The Peter Attia Drive - #47 – Matthew Walker, Ph.D., on sleep – Part I of III: Dangers of poor sleep, Alzheimer's risk, mental health, memory consolidation, and more.

Episode Date: April 1, 2019

In part 1 of this 3 part series, Matthew Walker, professor of neuroscience at UC Berkeley and expert on sleep, describes the different stages and cycles of sleep, including what he calls the 4 pillars of sleep, and how they contribute to memory consolidation and numerous important pathways to mental health. We also get into the dangers of chronic sleep deprivation, such as the development of dementia, and the more acute dangers of sleep deprivation like fatal car crashes which are most often caused by drowsy driving. We also discuss the different and important roles of REM vs. non-REM sleep, and the impact that bad sleep habits can have specifically on those sleep stages.    We discuss: Matthew’s background and interest in sleep [6:03]; Sleep and Alzheimer’s disease, and the 4 pillars of sleep [12:18]; Stages of sleep, sleep cycles, and brain waves [41:18]; Memory and sleep, and the risk of insufficient REM sleep [55:48]; Evolutionary reasons to sleep [1:02:03]; The early riser vs. the night owl, and tips for overcoming jet lag [1:10:18]; Is there one type or stage of sleep that is most important? [1:17:33]; The dangers of drowsy driving [1:28:48]; The timeliness of Matthew’s book, and how the conversation of sleep has changed over the past several years [1:35:18]; and More. Learn more at www.PeterAttiaMD.com Connect with Peter on Facebook | Twitter | Instagram.

Hey everyone, welcome to the Peter Atia Drive. I'm your host, Peter Atia. 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 peteratia-md.com.

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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 from monthly subscription. Welcome to the kickoff of this Matthew Walker 3 part series Unsleep. 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 being the first. Now, at the end of this 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 peteratiamd.com forward slash subscribe. I guess 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 in 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. Today he has published over over 100 scientific studies.

He has received numerous funding awards from the National Science Foundation, National Institutes of Health, and he's a fellow with the National Academy of Sciences. He's the author of the International Best Seller, 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, Iarthin Center. 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 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. Hey Matt, thank you so much for making time to meet on a Sunday. Absolutely privilege and a delight to be with you, Peter. What's with the weather in Berkeley? Is it always this bad? Now, when Peter says it's always this bad, it's probably in the low 60s and there isn't much blue sky. It's dry and there's a very pleasant breeze and there is some wonderful blossom. So, I know it's not San Diego.

Everything is utopian and people are singing Come By Are at the end of the day and holding hands, but it's pretty good day when you consider it still February. Right, I know. I live in these extremes. Like 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 when it stuck. But I mean, all three of those are best

than the United Kingdom. You know, my home country were essentially have nine months of really bad weather and then three months of winter. And then that's you, you know, that's your year. So this day February, like this, low 60s, I'm happy, man. 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 I never occurred to me that you could choose to do that. So, when now speaking of this, so what brought you to the US? 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 to 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 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 winter has 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 reproductivity 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 who is much more collaborative and collegial rather than combative and competitive. So Berkeley fit my mentality better, came out here, whether it was great, California, it's

an immensely easy place to arrive in a very difficult place to leave. And I think I probably won't. I know that feeling. I'm probably leaving California. I'm going through the morning process of accepting the departure because you're back. You'll be back. It's a hard place to leave. When did the switch flip in terms of your passion for sleep? 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 actually went out 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 sleep. 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 procreating. For tens, if not hundreds of years, but the fourth main biological drive,

the drive to sleep, had continued to elude scientific judgment. Was that possible? And back then, 20 years ago, if someone were to ask you, why do we sleep? The crash answer was, we sleep to cure sleepiness. And that's the fattuous equivalent of saying, well, we eat to cure hunger. Well, that tells you nothing about the fundamental nutritional benefits of macro-nutrition. 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 nut. It was one of the last great remaining scientific mysteries. I thought, well, you know, if you want to pick something that's going to sustain you for the rest of your life, and some of the most assertive brilliant minds in science had tried to crack this nut and failed, including Francis Crick, wonderful scientists 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 patents 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 Louis 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 egg lieu of journals that you used to sit in on a Sunday, just this kind of like sort of sanctified circle 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. Even within forms of dementia that clinically presented very similarly. 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 asleep generating centers. Whilst in other of those pathologies, those centers were spurred 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 the 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 the sleep is so disrupted, is it not just a symptom of dementia? Could sleep disruption actually be a biomarker of dementia? Could it actually foretell when you are going to develop dementia in which type, or even more profound, is sleep disruption and 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, 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 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. 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. That's right. So, do you think that sleep disruption or poor sleep, and I want to 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? 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 wakefulness. Sleep is the price that we pay for wakefulness, essentially. And you know, something I mentioned in a book that I put out was, and I got a little bit of sleep. Just a little book, 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.

