Why We Sleep / Почему мы спим (by Matthew Walker, 2017) - аудиокнига на английском

To Dacher Keltner, for inspiring me to write.? PART 1 This Thing Called Sleep? CHAPTER 1 To Sleep . . . Do you think you got enough sleep this past week? Can you recall the last time you woke up without an alarm clock feeling refreshed, not needing caffeine? If the answer to either of these questions is “no,” you are not alone. Two-thirds of adults throughout all developed nations fail to obtain the recommended eight hours of nightly sleep.I I doubt you are surprised by this fact, but you may be surprised by the consequences. Routinely sleeping less than six or seven hours a night demolishes your immune system, more than doubling your risk of cancer. Insufficient sleep is a key lifestyle factor determining whether or not you will develop Alzheimer’s disease. Inadequate sleep—even moderate reductions for just one week—disrupts blood sugar levels so profoundly that you would be classified as pre-diabetic. Short sleeping increases the likelihood of your coronary arteries becoming blocked and brittle, setting you on a path toward cardiovascular disease, stroke, and congestive heart failure. Fitting Charlotte Bront?’s prophetic wisdom that “a ruffled mind makes a restless pillow,” sleep disruption further contributes to all major psychiatric conditions, including depression, anxiety, and suicidality. Perhaps you have also noticed a desire to eat more when you’re tired? This is no coincidence. Too little sleep swells concentrations of a hormone that makes you feel hungry while suppressing a companion hormone that otherwise signals food satisfaction. Despite being full, you still want to eat more. It’s a proven recipe for weight gain in sleep-deficient adults and children alike. Worse, should you attempt to diet but don’t get enough sleep while doing so, it is futile, since most of the weight you lose will come from lean body mass, not fat. Add the above health consequences up, and a proven link becomes easier to accept: the shorter your sleep, the shorter your life span. The old maxim “I’ll sleep when I’m dead” is therefore unfortunate. Adopt this mind-set, and you will be dead sooner and the quality of that (shorter) life will be worse. The elastic band of sleep deprivation can stretch only so far before it snaps. Sadly, human beings are in fact the only species that will deliberately deprive themselves of sleep without legitimate gain. Every component of wellness, and countless seams of societal fabric, are being eroded by our costly state of sleep neglect: human and financial alike. So much so that the World Health Organization (WHO) has now declared a sleep loss epidemic throughout industrialized nations.II It is no coincidence that countries where sleep time has declined most dramatically over the past century, such as the US, the UK, Japan, and South Korea, and several in western Europe, are also those suffering the greatest increase in rates of the aforementioned physical diseases and mental disorders. Scientists such as myself have even started lobbying doctors to start “prescribing” sleep. As medical advice goes, it’s perhaps the most painless and enjoyable to follow. Do not, however, mistake this as a plea to doctors to start prescribing more sleeping pills—quite the opposite, in fact, considering the alarming evidence surrounding the deleterious health consequences of these drugs. But can we go so far as to say that a lack of sleep can kill you outright? Actually, yes—on at least two counts. First, there is a very rare genetic disorder that starts with a progressive insomnia, emerging in midlife. Several months into the disease course, the patient stops sleeping altogether. By this stage, they have started to lose many basic brain and body functions. No drugs that we currently have will help the patient sleep. After twelve to eighteen months of no sleep, the patient will die. Though exceedingly rare, this disorder asserts that a lack of sleep can kill a human being. Second is the deadly circumstance of getting behind the wheel of a motor vehicle without having had sufficient sleep. Drowsy driving is the cause of hundreds of thousands of traffic accidents and fatalities each year. And here, it is not only the life of the sleep-deprived individuals that is at risk, but the lives of those around them. Tragically, one person dies in a traffic accident every hour in the United States due to a fatigue-related error. It is disquieting to learn that vehicular accidents caused by drowsy driving exceed those caused by alcohol and drugs combined. Society’s apathy toward sleep has, in part, been caused by the historic failure of science to explain why we need it. Sleep remained one of the last great biological mysteries. All of the mighty problem-solving methods in science—genetics, molecular biology, and high-powered digital technology— have been unable to unlock the stubborn vault of sleep. Minds of the most stringent kind, including Nobel Prize–winner Francis Crick, who deduced the twisted-ladder structure of DNA, famed Roman educator and rhetorician Quintilian, and even Sigmund Freud had all tried their hand at deciphering sleep’s enigmatic code, all in vain. To better frame this state of prior scientific ignorance, imagine the birth of your first child. At the hospital, the doctor enters the room and says, “Congratulations, it’s a healthy baby boy. We’ve completed all of the preliminary tests and everything looks good.” She smiles reassuringly and starts walking toward the door. However, before exiting the room she turns around and says, “There is just one thing. From this moment forth, and for the rest of your child’s entire life, he will repeatedly and routinely lapse into a state of apparent coma. It might even resemble death at times. And while his body lies still his mind will often be filled with stunning, bizarre hallucinations. This state will consume one-third of his life and I have absolutely no idea why he’ll do it, or what it is for. Good luck!” Astonishing, but until very recently, this was reality: doctors and scientists could not give you a consistent or complete answer as to why we sleep. Consider that we have known the functions of the three other basic drives in life—to eat, to drink, and to reproduce—for many tens if not hundreds of years now. Yet the fourth main biological drive, common across the entire animal kingdom—the drive to sleep—has continued to elude science for millennia. Addressing the question of why we sleep from an evolutionary perspective only compounds the mystery. No matter what vantage point you take, sleep would appear to be the most foolish of biological phenomena. When you are asleep, you cannot gather food. You cannot socialize. You cannot find a mate and reproduce. You cannot nurture or protect your offspring. Worse still, sleep leaves you vulnerable to predation. Sleep is surely one of the most puzzling of all human behaviors. On any one of these grounds—never mind all of them in combination— there ought to have been a strong evolutionary pressure to prevent the emergence of sleep or anything remotely like it. As one sleep scientist has said, “If sleep does not serve an absolutely vital function, then it is the biggest mistake the evolutionary process has ever made.”III Yet sleep has persisted. Heroically so. Indeed, every species studied to date sleeps.IV This simple fact establishes that sleep evolved with—or very soon after—life itself on our planet. Moreover, the subsequent perseverance of sleep throughout evolution means there must be tremendous benefits that far outweigh all of the obvious hazards and detriments. Ultimately, asking “Why do we sleep?” was the wrong question. It implied there was a single function, one holy grail of a reason that we slept, and we went in search of it. Theories ranged from the logical (a time for conserving energy), to the peculiar (an opportunity for eyeball oxygenation), to the psychoanalytic (a non-conscious state in which we fulfill repressed wishes). This book will reveal a very different truth: sleep is infinitely more complex, profoundly more interesting, and alarmingly more health-relevant. We sleep for a rich litany of functions, plural—an abundant constellation of nighttime benefits that service both our brains and our bodies. There does not seem to be one major organ within the body, or process within the brain, that isn’t optimally enhanced by sleep (and detrimentally impaired when we don’t get enough). That we receive such a bounty of health benefits each night should not be surprising. After all, we are awake for two-thirds of our lives, and we don’t just achieve one useful thing during that stretch of time. We accomplish myriad undertakings that promote our own well-being and survival. Why, then, would we expect sleep—and the twenty-five to thirty years, on average, it takes from our lives—to offer one function only? Through an explosion of discoveries over the past twenty years, we have come to realize that evolution did not make a spectacular blunder in conceiving of sleep. Sleep dispenses a multitude of health-ensuring benefits, yours to pick up in repeat prescription every twenty-four hours, should you choose. (Many don’t.) Within the brain, sleep enriches a diversity of functions, including our ability to learn, memorize, and make logical decisions and choices. Benevolently servicing our psychological health, sleep recalibrates our emotional brain circuits, allowing us to navigate next-day social and psychological challenges with cool-headed composure. We are even beginning to understand the most impervious and controversial of all conscious experiences: the dream. Dreaming provides a unique suite of benefits to all species fortunate enough to experience it, humans included. Among these gifts are a consoling neurochemical bath that mollifies painful memories and a virtual reality space in which the brain melds past and present knowledge, inspiring creativity. Downstairs in the body, sleep restocks the armory of our immune system, helping fight malignancy, preventing infection, and warding off all manner of sickness. Sleep reforms the body’s metabolic state by fine-tuning the balance of insulin and circulating glucose. Sleep further regulates our appetite, helping control body weight through healthy food selection rather than rash impulsivity. Plentiful sleep maintains a flourishing microbiome within your gut from which we know so much of our nutritional health begins. Adequate sleep is intimately tied to the fitness of our cardiovascular system, lowering blood pressure while keeping our hearts in fine condition. A balanced diet and exercise are of vital importance, yes. But we now see sleep as the preeminent force in this health trinity. The physical and mental impairments caused by one night of bad sleep dwarf those caused by an equivalent absence of food or exercise. It is difficult to imagine any other state—natural or medically manipulated—that affords a more powerful redressing of physical and mental health at every level of analysis. Based on a rich, new scientific understanding of sleep, we no longer have to ask what sleep is good for. Instead, we are now forced to wonder whether there are any biological functions that do not benefit by a good night’s sleep. So far, the results of thousands of studies insist that no, there aren’t. Emerging from this research renaissance is an unequivocal message: sleep is the single most effective thing we can do to reset our brain and body health each day—Mother Nature’s best effort yet at contra-death. Unfortunately, the real evidence that makes clear all of the dangers that befall individuals and societies when sleep becomes short have not been clearly telegraphed to the public. It is the most glaring omission in the contemporary health conversation. In response, this book is intended to serve as a scientifically accurate intervention addressing this unmet need, and what I hope is a fascinating journey of discoveries. It aims to revise our cultural appreciation of sleep, and reverse our neglect of it. Personally, I should note that I am in love with sleep (not just my own, though I do give myself a non-negotiable eight-hour sleep opportunity each night). I am in love with everything sleep is and does. I am in love with discovering all that remains unknown about it. I am in love with communicating the astonishing brilliance of it to the public. I am in love with finding any and all methods for reuniting humanity with the sleep it so desperately needs. This love affair has now spanned a twenty-plus-year research career that began when I was a professor of psychiatry at Harvard Medical School and continues now that I am a professor of neuroscience and psychology at the University of California, Berkeley. It was not, however, love at first sight. I am an accidental sleep researcher. It was never my intent to inhabit this esoteric outer territory of science. At age eighteen I went to study at the Queen’s Medical Center in England: a prodigious institute in Nottingham boasting a wonderful band of brain scientists on its faculty. Ultimately, medicine wasn’t for me, as it seemed more concerned with answers, whereas I was always more enthralled by questions. For me, answers were simply a way to get to the next question. I decided to study neuroscience, and after graduating, obtained my PhD in neurophysiology supported by a fellowship from England’s Medical Research Council, London. It was during my PhD work that I began making my first real scientific contributions in the field of sleep research. I was examining patterns of electrical brainwave activity in older adults in the early stages of dementia. Counter to common belief, there isn’t just one type of dementia. Alzheimer’s disease is the most common, but is only one of many types. For a number of treatment reasons, it is critical to know which type of dementia an individual is suffering from as soon as possible. I began assessing brainwave activity from my patients during wake and sleep. My hypothesis: there was a unique and specific electrical brain signature that could forecast which dementia subtype each individual was progressing toward. Measurements taken during the day were ambiguous, with no clear signature of difference to be found. Only in the nighttime ocean of sleeping brainwaves did the recordings speak out a clear labeling of my patients saddening disease fate. The discovery proved that sleep could potentially be used as a new early diagnostic litmus test to understand which type of dementia an individual would develop. Sleep became my obsession. The answer it had provided me, like all good answers, only led to more fascinating questions, among them: Was the disruption of sleep in my patients actually contributing to the diseases they were suffering from, and even causing some of their terrible symptoms, such as memory loss, aggression, hallucinations, delusions? I read all I could. A scarcely believable truth began to emerge—nobody actually knew the clear reason why we needed sleep, and what it does. I could not answer my own question about dementia if this fundamental first question remained unanswered. I decided I would try to crack the code of sleep. I halted my research in dementia and, for a post-doctoral position that took me across the Atlantic Ocean to Harvard, set about addressing one of the most enigmatic puzzles of humanity—one that had eluded some of the best scientists in history: Why do we sleep? With genuine na?vet?, not hubris, I believed I would find the answer within two years. That was twenty years ago. Hard problems care little about what motivates their interrogators; they meter out their lessons of difficulty all the same. Now, after two decades of my own research efforts, combined with thousands of studies from other laboratories around the world, we have many of the answers. These discoveries have taken me on wonderful, privileged, and unexpected journeys inside and outside of academia—from being a sleep consultant for the NBA, NFL, and British Premier League football teams; to Pixar Animation, government agencies, and well-known technology and financial companies; to taking part in and helping make several mainstream television programs and documentaries. These sleep revelations, together with many similar discoveries from my fellow sleep scientists, will offer all the proof you need about the vital importance of sleep. A final comment on the structure of this book. The chapters are written in a logical order, traversing a narrative arc in four main parts. Part 1 demystifies this beguiling thing called sleep: what it is, what it isn’t, who sleeps, how much they sleep, how human beings should sleep (but are not), and how sleep changes across your life span or that of your child, for better and for worse. Part 2 details the good, the bad, and the deathly of sleep and sleep loss. We will explore all of the astonishing benefits of sleep for brain and for body, affirming what a remarkable Swiss Army knife of health and wellness sleep truly is. Then we turn to how and why a lack of sufficient sleep leads to a quagmire of ill health, disease, and untimely death—a wakeup call to sleep if ever there was one. Part 3 offers safe passage from sleep to the fantastical world of dreams scientifically explained. From peering into the brains of dreaming individuals, and precisely how dreams inspire Nobel Prize–winning ideas that transform the world, to whether or not dream control really is possible, and if such a thing is even wise—all will be revealed. Part 4 seats us first at the bedside, explaining numerous sleep disorders, including insomnia. I will unpack the obvious and not-so-obvious reasons for why so many of us find it difficult to get a good night’s sleep, night after night. A frank discussion of sleeping pills then follows, based on scientific and clinical data rather than hearsay or branding messages. Details of new, safer, and more effective non-drug therapies for better sleep will then be advised. Transitioning from bedside up to the level of sleep in society, we will subsequently learn of the sobering impact that insufficient sleep has in education, in medicine and health care, and in business. The evidence shatters beliefs about the usefulness of long waking hours with little sleep in effectively, safely, profitably, and ethically accomplishing the goals of each of these disciplines. Concluding the book with genuine optimistic hope, I lay out a road map of ideas that can reconnect humanity with the sleep it remains so bereft of—a new vision for sleep in the twenty-first century. I should point out that you need not read this book in this progressive, four-part narrative arc. Each chapter can, for the most part, be read individually, and out of order, without losing too much of its significance. I therefore invite you to consume the book in whole or in part, buffet-style or in order, all according to your personal taste. In closing, I offer a disclaimer. Should you feel drowsy and fall asleep while reading the book, unlike most authors, I will not be disheartened. Indeed, based on the topic and content of this book, I am actively going to encourage that kind of behavior from you. Knowing what I know about the relationship between sleep and memory, it is the greatest form of flattery for me to know that you, the reader, cannot resist the urge to strengthen and thus remember what I am telling you by falling asleep. So please, feel free to ebb and flow into and out of consciousness during this entire book. I will take absolutely no offense. On the contrary, I would be delighted. I.The World Health Organization and the National Sleep Foundation both stipulate an average of eight hours of sleep per night for adults. II.Sleepless in America, National Geographic, http://channel.nationalgeographic.com/sleepless-inamerica/episode/sleepless-in-america. III.Dr. Allan Rechtschaffen. IV.Kushida, C. Encyclopedia of Sleep, Volume 1 (Elsever, 2013).? CHAPTER 2 Caffeine, Jet Lag, and Melatonin Losing and Gaining Control of Your Sleep Rhythm How does your body know when it’s time to sleep? Why do you suffer from jet lag after arriving in a new time zone? How do you overcome jet lag? Why does that acclimatization cause you yet more jet lag upon returning home? Why do some people use melatonin to combat these issues? Why (and how) does a cup of coffee keep you awake? Perhaps most importantly, how do you know if you’re getting enough sleep? There are two main factors that determine when you want to sleep and when you want to be awake. As you read these very words, both factors are powerfully influencing your mind and body. The first factor is a signal beamed out from your internal twenty-four-hour clock located deep within your brain. The clock creates a cycling, day-night rhythm that makes you feel tired or alert at regular times of night and day, respectively. The second factor is a chemical substance that builds up in your brain and creates a “sleep pressure.” The longer you’ve been awake, the more that chemical sleep pressure accumulates, and consequentially, the sleepier you feel. It is the balance between these two factors that dictates how alert and attentive you are during the day, when you will feel tired and ready for bed at night, and, in part, how well you will sleep. GOT RHYTHM? Central to many of the questions in the opening paragraph is the powerful sculpting force of your twenty-four-hour rhythm, also known as your circadian rhythm. Everyone generates a circadian rhythm (circa, meaning “around,” and dian, derivative of diam, meaning “day”). Indeed, every living creature on the planet with a life span of more than several days generates this natural cycle. The internal twenty-four-hour clock within your brain communicates its daily circadian rhythm signal to every other region of your brain and every organ in your body. Your twenty-four-hour tempo helps to determine when you want to be awake and when you want to be asleep. But it controls other rhythmic patterns, too. These include your timed preferences for eating and drinking, your moods and emotions, the amount of urine you produce,I your core body temperature, your metabolic rate, and the release of numerous hormones. It is no coincidence that the likelihood of breaking an Olympic record has been clearly tied to time of day, being maximal at the natural peak of the human circadian rhythm in the early afternoon. Even the timing of births and deaths demonstrates circadian rhythmicity due to the marked swings in key life-dependent metabolic, cardiovascular, temperature, and hormonal processes that this pacemaker controls. Long before we discovered this biological pacemaker, an ingenious experiment did something utterly remarkable: stopped time—at least, for a plant. It was in 1729 when French geophysicist JeanJacques d’Ortous de Mairan discovered the very first evidence that plants generate their own internal time. De Mairan was studying the leaf movements of a species that displayed heliotropism: when a plant’s leaves or flowers track the trajectory of the sun as it moves across the sky during the day. De Mairan was intrigued by one plant in particular, called Mimosa pudica.II Not only do the leaves of this plant trace the arching daytime passage of the sun across the sky’s face, but at night, they collapse down, almost as though they had wilted. Then, at the start of the following day, the leaves pop open once again like an umbrella, healthy as ever. This behavior repeats each and every morning and evening, and it caused the famous evolutionary biologist Charles Darwin to call them “sleeping leaves.” Prior to de Mairan’s experiment, many believed that the expanding and retracting behavior of the plant was solely determined by the corresponding rising and setting of the sun. It was a logical assumption: daylight (even on cloudy days) triggered the leaves to open wide, while ensuing darkness instructed the leaves to shut up shop, close for business, and fold away. That assumption was shattered by de Mairan. First, he took the plant and placed it out in the open, exposing it to the signals of light and dark associated with day and night. As expected, the leaves expanded during the light of day and retracted with the dark of night. Then came the genius twist. De Mairan placed the plant in a sealed box for the next twenty-fourhour period, plunging it into total dark for both day and night. During these twenty-four hours of blackness, he would occasionally take a peek at the plant in controlled darkness, observing the state of the leaves. Despite being cut off from the influence of light during the day, the plant still behaved as though it were being bathed in sunlight; its leaves were proudly expanded. Then, it retracted its leaves as if on cue at the end of the day, even without the sun’s setting signal, and they stayed collapsed throughout the entire night. It was a revolutionary discovery: de Mairan had shown that a living organism kept its own time, and was not, in fact, slave to the sun’s rhythmic commands. Somewhere within the plant was a twenty-four-hour rhythm generator that could track time without any cues from the outside world, such as daylight. The plant didn’t just have a circadian rhythm, it had an “endogenous,” or selfgenerated, rhythm. It is much like your heart drumming out its own self-generating beat. The difference is simply that your heart’s pacemaker rhythm is far faster, usually beating at least once a second, rather than once every twenty-four-hour period like the circadian clock. Surprisingly, it took another two hundred years to prove that we humans have a similar, internally generated circadian rhythm. But this experiment added something rather unexpected to our understanding of internal timekeeping. It was 1938, and Professor Nathaniel Kleitman at the University of Chicago, accompanied by his research assistant Bruce Richardson, were to perform an even more radical scientific study. It required a type of dedication that is arguably without match or comparison to this day. Kleitman and Richardson were to be their own experimental guinea pigs. Loaded with food and water for six weeks and a pair of dismantled, high-standing hospital beds, they took a trip into Mammoth Cave in Kentucky, one of the deepest caverns on the planet—so deep, in fact, that no detectable sunlight penetrates its farthest reaches. It was from this darkness that Kleitman and Richardson were to illuminate a striking scientific finding that would define our biological rhythm as being approximately one day (circadian), and not precisely one day. In addition to food and water, the two men brought a host of measuring devices to assess their body temperatures, as well as their waking and sleeping rhythms. This recording area formed the heart of their living space, flanked either side by their beds. The tall bed legs were each seated in a bucket of water, castle-moat style, to discourage the innumerable small (and not so small) creatures lurking in the depths of Mammoth Cave from joining them in bed. The experimental question facing Kleitman and Richardson was