Intro. [Recording date: September 5, 2023.]
Russ Roberts: Today is September 5th, 2023, and my guest is Dr. Peter Attia. His podcast is The Drive and he's the author, with Bill Gifford, of Outlive: The Science and Art of Longevity, which is our topic for today.
Peter, welcome to EconTalk.
Peter Attia: Thanks for having me, Russ.
Russ Roberts: Now, the book is a combination of advice for the reader: how to live in a different way. It also is a critique of advice for the field of medicine. And I'm sure we'll bounce back and forth between those.
I want to start with an early part of the book, which is a dream you had, maybe more of a nightmare, that involved eggs. Tell us what that was about.
Peter Attia: Yeah. So in this dream, I was sort of tasked with catching eggs before they hit the ground. And so, there's a tall building--not that tall, maybe two or three stories tall--and there's a guy on the top, and he's tossing eggs out of a basket. And I have a padded basket beneath him on the street level, and I'm running around trying to catch them all. And, truthfully, I'm not doing that well. I'm catching some, but many of them I miss and they splat all over the pavement.
And, of course, this dream, I realized many years later--I mean, probably a decade later--probably spoke to how I felt in my medical training. I had this dream during Residency, and it probably spoke to the feeling that we were doing so much at the last minute to try to save lives. And, of course, we could. We had some remarkably heroic things that we could do. But, ultimately, they were typically futile, and they merely extended lifespan slightly without really meaningfully impacting healthspan.
And, of course, in the dream, I come to realize that the only way to stop this is to go to the top of the building and take the basket of eggs from the guy who is tossing them.
Russ Roberts: Explain the difference between lifespan and healthspan.
Peter Attia: So, lifespan, I think, is the easier of these two to understand. It's certainly the easier to measure, because it is binary. It's discrete. And it's the period of life in which you are alive: you're respiring.
And so, we measure lifespan. And most of the data that is collected with respect to health is lifespan-based.
And, you think about it this way, Russ: Everybody says, 'Well, median lifespan or maximal lifespan has extended by such and such amount over the past hundred years.' And, if we look at those metrics, we can clearly see successes. So, if you look 150 years ago versus today, we have indeed doubled the expected lifespan of a person living in the developed world from approximately 40 to 80. We can talk a little bit about why that's happened.
Healthspan, however, is the analog measure. It really speaks to quality of life.
Now, I tend to have a more nuanced definition to this than the medical establishment would today.
The medical definition of healthspan is the period of time in which you are free from disability and disease. I don't find that to be a particularly helpful definition. It, maybe, lends itself to slightly better measurement than my definition, but I don't think it truly captures what people care about.
I think what healthspan really comes down to is the quality of your physical life. So, your ability to move around, do things, be free of pain. It's the difference between the 80-year-old and the 30-year-old from a physical activity-level standpoint. There's a cognitive component to healthspan, and this is absent disease, so we're not talking about dementia, but we're still talking about executive power, processing speed, memory, those things.
And then there's an emotional component. And this is the more interesting one, in a sense, because it's the only one that doesn't decline with age. It doesn't necessarily have to decline.
I think, unless you're living in a sci-fi land, we have to accept that our physical and cognitive healthspan is inevitably going to decline as we age. This does not have to be true with our emotional health, which includes everything from our sense of purpose, the quality of our relationships with others, with ourselves, our happiness, joy, spontaneity--all these things.
And so, to me, those are a basket of things that encompass healthspan. And, I will say this, Russ: when patients come to me, virtually without exception--because I always ask my patients on the first day, 'What is your goal for the last decade of your life, this marginal decade?'--they virtually never talk about lifespan. They only talk about healthspan.
And, I think therein lies one of the biggest problems with our healthcare system today is the relentless focus on lifespan. By the way, we're not even doing that well, so we can talk about that. But, to the exclusion of healthspan.
Russ Roberts: Yeah. I love--the fundamental idea behind this book, is that of course, we don't want to just live long. We want to live in a meaningful way, as you say. We want to live in a way that brings delight and that is--maybe diminished relative to our youth, but it still at least reminds us of some of the aspects of our youth in terms of what we care about doing and how we spend our time. And, so much of our focus is on saving lives and not on the quality of life. And, you make the distinction between Medicine 2.0 and Medicine 3.0, and you can also start with Medicine 1.0. So, give us those three eras.
Peter Attia: So, Medicine 1.0 represents the longest in terms of time because it's basically medicine for all of human history until about the transition that occurred from, say, Francis Bacon to germ theory. That's really the transition to Medicine 2.0.
So, in Medicine 1.0, we didn't understand the natural universe. Right? The scientific method had not been created; and while we can look back at what people thought at the time and laugh, I think we have to be a little bit kinder and realize that you can't use a tool that doesn't exist. And so, if a person was ill, you had to assume this was the gods or there were bad humors in the air that were causing this.
All of this changed, of course, in the 17th century when Francis Bacon began the work that I think led to the elucidation of the scientific method. There were also some really big technological breakthroughs. I'm sure you've read Sidd Mukherjee's book The Cell, and I think he does perhaps the best job of anyone in kind of explaining what really took place in this cellular revolution, where we finally began to understand that there were microscopic organisms that played a role in our illness. And so, the development of the light microscope and ultimately the discovery of antimicrobial agents completely changed the face of medicine.
And that is where I really think Medicine 2.0 took hold, in the late 19th century. And by the way, that is really the thing that is accounting for the doubling of human lifespan in the past 120 to 140 years.
There is, of course, another very important tool in Medicine 2.0 that was not introduced until about the 1940s, and that was the statistical and conceptual tool of the Randomized Control Trial [RCT]. This is what really allowed Medicine 2.0 to take off and to continue to make advances in other areas such as oncology. And in particular, I would say the poster child for Medicine 2.0, beyond the obvious--which is communicable and infectious diseases--is in cardiovascular disease.
So, we have Medicine 2.0, which is currently the system that we're in. It does very well, again, for infectious and communicable diseases, and it also does very well for acute injuries. So, our ability to actually deal with a heart attack when it's happening today is remarkable compared to 50 years ago. Our ability to take care of trauma patients, to take care of patients in sepsis, it's unparalleled.
However, what this has all shown us is that Medicine 2.0 has an enormous blind spot, and that is to the treatment of chronic diseases. We've made virtually no progress in the management of chronic diseases, and that's why today we see that the majority of people living in the developed world are going to die, indeed, from chronic diseases.
Russ Roberts: Yeah. When we think about that expansion, that doubling of lifespan, it's overwhelmingly two factors: the incredible improvement in childbirth--you talk about Semmelweis. We've talked about Semmelweis many times in this program--a tragic figure, incredibly poignant--who understood that it was washing your hands after you went to the morgue; and no one believed him. And the tragedy for me has always been he was careless about his study because he was so confident he was right, and so it made it easier for people to dismiss it; along with his personality; and of course, that led to the deaths of thousands of women prematurely. Such a sad story.
But, we have the improvement in childbirth and in childhood death--death before the age of five. So, once you reached a certain age, six, ten, fifteen, whatever it was in the data--I'm not sure, but five is a good round starting point--the improvement isn't anything close to a doubling. Once in 1900 you reached age of five, many people lived to be 70 and 80 years old. It wasn't everybody died at 40, even though that was the average. That's because you had a lot of zeros and point fours for the people who died as infants.
The second improvement, though, that--I knew that before, but what I learned from your book, which I didn't realize or appreciate--is that most of the improvement since then is in fighting sepsis, infection and the use of antibiotics. Which is a miracle, an extraordinary revolution in human creativity. But, the other things, very, very, very, very slow progress or none, and it's easy to forget that. We hear lots of statistics about improved mortality from certain conditions. They're somewhat misleading in that sometimes it's due to earlier detection rather than actual improvement in outcome and mortality outcome.
And then, there's the question that you focus on in the book, which I find really a totally different perspective, which is that our goal isn't to keep people alive. It's a cliché, but it's so easy to forget it. It's to have a good life. And, it's not just, 'Oh, take risks and enjoy things, because of course you're not going to live forever.' It's that we may have the potential, and medicine could focus instead on making sure that you maintain function further and further into your lifespan. It's a beautiful idea.
Peter Attia: Yeah, and I think I want to reiterate a point I made very quickly, but I think it's the jugular issue here, which is the old cliché, what gets measured gets managed, could not be more true. And, in Medicine 2.0, understandably, the benchmark is lifespan, and therefore, everything works towards the management of lifespan. If we instead chose to focus more on healthspan, I believe we could be more effective. But, it's also understandable why we're not focusing on healthspan. It is much harder to measure, and therefore, I think it's easy to understand why we as doctors will instead focus on the metric that we can measure.
Russ Roberts: And we've had recent episodes with a number of folks we'll link to, pointing out that a lot of end-of-life care, it isn't just that it extends your life a small amount: it extends it in unpleasant ways often that take out the opportunity to do the things we love. And, maybe we'll talk more about that later. But, what are the Four Horsemen of the Apocalypse? What are the four things that kill us slowly?
