to completely eliminate cancer, which I don’t think are going to happen anytime soon, we have to take a much more aggressive posture towards screening and acknowledge, by the way, the downside of that. There’s a significant downside to more aggressive screening, but if you can come to grips with that, you have a better chance of beating cancer by far.

And to your question, now, GRAIL becomes one of the tools we would think about doing that. GRAIL is a company, I guess it’s currently or now probably owned by Illumina, and it uses something called cell-free DNA. It takes a blood, couple tubes of blood and looks in there for tiny, tiny, tiny amounts of DNA that are out of the cell.

Most of the DNA, Tim, if you went and did a DNA test and they took blood, they would take the DNA out of cells in your blood, they’d break down red blood cells and white blood cells and take the DNA. But this technique looks at all the DNA which is not in cells, which is a fraction of a fraction of a fraction of a percent. They look at that DNA and by looking at the methylation pattern of it, so these little methyl groups that are stuck to it, they impute two things.

One, is cancer likely to be present, yes or no? And if yes, can we figure out what organ it is? Where did it come from? These tests have a relatively low sensitivity, meaning if a cancer is present, their ability to detect it is not that high. They have a very high specificity, which means if no cancer is present, they’re very likely to tell you that.

Every screening test has to be tuned towards sensitivity versus specificity. And this test is tuned to very high specificity, very low sensitivity. 

The implication of this is for a low prevalence cancer, so for general screening, by general screening — so let me take one step back. Knowing the sensitivity and specificity of a diagnostic test is only slightly useful. If you don’t know the prevalence of the condition you’re testing for, which is called the pretest probability, you can’t actually impute what’s called positive and negative predictive value.

In other words, what you really want to know when you look at a diagnostic test before you take it is if it’s positive, how likely is it that I have the condition? If it’s negative, how likely is it that I don’t have the condition? That’s positive and negative predictive value respectively. And you can only answer that question when not only the sensitivity and specificity, but what your pretest probability is. And if you don’t know that, you would just say, “Well, what’s the prevalence of the condition in where I’m looking?”

When you take cancer screening in a general population, the prevalence is very low. That’d be one percent, two percent. 100 people that walk into for a random cancer screening, you wouldn’t expect more than one or two of them have cancer. With a low sensitivity and a high specificity test you have, if you do the math, you’ll see, very low positive predictive value and very high negative predictive value.

And for that reason, I think initially was not blown away by the test because of how low the sensitivity was. For low stage cancers, like stage one and stage two, the sensitivity was like 20 percent. And that’s the metric that I cared most about. I don’t really care about your sensitivity at detecting stage four cancer. We’ve blown it if we’re waiting until that point. What is very interesting to me though, is when you start to look at this by histology, and this to me is interesting.

If you look at all breast cancer, the stage one, stage two sensitivity for detection is 20-ish percent. But if you look at hormone negative breast cancer, it’s 75 percent. If you look at hormone positive cancer, it’s 20 percent, basically.

Tim Ferriss: What do you mean by hormone negative and positive?

Dr. Peter Attia: One of the most important ways that we identify breast cancer is by its hormone profile. Is it estrogen, progesterone, and/or HER2 neu positive? Triple negative breast cancer has the worst prognosis. A breast cancer that does not express the progesterone estrogen or HER2 neu receptors has the worst outcome. It’s the most aggressive breast cancer. And those cancers even at the same stage are far more detectable. They have a 75 percent sensitivity in low stage cancer. This tells us that we need to think of liquid biopsies in a very different way from how we think about “anatomic screening.”

A mammogram or an MRI or an ultrasound are agnostic to the properties of the cancer. They are simply looking at its presence and size. What this liquid biopsy might be giving us a window into is the behavior of a cancer. Why is it that a triple negative, I have a 75 percent chance of — I’m using the terminology looser, but let’s just say I got a 75 percent chance of catching it in the bloodstream even at an early stage. Whereas if it’s triple positive, which has a much better outcome, I’m not going to catch it very likely at that stage.