simple: When cut off from the daily cycle of light and dark, would their biological rhythms of sleep and wakefulness, together with body temperature, become completely erratic, or would they stay the same as those individuals in the outside world exposed to rhythmic daylight? In total, they lasted thirty-two days in complete darkness. Not only did they aggregate some impressive facial hair, but they made two groundbreaking discoveries in the process. The first was that humans, like de Mairan’s heliotrope plants, generated their own endogenous circadian rhythm in the absence of external light from the sun. That is, neither Kleitman nor Richardson descended into random spurts of wake and sleep, but instead expressed a predictable and repeating pattern of prolonged wakefulness (about fifteen hours), paired with consolidated bouts of about nine hours of sleep. The second unexpected—and more profound—result was that their reliably repeating cycles of wake and sleep were not precisely twenty-four hours in length, but consistently and undeniably longer than twenty-four hours. Richardson, in his twenties, developed a sleep-wake cycle of between twentysix and twenty-eight hours in length. That of Kleitman, in his forties, was a little closer to, but still longer than, twenty-four hours. Therefore, when removed from the external influence of daylight, the internally generated “day” of each man was not exactly twenty-four hours, but a little more than that. Like an inaccurate wristwatch whose time runs long, with each passing (real) day in the outside world, Kleitman and Richardson began to add time based on their longer, internally generated chronometry. Since our innate biological rhythm is not precisely twenty-four hours, but thereabouts, a new nomenclature was required: the circadian rhythm—that is, one that is approximately, or around, one day in length, and not precisely one day.III In the seventy-plus years since Kleitman and Richardson’s seminal experiment, we have now determined that the average duration of a human adult’s endogenous circadian clock runs around twenty-four hours and fifteen minutes in length. Not too far off the twenty-four-hour rotation of the Earth, but not the precise timing that any self-respecting Swiss watchmaker would ever accept. Thankfully, most of us don’t live in Mammoth Cave, or the constant darkness it imposes. We routinely experience light from the sun that comes to the rescue of our imprecise, overrunning internal circadian clock. Sunlight acts like a manipulating finger and thumb on the side-dial of an imprecise wristwatch. The light of the sun methodically resets our inaccurate internal timepiece each and every day, “winding” us back to precisely, not approximately, twenty-four hours.IV It is no coincidence that the brain uses daylight for this resetting purpose. Daylight is the most reliable, repeating signal that we have in our environment. Since the birth of our planet, and every single day thereafter without fail, the sun has always risen in the morning and set in the evening. Indeed, the reason most living species likely adopted a circadian rhythm is to synchronize themselves and their activities, both internal (e.g., temperature) and external (e.g., feeding), with the daily orbital mechanics of planet Earth spinning on its axis, resulting in regular phases of light (sun facing) and dark (sun hiding). Yet daylight isn’t the only signal that the brain can latch on to for the purpose of biological clock resetting, though it is the principal and preferential signal, when present. So long as they are reliably repeating, the brain can also use other external cues, such as food, exercise, temperature fluctuations, and even regularly timed social interaction. All of these events have the ability to reset the biological clock, allowing it to strike a precise twenty-four-hour note. It is the reason that individuals with certain forms of blindness do not entirely lose their circadian rhythm. Despite not receiving light cues due to their blindness, other phenomena act as their resetting triggers. Any signal that the brain uses for the purpose of clock resetting is termed a zeitgeber, from the German “time giver” or “synchronizer.” Thus, while light is the most reliable and thus the primary zeitgeber, there are many factors that can be used in addition to, or in the absence of, daylight. The twenty-four-hour biological clock sitting in the middle of your brain is called the suprachiasmatic (pronounced soo-pra-kai-as-MAT-ik) nucleus. As with much of anatomical language, the name, while far from easy to pronounce, is instructional: supra, meaning above, and chiasm, meaning a crossing point. The crossing point is that of the optic nerves coming from your eyeballs. Those nerves meet in the middle of your brain, and then effectively switch sides. The suprachiasmatic nucleus is located just above this intersection for a good reason. It “samples” the light signal being sent from each eye along the optic nerves as they head toward the back of the brain for visual processing. The suprachiasmatic nucleus uses this reliable light information to reset its inherent time inaccuracy to a crisp twenty-four-hour cycle, preventing any drift. When I tell you that the suprachiasmatic nucleus is composed of 20,000 brain cells, or neurons, you might assume it is enormous, consuming a vast amount of your cranial space, but actually it is tiny. The brain is composed of approximately 100 billion neurons, making the suprachiasmatic nucleus minuscule in the relative scheme of cerebral matter. Yet despite its stature, the influence of the suprachiasmatic nucleus on the rest of the brain and the body is anything but meek. This tiny clock is the central conductor of life’s biological rhythmic symphony—yours and every other living species. The suprachiasmatic nucleus controls a vast array of behaviors, including our focus in this chapter: when you want to be awake and asleep. For diurnal species that are active during the day, such as humans, the circadian rhythm activates many brain and body mechanisms in the brain and body during daylight hours that are designed to keep you awake and alert. These processes are then ratcheted down at nighttime, removing that alerting influence. Figure 1 shows one such example of a circadian rhythm—that of your body temperature. It represents average core body temperature (rectal, no less) of a group of human adults. Starting at “12 pm” on the far left, body temperature begins to rise, peaking late in the afternoon. The trajectory then changes. Temperature begins to decline again, dropping below that of the midday start-point as bedtime approaches. Your biological circadian rhythm coordinates a drop in core body temperature as you near typical bedtime (figure 1), reaching its nadir, or low point, about two hours after sleep onset. However, this temperature rhythm is not dependent upon whether you are actually asleep. If I were to keep you awake all night, your core body temperature would still show the same pattern. Although the temperature drop helps to initiate sleep, the temperature change itself will rise and fall across the twenty-four-hour period regardless of whether you are awake or asleep. It is a classic demonstration of a preprogrammed circadian rhythm that will repeat over and over without fail, like a metronome. Temperature is just one of many twenty-four-hour rhythms that the suprachiasmatic nucleus governs. Wakefulness and sleep are another. Wakefulness and sleep are therefore under the control of the circadian rhythm, and not the other way around. That is, your circadian rhythm will march up and down every twenty-four hours irrespective of whether you have slept or not. Your circadian rhythm is unwavering in this regard. But look across individuals, and you discover that not everyone’s circadian timing is the same. MY RHYTHM IS NOT YOUR RHYTHM Although every human being displays an unyielding twenty-four-hour pattern, the respective peak and trough points are strikingly different from one individual to the next. For some people, their peak of wakefulness arrives early in the day, and their sleepiness trough arrives early at night. These are “morning types,” and make up about 40 percent of the populace. They prefer to wake at or around dawn, are happy to do so, and function optimally at this time of day. Others are “evening types,” and account for approximately 30 percent of the population. They naturally prefer going to bed late and subsequently wake up late the following morning, or even in the afternoon. The remaining 30 percent of people lie somewhere in between morning and evening types, with a slight leaning toward eveningness, like myself. You may colloquially know these two types of people as “morning larks” and “night owls,” respectively. Unlike morning larks, night owls are frequently incapable of falling asleep early at night, no matter how hard they try. It is only in the early-morning hours that owls can drift off. Having not fallen asleep until late, owls of course strongly dislike waking up early. They are unable to function well at this time, one cause of which is that, despite being “awake,” their brain remains in a more sleep-like state throughout the early morning. This is especially true of a region called the prefrontal cortex, which sits above the eyes, and can be thought of as the head office of the brain. The prefrontal cortex controls high-level thought and logical reasoning, and helps keep our emotions in check. When a night owl is forced to wake up too early, their prefrontal cortex remains in a disabled, “offline” state. Like a cold engine after an early-morning start, it takes a long time before it warms up to operating temperature, and before that will not function efficiently. An adult’s owlness or larkness, also known as their chronotype, is strongly determined by genetics. If you are a night owl, it’s likely that one (or both) of your parents is a night owl. Sadly, society treats night owls rather unfairly on two counts. First is the label of being lazy, based on a night owl’s wont to wake up later in the day, due to the fact that they did not fall asleep until the early-morning hours. Others (usually morning larks) will chastise night owls on the erroneous assumption that such preferences are a choice, and if they were not so slovenly, they could easily wake up early. However, night owls are not owls by choice. They are bound to a delayed schedule by unavoidable DNA hardwiring. It is not their conscious fault, but rather their genetic fate. Second is the engrained, un-level playing field of society’s work scheduling, which is strongly biased toward early start times that punish owls and favor larks. Although the situation is improving, standard employment schedules force owls into an unnatural sleep-wake rhythm. Consequently, job performance of owls as a whole is far less optimal in the mornings, and they are further prevented from expressing their true performance potential in the late afternoon and early evening as standard work hours end prior to its arrival. Most unfortunately, owls are more chronically sleep-deprived, having to wake up with the larks, but not being able to fall asleep until far later in the evening. Owls are thus often forced to burn the proverbial candle at both ends. Greater ill health caused by a lack of sleep therefore befalls owls, including higher rates of depression, anxiety, diabetes, cancer, heart attack, and stroke. In this regard, a societal change is needed, offering accommodations not dissimilar to those we make for other physically determined differences (e.g., sight impaired). We require more supple work schedules that better adapt to all chronotypes, and not just one in its extreme. You may be wondering why Mother Nature would program this variability across people. As a social species, should we not all be synchronized and therefore awake at the same time to promote maximal human interactions? Perhaps not. As we’ll discover later in this book, humans likely evolved to co-sleep as families or even whole tribes, not alone or as couples. Appreciating this evolutionary context, the benefits of such genetically programmed variation in sleep/wake timing preferences can be understood. The night owls in the group would not be going to sleep until one or two a.m., and not waking until nine or ten a.m. The morning larks, on the other hand, would have retired for the night at nine p.m. and woken at five a.m. Consequently, the group as a whole is only collectively vulnerable (i.e., every person asleep) for just four rather than eight hours, despite everyone still getting the chance for eight hours of sleep. That’s potentially a 50 percent increase in survival fitness. Mother Nature would never pass on a biological trait—here, the useful variability in when individuals within a collective tribe go to sleep and wake up—that could enhance the survival safety and thus fitness of a species by this amount. And so she hasn’t. MELATONIN Your suprachiasmatic nucleus communicates its repeating signal of night and day to your brain and body using a circulating messenger called melatonin. Melatonin has other names, too. These include “the hormone of darkness” and “the vampire hormone.” Not because it is sinister, but simply because melatonin is released at night. Instructed by the suprachiasmatic nucleus, the rise in melatonin begins soon after dusk, being released into the bloodstream from the pineal gland, an area situated deep in the back of your brain. Melatonin acts like a powerful bullhorn, shouting out a clear message to the brain and body: “It’s dark, it’s dark!” At this moment, we have been served a writ of nightime, and with it, a biological command for the timing of sleep onset.V In this way, melatonin helps regulate the timing of when sleep occurs by systemically signaling darkness throughout the organism. But melatonin has little influence on the generation of sleep itself: a mistaken assumption that many people hold. To make clear this distinction, think of sleep as the Olympic 100-meter race. Melatonin is the voice of the timing official that says “Runners, on your mark,” and then fires the starting pistol that triggers the race. That timing official (melatonin) governs when the race (sleep) begins, but does not participate in the race. In this analogy, the sprinters themselves are other brain regions and processes that actively generate sleep. Melatonin corrals these sleep-generating regions of the brain to the starting line of bedtime. Melatonin simply provides the official instruction to commence the event of sleep, but does not participate in the sleep race itself. For these reasons, melatonin is not a powerful sleeping aid in and of itself, at least not for healthy, non-jet-lagged individuals (we’ll explore jet lag—and how melatonin can be helpful—in a moment). There may be little, if any, quality melatonin in the pill. That said, there is a significant sleep placebo effect of melatonin, which should not be underestimated: the placebo effect is, after all, the most reliable effect in all of pharmacology. Equally important to realize is the fact that over-the-counter melatonin is not commonly regulated by governing bodies around the world, such as the US Food and Drug Administration (FDA). Scientific evaluations of over-the-counter brands have found melatonin concentrations that range from 83 percent less than that claimed on the label, to 478 percent more than that stated.VI Once sleep is under way, melatonin slowly decreases in concentration across the night and into the morning hours. With dawn, as sunlight enters the brain through the eyes (even through the closed lids), a brake pedal is applied to the pineal gland, thereby shutting off the release of melatonin. The absence of circulating melatonin now informs the brain and body that the finish line of sleep has been reached. It is time to call the race of sleep over and allow active wakefulness to return for the rest of the day. In this regard, we human beings are “solar powered.” Then, as light fades, so, too, does the solar brake pedal blocking melatonin. As melatonin rises, another phase of darkness is signaled and another sleep event is called to the starting line. You can see a typical profile of melatonin release in figure 2. It starts a few hours after dusk. Then it rapidly rises, peaking around four a.m. Thereafter, it begins to drop as dawn approaches, falling to levels that are undetectable by early to midmorning. HAVE RHYTHM, WON’T TRAVEL The advent of the jet engine was a revolution for the mass transit of human beings around the planet. However, it created an unforeseen biological calamity: jet planes offered the ability to speed through time zones faster than our twenty-four-hour internal clocks could ever keep up with or adjust to. Those jets caused a biological time lag: jet lag. As a result, we feel tired and sleepy during the day in a distant time zone because our internal clock still thinks it is nighttime. It hasn’t yet caught up. If that were not bad enough, at night, we are frequently unable to initiate or maintain sleep because our internal clock now believes it to be daytime. Take the example of my recent flight home to England from San Francisco. London is eight hours ahead of San Francisco. When I arrive in England, despite the digital clock in London’s Heathrow Airport telling me it is nine a.m., my internal circadian clock is registering a very different time— California time, which is one a.m. I should be fast asleep. I will drag my time-lagged brain and body through the London day in a state of deep lethargy. Every aspect of my biology is demanding sleep; sleep that most people back in California are being swaddled in at this time. The worst, however, is yet to come. By midnight London time, I am in bed, tired and wanting to fall asleep. But unlike most people in London, I can’t seem to drift off. Though it is midnight in London, my internal biological clock believes it to be four p.m., which it is in California. I would normally be wide awake, and so I am, lying in bed in London. It will be five or six hours before my natural tendency to fall asleep arrives . . . just as London is starting to wake up, and I have to give a public lecture. What a mess. This is jet lag: you feel tired and sleepy during the day in the new time zone because your body clock and associated biology still “think” it is nighttime. At night, you are frequently unable to sleep solidly because your biological rhythm still believes it to be daytime. Fortunately, my brain and body will not stay in this mismatched limbo forever. I will acclimatize to London time by way of the sunlight signals in the new location. But it’s a slow process. For every day you are in a different time zone, your suprachiasmatic nucleus can only readjust by about one hour. It therefore took me about eight days to readjust to London time after having been in San Francisco, since London is eight hours ahead of San Francisco. Sadly, after such epic efforts by my suprachiasmatic nucleus’s twenty-four-hour clock to drag itself forward in time and get settled in London, it faces some depressing news: I now have to fly back to San Francisco after nine days. My poor biological clock has to suffer this struggle all over again in the reverse direction! You may have noticed that it feels harder to acclimate to a new time zone when traveling eastward than when flying westward. There are two reasons for this. First, the eastward direction requires that you fall asleep earlier than you would normally, which is a tall biological order for the mind to simply will into action. In contrast, the westward direction requires you to stay up later, which is a consciously and pragmatically easier prospect. Second, you will remember that when shut off from any outside world influences, our natural circadian rhythm is innately longer than one day—about twenty-four hours and fifteen minutes. Modest as this may be, this makes it somewhat easier for you to artificially stretch a day than shrink it. When you travel westward—in the direction of your innately longer internal clock—that “day” is longer than twenty-four hours for you and why it feels a little easier to accommodate to. Eastward travel, however, which involves a “day” that is shorter in length for you than twenty-four hours, goes against the grain of your innately long internal rhythm to start with, which is why it is rather harder to do. West or east, jet lag still places a torturous physiological strain on the brain, and a deep biological stress upon the cells, organs, and major systems of the body. And there are consequences. Scientists have studied airplane cabin crews who frequently fly on long-haul routes and have little chance to recover. Two alarming results have emerged. First, parts of their brains—specifically those related to learning and memory—had physically shrunk, suggesting the destruction of brain cells caused by the biological stress of time-zone travel. Second, their short-term memory was significantly impaired. They were considerably more forgetful than individuals of similar age and background who did not frequently travel through time zones. Other studies of pilots, cabin crew members, and shift workers have reported additionally disquieting consequences, including far higher rates of cancer and type 2 diabetes than the general population—or even carefully controlled match individuals who do not travel as much. Based on these deleterious effects, you can appreciate why some people faced with frequent jet lag, including airline pilots and cabin crew, would want to limit such misery. Often, they choose to take melatonin pills in an attempt to help with the problem. Recall my flight from San Francisco to London. After arriving that day, I had real difficulty getting to sleep and staying asleep that night. In part, this was because melatonin was not being released during my nighttime in London. My melatonin rise was still many hours away, back on California time. But let’s imagine that I was going to use a legitimate compound of melatonin after arriving in London. Here’s how it works: at around seven to eight p.m. London time I would take a melatonin pill, triggering an artificial rise in circulating melatonin that mimics the natural melatonin spike currently occurring in most of the people in London. As a consequence, my brain is fooled into believing it’s nighttime, and with that chemically induced trick comes the signaled timing of the sleep race. It will still be a struggle to generate the event of sleep itself at this irregular time (for me), but the timing signal does significantly increase the likelihood of sleep in this jet-lagged context. SLEEP PRESSURE AND CAFFEINE Your twenty-four-hour circadian rhythm is the first of the two factors determining wake and sleep. The second is sleep pressure. At this very moment, a chemical called adenosine is building up in your brain. It will continue to increase in concentration with every waking minute that elapses. The longer you are awake, the more adenosine will accumulate. Think of adenosine as a chemical barometer that continuously registers the amount of elapsed time since you woke up this morning. One consequence of increasing adenosine in the brain is an increasing desire to sleep. This is known as sleep pressure, and it is the second force that will determine when you feel sleepy, and thus should go to bed. Using a clever dual-action effect, high concentrations of adenosine simultaneously turn down the “volume” of wake-promoting regions in the brain and turn up the dial on sleepinducing regions. As a result of that chemical sleep pressure, when adenosine concentrations peak, an irresistible urge for slumber will take hold.VII It happens to most people after twelve to sixteen hours of being awake. You can, however, artificially mute the sleep signal of adenosine by using a chemical that makes you feel more alert and awake: caffeine. Caffeine is not a food supplement. Rather, caffeine is the most widely used (and abused) psychoactive stimulant in the world. It is the second most traded commodity on the planet, after oil. The consumption of caffeine represents one of the longest and largest unsupervised drug studies ever conducted on the human race, perhaps rivaled only by alcohol, and it continues to this day. Caffeine works by successfully battling with adenosine for the privilege of latching on to adenosine welcome sites—or receptors—in the brain. Once caffeine occupies these receptors, however, it does not stimulate them like adenosine, making you sleepy. Rather, caffeine blocks and effectively inactivates the receptors, acting as a masking agent. It’s the equivalent of sticking your fingers in your ears to shut out a sound. By hijacking and occupying these receptors, caffeine blocks the sleepiness signal normally communicated to the brain by adenosine. The upshot: caffeine tricks you into feeling alert and awake, despite the high levels of adenosine that would otherwise seduce you into sleep. Levels of circulating caffeine peak approximately thirty minutes after oral administration. What is problematic, though, is the persistence of caffeine in your system. In pharmacology, we use the term “half-life” when discussing a drug’s efficacy. This simply refers to the length of time it takes for the body to remove 50 percent of a drug’s concentration. Caffeine has an average half-life of five to seven hours. Let’s say that you have a cup of coffee after your evening dinner, around 7:30 p.m. This means that by 1:30 a.m., 50 percent of that caffeine may still be active and circulating throughout your brain tissue. In other words, by 1:30 a.m., you’re only halfway to completing the job of cleansing your brain of the caffeine you drank after dinner. There’s nothing benign about that 50 percent mark, either. Half a shot of caffeine is still plenty powerful, and much more decomposition work lies ahead throughout the night before caffeine disappears. Sleep will not come easily or be smooth throughout the night as your brain continues its battle against the opposing force of caffeine. Most people do not realize how long it takes to overcome a single dose of caffeine, and therefore fail to make the link between the bad night of sleep we wake from in the morning and the cup of coffee we had ten hours earlier with dinner. Caffeine—which is not only prevalent in coffee, certain teas, and many energy drinks, but also foods such as dark chocolate and ice cream, as well as drugs such as weight-loss pills and pain relievers—is one of the most common culprits that keep people from falling asleep easily and sleeping soundly thereafter, typically masquerading as insomnia, an actual medical condition. Also be aware that de-caffeinated does not mean non-caffeinated. One cup of decaf usually contains 15 to 30 percent of the dose of a regular cup of coffee, which is far from caffeine-free. Should you drink three to four cups of decaf in the evening, it is just as damaging to your sleep as one regular cup of coffee. The “jolt” of caffeine does wear off. Caffeine is removed from your