Peter Attia: So, if you're a non-smoker--and that's an important distinction because if you're a smoker, there's a fifth really big bucket here, which is chronic lung disease. But, if you take out lung disease, aside from lung cancer, the Four Horsemen, in order, are: cardiovascular disease or the diseases of atherosclerosis--so that includes cerebrovascular disease, strokes, heart attacks, heart failure, all of those things.
That's hands-down Number One, Russ, and it's funny how little attention it gets. At least in America, I think cancer gets a lot more attention, perhaps because it's scarier. But, the truth of it is, heart disease has always been Number One. And, by the way, globally, that gap is even larger. So, globally, that gap is about 19 million versus 13 million. That's deaths per year.
Disease Number Two is cancer; and again, we have to be careful when we talk about cancer. It's not a disease, right? Cancer is a very, very heterogeneous set of diseases that only have two things in common--which we can talk about--but aside from that, completely different process. Right? So, breast cancer and colon cancer are so different that to compare them--to say that they're one disease called cancer--is a little bit misleading.
The Third Pillar, or the Third Horseman, would be all of the neurodegenerative diseases and all of the diseases of dementia. This is a bit of a two-bucket, if you will, because not all forms of dementia are neurodegenerative. For example, vascular dementia, which is a significant driver of dementia, is not neurodegenerative the way Alzheimer's is; and of course, Parkinson's disease is not typically a dementing disease in the way that Lewy body dementia or Alzheimer's is. But collectively, taken together, this would be the Third Horseman.
The Fourth and final Horseman is one that doesn't really directly kill an enormous number of people, but indirectly, I would argue, is the gasoline that is poured on the fire of all of them, and it's the cluster of metabolic diseases, or maybe a better way to think about it is the continuum of metabolic diseases that ranges from insulin resistance all the way to Type 2 diabetes. Now, Type 2 diabetes is indeed an epidemic in the United States. I apologize: I can't quote worldwide statistics. But, if you just go back in time 50 years to when I was born, the prevalence of this condition was less than 1% in the United States. Today it's over 10%.
So, when you have a log-fold increase in a disease in a decade--and that is not a diagnostic difference; I mean, it's crystal clear that using the same diagnostic criteria, we have this log-fold increase--it's clear that there's a problem. And that problem, while it does kill people directly--people do die directly from Type 2 diabetes--far more likely they're dying as a result of it's doubling of risk of these other Horsemen.
Russ Roberts: Yeah. That's a fascinating point.
Russ Roberts: I have to say, when I started your book--and it's very entertaining. It's very well-written. Besides the medical insights and advice you give, there's a great deal of you in the book, which is riveting. I have to say, when I started it, I had a lot of skepticism, because if you asked me before I read your book, 'These four things, we want to avoid them and we want to do better,' I would say, 'You know, other than maybe obesity,'--which we're going to talk a lot about--'and diet and nutrition, these things are overwhelmingly driven by genetics. And, right now I can't change my genetics, at least in our current medical knowledge, scientific knowledge, but I can be kind of cavalier about these risks, because it's already written into my DNA [Deoxyribonucleic acid].
And, in fact, ironically, you start with an analysis--after the introductory parts of the book--you start with analysis of people who live very, very long. They live over a hundred. Centenarians. And, they smoke. They drink. There doesn't seem to be anything they have in common behaviorally. So it kind of reinforces my bias.
And yet, you come up with a very clever insight about those folks and use that as an example of why my initial skepticism might be misplaced. So, while it's true that genetics have a lot to do with our risk of heart attack, cancer, Alzheimer's, etc., it's not the whole story.
Peter Attia: Yeah. So, this is an area where, Russ, I had no idea what the answer was going to be ten years ago. So, I didn't start writing this book till seven years ago. But of course, the topic was my life's work.
And so, 10 years ago, I was really digging into this particular question around centenarians. So, these are the people who--as you point out--live to be a hundred and beyond. And there's something very special about them. And understandably, there are no shortage of studies being done on them. But the two people who have done the lion's share of this work are Tom Perls at Boston University and Nir Barzilai at Albert Einstein.
And I'll never forget the day when I finally--you know when Neo in the Matrix finally sees the connection and everything? I'll never forget my Neo-in-the-Matrix moment, which was literally, I don't know, circa 2011. And, up until that point, there was a very important question I wanted to understand, which was: did centenarians somehow have immunity from chronic disease, and therefore, it was just a matter of time before something else killed them that was not part of the chronic-disease playbook? Or did they just delay the onset?
And, it became really clear, again, just through putting all this work together 10, 12 years ago, that the answer was: No, they're actually not immune to chronic disease. They just have a phase shift in time of 20 to 30 years, but then they basically die in the exact same distribution as the rest of us, with a slight difference. They get slightly more cardiovascular disease and slightly less cancer. But--and I talk about all this in the book--when they get their first heart attack, it's about 20 to 25 years later; but then they go down the exact same path to demise of cardiovascular disease. When they get cancer, they just get diagnosed 20 to 25 years later, but then their path towards death is the exact same.
So, the insight here--the first insight--was centenarians' gift is indeed delaying the onset of chronic disease. Not avoiding it indefinitely, simply delaying it.
The second insight, and this is the second part that the chapter focuses on, is--and you led with this--it's not due to any behavior. It truly is a genetic lottery. Contrary to popular belief, however, it's very polygenic. It is not like there is a longevity gene. Now, there are some that show up more frequently, and I talk about the top four or five in that chapter, but I talk about them not because you and I can do anything about them.
You and I are not going to go change our APOE [apolipoprotein E], our CETP [cholesteryl ester transfer protein] gene, our FOXO [Forkhead Box O] gene, or any of those genes. However, what we can do is copy the phenotype. We can't change the genotype. We can't change the actual gene to match theirs, but we can learn what that gene is doing.
So for example, a [?]--a mutation in a gene or a snip in a gene, a difference in a gene that changes or lowers the burden of their lipoproteins, the causative driver of atherosclerosis, is going to lead to a delay in the onset of atherosclerosis. That's something we can mimic.
So, the other thing that came out of this study for me was the understanding of where and when genetics play a role in lifespan. And it turns out that up until about the 8th decade of life, genes play virtually no role. You can never say no role, because there are examples I could give where genes do indeed--are almost deterministic in lifespan. But those are absolutely marginal cases. For the most part, into your 8th decade, genes don't play any impact on lifespan. However, as you get into the 9th, 10th, and 11th decade, genes start to matter.
All of this comes back to, though: So what? Why does this matter? Well, I'm not here to suggest you or I--I don't know your family history, Russ, but let's just assume you don't have centenarian parents or grandparents or siblings. Well, you wouldn't have siblings, but parents or grandparents, aunts and uncles. And, I certainly don't. I have very little belief that anything I'm going to do is going to get me to live to be 100, but that doesn't mean I can't live, say, five, six, seven years longer than my, quote-unquote, "genetic predisposition." And again, and more importantly, it's: What can I do for my healthspan? What can I do such that at 80, instead of looking and functioning like the average 80-year-old, I could look and function like the average 65-year-old? That's the really important thing to consider.
Russ Roberts: And, that's very inspiring and very moving.
Russ Roberts: I want to raise a question you don't talk about in the book. It feels to me that--my mom is 90. My dad died at 89, and he was a smoker, and he had about five horrible cancers over the last 15 years he was alive. They didn't eliminate his ability to play tennis, ride his bicycle, spend time with his grandchildren, but it took a lot of the fun out of it. He hated the phrase 'he battled cancer,' like it was a military campaign. In his view, it was just you were stuck with it, and you did what you could. And, he was lucky in a sense that he overcame them for a while, but while he was overcoming them, it was really unpleasant. So, that theme of your book really resonates--really resonated with me.
But, let's take my mom. My mom is 90. She lives on her own. Until about a month ago, she drove--until she knocked her side mirror off. Her car misbehaved. It accelerated suddenly when she put her foot on the brake; and she decided it was a design malfunction. Her children thought otherwise.
But, she's lucid. She takes walks every day. She lives a very good life doing the things that she still enjoys. At 90. My wife's mother just turned 80, and she's also very active. It feels to me that 90 is the new 80, and 80 is the new 70. Is that a misperception on my part, because when I was younger, old people just looked really old, and a 70-year-old seemed decrepit and hopelessly having a hard life? Or have we made some improvement in healthspan already?
Peter Attia: No. I wish you were right, Russ. I think that's a sampling bias. I think you have a couple of really great examples.
Russ Roberts: Small samples.
Peter Attia: Yeah. I think you have a couple of wonderful examples in front of you; but sadly, I don't think that's the case. I think we've done the opposite, actually.
So, there's two things going on, actually. Let's go back to the example that you gave. Believe it or not, if in the 1940s someone managed to escape childhood mortality, managed to escape all of the infections that probably would have killed them along the way--managed to not get a heart attack, i.e., managed not to die by the time they were 85--they were on balance, far more robust than the 85-year-old today, in large part because of their lifestyle. Right? They were a far more active person, they were sleeping better, they were probably under far less stress. There's a lot of things that they had going for them. Whereas I think today, yes, we do have more people living to that age, but they're living at probably a much lower quality of life. So, I think the two women in your life are excellent examples of what we would aspire to.
