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Peter Attia MD#47–Matt Walker, Ph.D. on Sleep (Part 1 of 3): Dangers of poor sleep, dementia risk, mental health..
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EVERY SPOKEN WORD
95 min read · 18,769 words- 0:00 – 0:04
Intro
- PAPeter Attia
[intro music]
- 0:04 – 6:11
Why Peter Doesn't Run Ads, and Series Introduction
- PAPeter Attia
Hey everyone, welcome to The Peter Attia Drive. I'm your host, Peter Attia. The Drive is a result of my hunger for optimizing performance, health, longevity, critical thinking, along with a few other obsessions along the way. I've spent the last several years working with some of the most successful top-performing individuals in the world, and this podcast is my attempt to synthesize what I've learned along the way to help you live a higher quality, more fulfilling life. If you enjoy this podcast, you can find more information on today's episode and other topics at peterattiamd.com. [upbeat music] Hey everybody, welcome to this week's episode of The Drive. I'd like to take a couple of minutes to talk about why we don't run ads on this podcast and why instead we've chosen to rely entirely on listener support. If you're listening to this, you probably already know, but the two things I care most about professionally are how to live longer and how to live better. I have a complete fascination and obsession with this topic. I practice it professionally, and I've seen firsthand how access to information is basically all people need to make better decisions and improve the quality of their lives. Curating and sharing this knowledge is not easy, and even before starting the podcast, that became clear to me. The sheer volume of material published in this space is overwhelming. I'm fortunate to have a great team that helps me continue learning and sharing this information with you. To take one example, our show notes are in a league of their own. In fact, we now have a full-time person that is dedicated to producing those, and the feedback has mirrored this. So all of this raises a natural question. How will we continue to fund the work necessary to support this? As you probably know, the tried and true way to do this is to sell ads. But after a lot of contemplation, that model just doesn't feel right to me for a few reasons. Now, the first and most important of these is trust. I'm not sure how you can trust me if I'm telling you about something when you know I'm being paid by the company that makes it to tell you about it. Another reason selling ads doesn't feel right to me is because I, I, I just know myself. I have a really hard time advocating for something that I'm not absolutely nuts for. So if I don't feel that way about something, I don't know how I can talk about it enthusiastically. So instead of selling ads, I've chosen to do what a handful of others have proved can work over time, and that is to create a subscriber support model for my audience. This keeps my relationship with you both simple and honest. If you value what I'm doing, you can become a member and support us at whatever level works for you. In exchange, you'll get the benefits above and beyond what's available for free. It's that simple. It's my goal to ensure that no matter what level you choose to support us at, you will get back more than you give. So for example, members will receive full access to the exclusive show notes, including other things that we plan to build upon, such as the downloadable transcripts for each episode. These are useful beyond just the podcast, especially given the technical nature of many of our shows. Members also get exclusive access to listen to and participate in the regular Ask Me Anything episodes. That means asking questions directly into the AMA portal and also getting to hear these podcasts when they come out. Lastly, and this is something I'm really excited about, I want my supporters to get the best deals possible on the products that I love. And as I said, we're not taking ad dollars from anyone. But instead, what I'd like to do is work with companies who make the products that I already love and would already talk about for free and have them pass savings on to you. Again, the podcast will remain free to all. But my hope is that many of you will find enough value in, one, the podcast itself, and two, the additional content exclusive for members to support us at a level that makes sense for you. I want to thank you for taking a moment to listen to this. If you learn from and find value in the content I produce, please consider supporting us directly by signing up for a monthly subscription. Welcome to the kickoff of this Matthew Walker three-part series on sleep. This is one of the topics we are asked about the most, and I think this will be a fan favorite. This series of podcasts will be released over three weeks, with this one being the first. Now, at the end of the series, we're going to take questions for a follow-up AMA with Matthew. Asking questions on the AMA forum and listening to the AMA podcast with Matthew, along with all AMAs, will only be available to subscribers. So if you haven't signed up yet, you can do so now at peterattiamd.com/subscribe. My guest this week is Matthew Walker, professor of neuroscience and psychology at the University of California, Berkeley, and the founder and director of the Center for Human Sleep Science. Matthew earned his undergraduate degree and PhD in neurophysiology in London and subsequently became a professor of psychiatry at Harvard Medical School before moving to Berkeley. His research examines the impact of sleep on human brain function in healthy and diseased populations. To date, he has published over a hundred scientific studies. He has received numerous funding awards from the National Science Foundation, National Institutes of Health, and he's a fellow of the National Academy of Sciences. He's the author of the international bestseller Why We Sleep, which also happens to be the favorite book of my not yet two-year-old son. He holds many patents covering various consumer-based sleep recordings, sleep tracking, and sleep simulation. He's a sleep scientist at Google, where he helps the scientific exploration of sleep in health and disease. He is also an enormous fan of Formula One and my hero, Ayrton Senna. And in the third part of this installment, we actually spend quite a bit of time discussing this. Here in the first part of this series, we discuss the relationship between sleep, dementia, and Alzheimer's disease, the four pillars of sleep, sleep stages, measurements, and the overall importance of sleep, the lack of sleep and dangers of drowsy driving, and how the conversation of sleep has changed over the past several years. So without further delay, here is the first installment of my three-part series with Professor Matthew Walker. [upbeat music]
- 6:11 – 15:18
Walker's Path from Medical School to Sleep Science
- PAPeter Attia
Hey, Matt, thank you so much for making time to meet on a Sunday
- MWMatthew Walker
Absolute privilege and a delight to be with you, Peter
- PAPeter Attia
What's with the weather in Berkeley? Is it always this bad?
- MWMatthew Walker
[laughs] Now, when Peter says, "Is it always this bad?" it's probably in the low 60s and it's-- there isn't much blue sky.
- PAPeter Attia
[laughs]
- MWMatthew Walker
It's dry, and there's a very pleasant breeze, and there is some wonderful blossom. So [laughs] I know it's not San Diego, where everything is utopian and people are singing Kumbaya at the end of the day and holding hands. But it's a pretty good day when you consider it's still February
- PAPeter Attia
Right. Right. I know. It's like I live in these extremes. Like in, you know, in San Diego, the bar is like it has to be perfect, and then in New York, you just sort of expect it to be sort of, you know... Like I was there two days ago and it stunk. But, um-
- MWMatthew Walker
I mean, all three of those are better than the United Kingdom, my, you know, my home country, where essentially you have nine months of really bad weather and then three months of winter.
- PAPeter Attia
[laughs]
- MWMatthew Walker
And then that's your, you know, that's your year. So this day, February, like this low 60s, I'm a happy man
- PAPeter Attia
I came from Canada, where it's bad in a different way, but the first time I saw California was my interview for med school, and it was a February day, and it was 76 degrees, and that was the first time it occurred to me that you didn't have to suffer. You know? Like I just, I never realized-- I mean, I guess intellectually I understood that it could be warm in the winter, but it never occurred to me that you could choose to do that, so. Well, now speaking of this, so what brought you to the US?
- MWMatthew Walker
It was science. I did all of my education back in United Kingdom. I actually started off at medical school. So back in the UK at age 18, you can actually go to medical school. It's a five-year program. And after about two years, this wonderful professor came up and said, "Look, you're a nice guy, but you're always asking questions, and you're asking them, I think, genuinely. You're not asking them to be an ass. But I think you're actually a scientist, not a doctor." Because at the time, you know, he was thinking doctors are interested in answers, scientists are interested in questions. "I think you're a scientist, not a doctor." So we didn't have MD-PhD programs back at that time. So then, you know, I thought about it for the summer, came back, switched to neuroscience, so essentially brain science. Did that as an undergraduate, then went on to do my PhD at the Medical Research Council in London, and then came to Harvard for my first faculty position there, and I was there for seven years as faculty in psychiatry at Harvard. And the winters just got to me, and, you know, the environment at times as well, academic was perhaps more combative and competitive, and I think that's one way to breed productivity in a department, and I'm not shaking a finger at it. But by nature, I'm just a person who is much more collaborative and collegial rather than combative and competitive. So Berkeley fit my mentality better. Came out here, weather was great. California, it's an immensely easy place to arrive and a very difficult place to leave, and I think I probably won't. [laughs]
- PAPeter Attia
I know that feeling. I'm probably leaving California. I'm going through the mourning process of accepting the departure, 'cause you're right-
- MWMatthew Walker
You'll be back. You'll be back. [laughs]
- PAPeter Attia
It's, it's a hard place to leave. When did the switch sort of flip in terms of your passion for sleep?