system by an enzyme within your liver,VIII which gradually degrades it over time. Based in large part on genetics,IX some people have a more efficient version of the enzyme that degrades caffeine, allowing the liver to rapidly clear it from the bloodstream. These rare individuals can drink an espresso with dinner and fall fast asleep at midnight without a problem. Others, however, have a slower-acting version of the enzyme. It takes far longer for their system to eliminate the same amount of caffeine. As a result, they are very sensitive to caffeine’s effects. One cup of tea or coffee in the morning will last much of the day, and should they have a second cup, even early in the afternoon, they will find it difficult to fall asleep in the evening. Aging also alters the speed of caffeine clearance: the older we are, the longer it takes our brain and body to remove caffeine, and thus the more sensitive we become in later life to caffeine’s sleepdisrupting influence. If you are trying to stay awake late into the night by drinking coffee, you should be prepared for a nasty consequence when your liver successfully evicts the caffeine from your system: a phenomenon commonly known as a “caffeine crash.” Like the batteries running down on a toy robot, your energy levels plummet rapidly. You find it difficult to function and concentrate, with a strong sense of sleepiness once again. We now understand why. For the entire time that caffeine is in your system, the sleepiness chemical it blocks (adenosine) nevertheless continues to build up. Your brain is not aware of this rising tide of sleep-encouraging adenosine, however, because the wall of caffeine you’ve created is holding it back from your perception. But once your liver dismantles that barricade of caffeine, you feel a vicious backlash: you are hit with the sleepiness you had experienced two or three hours ago before you drank that cup coffee plus all the extra adenosine that has accumulated in the hours in between, impatiently waiting for caffeine to leave. When the receptors become vacant by way of caffeine decomposition, adenosine rushes back in and smothers the receptors. When this happens, you are assaulted with a most forceful adenosine-trigger urge to sleep—the aforementioned caffeine crash. Unless you consume even more caffeine to push back against the weight of adenosine, which would start a dependency cycle, you are going to find it very, very difficult to remain awake. To impress upon you the effects of caffeine, I footnote esoteric research conducted in the 1980s by NASA. Their scientists exposed spiders to different drugs and then observed the webs that they constructed.X Those drugs included LSD, speed (amphetamine), marijuana, and caffeine. The results, which speak for themselves, can be observed in figure 3. The researchers noted how strikingly incapable the spiders were in constructing anything resembling a normal or logical web that would be of any functional use when given caffeine, even relative to other potent drugs tested. It is worth pointing out that caffeine is a stimulant drug. Caffeine is also the only addictive substance that we readily give to our children and teens—the consequences of which we will return to later in the book. IN STEP, OUT OF STEP Setting caffeine aside for a moment, you may have assumed that the two governing forces that regulate your sleep—the twenty-four-hour circadian rhythm of the suprachiasmatic nucleus and the sleep-pressure signal of adenosine—communicate with each other so as to unite their influences. In actual fact, they don’t. They are two distinct and separate systems that are ignorant of each other. They are not coupled; though, they are usually aligned. Figure 4 encompasses forty-eight hours of time from left to right—two days and two nights. The dotted line in the figure is the circadian rhythm, also known as Process-C. Like a sine wave, it reliably and repeatedly rises and falls, and then rises and falls once more. Starting on the far left of the figure, the circadian rhythm begins to increase its activity a few hours before you wake up. It infuses the brain and body with an alerting energy signal. Think of it like a rousing marching band approaching from a distance. At first, the signal is faint, but gradually it builds, and builds, and builds with time. By early afternoon in most healthy adults, the activating signal from the circadian rhythm peaks. Now let us consider what is happening to the other sleep-controlling factor: adenosine. Adenosine creates a pressure to sleep, also known as Process-S. Represented by the solid line in figure 4, the longer you are awake, the more adenosine builds up, creating an increasing urge (pressure) to sleep. By mid- to late morning, you have only been awake for a handful of hours. As a result, adenosine concentrations have increased only a little. Furthermore, the circadian rhythm is on its powerful upswing of alertness. This combination of strong activating output from the circadian rhythm together with low levels of adenosine result in a delightful sensation of being wide awake. (Or at least it should, so long as your sleep was of good quality and sufficient length the night before. If you feel as though you could fall asleep easily midmorning, you are very likely not getting enough sleep, or the quality of your sleep is insufficient.) The distance between the curved lines above will be a direct reflection of your desire to sleep. The larger the distance between the two, the greater your sleep desire. For example, at eleven a.m., after having woken up at eight a.m., there is only a small distance between the dotted line (circadian rhythm) and solid line (sleep pressure), illustrated by the vertical double arrow in figure 5. This minimal difference means there is a weak sleep drive, and a strong urge to be awake and alert. However, by eleven p.m. it’s a very different situation, as illustrated in figure 6. You’ve now been awake for fifteen hours and your brain is drenched in high concentrations of adenosine (note how the solid line in the figure has risen sharply). In addition, the dotted line of the circadian rhythm is descending, powering down your activity and alertness levels. As a result, the difference between the two lines has grown large, reflected in the long vertical double arrow in figure 6. This powerful combination of abundant adenosine (high sleep pressure) and declining circadian rhythm (lowered activity levels) triggers a strong desire for sleep. What happens to all of the accumulated adenosine once you do fall asleep? During sleep, a mass evacuation gets under way as the brain has the chance to degrade and remove the day’s adenosine. Across the night, sleep lifts the heavy weight of sleep pressure, lightening the adenosine load. After approximately eight hours of healthy sleep in an adult, the adenosine purge is complete. Just as this process is ending, the marching band of your circadian activity rhythm has fortuitously returned, and its energizing influence starts to approach. When these two processes trade places in the morning hours, wherein adenosine has been removed and the rousing volume of the circadian rhythm is becoming louder (indicated by the meeting of the two lines in figure 6), we naturally wake up (seven a.m. on day two, in the figure example). Following that full night of sleep, you are now ready to face another sixteen hours of wakefulness with physical vigor and sharp brain function. INDEPENDENCE DAY, AND NIGHT Have you ever pulled an “all-nighter”—forgoing sleep and remaining awake throughout the following day? If you have, and can remember much of anything about it, you may recall that there were times when you felt truly miserable and sleepy, yet there were other moments when, despite having been awake for longer, you paradoxically felt more alert. Why? I don’t advise anyone to conduct this selfexperiment, but assessing a person’s alertness across twenty-four hours of total sleep deprivation is one way that scientists can demonstrate that the two forces determining when you want to be awake and asleep—the twenty-four-hour circadian rhythm and the sleepiness signal of adenosine—are independent, and can be decoupled from their normal lockstep. Let’s consider figure 7, showing the same forty-eight-hour slice of time and the two factors in question: the twenty-four-hour circadian rhythm and the sleep pressure signal of adenosine, and how much distance there is between them. In this scenario, our volunteer is going to stay awake all night and all day. As the night of sleep deprivation marches forward, the sleep pressure of adenosine (upper line) rises progressively, like the rising water level in a plugged sink when a faucet has been left on. It will not decline across the night. It cannot, since sleep is absent. By remaining awake, and blocking access to the adenosine drain that sleep opens up, the brain is unable to rid itself of the chemical sleep pressure. The mounting adenosine levels continue to rise. This should mean that the longer you are awake, the sleepier you feel. But that’s not true. Though you will feel increasingly sleepy throughout the nighttime phase, hitting a low point in your alertness around five to six a.m., thereafter, you’ll catch a second wind. How is this possible when adenosine levels and corresponding sleep pressure continue to increase? The answer resides with your twenty-four-hour circadian rhythm, which offers a brief period of salvation from sleepiness. Unlike sleep pressure, your circadian rhythm pays no attention to whether you are asleep or awake. Its slow, rhythmic countenance continues to fall and rise strictly on the basis of what time of night or day it is. No matter what state of adenosine sleepiness pressure exists within the brain, the twenty-four-hour circadian rhythm cycles on as per usual, oblivious to your ongoing lack of sleep. If you look at figure 7 once again, the graveyard-shift misery you experience around six a.m. can be explained by the combination of high adenosine sleep pressure and your circadian rhythm reaching its lowest point. The vertical distance separating these two lines at three a.m. is large, indicated by the first vertical arrow in the figure. But if you can make it past this alertness low point, you’re in for a rally. The morning rise of the circadian rhythm comes to your rescue, marshaling an alerting boost throughout the morning that temporarily offsets the rising levels of adenosine sleep pressure. As your circadian rhythm hits its peak around eleven a.m., the vertical distance between the two respective lines in figure 7 has been decreased. The upshot is that you will feel much less sleepy at eleven a.m. than you did at three a.m., despite being awake for longer. Sadly, this second wind doesn’t last. As the afternoon lumbers on, the circadian rhythm begins to decline as the escalating adenosine piles on the sleep pressure. Come late afternoon and early evening, any temporary alertness boost has been lost. You are hit by the full force of an immense adenosine sleep pressure. By nine p.m., there exists a towering vertical distance between the two lines in figure 7. Short of intravenous caffeine or amphetamine, sleep will have its way, wrestling your brain from the now weak grip of blurry wakefulness, blanketing you in slumber. AM I GETTING ENOUGH SLEEP? Setting aside the extreme case of sleep deprivation, how do you know whether you’re routinely getting enough sleep? While a clinical sleep assessment is needed to thoroughly address this issue, an easy rule of thumb is to answer two simple questions. First, after waking up in the morning, could you fall back asleep at ten or eleven a.m.? If the answer is “yes,” you are likely not getting sufficient sleep quantity and/or quality. Second, can you function optimally without caffeine before noon? If the answer is “no,” then you are most likely self-medicating your state of chronic sleep deprivation. Both of these signs you should take seriously and seek to address your sleep deficiency. They are topics, and a question, that we will cover in depth in chapters 13 and 14 when we speak about the factors that prevent and harm your sleep, as well as insomnia and effective treatments. In general, these un-refreshed feelings that compel a person to fall back asleep midmorning, or require the boosting of alertness with caffeine, are usually due to individuals not giving themselves adequate sleep opportunity time—at least eight or nine hours in bed. When you don’t get enough sleep, one consequence among many is that adenosine concentrations remain too high. Like an outstanding debt on a loan, come the morning, some quantity of yesterday’s adenosine remains. You then carry that outstanding sleepiness balance throughout the following day. Also like a loan in arrears, this sleep debt will continue to accumulate. You cannot hide from it. The debt will roll over into the next payment cycle, and the next, and the next, producing a condition of prolonged, chronic sleep deprivation from one day to another. This outstanding sleep obligation results in a feeling of chronic fatigue, manifesting in many forms of mental and physical ailments that are now rife throughout industrialized nations. Other questions that can draw out signs of insufficient sleep are: If you didn’t set an alarm clock, would you sleep past that time? (If so, you need more sleep than you are giving yourself.) Do you find yourself at your computer screen reading and then rereading (and perhaps rereading again) the same sentence? (This is often a sign of a fatigued, under-slept brain.) Do you sometimes forget what color the last few traffic lights were while driving? (Simple distraction is often the cause, but a lack of sleep is very much another culprit.) Of course, even if you are giving yourself plenty of time to get a full night of shut-eye, next-day fatigue and sleepiness can still occur because you are suffering from an undiagnosed sleep disorder, of which there are now more than a hundred. The most common is insomnia, followed by sleepdisordered breathing, or sleep apnea, which includes heavy snoring. Should you suspect your sleep or that of anyone else to be disordered, resulting in daytime fatigue, impairment, or distress, speak to your doctor immediately and seek a referral to a sleep specialist. Most important in this regard: do not seek sleeping pills as your first option. You will realize why I say this come chapter 14, but please feel free to skip right to the section on sleeping pills in that chapter if you are a current user, or considering using sleeping pills in the immediate future. In the event it helps, I have provided a link to a questionnaire that has been developed by sleep researchers that will allow you to determine your degree of sleep fulfillment.XI Called SATED, it is easy to complete, and contains only five simple questions. I.I should note, from personal experience, that this is a winning fact to dispense at dinner parties, family gatherings, or other such social occasions. It will almost guarantee nobody will approach or speak to you again for the rest of the evening, and you’ll also never be invited back. II.The word pudica is from the Latin meaning “shy” or “bashful,” since the leaves will also collapse down if you touch or stroke them. III.This phenomenon of an imprecise internal biological clock has now been consistently observed in many different species. However, it is not consistently long in all species, as it is in humans. For some, the endogenous circadian rhythm runs short, being less than twentyfour hours when placed in total darkness, such as hamsters or squirrels. For others, such as humans, it is longer than twenty-four hours. IV.Even sunlight coming through thick cloud on a rainy day is powerful enough to help reset our biological clocks. V. For nocturnal species like bats, crickets, fireflies, or foxes, this call happens in the morning. VI.L. A. Erland and P. K. Saxena, “Melatonin natural health products and supplements: presence of serotonin and significant variabilityof melatonin content,” Journal of Clinical Sleep Medicine 2017;13(2):275–81. VII.Assuming you have a stable circadian rhythm, and have not recently experienced jet travel through numerous time zones, in which case you can still have difficulty falling asleep even if you have been awake for sixteen hours. VIII.There are other factors that contribute to caffeine sensitivity, such as age, other medications currently being taken, and the quantity and quality of prior sleep. A. Yang, A. A. Palmer, and H. de Wit, “Genetics of caffeine consumption and responses to caffeine,” Psychopharmacology 311, no. 3 (2010): 245–57, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4242593/. IX.The principal liver enzyme that metabolizes caffeine is called cytochrome P450 1A2. X.R. Noever, J. Cronise, and R. A. Relwani, “Using spider-web patterns to determine toxicity,” NASA Tech Briefs 19, no. 4 (1995): 82; and Peter N. Witt and Jerome S. Rovner, Spider Communication: Mechanisms and Ecological Significance (Princeton University Press, 1982). XI.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3902880/bin/aasm.37.1.9s1.tif (source: D. J. Buysse, “Sleep Health: Can we define it? Does it matter?” SLEEP 37, no. 1 [2014]: 9–17).? CHAPTER 3 Defining and Generating Sleep Time Dilation and What We Learned from a Baby in 1952 Perhaps you walked into your living room late one night while chatting with a friend. You saw a family member (let’s call her Jessica) lying still on the couch, not making a peep, body recumbent and head lolling to one side. Immediately, you turned to your friend and said, “Shhhhh, Jessica’s sleeping.” But how did you know? It took a split second of time, yet there was little doubt in your mind about Jessica’s state. Why, instead, did you not think Jessica was in a coma, or worse, dead? SELF-IDENTIFYING SLEEP Your lightning-quick judgment of Jessica being asleep was likely correct. And perhaps you accidentally confirmed it by knocking something over and waking her up. Over time, we have all become incredibly good at recognizing a number of signals that suggest that another individual is asleep. So reliable are these signs that there now exists a set of observable features that scientists agree indicate the presence of sleep in humans and other species. The Jessica vignette illustrates nearly all of these clues. First, sleeping organisms adopt a stereotypical position. In land animals, this is often horizontal, as was Jessica’s position on the couch. Second, and related, sleeping organisms have lowered muscle tone. This is most evident in the relaxation of postural (antigravity) skeletal muscles—those that keep you upright, preventing you from collapsing to the floor. As these muscles ease their tension in light and then deep sleep, the body will slouch down. A sleeping organism will be draped over whatever supports it underneath, most evident in Jessica’s listing head position. Third, sleeping individuals show no overt displays of communication or responsivity. Jessica showed no signs of orienting to you as you entered the room, as she would have when awake. The fourth defining feature of sleep is that it’s easily reversible, differentiating it from coma, anesthesia, hibernation, and death. Recall that upon knocking the item over in the room, Jessica awoke. Fifth, as we established in the previous chapter, sleep adheres to a reliable timed pattern across twenty-four hours, instructed by the circadian rhythm coming from the brain’s suprachiasmatic nucleus pacemaker. Humans are diurnal, so we have a preference for being awake throughout the day and sleeping at night. Now let me ask you a rather different question: How do you, yourself, know that you have slept? You make this self-assessment even more frequently than that of sleep in others. Each morning, with luck, you return to the waking world knowing that you have been asleep.I So sensitive is this self-assessment of sleep that you can go a step further, gauging when you’ve had good- or bad-quality sleep. This is another way of measuring sleep—a first-person phenomenological assessment distinct from signs that you use to determine sleep in another. Here, also, there are universal indicators that offer a convincing conclusion of sleep—two, in fact. First is the loss of external awareness—you stop perceiving the outside world. You are no longer conscious of all that surrounds you, at least not explicitly. In actual fact, your ears are still “hearing”; your eyes, though closed, are still capable of “seeing.” This is similarly true for the other sensory organs of the nose (smell), the tongue (taste), and the skin (touch). All these signals still flood into the center of your brain, but it is here, in the sensory convergence zone, where that journey ends while you sleep. The signals are blocked by a perceptual barricade set up in a structure called the thalamus (THAL-uh-muhs). A smooth, oval-shaped object just smaller than a lemon, the thalamus is the sensory gate of the brain. The thalamus decides which sensory signals are allowed through its gate, and which are not. Should they gain privileged passage, they are sent up to the cortex at the top of your brain, where they are consciously perceived. By locking its gates shut at the onset of healthy sleep, the thalamus imposes a sensory blackout in the brain, preventing onward travel of those signals up to the cortex. As a result, you are no longer consciously aware of the information broadcasts being transmitted from your outer sense organs. At this moment, your brain has lost waking contact with the outside world that surrounds you. Said another way, you are now asleep. The second feature that instructs your own, self-determined judgment of sleep is a sense of time distortion experienced in two contradictory ways. At the most obvious level, you lose your conscious sense of time when you sleep, tantamount to a chronometric void. Consider the last time you fell asleep on an airplane. When you woke up, you probably checked a clock to see how long you had been asleep. Why? Because your explicit tracking of time was ostensibly lost while you slept. It is this feeling of a time cavity that, in waking retrospect, makes you confident you’ve been asleep. But while your conscious mapping of time is lost during sleep, at a nonconscious level, time continues to be cataloged by the brain with incredible precision. I’m sure you have had the experience of needing to wake up the next morning at a specific time. Perhaps you had to catch an early-morning flight. Before bed, you diligently set your alarm for 6:00 a.m. Miraculously, however, you woke up at 5:58 a.m., unassisted, right before the alarm. Your brain, it seems, is still capable of logging time with quite remarkable precision while asleep. Like so many other operations occurring within the brain, you simply don’t have explicit access to this accurate time knowledge during sleep. It all flies below the radar of consciousness, surfacing only when needed. One last temporal distortion deserves mention here—that of time dilation in dreams, beyond sleep itself. Time isn’t quite time within dreams. It is most often elongated. Consider the last time you hit the snooze button on your alarm, having been woken from a dream. Mercifully, you are giving yourself another delicious five minutes of sleep. You go right back to dreaming. After the allotted five minutes, your alarm clock faithfully sounds again, yet that’s not what it felt like to you. During those five minutes of actual time, you may have felt like you were dreaming for an hour, perhaps more. Unlike the phase of sleep where you are not dreaming, wherein you lose all awareness of time, in dreams, you continue to have a sense of time. It’s simply not particularly accurate—more often than not dream time is stretched out and prolonged relative to real time. Although the reasons for such time dilation are not fully understood, recent experimental recordings of brain cells in rats give tantalizing clues. In the experiment, rats were allowed to run around a maze. As the rats learned the spatial layout, the researchers recorded signature patterns of brain-cell firing. The scientists did not stop recording from these memory-imprinting cells when the rats subsequently fell asleep. They continued to eavesdrop on the brain during the different stages of slumber, including rapid eye movement (REM) sleep, the stage in which humans principally dream. The first striking result was that the signature pattern of brain-cell firing that occurred as the rats were learning the maze subsequently reappeared during sleep, over and over again. That is, memories were being “replayed” at the level of brain-cell activity as the rats snoozed. The second, more striking finding was the speed of replay. During REM sleep, the memories were being replayed far more slowly: at just half or quarter the speed of that measured when the rats were awake and learning the maze. This slow neural recounting of the day’s events is the best evidence we have to date explaining our own protracted experience of time in human REM sleep. This dramatic deceleration of neural time may be the reason we believe our dream life lasts far longer than our alarm clocks otherwise assert. AN INFANT REVELATION—TWO TYPES OF SLEEP Though we have all determined that someone is asleep, or that we have been asleep, the gold-standard scientific verification of sleep requires the recording of signals, using electrodes, arising from three different regions: (1) brainwave activity, (2) eye movement activity, and (3) muscle activity. Collectively, these signals are grouped together under the blanket term “polysomnography” (PSG), meaning a readout (graph) of sleep (somnus) that is made up of multiple signals (poly). It was using this collection of measures that arguably the most important discovery in all of sleep research was made in 1952 at the University of Chicago by Eugene Aserinsky (then a graduate student) and Professor Nathaniel Kleitman, famed for the Mammoth Cave experiment discussed in chapter 2. Aserinsky had been carefully documenting the eye movement patterns of human infants during the day and night. He noticed that there were periods of sleep when the eyes would rapidly dart from side to side underneath their lids. Furthermore, these sleep phases were always accompanied by remarkably active brainwaves, almost identical to those observed from a brain that is wide awake. Sandwiching these earnest phases of active sleep were longer swaths of time when the eyes would calm and rest still. During these quiescent time periods, the brainwaves would also become calm, slowly ticking up and down. As if that weren’t strange enough, Aserinsky also observed that these two phases of slumber (sleep with eye movements, sleep with no eye movements) would repeat in a somewhat regular pattern throughout the night, over, and over, and over again. With classic professorial skepticism, his mentor, Kleitman, wanted to see the results replicated before he would entertain their validity. With his propensity for including his nearest and