Russ Roberts: Yeah. And, I'm, of course, well aware that they just could be lucky, and I may not be, or may be, no way of knowing in advance.
Russ Roberts: Now, you talk about five tactics that we're going to talk about: Exercise, nutritional biochemistry, sleep, emotional health, exogenous molecules. And, you have interesting things to say about all of them, and we'll get to that. But, before we do, I want to talk about screening, because you make a case for--one of the Four Horsemen is cancer, obviously. We've made tragically little progress in, quote, "curing" it, or with a couple exceptions, we've made very little progress in reducing mortality dramatically.
Vinay Prasad, recently on the program, very skeptical of all-mortality impact for screening for breast cancer and colon cancer. We can talk about many other things, but he's certainly skeptical of those. I think you're less skeptical on the colon cancer front. You have a different interpretation of the NordICC [Nordic-European Initiative on Colorectal Cancer] trials. I'm going to give you a chance to talk about that. I have a thought in response. But, talk about your view of screening and in fighting cancer, and then we'll turn to this question of tactics for better health span.
Peter Attia: Yeah. I think my thinking on screening has really changed so much over the past decade. I trained in cancer--so I did my fellowship at the National Cancer Institute in immunotherapy, and got to see firsthand what I think and what I believe is the most promising therapy we have for cancer, going forward.
So, everything you said about the lack of progress in cancer so far is true, and I'll put some statistics to that in a moment. But, when I think about the next decade, I'm actually much more optimistic; and we can talk about why. But, let's talk about some facts.
So, 50 years ago--a little over 50 years ago--Richard Nixon declared a war on cancer. The goal, if you recall--this is coming on the heels of the success of the space project where Kennedy declares, 'We're going to go to the moon,' in 1961; and in 1969 we're there. And, let's be clear: it was a very reasonable, although naïve, thing to assume that we could do the same thing with cancer.
In the early 1970s, if you had metastatic, solid-organ cancer--so epithelial cancers mean cancers of breast, prostate, colon, pancreas, lung, brain, all those things essentially--if you had metastatic, solid-organ tumor, the probability you would be alive in 10 years, was zero. That's the metrics that matters. Not median survival. Median survival might have been 12 months. Today it's longer. But, overall survival, zero.
What is it today? Today it's slightly better than zero, but in solid-organ tumor, there's only two solid organ cancers that are being cured today: testicular cancer--which was not cured back then--and a very rare type of stomach cancer called GI stromal tumors [gastrointestinal stromal tumors]. This is not the stomach cancer that killed most people. This is a rare cancer because it happens to arise from one mutation for which there's a beautiful, targeted drug.
So, we'll make the math easy and say 50 years ago, a hundred percent of people with metastatic cancer died in 10 years, or [0%?--Econlib Ed.] were still alive in 10 years, and today 1% of those people might be alive. So, that's really low progress. Now, median survival has increased significantly. It's probably more than doubled, and some non-solid organ tumors have become cured. So, the success against leukemias and lymphomas has also been remarkable.
Again, I think for the space of time, we don't need to go into all of those, but I just want to make sure people understand that: look, overall survival for cancer--overall survival--is probably up by 8-10% from 50 years ago.
But, why so little? Well, I would say that there are a couple of things going on, but one of them is--the obvious is--we don't have great treatments. So, we don't have great treatments once cancers reach a certain size and a certain mutagenic burden. The cancers seem very good at outmaneuvering therapies.
But, the other thing I would argue, is we're intervening very late, because we intervene at a time when the cancer is quite visible. Now, if you consider, I don't know, a lump in a breast that turns out to be cancerous, it's already, even just at that one lump, well over a billion cells. Now, the question is: What's the probability in a billion cells that you are going to have heterogeneous pools of cells that are not going to respond to the same therapy? It's actually pretty high. It's much higher when that number is a hundred billion cells.
So, enter the discussion of screening, which is something I used to really be a stronger skeptic of. I really used to think that screening wasn't doing much. In fact, I even worked on a lengthy project on this when I was in medical school, and I used to think that most of the effective screening was lead-time bias. So, you kind of alluded to this actually a few minutes ago, Russ, when you said if you catch a cancer two years earlier, it could look like you're living two years longer, when in fact you're not.
I think--a couple of things now, I feel different about this. So, the first is the following. If you look at colon cancer and breast cancer, which are two easy examples to look at--and I write about this in the book--we compare the success of adjuvant treatment versus metastatic treatment--so I'll define those terms in a second--you see an important pattern. Adjuvant treatment is the treatment you give a patient after you have removed all visible cancer. So, this is what's done in Stage II, Stage III colon cancer.
So, a Stage III colon cancer--let's use that as an example. A person has a colonoscopy and you see a tumor; they sample it, they biopsy it. Yep, they know it's cancer. That person goes to the operating room; they have a section of their colon removed and a section of the adjacent tissue, and you actually see that the cancer even went to the lymph nodes. So, that's a pretty aggressive cancer. But, during the surgical exploration, the surgeon looks; there's no visible tumor in the liver. You can see that. You do a scan of that person, there's no visible tumor anywhere in the body. So, the term in oncology is: that person is NED--No Evidence of Disease. Do we just leave that person alone? No, we don't. We give them a cocktail of chemotherapy. What's the survival of that person five or 10 years later, call it 10 years later? It's a little over 50%, meaning half those people are alive--a little over half those people are alive--but half those people had a recurrence, typically in the liver or in the lung, and they don't survive.
Now, what about the patients who have metastatic cancer on that same day that these persons had their surgical resection? It turns out we give them the exact same chemotherapy. How many of those people are alive?
Russ Roberts: Explain what metastatic cancer is. In other words, the first one was no visible tumors, but the cells nearby have some--have cancer.
Peter Attia: That's right. In the metastatic case, it's visible to the naked eye. Either at the time that the surgeon removes the colon, he or she can actually see cancer in the liver, or even just doing a scan on the person you see that the cancer has spread to the liver, lungs, where else. We give those people the exact same therapy. Zero of those people are alive. So, what's the difference--
Russ Roberts: Five to 10 years later, you said--
Peter Attia: That's correct.
Russ Roberts: Right.
Peter Attia: That's correct, yeah. What's the difference? Why is it that the people who present with metastatic disease cannot survive for 10 years, where those that present with Stage III disease and you give them the exact same therapy, you could save half of those people permanently? That's a cure, by the way.
I believe--and many others as well--believe that the difference is in tumor burden. The difference is that when you're treating that patient with adjuvant therapy--i.e., when you don't have visible tumor--you probably only have a few billion cells scattered throughout the body. When you're treating that patient with abject metastatic disease, there are hundreds of billions of cells throughout the body. It's a numbers game, and the numbers are not in your favor.
The same example, by the way, is true with breast cancer. So, if you go hormone receptor for hormone receptor and do the same exercise, when you treat women for adjuvant therapy versus treat women for metastatic therapy using similar regimens, you're going to get similar outcomes [similar to those when treating colon cancer--Econlib Ed.].
All of this leads me to the inevitable conclusion that the earlier one can detect a cancer and treat it, the better your odds are. Does it mean that there's a guarantee? Absolutely not. The biology of this is very complicated.
And by the way, I think if we want to talk about breast and colon, those are two great examples, because they have very different biology. So, colon cancer develops in a Halstedian manner. So, William Stewart Halsted, the modern architect of American surgery, proposed this idea--which is not true for all cancers, but is true for colon cancer--and that is the stepwise progression from adenoma to cancer to distant spread. So, every single colon cancer comes from a polyp, though most polyps do not become cancer.
This is not true in breast cancer, and this is why I believe breast cancer is a much more complicated cancer--right?--we don't fully understand. Not every breast cancer comes from a ductal carcinoma in situ. So, there's something going on in the biology of breast cancer that makes it more complicated.
But, the reason I do feel very strongly about colonoscopy, is it's also one of the few cancers you can look directly at. You can't look at breast cancer. You have to infer it from a mammogram, an ultrasound, an MRI [Magnetic Resonance Imaging]. Those are all flawed. They all have limitations in sensitivity and specificity, the way a colonoscopy does not.
So with colonoscopy, I think what we really need to be considering, is: At what frequency would you need to do this, given that you know every cancer came from an adenoma, to justify the risk? Because, we'll have to talk about the three risks of colonoscopy. And it's not a benign procedure--unlike a mammogram which has a trivial amount of radiation and is effectively a benign procedure.
So, I don't want to suggest that this is an easy problem to solve, and that's why I write about it at length. But it is--and again, I have yet to see evidence that suggests that treating advanced cancer is better than treating early cancer, or treating a hundred billion cells is better than treating a billion cells. Or as good as: let's put it that way.