- MWMatthew Walker
I think back at medical school, I was always interested in states of consciousness, I guess you would describe it as. I was fascinated by anesthesia. I was fascinated by even hypnosis. I remember I actually went out to, to meet this hypnotist to try and understand not, you know, the act and the show. I wasn't interested in that. I fundamentally wanted to understand what did he think happened within the brain to produce this altered state of consciousness. So I got really interested in how the brain can switch between sort of states, mental states, and then just fundamental awareness states. That then naturally led me to just become fascinated by sleep. I mean, there is no better demonstration of a gigantic shift in conscious state that happens to almost every single living creature on this planet every 24 hours. And back then, this was 20 years ago, we had this fundamental question: Why do we sleep? And what was staggering to me is that it took a third of our lives. Every species that we've studied to date does it, sleeps. It seems to have evolved with life itself on this planet. Even more, we've understood the functions of the other main biological drives, eating, drinking, and [chuckles] procreating-
- PAPeter Attia
Mating. [laughs]
- MWMatthew Walker
[laughs] for tens if not hundreds of years. But the fourth main biological drive, the drive to sleep, had continued to elude scientific judgment. How was that possible? And back then, 20 years ago, if someone were to ask you, you know, "Why do we sleep?" the crass answer was we sleep to cure sleepiness. And that's the fatuous equivalent of saying, "Well, we eat to cure hunger." Well, that tells you nothing about the fundamental nutritional benefits of macro nutrition. [laughs] But that's where we were at with sleep. So it was, for me, this perfect collision of a fascination in an innate biological problem and universal behavior conserved across evolution, together with the fact that we did it for a third of our lives, plus the fact that science had not been able to crack this, this nut. It was one of the last great remaining scientific mysteries. I thought, well, you know, if you want to pick something that's gonna sustain you for the rest of your life, and some of the most acerbic, brilliant minds in science had tried to crack this nut and failed, including Francis Crick, wonderful scientist who discovered the helical structure of DNA, it's unlikely I'm going to do it in my lifetime, but at least it will sustain me as a problem, and I could not let it go. And so That was where the intellectual bite happened. The data, the empirical scientific bite happened when I was doing my PhD. I was studying brainwave patterns in people with dementia, and I was trying to do differential diagnosis very early on in the course of cognitive decline, seeing which type of dementia did they have. Was it frontal lobe dementia? Was it Lewy body dementia? Was it Alzheimer's dementia? And I was failing miserably for two years. I was getting nothing. I used to go home, I was living in this doctor's residence, and I had this sort of, in the middle of my room, this little igloo of journals that used to sit in on a Sunday, just this kind of like sort of sanctified circle of, of knowledge. And I was reading one Sunday and I realized that the different pathologies in these different dementias, some would hit the sleep centers and others would leave those sleep centers completely untouched.
- PAPeter Attia
Even within forms of dementia that clinically presented very similarly?
- MWMatthew Walker
That's right. Yeah. You could see certain brainstem nuclei, certain centers within the basic base of the brain. Some of those were getting eroded by the dementia, and those are sleep-generating centers. Whilst in other of those pathologies, those centers were spared until very late in the disorder, so they probably weren't affecting my early patients. So I realized I was measuring their brainwave activity at the wrong time. I was measuring my patients whilst they were awake. What I should have been doing is measuring them whilst they were asleep. Got a small grant, set up a sleep lab, learned how to do it, got some great results, and then the question became, if their sleep is so disrupted, is it not just a symptom of de- dementia? Could sleep disruption actually be a biomarker of dementia? Could it actually foretell when you are going to develop dementia and which type? Or even more profound, is sleep disruption an underlying cause of Alzheimer's disease? And I think right now, based on the weight of the data that we have, and we and others have got large research programs doing this work, the evidence I think is causal. I think that sleep at this stage may be one of the most significant lifestyle factors at least that determines your risk ratio for Alzheimer's disease. I, I feel the causal evidence for that now in humans and animals is strong enough to make that statement, and I don't make that statement lightly.
- PAPeter Attia
Yeah, that is profound because when you think about the other really big ones, vascular disease and insulin resistance, they both feed into a very similar mechanism, which is neuronal energy deprivation.
- MWMatthew Walker
That's right.
- PAPeter Attia
So do you think that sleep disruption or poor sleep, and I wanna come back to the semantics around that because I don't actually think I'm well-equipped to talk about this intelligently, but do you think that that also disrupts some aspect of energy metabolism in the brain? Or where in the sort of chain of events do you think that that impacts?
- 15:18 – 23:05
Sleep as a Causal Factor in Alzheimer's Disease
- MWMatthew Walker
I think one of the places that it impacts is in oxidative stress. I think it's safe to say that wakefulness is low-level brain damage, and we need sleep to avert some of that low-level brain damage that wakeful-- Sleep is the price that we pay for wakefulness [chuckles] essentially. And you know, something I mentioned in a book that I put out was, and I got a lot of-
- PAPeter Attia
Just a little book. Just a, just a little, just a little New York Times bestseller, yeah. Which by the way, before we're done, I brought my copy because my youngest son, who's named after our mutual favorite race car driver, loves moons. It's all he thinks about. Moons, moons. Every-- His pajamas moons, everything. And he loves your book except for the fact that on the inside there are no pictures of moons.
- MWMatthew Walker
[chuckles]
- PAPeter Attia
So he'll sit there and he'll look at the cover and he'll go, "Moon, moon, moon." And then he flips through it and he gets so frustrated that there's no moon pictures inside.
- MWMatthew Walker
I will course correct that if there's a second edition-
- PAPeter Attia
[chuckles]
- MWMatthew Walker
... and, and I will just try to place the words underneath there-
- PAPeter Attia
[chuckles]
- MWMatthew Walker
... that it is for the benefit of Ayrton.
- PAPeter Attia
Yes. Yes, sir.
- MWMatthew Walker
Um, but in the book, you know, I proposed that we didn't evolve sleep, that perhaps we've got it the wrong way round. Perhaps the default state of life on the planet was sleep, and it was from sleep that wakefulness emerged.
- PAPeter Attia
Wow.
- MWMatthew Walker
Why could it not have been that way? Now, I don't have any good evidence to support my hypothesis. I think it could be utter nonsense, but I think it's a tenable hypothesis. It's just one that's difficult to test. But to come back to your question about Alzheimer's, which I think is critical, I think the first thing is that we see that with insufficient sleep you get increases in oxidative stress. Those oxidative stress processes lead to a whole cascade of kind of a finger flick domino effect of things that lead to neuronal death. One of the areas in the brain that is most sensitive to that is an area that we call the hippocampus, which is a critical memory center. It's probably one of the first structures to undergo damage in Alzheimer's disease. It's part of the reason why the sort of the phenotype of Alzheimer's is forgetfulness, problems with memory. I think perhaps the stronger evidence though, in terms of sleep and Alzheimer's disease risk, is a remarkable discovery that was made probably about five or six years ago now by some folks at Rochester University in rats. And what they discovered is that the brain actually has a sewage system inside of it. Now, your body has one that you're all familiar with called the lymphatic system. But it turns out the brain has one, and it's called the glymphatic system, named after the cells in the brain that form this system called the glial cells, also known by sort of from a Greek derivative meaning glue. So they used to be just thought as the, the sort of the cells that-
- PAPeter Attia
The sort of irrelevant stuff between the neurons.
- MWMatthew Walker
[chuckles] Exactly. You know? Yeah, it was like junk DNA. And of course, what we always learn is that Mother Nature is far too efficient to leave inefficiency on the table like glue or junk. And it turns out they form, uh, this sanitization system within the brain. And what happens they discovered is that when you go into deep sleep at night This sewage system kicks into high gear, and essentially those glial cells which surround the brain cells themselves, the neurons proper, they shrink in size by up to 200%. And then all of a sudden it leaves a vast amount of room for cerebrospinal fluid to start perfusing the brain and washing out the detri- the metabolic detritus of wakefulness. So it would be like New York City at night, all of the buildings shrunk down to 200%. You know, they became miniaturized, and then there was this big effluent flush that just happened across Manhattan to clear out all the debris, and it's essentially good night, sleep clean, that you get this power cleanse at night. Why is this related to Alzheimer's? Well, one of the critical ingredients that they found that the glymphatic system washed away was a sticky toxic protein called beta amyloid. Beta amyloid is probably one of the two core proteins that we know underlie your risk for the development of Alzheimer's. Ergo, if you're not getting your sleep at night, you're not getting that washing away of the toxic Alzheimer's protein. Every night then you are building up more amyloid within the brain. If you keep doing that night after night, it's like compounding interest on a loan. It's just escalating your Alzheimer's risk. That's why we can then explain the associational evidence, which I, I don't like associational evidence in epidemiological studies, and I don't think you're a huge fan of it perhaps either. Um-
- PAPeter Attia
Just don't tell anybody at the Harvard School of Public Health.
- MWMatthew Walker
Yeah, or maybe the NIH when I'm applying for grants for epidemiological studies [chuckles] . But what we certainly see is that if you bucket people into the amount of sleep on average that they've got across their lifespan, and at the end of their sort of life or in late life, in their 70s, in their 80s, we do a special type of PET scan to map the amount of amyloid in their brain, and then you just sort of look at those brain scans. Anyone on the street would not need any statistics, they would not need any training in brain science to see that one of these maps is different to the other. It's like Sesame Street. And what is remarkable is people who are getting, you know, seven hours of sleep or less compared to seven hours of sleep or more, there is marked differences in the amount of amyloid that's built up. Now, that's just associational evidence. But then when you take it down to the level of animal studies, where they selectively deprive animals of either deep non-REM sleep or they fragment their sleep, you get an immediate amyloid buildup centrally within the brain. You start to have what looks like a sort of, you know, an amyloid sort of genic process that's happening. That's rats, so then we can all wave our hands if we want because we would like to beat our chests and sort of, you know, say, "I don't need my sleep," and that's just rat stuff. Well, the studies have now been done in humans, where we will take a human being and for one single night we will take away their deep sleep. And the way that you do that is that you just play these auditory tones at night. So they never wake up, so the total amount of sleep that they get is still eight hours, but I can just selectively excise your deep sleep when that, that sewage system should be kicking into gear. And then the next day we do something that's r- really rather unpleasant. We do a spinal cord puncture, and we suck out some cerebrospinal fluid, and we can measure the amount of the two toxic proteins linked to Alzheimer's. One is called beta amyloid that we've discussed. The other is called tau protein. And we see the next day after one night of sleep disruption a significant increase in circulating levels of amyloid and tau. For me, that was kind of like the turning point where I finally felt comfortable going on record and saying, "At this point, folks, I really feel comfortable saying that your sleep is a critical component of your prevention of Alzheimer's disease." I really think the, the evidence is now, you know, in that direction and way in that direction. It's not just epidemiological. It's not just prospective longitudinal studies which are better than cross-sectional sort of epidemiological. It's not just causal in rats. It's experimentally causal in humans after one night of sleep.