So he'll sit there and he'll look at the cover and he'll go, moo, moo, moo. And then he flips through it and he gets so frustrated that there's no moon pictures inside. I will course correct that if there's a second edition and I will just try to place the words underneath that it is for the benefit of Iatim. Yes, yes.

But in the book, I proposed that we didn't evolve sleep. That perhaps we've got it the wrong way around. Perhaps the default state of life on the planet was sleep. And it was from sleep that wakefulness emerged. Wow. 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 within sufficient sleep, you get increases in oxidative

stress. Those oxidative stress processes lead to 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, it's called the glimphatic 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 sort of the cell.

Sort of irrelevant stuff between the neurons. Exactly, you know, 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 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 cerebral spinal fluid to start perfusing the brain and washing out the metabolic detritus of wakefulness. So it would be like New York City at night, all of the building shrunk down to 200%. 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. Ago, 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 alone. It's just escalating your Alzheimer as risk. That's why we can then explain

the associational evidence, which I don't like associational evidence in epidemiological studies, and I don't think you're a huge fan of it, perhaps either. Just don't tell anybody at the Harvard School of Public Health. Yeah, or maybe the NIH, and I'm applying for grants for epidemiological studies, but what we certainly see is that if you bucket people into the amount of sleep on average that they've got across the lifespan, and at the end of the sort of life, or in late life in their 70s and 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, 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 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-rhym sleep or they fragment their sleep, you get an immediate amyloid buildup, essentially 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 really rather unpleasant. We do a spinal cord puncture and we suck out some cerebral spinal fluid and we can measure

the amount of the two toxic proteins linked to Alzheimer's. One is called beta-amoloid 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 amoloid and tau. 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 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. 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 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 miss things that you would see in an otherwise homogenous population. So for example, when you look at the coin edge of the term Alzheimer's disease, it's quite likely that that was coined based on a patient who probably had a PSN1 or two mutation, such an early onset of the disease versus the disease we typically see. I mean, today, those patients make up less than 1%.

And it's almost a different disease from the, you know, these are people 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, at least from the perspective of no obvious

disease. So your analogy is really interesting because I don't really find myself hugely in the M.O.I. beta camp as the main causal driver. I think it's more of a result, but it's interesting what you pos it 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. 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. Yeah, imagine it's like cancer, right? Where in 30 years, hopefully the rate of growth has slowed that it's not, you know, a pandemic, but yeah, you might have five subtypes or something for that. That's right. You know, and I think we will see that. I think, and then we will start to patent match what features.

I think the fact that sleep already, let's just call Alzheimer's disease, the 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, I think the data are better stronger than any of those. 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 tower aggregation too, I think, 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 grade matterball 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. Sleep fragmentation, which is more about sleep quality than it is about physiological quantity. Sleep fragmentation will be predictive of something else, another subtype of Alzheimer's disease. Then I think basic duration could matter. I think there are probably 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, 1am, then 10pm

and all over the map. So there's sort of regularity. There is the continuity of your sleep, is it fragmented? 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 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 come 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 I hope that we get the chance to speak about 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 love the way that you think about that problem. And I agree with it very much that Alzheimer's disease is probably going to be a 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, it's a media 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 10-year decades and you ask, what was the quantity and quality of their sleep from their 30s and 40s, 40s and 50s, 50s and 60s, 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 towers in the brain, which is what we can do here at the sleep center. And then you essentially can, in retrospective manners 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 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? 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 polysumnography, 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 hopskip 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. 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. Right. Exactly. 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? 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 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 because 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, unfortunately, he's four and a half, but he got a, probably about a 12 minute lecture on epidemiology and the hazard ratio of small cell lung cancer and smoking. But the punchline in my story to him,

pizza or tea ladies and gentlemen, pizza, tea. Yeah. I was trying to story to him, pizza or tea, ladies and gentlemen, pizza, a tea. 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, as you describe it, I love, whenever you can get these things, that's statistics are necessary. When you don't need the p-value to figure it out, that's it. So, does your intuition, and 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, wow, this isn't a subtle change. Yeah, I mean, we're up in the region of, you know, from 0.45 to 0.6. So it's, you know, it's in risk reduction for those doing it correct. Correct. 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, 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, 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 amyloids you get a very strong predictive signal, you know, 30s to 40s and then again, sort of 60s to 70s. And for Tao, it's actually somewhere in sort of the starts in the 50s to 60s and then goes through until the 80s. So what about child? So we actually, we didn't go back in terms of child just because at that point,