Might it be that because the latter is not that lethal and therefore it’s not shedding, and the former is much more lethal and that’s why the cancer is spreading? I think it’s super early days on this, and I think these cancer screening is definitely one of the most contentious things that I probably talk about in the book, because I do take, I think, a very different view from the mainstream, which is that we have to do this aggressively, we have to do this early.

I mean, I’m just 50 years old. I’m three colonoscopies in at 50. To me, just as it’s unacceptable I think, to die of cardiovascular disease in the year 2023, I think it’s unacceptable to die of colon cancer, and yet colon cancer is the third leading cause of cancer death.

Tim Ferriss: I will just say, I’m not going to name names, but a friend of mine put off colonoscopy for a few years, older guy and — 

Dr. Peter Attia: Yeah, I know who you’re talking about.

Tim Ferriss: Yeah, stage four. Early counts, early counts a lot. And I’m just going to leave a couple of gingerbread trails for folks because I do want them to pick up the book. I mean, there’s so much, we couldn’t even scratch the surface in our conversation.

But the contrast between say, CT angiogram over calcium score or calcium scan, I mean, there’s so much we could dig into, immunotherapy and many other things. But what I’d like to do, you’ll probably get a kick out of this. 

Number one, I think you have some of the best chapter names I’ve seen in a long time. I want to give you credit where credit is due. And then where I think I’d like to go is to ask you about — 

Dr. Peter Attia: By the way, some of those might be — Bill Gifford might deserve some of the credit, my co-author. I was really struggling for some chapters with quotes. As you probably noticed, each chapter has a quote, and I think Bill probably came up with three quarters of them.

Tim Ferriss: Oh, nice.

Dr. Peter Attia: I was really struggling with the quotes because I had some that were okay, but he would always come through in the end with a better one.

Tim Ferriss: Well, credit to Bill. But what I’d like to do, just to give people a lay of the land is actually, this is going to sound ridiculous, but just read through these briefly. And then what I’d like to talk about is how and why you decided to include the chapter “The High Price of Ignoring Emotional Health.” If you bear with me here, I’ll just do a little recital.

Chapter one, “The Long Game from Fast Death to Slow Death.” And I’m not going to give the chapter numbers, I’m just going to go through these. “Medicine 3.0: Rethinking Medicine for the Age of Chronic Disease.” We touched on this briefly. “Objective Strategy Tactics: A Roadmap for Reading This Book.” “Centenarians” — this is coming into part two — “The Older You Get, the Healthier You’ve Been.” “Eat Less, Live Longer? The Science of Hunger and Health.”

“One Disease to Rule Them All.” “The Crisis of Abundance.” “The Ticker: Confronting and Preventing Heart Disease, the Deadliest Killer on the Planet.” That’s my chapter, as you know. If anything is going to kill me that isn’t an accident, it is probably heart disease. “The Runaway Cell: New Ways to Address the Killer That is Cancer.” “Chasing Memory: Understanding Alzheimer’s Disease.” Also something in my family and other neurodegenerative diseases.

Part three, we’re rounding the bend here, coming into home here. “Thinking Tactically: Building a Framework of Principles That Work For You.” “Exercise” Nature’s Longevity Drug.” “Training 101: Training for the Centenarian Decathlon,” which for those long-term, long-term podcast listeners, that may sound familiar, and it’s certainly been refined and developed in the form that you find in this book.

“The Gospel of Stability.” Let me try that — the fact that I stumbled on that is funny. “The Gospel of Stability: Relearning How to Move to Prevent Injury.” Jesus Christ, Tim Ferriss, hold on one second. Pull it together. “The Gospel of Stability: Relearning How to Move to Prevent Injury.” “Nutrition 3.0: You Say Potato, I Say Nutritional Biochemistry.” That’s the most Peter thing I’ve ever read. “Putting Nutritional Biochemistry into Practice: New Rules for Changing the Way You Eat.” “The Awakening: Tap into the Power of Sleep.” 

Then last but not least, “Work in Progress: The High Price of Ignoring Emotional Health.” Why the last chapter?