- 23:05 – 35:26
Alzheimer's Heterogeneity, the Four Pillars of Sleep, and Life-Stage Windows
- PAPeter Attia
Do you, do you see variation there? Because one of the things that I find difficult with understanding all diseases and Alzheimer's would be sort of more so than even cardiovascular disease, because it, we still have so much less data, is there must clearly be enough variation between people that it's very easy at the heterogeneous level to, um, miss things that you would see in an otherwise homogeneous population. So for example, when you look at the coinage of the term Alzheimer's disease, it's quite likely that that was coined based on a patient who probably had a, a PSEN1 or 2 mutation, such an early onset of the disease-
- MWMatthew Walker
Yeah
- PAPeter Attia
... versus the disease we typically see. I mean, today, those patients make up less than 1%, and it's, it's almost a different disease from the o- you know, these are people-
- MWMatthew Walker
I agree. Yeah
- PAPeter Attia
... that are presenting in their 50s, and they're usually dead before they're 60, whereas the, 99% of the population are getting a sort of later onset disease. And even, of course, then within that population, all of the variation with ApoE genotype, it almost makes you wonder if there's different susceptibilities to this deprivation because everybody and their brother can point to the exceptions to these rules, right? The person who did everything right, slept like a baby every night, and ends up down this one path, and then of course the person who does everything incorrect and seems to be, you know, completely fine, or at least from the perspective of, you know, no obvious disease. So your analogy's really interesting because I don't really find myself hugely in the amyloid beta camp as the main causal driver. I think it's more of a result, but it's interesting what you posit is if it's more about the clearance of that than the generation of that- That would be a congruent view with this idea that, you know, there could be other things on the back end that are driving this primarily. But of course, I think with Alzheimer’s disease, it strikes me as just so complicated because of the genetic predisposition coupled with the multiple pathways that can seem to drive comparable insults to an otherwise incredibly sensitive organ.
- MWMatthew Walker
I hugely cleave to the idea that probably what we call Alzheimer’s right now is going to be subtyped at some point in the future that we’ll have-
- PAPeter Attia
Yeah, imagine it’s like cancer, right? Where in thirty years, hopefully the rate of growth has slowed, that it’s not, you know, a pandemic. But yeah.
- MWMatthew Walker
Yeah.
- PAPeter Attia
You might have five subtypes or something for that.
- MWMatthew Walker
That’s right. You know, and I think we will see that, I think, and then we will start to pattern match what features. I think the fact that sleep already, let’s just call Alzheimer’s disease this strange heterogeneous sort of mix right now that we feel uncomfortable about in terms of pinning one exact pathological ingredient as the causal trigger for that. In fact, I actually probably think tau is, if you look at the data-
- PAPeter Attia
I think the data are better for tau than amyloid
- MWMatthew Walker
... probably stronger in terms of predicting cognitive decline at least than amyloid is. But the fact that, you know, we’ve now found that insufficient sleep will also lead to tau aggregation, too, I think i- is concerning and worrying. But let’s accept that this Alzheimer’s thing, this disease state, is heterogeneous. The fact that sleep and we can find such a strong predictive sleep signal in terms of that risk, despite it being such a diffuse gray matter ball itself of a disease, must mean that the links between insufficient sleep and this heterogeneous thing are, I think, probably quite strong. Otherwise, the dirtiness of the equation would be such that those associations would be far weaker rather than stronger. The fact that they’re already present leads me to believe that when we do eventually subtype Alzheimer’s disease, we will then find that there are subsets of sleep features that are deterministic of those subsets of Alzheimer’s. So for example, deep sleep will be predictive of one form of Alzheimer’s. Sleep fragmentation, which is more about sleep quality than it is about physiological quantity, you know, sleep fragmentation will be predictive of something else, another sort of subtype of Alzheimer’s disease. Then I think, you know, basic-
- PAPeter Attia
Duration could matter
- MWMatthew Walker
I think there probably are four pillars of sleep. There is probably regularity. How consistent is your sleep schedule from, are you undergoing what we call social jet lag, which is where you’re bouncing around, you’re going to sleep at, you know, one AM, then ten PM, and all over the map. So there’s sort of regularity. There is the continuity of your sleep. Is it fragmented? Uh, are you waking up many more times or is it just nice one long shot? That’s a second feature. I think the third feature is quantity, how much sleep are you getting and how much of the different stages of you g- are you getting? And then independent of how regular your sleep is, how continuous your sleep is, and the amount, the quantity, the final is quality, and quality has become big in the last five years in the sleep field. In other words, what is the electrical signature of your sleep? And just because you’re getting eight hours of sleep doesn’t mean that you’re getting eight hours of good electrical quality deep sleep. And you know, I hope that we get the chance to speak about sort of things like caffeine and alcohol, other substances of abuse that can make you feel like you’re sleeping eight hours. But so quantity just fine, quality poor. So to come back to your question, I, I love the, the way that you think about that problem and, and I agree with it very much that Alzheimer’s disease is probably going to be heterogeneous. I think the pathology already points to that and its complexity. The way that sleep plugs into that heterogeneous disorder that we call Alzheimer’s is also going to be heterogeneous in nature. Different sleep features will be predictive of different aspects of the amyloid pathology cascade. And we’re, we just submitted a paper which I’m going to blow now in terms of media, um, sort of outlet, which hasn’t been accepted yet, but we just tried to ask the question across someone’s lifespan, if you bucket them into ten-year decades and you ask what was the quantity and quality of their sleep from their thirties and forties, forties and fifties, fifties and sixties, so on and so forth. And then at the end of their life, you stick them in a brain scanner and you map how much amyloid is in the brain and how much tau is in the brain, which is what we can do here at the sleep center, and then you essentially can, in a retrospective manner say, "Was sleep at certain times of life more critical in predicting how much amyloid you will have late in life?" So in other words, are there certain decades during an adult’s lifespan where sleep is even more important for determining your-
- PAPeter Attia
How can you do that retrospectively? So let’s say you had this cohort of patients. Maybe at best you could, through questionnaires, infer duration, but how would you be able to infer anything about depth or quality?
- MWMatthew Walker
So depth we can’t do, but quality we can do. So we’ve got a set of standardized questionnaires that have been essentially validated against gold standard, what we call polysomnography, which essentially is sleep laboratory grade recording with electrodes. And what we find is that those questionnaires have good predictive validity relative to objective gold standard measures. So it’s a hop, skip, and a jump, but you can say, look, these subjective questionnaires seem to go pretty well hand in hand with sleep quantity and quality. Let’s take those questionnaires and then let’s ask of those patients what they were doing in terms of their sleep quantity and quality in those different bucket decades of their life, and it has all of the problems that you can imagine.
- PAPeter Attia
Yeah, because this seems like a slightly better version of a food frequency questionnaire, which your peers would be relying on to do the same question about nutrition.
- MWMatthew Walker
Right, exactly.
- PAPeter Attia
You know?
- MWMatthew Walker
So it’s reliant on an individual. You know, it’s got problems with history because, you know, the further you go back, does that signal of accuracy degrade?
- PAPeter Attia
How big are the hazard ratios? Because I guess this is where one of those things where If sleep could account for 25% of this disease or, or if it, if it increased the risk by, say, 25% would be a better way to say that, it strikes me as unlikely that you could see that signal 'cause that's not a big enough signal with all the noise you've just described. But if you were talking about a hazard ratio of six or seven or, you know... It's so funny, today one of my kids asked me about smoking, like, "Why do people smoke?" And this, I couldn't resist going down the Bradford Hill pathway of-
- MWMatthew Walker
[laughs]
- PAPeter Attia
Unfortunately, he's four and a half, but he got a probably about a 12-minute lecture on epidemiology and the hazard ratio of, uh, small cell lung cancer and smoking. But the punchline in my story to him-
- MWMatthew Walker
Peter Attia, ladies and gentlemen. Peter Attia. [laughs]
- PAPeter Attia
[laughs] Yeah. I was trying to explain to him what it would mean to have a 14x increase in risk, which was basically what was observed in the first physician study of smoking. And, you know, the point there is that is such a massive signal that, I mean, y- as you describe it, I love whenever you can get these things that s- statistics that aren't necessary. When you don't need the P value to figure it out, that's it. So does your intuition, and if, again, I don't want you to scoop what's already in this paper, so if you can't speak about it, no problem, but do you have a sense of that magnitude and therefore if even a crude backwards-looking metric is directionally pointing you at something that you think, uh, wow, this isn't a subtle change?
- MWMatthew Walker
Yeah, I mean, we're up in the region of, you know, from .45 to .6, so it's, you know, it's-
- PAPeter Attia
In risk reduction for those doing it correctly.
- MWMatthew Walker
Correct.
- PAPeter Attia
Okay.