Russ Roberts: So, the question is--as we talked about in the episode with Vinay Prasad, the all-cause mortality--which I misspoke a minute ago--all-cause mortality for colonoscopy seems to be relatively unchanged by the procedure: either because it doesn't matter--meaning it's not that important to get it early. Probably not the reason. There are side effects that you alluded to, the three things. There's perforation, there's infection; I assume there are other things. And, while you're skeptical, I know of some of those all-cause mortality results, they are discouraging. And attempts to--it does call into question the--it's complicated, but--
Peter Attia: Well, let's talk about the NordICC trial, because I think that's the trial that would be looked at as the case against colonoscopy from an all-cause mortality standpoint. So, the NordICC trial, just for folks listening, is an enormous trial that was done in Europe, published recently. It was about a year ago; I think it was published last summer. And it looked at two groups of people. Half the group was randomized to usual care, which meant not doing anything. The other half was randomized to a recommended colonoscopy in a 10-year window of time.
Well, let's pause for a moment and make sure people understand the difference between effectiveness trials and efficacy trials.
So, an efficacy trial says--let's use a different example to make this easier. Let's say, Russ, we wanted to study the effect of a certain diet on weight. So, we get our people, we randomize them, and we tell one group, 'Look, you're going to have to eat lettuce and carrots and lima beans and Fiber One cereal for the next five years. That's all you're allowed to eat.' And the other group, 'You can eat whatever you want.' And, five years later we go and see how they're doing.
Well, the efficacy of that is only determined if the people are able to adhere to the right diet. And, the notorious challenge of dietary studies, is: it's almost impossible to do efficacy studies if the intervention is quite extreme.
For the most part, we give up on doing that, and we only focus on effectiveness studies, which is: how effective is this intervention in the real world, i.e., how effectively can people follow the advice that is given? So, again, when you tell people, 'Go on a low fat diet, go on a Mediterranean diet,' they're going to adhere to it at some level, but it's nowhere near the prescribed level.
So, this was an effectiveness trial of colonoscopy: We're going to recommend that you guys get a colonoscopy once in 10 years. 40% of them did. A). I'm not convinced that every 10 years is nearly sufficient enough. There's literature showing that people can develop colon cancer as little as one to two years after a completely normal colonoscopy. Again, we could argue maybe in those cases the adenoma was missed a year earlier. It's hard to say. But what I would say is 10 years is far too infrequent.
And furthermore, we didn't have very good compliance, despite a statistical analysis that suggested that didn't matter. I don't buy it because I also don't think that the 10 years was sufficient.
So, I think that what we really ought to be doing is asking: What is the probability of one of those three risks?
So: What are the three risks of colonoscopy? There's the risk of the bowel prep--which for people like you and I is not an issue, Russ, but it would be for your mom. And by the way, I'd have reservations about your mom doing a colonoscopy because of the preparation. She could get so dehydrated that she could fall and knock her head, right? The bowel prep is a big deal. But that's risk number one.
Risk number two is the risk of the sedation. It's a low risk, but it's not zero.
And then risk number three is the procedural risk of bleeding and perforation. And, I always advise people, when you're getting a colonoscopy, you must ask the endoscopist what his or her risk is of perforation.
Russ Roberts: I'm sorry for laughing, I apologize, because I think I recently, in the Prasad episode--I don't know if it was in that episode or not--but a friend of mine was recently encouraged to do a particular procedure, and I was worried about it, about a bad outcome, and I said, 'You should ask about it.' And the guy said, 'Well, the odds of it are only,' blah, blah, blah. And I said, 'You don't want the national odds. You want his or her odds'--
Russ Roberts: 'the person doing it.' And, I assume they're not so eager to tell you, sometimes.
Peter Attia: Yeah, but, you know, look: we were encouraged in my surgical training to be very open about that. Even for the simplest procedure, like putting a central line into somebody, I could quote the national average, but I could also tell you that in the last 300 of these, I punctured one lung. In the last hundred times you take out somebody's gallbladder, you accidentally nick the common bile duct--whatever the number might be. So, I don't want to downplay any of those risks, and they must be taken seriously.
But, what we really need to do is ask the question: What is the cost of those versus the cost of missing a colon cancer?
So, here's the thought experiment. So, as an economist, you'll appreciate this, because the only way you can do this thought experiment is to throw money out the door for a minute. So, we're not going to talk about the economics of this.
Here's the thought experiment. If you did a colonoscopy every three months on a person, could they ever die of colon cancer? If you did a proper bowel prep and did a colonoscopy, the answer is No. Right? There's no chance that in three months an adenoma could develop and become cancerous in three months.
So, the question then is: Okay, so you take the 53,000 people a year in the United States who die of colon cancer, you took that number down to zero. You have to, because it's a Halstedian cancer. Now the question is: How many more people did you kill from the bowel prep, the sedation, and the perforation?
By the way, I did this calculation on the back of my napkin one day: I got about 5,000. You would kill about 5,000 people doing procedures.
Should we make that change? I'm not suggesting that at all. I'm suggesting that's an extreme way to think about it, right? You take--
Russ Roberts: Yeah, that's a nice--
Russ Roberts: There's also the stress, which is, I'm not sure how that factors in, how important it is, [inaudible 00:43:44]--
Peter Attia: And that's a bigger issue with some of the other cancers, Russ, I think. I think that's less of an issue with the colon cancer, because you get the answer right away. But, I think your point about stress is significant when it comes to the more vague imaging modalities. I'll warn all of our patients--
Russ Roberts: You get false positives--
Russ Roberts: You get false positives. I'm thinking more of the stress of the procedure. A lot of people, because of our cultural taboos, the idea of a colonoscopy is so unpleasant that some of the 60% who didn't get that, even though it was recommended in that NordICC trial, just didn't want to think about it. And if you'd forced them to have it, or in some measure incentivize them, it would come with an additional burden. But, it's probably pretty small. So, I think Vinay disagrees with you, but I'm not sure why. He has reported on--
Peter Attia: Well, I'll tell you why, I think, having not spoken about this with Vinay, though I'd be happy to. I think Vinay and Peter come at this through totally different lenses, and neither is right and neither is wrong. Right? Vinay is coming at this through the lens of policy. He's coming at this through the lens of: What is the recommendation to all?
I'm coming at this through the lens of the individual. I'm giving you, as a person, a way to think about this for your decision around colon cancer. I'm going to get a colonoscopy every three to four years, because I am comfortable with the additional risk that I'm taking of the procedure. By the way, the additional cost I'm bearing--because my insurance will not pay for it more than every five years, so I'm personally on the hook; and it's not cheap; I mean, I just paid for my last colonoscopy--I think it was about $2,000. So, that's a big sum of money. But, at the individual level, I can do the math and make that determination.
I think Vinay is saying we're trying to make recommendations to millions of people here. It can't be that nuanced. It has to be based on effectiveness trials, not efficacy.
Russ Roberts: He claims they're the same: that after a statistical analysis, that 40% or 60% difference wasn't important. But, that's a separate statistical question. Reasonable economists and data analysts can disagree on it, I'm sure.
But, I think it's important for our listeners who may have, after the previous episode said, 'Well, I'll never do that again,' should think twice. And I appreciate your view on this.
Russ Roberts: I want to turn to nutrition, which is one of the tactics you talk about. First, let's get it off the table: You're not a big fan of epidemiology; and you and I share a deep, I think, brotherhood there.
Peter Attia: Yeah. I used to be far more outspoken about it, although I do devote some real estate in this book to talking about how we need to be very skeptical of nutritional epidemiology. I think epidemiology has had some enormous wins, and I always try to point those out--to sort of say: Look, the field in and of itself has done some good. I mean, we can point to cholera and other things like that. And certainly smoking, by the way: We were never going to do the definitive randomized control trial to demonstrate the harm of tobacco smoke.
But, I also have to explain the Bradford Hill criteria to make sense of when can you increase your confidence in the causal nature of an observation? And, I think it is very safe to say, Russ, that the ability to infer cause from nutritional epidemiology is somewhere between zero and epsilon, where epsilon is a very, very, very small number.
Russ Roberts: Yeah. So, but: that does not mean we have nothing to learn about nutrition. And I want to give you my takeaways from your book and let you elaborate on them.
So, I would say a huge theme of the tactical part of your book--what we would call advice--and it's wonderful, because you don't say, 'Go Paleo. Lift weights. Do this with kettlebells.' You are a wise man. You understand that everybody is different, and a lot of those things, those disputes about various diets and exercise regimes are, as you say in the book, religious, rather than intellectual. And, it's a wonderful insight, very important.
But, you spend a lot of time on exercise and nutrition without giving explicit--without joining a church, which I really appreciated--but, they're quite complicated, a lot of your suggestions. And I want to start with the simplest recommendation I would take away from your nutrition, and then see if you can make me go a little further.
So, kind of simple, actually: Don't be obese, take in fewer calories, stay away from sugar and junk food, and you've gone a long way toward what nutritionally you can do. There's more to say, and I want to let you say it, but I think that's an enormously big step for most people. And I would say, as a person on a diet right now, I've been deeply inspired by the section of your book on calorie reduction, to stick with it. So, I'm guardedly optimistic: you've had a powerful impact on my beliefs. It may be a placebo effect, but that works, too. So, I'm okay with it.