Dr. Peter Attia: I’ll tell you something funny. When I had an early draft of the book, I shared it with a mutual friend of ours, Hugh Jackman, and Hugh read it, and his only feedback was that should be the first chapter. And Hugh had a really solid argument for why that was the case. The publisher absolutely said, “No chance in hell.” And so it was either nowhere or at the very end of the book.

Look, I think that this was the hardest chapter to write, unquestionably. It’s the 17th chapter that has very little to do with the other 16 for reasons I won’t necessarily explain here. But it’s a very different format. It’s a very different structure and it tells a very different story.

But look, I think for some people it might be the most important chapter in the book. And I think for others it might be totally irrelevant. But that was a risk I think that was worth taking. And I’ll just say this, I think you alluded to this earlier on several occasions, longevity without health span is the greatest curse in the world. To live a long life and to suffer is not to live. And that suffering, that loss of health span can be cognitive, it can be physical, and it can be emotional. And that last one is so squishy that it’s hard to talk about in a medical book, but that chapter is basically my way of trying to do that.

Tim Ferriss: I just want to give some, if you don’t mind, I’ll give a teaser. Now, there’s a lot to this chapter. We’re not going to dig into all of it, but maybe we could start with, and we won’t spend too much time as I’m watching the lighting in the sun and the moon and the stars changing your video, because I know we’ve been going for a while, but are you open to discussing the 47 affirmations that you had to write and the context, a little bit of the context around that? Because I think a lot of people listening to this will identify with certainly that particular instance of your experience.

Dr. Peter Attia: Yeah. Boy, it’s hard to explain that without explaining where I was when I was being asked to do that. But — 

Tim Ferriss: Sure, whatever you’d like to.

Dr. Peter Attia: Again, the sun is low. Let’s just say I was in a rehabilitation center where one of my homework assignments on the first day was to write an affirmation for each year I’d been alive. At the time I was 47, this was three years ago. So it was, you’ve got to come up with 47 things to say about yourself that are positive. And I couldn’t come up with more than a few. I was stuck at four or five until the 19th day. Then I really had an enormous breakthrough that honestly, in the book is — I don’t devote a lot of real estate to it, as profound as it is.

But I think if you’re a person reading this who’s been where I’m taking you will understand it. But I think once I reached that point, once I had that breakthrough, as I described in the book, I was able to write the remaining 43 of them in 20 minutes. Those 47 affirmations then became a very big part of my recovery contract. And for a period of about six months, I would read those twice a day, every day, standing in front of a mirror, which sounds very Stuart Smalley or whatever that character’s name was. What was his name? Smiley?

Tim Ferriss: It was something like that. “I’m good enough,” and — 

Dr. Peter Attia: “I’m good enough.”

Tim Ferriss: “Gosh darn it, people like me.”

Dr. Peter Attia: That’s right. But I think for my problems, this was such an important step, this fake it until you make it. I was able to basically use that in my — the term fake it until you make it has such a negative connotation from Silicon Valley and companies like Theranos. But in psychology, it can actually be pretty valuable. If you start to say something enough, you will believe it. And we think about that a lot in the negative but it works also in the positive. And I think that in some ways, that one exercise became a very important brick in the wall of fundamentally altering my view of myself and fundamentally altering the stories I told myself.

Tim Ferriss: And I must say, as someone who was there in your life for that period, and also watching the steps that you took, including what you just described, I am so glad that you included the chapter in this book because I think a lot of people who would like to optimize lifespan and health span nonetheless find it easier to think about the maybe hard measurable edges of something that is physical versus that which is currently giving them the most suffering, which is some lack of equilibrium or a set of proper, I shouldn’t say proper, constructive lenses through which to view life and themselves.

I think it’s a real gift and not one without, I’m sure, some trepidation on your part to include this in the book. I just wanted to commend and thank you for including that. Because I think it’ll help a lot of people. And so I hope you feel good about it. 

Dr. Peter Attia: Thank you so much.

