Dr Rupy: Why do we sleep? It seems like such a luxury, an evolutionary oversight, a privilege some might say. But on today's episode with Professor Russell Foster, you're going to learn about why sleep is having a renaissance in both the way we think about it as a means to health, as well as how the workforce should really embrace it for enhanced creativity and productivity. Russell Foster is Professor of Circadian Neuroscience, Director of the Sleep and Circadian Neuroscience Institute, SCNI, and Head of the Nuffield Laboratory of Ophthalmology at the University of Oxford. And his latest book, Lifetime, is a fantastic dive into everything circadian clock related, and I absolutely loved reading it. On today's show, you're going to learn all about circadian rhythms, sleep pressure, why we sleep and what happens when we sleep, how the visual system interacts with the brain. We're also going to talk about this concept of circadian entrainment, how we can entrain our circadian rhythm to our benefit as well as our physiology's benefit. And we talk about chronotherapeutics, sleep, shift work, mental health, how to figure out your chronotype, and Professor Russell's top 10 tips for entraining your clock right at the end as well. It's a brilliant episode. It's a little bit on the longer side, but I thoroughly enjoyed it myself and I know you're going to love it too. Remember, you can download the Doctor's Kitchen app for free to get access to all of our recipes with specific suggestions tailored to your health needs and new recipes added every month. We're adding about 15 to 20 every single month. All of them have got step-by-step images. You can choose from different health goals. You can also share lists to your friends now as well or share ingredients to your notes that you can go shopping with. And we're adding new features all the time. I'm really excited about our latest category of food, which is summer celebrations. So anything that you're celebrating today or in the future and you want to keep it healthy for all your guests, summer celebrations is a category with some delicious, beautiful salads. We also share recipes every single week for free on the newsletter, which is eat, read, listen. You can sign up for that at thedoctorskitchen.com. But for now, here is my conversation with Professor Russell Foster. Great. Professor, it's so lovely to have you on the podcast. Thanks so much for taking the time. Um, I'm really excited to.
Professor Russell Foster: Really delighted to join you, Rupy.
Dr Rupy: Oh, brilliant. Brilliant. I'm, I'm, yeah, I'm, I'm really excited to chat to you about this. As you know, sleep is almost having a bit of a renaissance. I think we're all becoming a lot more aware about how important it is to, to make sure that we're getting enough of it. Um, but I wanted to start by, by getting into a bit about your history and how you started studying, uh, and sleep and, and why this has become sort of your, your, your area of expertise.
Professor Russell Foster: Well, it goes, it goes back quite some way, actually. I mean, uh, frighteningly to undergraduate years. I was always fascinated with clocks, um, how they're regulated by light. And of course, one of the most obvious of our 24-hour rhythms is the sleep-wake rhythm. Is the sleep-wake rhythm. So, in a sense, they all sort of blended together. But, but in fact, um, if we go right back, you know, to, uh, the early years, I was sort of remedial in classes. I used to sort of sit in my own little bubble, um, and, and my parents were, you know, absolutely despairing because I remember the headmaster, I was a good swimmer, and I just sort of, you know, captained this sort of swimming team and the headmaster came, you know, gave me this cup and he said to my parents, at the same time, of course, you do realise Russell is an entirely non-academic child. Um, and so, you know, and it was, it's fascinating. I think sort of, and then I, I sort of fell into this, into this, this groove of neuroscience and, and loving, you know, all this, this, this sort of science and then realised, well, perhaps I, if I really want to continue in this way, I ought to sort of pull my finger out and actually pay attention in class. And it was just like a light bulb moment because it went from being, you know, in the bottom of the class, you know, in a low, um, sort of stream to, to the top of the top stream. And it's, it's, it's weird. Um, however, to answer your question, um, getting into sleep specifically, there, there was another pivotal moment. I was, um, I was in a lift with a psychiatrist, uh, in, in a hospital in West London where I, I used to work before, um, before Oxford. And this chap said to me, oh, you know, um, my patients with schizophrenia, they don't have a job. So they go to bed late, get up late, miss my clinic and don't have friends. And I was really irritated by that. And I thought that just doesn't make any sense to me. Um, and so we teamed up with another psychiatrist and we started to look systematically at the sleep-wake rhythms of these individuals with a diagnosis of schizophrenia. And these rhythms were so completely and utterly smashed. You know, there was no 24-hour, um, sort of rhythmicity in some of these individuals. And that really fascinated me. I mean, and so many of the, the problems that these individuals were having, you know, cognitive problems, health problems, were probably as a result of the appalling sleep that they were experiencing. And so, really that was the, the trigger that got me into human research and indeed specifically, uh, sleep, uh, and the, and the abnormal patterns of sleep in mental illness, which we've, we've continued to work on really for the past, crikey, um, 20, almost 20 years.
Dr Rupy: It's, it's so interesting. I mean, um, when you told that story in your book, actually, I went to Imperial, so I know Charing Cross Hospital well and the, uh, lifts that are really, uh, unreliable as well in that building. Unfortunately, I don't think they've, they've updated it. It's really in need.
Professor Russell Foster: No. I, I think, I think we had, we, we had a, an external examiner coming in to examine a PhD. I think they were stuck in the lift for about an hour before we thought, oh my goodness, they're probably, you know, there's probably some transport issue. No, they were banging on the doors of the lift trying to get out.
Dr Rupy: Yeah, crazy. It brought back so many memories of the medical student for me, actually, when you, when you told that story. I, I, I think, um, why don't we anchor the listener with a couple of definitions? Because I think circadian rhythm is going to come up quite a bit, the sleep-wake cycle. Um, so maybe we can establish exactly what we mean by those terms and, and the definitions. And then we can go into how that applies to a fascinating area of mental well-being, um, as well as all the other areas as well that it can affect.