- MWMatthew Walker
Yeah. So it's substantial, but what was interesting to me which gave me more confidence was that the windows of sleep sensitivity were -- now, by the way, across the entire lifespan, the, if you're getting less sleep at almost any point in the lifespan, the risk that you're going to have higher amounts of these Alzheimer's disease proteins in your brain is greater. That's what we find across the board. But what's interesting is that when it comes to those two different proteins, al- um, amyloid and tau, there are different decades that are predictive. So if it's just one global subjective bias in your questionnaire, that you shouldn't see that result. So there is a sensitivity and specificity to these two different proteins that to me got me more excited that it transcended some of the limitations that are inherent in this approach. And also the fact that for amyloid you get a very strong predictive signal, you know, thirties to forties and then again sort of sixties to seventies. And for tau, it's actually somewhere in sort of the, starts in the fifties to sixties and then goes through until the eighties-
- 35:26 – 40:31
Necessary but Not Sufficient: Prevention and Walker's Own Eight Hours
- PAPeter Attia
See, this is kind of interesting too because, uh, one of the reasons I've been a little less excited about amyloid, there's two reasons. One is what can only be I think described as just the abject failure of the pharmacologic approach to amyloid reduction. At our last counting, oh, I don't want to mis- be misquoted on this. We'll include it in the show notes what the actual number is, but it's basically one amyloid antibody quasi success at disease stabilization to the tune of 2,000 failures. That's one thing. The second is the autopsy studies of people who died without any clinical evidence of Alzheimer's disease who still have amyloid making me wonder if amyloid is necessary but not sufficient.
- MWMatthew Walker
Yeah.
- PAPeter Attia
And therefore, what if there's something else going on? And of course, the third thing I would now add just based on thinking about it for two seconds, so this might not be well thought out, is in the next couple of hours we're gonna talk about a whole bunch of other things that sleep does that are in and of themselves completely devastating to your health that also would feed into that. For example-
- MWMatthew Walker
Exactly
- PAPeter Attia
... the impact that negative sleep has on cardiovascular disease, and it's become quite clear that if you're doing bad things to your heart, you're doing bad things to your brain. And of course, we're gonna talk about glucose disposal, hyperinsulinemia, and all of those things which also have a clear impact. So I think this would only strengthen the case that sleep deprivation is bad for you and bad for your brain. It to me makes it harder to tease out potentially the mechanistic links, although there's no reason, as you said, that it can't be multifaceted.
- MWMatthew Walker
Yeah. And I think there are certainly those conundrums where you see patients with non-trivial amounts of amyloid in the brain, let's say at postmortem, who are even only in the early stages of MCI, of what we call mild cognitive impairment. They haven't transitioned yet to Alzheimer's disease.
- PAPeter Attia
I'm glad you remembered to explain these things 'cause I'm nodding away like-
- MWMatthew Walker
[laughs]
- PAPeter Attia
Yeah, of course I know what MCI is. So yeah.
- MWMatthew Walker
But that aside, I think th- the idea that it's, it's necessary, maybe not sufficient, but necessary, if you truly don't want necessary in your life And if you're getting insufficient sleep, you're placing a necessary there where it doesn't necessarily have to be [laughs]
- PAPeter Attia
No, no, the analogy could be with lipoproteins. You know, there's a-
- MWMatthew Walker
Oh, that's a very... Yeah.
- PAPeter Attia
Right? I mean-
- MWMatthew Walker
Yeah
- PAPeter Attia
... lipoproteins are absolutely necessary but not sufficient for atherosclerosis, and so some people say, "Well, there's no efficacy in reducing lipoproteins," and I think part of it is it's diffuse, right? You're only tackling one of the four constitutive elements. Four things have to happen for you to get atherosclerosis, the lipoproteins being one. So that's actually an interesting idea, and it's a great argument for why would you want something that's necessary but not sufficient there? Why would you decrease your odds?
- MWMatthew Walker
Yeah. I mean, you know, think about it like this. If your goal -- the two most feared diseases in developed nations right now, I believe, are cancer and Alzheimer's disease.
- PAPeter Attia
And I would say it's in the other order.
- MWMatthew Walker
And yeah, and I think Alzheimer's is, is, you know, top of the list there. Do you want to de-risk the probability of Alzheimer's disease in your life? If you truly don't want to invite right to, you know, this thing called Alzheimer's disease and invite it in, in the mail coming at you, but you're getting, you know, less than seven hours of sleep a night, you're not working in the direction that you wish. You're going against Alzheimer's disease prevention, and you're working well towards Alzheimer's invitation.
- PAPeter Attia
Yeah.
- MWMatthew Walker
People will often say, "You know, how much sleep do you get?" And I'll, I'll, I'll say like, "I give myself a non-negotiable eight-hour sleep opportunity," and that's not because I'm trying to practice what I preach. I don't want to be some poster child for sleep. If you understood what I knew about sleep and all-cause mortality as well as most disease processes, you would realize that I'm being nothing short of utterly selfish in my preservation of an eight-hour sleep opportunity. I don't want to die young, and I don't want sickness and disease in my life. My family, for example, has got a very strong history of cardiovascular disease, and we know that deep sleep is probably the best form of blood pressure medication that you could ever wish for.
- PAPeter Attia
That would be an easier one to study. I'm guessing we'll come to that later.
- MWMatthew Walker
Yeah. The data there is-
- PAPeter Attia
The ability to perturb deep sleep and then see the change in blood pressure.
- MWMatthew Walker
The constraints.
- PAPeter Attia
Yeah.
- MWMatthew Walker
Yeah. I think the point is, is I think I've bashed people over the head with this, uh, sufficiently, but the link between a lack of sleep and Alzheimer's now, I think, is very strong. And what I find, though, positive about that is with Alzheimer's disease, just as you mentioned, when it comes to pharmacological approaches, we just don't have anything that looks robust right now. So medicine, in many ways, and especially for Alzheimer's disease, has started to shift from a model of late-stage treatment to early-stage prevention, and I think I feel comfort- very comfortable saying that one of the best preventative actions that you can take on the basis of the science right now is start to capitalize on your sleep at night.
- 40:31 – 52:42
Brainwaves and the Stages of Sleep
- PAPeter Attia
So let's shift gears just a little bit and go back to the polysome. Let's explain to people, 'cause we're gonna eventually have to talk about tracking these things, and I wanna bring up some of the sort of commercially available ways that people do that, which I think by definition are still not accurate enough for people to, you know, compare them to their polysome. But if I came into your lab tonight and I was willing to go to sleep there and you would hook me up to an EEG, what are the different patterns of brainwaves, and how would you morphologically describe them and then bucket them by these stages? You've already sort of touched on a little bit is deep, REM, deep REM, deep non-REM, et cetera.
- MWMatthew Walker
Yeah. So upon falling asleep, human beings, and in fact all mammals, will experience two different stages of sleep. One of them is called non-rapid eye movement sleep. The other is rapid eye movement sleep. Non-REM sleep has been further subdivided into four separate stages, which are unimaginatively called stages one through four.
- PAPeter Attia
Thank God.
- MWMatthew Walker
I mean, [laughs] I know, yeah. I think that's all that the sleep-deprived people who are, you know, experimenting could come up with at that time.
- PAPeter Attia
[laughs]
- MWMatthew Walker
Um, so increasing in their depth of steep, sleep, so stages three and four of non-REM sleep are the really deep restorative stages of sleep. Stages one and two are the lighter stages of sleep. And then on the other hand, we have rapid eye movement sleep or REM sleep, which is named not after the popular Michael Stipe pop band but because of these bizarre horizontal shuttling eye movements that occur during this stage of sleep, these rapid eye movements. So you have these two different types of sleep, and they will essentially, as you fall asleep here in, at the sleep center at Berkeley, they will go into essentially a battle for brain domination throughout the night, and that cerebral war between non-REM and REM is going to be won and lost every 90 minutes and then replayed every 90 minutes to create what we call a standard cycling architecture of sleep or what we call a hypnogram of sleep. And so what you will see is that upon falling asleep, you'll go into the light stages of non-REM, stages one and two.
- PAPeter Attia
Oh, before we do that, let's say before I fall asleep, when I'm just laying in the bed, how would you describe my brainwaves under the wakeful condition?
- MWMatthew Walker
So at that point, what we typically see is that when you close your eyes, the back of the brain goes into what's called an alpha rhythm. So when you're awake, your brain shows this remarkably frenetic high-frequency electrical activity. In other words, your brain is going, in terms of its brainwaves, it's going up and down many, many times a second. And it's-
- PAPeter Attia
And, and the amplitude is-
- MWMatthew Walker
And the amplitude is very small.
- PAPeter Attia
Small.
- MWMatthew Walker
Which kind of is paradoxically you think if I'm awake, then my brain is active, and so the size of those brainwaves should be big. It's not. It's actually very small, and here's the reason. Different parts of your brain are doing different things at different times, so those brainwaves sort of are all canceling each other out. So what... The, the analogy would be if I were to dangle a microphone above a sports stadium What I'm picking up is the signal from the, the crowd of 100,000 individual neurons that sit underneath it. That's how an EEG electrode is. Now, before the game starts, that's wakefulness, and at that point, the 100,000 people in the stadium, the 100,000 brain cells, they're all speaking to each other at different moments in time.
- PAPeter Attia
So there's a lot of cancellation.
- MWMatthew Walker
So there's a lot of cancellation. They're not all coordinated. But it's very fast and frenetic, so I just get this signal that is very desynchronized, and it's not synchronous, so they're not summing their power together. So the size of that brainwave is not very big, but it's going up and down-
- PAPeter Attia
But that's why the frequency is so high.
- MWMatthew Walker
The frequency is high, meaning that you're sort of going up and down maybe 50, 60 times per second. Now, as you start to fall asleep, or actually even before you start to fall asleep, as you're lying in bed awake, the back of the brain is the first part of the brain that really starts to settle down. It goes into what we call alpha rhythm when you close your eyes.