dearest in his experimentation, he chose his infant daughter, Ester, for this investigation. The findings held up. At that moment Kleitman and Aserinsky realized the profound discovery they had made: humans don’t just sleep, but cycle through two completely different types of sleep. They named these sleep stages based on their defining ocular features: non–rapid eye movement, or NREM, sleep, and rapid eye movement, or REM, sleep. Together with the assistance of another graduate student of Kleitman’s at the time, William Dement, Kleitman and Aserinsky further demonstrated that REM sleep, in which brain activity was almost identical to that when we are awake, was intimately connected to the experience we call dreaming, and is often described as dream sleep. NREM sleep received further dissection in the years thereafter, being subdivided into four separate stages, unimaginatively named NREM stages 1 to 4 (we sleep researchers are a creative bunch), increasing in their depth. Stages 3 and 4 are therefore the deepest stages of NREM sleep you experience, with “depth” being defined as the increasing difficulty required to wake an individual out of NREM stages 3 and 4, compared with NREM stages 1 or 2. THE SLEEP CYCLE In the years since Ester’s slumber revelation, we have learned that the two stages of sleep—NREM and REM—play out in a recurring, push-pull battle for brain domination across the night. The cerebral war between the two is won and lost every ninety minutes,II ruled first by NREM sleep, followed by the comeback of REM sleep. No sooner has the battle finished than it starts anew, replaying every ninety minutes. Tracing this remarkable roller-coaster ebb and flow across the night reveals the quite beautiful cycling architecture of sleep, depicted in figure 8. On the vertical axis are the different brain states, with Wake at the top, then REM sleep, and then the descending stages of NREM sleep, stages 1 to 4. On the horizontal axis is time of night, starting on the left at about eleven p.m. through until seven a.m. on the right. The technical name for this graphic is a hypnogram (a sleep graph). Had I not added the vertical dashed lines demarcating each ninetyminute cycle, you may have protested that you could not see a regularly repeating ninety-minute pattern. At least not the one you were expecting from my description above. The cause is another peculiar feature of sleep: a lopsided profile of sleep stages. While it is true that we flip-flop back and forth between NREM and REM sleep throughout the night every ninety minutes, the ratio of NREM sleep to REM sleep within each ninety-minute cycle changes dramatically across the night. In the first half of the night, the vast majority of our ninety-minute cycles are consumed by deep NREM sleep, and very little REM sleep, as can be seen in cycle 1 of the figure above. But as we transition through into the second half of the night, this seesaw balance shifts, with most of the time dominated by REM sleep, with little, if any, deep NREM sleep. Cycle 5 is a perfect example of this REM-rich type of sleep. Why did Mother Nature design this strange, complex equation of unfolding sleep stages? Why cycle between NREM and REM sleep over and over? Why not obtain all of the required NREM sleep first, followed by all of the necessary REM sleep second? Or vice versa? If that’s too much a gamble on the off chance that an animal only obtains a partial night of sleep at some point, then why not keep the ratio within each cycle the same, placing similar proportions of eggs in both baskets, as it were, rather than putting most of them in one early on, and then inverting that imbalance later in the night? Why vary it? It sounds like an exhausting amount of evolutionary hard work to have designed such a convoluted system, and put it into biological action. We have no scientific consensus as to why our sleep (and that of all other mammals and birds) cycles in this repeatable but dramatically asymmetric pattern, though a number of theories exist. One theory I have offered is that the uneven back-and-forth interplay between NREM and REM sleep is necessary to elegantly remodel and update our neural circuits at night, and in doing so manage the finite storage space within the brain. Forced by the known storage capacity imposed by a set number of neurons and connections within their memory structures, our brains must find the “sweet spot” between retention of old information and leaving sufficient room for the new. Balancing this storage equation requires identifying which memories are fresh and salient, and which memories that currently exist are overlapping, redundant, or simply no longer relevant. As we will discover in chapter 6, a key function of deep NREM sleep, which predominates early in the night, is to do the work of weeding out and removing unnecessary neural connections. In contrast, the dreaming stage of REM sleep, which prevails later in the night, plays a role in strengthening those connections. Combine these two, and we have at least one parsimonious explanation for why the two types of sleep cycle across the night, and why those cycles are initially dominated by NREM sleep early on, with REM sleep reigning supreme in the second half of the night. Consider the creation of a piece of sculpture from a block of clay. It starts with placing a large amount of raw material onto a pedestal (that entire mass of stored autobiographical memories, new and old, offered up to sleep each night). Next comes an initial and extensive removal of superfluous matter (long stretches of NREM sleep), after which brief intensification of early details can be made (short REM periods). Following this first session, the culling hands return for a second round of deep excavation (another long NREM-sleep phase), followed by a little more enhancing of some fine-grained structures that have emerged (slightly more REM sleep). After several more cycles of work, the balance of sculptural need has shifted. All core features have been hewn from the original mass of raw material. With only the important clay remaining, the work of the sculptor, and the tools required, must shift toward the goal of strengthening the elements and enhancing features of that which remains (a dominant need for the skills of REM sleep, and little work remaining for NREM sleep). In this way, sleep may elegantly manage and solve our memory storage crisis, with the general excavatory force of NREM sleep dominating early, after which the etching hand of REM sleep blends, interconnects, and adds details. Since life’s experience is ever changing, demanding that our memory catalog be updated ad infinitum, our autobiographical sculpture of stored experience is never complete. As a result, the brain always requires a new bout of sleep and its varied stages each night so as to auto-update our memory networks based on the events of the prior day. This account is one reason (of many, I suspect) explaining the cycling nature of NREM and REM sleep, and the imbalance of their distribution across the night. A danger resides in this sleep profile wherein NREM dominates early in the night, followed by an REM sleep dominance later in the morning, one of which most of the general public are unaware. Let’s say that you go to bed this evening at midnight. But instead of waking up at eight a.m., getting a full eight hours of sleep, you must wake up at six a.m. because of an earlymorning meeting or because you are an athlete whose coach demands earlymorning practices. What percent of sleep will you lose? The logical answer is 25 percent, since waking up at six a.m. will lop off two hours of sleep from what would otherwise be a normal eight hours. But that’s not entirely true. Since your brain desires most of its REM sleep in the last part of the night, which is to say the late-morning hours, you will lose 60 to 90 percent of all your REM sleep, even though you are losing 25 percent of your total sleep time. It works both ways. If you wake up at eight a.m., but don’t go to bed until two a.m., then you lose a significant amount of deep NREM sleep. Similar to an unbalanced diet in which you only eat carbohydrates and are left malnourished by the absence of protein, short-changing the brain of either NREM or REM sleep—both of which serve critical, though different, brain and body functions—results in a myriad of physical and mental ill health, as we will see in later chapters. When it comes to sleep, there is no such thing as burning the candle at both ends—or even at one end—and getting away with it. HOW YOUR BRAIN GENERATES SLEEP If I brought you into my sleep laboratory this evening at the University of California, Berkeley, placed electrodes on your head and face, and let you fall asleep, what would your sleeping brainwaves look like? How different would those patterns of brain activity be to those you are experiencing right now, as you read this sentence, awake? How do these different electrical brain changes explain why you are conscious in one state (wake), non-conscious in another (NREM sleep), and delusionally conscious, or dreaming, in the third (REM sleep)? Assuming you are a healthy young/midlife adult (we will discuss sleep in childhood, old age, and disease a little later), the three wavy lines in figure 9 reflect the different types of electrical activity I would record from your brain. Each line represents thirty seconds of brainwave activity from these three different states: (1) wakefulness, (2) deep NREM sleep, and (3) REM sleep. Prior to bed, your waking brain activity is frenetic, meaning that the brainwaves are cycling (going up and down) perhaps thirty or forty times per second, similar to a very fast drumbeat. This is termed “fast frequency” brain activity. Moreover, there is no reliable pattern to these brainwaves—that is, the drumbeat is not only fast, but also erratic. If I asked you to predict the next few seconds of the activity by tapping along to the beat, based on what came before, you would not be able to do so. The brainwaves are really that asynchronous—their drumbeat has no discernible rhythm. Even if I converted the brainwaves into sound (which I have done in my laboratory in a sonification-of-sleep project, and is eerie to behold), you would find it impossible to dance to. These are the electrical hallmarks of full wakefulness: fast-frequency, chaotic brainwave activity. You may have been expecting your general brainwave activity to look beautifully coherent and highly synchronous while awake, matching the ordered pattern of your (mostly) logical thought during waking consciousness. The contradictory electrical chaos is explained by the fact that different parts of your waking brain are processing different pieces of information at different moments in time and in different ways. When summed together, they produce what appears to be a discombobulated pattern of activity recorded by the electrodes placed on your head. As an analogy, consider a large football stadium filled with thousands of fans. Dangling over the middle of the stadium is a microphone. The individual people in the stadium represent individual brain cells, seated in different parts of the stadium, as they are clustered in different regions of the brain. The microphone is the electrode, sitting on top of the head—a recording device. Before the game starts, all of the individuals in the stadium are speaking about different things at different times. They are not having the same conversation in sync. Instead, they are desynchronized in their individual discussions. As a result, the summed chatter that we pick up from the overhead microphone is chaotic, lacking a clear, unified voice. When an electrode is placed on a subject’s head, as done in my laboratory, it is measuring the summed activity of all the neurons below the surface of the scalp as they process different streams of information (sounds, sights, smells, feelings, emotions) at different moments in time and in different underlying locations. Processing that much information of such varied kinds means that your brainwaves are very fast, frenetic, and chaotic. Once settled into bed at my sleep laboratory, with lights out and perhaps a few tosses and turns here and there, you will successfully cast off from the shores of wakefulness into sleep. First, you will wade out into the shallows of light NREM sleep: stages 1 and 2. Thereafter, you will enter the deeper waters of stages 3 and 4 of NREM sleep, which are grouped together under the blanket term “slow-wave sleep.” Returning to the brainwave patterns of figure 9, and focusing on the middle line, you can understand why. In deep, slowwave sleep, the up-and-down tempo of your brainwave activity dramatically decelerates, perhaps just two to four waves per second: ten times slower than the fervent speed of brain activity you were expressing while awake. As remarkable, the slow waves of NREM are also far more synchronous and reliable than those of your waking brain activity. So reliable, in fact, that you could predict the next few bars of NREM sleep’s electrical song based on those that came before. Were I to convert the deep rhythmic activity of your NREM sleep into sound and play it back to you in the morning (which we have also done for people in the same sonification-of-sleep project), you’d be able to find its rhythm and move in time, gently swaying to the slow, pulsing measure. But something else would become apparent as you listened and swayed to the throb of deep-sleep brainwaves. Every now and then a new sound would be overlaid on top of the slow-wave rhythm. It would be brief, lasting only a few seconds, but it would always occur on the downbeat of the slowwave cycle. You would perceive it as a quick trill of sound, not dissimilar to the strong rolling r in certain languages, such as Hindi or Spanish, or a very fast purrr from a pleased cat. What you are hearing is a sleep spindle—a punchy burst of brainwave activity that often festoons the tail end of each individual slow wave. Sleep spindles occur during both the deep and the lighter stages of NREM sleep, even before the slow, powerful brainwaves of deep sleep start to rise up and dominate. One of their many functions is to operate like nocturnal soldiers who protect sleep by shielding the brain from external noises. The more powerful and frequent an individual’s sleep spindles, the more resilient they are to external noises that would otherwise awaken the sleeper. Returning to the slow waves of deep sleep, we have also discovered something fascinating about their site of origin, and how they sweep across the surface of the brain. Place your finger between your eyes, just above the bridge of your nose. Now slide it up your forehead about two inches. When you go to bed tonight, this is where most of your deep-sleep brainwaves will be generated: right in the middle of your frontal lobes. It is the epicenter, or hot spot, from which most of your deep, slow-wave sleep emerges. However, the waves of deep sleep do not radiate out in perfect circles. Instead, almost all of your deep-sleep brainwaves will travel in one direction: from the front of your brain to the back. They are like the sound waves emitted from a speaker, which predominantly travel in one direction, from the speaker outward (it is always louder in front of a speaker than behind it). And like a speaker broadcasting across a vast expanse, the slow waves that you generate tonight will gradually dissipate in strength as they make their journey to the back of the brain, without rebound or return. Back in the 1950s and 1960s, as scientists began measuring these slow brainwaves, an understandable assumption was made: this leisurely, even lazy-looking electrical pace of brainwave activity must reflect a brain that is idle, or even dormant. It was a reasonable hunch considering that the deepest, slowest brainwaves of NREM sleep can resemble those we see in patients under anesthesia, or even those in certain forms of coma. But this assumption was utterly wrong. Nothing could be further from the truth. What you are actually experiencing during deep NREM sleep is one of the most epic displays of neural collaboration that we know of. Through an astonishing act of self-organization, many thousands of brain cells have all decided to unite and “sing,” or fire, in time. Every time I watch this stunning act of neural synchrony occurring at night in my own research laboratory, I am humbled: sleep is truly an object of awe. Returning to the analogy of the microphone dangling above the football stadium, consider the game of sleep now in play. The crowd—those thousands of brain cells—has shifted from their individual chitter-chatter before the game (wakefulness) to a unified state (deep sleep). Their voices have joined in a lockstep, mantra-like chant—the chant of deep NREM sleep. All at once they exuberantly shout out, creating the tall spike of brainwave activity, and then fall silent for several seconds, producing the deep, protracted trough of the wave. From our stadium microphone we pick up a clearly defined roar from the underlying crowd, followed by a long breathpause. Realizing that the rhythmic incantare of deep NREM slow-wave sleep was actually a highly active, meticulously coordinated state of cerebral unity, scientists were forced to abandon any cursory notions of deep sleep as a state of semi-hibernation or dull stupor. Understanding this stunning electrical harmony, which ripples across the surface of your brain hundreds of times each night, also helps explain your loss of external consciousness. It starts below the surface of the brain, within the thalamus. Recall that as we fall asleep, the thalamus—the sensory gate, seated deep in the middle of the brain—blocks the transfer of perceptual signals (sound, sight, touch, etc.) up to the top of the brain, or the cortex. By severing perceptual ties with the outside world, not only do we lose our sense of consciousness (explaining why we do not dream in deep NREM sleep, nor do we keep explicit track of time), this also allows the cortex to “relax” into its default mode of functioning. That default mode is what we call deep slow-wave sleep. It is an active, deliberate, but highly synchronous state of brain activity. It is a near state of nocturnal cerebral meditation, though I should note that it is very different from the brainwave activity of waking meditative states. In this shamanistic state of deep NREM sleep can be found a veritable treasure trove of mental and physical benefits for your brain and body, respectively—a bounty that we will fully explore in chapter 6. However, one brain benefit—the saving of memories—deserves further mention at this moment in our story, as it serves as an elegant example of what those deep, slow brainwaves are capable of. Have you ever taken a long road trip in your car and noticed that at some point in the journey, the FM radio stations you’ve been listening to begin dropping out in signal strength? In contrast, AM radio stations remain solid. Perhaps you’ve driven to a remote location and tried and failed to find a new FM radio station. Switch over to the AM band, however, and several broadcasting channels are still available. The explanation lies in the radio waves themselves, including the two different speeds of the FM and AM transmissions. FM uses faster-frequency radio waves that go up and down many more times per second than AM radio waves. One advantage of FM radio waves is that they can carry higher, richer loads of information, and hence they sound better. But there’s a big disadvantage: FM waves run out of steam quickly, like a muscle-bound sprinter who can only cover short distances. AM broadcasts employ a much slower (longer) radio wave, akin to a lean long-distance runner. While AM radio waves cannot match the muscular, dynamic quality of FM radio, the pedestrian pace of AM radio waves gives them the ability to cover vast distances with less fade. Longerrange broadcasts are therefore possible with the slow waves of AM radio, allowing far-reaching communication between very distant geographic locations. As your brain shifts from the fast-frequency activity of waking to the slower, more measured pattern of deep NREM sleep, the very same longrange communication advantage becomes possible. The steady, slow, synchronous waves that sweep across the brain during deep sleep open up communication possibilities between distant regions of the brain, allowing them to collaboratively send and receive their different repositories of stored experience. In this regard, you can think of each individual slow wave of NREM sleep as a courier, able to carry packets of information between different anatomical brain centers. One benefit of these traveling deep-sleep brainwaves is a file-transfer process. Each night, the long-range brainwaves of deep sleep will move memory packets (recent experiences) from a shortterm storage site, which is fragile, to a more permanent, and thus safer, longterm storage location. We therefore consider waking brainwave activity as that principally concerned with the reception of the outside sensory world, while the state of deep NREM slow-wave sleep donates a state of inward reflection—one that fosters information transfer and the distillation of memories. If wakefulness is dominated by reception, and NREM sleep by reflection, what, then, happens during REM sleep—the dreaming state? Returning to figure 9, the last line of electrical brainwave activity is that which I would observe coming from your brain in the sleep lab as you entered into REM sleep. Despite being asleep, the associated brainwave activity bears no resemblance to that of deep NREM slow-wave sleep (the middle line in the figure). Instead, REM sleep brain activity is an almost perfect replica of that seen during attentive, alert wakefulness—the top line in the figure. Indeed, recent MRI scanning studies have found that there are individual parts of the brain that are up to 30 percent more active during REM sleep than when we are awake! For these reasons, REM sleep has also been called paradoxical sleep: a brain that appears awake, yet a body that is clearly asleep. It is often impossible to distinguish REM sleep from wakefulness using just electrical brainwave activity. In REM sleep, there is a return of the same fasterfrequency brainwaves that are once again desynchronized. The many thousands of brain cells in your cortex that had previously unified in a slow, synchronized chat during deep NREM sleep have returned to frantically processing different informational pieces at different speeds and times in different brain regions—typical of wakefulness. But you’re not awake. Rather, you are sound asleep. So what information is being processed, since it is certainly not information from the outside world at that time? As is the case when you are awake, the sensory gate of the thalamus once again swings open during REM sleep. But the nature of the gate is different. It is not sensations from the outside that are allowed to journey to the cortex during REM sleep. Rather, signals of emotions, motivations, and memories (past and present) are all played out on the big screens of our visual, auditory, and kinesthetic sensory cortices in the brain. Each and every night, REM sleep ushers you into a preposterous theater wherein you are treated to a bizarre, highly associative carnival of autobiographical themes. When it comes to information processing, think of the wake state principally as reception (experiencing and constantly learning the world around you), NREM sleep as reflection (storing and strengthening those raw ingredients of new facts and skills), and REM sleep as integration (interconnecting these raw ingredients with each other, with all past experiences, and, in doing so, building an ever more accurate model of how the world works, including innovative insights and problem-solving abilities). Since the electrical brainwaves of REM sleep and wake are so similar, how can I tell which of the two you are experiencing as you lie in the bedroom of the sleep laboratory next to the control room? The telltale player in this regard is your body—specifically its muscles. Before putting you to bed in the sleep laboratory, we would have applied electrodes to your body, in addition to those we affix to your head. While awake, even lying in bed and relaxed, there remains a degree of overall tension, or tone, in your muscles. This steady muscular hum is easily detected by the electrodes listening in on your body. As you pass into NREM sleep, some of that muscle tension disappears, but much remains. Gearing up for the leap into REM sleep, however, an impressive change occurs. Mere seconds before the dreaming phase begins, and for as long as that REM-sleep period lasts, you are completely paralyzed. There is no tone in the voluntary muscles of your body. None whatsoever. If I were to quietly come into the room and gently lift up your body without waking you, it would be completely limp, like a rag doll. Rest assured that your involuntary muscles— those that control automatic operations such as breathing—continue to operate and maintain life during sleep. But all other muscles become lax. This feature, termed “atonia” (an absence of tone, referring here to the muscles), is instigated by a powerful disabling signal that is transmitted down the full length of your spinal cord from your brain stem. Once put in place, the postural body muscles, such as the biceps of your arms and the quadriceps of your legs, lose all tension and strength. No longer will they respond to commands from your brain. You have, in effect, become an embodied prisoner, incarcerated by REM sleep. Fortunately, after serving the detention sentence of the REM-sleep cycle, your body is freed from physical captivity as the REM-sleep phase ends. This striking dissociation during the dreaming state, where the brain is highly active but the body is immobilized, allows sleep scientists to easily recognize—and therefore separate—REMsleep brainwaves from wakeful ones. Why did evolution decide to outlaw muscle activity during REM sleep? Because by eliminating muscle activity you are prevented from acting out your dream experience. During REM sleep, there is a nonstop barrage of motor commands swirling around the brain, and they underlie the movement-rich experience of dreams. Wise, then, of Mother Nature to have tailored a physiological straitjacket that forbids these fictional movements from becoming reality, especially considering that you’ve stopped consciously perceiving your surroundings. You can well imagine the calamitous upshot of falsely enacting a dream fight, or a frantic sprint from an approaching dream foe, while your eyes are closed and you have no comprehension of the world around you. It wouldn’t take long before you quickly left the gene pool. The brain paralyzes the body so the mind can dream safely. How do we know these movement commands are actually occurring while someone dreams, beyond the individual simply waking up and telling you they were having a running dream or a fighting dream? The sad answer is