Tim Ferriss: Yeah, I hope you feel good about it, Peter. Peter, we talked about a lot. The sun has come. The sun is gone. Is there anything else that you would like to mention before we close any requests to people? The book is Outlive: The Science and Art of Longevity. I never say this, long-term listeners will know this, go get the book. This is a very, very solid book that many years have gone into, not just in the writing, but in the living and experimenting and refining and changing of mind that is reflected in the adaptability and principles in the book. I do recommend everybody check out the book. Of course, There are many other places on Instagram, @PeterAttiaMD. Is there anything else that you’d like to mention, Peter, before we wrap up?

Dr. Peter Attia: No, other than just to really thank people. I think there’s a lot of noise out there in the world today. And I think that anyone who’s going to buy this book and devote the time to read it or listen to it on the audiobook, this is not a two-crapper. This is not a book you’re going to read on the toilet in taking two craps. I just want to thank everybody who — 

Tim Ferriss: Never heard that expression.

Dr. Peter Attia: Oh, I think of all books as how many craps. Every book is like, it’s a four-crapper, it’s a two-crapper. It’s an amazing honor. Little things I’ve been doing for the book prep that would’ve ordinarily annoyed me to no end, haven’t annoyed me at all, because I’m realizing that it is a special thing that you have a relationship with someone you’re not necessarily meeting but they’re doing something that is giving of themselves, which is taking the time to read this thing. And in exchange, you’re giving them something that’s hopefully valuable. Anyway, thank you for having me on the show, Tim. And thanks for people who are going to maybe go out and get this thing.

Tim Ferriss: All right, guys, it’s no two-crapper. That’s my quote on the back of the book. You’ll find it featured prominently on Amazon. And Peter, congratulations, man. I know this has been a long time coming. I’m excited for you. I am even more excited for the people who will read this and hopefully derive from it some clarity and focus amidst an overwhelming amount of noise and bullshit out there.

I do see this as a very strong signal in a sea of noise, so I encourage people to check it out. Outlive: The Science and Art of Longevity. Dr. Peter Attia, nice to see you, man, and to be continued in person soon. Maybe we’ll have those two drinks a piece with some red wine and some nice selects of axis deer from your freezer. And best of luck with the launch, man. Thanks for making the time.

Dr. Peter Attia: Thanks man, appreciate it. Thank you so much.

The Tim Ferriss Show is one of the most popular podcasts in the world with more than 900 million downloads. It has been selected for "Best of Apple Podcasts" three times, it is often the #1 interview podcast across all of Apple Podcasts, and it's been ranked #1 out of 400,000+ podcasts on many occasions. To listen to any of the past episodes for free, check out this page.

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One Reply to “The Tim Ferriss Show Transcripts: Dr. Peter Attia — The Science and Art of Longevity, Optimizing Protein, Alcohol Rules, Lessons from Glucose Monitoring with CGMs, Boosting Your VO2 Max, Preventing Alzheimer’s Disease, Early Cancer Detection, How to Use DEXA Scans, Nature’s Longevity Drug, and More (#661)”

  1. Re “the war on cancer”

    Most people would be much smarter and better informed if they had awareness of what the “war on cancer” movement (and the “Breast Cancer Awareness” movement, etc) does NOT raise awareness about.

    The official mainstream “war on cancer” has been an unofficial “war” on the unsuspecting public: to keep them misinformed and misguided about the real truth of this “war.” The latest program/”promise” is an extension or reincarnation of the enduring deep racket.

    This PHONY official “war” was never meant to be won but to be CONTINUED (preferably endlessly, at least for decades) so that the criminal BIG allopathic medical business (the medical mafia) built around them makes insane profits and defraud the general naive/stupid public, which they’ve been doing successfully … so “THEY ARE winning THEIR war against the general forever-naive/forever-stupid public”..

    The orthodox cancer establishment has been saying a cure for cancer “is just around the corner” and “we’re winning the war on cancer” for decades. It’s all hype and lies (read Dr. Guy Faguet’s ‘War on cancer,” Dr. Sam Epstein’s work, or Clifton Leaf’s book, or Dr. Siefried’s work on this bogus ‘war’, etc). The criminal medical establishment deliberate and falsely self-servingly claims and distorts a ‘win’ in the bogus ‘war on cancer’ when the only truly notably win is a reduction in lung cancer due to a huge reduction in smoking, which has NOTHING to do with their cancer treatments. Lying is their mode of operation.