- PAPeter Attia
And I assume that's just because the occipital cortex is in the back and you've closed your eyes.
- MWMatthew Walker
Brilliant. So the back of the brain, visual brain, if you close your eyes, that part of the brain essentially stops processing the outside world, and it goes into its sort of default state when it's awake of slowed frequency. It drops down from maybe 50 times per second down to about, let's say, 10 cycles per second.
- PAPeter Attia
But still relatively low amplitude?
- MWMatthew Walker
But still relatively low amplitude. Then once you start to actually transition, when you make that bridge from the world of wakefulness to sleep, as you sort of cross through that window from one of those worlds to the next, something bizarre happens, and if anyone out there is lucky enough, um, to be listening to this and they have a bed partner, you can actually see this. Just look at their eyelids as they're falling asleep, and what you'll see is that their eyeballs start to roll in their sockets, and they're called slow rolling eye movements. Now, we don't know why the eyes roll in the sockets like that, but it's the first sign that you're making the transition from the world of wakefulness into sleep. We use it as almost an indicator of the transition into sleep. Now, by the way, if your partner wakes up, sometimes people wa- will wake up from that state, and they see you just looking over them in bed, staring at their eyelids. If you're in early in a relationship, it- it's usually the end of the relationship.
- PAPeter Attia
Yeah. Yeah, that's-
- MWMatthew Walker
Just a point of note. Please don't blame me. Usually wait till you're married and then start to do that one. [laughs] The divorce usually is harder to come by. So then you start to go down into the light stages of non-REM sleep stages one and two. Then after about 20 or so minutes, you'll go down deep into stages three and four of non-REM sleep.
- PAPeter Attia
And in, and in one and two, have we transitioned out of that alpha wave? I mean-
- MWMatthew Walker
Yes
- PAPeter Attia
... where do we start to see the-
- MWMatthew Walker
Already
- PAPeter Attia
... thetas and-
- MWMatthew Walker
Theta already happening in stage one. In stage two, you actually go into theta activity, which is now down from 50 cycles per second, maybe down to just sort of six or seven cycles per second.
- PAPeter Attia
And the amplitude's getting a bit bigger, isn't it?
- MWMatthew Walker
It is getting a bit bigger, yeah. And then every now and again during stage two, the way that I know that you're in this lighter stage of non-REM sleep, stage two, is that you'll get these synchronous bursts of electrical activity that we call sleep spindles.
- 52:42 – 58:23
Sleep Architecture Across the Night and Memory
- PAPeter Attia
And do people always progress monotonically through these, or do sometimes people go one, two, four, three REM, for example?
- MWMatthew Walker
No, you will-
- PAPeter Attia
You have to go through three to get to four?
- MWMatthew Walker
You have to go to three to get to four. You have to go from two to get to three to get to four, with the exception of probably, let's say, two examples. One is pathological. If you suffer from narcolepsy, one of the things that typically happens is that you go from being awake straight into REM sleep. So to sort of finish the 90-minute cycle, and this will make sense, you go sort of stage one to stage two, stage two, three, three, four. Then after about 70 minutes, you'll rise back up into stage two, and then finally you'll pop up into REM sleep, and then you'll have a short REM sleep period, and then you'll go back down again, down into non-REM sleep, up into REM, down into non-REM sleep, up into REM. And you do that, as I said, every 90 minutes. However, what changes is the ratio of non-REM to REM within that 90-minute period as you move across the night, such that in the first half of the night, the majority of your 90-minute sleep cycles are comprised of lots of deep non-REM sleep and very little REM sleep. But as you push through to the second half of the night, now the seesaw balance changes, and the majority of those sleep cycles are comprised much more of rapid eye movement sleep and almost no deep sleep. And that's why it's always dangerous when people say, you know, "I'm one of those who survives on, you know, six, six and a half hours of sleep at night. I wake up, you know, 5:00, 5:30 to get a jump start on the day." And you can ask, "Well, let's say you're getting six hours of sleep. How much sleep are you losing?" And they will say, "Well, according to your definition of eight hours of sleep, well, I'm 25% off because I'm getting-- I lose two hours at the end of an eight-hour night of sleep, so I'm sleeping 75-- I'm losing 25%." Yes and no, because yes, you're-
- PAPeter Attia
It's disproportionate.
- MWMatthew Walker
Exactly. So yes, you're losing 25% of total sleep, but you could be losing up to 70% of all of your REM sleep because it's the REM sleep rich phase that you are short-changing to get a jump start on the day. So you've got to be very careful when you try to think of your sleep dynamics. But to come back to your point, sorry, yes, you always have to go through that linear progression. Narcolepsy is a standout case there. You'll usually go from wakefulness sometimes immediately into REM sleep. Very frightening.
- PAPeter Attia
Yeah.
- MWMatthew Walker
Most people don't experience, you know, logical, rational waking consciousness and then go immediately into irrational hallucinogenic consciousness, which is what REM sleep is. It's very disturbing when you speak to these patients. The other is if you are horrifically REM sleep deprived or chronically sleep deprived, occasionally you can make the transition straight into REM sleep. We see this in people who are abusing alcohol heavily, who are alcoholics. Alcohol, and we'll come onto this, blocks your REM sleep. You can build up such a hunger for REM sleep that the brain says, "Well, tonight I'm gonna forego the non-REM sleep. I'm just gonna go and feast on REM sleep straight away." There's hysteresis in the system, maladaptively so. That's a bad sign when you get hysteresis like that, that type of pressure.
- PAPeter Attia
Does this explain, and maybe this is not even really correct, but, but you could see that someone who's constitutively sleeping six hours a night would suffer perhaps fewer of the memory consolidation issues because they're still getting much of their deeper sleep earlier in the evening, presumably where that hippocampal consolidation takes place, and the lack of REMs manifestations are just harder to see. Like, does that partially explain any of that, or is that, is that even accurate?
- MWMatthew Walker
It turns out that different types of memory rely on different stages of sleep at different times of night. So what we found is that you need sleep after learning to essentially hit the save button on new memories so that you don't forget. And for that, it's all about deep non-REM sleep. So as long as you were getting, let's say, the first, you know, half of the night, the first five hours, then it's likely that you may have been able to protect those memories. But here's the other problem, that stage two non-REM sleep, which actually happens most in the second half of the night, in the second half of the night you're having either REM sleep or stage two, and in fact if you look at those sleep spindles, they exponentially increase towards the end of the night, so you get most of your sleep spindle rich sleep in the last two hours of the night. The reason that's important is because you not only need sleep after learning to consolidate, to save those memories, you also need sleep before learning to get your brain ready in preparation to actually lay down new memories, and there it's stage two non-REM sleep and these spindles. So what we've discovered is that the more of those sleep spindles that you have, the greater refreshment of your memory encoding ability to-- so think about it like this-
- PAPeter Attia
Yeah, and, and this is a very beautiful experimental demonstration because you can surgically deprive people of each of those. And, you know, I've seen other talks you've given, of course, and in your book you, you touch on this where you could preferentially from an experimental standpoint prevent somebody from consolidating memory, and you could similarly prevent them from forming new memory.
- MWMatthew Walker
Even though we can keep the total amount of sleep consistent.
- PAPeter Attia
Yeah.
- MWMatthew Walker
So it's not a stressor, it's not that wakefulness, it's you can selectively excise, just like you said, individual stages of sleep.
- 58:23 – 1:08:44
REM Sleep, Mental Health, and the Foundation of Health
- PAPeter Attia
What's the biggest detriment that persons face clinically with the reduction of REM?
- MWMatthew Walker
I think right now, based on the weight of the evidence, it probably starts with mental health.
- PAPeter Attia
Anything from depression, anxiety through to disease.
- MWMatthew Walker
Mood, anxiety, depression, and then suicidality. I think one of the most striking things that we've been seeing in our hands and other people have demonstrated too, and this is probably the second other big area of work that we do here at the sleep center is sleep and mental health. You know, sleep is emotional first aid, bottom line, period. And what you find is that in young teenagers, one of the strongest predictors of firstly suicidal ideation, in other words, thoughts of taking their own life, strongest predictors of suicide attempts, and tragically a very strong predictor of suicide completion is insufficient sleep and sleep fragmentation. And what we've been finding is that it's REM sleep that seems to provide essentially a form of overnight therapy, and it's REM sleep that resets or recalibrates the emotional networks in the brain. And there's a series, there's a network of them that involves an area called the prefrontal cortex, and particularly the middle part of the prefrontal cortex, which acts like a top-down regulator of your emotions. So there's deep emotional brain centers, centers like the amygdala, which is a centerpiece region for the generation of strong, impulsive, aversive, negative, uh, reactions.
- PAPeter Attia
Anyone with a young boy knows what the amygdala does.
- MWMatthew Walker
Right. [laughs] Exactly. If they have a ten- temper tantrum in the middle of, you know, the supermarket, it's because firstly their prefrontal cortex, you know, has not developed yet.
- PAPeter Attia
It's just not developed yet.
- MWMatthew Walker
And what little of it that there is, if they haven't slept well, is obliterated.
- PAPeter Attia
That's actually a really great example of one of the most obvious observations. Like we, we ta- you know, I mean any, any parent listening to this knows how emphatically you protect the nap.
- MWMatthew Walker
Correct.
- PAPeter Attia
You know? And it's like-
- MWMatthew Walker
For mental, for emotional mental health.