Professor Russell Foster: So it's, I think it's quite remarkable. We have an internal biological day, um, often called the body clock, uh, and, and also called circadian rhythms. And, and what these circadian rhythms represent is essentially a biological process which, which produces a cycle of around about 24 hours. Now, it's not exactly 24 hours. In fact, circadian rhythm means about 24 hours. And so in addition to this internal representation of a day, we also need to set that day to the external world. And the most important, um, factor for setting or for aligning the internal and the external day is exposure to the light-dark cycle. So that's the core of our circadian rhythms. We often talk about a sleep-wake cycle. And, and of course that's the most obvious of our 24-hour rhythms. But the sleep-wake cycle is, is more than just the circadian system. The circadian system times a whole bunch of processes within the brain. In fact, the sleep-wake flip-flop from consciousness to, to sleep is extraordinary. It involves a realignment of all the key brain neurotransmitter systems and multiple brain structures all interacting. And this flip-flop between the two states is then timed by the clock, the circadian system, which says, now's the appropriate time to be awake, now's the appropriate time to be asleep. But there's yet another timer for the sleep-wake cycle, which is probably the most intuitive part about sleep, which is called the homeostatic drive or sleep pressure. And what that represents is essentially the longer you've been awake, the greater the build-up of sleep pressure and, and, and the greater the need for sleep. So what happens is that first thing in the morning, the clock has, has woken you up, ideally, your, your, your biological clock, not your alarm clock. Um, and, and sleep pressure builds throughout the day, and it's really high towards sleep. And we don't fall asleep because the clock is saying, no, it's daytime, keep awake, keep awake, keep awake. And in fact, the highest drive from the clock for wakefulness is just before we fall asleep, because it's counteracting that build-up of sleep pressure throughout the day. So we have these wonderful timers all interacting to flip-flop us between consciousness and the sleep state.
Dr Rupy: So we have this, this rough 24-hour cycle, um, that, that, uh, we operate on. We have sleep pressure. I think that's a really important, um, uh, concept as well for people to understand as it builds throughout the whole day and, and, and, uh, affects our, our, our rhythm. How do we entrain this, uh, rhythm such that it's, uh, consistent and actually in line with how we should be, um, working with the, the day and night cycles?
Professor Russell Foster: Well, of course, Rupy, that's one of my favourite questions because that's where I've spent a lot of my, my time researching. And, and in fact, you know, we, we, we knew that, that in, in humans and in fact all mammals, the eye is critical for detecting the dawn-dusk cycle to set the internal clock. But it, it always puzzled me because if you think about the visual system, what the visual system does is grab light in a fraction of a second and then forget it's seen it. So we're, we're talking about light sensing in the millisecond, the sub-second range. But the clock doesn't need information like that. It needs a sort of a global measure of light intensity around about dawn and dusk. And I couldn't work out how the classical visual system was grabbing light to regulate internal time. So we started working on mice with hereditary retinal disorders. They had gene defects which had rendered their rods and cones, the visual cells within the eye, it had effectively turned them off. And in fact, these are really interesting animal models because they were being used at the time to understand the genetics of human eye disease. So these animals existed and we put them into little running wheels and we hooked up the running wheels to a computer and we just measured their rest-activity cycles. And what was truly remarkable, and I can, I still get a tingle when I think about these, these early observations, is that these mice were visually blind. They, they simply showed no visual response at all, and yet they regulated their, their clock, their circadian system to the light-dark cycle perfectly. They showed, they, they, they showed that they could not only entrain, but they did so with the same sensitivity as a mouse with all of its rods and cones. And I remember, uh, when I first sort of presented these, these data, actually at a vision meeting, I said, so the data are, are consistent with the fact that there's another light sensor within the eye. And the consternation, uh, in response to this heresy was extraordinary. I mean, one talk I gave, uh, and, and a chap stood up at the, at the back of the, of the auditorium, and I thought he was sort of interrupting to ask a question, so I sort of, I sort of paused, and he just looked at me and shouted, bullshit, and walked, and walked out. Um, and another person, I remember, was absolutely infuriated. They said, do you think after 150 years of research on the eye, all of us here have missed a completely new photoreceptor system? And of course, I was quite young in my career and quite bullish, and I said, well, I'm sorry, but yes, you have. Um, and so, I mean, but, but, but as, you know, it's never black and white. Um, and, and so there was, there was a, a grain of, of, of, of truth in the criticism, which was, okay, there could be just a few visual cells, rods and cones left within the eye regulating these, these circadian systems. And so what we then did was genetically engineer a mouse where all the rods and all the cones had been absolutely turned off. There was no way that they could signal at all. And those mice were just like the other mice. They showed perfectly normal circadian entrainment to the light-dark cycle. And that then led to the realisation that there's another light-sensing cell, and in fact, it's based upon the ganglion cells within the retina. Now, the ganglion cells are wonderful because they have their axons, and those axons form the optic nerve. They're, they're the last layer in the retina, and they, they project off into the brain. And what, what we were able to show in the mouse, um, working closely with my, my colleague Mark Hankins, um, and David Berson was able to show in the rat, is that a small number of these ganglion cells are directly light-sensitive. They, they are photosensitive retinal ganglion cells, using a completely new light-sensing molecule or photopigment that we showed that was maximally sensitive in the blue part of the spectrum. So it's a great example where really completely curiosity-driven, uh, research has resulted in an extraordinary finding. And in fact, it, it's, it's changed our view of the eye. We now appreciate that the eye is, is an organ of, of, of, of space. It gives us our sense of space through vision, but it's also an organ of time because of its ability to regulate the internal clock. And indeed, it's, it's, to some extent, redefining our understanding of blindness. You can be visually blind because you've lost your, let's say, visual cells, your rods and cones, but you can still be, um, able to regulate the clock by light because you've got those photosensitive retinal ganglion cells. And so, yes, it's been, uh, really exciting. And in fact, what we're up to at the moment, um, uh, with, with my colleagues, is trying to understand how those novel photosensitive retinal ganglion cells actually interact with the molecular clockwork. And we, we've produced actually some quite exciting stuff over the past couple of years, and I've got, as, as all, when you talk to other scientists, oh, my best paper is just around the corner, you know, we're actually working on this, this new, this new paper, which we hope to submit fairly shortly. And, and by understanding those pathways in, what we can also do is think about drugs that will interact with key nodes in that pathway that will then fool the clock that it's seen light. So I work very closely with Blind Veterans UK. These extraordinary individuals who as a result of, um, trauma, uh, have lost their eyes, um, in combat, um, and so they have no eyes. And so they drift through time completely. And, uh, the work that we're doing on mice, um, and now in, in early stage human trials, we think will be able to give back a sense of time to these individuals because we will fool their biological clock that it's seen light. And, and I think that's so cool. If I can finish my career by giving back a sense of time to those individuals. And in fact, it relates to, to a bigger population because rhythms, sleep-wake rhythms are smashed in mental illness, neurodevelopmental diseases, and other conditions, um, really which are, are very, very difficult. And some childhood illnesses, for example, where there's no sense of time. And so there's a thought that perhaps we can, we can use these drugs which are originally being developed for the blind, but in other clinical cases as well, whereby we can, um, uh, consolidate sleep-wake and then, uh, maybe just short-term use of these drugs and then move on to light and, and other agents. So, yeah, it's a really exciting time because we're developing new drugs to help individuals.