that this paralysis mechanism can fail in some people, particularly later in life. Consequentially, they convert these dream-related motor impulses into real-world physical actions. As we shall read about in chapter 11, the repercussions can be tragic. Finally, and not to be left out of the descriptive REM-sleep picture, is the very reason for its name: corresponding rapid eye movements. Your eyes remain still in their sockets during deep NREM sleep.III Yet electrodes that we place above and below your eyes tell a very different ocular story when you begin to dream: the very same story that Kleitman and Aserinsky unearthed in 1952 when observing infant sleep. During REM sleep, there are phases when your eyeballs will jag, with urgency, left-to-right, left-to-right, and so on. At first, scientists assumed that these rat-a-tat-tat eye movements corresponded to the tracking of visual experience in dreams. This is not true. Instead, the eye movements are intimately linked with the physiological creation of REM sleep, and reflect something even more extraordinary than the passive apprehension of moving objects within dream space. This phenomenon is chronicled in detail in chapter 9. Are we the only creatures that experience these varied stages of sleep? Do any other animals have REM sleep? Do they dream? Let us find out. I.Some people with a certain type of insomnia are not able to accurately gauge whether they have been asleep or awake at night. As a consequence of this “sleep misperception,” they underestimate how much slumber they have successfully obtained—a condition that we will return to later in the book. II.Different species have different NREM–REM cycle lengths. Most are shorter than that of humans. The functional purpose of the cycle length is another mystery of sleep. To date, the best predictor of NREM–REM sleep cycle length is the width of the brain stem, with those species possessing wider brain stems having longer cycle lengths. III.Oddly, during the transition from being awake into light stage 1 NREM sleep, the eyes will gently and very, very slowly start to roll in their sockets in synchrony, like two ocular ballerinas pirouetting in perfect time with each other. It is a hallmark indication that the onset of sleep is inevitable. If you have a bed partner, try observing their eyelids the next time they are drifting off to sleep. You will see the closed lids of the eyes deforming as the eyeballs roll around underneath. Parenthetically, should you choose to complete this suggested observational experiment, be aware of the potential ramifications. There is perhaps little else more disquieting than aborting one’s transition into sleep, opening your eyes, and finding your partner’s face looming over yours, gaze affixed. CHAPTER 4 Ape Beds, Dinosaurs, and Napping with Half a Brain Who Sleeps, How Do We Sleep, and How Much? WHO SLEEPS When did life start sleeping? Perhaps sleep emerged with the great apes? Maybe earlier, in reptiles or their aquatic antecedents, fish? Short of a time capsule, the best way to answer this question comes from studying sleep across different phyla of the animal kingdom, from the prehistoric to the evolutionarily recent. Investigations of this kind provide a powerful ability to peer far back in the historical record and estimate the moment when sleep first graced the planet. As the geneticist Theodosius Dobzhansky once said, “Nothing in biology makes sense except in light of evolution.” For sleep, the illuminating answer turned out to be far earlier than anyone anticipated, and far more profound in ramification. Without exception, every animal species studied to date sleeps, or engages in something remarkably like it. This includes insects, such as flies, bees, cockroaches, and scorpions;I fish, from small perch to the largest sharks;II amphibians, such as frogs; and reptiles, such as turtles, Komodo dragons, and chameleons. All have bona fide sleep. Ascend the evolutionary ladder further and we find that all types of birds and mammals sleep: from shrews to parrots, kangaroos, polar bears, bats, and, of course, we humans. Sleep is universal. Even invertebrates, such as primordial mollusks and echinoderms, and even very primitive worms, enjoy periods of slumber. In these phases, affectionately termed “lethargus,” they, like humans, become unresponsive to external stimuli. And just as we fall asleep faster and sleep more soundly when sleep-deprived, so, too, do worms, defined by their degree of insensitivity to prods from experimenters. How “old” does this make sleep? Worms emerged during the Cambrian explosion: at least 500 million years ago. That is, worms (and sleep by association) predate all vertebrate life. This includes dinosaurs, which, by inference, are likely to have slept. Imagine diplodocuses and triceratopses all comfortably settling in for a night of full repose! Regress evolutionary time still further and we have discovered that the very simplest forms of unicellular organisms that survive for periods exceeding twenty-four hours, such as bacteria, have active and passive phases that correspond to the light-dark cycle of our planet. It is a pattern that we now believe to be the precursor of our own circadian rhythm, and with it, wake and sleep. Many of the explanations for why we sleep circle around a common, and perhaps erroneous, idea: sleep is the state we must enter in order to fix that which has been upset by wake. But what if we turned this argument on its head? What if sleep is so useful—so physiologically beneficial to every aspect of our being—that the real question is: Why did life ever bother to wake up? Considering how biologically damaging the state of wakefulness can often be, that is the true evolutionary puzzle here, not sleep. Adopt this perspective, and we can pose a very different theory: sleep was the first state of life on this planet, and it was from sleep that wakefulness emerged. It may be a preposterous hypothesis, and one that nobody is taking seriously or exploring, but personally I do not think it to be entirely unreasonable. Whichever of these two theories is true, what we know for certain is that sleep is of ancient origin. It appeared with the very earliest forms of planetary life. Like other rudimentary features, such as DNA, sleep has remained a common bond uniting every creature in the animal kingdom. A long-lasting commonality, yes; however, there are truly remarkable differences in sleep from one species to another. Four such differences, in fact. ONE OF THESE THINGS IS NOT LIKE THE OTHER Elephants need half as much sleep as humans, requiring just four hours of slumber each day. Tigers and lions devour fifteen hours of daily sleep. The brown bat outperforms all other mammals, being awake for just five hours each day while sleeping nineteen hours. Total amount of time is one of the most conspicuous differences in how organisms sleep. You’d imagine the reason for such clear-cut variation in sleep need is obvious. It isn’t. None of the likely contenders—body size, prey/predator status, diurnal/nocturnal—usefully explains the difference in sleep need across species. Surely sleep time is at least similar within any one phylogenetic category, since they share much of their genetic code. It is certainly true for other basic traits within phyla, such as sensory capabilities, methods of reproduction, and even degree of intelligence. Yet sleep violates this reliable pattern. Squirrels and degus are part of the same family group (rodents), yet they could not be more dissimilar in sleep need. The former sleeps twice as long as the latter—15.9 hours for the squirrel versus 7.7 hours for the degu. Conversely, you can find near-identical sleep times in utterly different family groups. The humble guinea pig and the precocious baboon, for example, which are of markedly different phylogenetic orders, not to mention physical sizes, sleep precisely the same amount: 9.4 hours. So what does explain the difference in sleep time (and perhaps need) from species to species, or even within a genetically similar order? We’re not entirely sure. The relationship between the size of the nervous system, the complexity of the nervous system, and total body mass appears to be a somewhat meaningful predictor, with increasing brain complexity relative to body size resulting in greater sleep amounts. While weak and not entirely consistent, this relationship suggests that one evolutionary function that demands more sleep is the need to service an increasingly complex nervous system. As millennia unfolded and evolution crowned its (current) accomplishment with the genesis of the brain, the demand for sleep only increased, tending to the needs of this most precious of all physiological apparatus. Yet this is not the whole story—not by a good measure. Numerous species deviate wildly from the predictions made by this rule. For example, an opossum, which weighs almost the same as a rat, sleeps 50 percent longer, clocking an average of eighteen hours each day. The opossum is just one hour shy of the animal kingdom record for sleep amount currently held by the brown bat, who, as previously mentioned, racks up a whopping nineteen hours of sleep each day. There was a moment in research history when scientists wondered if the measure of choice—total minutes of sleep—was the wrong way of looking at the question of why sleep varies so considerably across species. Instead, they suspected that assessing sleep quality, rather than quantity (time), would shed some light on the mystery. That is, species with superior quality of sleep should be able to accomplish all they need in a shorter time, and vice versa. It was a great idea, with the exception that, if anything, we’ve discovered the opposite relationship: those that sleep more have deeper, “higher”-quality sleep. In truth, the way quality is commonly assessed in these investigations (degree of unresponsiveness to the outside world and the continuity of sleep) is probably a poor index of the real biological measure of sleep quality: one that we cannot yet obtain in all these species. When we can, our understanding of the relationship between sleep quantity and quality across the animal kingdom will likely explain what currently appears to be an incomprehensible map of sleep-time differences. For now, our most accurate estimate of why different species need different sleep amounts involves a complex hybrid of factors, such as dietary type (omnivore, herbivore, carnivore), predator/prey balance within a habitat, the presence and nature of a social network, metabolic rate, and nervous system complexity. To me, this speaks to the fact that sleep has likely been shaped by numerous forces along the evolutionary path, and involves a delicate balancing act between meeting the demands of waking survival (e.g., hunting prey/obtaining food in as short a time as possible, minimizing energy expenditure and threat risk), serving the restorative physiological needs of an organism (e.g., a higher metabolic rate requires greater “cleanup” efforts during sleep), and tending to the more general requirements of the organism’s community. Nevertheless, even our most sophisticated predictive equations remain unable to explain far-flung outliers in the map of slumber: species that sleep much (e.g., bats) and those that sleep little (e.g., giraffes, which sleep for just four to five hours). Far from being a nuisance, I feel these anomalous species may hold some of the keys to unlocking the puzzle of sleep need. They remain a delightfully frustrating opportunity for those of us trying to crack the code of sleep across the animal kingdom, and within that code, perhaps as yet undiscovered benefits of sleep we never thought possible. TO DREAM OR NOT TO DREAM Another remarkable difference in sleep across species is composition. Not all species experience all stages of sleep. Every species in which we can measure sleep stages experiences NREM sleep—the non-dreaming stage. However, insects, amphibians, fish, and most reptiles show no clear signs of REM sleep —the type associated with dreaming in humans. Only birds and mammals, which appeared later in the evolutionary timeline of the animal kingdom, have full-blown REM sleep. It suggests that dream (REM) sleep is the new kid on the evolutionary block. REM sleep seems to have emerged to support functions that NREM sleep alone could not accomplish, or that REM sleep was more efficient at accomplishing. Yet as with so many things in sleep, there is another anomaly. I said that all mammals have REM sleep, but debate surrounds cetaceans, or aquatic mammals. Certain of these ocean-faring species, such as dolphins and killer whales, buck the REM-sleep trend in mammals. They don’t have any. Although there is one case in 1969 suggesting that a pilot whale was in REM sleep for six minutes, most of our assessments to date have not discovered REM sleep—or at least what many sleep scientists would believe to be true REM sleep—in aquatic mammals. From one perspective, this makes sense: when an organism enters REM sleep, the brain paralyzes the body, turning it limp and immobile. Swimming is vital for aquatic mammals, since they must surface to breathe. If full paralysis was to take hold during sleep, they could not swim and would drown. The mystery deepens when we consider pinnipeds (one of my all-time favorite words, from the Latin derivatives: pinna “fin” and pedis “foot”), such as fur seals. Partially aquatic mammals, they split their time between land and sea. When on land, they have both NREM sleep and REM sleep, just like humans and all other terrestrial mammals and birds. But when they enter the ocean, they stop having REM sleep almost entirely. Seals in the ocean will sample but a soup?on of the stuff, racking up just 5 to 10 percent of the REM sleep amounts they would normally enjoy when on land. Up to two weeks of ocean-bound time have been documented without any observable REM sleep in seals, who survive in such times on a snooze diet of NREM sleep. These anomalies do not necessarily challenge the usefulness of REM sleep. Without doubt, REM sleep, and even dreaming, appears to be highly useful and adaptive in those species that have it, as we shall see in part 3 of the book. That REM sleep returns when these animals return to land, rather being done away with entirely, affirms this. It is simply that REM sleep does not appear to be feasible or needed by aquatic mammals when in the ocean. During that time, we assume they make do with lowly NREM sleep—which, for dolphins and whales, may always be the case. Personally, I don’t believe aquatic mammals, even cetaceans like dolphins and whales, have a total absence of REM sleep (though several of my scientific colleagues will tell you I’m wrong). Instead, I think the form of REM sleep these mammals obtain in the ocean is somewhat different and harder to detect: be it brief in nature, occurring at times when we have not been able to observe it, or expressed in ways or hiding in parts of the brain that we have not yet been able to measure. In defense of my contrarian point of view, I note that it was once believed that egg-laying mammals (monotremes), such as the spiny anteater and the duck-billed platypus, did not have REM sleep. It turned out that they do, or at least a version of it. The outer surface of their brain—the cortex—from which most scientists measure sleeping brainwaves, does not exhibit the choppy, chaotic characteristics of REM-sleep activity. But when scientists looked a little deeper, beautiful bursts of REM-sleep electrical brainwave activity were found at the base of the brain—waves that are a perfect match for those seen in all other mammals. If anything, the duck-billed platypus generates more of this kind of electrical REM-sleep activity than any other mammal! So they did have REM sleep after all, or at least a beta version of it, first rolled out in these more evolutionarily ancient mammals. A fully operational, whole-brain version of REM sleep appears to have been introduced in more developed mammals that later evolved. I believe a similar story of atypical, but nevertheless present, REM sleep will ultimately be observed in dolphins and whales and seals when in the ocean. After all, absence of evidence is not evidence of absence. More intriguing than the poverty of REM sleep in this aquatic corner of the mammalian kingdom is the fact that birds and mammals evolved separately. REM sleep may therefore have been birthed twice in the course of evolution: once for birds and once for mammals. A common evolutionary pressure may still have created REM sleep in both, in the same way that eyes have evolved separately and independently numerous times across different phyla throughout evolution for the common purpose of visual perception. When a theme repeats in evolution, and independently across unrelated lineages, it often signals a fundamental need. However, a very recent report has suggested that a proto form of REM sleep exists in an Australian lizard, which, in terms of the evolutionary timeline, predates the emergence of birds and mammals. If this finding is replicated, it would suggest that the original seed of REM sleep was present at least 100 million years earlier than our original estimates. This common seed in certain reptiles may have then germinated into the full form of REM sleep we now see in birds and mammals, including humans. Regardless of when true REM sleep emerged in evolution, we are fast discovering why REM-sleep dreaming came into being, what vital needs it supports in the warm-blooded world of birds and mammals (e.g., cardiovascular health, emotional restoration, memory association, creativity, body-temperature regulation), and whether other species dream. As we will later discuss, it seems they do. Setting aside the issue of whether all mammals have REM sleep, an uncontested fact is this: NREM sleep was first to appear in evolution. It is the original form that sleep took when stepping out from behind evolution’s creative curtain—a true pioneer. This seniority leads to another intriguing question, and one that I get asked in almost every public lecture I give: Which type of sleep—NREM or REM sleep—is more important? Which do we really need? There are many ways you can define “importance” or “need,” and thus numerous ways of answering the question. But perhaps the simplest recipe is to take an organism that has both sleep types, bird or mammal, and keep it awake all night and throughout the subsequent day. NREM and REM sleep are thus similarly removed, creating the conditions of equivalent hunger for each sleep stage. The question is, which type of sleep will the brain feast on when you offer it the chance to consume both during a recovery night? NREM and REM sleep in equal proportions? Or more of one than the other, suggesting greater importance of the sleep stage that dominates? This experiment has now been performed many times on numerous species of birds and mammals, humans included. There are two clear outcomes. First, and of little surprise, sleep duration is far longer on the recovery night (ten or even twelve hours in humans) than during a standard night without prior deprivation (eight hours for us). Responding to the debt, we are essentially trying to “sleep it off,” the technical term for which is a sleep rebound. Second, NREM sleep rebounds harder. The brain will consume a far larger portion of deep NREM sleep than of REM sleep on the first night after total sleep deprivation, expressing a lopsided hunger. Despite both sleep types being on offer at the finger buffet of recovery sleep, the brain opts to heap much more deep NREM sleep onto its plate. In the battle of importance, NREM sleep therefore wins. Or does it? Not quite. Should you keep recording sleep across a second, third, and even fourth recovery night, there’s a reversal. Now REM sleep becomes the primary dish of choice with each returning visit to the recovery buffet table, with a side of NREM sleep added. Both sleep stages are therefore essential. We try to recover one (NREM) a little sooner than the other (REM), but make no mistake, the brain will attempt to recoup both, trying to salvage some of the losses incurred. It is important to note, however, that regardless of the amount of recovery opportunity, the brain never comes close to getting back all the sleep it has lost. This is true for total sleep time, just as it is for NREM sleep and for REM sleep. That humans (and all other species) can never “sleep back” that which we have previously lost is one of the most important take-homes of this book, the saddening consequences of which I will describe in chapters 7 and 8. IF ONLY HUMANS COULD A third striking difference in sleep across the animal kingdom is the way in which we all do it. Here, the diversity is remarkable and, in some cases, almost impossible to believe. Take cetaceans, such as dolphins and whales, for example. Their sleep, of which there is only NREM, can be unihemispheric, meaning they will sleep with half a brain at a time! One half of the brain must always stay awake to maintain life-necessary movement in the aquatic environment. But the other half of the brain will, at times, fall into the most beautiful NREM sleep. Deep, powerful, rhythmic, and slow brainwaves will drench the entirety of one cerebral hemisphere, yet the other half of the cerebrum will be bristling with frenetic, fast brainwave activity, fully awake. This despite the fact that both hemispheres are heavily wired together with thick crisscross fibers, and sit mere millimeters apart, as in human brains. Of course, both halves of the dolphin brain can be, and frequently are, awake at the very same time, operating in unison. But when it is time for sleep, the two sides of the brain can uncouple and operate independently, one side remaining awake while the other side snoozes away. After this one half of the brain has consumed its fill of sleep, they switch, allowing the previously vigilant half of the brain to enjoy a well-earned period of deep NREM slumber. Even with half of the brain asleep, dolphins can achieve an impressive level of movement and even some vocalized communication. The neural engineering and tricky architecture required to accomplish this staggering trick of oppositional “lights-on, lights-off ” brain activity is rare. Surely Mother Nature could have found a way to avoid sleep entirely under the extreme pressure of nonstop, 24/7 aquatic movement. Would that not have been easier than masterminding a convoluted split-shift system between brain halves for sleep, while still allowing for a joint operating system where both sides unite when awake? Apparently not. Sleep is of such vital necessity that no matter what the evolutionary demands of an organism, even the unyielding need to swim in perpetuum from birth to death, Mother Nature had no choice. Sleep with both sides of the brain, or sleep with just one side and then switch. Both are possible, but sleep you must. Sleep is non-negotiable. The gift of split-brain deep NREM sleep is not entirely unique to aquatic mammals. Birds can do it, too. However, there is a somewhat different, though equally life-preserving, reason: it allows them to keep an eye on things, quite literally. When birds are alone, one half of the brain and its corresponding (opposite-side) eye must stay awake, maintaining vigilance to environmental threats. As it does so, the other eye closes, allowing its corresponding half of the brain to sleep. Things get even more interesting when birds group together. In some species, many of the birds in a flock will sleep with both halves of the brain at the same time. How do they remain safe from threat? The answer is truly ingenious. The flock will first line up in a row. With the exception of the birds at each end of the line, the rest of the group will allow both halves of the brain to indulge in sleep. Those at the far left and right ends of the row aren’t so lucky. They will enter deep sleep with just one half of the brain (opposing in each), leaving the corresponding left and right eye of each bird wide open. In doing so, they provide full panoramic threat detection for the entire group, maximizing the total number of brain halves that can sleep within the flock. At some point, the two end-guards will stand up, rotate 180 degrees, and sit back down, allowing the other side of their respective brains to enter deep sleep. We mere humans and a select number of other terrestrial mammals appear to be far less skilled than birds and aquatic mammals, unable as we are to take our medicine of NREM sleep in half-brain measure. Or are we? Two recently published reports suggest humans have a very mild version of unihemispheric sleep—one that is drawn out for similar reasons. If you compare the electrical depth of the deep NREM slow brainwaves on one half of someone’s head relative to the other when they are sleeping at home, they are about the same. But if you bring that person into a sleep laboratory, or take them to a hotel—both of which are unfamiliar sleep environments—one half of the brain sleeps a little lighter than the other, as if it’s standing guard with just a tad more vigilance due to the potentially less safe context that the conscious brain has registered while awake. The more nights an individual sleeps in the new location, the more similar the sleep is in each half of the brain. It is perhaps the reason why so many of us sleep so poorly the first night in a hotel room. This phenomenon, however, doesn’t come close to the complete division between full wakefulness and truly deep NREM sleep achieved by each side of birds’ and dolphins’ brains. Humans always have to sleep with both halves of our brain in some state of NREM sleep. Imagine, though, the possibilities that would become available if only we could rest our brains, one half at a time. I should note that REM sleep is strangely immune to being split across sides of the brain, no matter who you are. All birds, irrespective of the environmental situation, always sleep with both halves of the brain during REM sleep. The same is true for every species that experiences dream sleep, humans included. Whatever the functions of REM-sleep dreaming—and there appear to be many—they require participation of both sides of the brain at the same time, and to an equal degree. UNDER PRESSURE The fourth and final difference in sleep across the animal kingdom is the way in which sleep patterns can be diminished under rare and very special circumstances, something that the US government sees as a matter of national security, and has spent sizable taxpayer dollars investigating. The infrequent situation happens only in response to extreme environmental pressures or challenges. Starvation is one example. Place an organism under conditions of severe famine, and foraging for food will supersede sleep. Nourishment will, for a time, push aside the need for sleep, though it cannot be sustained for long. Starve a fly and it will stay awake longer, demonstrating a pattern of food-seeking behavior. The same is true for humans. Individuals who are deliberately