Peter Attia: Well, I'm glad to hear that, Russ. I think the easiest way to talk about nutrition is to maybe do it through the clinical lens in which I will look at a patient. So, every time I interact with a patient, I'm asking myself three questions. I mean, I'm asking myself hundreds of questions, but these are the three questions that factor into the thinking around a nutritional strategy. The first question is: 'Is this person over-nourished, or adequately nourished?' That's a way of saying, 'Are they storing excess energy or not.
Let's understand something here, which is up until about 150 years ago, i.e., from 250,000 years ago until 150 years ago, the ability to store excess energy was very good. Right? This was our Darwinian superpower. This is what allowed us to leap forward. Our brains, which weigh 2% of our body weight, consume 20 to 25% of our metabolic demand. There is no way our species could have evolved to where it did, did we not have the capacity to store enormous amounts of energy. So, this was a very good thing--until very recently when we entered such an energy dense environment.
So, Question One is: Are you storing excess energy or not?
Question Two is: Are you adequately muscled or not?
And, Question Three, which is often related to the first two: Is are you metabolically healthy or not?
Now, the good news is all three of those questions have objective answers. There's nothing subjective about this.
Now, you can't measure them on a bathroom scale. You do need more complicated testing called DEXA [Dual X-ray Absorptiometry] testing, but that's readily available. It's about a $100 test. Everybody can get a DEXA scan, and understand the extent to which they're over-nourished/under-nourished, adequately muscled/under-muscled. And I explain all the parameters for these things, and if they're metabolically healthy or not--which can be done with blood testing.
When you know the answer to that question, you basically now can draft out an algorithm which says: Do you need to maintain caloric intake or decrease it? And by the way, in some cases, increase it. Do you need to maintain protein intake specifically or increase it? And, do you need to undertake additional tools to improve your metabolic health? And, that's where exercise fits in. By the way, it also fits into the muscle balance.
Now, most people listening to this, if they go through this exercise, more than 50% of people are going to wind up in the overnourished camp. So, if you're in the overnourished camp, the strategy must be some form of energy reduction. And, what I outline in the book is, there's only three strategies to reduce energy. In other words, only three ways to go about reducing intake.
One is directly. We call that caloric restriction. You directly reduce caloric intake without necessarily paying attention to what you're eating and when you're eating. You just say: Total pool of energy must go down. So, if I'm eating 3,000 calories a day, it's got to be 2,400 calories per day. But, if you're willing to track that--and that's the challenge of this approach, you have great flexibility in what you eat and when you eat.
The second approach is time restriction. This has become very popular lately and also very cult-like. But, this says the key is just fasting throughout the day. So, Russ, you might say, 'Well, okay, the way I'm going to do this is I'm only going to eat between 2:00 and 7:00 in the afternoon. So, 2:00 in the afternoon, 7:00 in the evening, and by starving myself for 19 hours a day, it's going to induce--indirectly--a state of caloric restriction. And, that's fine.
The data on this, by the way, are crystal clear. There's nothing magical about time restriction metabolically or from a health perspective. All of the benefits that are accrued through time restriction are through the direct effects on calorie restriction.
The third and most contentious of this--and I say 'most contentious' because it's the one where most of the attention is; it's the one where most of the books are written--is called dietary restriction. So, you pick a boogeyman in the diet and you take it out. And, the more restrictive the boogeyman, the more calorically dense it is, the more ubiquitous it is, the more restrictive you'll be.
So, again--I use this example--but if you go on the all-lettuce diet, you're going to lose a lot of weight. If you go on the no-lettuce diet, you're going to lose no weight. But, that's where paleo and vegan and low-carb and South Beach and all those things come in: they're restrictive diets. And the more you restrict, the more you will lose.
None of these, in my opinion, are really superior to the other. The data just doesn't bear it out. What the data suggests is: The one that you can adhere to is the best one.
Again, it's not a very satisfying answer because I think people want to believe that there is one true answer here, but at the level of our capacity to measure these things, that doesn't seem to be the case.
Russ Roberts: So, here's what's interesting to me--and let's move away from the individual for a minute and talk about the practice of medicine, and I want your take. Past doctor of mine in a different city, different country than where I am now; I liked him a lot, he was thoughtful, sensible, clearly well-educated, understood a lot of things. I would get a physical. The physical would go something like this: I would say, 'I don't want a PSA [Prostate-Specific Antigen] test because I know there's a lot of false positives.' And, he'd say, 'Oh, okay.' And then, he would do the rest of the--what do we call it?--workup. And, I'd get a PSA test anyway, even though I told him not to; they'd throw it in for free. And I'd say, 'I didn't want that.' 'Oh yeah, sorry about that.' Fortunately, it was always a relatively low number, didn't lead to anything bad.
Then we look at all the 60, 40, 28 things that came back; and there's a range, called Healthy/Abnormal. If you stayed within the range, nothing else happened. We never had a conversation. Again, smart man. This was a while ago, so maybe things have improved. But, in general, the doctors that I've encountered and talked to tend to just view it as a binary thing. 'Your HDL [High-Density Lipoprotein] is okay. Your such and such is okay.' And, they go down the list, and if something's not okay, they might say, 'Oh, your glucose is a little high, your sugar's a little high. You should probably cut out candy bars or eat less dessert.' That would be the--that's the most radical thing I've ever learned from a physical except for the occasional--the last time, because I'm getting older now and I get more things outside the range, they say things like, 'Well, yeah, keep an eye on it, but it's probably okay.'
You have a different approach. So, talk about that and why your approach isn't everybody's approach. What's going on?
Peter Attia: Well, I guess there's a couple of things I'd like to unpack.
Russ Roberts: And, excuse me, I know we could spend the whole rest of the time on your approach. Not the rest of time, we could spend three, four hours on it, a lifetime. So, try to summarize, give us a thumbnail of why you look at that number differently than I just described it.
Peter Attia: So, I think a couple of things. One is let's talk about what that range means.
So, when you go to a doctor and the doctor does a blood test on you and you look at the range, it's very misleading to editorialize that the way we do by saying, 'This is normal/this is not normal.' We should be more accurate and simply talk about what it is, which is: This is the interquartile range.
For example, if you look at your liver function tests, your AST [aspartate aminotransferase] and your ALT [alanine transaminase], it might say less than 40, less than 40. That doesn't mean less than 40 is normal, and that 39 is good and 41 is bad. It simply means that, in that case, 80% of the people are below 40. Right? Or, if you look at your testosterone level and it says 300 to 1200 is, quote-unquote, "normal," no. It means that 5% of people are at 300, the 95th percentile is at 1200. So, the 5th to 95th percentile is between 300 and 1200.
And so, again, I think the problem starts when we take a binary look at any of these metrics.
Again, I'll use one more example, which is the hemoglobin A1C [hemoglobin A1C or HbA1C], which everybody I'm sure is familiar with. That's the test that's used to diagnose Type 2 diabetes. So, the diagnosis of Type 2 diabetes is made today--this is not the way it used to be done--but it's made today when you have that number exceed 6.5%. Because that number is an estimate of your average blood glucose. So, 6.5% represents or estimates an average blood glucose of 140 milligrams per deciliter. We would all agree today that if you have that number or greater, 6.5% or above, you have Type 2 diabetes.
But, does that mean that if you're at 5.7% versus 5% that it's the same? No, not at all. This is a continuum.
And we know, by the way, that there is a monotonic improvement in health outcomes as that number gets lower. So, 5% is better than 5.5% is better than 6%, even though none of those have diabetes.
So, that's Problem One.
Problem Two is--and I went to a good medical school in your backyard, Stanford, and I think I had a very good medical education. I mean, I had amazing professors, and I thought it was amazing to be lectured by Nobel Laureates and all of that stuff. You talked at the outset about five tactics. In the four years of my medical school, Russ, I want you to estimate for me how much time did I receive training in nutrition, exercise, emotional health, and sleep, which were four of the five tactics. And, just round it to the nearest hour.
Russ Roberts: Yeah, that's zero-one maybe.
Peter Attia: It's exactly right. I would give you a confidence interval of 95% if you said zero to one.
Now, this is a problem. And I want to juxtapose this with the problem I stated at the outset of our discussion: What gets measured gets managed, and all we're measuring is lifespan, and that's all we're managing.
And then we're educating people in one-fifth of the tools we have at our disposal to impact these things, which is the exogenous molecules piece.
And, again, I don't want to suggest that medications aren't valuable. I can talk for hours about all the places where medications are valuable.
But the truth of it is--and this is borne out by data--it's not as valuable as exercise. Exercise is far more potent at extending lifespan and improving health span than any medication.
Russ Roberts: I misremembered my doctor I was mentioning. I remember I had a Vitamin D deficiency, which of course I suspect an enormous part of the American population does because they work indoors and don't play outside much. So, he prescribed a megadose of Vitamin D, and I thought, 'I'm not sure taking vitamin D does the same thing to my body as sunshine does in terms of reducing my risk of,'--I think it was shingles. And, it looks like it's correlated with kidney stones, and I really don't want to get a kidney stone. So, I remain, I am sure, very Vitamin D deficient, although now that I live in Jerusalem and walk to work every day, I think I'm probably up a bit; I hope I'm into, quote, a "healthy" range.