Dr Rupy: Yeah, that is absolutely fascinating. I mean, I, I not to derail our conversation, but I did want to ask you about that incident, uh, where you had a number of probably senior colleagues standing up and actually sort of publicly shaming you in front of everyone at this conference. I mean, how did you get over that sort of public shaming and that, you know, the fact that you were going against what a lot of people believed in that there was a another photoreceptor that somehow everyone had, had overseen?
Professor Russell Foster: Yeah. And I think this does happen, you know, quite a bit in, in science when there's a sort of a, a change in, in the mindset. And what you've got to do is just generate better and better data. In fact, those public challenges, whilst they're, they're emotionally difficult to deal with, what they do is they stimulate you to do better experiments and to just genuinely nail it. And that's what we did. It took us 10 years from the sort of original idea to absolutely showing there was something else. And, and, and you just keep on, the expression I used to my, to my, um, wonderful younger colleagues is, you just keep on kicking the door until they bloody well let you in. Um, and, and that's, that's the approach. I mean, I do remember having some anxious moments. Um, I do remember I gave a seminar in, in Germany, um, and one of the very distinguished vision people stood up and basically harangued me. Um, and, uh, it was still early days where, you know, there was this possibility. But, but my, my first degree actually wasn't in vision science, it, it wasn't in medicine, it was actually zoology. And so I've always had this sort of comparative interest in, in how evolution solves similar problems. And what we had in our back pocket was the discovery that in fish, there is a non-rod, non-cone photoreceptor. We discovered a completely new gene and a new photoreceptor within the eye of fish, completely different from the rods and cones. And I remember thinking, oh my god, could we have got it wrong? Have I missed something? And I remember thinking, no, we've got proof of principle. We found it in a fish. Okay, a fish isn't a mammal, but, you know, it's not such a daft hypothesis. So, so to answer your, your question, you just get more and more data to, to, to deal with the critics. Yeah, yeah. But it can be painful. I can imagine. Yeah, yeah, no, I can. Absolutely. Yeah, yeah. Well, that, that's good. That's good to know. And I think, you know, any budding scientists listening to this, I think that will be really inspirational for them too. I, I wanted to talk about,
Professor Russell Foster: So just, just to go back, I mean, I think that what, what happened is this, is, is this, this happened sort of fairly early on in my career. And I remember sending a grant off to the Eye Institute. Um, and in those days, because I was based in the States for these, these early, early studies. And, um, it came back and the grant was utterly rejected. It was just awful. And I remember sitting at my desk thinking, oh God, you know. Um, and my head of department, you know, called me and I thought, well, I'm just about to get a roasting. And he was wonderful, Mike Menaker, uh, who sadly died last year. And he said to me, look, you're right. This is wonderful stuff. You know, stick with it. And so he said, just send the grant to another section. So instead of it going to the Eye Institute, I sent it to the Institutes of Mental Health. Um, uh, which, which looked at biological questions broadly. And six months later or so, I got this call from the head of the section saying, oh, congratulations, Dr. Foster. Um, your, your study has, your grant has come top of the study section, and we like it so much, we'd like to get permission from you to, to bind it up and, and exhibit it at the Society for Neuroscience, which is the, you know, the, the big thing, as, as an example of how you should write a research grant. And that was so useful because it went from the outer darkness to the highest it could get, um, with the same day. I barely changed a word. And so it's that business of sticking to it and getting the, as long as the data are right and they support the, the hypothesis, you just plough on.
Dr Rupy: Yeah, absolutely. Yeah, that's a really good example of backing yourself as well. That's brilliant. I, I wanted to ask about, okay, so now, now we have this idea of, uh, the visual system being very important in training, uh, the sleep-wake cycle. Um, how does this interact with the, uh, quote-unquote master clock? And how does that filter down into all the other, uh, elements, the, the, the organs, our pancreas, our digestive system, etc, etc. But I, I thought we'd, we'd focus on the master clock, um, at first.
Professor Russell Foster: So we actually have a, a physical structure deep within the brain, within the hypothalamus, that represents a master clock. It's called the suprachiasmatic nuclei. It's a paired structure either side of where the optic nerves go into the brain and fuse. And so it sits right at the base of the brain. And there were rumbles that this bit of the brain was very important in circadian organisation. Studies going back to the, the 20s and 30s identified something within the base of the brain because when that part of the brain was destroyed, these 24-hour activity patterns that rats and mice were showing were lost. So there was some stuff going down there. Um, I was involved actually with some experiments with Martin Ralph, um, in University of Virginia and Mike Menaker. But Martin led these experiments showing that you could destroy that little bit of the brain in a mouse. Um, well, actually it wasn't a mouse, it was a hamster. Um, and I can tell you why it was a hamster later on. But anyway, it was this hamster. And then transplant in, um, an SCN from another hamster, but it was a mutant hamster. So instead of having a clock of about 24 hours, it had a clock of about 20 hours. And what was truly remarkable is that that mutant SCN actually restored rhythms to the host where the SCN had been lesioned, uh, but with a period of 20 hours. And that was just so cool because, you know, here we have, you've transplanted an essential element of the clock, which is its period. And so, uh, further work went on and it was discovered by other groups that you could take one of those individual clock cells out, and there's about 50,000 in a human SCN, and it would tick away in a dish. It would show 24-hour oscillations. And, and that was immensely exciting. Um, and then it, it became clear how that, that clock was actually generated. Now, it wasn't originally shown in mammals at all. It was shown in the fruit fly. And in fact, in 2017, I was lucky enough to see my, my colleagues, um, Rosbash, Hall and Young get the Nobel Prize for discovering how the clock tick, ticked in, in fruit flies. And, and of course, in essence, what you've got is a bunch of clock genes, which encode proteins. Those proteins then form a complex, which move into the nucleus and turn off their own genes. That complex then gets degraded, the genes can then turn on again. So you've got this extraordinary feedback loop, a molecular feedback loop. Um, and so more recently, it's been shown that that subtle changes in some of those clock genes can either speed up the clock or slow the clock down. And so part of whether you're a morning person or an evening person, or somebody in the middle, is actually due to how fast your clock runs, which is in turn related to subtle changes in some of those genes, um, that are part of the molecular clockwork. Okay. So, we have this master clock within the brain, these molecular clocks ticking away. It's regulated by the eye and the light-dark cycle. And what we thought was