it's really difficult to feel confident about that data. You'd have to get parents who are not living at that stage. But to me, I think the fact that you got the strange kind of... And you have a... You've just tried the bimodal distribution for M-Oid. Exactly. For M-Oid, yeah. Which then lends me to believe that that result is difficult to explain

by sort of just general memory biases, which would be kind of more of a linear approach. But I don't, I mean, I think the point is that, you know, the evidence that continues to build in favor of this story that insufficient sleep is a significant lifestyle factor in your deterministic ratio, odds of developing Alzheimer's disease is ever stronger now. And the fact that unlike many of the other lifestyle factors, the mechanism underlying it has now been demonstrated causally in humans and adults and it's been done so acutely within a 24-hour period of time, that to me just knocked me sideways.

And the controls did not have, so if you controlled for everything except the perturbation, you didn't see the amyloid or towel rise in controls. See, this is kind of interesting too, because 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 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 2000 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, 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, 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 going to talk about glucose disposal, hyperinsulinemia, and all 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. 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 post-mortem, who are even only in the

early stages of MCI, of what we call mild cognitive impairment. They haven't transitioned yet to that. I'm glad you remembered it, explain these things, because I'm nodding away like, first I know what MCI is. But that aside, I think the idea that 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 where it doesn't necessarily have to be. No, the analogy could be with lipoproteins.

There's a... Oh, that's a very... Right. I mean, lipoproteins are absolutely necessary a... Oh, that's a very... Right. I mean, 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. You're only attacking 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? 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. And I would say it's in the other order. And yeah, and I think Alzheimer's is, you know, top of the list that, 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. People will often say, you know, how much sleep do you get? And 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 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. That would be an easier one to study. I'm guessing we'll come to that later to the ability to perturb deep sleep and then see the change in the consequence. Yeah, I think the point is I think I've bashed people over the head with this sufficiently, but the link between a lack of sleep and

Alzheimer's now, I think is very strong. And what I find the positive about that is without times to see it's 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 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. So let's shift gears just a little bit and go back to the polysum. Let's explain to people because we're going to eventually have to talk about tracking these things and I want to 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 compare them to their polysum. 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 brain waves? And how would you morphologically describe them and then bucket them by these stages? You've already sort of touched on a little bit as deep, ram, deep, ram, deep, non-ram, etc.

Yes, 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-rhym sleep has been further subdivided into four separate stages, which are unimaginatively called stages one through four. Thank God.

I know, yeah. I think that's all at the sleep deprived people who are experimenting, could come up at that time. 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 Steipop Ben, but because of these bizarre horizontal shuttling eye movements that occur during the 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-rhym and REM is going to be one and last 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-ramp stages. Before we do that, let's say before I fall asleep, when I'm just laying in the bed, how would you describe my brain waves under the wakeful condition? 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 alpharithm. 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 brain waves. It's going up and down many, many times a second. And the amplitude is very small, which kind of is paradoxically you think, if I'm awake, then my brain is active. And so the size of those brain waves 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 brain waves sort of are all cancelling each other out. So the analogy would be, if I were to dangle a microphone above a sport stadium, what I'm picking up is the signal from 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. So there's a lot of cancellation. 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 brain wave is not very big, but it's going up and down. But that's why the frequency is so high. 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. And I assume that's just because the occipital cortex is in the back and you've closed your eyes. 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. But still relatively low amplitude. 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 looking enough 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 their 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 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's usually the end of the relationship. It's just a point of note. Please don't blame me. Usually, wait till you're married and then start to do that one. The divorce usually is harder to come by. So then you start to go down into the light stages of non-ramp sleep stages one and two. Then after about 20 or so minutes, you'll go down deep into stages three and four and an hour. And in one and two, have we transitioned out of that alpha wave?

I mean, where do we start to see the theta's and theta already happening in stage one? In stage two, you actually go into theater activity, which is now down from 50 cycles per second, maybe down to just sort of six or seven cycles per second. And the amplitude's getting a bit bigger. It is getting a bit bigger. And then every now and again, during stage two, the way that I know that you're in this lighter stage of non-ramp sleep stage two

is that you'll get these synchronous bursts of electrical activity that we call sleep spindles. That's the K spindle. And that sort of yeah, where you get this, actually you get a nice big slow wave, like almost like a single slow wave, and then you get this burst of a sleep spindle. And we actually did this great project here at the sleep center where we did the sonification of sleep. And we extracted brainwaves from human beings.