    Since the war on cancer began orthodox medicine hasn’t progressed in their basic highly profitable therapies: it still uses primarily and almost exclusively highly toxic, deadly things like radiation, chemo, surgery, and drugs that have killed millions of people instead of the disease.

    As long as the official “war on cancer” is a HUGE BUSINESS based on expensive TREATMENTS (INTERVENTIONS) of a disease instead of its PREVENTION, logically, they will never find a cure for cancer. The moonshot-war on cancer inventions, too, includes industry-profitable gene therapies of cancer treatment that are right in line with the erroneous working model of mechanistic reductionism of allopathic medicine.

    The lucrative game of the medical business is to endlessly “look for” a cure but not “find” a cure. Practically all resources in the phony ‘war on cancer’ are poured into TREATMENT of cancer but almost none in the PREVENTION of the disease. Eg, Heidi Williams, the director of science policy at the Institute for Progress, explained that from the time the “War on Cancer” was announced, in 1971, until 2015, only six drugs were approved to prevent any cancer. From 1973 to 2011, nearly 30,000 trials were run for drugs that treated recurrent or metastatic cancer, compared with fewer than 600 for cancer prevention.

    It’s IRREFUTABLE PROOF POSITIVE that BIG MONEY and a TOTAL LACK OF ETHICS rule the official medical establishment.

    It’s just like with any bogus official “war” (‘war on drugs’, ‘war on terrorism’, ‘war on covid’ etc) — it’s not about winning these wars but to primarily prolong them because behind any of these fraudulent “war” rackets of the criminal establishment is a Big Business, such as the massive cancer industry. The very profitable TREATMENT focus of conventional medicine, instead of a PREVENTION focus which these official medical quacks (or rather crooks) can hardly make any money off, is a major reason why today 1 of 2 men and 1 in 3 women can expect a cancer diagnosis at some point in their lifetimes yet that rate was multiple times lower 5 decades ago when the phony ‘war on cancer’ began (1 in about 16). And 5 decades ago when this bogus war began cancer was the second leading cause of death and 50 years later it is STILL the second leading cause of death in the country this “war” was declared in. These facts alone prove we are NOT winning the war on cancer.

    At the same time, this same orthodox cancer cartel has been suppressing and squashing a number of very effective and beneficial alternative cancer approaches. You probably guessed why: effective, safe, inexpensive cancer therapies are cutting into the astronomical profits of the medical mafia’s lucrative treatments. That longstanding decadent activity is part of the fraud of the war on cancer.

    If the public were to scrutinize what the medical industry and its government pawns are telling them about the ‘war on cancer’ instead of blindly believing what they’re saying, they’d find that the cancer industry and the cancer charities have been dismissing, ignoring, and obfuscating the true causes of cancer while mostly putting the blame for cancer on the individual, denying or dismissing the serious harms from orthodox cancer treatments and chemical toxicants, and resorting to deceptive cancer statistics to “educate” (think: mislead) the public that their way of treatment is actually successful — read this well referenced scholarly article’s (“A Mammogram Letter The British Medical Journal Censored”) afterword on the war on cancer at [Moderator: link removed per link policy.] (scroll down to the afterword that addresses the fraudulent ‘war on cancer’).

    What the medical establishment “informs” the public about is about as truthful as what the political establishment keeps telling them. Not to forget, the corporate media (the mainstream fake news media) is a willing tool to spread these distortions, lies, and the scam of the war on cancer.

    Does anyone really think it’s a coincidence that double Nobel laureate Linus Pauling called the ‘war on cancer’ a fraud? If you look closer you’ll come to the same conclusion. But…politics and self-serving interests of the conventional medical cartel, and their allied corporate media, keep the real truth far away from the public at large. Or people’s own denial or indifference of the real truth.