that the SCN then imposed 24-hour rhythms on, uh, activity, whether it was the, the hormonal systems, whether it was the digestive enzymes, whether it was liver function, muscle function, we just assumed it was a signal from the master clock imposing this, these rhythms. And then Ueli Schibler, um, did some amazing experiments, and I was, I was in the audience when, when these data were first, uh, first presented. And he showed that other cells in the body had clocks, and they were ticking in a way that was just like those clocks within the SCN. And from that early observation, it became clear that essentially every cell in the body has the capacity to generate its own 24-hour molecular oscillation. And so our concept of the circadian system changed almost overnight from an SCN forcing rhythmicity on the rest of the body to a system more like, more akin to an orchestra, where you have the conductor of the orchestra, the SCN, producing a rhythmic temporal beat from which the members of the orchestra, the cells in the body, take a reference cue and align their rhythmicity, um, uh, in, in, in alignment with, with the master clock. So, so we've moved from saying the circadian system, uh, to, to this sort of circadian network, uh, which is what's generating our 24-hour biology, including of course, the sleep-wake cycle. So it's, it's been, it's been a really exciting time. And, and I do feel that this, this sort of work is one of the great achievements in, in, in biology. I mean, to simply understand how genes and their protein products can interact to generate complex behaviour and contribute to so much of, of our embedded biology. I think is an extraordinary achievement. And I think, you know, uh, Rosbash, Hall and Young deserved their, their, their Nobel Prize, um, absolutely, for getting this sorted out, not in us, of course, but in fruit, in flies, but that then informed, uh, how the molecular clock is working across the animal kingdom. I mean, what's also extraordinary is that the way that a fly generates its circadian rhythm, its genes and those proteins are broadly similar, similar to the sorts of things ticking away in you and I. So the whole of the animal lineage is, is ticking away using genes and proteins which are broadly similar. And it's what's fascinating, of course, is that the different groups, the plants, for example, um, the bacteria, they also have clocks, but they're built slightly differently. So it's likely that circadian rhythms have evolved more than once, using different sorts of, they all are based upon a feedback loop, but they're using different genes and different proteins to, to achieve that oscillation.
Dr Rupy: Yeah, that, that point actually leads me nicely on to the more broader question about why we sleep. I mean, I, I, to echo your point, I think if you think about the ramifications of sleep, uh, more generally, absolutely, that Nobel Prize was really well deserved because we have a deeper understanding about how it affects everything from mental health, hormonal health, uh, digestive health, uh, metabolic health, obesity, all the things that you've just rattled off there. And in part, that's definitely due to, um, shift workers because we're all shift workers essentially. Um, I, I wanted to, actually, before we go on to that, because we were mentioning teenagers, I wanted to talk a little bit about social media actually, and this idea that the reason why teenagers are waking up later is potentially because of the use of their mobile phones at night. Now, I know you've got some, some views on this that it might not be necessarily due to the light, but more so due to the content. Um, and, and perhaps we could talk about the spectrum of light as well that we have indoors versus outdoors.
Professor Russell Foster: It's, it's really important because there are, in, embedded in the media is the concept that blue light at night, um, from computer screens and Kindles and all the rest of it, is delaying the circadian clock. Remember, nighttime light delays the clock. Um, the evidence for that is, uh, scant at best. A classic study that was undertaken by a group at Harvard got people to look at a Kindle on its brightest intensity for four hours on five consecutive nights. And after five nights, yeah, I mean, it's a, it's a brutal hit. After five nights with that sort of experience, sleep time was just statistically significantly delayed by 10 minutes. And as Mary Casden, you know, I think said at the time, well, it may be statistically significant, but it's biologically meaningless. It's within the wobble. Now, the problem with device, and I, and while we're talking about it, computer screens, um, and the shift from sort of a blue enriched to a sort of a red enriched screen. There's very little evidence that that, uh, works at all in terms of the circadian system. And, and it really goes back to our understanding of how light interacts with the clock. You need a lot of light of a long duration to actually, um, shift the clock. So for example, um, light treatments use 10,000 lux for 30 minutes. Um, the sorts of light you're getting from a Kindle is going to be 30 lux. Uh, and from a computer screen, it's probably going to be something like maybe 70 lux, 100 lux if you, if you're lucky. And I remember talking to a, a teenager about, um, the use of, of screens at night. And he said, okay, just, just stop right there, because I have a device which shifts the colour of my screen from blue to orange, and therefore I'm not going to shift my circadian rhythms. I said, okay, that's great. There's not much evidence that it really works very well. But by the way, what time do you think you're getting off to sleep? And he said, well, about 2:30 a.m. So, you know, there's this idea that you can actually dodge the bullets with technology, but actually you're not. Um, and so, uh, yeah, I, I, I think the danger, and where we do have good data with devices, and particularly devices that you're interacting with, they have an alerting effect upon the brain and they delay sleep onset. Um, and particularly if you're doing multimedia, you know, you're doing your emails, you're doing your, your, your, your WhatsApps and all the rest of it. It's a highly dynamic, very brain alerting. And, and I think really what you've got to do is turn the devices off, um, you know, at least 30 minutes before you want to go to sleep. And you, if you don't have the strength to, um, uh, not turn them back on if you wake up, um, leave them in another room. I mean, I, I know what it's like. I remember when I first got a BlackBerry, I was in, I was in Western Australia. And, and those of us that remember this sort of little light that would flash slowly when, when a message. And so I was in Australia, so I deal with the Australian, you know, emails and stuff. And then of course, the European ones would come in. And then of course, the American ones would come in. So, you know, it's spanned. And I sort of got there, I had jet lag, it was difficult to get to sleep. And, uh, I, I thought, okay, well, I'll, I'll put the BlackBerry in, in, in the next room, woke up, wandered into the next room. So I, in the end, I had to leave this damn thing in the lab because I had no control over, over looking at this, this thing. And so I, you know, I do, I do speak with experience. I do know how difficult it is, but, but actually leaving it in the lab worked, you know, I'd wake up, I'd then fall back to sleep again.
Dr Rupy: Yeah, definitely. So, so rather than the, uh, the light emitted from these devices, uh, from, from what I gather, it's more the attention, uh, or the alerting effect of the content that you're consuming and the attention switching between different applications and tasks that can be alerting to the brain.