And then we sort of, you know, smooth them a little bit with some sort of audio software. And then you can play them back. And it's beautiful because when you hear these sleep spindles, they are the short synchronous bursts of electrical activity that lasts for about a second and a half, and they go up to about 10 or 15 cycles per second. So it's almost like that beautiful rolling R in sort of in the Hindi language, you know, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, rrr, r, rrr, r, r, r, rrr, rrr, shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh shh the brain goes into this incredible synchronous mantra chant of these slow waves. So the brain wave slow down. You go down to maybe just one or two cycles per second. Very, very slow brain wave activity, but the size of those waves, crashing on the beach of the cortex, as it were, they are huge. And the reason is this, go back to the sports stadium analogy.

Let's say that we're here at Berkeley and we're playing Stanford arch rivals. Yeah, which hopefully you're going to kick their butt. Fingers crossed. Just make sure there's no band anywhere to be found. It always does as a terrible dissent. But at that point, they're chanting in unison. They're all chanting in unison. So it's louder, but they're now making the same sound together. And you can actually hear what's being said. Exactly. So now in that single microphone, you can hear Stanford sucks.

Stanford sucks. So all of a sudden, all of the reasons that we are only now starting to understand, the brain coordinates hundreds of thousands of neurons, unlike it does at any moment elsewhere in the 24-hour period, hundreds of thousands of brain cells all decide to join hands as it were physiologically, metaphorically, and they all fire together, and then they all go silent. They all fire together, and then they all go silent. And what I find amazing about that, by the way,

is how slow that frequency is. You're basically, you could be, this could be only happening once a second, right? That's right, and that's why it got a terrible rap for 20 or 30 years, because it actually looked not dissimilar to some aspects of coma. That's how slow those brainwaves were.

So sleep scientists were, you know, understandably fooled into thinking that deep sleep was a time when the brain essentially was just doing nothing. Now we realize the exact opposite is true because it's during that deep sleep that you get essentially information transfer within the brain, It's a file transfer

mechanism. And the way to think about this is, let's say it's like long wave radio. If you're in the city, you tune into FM, which is short wave radio, you can pick up a bunch of signals. And the further you drive out into the desert, let's say here in California, you just lose those channels because the range from the tower is so short that you just lose that range. But if you go on to the long wave radio stations, you can still pick up stations for hundreds of miles. Why?

Because the carrier frequency of those radio waves is much slower. And so the distance over which you can transfer information is much further. Deep sleep is a brain state of long distance information transfer. Is there more philagically a difference that you can see between stages 3 and 4, which are obviously both delta waves, but how do you distinguish those two? Technically no. The way it's defined is that what proportion of a 30-second period of time, and that's the way that we score sleep, I'll have you sleep for eight hours, then I'll chop up that eight

hours into 30-second bits of information, and for each 30 seconds you'll get a sleep score, and then we add them all up. And what differentiates stage three of deep non-ramps sleep from the very deepest stage, which is stage four non-ramps sleep, is simply what proportion of that 30 seconds is consumed by that deep slow brain wave activity. If it's sort of less than 50%, then it's stage 3. If it's more than 50% stage 4. So morphologically know, although if you really look at it morphologically on average, yes, the waves are typically larger in amplitude and slower in frequency in stage 4 than they are in stage 3. And do people always progress monotonically through these

or do sometimes people go one, two, four, three, REM, for example? No, you have to go through three to get to four. 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 see, 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

2 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 sea-saw 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, 6, 6 and a half hours of sleep at night, I wake up, you know, 5, 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 no because yes, it does proportionate 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 Changing to get a jumpstart 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 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. Noclepsy is a standout case there. You'll usually go from wakefulness sometimes immediately into REM sleep, very frightening, because 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 will come onto this block, your REM sleep. You can build up such a hunger for REM sleep that the brain says, well tonight, I'm going to forego the non-REM sleep. I'm just going to go and feast on REM sleep straight away.

This hysteresis in the system, maladaptively. So that's a bad sign when you get hysteresis like that, that type of pressure. Does this explain, and maybe this is not even really correct, 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. Is that partially explained any of that?

Or is that even accurate? 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 your 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 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-M 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 2, 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 that, 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. So think

about it like this. And this is a very beautiful experimental demonstration because you can surgically deprive people of each of those. And I've seen other talks you've given, of course, and in your book, you touch on this where you could prefer eventually from an experimental standpoint, prevent somebody from consolidating memory, and you could similarly prevent them from forming new memory. Even though we can keep the total amount of sleep consistent, so it's not a stressor,

it's not that wakefulness, you can selectively excise, just like you said, individual stages of sleep. What's the biggest detriment that persons face clinically with the reduction of REM? I think right now, based on the weight of the evidence, it probably starts with mental health. Anything from depression, anxiety, through to disease. 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 to them, this is probably the second other big area of work that we do here at the Sleep Center is sleep and mental health. 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 reactions. Anyone with a young boy knows what the amygdala does? Right, exactly. If they have a temper tantrum in the middle of the supermarket, it's because firstly, their prefrontal cortex has developed, and what little of it that there is, if they haven't slept well, is obliterated.