- PAPeter Attia
For, for, for, yeah, just for behavioral health of the child, right?
- MWMatthew Walker
Correct.
- PAPeter Attia
And it's sort of like your day revolves around the nap. Like can you go to Disneyland today? I don't know. Depends. If we get the nap schedule and, you know, yes or no. And what you're basically providing is a technical explanation for something that is so empirically obvious, it's undeniable. A- and it's not the opposite, right? So bear with me for a moment. When it comes to the broader mental health stuff, you could easily construct an argument that says the arrow of causality is the other way.
- MWMatthew Walker
Yeah.
- PAPeter Attia
The person who is anxious, it's the anxiety that's keeping them awake.
- MWMatthew Walker
Mm-hmm.
- PAPeter Attia
Now, my guess is in reality these two feed off each other constantly. So-
- MWMatthew Walker
I think you're absolutely right. It's-
- PAPeter Attia
You might be predisposed to anxiety that fosters lack of sleep. The lack of sleep amplifies and boom, boom, boom, boom.
- MWMatthew Walker
It's a two-way street, but is the traffic flowing more dominantly in one direction than the other? And I think this is what your point you're gonna make.
- PAPeter Attia
But then the behavior of a four-year-old is a perfect example of you only need to screw that up one night. You give a four-year-old one bad night or miss one nap, y- I mean, it's very obvious how that translates into the behavior. So that would point in the direction of the sleep can really be the driver of the pathology, if you want to use pathology to describe that, which of course is a strong term to describe, you know, outbursts of four-year-olds. But, but just to make the point, right? That's, that, that to me is one of the most interesting, albeit somewhat glib examples.
- MWMatthew Walker
But I think it's so consistent, you know, and I use that frequently where you often see a parent with a child and the child is crying and they look at you and they say, "Well, they just didn't sleep well last night." As if there's this universal parental knowledge that bad sleep the night before equals bad mood and emotional reactivity the next day. And what's striking is that if you look at the data somewhere between infancy and even now childhood, not only do we abandon the notion that sleep is absolutely essential and non-negotiable, but we start to stigmatize it with this label of laziness, that you're slothful or that your child is slothful for getting sufficient sleep. And the reason that upsets me, and I, I, I am, I'm getting a little bit [chuckles] I'm getting a little bit animated, um, s- which is odd for a British man, but the-
- PAPeter Attia
[laughs]
- MWMatthew Walker
... you know, the, the reason I, I do is because firstly, you know, it took Mother Nature three point six million years to put this eight-hour thing called a night of sleep in place, and within the space of seventy years, if you look at the data, we've lopped off almost twenty to twenty-five percent of that. You know, imagine coming along and saying, "You know, in the next hundred years, I think what I'm going to do is for the entirety of human society, I'm going to reduce their oxygen saturation by about twenty to twenty-five percent." Do you think that's a good idea? And the answer is no. [chuckles]
- PAPeter Attia
No, it, it's such a great example. I'm, I'll pause for a moment just to tell a funny story that you, you and I have talked about off mic, which is up until about 2012, I was in the I'll sleep when I'm dead camp, and I, I know what led to that. It wasn't... It, it was a very deliberate decision at the end of medical school when a, a good friend of mine with all the best intentions, who was a year ahead of me, so he was now in, at the end of his internship as I was about to begin mine. He said-- And this is in the days when we didn't have the eighty-hour work week requirement in residency, so we averaged, I think, about a hundred and fourteen hours a week in the hospital. So he said to me, "Look, Peter, you're, you're signing up for, you know, whatever, five, seven years of this thing. If you spent every moment outside of the hospital sleeping, you would still be tired. The only difference is you wouldn't have any fun. So make sure you live every moment that you're not in the hospital to the fullest." And so for me, that basically meant if I wasn't in the hospital, I was swimming, I was going out with my friends, I was trying to meet girls, like an- I was doing anything and everything, such that during that period of my life, I, I just know 'cause I was pretty adamant about recording how much time... Like, I was very wed to this idea there's a hundred and sixty-eight hours in a week. If I'm spending, you know, a hundred and fourteen of them here, and I spend this many driving, and I spend this many getting groceries, and I spend this many swimming, and blah, blah, blah, blah, blah, I think I, I was about twenty-eight hours a week of sleep. So it wasn't four every night because you'd have none, and then six, and then three, and then eight. Like, you, you could binge sleep from time to time.
- MWMatthew Walker
Right.
- PAPeter Attia
But it was pretty much twenty-eight a week. I'll come back to some of the implications of that, but fast-forward a few years, I'm talking to a good friend of mine, Kirk Parsley, who's a physician who, like you, is adamant about, you know, the importance of sleep. And we're having dinner one night, and he says-- He's challenging me on this, and he says, "So let me get this straight. You've just decided that you're gonna sleep half of what is evolutionarily programmed." And I said, "Yeah." He goes, "Does it strike you as odd that evolution would have designed us to spend a third of our life not mating, not watching out for predators, not hunting for food, but doing this thing for some other purpose? Do you think that thing must have been important?" And it was, it was such an obvious argument, but it really overnight changed the way I thought about this, which was evolution went to great lengths to do this and superficially at great cost to us, right? I mean, you could argue, well, imagine you didn't need to sleep, and you could spend twenty-four hours a day foraging for food or a mate or some other thing, but it didn't. So it's sort of, it's sort of like there's probably a reason we are not anaerobic [chuckles] to your point about reducing oxygen saturation by twenty-five percent.
- MWMatthew Walker
You know, if you were to think about that, you know, during sleep, just as you said, you're not eating, you're not finding food, you're not finding a mate, you're not reproducing, you're not caring for your young, you're vulnerable to predation on any one of those grounds, but especially all of them put together as a collective-
- 1:08:44 – 1:11:12
Sleep Deprivation Studies, REM Evolution, and Fatal Familial Insomnia
- MWMatthew Walker
And those studies have been done in rats.
- PAPeter Attia
Yeah, and actually we know some of this from humans who have been trying to... I, in fact, didn't the Guinness Book of World Records, I can't remember if I read this in your work, they've actually banned-
- MWMatthew Walker
Yep
- PAPeter Attia
... attempts at longest period of sleep deprivation.
- MWMatthew Walker
So I mentioned this, yeah, in the book that-
- PAPeter Attia
Yeah, you might, it even might be in the book, yeah
- MWMatthew Walker
... there was a time when you could still try and beat the world record of sleep deprivation, and it got up to about sort of, I think the last true effort was about 24 days, uh-
- PAPeter Attia
Oh my god
- MWMatthew Walker
... but I, I think it was debatable, that one. But based on the weight of the scientific data, the relationship with, between sleep loss and mental health, sleep loss and cancer, sleep loss, cardiovascular disease, sleep loss and metabolic syndrome, Guinness started to feel very, very uncomfortable. And then when suicide came on the table, it pulled it. So in other words, think about this. You know, there was a gentleman, Felix Baumgartner, I think his name was, who, sponsored by Red Bull, went up in a capsule-
- PAPeter Attia
Mm-hmm
- MWMatthew Walker
... in a hot air balloon to the outer surface of our planet.
- PAPeter Attia
This was about four years ago.
- MWMatthew Walker
Four years ago.
- PAPeter Attia
This was remarkable.
- MWMatthew Walker
He opened the door, and then he jumped out, and he fell back down to Earth at over 1,000 kilometers an hour. Using his body alone, he broke [chuckles] the sound barrier, and he successfully came down. And now Guinness says for that, just fine. [laughs] However, to sleep deprive yourself, no. Much more unsafe.
- PAPeter Attia
Right.
- MWMatthew Walker
We're not going to let it happen.
- PAPeter Attia
You are allowed up to-
- MWMatthew Walker
Just to put it in context, you know?
- PAPeter Attia
Yeah. You're, you're allowed up to 12 jumps off Niagara Falls.
- MWMatthew Walker
[laughs] Basically.
- PAPeter Attia
But that's okay. But no, no, you're not gonna... That's such a great point. I want to go back to one other thing to close the loop on this, and again, I, the listener may say, "Boy, this is... there's a lot of stuff going on here." But, but there really is. Like, this is... I think you have to have a lot-- And I'm trying to think about all the questions I can ask that others would have. If you took two individuals who are sleeping six hours a night, if you have one person who, just for the argument's sake, is doing it from 9:00 PM to 3:00 AM, and another person's doing it from midnight to 6:00 AM, would you expect... Or even if it were the, let's make it even more clear. It's the same individual, but you do it over a period of weeks. You transition them from 9:00 to 3:00 versus midnight to 6:00. Would their sleep wave cycles look the same? Would they still be truncating the same amount of REM at the tail end of that? Or would they start to do some
- 1:11:12 – 1:26:12
Timing of Sleep, Jet Lag, and Wearable Data
- PAPeter Attia
forward truncation?
- MWMatthew Walker
Forward truncation. So essentially what happens is that your brain has a different hunger or different appetite for different types of sleep. So think of those different stages of sleep like a finger buffet. And at different times of the night, that buffet is going to be sort of, you know, consumed more heavily in terms of, you know, the deep non-REM sleep phase, which would probably be the hours from 9:00 PM through until about sort of 3:00 AM.
- PAPeter Attia
Mm-hmm.