Professor Russell Foster: Absolutely. And I think, and it will depend upon the device. So for example, a Kindle, you know, we've got the data which suggests it's not going to delay sleep onset. Um, and a Kindle is, is kind of what one-dimensional, it's an electronic book. You know, you're not, you're, you're reading. Um, so a smartphone or a gaming or something else is very different in that there, you're, it's a much more dynamic and complex set of interactions, which is going to be more alerting. So I think it's, it's those electronic devices which I think one has to be particularly, um, uh, careful about in terms of their alerting effects because of the, of, of what you're doing on the brain and therefore delaying sleep.
Dr Rupy: Brilliant. Um, and on the note back to shift work, sorry, we're shifting, attention shifting across different topics here ourselves. There's just so much to talk about with you. So shift workers, um, it's not going to go away. It's, uh, it's going to be a part of, uh, frontline workers' life in, in medicine, in, you know, in supermarkets, lorry drivers, etc, etc. What kind of things can we do to mitigate the effect, the inevitable disruption, uh, that, that these entail? I mean, it's a very difficult question. And, and perhaps we could, uh, draw down in some, into some of the processes that are actually disturbed as a result of shift work, um, before we provide some solutions.
Professor Russell Foster: We touched on this within the context of, of, um, so higher frequency health checks, uh, the appropriate nutrition, uh, education. Um, one idea which I think is really interesting, and I, and it sounds a bit crazy, but I think it's worth thinking about. We talked about chronotype. And so, wouldn't it be smart to chronotype the workforce and those who were the morning types would do the morning shift, those that did the, that were the late, that were the late chronotypes did the late shifts. What you really want to avoid is somebody like me, who's a late type, doing the morning shift, uh, and vice versa. So I think that we can actually use one's chronotype to try and match, uh, onto the sorts of shift schedule that you would, you would want to try. And it's not the whole solution, but it will, will mitigate to some extent. So, so I think that, uh, you know, those approaches are, are really important. They're not going to, they're not going to get rid of the problems, but they will mitigate some of the problems. Uh, and not, not least the educational component. I think that the various sectors, you know, warning, you know, that, that knowledge, you know, for junior doctors, for example, that 50, 57% have either had a crash or a near miss on the drive home. So what, what can you, how can you deal with that information? And as we said, you know, looking at devices which detect drowsiness, uh, uh, and alert you to the fact that you're falling asleep at the wheel. And, and these microsleeps that you mentioned, Rupy, they're uncontrollable. Uh, you can, you know, you're, you're going along, you think you're okay, and then you just fall asleep uncontrollably. And, and of course, that's why they're so dangerous because you've lost any consciousness and so you can't even put the brake on when you're ploughing into the car in front of you or to the, into, into the middle of the road because you, you, you've lost consciousness. And that's why they're so very dangerous in terms of, of, of, um, causing, uh, severe, um, uh, uh, trauma and indeed death.
Dr Rupy: Yeah. And, and so with, um, with sleep disruption, you have, uh, poor immune health, higher cortisol levels, uh, greater risks of cardiovascular disease, etc. One of the elements, uh, one of the things that I think is getting a bit more attention these days is, um, the impact on mental health. Um, so I wonder if we can do a bit of a dive into how sleep disruption can relate to mental health in either an associative role or, or in a potentially causative manner.
Professor Russell Foster: Yeah. I think the relationship between sleep and circadian rhythm disruption and mental health is very, very important. And, you know, I mentioned those studies right at the beginning that I did on, with colleagues on schizophrenia. And I was just completely gobsmacked at the, at the appalling sleep-wake problems. And of course, the longevity of people with severe mental illness is much reduced. And what do they have? They have obesity, diabetes two, uh, cognitive problems, and these are all the sorts of things that you get as a result of chronic sleep disruption. And it's never, it's never thought about as a treatment option. Um, you know, the poor sleep. It's thought of as, well, uh, an unavoidable consequence of antipsychotics, for example, or lack of employment. And I've, and again, I think this is not the right way to think about it. And so we sort of developed a sort of a conceptual model, you know, because everybody says, what is it chicken and egg? You know, is it, is the sleep problem, you know, causing the mental health and the mental health, it, it's, it's actually, you shouldn't look at it in that way. What we, um, because of our increased understanding of how the sleep and circadian systems are generated, they involve all those key brain neurotransmitter systems, multiple brain structures. So the hypothesis is that the, the heart of the problem is an overlap between the brain circuits, the neurotransmitter systems that are regulating mental health and those that are regulating normal sleep-wake. And if there's a change in a neurotransmitter pathway that predisposes you to mental illness, let's say serotonin, let's say dopamine, whatever, it's going to have an impact upon the sleep-wake system at some level. And what evidence do we have for that? Well, it's been so interesting because genes that have been linked to human schizophrenia, for example, SNAP25, we, we looked at a mouse with a mutation in SNAP25, which shows sort of odd, you know, mice can't have schizophrenia, but it shows some patterns of behaviour which, which you can associate with schizophrenia. But what's its sleep-wake like? Well, it's smashed, completely smashed, just like the patients. And increasingly, we're finding genes which have been originally associated with the clock, which are now being linked to, uh, mental health issues and mental health, um, genes which are now being shown to have a role in the circadian and the sleep system. So there is that mechanistic overlap at the beginning. Okay. But it's more than that. Because of course, the distorting effect of sleep and circadian rhythm disruption on our physiology, uh, and our, and our, and our cognitive behaviours and our emotional pathways will exacerbate the mental health condition. And of course, the mental health condition will then feed back, let's say via anxiety, psychosocial stress, maybe even the medications, can feed back and then affect the sleep and circadian rhythm disruption. So you've, and of course, you, you have this stuff at the heart, but very rapidly, you can, you can, as a result of a positive feedback loop, distort both the worsening sleep situation and the worsening, worsening mental health situation. So that's the conceptual framework, um, that we came up with. And we thought, okay, well, if that's the case, um, do you see changes in, in, in, in sleep-wake prior to a, let's say, a depressive episode? And you do. And what about those individuals who are at risk from developing bipolar? So, working with Guy Goodwin, um, Guy had developed a bunch of questionnaires, uh, about vulnerability to develop bipolar. And we were able to show that those young people who were at risk of developing bipolar, but did not have a clinical diagnosis of bipolar, were already showing sleep-wake problems. So again, further evidence for this relationship. Um, and so anyway, the explicit test was, and this was led by Dan Freeman in psychiatry in Oxford, a wonderful set of, um, experiments. And using, um, a, a, a digital, um, uh, cognitive behavioural therapy, uh, for insomnia program, and looked at thousands of individuals. Um, and these individuals were showing insomnia and high levels of paranoia and hallucinatory experiences. And what was extraordinary is that by just partially stabilising the sleep-wake cycle with digital, you know, cognitive behavioural therapy for insomnia, it was able to reduce the levels of paranoia and hallucinatory experiences. And so I think we can think about the, the sleep circadian system as a new therapeutic target in mental health. Stabilise that, and you'll hopefully reduce the severity of symptoms. And there will be a number of ways of, of course, that you could, you could use to stabilise sleep-wake in those groups. But, but I think that's, it's, it's really fascinating. The other thing that I think is so important, and I've been talking to a, a tech company about this, is I've long had the idea that because you see a change in sleep-wake prior to a depressive episode or a psychotic episode, you could use a very simple device that would measure when you got up, when you went to bed, um, how many times you woke up in the middle of the night. And if you see a change in that, it signals to your smartphone, um, and that then goes to a clinical, uh, individual who, who says, who, who can then ring up the individual and say, how's it going? Noticed some changes in your sleep-wake. Do you want to come in? Should we, should we think about, you know, do you find that your mental health state is, is sliding? Do we need to sort of, so you can then, uh, very light touch, monitor individuals who are vulnerable within the community and try and head off a mental health crisis by looking at changes in the sleep-wake pattern. And I think that's, that's potentially very exciting. We don't have that device. Nobody's built the device. It's quite a simple technology. It could be done now. And, and I'm, I hope, I hope this group will do it finally.