That's actually a really great example of one of the most obvious observations. We taught, I mean, any parent listening to this knows how emphatically you protect the nap. Correct. And it's for- Full mental, emotional, yeah, just for behavioral health of the child, right?

Correct. 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, 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 era of causality is the other way. The person who is anxious, it's the anxiety that's keeping them awake. Now, my guess is in reality, these two feet off each other constantly. I think you're absolutely right. You might be predisposed to anxiety that fosters lack of sleep, the lack of sleep amplifies and boom, boom, boom, boom.

It's a two-way street, but is the traffic flowing more dominantly in one direction than the other? I think this is what you're pointing at, 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 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.

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, outbursts of four-year-olds, but just to make the point, right? That, to me, is one of the most interesting, albeit somewhat, glib examples. 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, actually. 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 stigmatise it with this label of laziness that your child is sloffful for getting sufficient sleep. And the reason that upsets me,

and I'm getting a little bit animated, which is off for a British man, but the reason I do is because firstly, it took Mother Nature 3.6 million years to put this eight-hour thing called a night of sleep in place. And within the space of 70 years, if you look at the data, we've locked off almost 20 to 25 percent of that. Imagine coming along and saying, 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 20 to 25 percent. Do you think that's a good idea? I'm not sure, isn't that all? It's such a great example. I'll pause for a moment just to tell a funny story that you and I have talked about off-mic, which is, until about 2012, I was in the, I'll sleep when I'm dead camp.

And I know what led to that. It wasn't, it was a very deliberate decision at the end of medical school when a good friend of mine, with all the best intentions, who was a year ahead of me. So he was now in, that 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 80-hour work week requirement and residency. So we averaged I think about 114 hours a week in the hospital. So he said to me, look, Peter, you're signing up for whatever, five, seven years of this thing, if you spent every moment outside of the hospital sleeping, you would still be tired.

And 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 and, and I was doing anything, everything. Such that during that period of my life, I just know, because I was pretty adamant about recording how much time,

like I was very wed to this idea, there's 168 hours in a week, if I'm spending, you know, 114 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 was about 28 hours a week of sleep. So it wasn't for every night because you'd have none and then six and then three and then

eight. You could binge sleep from time to time, but it was pretty much 28 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 going to sleep half of what is evolutionarily programmed. And I said, yeah, because 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 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 24 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 to your point about reducing oxygen saturation by 25%.

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. It's completely anti-evolutionary. It sounds like the dumbest thing. I often said, and it has been said before, if sleep doesn't serve an absolutely vital set of functions, it's the biggest mistake that the evolutionary process has ever made.

And we now realize from this constellation of evidence that Mother Nature did not make a spectacular blunder in putting this thing called an eight hour sort of need of sleep in place. It is the greatest life support system that you could ever wish for. It is a remarkable health insurance policy. And what's great is that it's largely democratic, it's mostly free, and in terms of a prescription from a doctor, it's largely painless. So I almost wanted to title a book, Consciousness is Overrated, or just sometimes, dot, dot,

consciousness is overrated. But when you really look at the evidence, in terms of risk-d-risking, just about every disease that is killing us in the developed world, it's very hard to look no further than sleep, and that's why I don't want to trivialize diet and I don't want to trivialize movement and activity. But what I would say is that if you want to put sleep up against either one of those two and kind of play the whole head-to-head game, which I don't think we need to do here, I would simply say that sleep is the foundation on which those two other things sit. It's not the third pillar of good health.

I think it is the foundation. That's a really interesting way to think about it, because I typically describe four pillars or five if you include all of the exogenous molecules that you could lump together. But another way to think about it, which again, I don't think is necessarily the right way to think about it, but sometimes it makes the point. If you deprive yourself of food, how long can you survive? Well, we have one person up to 382 days, even someone who's as lean as you could survive 30 days with

no food. How long could you survive without water? Depends greatly on the temperature, etc. But you could make the case that deprivation of sleep would result in the quickest reduction of health. Certainly more than not eating or not exercising for a period of time. And those studies have been done in rats Yeah, and actually we know some of this from humans who have been trying to 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 Attempts at longest period of sleep deprivation so I mentioned this yeah

Yeah, you know, it 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 I think the last true effort was about 24 days. Oh my. But 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 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 Baumgardner, I think his name was, who sponsored by Red Bull,

went up in a capsule in a hot air balloon to the outer surface of our planet. This was about four years ago. Four years ago. It was remarkable. He opened the door and then he jumped out and he fell back down to earth at over a thousand kilometers an hour

using his body alone. He broke the sound barrier and he successfully came down. And now Guinness says for that, just fine. However, to sleep deprived yourself, no, much more unsafe, we're not going to let it happen. You are allowed to put it in context. You're allowed up to 12 jumps off Niagara Falls. Basically.