fasting will sleep less as the brain is tricked into thinking that food has suddenly become scarce. Another rare example is the joint sleep deprivation that occurs in female killer whales and their newborn calves. Female killer whales give birth to a single calf once every three to eight years. Calving normally takes place away from the other members of the pod. This leaves the newborn calf incredibly vulnerable during the initial weeks of life, especially during the return to the pod as it swims beside its mother. Up to 50 percent of all new calves are killed during this journey home. It is so dangerous, in fact, that neither mother nor calf appear to sleep while in transit. No mother-calf pair that scientists have observed shows signs of robust sleep en route. This is especially surprising in the calf, since the highest demand and consumption of sleep in every other living species is in the first days and weeks of life, as any new parent will tell you. Such is the egregious peril of long-range ocean travel that these infant whales will reverse an otherwise universal sleep trend. Yet the most incredible feat of deliberate sleep deprivation belongs to that of birds during transoceanic migration. During this climate-driven race across thousands of miles, entire flocks will fly for many more hours than is normal. As a result, they lose much of the stationary opportunity for plentiful sleep. But even here, the brain has found an ingenious way to obtain sleep. In-flight, migrating birds will grab remarkably brief periods of sleep lasting only seconds in duration. These ultra–power naps are just sufficient to avert the ruinous brain and body deficits that would otherwise ensue from prolonged total sleep deprivation. (If you’re wondering, humans have no such similar ability.) The white-crowned sparrow is perhaps the most astonishing example of avian sleep deprivation during long-distance flights. This small, quotidian bird is capable of a spectacular feat that the American military has spent millions of research dollars studying. The sparrow has an unparalleled, though time-limited, resilience to total sleep deprivation, one that we humans could never withstand. If you sleep-deprive this sparrow in the laboratory during the migratory period of the year (when it would otherwise be in flight), it suffers virtually no ill effects whatsoever. However, depriving the same sparrow of the same amount of sleep outside this migratory time window inflicts a maelstrom of brain and body dysfunction. This humble passerine bird has evolved an extraordinary biological cloak of resilience to total sleep deprivation: one that it deploys only during a time of great survival necessity. You can now imagine why the US government continues to have a vested interest in discovering exactly what that biological suit of armor is: their hope for developing a twenty-four-hour soldier. HOW SHOULD WE SLEEP? Humans are not sleeping the way nature intended. The number of sleep bouts, the duration of sleep, and when sleep occurs have all been comprehensively distorted by modernity. Throughout developed nations, most adults currently sleep in a monophasic pattern—that is, we try to take a long, single bout of slumber at night, the average duration of which is now less than seven hours. Visit cultures that are untouched by electricity and you often see something rather different. Hunter-gatherer tribes, such as the Gabra in northern Kenya or the San people in the Kalahari Desert, whose way of life has changed little over the past thousands of years, sleep in a biphasic pattern. Both these groups take a similarly longer sleep period at night (seven to eight hours of time in bed, achieving about seven hours of sleep), followed by a thirty- to sixty-minute nap in the afternoon. There is also evidence for a mix of the two sleep patterns, determined by time of year. Pre-industrial tribes, such as the Hadza in northern Tanzania or the San of Namibia, sleep in a biphasic pattern in the hotter summer months, incorporating a thirty- to forty-minute nap at high noon. They then switch to a largely monophasic sleep pattern during the cooler winter months. Even when sleeping in a monophasic pattern, the timing of slumber observed in pre-industrialized cultures is not that of our own, contorted making. On average, these tribespeople will fall asleep two to three hours after sunset, around nine p.m. Their nighttime sleep bouts will come to an end just prior to, or soon after, dawn. Have you ever wondered about the meaning of the term “midnight”? It of course means the middle of the night, or, more technically, the middle point of the solar cycle. And so it is for the sleep cycle of hunter-gatherer cultures, and presumably all those that came before. Now consider our cultural sleep norms. Midnight is no longer “mid night.” For many of us, midnight is usually the time when we consider checking our email one last time—and we know what often happens in the protracted thereafter. Compounding the problem, we do not then sleep any longer into the morning hours to accommodate these later sleep-onset times. We cannot. Our circadian biology, and the insatiable early-morning demands of a post-industrial way of life, denies us the sleep we vitally need. At one time we went to bed in the hours after dusk and woke up with the chickens. Now many of us are still waking up with the chickens, but dusk is simply the time we are finishing up at the office, with much of the waking night to go. Moreover, few of us enjoy a full afternoon nap, further contributing to our state of sleep bankruptcy. The practice of biphasic sleep is not cultural in origin, however. It is deeply biological. All humans, irrespective of culture or geographical location, have a genetically hardwired dip in alertness that occurs in the midafternoon hours. Observe any post-lunch meeting around a boardroom table and this fact will become evidently clear. Like puppets whose control strings were let loose, then rapidly pulled taut, heads will start dipping then quickly snap back upright. I’m sure you’ve experienced this blanket of drowsiness that seems to take hold of you, midafternoon, as though your brain is heading toward an unusually early bedtime. Both you and the meeting attendees are falling prey to an evolutionarily imprinted lull in wakefulness that favors an afternoon nap, called the postprandial alertness dip (from the Latin prandium, “meal”). This brief descent from high-degree wakefulness to low-level alertness reflects an innate drive to be asleep and napping in the afternoon, and not working. It appears to be a normal part of the daily rhythm of life. Should you ever have to give a presentation at work, for your own sake—and that of the conscious state of your listeners—if you can, avoid the midafternoon slot. What becomes clearly apparent when you step back from these details is that modern society has divorced us from what should be a preordained arrangement of biphasic sleep—one that our genetic code nevertheless tries to rekindle every afternoon. The separation from biphasic sleep occurred at, or even before, our shift from an agrarian existence to an industrial one. Anthropological studies of pre-industrial hunter-gatherers have also dispelled a popular myth about how humans should sleep.III Around the close of the early modern era (circa late seventeenth and early eighteenth centuries), historical texts suggest that Western Europeans would take two long bouts of sleep at night, separated by several hours of wakefulness. Nestled in-between these twin slabs of sleep—sometimes called first sleep and second sleep, they would read, write, pray, make love, and even socialize. This practice may very well have occurred during this moment in human history, in this geographical region. Yet the fact that no pre-industrial cultures studied to date demonstrate a similar nightly split-shift of sleep suggests that it is not the natural, evolutionarily programmed form of human sleep. Rather, it appears to have been a cultural phenomenon that appeared and was popularized with the western European migration. Furthermore, there is no biological rhythm—of brain activity, neurochemical activity, or metabolic activity—that would hint at a human desire to wake up for several hours in the middle of the night. Instead, the true pattern of biphasic sleep— for which there is anthropological, biological, and genetic evidence, and which remains measurable in all human beings to date—is one consisting of a longer bout of continuous sleep at night, followed by a shorter midafternoon nap. Accepting that this is our natural pattern of slumber, can we ever know for certain what types of health consequences have been caused by our abandonment of biphasic sleep? Biphasic sleep is still observed in several siesta cultures throughout the world, including regions of South America and Mediterranean Europe. When I was a child in the 1980s, I went on vacation to Greece with my family. As we walked the streets of the major metropolitan Greek cities we visited, there were signs hanging in storefront windows that were very different from those I was used to back in England. They stated: open from nine a.m. to one p.m., closed from one to five p.m., open five to nine p.m. Today, few of those signs remain in windows of shops throughout Greece. Prior to the turn of the millennium, there was increasing pressure to abandon the siesta-like practice in Greece. A team of researchers from Harvard University’s School of Public Health decided to quantify the health consequences of this radical change in more than 23,000 Greek adults, which contained men and women ranging in age from twenty to eighty-three years old. The researchers focused on cardiovascular outcomes, tracking the group across a six-year period as the siesta practice came to an end for many of them. As with countless Greek tragedies, the end result was heartbreaking, but here in the most serious, literal way. None of the individuals had a history of coronary heart disease or stroke at the start of the study, indicating the absence of cardiovascular ill health. However, those that abandoned regular siestas went on to suffer a 37 percent increased risk of death from heart disease across the six-year period, relative to those who maintained regular daytime naps. The effect was especially strong in workingmen, where the ensuing mortality risk of not napping increased by well over 60 percent. Apparent from this remarkable study is this fact: when we are cleaved from the innate practice of biphasic sleep, our lives are shortened. It is perhaps unsurprising that in the small enclaves of Greece where siestas still remain intact, such as the island of Ikaria, men are nearly four times as likely to reach the age of ninety as American males. These napping communities have sometimes been described as “the places where people forget to die.” From a prescription written long ago in our ancestral genetic code, the practice of natural biphasic sleep, and a healthy diet, appear to be the keys to a long-sustained life. WE ARE SPECIAL Sleep, as you can now appreciate, is a unifying feature across the animal kingdom, yet within and between species there is remarkable diversity in amount (e.g., time), form (e.g., half-brain, whole-brain), and pattern (monophasic, biphasic, polyphasic). But are we humans special in our sleep profile, at least, in its pure form when unmolested by modernity? Much has been written about the uniqueness of Homo sapiens in other domains—our cognition, creativity, culture, and the size and shape of our brains. Is there anything similarly exceptional about our nightly slumber? If so, could this unique sleep be an unrecognized cause of these aforementioned accomplishments that we prize as so distinctly human—the justification of our hominid name (Homo sapiens—Latin derivative, “wise person”)? As it turns out, we humans are special when it comes to sleep. Compared to Old- and New-World monkeys, as well as apes, such as chimpanzees, orangutans, and gorillas, human sleep sticks out like the proverbial sore thumb. The total amount of time we spend asleep is markedly shorter than all other primates (eight hours, relative to the ten to fifteen hours of sleep observed in all other primates), yet we have a disproportionate amount of REM sleep, the stage in which we dream. Between 20 and 25 percent of our sleep time is dedicated to REM sleep dreaming, compared to an average of only 9 percent across all other primates! We are the anomalous data point when it comes to sleep time and dream time, relative to all other monkeys and apes. To understand how and why our sleep is so different is to understand the evolution of ape to man, from tree to ground. Humans are exclusive terrestrial sleepers—we catch our Zs lying on the ground (or sometimes raised a little off it, on beds). Other primates will sleep arboreally, on branches or in nests. Only occasionally will other primates come out of trees to sleep on the ground. Great apes, for example, will build an entirely new treetop sleep nest, or platform, every single night. (Imagine having to set aside several hours each evening after dinner to construct a new IKEA bedframe before you can sleep!) Sleeping in trees was an evolutionarily wise idea, up to a point. It provided safe haven from large, ground-hunting predators, such as hyenas, and small blood-sucking arthropods, including lice, fleas, and ticks. But when sleeping twenty to fifty feet up in the air, one has to be careful. Become too relaxed in your sleep depth when slouched on a branch or in a nest, and a dangling limb may be all the invitation gravity needs to bring you hurtling down to Earth in a life-ending fall, removing you from the gene pool. This is especially true for the stage of REM sleep, in which the brain completely paralyzes all voluntary muscles of the body, leaving you utterly limp—a literal bag of bones with no tension in your muscles. I’m sure you have never tried to rest a full bag of groceries on a tree branch, but I can assure you it’s far from easy. Even if you manage the delicate balancing act for a moment, it doesn’t last long. This body-balancing act was the challenge and danger of tree sleeping for our primate forebears, and it markedly constrained their sleep. Homo erectus, the predecessor of Homo sapiens, was the first obligate biped, walking freely upright on two legs. We believe that Homo erectus was also the first dedicated ground sleeper. Shorter arms and an upright stance made tree living and sleeping very unlikely. How did Homo erectus (and by inference, Homo sapiens) survive in the predator- rich ground-sleeping environment, when leopards, hyenas, and saber-toothed tigers (all of which can hunt at night) are on the prowl, and terrestrial bloodsuckers abound? Part of the answer is fire. While there remains some debate, many believe that Homo erectus was the first to use fire, and fire was one of the most important catalysts—if not the most important—that enabled us to come out of the trees and live on terra firma. Fire is also one of the best explanations for how we were able to sleep safely on the ground. Fire would deter large carnivores, while the smoke provided an ingenious form of nighttime fumigation, repelling small insects ever keen to bite into our epidermis. Fire was no perfect solution, however, and ground sleeping would have remained risky. An evolutionary pressure to become qualitatively more efficient in how we sleep therefore developed. Any Homo erectus capable of accomplishing more efficient sleep would likely have been favored in survival and selection. Evolution saw to it that our ancient form of sleep became somewhat shorter in duration, yet increased in intensity, especially by enriching the amount of REM sleep we packed into the night. In fact, as is so often the case with Mother Nature’s brilliance, the problem became part of the solution. In other words, the act of sleeping on solid ground, and not on a precarious tree branch, was the impetus for the enriched and enhanced amounts of REM sleep that developed, while the amount of time spent asleep was able to modestly decrease. When sleeping on the ground, there’s no more risk of falling. For the first time in our evolution, hominids could consume all the body-immobilized REM-sleep dreaming they wanted, and not worry about the lasso of gravity whipping them down from treetops. Our sleep therefore became “concentrated”: shorter and more consolidated in duration, packed aplenty with high-quality sleep. And not just any type of sleep, but REM sleep that bathed a brain rapidly accelerating in complexity and connectivity. There are species that have more total REM time than hominids, but there are none who power up and lavish such vast proportions of REM sleep onto such a complex, richly interconnected brain as we Homo sapiens do. From these clues, I offer a theorem: the tree-to-ground reengineering of sleep was a key trigger that rocketed Homo sapiens to the top of evolution’s lofty pyramid. At least two features define human beings relative to other primates. I posit that both have been beneficially and causally shaped by the hand of sleep, and specifically our intense degree of REM sleep relative to all other mammals: (1) our degree of sociocultural complexity, and (2) our cognitive intelligence. REM sleep, and the act of dreaming itself, lubricates both of these human traits. To the first of these points, we have discovered that REM sleep exquisitely recalibrates and fine-tunes the emotional circuits of the human brain (discussed in detail in part 3 of the book). In this capacity, REM sleep may very well have accelerated the richness and rational control of our initially primitive emotions, a shift that I propose critically contributed to the rapid rise of Homo sapiens to dominance over all other species in key ways. We know, for example, that REM sleep increases our ability to recognize and therefore successfully navigate the kaleidoscope of socioemotional signals that are abundant in human culture, such as overt and covert facial expressions, major and minor bodily gestures, and even mass group behavior. One only needs to consider disorders such as autism to see how challenging and different a social existence can be without these emotional navigation abilities being fully intact. Related, the REM-sleep gift of facilitating accurate recognition and comprehension allows us to make more intelligent decisions and actions as a consequence. More specifically, the coolheaded ability to regulate our emotions each day—a key to what we call emotional IQ—depends on getting sufficient REM sleep night after night. (If your mind immediately jumped to particular colleagues, friends, and public figures who lack these traits, you may well wonder about how much sleep, especially late-morning REM-rich sleep, they are getting.) Second, and more critical, if you multiply these individual benefits within and across groups and tribes, all of which are experiencing an everincreasing intensity and richness of REM sleep over millennia, we can start to see how this nightly REM-sleep recalibration of our emotional brains could have scaled rapidly and exponentially. From this REM-sleep-enhanced emotional IQ emerged a new and far more sophisticated form of hominid socioecology across vast collectives, one that helped enable the creation of large, emotionally astute, stable, highly bonded, and intensely social communities of humans. I will go a step further and suggest that this is the most influential function of REM sleep in mammals, perhaps the most influential function of all types of sleep in all mammals, and even the most eminent advantage ever gifted by sleep in the annals of all planetary life. The adaptive benefits conferred by complex emotional processing are truly monumental, and so often overlooked. We humans can instantiate vast numbers of emotions in our embodied brains, and thereafter, deeply experience and even regulate those emotions. Moreover, we can recognize and help shape the emotions of others. Through both of these intra- and interpersonal processes, we can forge the types of cooperative alliances that are necessary to establish large social groups, and beyond groups, entire societies brimming with powerful structures and ideologies. What may at first blush have seemed like a modest asset awarded by REM sleep to a single individual is, I believe, one of the most valuable commodities ensuring the survival and dominance of our species as a collective. The second evolutionary contribution that the REM-sleep dreaming state fuels is creativity. NREM sleep helps transfer and make safe newly learned information into long-term storage sites of the brain. But it is REM sleep that takes these freshly minted memories and begins colliding them with the entire back catalog of your life’s autobiography. These mnemonic collisions during REM sleep spark new creative insights as novel links are forged between unrelated pieces of information. Sleep cycle by sleep cycle, REM sleep helps construct vast associative networks of information within the brain. REM sleep can even take a step back, so to speak, and divine overarching insights and gist: something akin to general knowledge—that is, what a collection of information means as a whole, not just an inert back catalogue of facts. We can awake the next morning with new solutions to previously intractable problems or even be infused with radically new and original ideas. Adding, then, to the opulent and domineering socioemotional fabric that REM sleep helps weave across the masses came this second, creativity benefit of dream sleep. We should (cautiously) revere how superior our hominid ingenuity is relative to that of any of our closest rivals, primate or other. The chimpanzees—our nearest living primate relatives—have been around approximately 5 million years longer than we have; some of the great apes preceded us by at least 10 million years. Despite aeons of opportunity time, neither species has visited the moon, created computers, or developed vaccines. Humbly, we humans have. Sleep, especially REM sleep and the act of dreaming, is a tenable, yet underappreciated, factor underlying many elements that form our unique human ingenuity and accomplishments, just as much as language or tool use (indeed, there is even evidence that sleep causally shapes both these latter traits as well). Nevertheless, the superior emotional brain gifts that REM sleep affords should be considered more influential in defining our hominid success than the second benefit, of inspiring creativity. Creativity is an evolutionarily powerful tool, yes. But it is largely limited to an individual. Unless creative, ingenious solutions can be shared between individuals through the emotionally rich, pro-social bonds and cooperative relationships that REM sleep fosters—then creativity is far more likely to remain fixed within an individual, rather than spread to the masses. Now we can appreciate what I believe to be a classic, self-fulfilling positive cycle of evolution. Our shift from tree to ground sleeping instigated an ever more bountiful amount of relative REM sleep compared with other primates, and from this bounty emerged a steep increase in cognitive creativity, emotional intelligence, and thus social complexity. This, alongside our increasingly dense, interconnected brains, led to improved daily (and nightly) survival strategies. In turn, the harder we worked those increasingly developed emotional and creative circuits of the brain during the day, the greater was our need to service and recalibrate these ever-demanding neural systems at night with more REM sleep. As this positive feedback loop took hold in exponential fashion, we formed, organized, maintained, and deliberatively shaped ever larger social groups. The rapidly increasing creative abilities could thus be spread more efficiently and rapidly, and even improved by that ever-increasing amount of hominid REM-sleep that enhances emotional and social sophistication. REM-sleep dreaming therefore represents a tenable new contributing factor, among others, that led to our astonishingly rapid evolutionary rise to power, for better and worse—a new (sleep-fueled), globally dominant social superclass. I.Proof of sleep in very small species, such as insects, in which recordings of electrical activity from the brain are impossible, is confirmed using the same set of behavioral features described in chapter 3, illustrated by the example of Jessica: immobility, reduced responsiveness to the outside world, easily reversible. A further criterion is that depriving the organism of what looks like sleep should result in an increased drive for more of it when you stop the annoying deprivation assault, reflecting “sleep rebound.” II.It was once thought that sharks did not sleep, in part because they never closed their eyes. Indeed, they do have clear active and passive phases that resemble wake and sleep. We now know that the reason they never close their eyes is because they have no eyelids. III.A. Roger Ekirch, At Day’s Close: Night in Times Past (New York: W. W. Norton, 2006).? CHAPTER 5 Changes in Sleep Across the Life Span SLEEP BEFORE BIRTH Through speech or song, expecting parents will often thrill at their ability to elicit small kicks and movements from their in utero child. Though you should never tell them this, the baby is most likely fast asleep. Prior to birth, a human infant will spend almost all of its time in a sleep-like state, much of which resembles the REM-sleep state. The sleeping fetus is therefore unaware of its parents’ performative machinations. Any co-occurring arm flicks and leg bops that the mother feels from her baby are most likely to be the consequence of random bursts of brain activity that typify REM sleep. Adults do not—or at least should not—throw out similar nighttime kicks and movements, since they are held back by the body-paralyzing mechanism of REM sleep. But in utero, the immature fetus’s brain has yet to construct the REM-sleep muscle-inhibiting system adults have in place. Other deep centers of the fetus brain have, however, already been glued in place, including those that generate sleep. Indeed, by the end of the second trimester of development (approximately week 23 of pregnancy), the vast majority of the neural dials and switches required to produce NREM and REM sleep have been sculpted out and wired up. As a result of this mismatch, the fetus brain still generates formidable motor commands during REM sleep, except there is no paralysis to hold them back. Without restraint, those commands are freely translated into frenetic body movements, felt by the mother as acrobatic kicks and featherweight punches. At this stage of in utero development, most of the time is spent in sleep. The twentyfour-hour period contains a mishmash of approximately six hours of NREM sleep, six hours of REM sleep, and twelve hours of an intermediary sleep state that we cannot confidently say is REM or NREM sleep, but certainly is not full wakefulness. It is only when the fetus enters the final trimester that the