Dr Rupy: Yeah, yeah, absolutely. I mean, what, what is your opinion of sleep tech in general? I mean, you've probably, I mean, you've definitely come across a number of consumer available tools these days that are, um, at least claiming to give you, uh, certain data on the quality of your sleep such that you can do things to inform it and improve it. What, what, what is your, yeah, what is your opinion of the accuracy of those and the utility?
Professor Russell Foster: Well, where should we start? Um, uh, so, so first of all, in principle, um, a device that gives you some feedback about when you went to sleep, how long you've slept, when you get up, could be very useful. It's rather like a diet. You know, you, you change your eating behaviour, you weigh yourself in the morning, you see a weight loss, you think, great, that's, I'm doing something right, and it reinforces the behaviour. And so they could be useful at that level. Um, the problem about the devices that are currently marketed, and I should say, none are endorsed by any of the, um, sleep federations, National Sleep Federation, for example, none of them are FDA approved at the moment. They can be very misleading because what they're good at, as I say, is telling you when you went to sleep, when you got up. But, but then giving you measures of, you had a good deep sleep, or you had lots of slow-wave sleep, or lots of REM sleep, they simply aren't accurate enough to, to report this. And I think it can generate anxiety. And I give you two examples. One young lad came to me and said, do you believe in slow-wave sleep? And I said, well, you're kind of. Um, uh, he said, well, I don't because my device is saying I'm not getting any. And I sort of, sort of explained why I thought that, um, I, I wouldn't put any trust in the device. But one chap, one chap, seriously, I kid you not. Again, this is a discussion prior to lockdown. Uh, he came up to me and, again, he said, I'm really worried. I'm not getting enough deep, slow-wave sleep. My, my app is telling me I'm just not. In fact, I'm so anxious about it, I wake, I set the alarm for 3:00 in the morning to check how much slow-wave sleep my app has recorded. And, and you know, this is just crazy. Uh, and, and so, um, take the information with a pinch of salt. Um, very, a good, good, good friend of mine, um, uh, from, from, uh, the States, he teaches a massive class in sleep. And he sort of starts the class by saying, who here has used a sleep app ever? And you know, the whole class puts its sort of hand up. And he said, who is now using them today? And you know, you've got three hands going up. You know, people, people very, get wise quickly that these devices, um, are, are inaccurate and actually can be under some circumstances unhelpful, particularly if you take the information too seriously. It's frustrating because they could work. It's, it's a difficult problem though, because, you know, they're based upon an algorithm trying to extract information. And as we've discussed, um, sleep is highly dynamic and very variable. So you'd have to have a deeply sophisticated algorithm, maybe AI will get there in the end, to try, you know, you plug in age, you plug in a whole bunch of factors, which could then modify the app that would make it more applicable to you. But, but you know, you say that these have been scientifically validated. Well, you look at the papers, and it was 800 undergraduates from California, um, with two nights in a sleep lab. That's not validation for me. Um, and so I, you know, it's a shame because this, this extraordinary technology, they could do a so much better job and they're doing it half-arsed, and that really upsets me.
Dr Rupy: I have used multiple different sleep trackers and I use a sleep tracker and I think the main takeaways for me are, don't look into it too much because it's highly inaccurate. B, for, for the type of analytical person I am and for someone who doesn't get too carried away with things like calorie counting and, you know, measuring steps and that kind of stuff, it gives me a rough idea of what, um, impacts my sleep, uh, the lateness of my meals, the amount of alcohol, the timing of exercise, all those kind of broad stroke things, but I wouldn't look into it to the point of measuring the amount of minutes that I've been in REM sleep because I know that's highly inaccurate. And I, I can't remember if it's via a lecture or in your book where you talk about EEGs, uh, inaccuracy, or the, the lack of information you can actually gather from it. And I was quite surprised about that. So I wonder if we could, we could talk about that.