But that's okay, but no, no, you're not going to, that's such a great point. I want to go back to one other thing to close the loop on this and again, the listener may say, boy, there's a lot of stuff going on here, 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 were sleeping six hours a night, if you have one person who just for the argument's sake is doing it from 9 p.m. to 3 a.m. and another person is doing it from midnight to 6 a.m. would you expect or even if it were, 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 to 3 versus midnight to 6. 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 forward truncation? 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 consumed more heavily in terms of the deep non-rem sleep phase, which would probably be the hours from 9 p.m. through until about 3 a.m. That's really 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 a.m. through until about midday, then

the brain shifts in terms of its pattern. If you let people just sleep it out, you know, if you look at sort of extreme owls who, I wish to 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 going to get hit hard in terms of REM sleep devouring. So I make that point that your brain has different taste sensitivities to non-remin 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 because most of your REM sleep happens in the late morning hours and you're already awake by 3 or 4 a.m. in the morning, and so you're not getting the chance to get into those REM sleep-rich phases. And which of those patients would develop more appetite for sleep the subsequent evening? The person who was deprived, and you know I'm asking by the way, it's exactly what we were talking about earlier. It's this jet lag question. If you know you've got that flight and you need to

force yourself to sleep at a time zone, it's not right. I'm just now thinking about, well, I always do the nine to three, right, would I be better off doing that? In other words, I'm depriving myself of REM, would I be better off just just driving just to, um, well, you're depriving yourself of REM, but you're also still depriving yourself of total sleep as well, you know, when it comes to the jet like modeling. And, you know, there are, there's some,

I think that that's an interesting model and I think it does work that you can try to, in the week before you start to fly, let's say you're 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 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 really early. And then I won't 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 the 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 speak probably a lot more about this when we speak about caffeine and

adenosine and pressure. But that's, 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 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, sort of early in the morning versus five hours late in the morning until later in 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. 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. And I think we both acknowledge that, look, I mean, these things are still not quite at the level of the polysum, 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 because I came back from New York last night, you know, went to bed at, I don't know, 8.30 pm and got up at 5 or, yeah, probably 4.30 or 5 in the morning. But had a huge deep sleep. Exactly. So you've dragged your eight hour window if you think about this sort of eight hour window and you slide it back on the clock face from midnight to 11 p.m. to 10 p.m. to in fact 9 p.m. you're dragging that eight hour sleep phase

back closer into the deeper sleep rich phase, the deep non-rem sleep that you want. So what your sort of aure ring will be telling you is you got more deep sleep and perhaps you may actually see a little bit of a reduction in REM sleep. As you go to New York, you may see the opposite. As you sleep later in the morning, you'll get more of that REM sleep pattern, which is I get, and it pisses me off too. I'm like, I didn't get as much deep sleep and I got more REM sleep and not that REM is bad, but I'm generally more

upset by the dearth of deep. You know, this is interesting. It's now really, I really need to think about that because, of course, on some level, our body is responding to cues in the environment. It's not just responding to the intellectual knowledge that, hey, in California, it's this time it's time to go to bed. I mean, light is playing a role. Meal timing is playing a role.

Huge meal, then. Yeah. I want to definitely talk with you about this, because this is, to me, this is such an important topic. And then, of course, the accumulation of a denocene and, of course, the melatonin stuff. So, by the way, I would just say that, you know, I think REM sleep, some people, I have this kind of bimodal distribution of questions, some people will say, you know, how do I maximize my REM sleep? And I say, why do you want to maximize your REM sleep?

I said, well, that's dream sleep. And that's the good stuff, right? As if, you know, it's like saying, you know, how do I maximize the amount of yolk in my egg? You know, do I get the like the, oh, can I go the ostrich egg? Whatever it is. I don't know what the analogy is. And the question is, Mother Nature has found this equilibrium. Don't mess with it. It's the Da Vinci code of sleep and stick to it, you're good to go. But also then other people will say, how do I get more deep sleep or, you know, I, you know, I could get upset by that lack of deep sleep. To come back on to REM sleep and how important it is,

the studies have been done were firstly they deprived. And by the way, these studies have never been done again since the 1980s, and they probably never will be because of the ethics regarding them, because they are just so devastating that we probably won't be allowed rightly so, I think, to do these studies to animals ever again. But they essentially deprived animals of sleep until they died. And what they found was that rats will firstly die as quickly if not quicker, almost by about 20% from total sleep deprivation as they will from total food deprivation.