Russ Roberts: But, I think the point you're making about--I mean, there's two things. You did mention the other one. The one is: Well, some of these, even if they're in the range, there's a big difference to what piece of the range you're in.
Second is: You should be looking at them over time because they tell you things about how your body is aging. And, I've never had a doctor do that.
So, I think it's a fascinating example about the training and the mindset of medicine, what you call the 2.0 mindset that--and I'm not sure why. I think it's a hard question to answer why it's so, I would call it, algorithmically-driven rather than craft- or art-driven. You have the word 'art' in your title, and I think the part that it's incredibly important, but it can't be measured precisely. So, I think it gets ignored.
Peter Attia: I think that's fair. You've said this, I'm sure, in the past, and I want to make sure it's clear. I think most doctors desperately want to practice medicine 3.0. And again, the term is meaningless: it's just a dumb idea I came up with. But, I think everybody understands the ethos of it, right? Everybody understands that they want to prevent their patients from getting ill. They want to keep people not just living longer, but more importantly, living better.
I think another point which can't be ignored here is the structural system of reimbursement. Now, again, this is a very U.S.-centric discussion, but unfortunately the United States and Canada are the two systems I understand best because I grew up in Canada, but I've lived over half my life now in the United States. Both of them are completely inappropriate to solve this problem for completely separate reasons.
But in the United States, because it is mostly a for-profit system--which is not always a bad thing--but in this case, it requires a system of diagnosis and billing code. And, this gets into a lot of problems, which is you couldn't fix the system today because you don't have a diagnostic code to bill for true preventive work.
So, again, I don't need to tell an economist what incentives do. And, there's nothing wrong with people who follow the incentive. But, if you're going to say to a physician, 'You have to see X number of patients in a day because that's the nature of the job, and that affords you 15 minutes per patient per day,' well, in that 15 minutes you have to see how many billing codes you can come up with, and they have to be in line with the tools you have to treat.
So, when you look at hypertension, which is a very important problem, that's diagnosis, it's a lot easier to give somebody a medication for hypertension than to explain to them how to exercise and change their nutrition, which could also be very effective there. And by the way, address their stress.
And, by the way, I don't want to suggest I could do a better job. There's zero chance I would be doing a better job, Russ, no chance at all. So, I have nothing but empathy for the doctors that are in that system. And, unfortunately the doctors--those of us who practice differently--have to do so outside of the reimbursement system.
Russ Roberts: Yeah; I don't want to go any deeper into this, although my first thought is that it would be nice to have an app where I could enter my results of my blood tests and then it would help me track them over time in a thoughtful way. I don't think that's very hard to do. I think there's some obvious things you could learn from that. It's shocking to me now that I think about that. I've never seen that done by a doctor. I understand no incentive to do it or limited incentive, but--
Peter Attia: Well, but I'm actually surprised. I mean that seems--I don't even think that that's the massive insight. The massive insight shouldn't be tracking it over time. It's really knowing what to do with it.
So, for example, let's use your PSA example. So, I think that the PSA I think has been demonized for the wrong reasons. It's a very, very low specificity test. There's no doubt about it. It's a high-sensitivity, low-specificity test, which means taken on face value it's not helpful for making the diagnosis of prostate cancer. But, again, a very good doctor understands that it's not PSA that matters. It's PSA velocity--which we calculate.
So, there's an app for that, by the way. There's literally an app online where you plug in all your PSA values and time and it calculates PSA velocity. And, if PSA velocity exceeds 0.45, meaning if it's changing at 0.45 units per year or greater, that's a problem.
We also calculate PSA density. So, you take the PSA and you divide it by prostate size, which can be determined easily from an ultrasound that costs about 10 cents. If the PSA density exceeds 0.1, that's also of concern. So, by looking at PSA velocity and PSA density, you can very easily catch it.
And, I'll tell you a very interesting story. A very close friend of mine was paying attention to his father's health. He's not a physician, by the way, but he works with me. He noticed that his dad had a PSA test and the number wasn't that high. People don't get alarmed until it's above three. It was below three. But, he did the calculation, because he works with me, and he saw that the PSA velocity was over 0.45. And so, they went, he told his dad, 'Hey, you got to tell your doctor this is a problem. You need to get an MRI to look at this.' And, the doctor said, 'No, no, no. There's nothing wrong with this.' And, to make a long story short, we went around the doctor, got the MRI; he ended up having prostate cancer. And so, his son, who is not a doctor, made the diagnosis by looking at the rate of change of PSA, which again is just time series data. So, it upsets me greatly to think that patients don't have access to that information.
Russ Roberts: Nassim Nicholas Taleb says when you go to a casino, you don't take gambling advice from the carpenter who built the roulette wheel, even though in theory he's an expert on roulette because he built the wheel. And, doctors are not trained sufficiently, in my view, in risk or this craft and art we're talking about. And of course, individuals who are not doctors can often give thoughtful advice. A friend of mine said--he had a vitamin D deficiency; he was going to take this vitamin D supplement. And I said, 'Well, you might worry about' blah, blah, blah. And he looked at me like I was insane. He said, 'You don't understand. A doctor told me to take it.' And I wanted to say, 'Okay, whatever.' I am a doctor. Just not the kind that helps people. Maybe an economist, but maybe in this case it could be helpful.
Russ Roberts: Anyway, a couple of other issues we don't have time to talk about. I just want to mention them and let you say a few things about them if you'd like. A couple of things in here that were helpful to me. You argue for the importance of protein. You argue for the importance of sleep, and you argue for the importance of exercise.
And, the exercise chapter is hard for me because I don't have the devotion that it sounds like I need to go to the level of customization that you're worrying about. So, for me, who sits at a desk and loves sitting at a desk, or a comfortable chair even better--or lying in bed--and would do it for 16 hours a day, I now walk to and from work. So, my step count in Israel is 10,000 plus and sometimes 20,000 when we go out at night because I don't own a car versus the 4,000 or 5,000 I had in suburban Maryland. I assume that's a good thing, but I had some guilt reading that chapter on exercise because I think I'm not doing enough and I'm worried I don't know how to get there from here. So, give me some thoughts on exercise; and if you want, throw in some protein and sleep.
Peter Attia: All right, I'll start with a specific piece of advice for you that without adding any more time to your day, could get you more benefit, provided you have a place to shower at your office, which is: you could, instead of just walking to and from work, you could ruck to and from work. I talk a little bit about rucking in the book, which is just putting a weighted backpack on. So, if you were carrying 30 pounds with you everywhere you went again, again, it wouldn't take any more time but what it's going to do is give you a more compressive load. Because, one of the things we have to think about here is we have to make sure you have strong bones, strong muscles as you age.
Once you hit the age of 65, if you fall and break your femur or your hip, your one-year mortality is anywhere from 15-30%. That's all-cause mortality. Because, what happens when a person breaks their hip, they don't just die immediately from blood loss or from a fat embolism or a blood clot. Those things can happen. But, it sets them on a trajectory towards all sorts of bad things happening.
So, even if you take the low end of that estimate, 15% of people age 65 or over fall and break their hip, they're going to be dead in a year. And, of the remaining survivors, 50% of them will see a full reduction in functionality. Meaning people who walked unassisted will now require a cane. People who were on a cane will require a walker. People who were on a walker will be in a wheelchair.
So, how do we avoid those things? Well, we avoid those things by working. We avoid those things by having strong muscles, strong bones, and improving our balance, which you get by practicing. So, again, that's just a very simple thing that says: Look, if you don't want to be in the gym doing all these other things, put that rucksack on your back when you make that walk and you'll get more bang for your buck.
Okay: now why do I harp on this so much? Because I think the data are unambiguously clear that exercise is hands down the heavyweight champion of interventions.
And, here's where the statistical tool of a Cox proportional hazard makes this case very clearly. So, I won't go into the explanation of it. I assume your listeners understand what a hazard ratio is? Sort of. Okay. A hazard ratio is an indication of relative risk.
So, let's start with things that are very obvious. Is smoking bad for people? Yes. How can we measure this? Well, when we look at all-cause mortality, if we compare a smoker to a non-smoker at any point in time, the smoker has a 40% increase in all-cause mortality in the coming year relative to the non-smoker. So, that's a hazard ratio of 1.40. That's a very big hazard ratio. And, it's not surprising, right? I mean, it's not just that smokers are more likely to die of lung cancer: they're more likely to die of all cancer. They're more likely to die of heart disease. All of these things. Okay.
If you look at the hazard ratio for high blood pressure, it's about 1.29, 1.3. So, 29 to 30% chance greater death in the following year than the non-smoker [?someone without high blood pressure?--Econlib Ed.].
At the very extreme levels, Russ, we look at people who have end-stage kidney disease. So, someone who's on dialysis compared to someone who's not on dialysis, that hazard ratio is about 2.75. That's enormous. That's 175% difference in all-cause mortality over the coming year.