Professor Russell Foster: EEG, of course, has dominated the sleep field from its, its origins. And it's worth bearing in mind that the circadian scientists and the sleep scientists didn't go to the same meetings for most of my career. Um, you know, the circadian people were often comparative biologists. They, you know, worked on pigeons and lizards and plants and, you know, just, you know, didn't really work on humans and we sort of didn't think about sleep that much. And then this other group, primarily based, you know, in the clinical realms, would measure, you know, the electrical activities from the surface of the skin covering the, the, the skull and look for change patterns and associate that with disease or, or whatever. Um, and it's only recently that the sleep people and the clock people have, have come together and are talking a similar language. And the problem about EEG is that it's, it also can be rather misleading. And, and I was speaking to a sleep colleague fairly recently, who shall remain nameless because he might get attacked by his colleagues. And he said, yeah, and I said to him, you know, EEG, what's, what's it good for? And he said, yeah, it's a good point. Um, uh, and he said, um, measuring, measuring the EEG to try and work out how the brain works is a bit like looking, um, at when the toilets are flushed and when the lights go on and off in a building to try and work out what's going on in the building. It's a very crude measure. And, and of course, it's tricky because EEG is correlative, you know. Um, and, and there's some very interesting correlations. So in, in schizophrenia, for example, you lose slow-wave sleep, you lose deep sleep. What does that mean, though? Well, it's complicated because we don't really know what slow-wave sleep and REM sleep are actually doing. What do they represent at a functional level? So, there's a suggestion, and the data aren't too bad, suggesting that slow-wave sleep is associated with memory consolidation and the processing of information while we sleep. REM sleep could well be emotional processing. But other than that sort of hand-waving, it hasn't taught us a huge amount about the fundamental mechanisms that generate the sleep-wake cycle. Um, and I think it's to some extent been a, a distraction. And what we've got now are young, early career, mid-career scientists who are electrophysiologists, who are now looking at sleep, um, using some of the incredibly sophisticated new tools to get a genuine understanding of what's going on. So, is a K-complex actually associated with memory transfer? I mean, they're beginning to sort of delve more deeply, and of course, using drugs can manipulate some of these patterns and see what effect it has on the individual's ability to perform during the day. So, yeah, um, I, I think, and of course, EEG is really tricky because the tricky, the way people have used it is to bring somebody into a sleep lab, wire them up, and then expect normal sleep overnight. And of course, it, it's a deeply abnormal sleep environment. There are some new devices, and I, and I'm, I'm very hopeful about this. And I think this may actually be really useful for the field, whereby you have truly ambulatory EEG with dry electrodes. So you can put a sort of little band round, um, and those devices look to be, I think, really interesting. They're not only, I think, good for looking at the, the EEG from the brain when you're asleep, but also the wake state, because the amplitude of some of the oscillations and the frequency that you get during wake can alert you to whether you're tired or you're fully alert. And that, of course, could be very useful within the workplace, um, to prevent accidents or indeed, as we've discussed on the drive home. So I think that the new, the new technologies, the new generation of dry electrodes, uh, for measuring EEG could actually be, be rather helpful. So you're not then bolted in to all the paraphernalia and the abnormal environment of a sleep clinic.
Dr Rupy: Yeah. This has been such a fascinating conversation. There's so many more things that I want to chat to you about as well, but I, I realise we've been going for well over an hour here. Um, I mean, in the book you talk about chronotherapeutics. I think that's a fascinating area of research that needs to be taken a lot more seriously within multiple specialties of medicine, you know, when we deliver chemotherapy and, sorry.
Professor Russell Foster: Yeah, I mean, I think that so interesting where, where it looks like the circadian clock actually provides a break on cell division. And the clocks, the circadian clocks of cancer cells seem to be turned off. And so that allows this, this unregulated cell division. And by putting clocks back into those cells, you can reduce tumour progression. And boy, is that exciting. So if you can turn clocks back on in a cancer cell, you, you can actually have, have another way of hitting these horrendous, uh, uh, conditions. So that's, you know, one area. We, we touched on earlier on our attempts to try and mimic the effects of light on the clock to regulate circadian rhythms in individuals with no eyes. Uh, and I think that it's all arising from this fundamental understanding of how these systems are generated. And that's, I think it's fascinating that so many of us who, you know, went into science, curiosity-driven science, um, and now see how we can use this new knowledge, uh, and apply it, um, for human, uh, therapeutics and well-being.
Dr Rupy: Absolutely. I think on the, on the subject of, um, health anxiety, particularly when people read and hear about the importance of sleep to all the different elements that we've discussed here, mental well-being, uh, metabolic health, we've spoken on the podcast actually before about, um, the timing of food as well and, and how that can impact your propensity towards glucose excursions, etc, etc. Um, what, what would you say are some of the key things that people need to get right without sounding too puritanical about things? People have a lot of struggles and sleep, as you've mentioned a number of times here, is a very much a dynamic process. What are the key things that you think we should be thinking about, listeners should be thinking about in terms of optimising or giving ourselves the best chance of having this restorative sleep that is super important for us?
Professor Russell Foster: It's a really important point because I think so many people feel that the sleep is what you get and they have no control over it. But actually, very simple tricks, if you like, um, can improve our sleep. And I think we can think about this in four domains. What we do during the day, what we do before bed, what we do in the bedroom, uh, uh, what we could do for the bedroom, and then when we've actually crawled into bed. So, during the day, the most important thing for me is getting that morning, that that morning light exposure, setting the internal clock to the external world. That will stabilise everything, physiology, and of course, the sleep-wake cycle. Napping is often, if people are tired, I mean, the first point to make is if you need a nap, you're not getting enough sleep at night, but let's not be too prescriptive. If you're going to nap, that it's been shown that a 20-minute nap, um, but not longer, can actually improve your ability to function during the second half of the day. So the occasional nap is not a problem, but, but, you know, make sure it's not, not, um, longer than 20 minutes. The problem with napping, we go back to our teenagers, is that, um, our teenagers are getting very little sleep at night. They're dragged out of bed by their frustrated parents, uh, well, not all of them, but some of them. Um, they struggle to school. Some actually, and I've talked to teachers, they're actually falling asleep on the, on the desk at school. They then go home, they're chronically tired, they'll then experience a two-hour nap fairly close to bedtime. That pushes back the sleep pressure, meaning it's more difficult to get to sleep that night, and then you get into a vicious circle of longer naps, shorter nighttime, uh, sleep. So be careful about napping. You know, uh, casual, short nap, not a problem. Exercise, again, not too close to, uh, to, to bedtime because that will increase core body temperature. And a drop in core body temperature has been associated, um, with, with, with getting to sleep. And we'll, we'll come back to temperature in a moment. We've talked about, we've touched on food intake. Uh, try and concentrate your main food intake morning, lunchtime rather than lunchtime, evening, um, because of the increased chances of obesity, diabetes two, and the development of conditions such as obstructive sleep apnoea, which are common in individuals who