So if you want to put sleep in the food. That's interesting that their gap is much narrower because for humans, the gap is very well, you'll die way earlier from sleep deprivation than food deprivation unless you're, you know, the leanest person on the planet. And there is a tragic disorder that I describe a little bit in the book. It's a very rude, genetically inherited disorder called fatal familial insomnia, and it's really the only evidence short of the disgusting travesty that is total sleep deprivation used in certain countries for interrogation tactics that we know of that has led to death. But with standing that, this disorder fatal familiar in Somnia says it in the name that essentially human beings. How old do people typically survive?

It usually takes about 18 to 24 months before they die. But the problem is this is not they wake up one day and they are no longer sleeping. They're gradual things. So it's kind of like it masquerades is just typically insomnia first, restless nights for the first two or three months. Then it gets worse. Then you're only sleeping four hours. Then you know, by month 12, you're already sleeping two hours. How much of this is genetic versus environmental versus we don't know? It's strongly heritable that we know. So it's within the Mendelian sort of, you know, pool of genetic disorders. And it's testable.

We know that gene, interestingly, it's what seems to be the single gene. Yeah. And it's a prion protein gene abnormality, which is if you don't know about prion proteins, you may have heard of mad cow disease, which was rife in the United Kingdom. That's another thing. That's another prion protein disorder. That's why you can't donate blood. And it's also why, yeah, I'll probably forget half of what I've been saying and start

repeating myself because I've been vegetarian for about 12 years, but before I went that route, I think I definitely was in the phase of eating beef when it was filled with these frowns in the United Kingdom. So my brain is probably Swiss cheese at the stage, but essentially this disorder, fatal familiar insomnia, it gives us some degree of disease proof that insufficient sleep is fatal for human beings, but we knew it in these rats studies because these rats would die as quickly from food deprivation as they did from sleep deprivation. But the most striking thing was then they did a second round of studies. They selectively deprive them of either just non-rapid eye movement sleep or rapid eye movement sleep. And what they found is that

the rats were dead within about 9- ten days with total sleep deprivation. They were dead within just about the same period of time from REM sleep deprivation. Duration was kept constant or also reduced. It was still reduced somewhat, but you could probably look at a control that had a same duration without a selective deprivation. Yeah, and there is a what's called a yoked paradigm. It's a very clever technique where you can mimic the total amount of sleep deprivation in one other animal, but the other animal is still getting the chance to get REM sleep. So REM sleep selectively removed, the rats died basically almost as quickly as they did

from total sleep deprivation. And then non-REM sleep deprivation was deathly. Ultimately, it just took longer, it took about 20 days. Total sleep deprivation, let's just say for argument, say you die in nine days. Sleep reduction, but selective rem deprivation, you die in the same period of time. Basically, yeah.

Sleep reduction, but deep deprivation, you live maybe twice as long. Yeah. So everything, definitely, everything fatal, just that one takes a little bit longer to kill you than the other. And what I find either strange or exciting about that is if you look from an evolutionary standpoint, those two types of sleep did not emerge at the same time. We only have observed true rapid eye movement sleep in birds and mammals. We don't see true rapid eye movement sleep

in reptiles amphibians fish or insects. Now birds and mammals evolved separately along the evolutionary path from amphibians fish and reptiles. So what this means is that when we went from the transition from being reptilian to either avian or mammalian, that's when REM sleep emerged because we see non-REM sleep in every species. Even in insects we can observe something that looks like non-rem sleep in reptiles, fish, amphibians, birds, and mammals. Every one of them has non-rem sleep. Not every one of them has REM sleep.

Only birds and mammals have REM sleep. In other words, REM sleep is the new kid on the block in the time course of evolution. REM sleep, firstly emerged later in the course of evolution, and secondly, what's kind of wonderful is it emerged twice independently, once in birds and once in mammals. So you could argue that, well, if deep non-rem sleep, which is much more evolutionary from an evolutionary perspective, it's in much older form of sleep. Wouldn't it be the much more necessary fundamental one?