- MWMatthew Walker
That's the really, the, the window of preferential appetite for your brain when it comes to deep non-REM sleep. That's when it will preferentially eat at that type of sleep. But then from about 3:00 AM through until about midday, then the brain shifts in terms of its pattern if you let people just sleep it out. You know, if, if you look at sort of extreme owls who, and we should speak about chronotypes at some point, but people who, you know, like to go to bed very late and wake up very late, essentially there, then the buffet is gonna get hit hard in terms of REM sleep devouring. So I make that point that your brain has different taste sensitivities to non-REM and REM across the 24-hour clock face because it means that if you're short-changing your sleep by two hours, but you're doing it by going to bed very early and waking up very early, then what's going to happen is that you're probably going to be losing most of your REM sleep, 'cause most of your REM sleep happens in the late morning hours, and you're already awake by 3:00 or 4:00 AM in the morning, and so you're not getting the chance to get into those REM sleep rich phases.
- PAPeter Attia
And which of those patients would develop more appetite for sleep the subsequent evening? The person who was deprived... And you know why I'm asking, by the way? It's exactly what we were talking about earlier. It's this jet lag question.
- MWMatthew Walker
Right.
- PAPeter Attia
If you know you've got that flight, and you need to force yourself to sleep at a time zone that's not right, I'm just now thinking about, well, I always do the 9:00 to 3:00.
- MWMatthew Walker
Right.
- PAPeter Attia
Would I be better off doing the... In other words, I'm depriving myself of REM. Would I be better off des- depriving, just, uh, um, restricting my-
- MWMatthew Walker
Well, you're, you're depriving yourself of REM, but you're also still depriving yourself of total sleep as well, you know, when it comes to-
- PAPeter Attia
Yeah, yeah
- MWMatthew Walker
... the jet lag model. And, you know, there are, there's some... I think that that's an interesting model, and I, I think it does work that you can try to, in the week before you start to fly, let's say you're f- going, I'm going home to London, which essentially is eight hours ahead, so I need to now essentially start to sort of, by the time I'm waking up, people in London have already been awake for essentially eight hours. So I need to start to get myself on the schedule. So I start to wake up, you know, 10 minutes earlier for about five days before. And, you know, so I'm only about an hour shifted, but it helps. And then the morning of the flight, I'll wake up-
- PAPeter Attia
Really early
- MWMatthew Walker
... especially early.
- PAPeter Attia
Yeah.
- MWMatthew Walker
And then I won't the, make the mistake that everyone makes on those transatlantic flights, which is they sleep in the second half of the flight. You shouldn't do that. You should sleep in the first half of the flight, which is when most people in the UK are asleep. And by the middle of that flight, most people in the UK, that's their time to wake up. And so you should be waking up that time so that you build up enough of this sleepiness pressure By the time that you want to get to bed once you've landed that evening in London, and this won't make too much sense right now, and I think we'll, we'll speak probably a lot more about this when we speak about caffeine and adenosine-
- PAPeter Attia
Adenosine, yeah
- MWMatthew Walker
... and sleep pressure. But that-- But to come to your point, you're building up what's called sleep pressure. The longer that you're awake, the more of that s- healthy sleepiness that builds up. But to come back to the real question at hand, yes, just because you sleep, you know, five hours from one point in the clock face, maybe earlier in the night to sort of early in the morning versus five hours late in the morning until later in that, that day, the type of sleep that you get will not be the same. You will be selectively short-changing yourself of sleep, either of deep sleep or of REM sleep on either side of that equation.
- PAPeter Attia
This points out another interesting observation, which I do want to spend some time talking about wearables, because of course, you know, we're both wearing our wearables at the moment.
- MWMatthew Walker
[laughs]
- PAPeter Attia
And I think we both acknowledge that, look, I mean, these things are still not quite at the level of the polysom, and maybe they never will be. I mean, that's a very difficult thing to replicate from, you know, something on your wrist or your finger. But it's so funny, this might explain an observation I always experience when I come from New York back to California, which is I generally try to stay on California time, even when I'm in New York, going to bed later, waking up later, and in California, I'm a very early sleeper and an early riser. So even if I'm trying to keep it at eight hours and eight hours, and I can do that very well in California, not as well in New York, my first night back, even my first two nights back in California, I have much higher deep sleep, and that would explain it. It's this phase shift that I'm capturing this -- I mean, last night was-- 'cause I came back from New York last night, you know, went to bed at, I don't know, eight thirty PM and got up at five or yeah, probably four thirty or five in the morning.
- MWMatthew Walker
So you have dragged your-
- PAPeter Attia
But had a huge deep sleep.
- MWMatthew Walker
Exactly. So you've dragged your eight-hour window, if you think about the sort of eight-hour window, and you slide it back on the clock face from midnight to eleven PM, to ten PM, to in fact nine PM, you're dragging that eight-hour sleep phase back closer into the deeper-
- PAPeter Attia
Yeah
- MWMatthew Walker
... sleep-rich phase, the deep non-REM sleep that you want. So what your sort of Oura Ring will be telling you is you got more deep sleep, and perhaps you may actually see a little bit of a reduction in-
- PAPeter Attia
In REM
- MWMatthew Walker
... REM sleep.
- PAPeter Attia
Yep.
- MWMatthew Walker
As you go to New York, you may see the opposite. As you sleep later in the morning, you'll get more of that-
- 1:26:12 – 1:35:34
Making the Case Beyond Alzheimer's: Sleep Machismo and Drowsy Driving
- PAPeter Attia
Now, before we go there, Matt, look, for me, I don't need any more of a case in the importance of sleep, and I, I think honestly the Alzheimer's thing alone should be sufficient for anyone to take this seriously because certainly my patients, that's the single most important thing to them. Now, there are some of them that are more high risk, you know, people that have, uh, you know, ApoE4 genotype that's in the, you know, the direction that would increase risk or family history. But I don't think I've met a patient yet who doesn't say on some level preserving cognition is their single highest priority in life. That said, can you spend even just a minute, couple of minutes, [chuckles] it's The Drive after all, we have all the time in the world, making the case, the similar case in the presence of cardiovascular disease and cancer?
- MWMatthew Walker
Yeah. And I want to touch on that point before we go on about this Alzheimer's disease risk. You know, a lot of people out there may be having this sort of like sleep machismo moment where they have this braggadocio attitude of getting insufficient sleep, and they say, "Look, I'm in my 50s and, you know, I'm fit as a fiddle, and my cognition is razor sharp, and I sleep five or six hours a night." So we've got, you know, heads of state, for example, who are saying this, people who, you know, have a huge impact on the public, and they're saying these things. And it makes me sad because you can look at two other heads of state who were very vociferous about their proclamation of the uselessness of sleep, Margaret Thatcher and Ronald Reagan. Both of them were chest beaters when it came to insufficient sleep. They were very proud of saying that they only got four or five hours of sleep, that they were immune to the effects of insufficient sleep, that sleep was for the weak, and that you can sleep when you're dead, which, PS, is mortally unwise advice based on the evidence. The shorter your sleep, the shorter your life. That's what all of the studies tell us. I don't think it's coincidental now looking back that both of them went on to develop Alzheimer's disease. And it, you know, makes me so sad because I saw pictures of Margaret Thatcher in an enfeebled state of dementia, and I'm just thinking, you know, if only when she was, you know, in her 50s and had that bravado about sleep, if she could see herself in that bed in that later state of life in such a crippled mental cognitive functioning state, would you be so brave about it? And I would hope that she wouldn't, that humility would come into place. So that's the first thing about, I think, the insufficient sleep argument and people rightly being frightened, having the daylights frightened out of them about preserved cognition. You should have that regarding your sleep. The other one, though, that frightens me, too, is the other way that a lack of sleep can get you is not chronically across the lifespan with Alzheimer's disease, but acutely with car crashes, and I know that we'll come onto this at, at some point, too. But the only thing I would say is that I get many emails from people who've read the book. And two months ago, I got an email from a gentleman, I won't name him, and he was in his late 30s, and he described how three months before that, he had lost his wife and his 18-month, 18-month-old child in a car crash. And it later became apparent that the person who hit them had basically been surviving on about five and a half hours of sleep for the two months prior, that they'd had what's called a microsleep. They actually lost control of their car at 60 miles an hour at a moderate drift angle. You are essentially in the next lane within less than a second, and you're in the ditch after a second, and they went straight head-on. And now he was going to have to raise his four-year-old son by himself without the wife that he loved, without the 18-month daughter that they'd invested in because someone perhaps had heard from someone vocally in the public that surviving on five hours of sleep was something that was okay to do. And to me, that just breaks my heart. I, I just don't feel comfortable in, you know, having the responsibility like the head of a state of a country and then speaking about this thing, this kind of magic attitude of insufficient sleep because that's what it can lead to. It can lead to the travesty of the explosion of a nuclear family.
- PAPeter Attia
And my guess is, even though it's gonna be very difficult to actually quantify this, I believe that the story you just shared is an especially tragic, poignant example of something that probably occurs much more than we are able to quantify. I sometimes say to patients, you know, the four horsemen of death would be these big chronic diseases that kill us, but, but we can never forget accidental death. And then when you look at accidental death, how do you quantify it? Well, it turns out that three forms of accidental death form 80% of them, and the biggest among them is motor vehicle.
- MWMatthew Walker
Car crashes, yeah.
- PAPeter Attia
Right. And so the question is, what can you do to reduce that risk? So if you look at it, some form of distraction, and I've included sleep deprivation in that, but now I almost feel like they need to be separated out. Distraction meaning you're putzing with your phone-
- MWMatthew Walker
Yeah
- PAPeter Attia
... you're checking Waze, you're, you doing something you shouldn't be doing with your phone, sleep deprivation, ethanol, failure to wear a seatbelt, and reckless driving. I mean, that basically accounts for it. It wouldn't surprise me if that's, that sleep deprivation bucket is bigger than we think.