Now, let's talk about the difference between being very fit and not being very fit. When you compare--so, there's a test called the VO2 max test [maximum volume of oxygen test]--it's a test you do on a treadmill or on a bike where you have a mask on your face and you're pushed to exertion, to failure actually. And, what's measured is the maximum amount of oxygen you can consume. And the higher the amount of oxygen you can consume, the fitter you are. When we divide people into quartiles and we compare the top to the bottom, etc., you see hazard ratios that look as follows: If you compare people at the very bottom, and this is by sex and by age, so if you take 60-year-old men in the bottom 25% and you compare them to 60-year-old men in the top 2.5%, the hazard ratio is five. That's 400% difference.
If you just compare the bottom 25% to the second quartile--these people are both still below average--the hazard ratio is 1.5. It's a 50% difference.
I could do the same exercise with muscle mass and strength. And, while the numbers aren't quite as big, they're still in the two- to three-X delta. And, the reason for this is that VO2 max strength and muscle mass are amazing integrals of work. Like, you can't just decide tomorrow you want to be strong and have a high VO2 max the way you could fix your vitamin D. If you took enough vitamin D, in two weeks you'd normalize your level. The reason I don't think that has much of an impact is that it's not a real change in your physiology the way--if we improved your VO2 max by 25%, which we could do in two years, it would have a bigger impact on your lifespan and the quality of your life than any other intervention. But, it would require work. So, this is the two-edged sword of exercise, which is it does require the most work by far, but it has the most bang for the buck.
Russ Roberts: I just want to say the other perspective you bring, which I love, is that you tend to think about, 'Well, I'll lift some weights; I'll get stronger,' or 'I'll just work out in the gym; I'll get stronger.' It's really an investment in those next 20 to 30 years for somebody in my situation--at 68--because as you point out--and you don't think about this enough, I didn't think about it enough--you're going to start declining, actually pretty young. And, there's an inevitable decline, and what you're trying to do is slow it down. And it's not about today: it's about 10, 20 years from now and having, again, the ability to live a healthy life.
You said if I carried a 30 pound rucksack, it wouldn't take any more time. That would not be true tomorrow. I would have trouble getting to work in my 35-minute walk with 30 pounds on my back. I'd rest more even if I had--I do have a shower here, so there's hope.
Russ Roberts: But, I think the basic idea, that there's some somewhat simple things we can do to improve our health and healthspan and lifespan is interesting.
Russ Roberts: My only problem with claims about exercise is that I thought you were a lot more skeptical of the nutritional literature than you were of the exercise literature. So, let's take the VO2 example. Somebody in the bottom quartile has a lot of things different about them than the people in the top 2 1/2%. Income, education. There's a lot of other stuff, which are called confounders--third things that interfere with the causal relationship.
So, I'm curious why you're so confident in the exercise. For example, the most obvious thing is that people with low VO2 I assume are on average more obese. So, if you control for weight: say, if it's two 60-year-old men of similar weight and height, BMI--body mass index, is it still going to be true that that hazard ratio is that large? What if you control for education? What if you control for income? Are we still going to get those impacts?
Peter Attia: Yeah, a couple thoughts on that. And, great point: I'm glad you brought it up.
So, VO2 max already controls for weight because it's normalized by weight. So, VO2 max is measured in liters per kilogram per minute. So, that takes care of that issue.
But, you're right that there is something fundamentally different about a person whose VO2 max is in the top 5% versus the bottom 5%. In other words, VO2 max is a proxy for health. At the end of the day, that's the biggest difference.
So, it's a bit of a circular argument, but here's what I would say. The same argument is true when we look at the smoking, when we look at the diabetes, when we look at the end-stage renal disease examples. So, really the only thing I can say is not that the hazard ratio is 2.8 for this group of fitness versus that group of fitness; because you're right, that has confounders in it, but those same confounders will exist when I'm looking at the person without diabetes to the person with diabetes. Having diabetes is a proxy for unhealthy behaviors. So, it's a relative change.
The other point I would make--and I actually devote a bit of space in the book to explain this, because I understand that this is an obvious point--is that when you go back and you look at those Bradford Hill criteria of epidemiology and you run it through--you run the exercise epidemiology through the Bradford Hill criteria--versus the way we did on the nutrition, everything points in the right direction.
So, with nutritional epidemiology, there are a lot of problems statistically. The hazard ratios are tiny. They're like 1.1, 1.12. They never go in the same direction twice. One day red meat causes cancer, the next week it doesn't. One week coffee is bad for you, the next week it's good for you. There's no dose effect, it appears. There's no biologic plausibility. You don't have the data to support this: you can't reproduce these results in randomized control trials.
All of that goes out the window when you looked at the exercise, Russ. So, in the exercise stuff, all the data point in the same direction. The magnitudes change a little bit from study to study. So, the two biggest studies looking at VO2 max ever--and these are studies that involve over a million people--you might have the difference: one study might have the highest hazard ratio of four while the other one is at five. But you see a dose effect for all levels of VO2 max.
You also see the biologic plausibility when you study these in a controlled setting. In other words, when you take individuals and you randomize them to treatment arms of different training for a period of six months or nine months, you see all of the health benefits come in line with the intervention directly, though they started without it.
So, all of this is to say that the epidemiology is far from perfect, but in the exercise literature it's consistent and in the nutrition world it is not. And the magnitudes, I think, give you much more of a buffer: you could put confidence intervals on those things and still know you're moving in the right direction.
So, none of this is to suggest that if you doubled your VO2 max, you'd live 20 years longer. That can't be imputed from the data. And, I've often said if all the exercise I did did not lengthen my life by one day, it would still be worth it because I want to be able to move freely and be active in the final decade of my life. And, there's no question that exercise is doing that.
Russ Roberts: I do want to say that although I think it's unlikely that I'm going to add 30 pounds to my backpack, I do often carry my laptop back and forth and I have a small MacBook Air. I think I need to go to an older IBM machine [International Business Machines] and thereby feel better about--anyway, it's just a bad joke.
Peter Attia: But, start with 10. Start with 10 pounds.
Russ Roberts: So, okay, I'll try. More books, I need to bring more books back and forth. And, I'm going to like this because I think I need a special rucking backpack and I have a small obsession with luggage, backpacks, and bags, so it'll feed that in a nice way.
Russ Roberts: There are a lot of interesting things in the book about sleep. We didn't have a chance to talk about protein, about exercise in more detail, certainly about calories and nutrition that we've touched on.
But I want to talk about the last part of the book, which is totally different. The fifth tactic of your book is emotional health, and I thought, 'Yeah, yeah, yeah. Okay. Yeah, it's good to have less stress in your life and that's lovely.' And, I found the last part of the book about emotional health quite overwhelming and quite powerful. It's worth the price of the book alone. I'm not encouraging readers to buy the book and skip to the last part, but it is a very, very powerful part of the book. And, I don't really care whether emotional health helps my physical health. I'm willing to accept the possibility that it's true. You can elaborate at that on that if you'd like.
But, I want to talk about the tricks you've been playing on your brain, as you got older, to be a more emotionally, mentally healthy person. And, I want to read an excerpt and let you expand on it. You write the following. Quote:
Another way in which mindfulness helps is by reminding us that when we are suffering, it is rarely because of some direct cause, like a rock that is crushing our leg at this very moment. Much more often, it's because we're thinking about some painful event that occurred in the past or worrying about something bad that may occur in the future. This, too, was an enormous revelation to me. Simply put, I experience less pain because I'm able to recognize when the source of that pain is inside my own head.
not an original insight, but it was nevertheless profound. I was about 2,500 years behind the Buddha, who said that "your worst enemy cannot harm you as much as your own unguarded thoughts." Seneca improved on that in the first century AD, observing that "we suffer more often in imagination than in reality." And later, in the sixteenth century, Shakespeare's Hamlet noted, "There is nothing either good or bad, but thinking makes it so."
If you could--end of quote--if you could, talk about why this wasn't just, 'Oh, you know, I have these thoughts and they do things to me,' but how they changed your life. And saved your life.
Peter Attia: Well, I'll never be able to explain it fully in just a few minutes. But, I think to that very specific point, one of the therapeutic modalities that I have found really powerful is something called Dialectical Behavioral Therapy, DBT. DBT is a form of therapy developed by a woman named Marsha Lineham that really teaches you to understand the relationship between thoughts and emotions. But, to do that, you have to create space between the emotion and the impulse or the reaction.
So, if there's an event that triggers you--for example, if my child does something which triggers me--I must create a pause between that stimulus and the response for me to then process the emotion and the thought and ultimately the action.
And, the only way to do that is to understand the things that--I know you're a lifelong meditator, Russ, or not lifelong, but I know that it's an enormous part of your practice. The only way to do that is to basically have the tool that allows you to hit pause.
And, I think that tool--Dan Harris describes this as kind of the bicep curl for the mind--is what you're learning when you do that.