glimmers of real wakefulness emerge. Far less than you would probably imagine, though—just two to three hours of each day are spent awake in the womb. Even though total sleep time decreases in the last trimester, a paradoxical and quite ballistic increase in REM-sleep time occurs. In the last two weeks of pregnancy, the fetus will ramp up its consumption of REM sleep to almost nine hours a day. In the last week before birth, REM-sleep amount hits a lifetime high of twelve hours a day. With near insatiable appetite, the human fetus therefore doubles its hunger for REM sleep just before entering the world. There will be no other moment during the life of that individual—prenatal, early post-natal, adolescence, adulthood, or old age—when they will undergo such a dramatic change in REM-sleep need, or feast so richly on the stuff. Is the fetus actually dreaming when in REM sleep? Probably not in the way most of us conceptualize dreams. But we do know that REM sleep is vital for promoting brain maturation. The construction of a human being in the womb occurs in distinct, interdependent stages, a little bit like building a house. You cannot crown a house with a roof before there are supporting wall frames to rest it on, and you cannot put up walls without a foundation to seat them in. The brain, like the roof of a house, is one of the last items to be constructed during development. And like a roof, there are sub-stages to that process—you need a roof frame before you can start adding roof tiles, for instance. Detailed creation of the brain and its component parts occurs at a rapid pace during the second and third trimesters of human development—precisely the time window when REM-sleep amounts skyrocket. This is no coincidence. REM sleep acts as an electrical fertilizer during this critical phase of early life. Dazzling bursts of electrical activity during REM sleep stimulate the lush growth of neural pathways all over the developing brain, and then furnish each with a healthy bouquet of connecting ends, or synaptic terminals. Think of REM sleep like an Internet service provider that populates new neighborhoods of the brain with vast networks of fiber-optic cables. Using these inaugural bolts of electricity, REM sleep then activates their high-speed functioning. This phase of development, which infuses the brain with masses of neural connections, is called synaptogenesis, as it involves the creation of millions of wiring links, or synapses, between neurons. By deliberate design, it is an overenthusiastic first pass at setting up the mainframe of a brain. There is a great deal of redundancy, offering many, many possible circuit configurations to emerge within the infant’s brain once born. From the perspective of the Internet service provider analogy, all homes, across all neighborhoods, throughout all territories of the brain have been gifted a high degree of connectivity and bandwidth in this first phase of life. Charged with such a herculean task of neuro-architecture—establishing the neural highways and side streets that will engender thoughts, memories, feelings, decisions, and actions—it’s no wonder REM sleep must dominate most, if not all, of early developmental life. In fact, this is true for all other mammals:I the time of life when REM sleep is greatest is the same stage when the brain is undergoing the greatest construction. Worryingly, if you disturb or impair the REM sleep of a developing infant brain, pre- or early post-term, and there are consequences. In the 1990s, researchers began studying newly born rat pups. Simply by blocking REM sleep, their gestational progress was retarded, despite chronological time marching on. The two should, of course, progress in unison. Depriving the infant rats of REM sleep stalled construction of their neural rooftop —the cerebral cortex of the brain. Without REM sleep, assembly work on the brain ground to a halt, frozen in time by the experimental wedge of a lack of REM sleep. Day after day, the half-finished roofline of the sleep-starved cerebral cortex shows no growth change. The very same effect has now been demonstrated in numerous other mammalian species, suggesting that the effect is probably common across mammals. When the infant rat pups were finally allowed to get some REM sleep, assembly of the cerebral rooftop did restart, but it didn’t accelerate, nor did it ever fully get back on track. An infant brain without sleep will be a brain ever underconstructed. A more recent link with deficient REM sleep concerns autism spectrum disorder (ASD) (not to be confused with attention deficit hyperactivity disorder [ADHD], which we will discuss later in the book). Autism, of which there are several forms, is a neurological condition that emerges early in development, usually around two or three years of age. The core symptom of autism is a lack of social interaction. Individuals with autism do not communicate or engage with other people easily, or typically. Our current understanding of what causes autism is incomplete, but central to the condition appears to be an inappropriate wiring up of the brain during early developmental life, specifically in the formation and number of synapses—that is, abnormal synaptogenesis. Imbalances in synaptic connections are common in autistic individuals: excess amounts of connectivity in some parts of the brain, deficiencies in others. Realizing this, scientists have begun to examine whether the sleep of individuals with autism is atypical. It is. Infants and young children who show signs of autism, or who are diagnosed with autism, do not have normal sleep patterns or amounts. The circadian rhythms of autistic children are also weaker than their non-autistic counterparts, showing a flatter profile of melatonin across the twenty-four-hour period rather than a powerful rise in concentration at night and rapid fall throughout the day.II Biologically, it is as if the day and night are far less light and dark, respectively, for autistic individuals. As a consequence, there is a weaker signal for when stable wake and solid sleep should take place. Additionally, and perhaps related, the total amount of sleep that autistic children can generate is less than that of non-autistic children. Most notable, however, is the significant shortage of REM sleep. Autistic individuals show a 30 to 50 percent deficit in the amount of REM sleep they obtain, relative to children without autism.III Considering the role of REM sleep in establishing the balanced mass of synaptic connections within the developing brain, there is now keen interest in discovering whether or not REM-sleep deficiency is a contributing factor to autism. Existing evidence in humans is simply correlational, however. Just because autism and REM-sleep abnormalities go hand in hand does not mean that one causes the other. Nor does this association tell you the direction of causality even if it does exist: Is deficient REM sleep causing autism, or is it the other way around? It is curious to note, however, that selectively depriving an infant rat of REM sleep leads to aberrant patterns of neural connectivity, or synaptogenesis, in the brain.IV Moreover, rats deprived of REM sleep during infancy go on to become socially withdrawn and isolated as adolescents and adults.V Irrespective of causality issues, tracking sleep abnormalities represents a new diagnostic hope for the early detection of autism. Of course, no expecting mother has to worry about scientists disrupting the REM sleep of their developing fetus. But alcohol can inflict that same selective removal of REM sleep. Alcohol is one of the most powerful suppressors of REM sleep that we know of. We will discuss the reason that alcohol blocks REM-sleep generation, and the consequences of that sleep disruption in adults, in later chapters. For now, however, we’ll focus on the impact of alcohol on the sleep of a developing fetus and newborn. Alcohol consumed by a mother readily crosses the placental barrier, and therefore readily infuses her developing fetus. Knowing this, scientists first examined the extreme scenario: mothers who were alcoholics or heavy drinkers during pregnancy. Soon after birth, the sleep of these neonates was assessed using electrodes gently placed on the head. The newborns of heavy-drinking mothers spent far less time in the active state of REM sleep compared with infants of similar age but who were born of mothers who did not drink during pregnancy. The recording electrodes went on to point out an even more concerning physiological story. Newborns of heavy-drinking mothers did not have the same electrical quality of REM sleep. You will remember from chapter 3 that REM sleep is exemplified by delightfully chaotic—or desynchronized—brainwaves: a vivacious and healthy form of electrical activity. However, the infants of heavy-drinking mothers showed a 200 percent reduction in this measure of vibrant electrical activity relative to the infants born of non-alcoholconsuming mothers. Instead, the infants of heavy-drinking mothers emitted a brainwave pattern that was far more sedentary in this regard.VI If you are now wondering whether or not epidemiological studies have linked alcohol use during pregnancy and an increased likelihood of neuropsychiatric illness in the mother’s child, including autism, the answer is yes.VII Fortunately, most mothers these days do not drink heavily during pregnancy. But what about the more common situation of an expectant mom having an occasional glass or two of wine during pregnancy? Using noninvasive tracking of heart rate, together with ultrasound measures of body, eye, and breathing movement, we are now able to determine the basic stages of NREM sleep and REM sleep of a fetus when it is in the womb. Equipped with these methods, a group of researchers studied the sleep of babies who were just weeks away from being born. Their mothers were assessed on two successive days. On one of those days, the mothers drank non-alcoholic fluids. On the other day, they drank approximately two glasses of wine (the absolute amount was controlled on the basis of their body weight). Alcohol significantly reduced the amount of time that the unborn babies spent in REM sleep, relative to the non-alcohol condition. That alcohol also dampened the intensity of REM sleep experienced by the fetus, defined by the standard measure of how many darting rapid eye movements adorn the REM-sleep cycle. Furthermore, these unborn infants suffered a marked depression in breathing during REM sleep, with breath rates dropping from a normal rate of 381 per hour during natural sleep to just 4 per hour when the fetus was awash with alcohol.VIII Beyond alcohol abstinence during pregnancy, the time window of nursing also warrants mention. Almost half of all lactating women in Western countries consume alcohol in the months during breastfeeding. Alcohol is readily absorbed in a mother’s milk. Concentrations of alcohol in breast milk closely resemble those in a mother’s bloodstream: a 0.08 blood alcohol level in a mother will result in approximately a 0.08 alcohol level in breast milk.IX Recently we have discovered what alcohol in breast milk does to the sleep of an infant. Newborns will normally transition straight into REM sleep after a feeding. Many mothers already know this: almost as soon as suckling stops, and sometimes even before, the infant’s eyelids will close, and underneath, the eyes will begin darting left-right, indicating that their baby is now being nourished by REM sleep. A once-common myth was that babies sleep better if the mother has had an alcoholic drink before a feeding— beer was the suggested choice of beverage in this old tale. For those of you who are beer lovers, unfortunately, it is just that—a myth. Several studies have fed infants breast milk containing either a non-alcoholic flavor, such as vanilla, or a controlled amount of alcohol (the equivalent of a mother having a drink or two). When babies consume alcohol-laced milk, their sleep is more fragmented, they spend more time awake, and they suffer a 20 to 30 percent suppression of REM sleep soon after.X Often, the babies will even try to get back some of that missing REM sleep once they have cleared it from their bloodstream, though it is not easy for their fledgling systems to do so. What emerges from all of these studies is that REM sleep is not optional during early human life, but obligatory. Every hour of REM sleep appears to count, as evidenced by the desperate attempt by a fetus or newborn to regain any REM sleep when it is lost.XI Sadly, we do not yet fully understand what the long-term effects are of fetal or neonate REMsleep disruption, alcohol-triggered or otherwise. Only that blocking or reducing REM sleep in newborn animals hinders and distorts brain development, leading to an adult that is socially abnormal. CHILDHOOD SLEEP Perhaps the most obvious and tormenting (for new parents) difference between the sleep of infants and young children and that of adults is the number of slumber phases. In contrast to the single, monophasic sleep pattern observed in adults of industrialized nations, infants and young kids display polyphasic sleep: many short snippets of sleep through the day and night, punctuated by numerous awakenings, often vocal. There is no better or more humorous affirmation of this fact than the short book of lullabies, written by Adam Mansbach, entitled Go the F**k to Sleep. Obviously, it’s an adult book. At the time of writing, Mansbach was a new father. And like many a new parent, he was run ragged by the constant awakenings of his child: the polyphasic profile of infant sleep. The incessant need to attend to his young daughter, helping her fall back to sleep time and time and time again, night after night after night, left him utterly exasperated. It got to the point where Mansbach just had to vent all the loving rage he had pent up. What came spilling out onto the page was a comedic splash of rhymes he would fictitiously read to his daughter, the themes of which will immediately resonate with many new parents. “I’ll read you one very last book if you swear,/You’ll go the fuck to sleep.” (I implore you to listen to the audiobook version of the work, narrated to perfection by the sensational actor Samuel L. Jackson.) Fortunately, for all new parents (Mansbach included), the older a child gets, the fewer, longer, and more stable their sleep bouts become.XII Explaining this change is the circadian rhythm. While the brain areas that generate sleep are molded in place well before birth, the master twenty-four-hour clock that controls the circadian rhythm—the suprachiasmatic nucleus—takes considerable time to develop. Not until age three or four months will a newborn show modest signs of being governed by a daily rhythm. Slowly, the suprachiasmatic nucleus begins to latch on to repeating signals, such as daylight, temperature change, and feedings (so long as those feedings are highly structured), establishing a stronger twenty-four-hour rhythm. By the one-year milestone of development, the suprachiasmatic nucleus clock of an infant has gripped the steering reins of the circadian rhythm. This means that the child now spends more of the day awake, interspersed with several naps and, mercifully, more of the night asleep. Mostly gone are the indiscriminate bouts of sleep and wake that once peppered the day and night. By four years of age, the circadian rhythm is in dominant command of a child’s sleep behavior, with a lengthy slab of nighttime sleep, usually supplemented by just a single daytime nap. At this stage, the child has transitioned from a polyphasic sleep pattern to a biphasic sleep pattern. Come late childhood, the modern, monophasic pattern of sleep is finally made real. What this progressive establishment of stable rhythmicity hides, however, is a much more tumultuous power struggle between NREM and REM sleep. Although the amount of total sleep gradually declines from birth onwards, all the while becoming more stable and consolidated, the ratio of time spent in NREM sleep and REM sleep does not decline in a similarly stable manner. During the fourteen hours of total shut-eye per day that a six-month-old infant obtains, there is a 50/50 timeshare between NREM and REM sleep. A five-year-old, however, will have a 70/30 split between NREM and REM sleep across the eleven hours of total daily slumber. In other words, the proportion of REM sleep decreases in early childhood while the proportion of NREM sleep actually increases, even though total sleep time decreases. The downgrading of the REM-sleep portion, and the upswing in NREM-sleep dominance, continues, throughout early and midchildhood. That balance will finally stabilize to an 80/20 NREM/REM sleep split by the late teen years, and remain so throughout early and midadulthood. SLEEP AND ADOLESCENCE Why do we spend so much time in REM sleep in the womb and early in life, yet switch to a heavier dominance of deep NREM sleep in late childhood and early adolescence? If we quantify the intensity of the deep-sleep brainwaves, we see the very same pattern: a decline in REM-sleep intensity in the first year of life, yet an exponential rise in deep NREM sleep intensity in mid- and late childhood, hitting a peak just before puberty, and then damping back down. What’s so special about this type of deep sleep at this transitional time of life? Prior to birth, and soon after, the challenge for development was to build and add vast numbers of neural highways and interconnections that become a fledgling brain. As we have discussed, REM sleep plays an essential role in this proliferation process, helping to populate brain neighborhoods with neural connectivity, and then activate those pathways with a healthy dose of informational bandwidth. But since this first round of brain wiring is purposefully overzealous, a second round of remodeling must take place. It does so during late childhood and adolescence. Here, the architectural goal is not to scale up, but to scale back for the goal of efficiency and effectiveness. The time of adding brain connections with the help of REM sleep is over. Instead, pruning of connections becomes the order of the day or, should I say, night. Enter the sculpting hand of deep NREM sleep. Our analogy of the Internet service provider is a helpful one to return to. When first setting up the network, each home in the newly built neighborhood was given an equal amount of connectivity bandwidth and thus potential for use. However, that’s an inefficient solution for the long term, since some of these homes will become heavy bandwidth users over time, while other homes will consume very little. Some homes may even remain vacant and never use any bandwidth. To reliably estimate what pattern of demand exists, the Internet service provider needs time to gather usage statistics. Only after a period of experience can the provider make an informed decision on how to refine the original network structure it put in place, dialing back connectivity to low-use homes, while increasing connectivity to other homes with high bandwidth demand. It is not a complete redo of the network, and much of the original structure will remain in place. After all, the Internet service provider has done this many times before, and they have a reasonable estimate of how to build a first pass of the network. But a use-dependent reshaping and downsizing must still occur if maximum network efficiency is to be achieved. The human brain undergoes a similar, use-determined transformation during late childhood and adolescence. Much of the original structure laid down early in life will persist, since Mother Nature has, by now, learned to create a quite accurate first-pass wiring of a brain after billions of attempts over many thousands of years of evolution. But she wisely leaves something on the table in her generic brain sculpture, that of individualized refinement. The unique experiences of a child during their formative years translate to a set of personal usage statistics. Those experiences, or those statistics, provide the bespoke blueprint for a last round of brain refinement,XIII capitalizing on the opportunity left open by nature. A (somewhat) generic brain becomes ever more individualized, based on the personalized use of the owner. To help with the job of refinement and downscaling of connectivity, the brain employs the services of deep NREM sleep. Of the many functions carried out by deep NREM sleep— the full roster of which we will discuss in the next chapter—it is that of synaptic pruning that features prominently during adolescence. In a remarkable series of experiments, the pioneering sleep researcher Irwin Feinberg discovered something fascinating about how this operation of downscaling takes place within the adolescent brain. His findings help justify an opinion you may also hold: adolescents have a less rational version of an adult brain, one that takes more risks and has relatively poor decision-making skills. Using electrodes placed all over the head—front and back, left side and right, Feinberg began recording the sleep of a large group of kids starting at age six to eight years old. Every six to twelve months, he would bring these individuals back to his laboratory and perform another sleep measurement. He didn’t stop for ten years. He amassed more than 3,500 all-night assessments: a scarcely believable 320,000 hours of sleep recordings! From these, Feinberg created a series of snapshots, depicting how deep-sleep intensity changed with the stages of brain development as the children made their often awkward transition through adolescence into adulthood. It was the neuroscience equivalent of time-lapse photography in nature: taking repeat pictures of a tree as it first comes into bud in the spring (babyhood), then bursts into leaf during the summer (late childhood), then matures in color come the fall (early adolescence), and finally sheds its leaves in the winter (late adolescence and early adulthood). During mid- and late childhood, Feinberg observed moderate deep-sleep amounts as the last neural growth spurts inside the brain were being completed, analogous to late spring and early summer. Then Feinberg began seeing a sharp rise in deep-sleep intensity in his electrical recordings, right at the time when the developmental needs of brain connectivity switch from growing connections to shedding them; the tree’s equivalent of fall. Just as maturational fall was about to turn to winter, and the shedding was nearly complete, Feinberg’s recordings showed a clear ramping back down in deep NREM-sleep intensity to lower intensity once more. The life cycle of childhood was over, and as the last leaves dropped, the onward neural passage of these teenagers had been secured. Deep NREM sleep had aided their transition into early adulthood. Feinberg proposed that the rise and fall of deep-sleep intensity were helping lead the maturational journey through the precarious heights of adolescence, followed by safe onward passage into adulthood. Recent findings have supported his theory. As deep NREM sleep performs its final overhaul and refinement of the brain during adolescence, cognitive skills, reasoning, and critical thinking start to improve, and do so in a proportional manner with that NREM sleep change. Taking a closer look at the timing of this relationship, you see something even more interesting. The changes in deep NREM sleep always precede the cognitive and developmental milestones within the brain by several weeks or months, implying a direction of influence: deep sleep may be a driving force of brain maturation, not the other way around. Feinberg made a second seminal discovery. When he examined the timeline of changing deep-sleep intensity at each different electrode spot on the head, it was not the same. Instead, the rise-and-fall pattern of maturation always began at the back of the brain, which performs the functions of visual and spatial perception, and then progressed steadily forward as adolescence progressed. Most striking, the very last stop on the maturational journey was the tip of the frontal lobe, which enables rational thinking and critical decision-making. Therefore, the back of the brain of an adolescent was more adult-like, while the front of the brain remained more child-like at any one moment during this developmental window of time.XIV His findings helped explain why rationality is one of the last things to flourish in teenagers, as it is the last brain territory to receive sleep’s maturational treatment. Certainly sleep is not the only factor in the ripening of the brain, but it appears to be a significant one that paves the way to mature thinking and reasoning ability. Feinberg’s study reminds me of a billboard advertisement I once saw from a large insurance firm, which read: “Why do most 16-year-olds drive like they’re missing part of their brain? Because they are.” It takes deep sleep, and developmental time, to accomplish the neural maturation that plugs this brain “gap” within the frontal lobe. When your children finally reach their mid-twenties and your car insurance premium drops, you can thank sleep for the savings. The relationship between deep-sleep intensity and brain maturation that Feinberg described has now been observed in many different populations of children and adolescents around the world. But how can we be sure that deep sleep truly offers a neural pruning service necessary for brain maturation? Perhaps changes in sleep and brain maturation simply occur at roughly the same time but are independent of each other? The answer is found in studies of juvenile rats and cats at the equivalent stage to human adolescence. Scientists deprived these animals of deep sleep. In doing so, they halted the maturational refinement of brain connectivity, demonstrating a causal role for deep NREM sleep in propelling the brain into healthy adulthood.XV Of concern is that administering caffeine to juvenile rats will also disrupt deep NREM sleep and, as a consequence, delay numerous measures of brain maturation and the development of social activity, independent grooming, and the exploration of the environment—measures of selfmotivated learning.XVI Recognizing the importance of deep NREM sleep in teenagers has been instrumental to our understanding of healthy development, but it has also offered clues as to what happens when things go wrong in the context of abnormal development. Many of the major psychiatric disorders, such as schizophrenia, bipolar disorder, major depression, and ADHD are now considered disorders of abnormal development, since they commonly emerge during childhood and adolescence. We will return to the issue of sleep and psychiatric illness several times in the course of this book, but schizophrenia deserves special mention at this juncture. Several studies have tracked neural development using brain scans every couple of months in hundreds of young teenagers as they make their way through adolescence. A proportion of these individuals went on to develop schizophrenia in their late teenage years and early adulthood. Those individuals who