have put on weight. And of course, obstructive sleep apnoea is when there's a cessation of, of breathing, um, during the sleep episode. Uh, essentially the musculature of the throat has collapsed onto the airway, and you're, you're suffocating. The brain realises it's being deprived of oxygen, wakes you up, and then you have these incredible, um, you know, surges in blood pressure, which can actually damage the small blood vessels within the eye and, and it's a really important condition. Obstructive sleep apnoea is associated with coronary heart disease and a whole range of other problems. So, so make sure, um, you're not eating, uh, your main meal of the day only at night. Um, avoid excessive consumption of, of caffeine, for example. And there's a, a very interesting cycle that people can get locked into. What caffeine does is really interesting because we talked about sleep pressure. Um, well, it actually blocks the receptors in the brain that are responding to some elements of sleep pressure. So, so it's a very interesting understanding of its physiological role. The problem is, of course, if you're fuelling the waking day with lots and lots of caffeine, it means you're wired when you need to get to sleep. Um, and so the first point is try not to drink coffee in the afternoon or caffeinated coffee in the afternoon. Um, and if you are drinking coffee throughout the day, then there's the tendency to reverse that stimulation with sedation. And so people will fall into a stimulant-sedative feedback loop. And that sedative, the first choice is alcohol. So many people will sedate themselves with alcohol. And it's really important to appreciate that sedatives, like alcohol, are sedatives. They, they mask some of the important things going on within the brain, such as memory formation and all the rest of it. So, really try and avoid that sort of stimulant-sedative, uh, feedback loop. Really important is after a stressful day, step back. Do something which detaches you from the stressful situation. The main enemy of sleep is stress. Many people don't have a sleep problem, they have a stress problem, which then prevents them getting the sleep that they're, they're, they're, they're wired to get. So, you know, do step back. Um, before bed, keep the levels of light low because that will increase levels of alertness. I think it's absolutely ironic. What's the last thing that we do before we go to bed? We stand in the most brightly lit room, the bathroom, looking into an illuminated mirror cleaning our teeth. And I, and again, maybe one of your listeners have will actually build the ideal bathroom mirror, which will have a switch. There'll be a morning setting with lots of bright light, increasing alertness, and then there'll be an evening setting, which will reduce the, the levels of light while you're cleaning your teeth. We've touched on electronic devices, you know, stop using them at least 30 minutes before your desired bedtime because they increase alertness and they reduce, uh, the chances of getting to sleep. We've talked about avoiding sedatives and prescription drugs. Short-term use, fine, but just be very careful that they don't become the way you try and induce a sleep-wake cycle because they, and particularly in the elderly, and you'll know this, Rupy, you know, with, with daytime sleepiness and the chances of falls because of, of, of sleeping, sleeping issues, um, induced by, uh, sedatives. Uh, going back, and I think it's worth, worth talking about, and there's the winding down at the end of the day, but it's also before bed is the time that many individuals, many couples, um, it's the only time that they have to talk about the important stuff going on. Um, and, and so what you find is that people slide into really stressful conversations. I mean, I remember, you know, um, that my, Lizzie, my wife, we, she wanted to discuss family finances, you know. And I'd say, no, this is, no, absolutely not. I, this is too terrifying. I don't want to, you know, we'll, we'll, we'll make another time for it. And I think it's true. I mean, I'm sort of trivialising it a bit, but actually, if it's stuff that stresses you out, don't do it before you, uh, go to bed. Um, uh, yeah, and, and you know, immediately before bed, you're adopting behaviours that, that relax you. It's sort of the, the, um, the book or, or the, or the music or whatever activity you, you find relaxing. The bedroom itself shouldn't be too warm. Uh, many, there's some very dodgy practices in British bedrooms with, with really overheated bedrooms. And of course, um, it shouldn't be, it shouldn't be cold, but it should be, you know, um, you should be able to lose core body temperature, um, to a slightly colder environment. Of course, it's difficult, keep it quiet, maybe white noise or, you know, the sound of the sea if, if there's traffic noise or you're in a flat with lots of other people around you. Uh, it's tricky. Keep it dark. Again, particularly if there's light from, uh, the window out, outside, uh, because light increases alertness. Uh, make the bedroom a place for sleep, a haven for sleep. And again, I appreciate it's difficult, but remove TVs, computers, smartphones, just get them out. This should be this wonderful cocoon, uh, of where you go for your glorious sleep. Um, don't clock watch. I think so we, we've talked about waking up at night. And, and many people will wake up. Yep, it's the natural thing. But then they'll look at their illuminated dial and they think, oh my god, I've only got two hours left. I'm never going to get back to sleep. And it doesn't matter. Just cover the face of the damn thing up. And, and it's the alarm that, that you're dependent upon, not roughly how many hours or less you've, you've got to sleep before you need to get up. Um, we've touched on sleep apps. Don't take them too seriously. I mean, they're fun, but really, uh, use them judiciously. In bed, keep to a routine, both on free days and, and work days. Try and keep that structure. And, and of course, it, it refers to other stuff. It's not only when you go to bed and when you get up, but also try and structure mealtimes. That can be useful as well. Um, considering that we spend more than 30% of our time in bed, we're really cheap in terms of, um, our bedding and our pillows. You know, there's, I don't know what it is, that you know, resentment in spending a lot of money on a mattress or a pillow. Um, but actually, it really helps and you should get the mattress and the pillows that enhance your sleep. There's some weird stuff going on there. Um, some people use relaxing oils. Now, the evidence that these are actually useful isn't really very robust. Um, it's probably having a placebo effect. But again, it's getting you into that, this is, this is the bed, this is the, the environment, I associate this smell with now it's sleepy time. Um, and incidentally, it can be very useful if you're doing a lot of travelling. You can have, you know, your partner's perfume or aftershave, and, and it can be quite nice because you essentially then define your space, um, as, as the place to sleep. Um, earplugs. Now, this is important. So, if your partner snores, it can be, it's one of the major problems and it gets worse as one gets older. And I think you need to take a pragmatic attitude towards it. Uh, if you don't like using earplugs, and many people don't, it's worth persevering, but many people don't like them, find an alternative sleeping place. It's not a reflection on the nature of your relationship. It just means that one of you is not going to be woken up by snoring and the other is not going to wake up with bruised ribs in the morning because you keep on sort of prodding them. Um, the key, the serious point about that though is that make sure your partner doesn't have obstructive sleep apnoea. And this occurs both in men and women. It's more prevalent in men, but it does occur in women as well. Um, so that's important. Um, now clearly, economically, one doesn't often have the chance of an alternative sleeping space. But if it does, it is an option and, and it's easier as one gets older, um, you know, you're more likely to have, have the space, then it's, it's go for it. Um, and, uh, the final bit, I suppose I'd say is if you wake, stay calm. Uh, we've talked about polyphasic, biphasic sleep. You will almost certainly get back to sleep if you don't let stress, um, social media, uh, and caffeine then, uh, blocking your ability to get back. Um, but the key point of all of this, this rant I've just, it's not really a rant, but all these tips, um, is that work out what works best for you. Uh, because everybody's going to be different and you need to take some ownership of your sleep. And with very simple things, you can actually enhance it enormously.