So, by the way, that's actually one of the things I really enjoy, doing when I ruck. So, if I'm carrying that heavy backpack and walking around the neighborhood, one of the things I really enjoy doing is focusing on a sensation. So, I never take a phone with me. So, even though I have lots of podcasts and audio books I'd like to listen to, that's one hour, you know, three or four times a week, when I have to be in total silence because it allows me to, for example, focus on the way the wind hits the edge of my hand as my arm swings. And, that's a sensation that is very difficult to notice normally. So, you have to really focus on it.
And, that's just one little example. Obviously, meditators will very frequently use the breath as the object of meditation, whether it be the movement of the abdomen or the air moving in and out of the nose.
So, again, I think of meditation, for me, not as a tool that in and of itself fixes the problems, but it's a skill that allows me to work on these other tools that, in the case of DBT, allows me to ask myself a series of questions. Why am I feeling this way? What is the purpose of this emotion? What is it trying to do for me? Is there a different emotion that's really underpinning the one that I think is going on right now?
Russ Roberts: And, that's obviously a good thing: to be thoughtful in responding to the events of the world around us. But it's much more profound.
Russ Roberts: And again--obviously we don't have time to go into it in the depth--but I want to give you a paradox that I think you have insight into that most people would find puzzling. In your book you describe--it's a powerful, tragic story. You get obsessed with your work. You struggle to spend time with your family. You're struggling in your marriage, you're struggling as a parent, as a father. And you're angry; and you recognize that. And, I have been angry, many different phases of my life. And, of course, when you're in that mode, it's a strange, addictive drug. You'd think you would say, 'Well, I don't like being angry. Who would want that?' I mean, there's nothing good about it. It could ruin your marriage. You could end up in jail because you get in a fight. Anger and rage seem so destructive, and yet they have an addictive quality.
And, what you suggest in your passage along--in this section--of the book is that you were having trouble forgiving yourself.
So, your anger at the outside world was not at the outside world, it was at yourself.
And, this is a paradox that I think is incredibly important, which is: people will tell you, 'You have to forgive yourself and love yourself before you can forgive and love others.' And, growing up as a so-called rational person, I always found that argument offensive. 'No, no, you don't understand. I'm judging myself because I need to get better. And, when I judge you, I'm just judging you the way I judge myself.'
And, this claim, 'Oh, you need to forgive yourself': Well, wait a minute. Doesn't that mean that I'm going to excuse all the things that I do imperfectly? 'No, I have high standards. I'm not going to do that. I'm going to live up to my expectations.'
And yet, I think that's false, and I think it's destructive. And, I'll just mention one thing: we have--we have the Jewish holiday of Yom Kippur coming up soon, which is about repentance and atonement. And, there's a strong flavor in Judaism that I have to berate myself. And yet, at the same time, there's a theology in Judaism--there's, there's a trend, a track of Jewish thought that says, 'Actually, no. If you beat yourself up all the time, you'll actually become a worse person.'
So, I want you to talk about--not the Jewish part--but about this seeming paradox that by forgiving yourself, you can then forgive others. By loving yourself, you can love others. That seems like cheating. And, as an economist, it seems: Oh, I'm going to ruin all the incentives I have to be a better person if I could always say, 'Oh, well, I'm going to forgive myself.' What have you learned about that?
Peter Attia: Oh, boy. I've learned a lot the hard way. I'll say that. Right? I've learned a lot the hard way. Which is for different reasons, we all kind of create different narratives. And, for whatever reason, at least in my case--and I should preface all of this by saying, Russ, I don't have a great answer to the questions broadly. There are 16 chapters in this book that have bits of me weaved into them, but they are primarily me speaking as a quasi-authority on a subject matter. But, this 17th and final chapter is not at all about that. It is purely an experiential chapter that is in the book, if for no other reason than to scratch or itch the scabs on the reader, to then go and do this type of exploration. Right?
It's a chapter that, to be clear, the publisher didn't even want in the book. Their view was it doesn't make sense. 'Go and write another book about this, but let's end it here on sleep and exercise,' or whatever.
So, what I came to realize, although it was not obvious at the time, because--I can't imagine you're not familiar with David Foster Wallace's beautiful commencement speech at Kenyon College, "This Is Water." He talks about the ubiquity of water around the fish. And, sometimes the most prevalent thoughts we have are the ones we're unaware of because they are so constant.
And similarly, I spent my entire life completely blind, oblivious to the self-talk. Even though, by the way, at times it was audible. Like, that's what's really remarkable, is: at times I could get so angry at myself, I would be screaming at myself as though there were another person there. And, yet somehow it just didn't register that that was happening.
And, what I learned through a very difficult stay in an inpatient residential therapy facility was that until I got that Bobby Knight--which is what I called him, he screamed at me like the famous basketball coach, Bobby Knight--until I got Bobby Knight out of the boardroom of my head, I was never going to be kind to myself, and therefore I could never be kind to another human being.
And, the therapist came up with a brilliant exercise that I think is--I still don't know how she came up with this and I'm even more amazed that it worked. Because, I did it because I had no choice, but I didn't think it could work. But, I'll share it with you. I know you've read the book so you know this, but just so listeners understand.
So, the exercise was: every time you're about to scream at yourself, either out loud or just in your head, take your phone out and record an alternative message as though you were speaking to your best friend who had just committed whatever the egregious act you just committed was. I'm being facetious, because it wasn't egregious, clearly. It was, like, I don't know: you overcooked a steak, or you missed a [inaudible 01:33:21]--
Russ Roberts: You burned the chicken--
Peter Attia: Yeah, yeah. Yeah, yeah. You weren't exceptional in archery practice today, or something like that. Right?
So, sure enough, three or four times a day--because that's the frequency with which I would want to berate myself--I would, I managed to do this. I managed to take out my phone and dictate a note. And, instead of saying it to me, I would pretend I was talking to you as a dear friend; and I would even say your name. Right? I would say, 'Hey, Russ, I know how frustrating it is right now that you just burnt that steak.' And, it's embarrassing. You have company over, and they're here for dinner, and you walked away from it because you got distracted, and now it's overcooked; and it's okay. You are distracted right now. You've got a lot on your mind. And, maybe when you heard your son calling you and you went over there to see what was wrong, you forgot to come back to the steak. And, I think people will understand, and it's not the end of the world.
And, that was it. And then, I would have to send that voice memo to my therapist. So, this poor woman is getting three or four of these messages a day.
But then, something happened, about four or five months later, which is: I stopped hearing Bobby Knight's voice. And to this day, Russ, I don't make any fewer mistakes than I did then. I'm no less likely to burn the steak, miss a shot in archery, spin my car on the racetrack, do any of the things that used to upset me; but I just don't hear Coach Knight at all.
And, that has had a bigger impact on my life than probably all the exercise, nutrition, sleep, or drugs, or cancer-screening that I could do.
Russ Roberts: Yeah. I have this fear that I'm hard on myself, so I'm justified of being hard on others. That's my fear. This is the flip side of that. And the argument is that if I can be nice to myself, maybe it'll be easier to be understanding of other people.
Everyone is in a battle. So: 'Be kind,' is fabulous, I think, advice. Except for me, of course: I win all the battles. I have to triumph. And, it is a fascinating aspect of human behavior that confronting my imperfection--and maybe it's a personality for certain kinds of people, but maybe it's every human being--confronting my imperfection, facing imposter syndrome, that this fear that I'll be discovered, that I'm a flawed human being. And, surely some of this anxiety and fear comes from the way we were raised--our childhood, or friends, or social circle when we were four and six and 10. But, somehow, my fear of imperfection somehow makes it harder for me to be aware that other people are in the battle.
And when I recognize it in myself, somehow it becomes easier to see it in others. And, I think: beautiful thing. It's great advice. And, I think it is the road to a much less stressful life, which probably is good for your health. And, it's a much better way to live, not just within your last few decades, but all the way along.
Peter Attia: Yeah. I think there's a lot there, Russ. I think first of all, I think of this the way I think of exercise, which is even if exercise didn't increase my life a day--even if it shortened my life by a year--it would still be worth it because of the quality of the life I get to live. And, truthfully, I feel the same way about this, which is it probably increases the length of your life simply on the basis of the impact that stress has on disease processes.
But, even if it didn't, it's really about the quality of life.
And, going back to what I said at the outset, I'm not delusional about the fact that my physical health is going to decline as I age, despite what I do. When I'm your age, Russ, I am not going to be able to do what I do today. I know that.
And a decade later, when I'm 78, if I'm still alive, it's going to be even less.
But there's no reason I need to be miserable throughout my life. There's no reason that I need to be angry constantly. And, what I'm excited about, frankly, this is--I'm just at the beginning of this journey. I'm only a few years into this fundamental change, into this rewiring.
And so, in many ways, I actually think I'm going to be--I hope I'm going to be--better off in a decade than I am today. And that's something to look forward to because in the other dimensions of my health, I likely won't be.
Russ Roberts: My guest today has been Peter Attia. His book is Outlive. Peter, thanks for being part of EconTalk.
Peter Attia: Thank you, Russ.