- MWMatthew Walker
I mean, we've got some decent data on this, and firstly, what we know is in the hour that we've been talking already, numerous people have lost their life in a drowsy driving-related accident based on the statistics. We know that already. And the way that we can tell that is both from speaking to the people who were involved in the accident, but you can also pick this apart from the dynamics of the accident as well, and here's the problem. When you are underslept, we're not talking about a night of total sleep deprivation. That's where you fall asleep at the wheel, and that's the obvious one. The much less obvious one, but the much more common one is what we call microsleeps. So when you are trying to survive on seven hours of sleep or s- six hours of sleep, and it really just takes that little of a dose -- By the way, I haven't forgotten our cardiovascular question. I will come back to it, but What you essentially have are these small lapses, we call them microsleeps, where the eyelid will partially close. And you can pick this up on a camera, and they've done these studies systematically where you dose people from getting nine hours of sleep to eight hours of sleep, seven, six, five, four, three, for one week, two weeks, three weeks. These studies have been essentially looked at, sliced and diced parametrically. They're probably the best studies done within the field of sleep. And so we know them very well, what your lapse rate is, what your microsleep rate is. And what you find is that the eyelid partially closes, and at that point, you no longer react. And the reason I'm bringing this point up is that drowsy driving accounts for more accidents on our roads than either drugs or alcohol combined. Combined. Now, I'm not condoning drink driving or driving inebriated under any circumstance. What I am saying, however, is that firstly, drowsy driving is a huge part of this problem on our roads. And the reason that it's not just problematic is because it's usually much more deathly. When you are drunk, you typically react, but you react too late. So you do something, but it's not enough, and you crash. When you have a microsleep-
- PAPeter Attia
Yeah, it's a projectile
- MWMatthew Walker
... you do nothing. That's why drowsy driving is more fatal than drunk driving typically, is because there is no reaction.
- PAPeter Attia
There's no application of brake.
- MWMatthew Walker
There is no application of brake, there's no course correction of steering wheel angle. There is nothing. There is simply a car with no one in control, and it's a two-ton missile on the freeway at 65 miles an hour with no one in charge. This is why I feel really uncomfortable about the idea of public proclamations of, of insufficient sleep. And I get that, and, you know, there are people, sports stars, p- all sorts of people who I respect hugely and, and I have a, a, an immense amount of sympathy for where they're coming from because I think there's a lot of public pressure to be this outspoken, "I'm gonna be crushing it on the sports field, and then I'm going to be, you know, back in the gym the next morning," and sleep is for, you know, X, Y, and Z. Who cares? But then you get someone in a car and you hear a story like that, and I can't help but just have my heart broken.
- 1:35:34 – 1:43:15
Why the Sleep Conversation Has Changed and Closing
- PAPeter Attia
But I think, you know, Matt, your work has come along at a really interesting point. I mean, I, I have to be honest with you. I remember when your book came out, and my initial thought was, does the world need another sleep book? 'Cause there's 2,000 of them out there.
- MWMatthew Walker
[chuckles]
- PAPeter Attia
And I think there's two things that are different. The first is your book is exceptional. Uh, actually I'd say three things. Your book is exceptional. The third is your understanding of the topic and your credibility is exceptional, and those aren't necessarily synonymous. You can have really credible, thoughtful people who write a book, but the book itself isn't exceptional or it doesn't hit the tone. And sim- and conversely, you can have someone who puts together a good book, but they themselves don't have the credibility. I think the... So, so you can take credit for the first two. I think the third is, is the little bit of luck, which is I think we are at a point in time where people are ready to hear this. In other words, if you, the exact same professor, wrote the exact same book 20 years ago, I'm not convinced it would have the same impact it is having today. Now, I don't know-- You probably have a better sense than me. I don't know exactly what accounts for that difference today. Is it that today we are more interested in... You know, the thin end of the wedge for this might have been our interest in performance.
- MWMatthew Walker
Mm-hmm.
- PAPeter Attia
Maybe that is the thing that first got people to think about this, which is, well, wait a minute, you know, if I wanna be better at X, Y, and Z, whether it be my sport, my craft, my whatever, is sleep a tool I need to be optimizing the way people have for many years realized, hey, what you eat and how you exercise absolutely impacts your performance. So I'm not, I'm not sure what it is, but I, I have a feeling, and I actually had this discussion with my daughter a couple of weeks ago, that we will look back at the way we think about nighttime electronics, sleep deprivation, and things like that. We will look back at that in 20 years, hopefully sooner, the way you and I would look back at, you know, a smoking mother being told by her doctor, "Smoke this brand versus that brand." Like, we, we, we can't even fathom that that was a discussion that took place as recently as about 1966 in the United States, and yet we're kind of in the, our infancy in the dark from a clinical perspective, from sort of a public health perspective-
- MWMatthew Walker
We are
- PAPeter Attia
... in functioning on this.
- MWMatthew Walker
So firstly, I mean, so much great stuff to unpack there. Um, I think you're absolutely right. I think the success of the book is largely despite my [chuckles] m- my ability to, to write and convey ideas. I think what happened is that it was a perfect storm where there has been this-
- PAPeter Attia
I gave you, I gave you two-thirds of the credit completely.
- MWMatthew Walker
Thank, thank you. And I ca-
- PAPeter Attia
[laughs]
- MWMatthew Walker
And, and I, I don't know if I can take them. I, I feel so a-ashamed, but I think the, the middle point is the erosion of sleep time has hit an all time high. We are now sleeping less than we have ever done in what seems to be the history of our species. Now, we can't say that for sure, but what we certainly can say is that back in the earliest record that we have of a systematic questionnaire, which was in 1942 by Gallup, what they found was that the average American adult was sleeping 7.9 hours a night. Now that number is down to six hours and 31 minutes. That's the average. 6,031. That must mean that-
- PAPeter Attia
How linear has that decline been, Matt? Has that been something that-
- MWMatthew Walker
Non-linear.
- PAPeter Attia
Yeah, it's accelerating, isn't it?
- MWMatthew Walker
It's accelerating, yeah. So I think you've, you've had this ballistic erosion of sleep time, this decimation of sleep throughout industrialized nations, and it's not just America, by the way. Japan is even worse. It's down to 6,021 minutes. You know, my home country, the United Kingdom, not much better, 6,049 minutes. And these are averages [laughs] . You know, you've got to imagine that, you know, a, at least a third of the people are probably s- trying to survive on five hours of sleep. Certainly during the week they are. It's that plus this incredible explosion of sleep science over the past 30 years, and this perfect storm has led to a collision where society is sleeping less, disease and sickness has been escalating in a manner that, you know, we've almost never seen before, and the knowledge of what sleep is doing, we know far more now. Sleep is not just curing sleepiness. Sleep is actually supporting... There is no physiological system in the body, and there is no operation of the brain that isn't wonderfully enhanced by sleep when you get it, or demonstrably impaired when you don't get enough. That knowledge and the causal knowledge of sleep in that, it's not just associational, it is, many of them are causal links with those disease states, I think led to this ability to write this book at this time that felt as though it was somewhat unequivocal, that it was very difficult to argue with. You know, you can pick apart one study from another, but when you build that blueprint manifesto, when you build the scientific, cold, hard, rational, emotion-free case for sleep, it's very difficult to argue with, and it just happened that we were at that time in our human history with sleep, and we were at that time in our scientific journey regarding our understanding of sleep. I think that's why the book felt like it was, it needed to be written and needed to be written now.
- PAPeter Attia
For what it's worth, you had many moons on the front and back covers, so my little Iarthan was delighted.
- MWMatthew Walker
Yeah [laughs] .
- PAPeter Attia
He loved that book.
- MWMatthew Walker
Yeah [laughs] . He's probably read from, literally from cover to back cover.
- PAPeter Attia
Back cover.
- MWMatthew Walker
But nothing-
- PAPeter Attia
Nothing in between.
- MWMatthew Walker
Yeah, exactly. That's just fine. I ask people they, please, you don't have to read the book. You just have to buy it. That's, that's all I ask [laughs] .
- PAPeter Attia
[laughs] Okay, there's, like, literally 100 more things I want to ask you about. So can you make the case for why cardiovascular disease is worsened by or accelerated by sleep deprivation? And then same question I'm going to ask you in a moment for cancer. You can find all of this information and more at peterattiamd.com/podcast. There you'll find the show notes, readings, and links related to this episode. You can also find my blog at peterattiamd.com. Maybe the simplest thing to do is to sign up for my subjectively non-lame once-a-week email where I'll update you on what I've been up to, the most interesting papers I've read, and all things related to longevity, science, performance, sleep, et cetera. On social, you can find me on Twitter, Instagram, and Facebook, all with the ID peterattiamd. But usually Twitter is the best way to reach me to share your questions and comments. Now for the obligatory disclaimer, this podcast is for general informational purposes only and does not constitute the practice of medicine, nursing, or other professional healthcare services, including the giving of medical advice. And note, no doctor-patient relationship is formed. The use of this information and the materials linked to the podcast is at the user's own risk. The content of this podcast is not intended to be a substitute for professional medical advice, diagnoses, or treatment. Users should not disregard or delay in obtaining medical advice for any medical condition they have and should seek the assistance of their healthcare professionals for any such conditions. Lastly, and perhaps most importantly, I take conflicts of interest very seriously. For all of my disclosures, the companies I invest in and/or advise, please visit peterattiamd.com/about.
Episode duration: 1:43:19
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