And therefore, wouldn't you die sooner? No, I see it seems. From the deep non-rem sleep. It seems the opposite, because you'd say, well, for the same reason that the cockroach can survive the nuclear disaster, the avian mammalian pathway is more evolved, neuronally, presumably, and therefore probably requires something essential in REM that when it deprives you, it takes away your superpower, which is a cortex. And I think that's exactly what it is, which is when you look at anything that has essentially

a complex nervous system, maybe that's where the pressure for this thing called REM sleep emerged, even though we know that non-REM sleep actually supports many essential central nervous system functions, like synaptic pruning and some great sort of neural thing, you know, the glimphatic system clearing up that he comes up with. It's sort of similar to your oxygen analogy, which is when you go from being an anaerobic

to a faculty of anaerobic to an A-robe, who's gonna be most sensitive to oxygen deprivation? To the E.A. Exactly. It's always a dangerous scientific hypothesis where you can argue it both ways, but I always found that interesting and it's uncommitted. But I just wanted to note that for 20 minutes ago in kind of indefense of REM sleep, that if we should all be worried about the amount of deep sleep that we're getting absolutely, but we also need to be worried about how much REM sleep that we're getting,

because from a pure mortality risk standpoint, REM sleep is arguably even more important than non-reps. And we'll come to this later, but my recollection of the literature is, and I think you even alluded to this earlier, ethanol's biggest hit is going to be on RAM, isn't it? Hands down. This is what we come on to. Substances that are misunderstood and misused when it comes to sleep. 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 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, you know, apoe for 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 as their single highest priority in life.

That said, can you spend even just a minute, couple of minutes? It's the drive after all. We have all the time in the world. Making the case, the similar case, been the presence of cardiovascular disease and cancer. Yeah, and I want to touch on that point before we go on about this Alzheimer's disease risk. A lot of people out there may be

having this sort of like sleep machismo moment where they have this bragadotio attitude of getting insufficient sleep and they say, look, I'm in my fifties and I'm fit as a fiddle, my cognition is raise a sharp and I sleep five or six hours a night. So we've got heads of state, for example, who are saying this, people who 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 chess 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 week, 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 makes me so sad because I saw pictures of Margaret Thatcher in an infeal 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 framed 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 without cymas disease, but acutely with car crashes. And I know that we'll come on to this at some point too. But the only thing I would say is that I get many emails from people who've read the

book. 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 hid them had basically been surviving on about five and a half hours

of sleep for the two months prior, that they had had what's called a micro-sleep. 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 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. And my guess is, even though it's going to 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 were able to quantify.

I sometimes say to patients, you know, the forehorsement of death would be these big chronic diseases that kill us, 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. 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 your puts in with your phone, your check-in ways, you're doing something,

you shouldn't be doing with your phone, sleep deprivation, ethanol, failure to wear to 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. 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 are involved in the accident, but you can also pick this apart from are 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 under-sled, 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 micro-sleeps. So when you are trying to survive

on seven hours of sleep or six hours of sleep, then 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 micro-sleeps, 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, four, 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 micro sleep 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 in the e-breated 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 micro-sleep, yeah, it's a projectile. You do nothing. That's why drowsy driving is more fatal than drunk driving typically, is because there is no action. There is no application of break,

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 insufficient sleep, and I get that. And, you know, there are people, sport stars, people, all sorts of people who I respect hugely. And I have 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 going to be crushing it on the sports field.

And then I'm going to be back in the gym the next morning and sleep is for 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. But I think, Matt, your work has come along at a really interesting point. I mean, I have to be honest with you. I remember when your book came out

and my initial thought was, does the world need another sleepbook? Because there's 2,000 of them out there. And I think there's two things that are different. The first is, your book is exceptional. I should 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 conversely, you can have someone who puts together a good book, but they themselves don't have the credibility. I think that so you can take credit for the first two. I think the third 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. Maybe that is the thing that first got people to think about this, which is, well, wait a minute. You know, if I want to 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 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. 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 our infancy and the dark from a clinical perspective, sort of a public health perspective and functioning on this. So firstly, I mean, so much great stuff to unpack there.

I think you're absolutely right. I think the success of the book is largely despite my my ability to to write and convey ideas. I think what happened is that it was a perfect storm. There is I gave you two thirds of the credit. Thank you. And I don't know if I can take them. I feel so ashamed, but I think 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, six hours and 31 minutes. That's the average six hours and 31. That must mean that how linear has that declined been met? Has that not been yet? Yeah, it's accelerating, isn't it? 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. These are averages. You've got to imagine that at least a third of the people are probably 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. You know, you can pick apart one street 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 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 needed to be written and needed to be written now. For what it's worth, you had many moons on the front and back covers, so my little Iarthian was delighted. He loved that. Yeah. He's probably read from, from cover to back cover.

Back cover, nothing in between. 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 all I ask. Good. Okay, there's like literally a hundred 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 peteratiamd.com forward slash podcast. There, you'll find the show notes, readings, and links related to this episode. You can also find my blog at peteratiamd.com.

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