developed schizophrenia had an abnormal pattern of brain maturation that was associated with synaptic pruning, especially in the frontal lobe regions where rational, logical thoughts are controlled—the inability to do so being a major symptom of schizophrenia. In a separate series of studies, we have also observed that in young individuals who are at high risk of developing schizophrenia, and in teenagers and young adults with schizophrenia, there is a two- to threefold reduction in deep NREM sleep.XVII Furthermore, the electrical brainwaves of NREM sleep are not normal in their shape or number in the affected individuals. Faulty pruning of brain connections in schizophrenia caused by sleep abnormalities is now one of the most active and exciting areas of investigation in psychiatric illness.XVIII Adolescents face two other harmful challenges in their struggle to obtain sufficient sleep as their brains continue to develop. The first is a change in their circadian rhythm. The second is early school start times. I will address the harmful and life-threatening effects of the latter in a later chapter; however, the complications of early school start times are inextricably linked with the first issue—a shift in circadian rhythm. As young children, we often wished to stay up late so we could watch television, or engage with parents and older siblings in whatever it was that they were doing at night. But when given that chance, sleep would usually get the better of us, on the couch, in a chair, or sometimes flat out on the floor. We’d be carried to bed, slumbering and unaware, by those older siblings or parents who could stay awake. The reason is not simply that children need more sleep than their older siblings or parents, but also that the circadian rhythm of a young child runs on an earlier schedule. Children therefore become sleepy earlier and wake up earlier than their adult parents. Adolescent teenagers, however, have a different circadian rhythm from their young siblings. During puberty, the timing of the suprachiasmatic nucleus is shifted progressively forward: a change that is common across all adolescents, irrespective of culture or geography. So far forward, in fact, it passes even the timing of their adult parents. As a nine-year-old, the circadian rhythm would have the child asleep by around nine p.m., driven in part by the rising tide of melatonin at this time in children. By the time that same individual has reached sixteen years of age, their circadian rhythm has undergone a dramatic shift forward in its cycling phase. The rising tide of melatonin, and the instruction of darkness and sleep, is many hours away. As a consequence, the sixteen-year-old will usually have no interest in sleeping at nine p.m. Instead, peak wakefulness is usually still in play at that hour. By the time the parents are getting tired, as their circadian rhythms take a downturn and melatonin release instructs sleep—perhaps around ten or eleven p.m., their teenager can still be wide awake. A few more hours must pass before the circadian rhythm of a teenage brain begins to shut down alertness and allow for easy, sound sleep to begin. This, of course, leads to much angst and frustration for all parties involved on the back end of sleep. Parents want their teenager to be awake at a “reasonable” hour of the morning. Teenagers, on the other hand, having only been capable of initiating sleep some hours after their parents, can still be in their trough of the circadian downswing. Like an animal prematurely wrenched out of hibernation too early, the adolescent brain still needs more sleep and more time to complete the circadian cycle before it can operate efficiently, without grogginess. If this remains perplexing to parents, a different way to frame and perhaps appreciate the mismatch is this: asking your teenage son or daughter to go to bed and fall asleep at ten p.m. is the circadian equivalent of asking you, their parent, to go to sleep at seven or eight p.m. No matter how loud you enunciate the order, no matter how much that teenager truly wishes to obey your instruction, and no matter what amount of willed effort is applied by either of the two parties, the circadian rhythm of a teenager will not be miraculously coaxed into a change. Furthermore, asking that same teenager to wake up at seven the next morning and function with intellect, grace, and good mood is the equivalent of asking you, their parent, to do the same at four or five a.m. Sadly, neither society nor our parental attitudes are well designed to appreciate or accept that teenagers need more sleep than adults, and that they are biologically wired to obtain that sleep at a different time from their parents. It’s very understandable for parents to feel frustrated in this way, since they believe that their teenager’s sleep patterns reflect a conscious choice and not a biological edict. But non-volitional, non-negotiable, and strongly biological they are. We parents would be wise to accept this fact, and to embrace it, encourage it, and praise it, lest we wish our own children to suffer developmental brain abnormalities or force a raised risk of mental illness upon them. It will not always be this way for the teenager. As they age into young and middle adulthood, their circadian schedule will gradually slide back in time. Not all the way back to the timing present in childhood, but back to an earlier schedule: one that, ironically, will lead those same (now) adults to have the same frustrations and annoyances with their own sons or daughters. By that stage, those parents have forgotten (or have chosen to forget) that they, too, were once adolescents who desired a much later bedtime than their own parents. You may wonder why the adolescent brain first overshoots in their advancing circadian rhythm, staying up late and not wanting to wake up until late, yet will ultimately return to an earlier timed rhythm of sleep and wake in later adulthood. Though we continue to examine this question, the explanation I propose is a socio-evolutionary one. Central to the goal of adolescent development is the transition from parental dependence to independence, all the while learning to navigate the complexities of peergroup relationships and interactions. One way in which Mother Nature has perhaps helped adolescents unbuckle themselves from their parents is to march their circadian rhythms forward in time, past that of their adult mothers and fathers. This ingenious biological solution selectively shifts teenagers to a later phase when they can, for several hours, operate independently—and do so as a peer-group collective. It is not a permanent or full dislocation from parental care, but as safe an attempt at partially separating soon-to-be adults from the eyes of Mother and Father. There is risk, of course. But the transition must happen. And the time of day when those independent adolescent wings unfold, and the first solo flights from the parental nest occur, is not a time of day at all, but rather a time of night, thanks to a forward-shifted circadian rhythm. We are still learning more about the role of sleep in development. However, a strong case can already be made for defending sleep time in our adolescent youth, rather than denigrating sleep as a sign of laziness. As parents, we are often too focused on what sleep is taking away from our teenagers, without stopping to think about what it may be adding. Caffeine also comes into question. There was once an education policy in the US known as “No child left behind.” Based on scientific evidence, a new policy has rightly been suggested by my colleague Dr. Mary Carskadon: “No child needs caffeine.” SLEEP IN MIDLIFE AND OLD AGE SLEEP IN MIDLIFE AND OLD AGE As you, the reader, may painfully know; sleep is more problematic and disordered in older adults. The effects of certain medications more commonly taken by older adults, together with coexisting medical conditions, result in older adults being less able, on average, to obtain as much sleep, or as restorative a sleep, as young adults. That older adults simply need less sleep is a myth. Older adults appear to need just as much sleep as they do in midlife, but are simply less able to generate that (still necessary) sleep. Affirming this, large surveys demonstrate that despite getting less sleep, older adults reported needing, and indeed trying, to obtain just as much sleep as younger adults. There are additional scientific findings supporting the fact that older adults still need a full night of sleep, just like young adults, and I will address those shortly. Before I do, let me first explain the core impairments of sleep that occur with aging, and why those findings help falsify the argument that older adults don’t need to sleep as much. These three key changes are: (1) reduced quantity/quality, (2) reduced sleep efficiency, and (3) disrupted timing of sleep. The postadolescent stabilization of deep-NREM sleep in your early twenties does not remain very stable for very long. Soon—sooner than you may imagine or wish—comes a great sleep recession, with deep sleep being hit especially hard. In contrast to REM sleep, which remains largely stable in midlife, the decline of deep NREM sleep is already under way by your late twenties and early thirties. As you enter your fourth decade of life, there is a palpable reduction in the electrical quantity and quality of that deep NREM sleep. You obtain fewer hours of deep sleep, and those deep NREM brainwaves become smaller, less powerful, and fewer in number. Passing into your mid- and late forties, age will have stripped you of 60 to 70 percent of the deep sleep you were enjoying as a young teenager. By the time you reach seventy years old, you will have lost 80 to 90 percent of your youthful deep sleep. Certainly, when we sleep at night, and even when we wake in the morning, most of us do not have a good sense of our electrical sleep quality. Frequently this means that many seniors progress through their later years not fully realizing how degraded their deep-sleep quantity and quality have become. This is an important point: it means that elderly individuals fail to connect their deterioration in health with their deterioration in sleep, despite causal links between the two having been known to scientists for many decades. Seniors therefore complain about and seek treatment for their health issues when visiting their GP, but rarely ask for help with their equally problematic sleep issues. As a result, GPs are rarely motivated to address the problematic sleep in addition to the problematic health concerns of the older adult. To be clear, not all medical problems of aging are attributable to poor sleep. But far more of our age-related physical and mental health ailments are related to sleep impairment than either we, or many doctors, truly realize or treat seriously. Once again, I urge an elderly individual who may be concerned about their sleep not to seek a sleeping pill prescription. Instead, I recommend you first explore the effective and scientifically proven non-pharmacological interventions that a doctor who is board certified in sleep medicine can provide. The second hallmark of altered sleep as we age, and one that older adults are more conscious of, is fragmentation. The older we get, the more frequently we wake up throughout the night. There are many causes, including interacting medications and diseases, but chief among them is a weakened bladder. Older adults therefore visit the bathroom more frequently at night. Reducing fluid intake in the mid- and late evening can help, but it is not a cure-all. Due to sleep fragmentation, older individuals will suffer a reduction in sleep efficiency, defined as the percent of time you were asleep while in bed. If you spent eight hours in bed, and slept for all eight of those hours, your sleep efficiency would be 100 percent. If you slept just four of those eight hours, your sleep efficiency would be 50 percent. As healthy teenagers, we enjoyed a sleep efficiency of about 95 percent. As a reference anchor, most sleep doctors consider good-quality sleep to involve a sleep efficiency of 90 percent or above. By the time we reach our eighties, sleep efficiency has often dropped below 70 or 80 percent; 70 to 80 percent may sound reasonable until you realize that, within an eight-hour period in bed, it means you will spend as much as one to one and a half hours awake. Inefficient sleep is no small thing, as studies assessing tens of thousands of older adults show. Even when controlling for factors such as body mass index, gender, race, history of smoking, frequency of exercise, and medications, the lower an older individual’s sleep efficiency score, the higher their mortality risk, the worse their physical health, the more likely they are to suffer from depression, the less energy they report, and the lower their cognitive function, typified by forgetfulness.XIX Any individual, no matter what age, will exhibit physical ailments, mental health instability, reduced alertness, and impaired memory if their sleep is chronically disrupted. The problem in aging is that family members observe these daytime features in older relatives and jump to a diagnosis of dementia, overlooking the possibility that bad sleep is an equally likely cause. Not all old adults with sleep issues have dementia. But I will describe evidence in chapter 7 that clearly shows how and why sleep disruption is a causal factor contributing to dementia in mid- and later life. A more immediate, though equally dangerous, consequence of fragmented sleep in the elderly warrants brief discussion: the nighttime bathroom visits and associated risk of falls and thus fractures. We are often groggy when we wake up during the night. Add to this cognitive haze the fact that it is dark. Furthermore, having been recumbent in bed means that when you stand and start moving, blood can race from your head, encouraged by gravity, down toward your legs. You feel light-headed and unsteady on your feet as a consequence. The latter is especially true in older adults whose control of blood pressure is itself often impaired. All of these issues mean that an older individual is at a far higher risk of stumbling, falling, and breaking bones during nighttime visits to the bathroom. Falls and fractures markedly increase morbidity and significantly hasten the end of life of an older adult. In the footnotes, I offer a list of tips for safer nighttime sleep in the elderly.XX The third sleep change with advanced age is that of circadian timing. In sharp contrast to adolescents, seniors commonly experience a regression in sleep timing, leading to earlier and earlier bedtimes. The cause is an earlier evening release and peak of melatonin as we get older, instructing an earlier start time for sleep. Restaurants in retirement communities have long known of this age-related shift in bedtime preference, epitomized (and accommodated) by the “early-bird special.” Changes in circadian rhythms with advancing age may appear harmless, but they can be the cause of numerous sleep (and wake) problems in the elderly. Older adults often want to stay awake later into the evening so that they can go to theater or the movies, socialize, read, or watch television. But in doing so, they find themselves waking up on the couch, in a movie theater seat, or in a reclining chair, having inadvertently fallen asleep mid-evening. Their regressed circadian rhythm, instructed by an earlier release of melatonin, left them no choice. But what seems like an innocent doze has a damaging consequence. The early-evening snooze will jettison precious sleep pressure, clearing away the sleepiness power of adenosine that had been steadily building throughout the day. Several hours later, when that older individual gets into bed and tries to fall asleep, they may not have enough sleep pressure to fall asleep quickly, or stay asleep as easily. An erroneous conclusion follows: “I have insomnia.” Instead, dozing off in the evening, which most older adults do not realize is classified as napping, can be the source of sleep difficulty, not true insomnia. A compounding problem arrives in the morning. Despite having had trouble falling asleep that night and already running a sleep debt, the circadian rhythm—which, as you’ll remember from chapter 2, operates independently of the sleep-pressure system—will start to rise around four or five a.m. in many elderly individuals, enacting its classic earlier schedule in seniors. Older adults are therefore prone to wake up early in the morning as the alerting drumbeat of the circadian rhythm grows louder, and corresponding hopes of returning back to sleep diminish in tandem. Making matters worse, the strengths of the circadian rhythm and amount of nighttime melatonin released also decrease the older we get. Add these things up, and a selfperpetuating cycle ensues wherein many seniors are battling a sleep debt, trying to stay awake later in the evening, inadvertently dozing off earlier, finding it hard to fall or stay asleep at night, only to be woken up earlier than they wish because of a regressed circadian rhythm. There are methods that can help push the circadian rhythm in older adults somewhat later, and also strengthen the rhythm. Here again, they are not a complete or perfect solution, I’m sad to say. Later chapters will describe the damaging influence of artificial light on the circadian twenty-four-hour rhythm (bright light at night). Evening light suppresses the normal rise in melatonin, pushing an average adult’s sleep onset time into the early-morning hours, preventing sleep at a reasonable hour. However, this same sleepdelaying effect can be put to good use in older adults, if timed correctly. Having woken up early, many older adults are physically active during the morning hours, and therefore obtain much of their bright-light exposure in the first half of the day. This is not optimal, as it reinforces the early-to-rise, early-to-decline cycle of the twenty-four-hour internal clock. Instead, older adults who want to shift their bedtimes to a later hour should get brightlight exposure in the late-afternoon hours. I am not, however, suggesting that older adults stop exercising in the morning. Exercise can help solidify good sleep, especially in the elderly. Instead, I advise two modifications for seniors. First, wear sunglasses during morning exercise outdoors. This will reduce the influence of morning light being sent to your suprachiasmatic clock that would otherwise keep you on an early-to-rise schedule. Second, go back outside in the late afternoon for sunlight exposure, but this time do not wear sunglasses. Make sure to wear sun protection of some sort, such as a hat, but leave the sunglasses at home. Plentiful later-afternoon daylight will help delay the evening release of melatonin, helping push the timing of sleep to a later hour. Older adults may also wish to consult with their doctor about taking melatonin in the evening. Unlike young or middle-age adults, where melatonin has not proved efficacious for helping sleep beyond the circumstance of jet lag, prescription melatonin has been shown to help boost the otherwise blunted circadian and associated melatonin rhythm in the elderly, reducing the time taken to fall asleep and improving self-reported sleep quality and morning alertness.XXI The change in circadian rhythm as we get older, together with more frequent trips to the bathroom, help to explain two of the three key nighttime issues in the elderly: early sleep onset/offset and sleep fragmentation. They do not, however, explain the first key change in sleep with advancing age: the loss of deep-sleep quantity and quality. Although scientists have known about the pernicious loss of deep sleep with advancing age for many decades, the cause has remained elusive: What is it about the aging process that so thoroughly robs the brain of this essential state of slumber? Beyond scientific curiosity, it is also a pressing clinical issue for the elderly, considering the importance of deep sleep for learning and memory, not to mention all branches of bodily health, from cardiovascular and respiratory, to metabolic, energy balance, and immune function. Working with an incredibly gifted team of young researchers, I set out to try and answer this question several years ago. I wondered whether the cause of this sleep decline was to be found in the intricate pattern of structural brain deterioration that occurs as we age. You will recall from chapter 3 that the powerful brainwaves of deep NREM sleep are generated in the middle-frontal regions of the brain, several inches above the bridge of your nose. We already knew that as individuals get older, their brains do not deteriorate uniformly. Instead, some parts of the brain start losing neurons much earlier and far faster than other parts of the brain—a process called atrophy. After performing hundreds of brain scans, and amassing almost a thousand hours of overnight sleep recordings, we discovered a clear answer, unfolding in a three-part story. First, the areas of the brain that suffer the most dramatic deterioration with aging are, unfortunately, the very same deep-sleep-generating regions—the middle-frontal regions seated above the bridge of the nose. When we overlaid the map of brain degeneration hot spots in the elderly on the brain map that highlighted the deep-sleep-generating regions in young adults, there was a near-perfect match. Second, and unsurprisingly, older adults suffered a 70 percent loss of deep sleep, compared with matched young individuals. Third, and most critical, we discovered that these changes were not independent, but instead significantly connected with one another: the more severe the deterioration that an older adult suffers within this specific mid-frontal region of their brain, the more dramatic their loss of deep NREM sleep. It was a saddening confirmation of my theory: the parts of our brain that ignite healthy deep sleep at night are the very same areas that degenerate, or atrophy, earliest and most severely as we age. In the years leading up to these investigations, my research team and several others around the world had demonstrated how critical deep sleep was for cementing new memories and retaining new facts in young adults. Knowing this, we had included a twist to our experiment in older adults. Several hours before going to sleep, all of these seniors learned a list of new facts (word associations), quickly followed by an immediate memory test to see how much information they had retained. The next morning, following the night of sleep recording, we tested them a second time. We could therefore determine the amount of memory savings that had occurred for any one individual across the night of sleep. The older adults forgot far more of the facts by the following morning than the young adults—a difference of almost 50 percent. Furthermore, those older adults with the greatest loss of deep sleep showed the most catastrophic overnight forgetting. Poor memory and poor sleep in old age are therefore not coincidental, but rather significantly interrelated. The findings helped us shed new light on the forgetfulness that is all too common in the elderly, such as difficulty remembering people’s names or memorizing upcoming hospital appointments. It is important to note that the extent of brain deterioration in older adults explained 60 percent of their inability to generate deep sleep. This was a helpful finding. But the more important lesson to be gleaned from this discovery for me was that 40 percent of the explanation for the loss of deep sleep in the elderly remained unaccounted for by our discovery. We are now hard at work trying to discover what that is. Recently, we identified one factor—a sticky, toxic protein that builds up in the brain called beta-amyloid that is a key cause of Alzheimer’s disease: a discovery discussed in the next several chapters. More generally, these and similar studies have confirmed that poor sleep is one of the most underappreciated factors contributing to cognitive and medical ill health in the elderly, including issues of diabetes, depression, chronic pain, stroke, cardiovascular disease, and Alzheimer’s disease. An urgent need therefore exists for us to develop new methods that restore some quality of deep, stable sleep in the elderly. One promising example that we have been developing involves brain stimulation methods, including controlled electrical stimulation pulsed into the brain at night. Like a supporting choir to a flagging lead vocalist, our goal is to electrically sing (stimulate) in time with the ailing brainwaves of older adults, amplifying the quality of their deep brainwaves and salvaging the health- and memory-promoting benefits of sleep. Our early results look cautiously promising, though much, much more work is required. With replication, our findings can further debunk the long-held belief that we touched on earlier: older adults need less sleep. This myth has stemmed from certain observations that, to some scientists, suggest that an eighty-year-old, say, simply needs less sleep than a fifty-year-old. Their arguments are as follows. First, if you deprive older adults of sleep, they do not show as dramatic an impairment in performance on a basic response-time task as a younger adult. Therefore, older adults must need sleep less than younger adults. Second, older adults generate less sleep than young adults, so by inference, older adults must simply need sleep less. Third, older adults do not show as strong a sleep rebound after a night of deprivation compared with young adults. The conclusion was that seniors therefore have less need for sleep if they have less of a recovery rebound. There are, however, alternative explanations. Using performance as a measure of sleep need is perilous in older adults, since older adults are already impaired in their reaction times to begin with. Said unkindly, older adults don’t have much further to fall in terms of getting worse, sometimes called a “floor effect,” making it difficult to estimate the real performance impact of sleep deprivation. Next, just because an older individual obtains less sleep, or does not obtain as much recovery sleep after sleep deprivation, does not necessarily mean that their need for sleep is less. It may just as easily indicate that they cannot physiologically generate the sleep they still nevertheless need. Take the alternative example of bone density, which is lower in older compared with younger adults. We do not assume that older individuals need weaker bones just because they have reduced bone density. Nor do we believe that older adults have bones that are weaker simply because they don’t recover bone density and heal as quickly as young adults after suffering a fracture or break. Instead, we realize that their bones, like the centers of the brain that produce sleep, deteriorate with age, and we accept this degeneration as the cause of numerous health issues. We consequently provide dietary supplements, physical therapy, and medications to try to offset bone deficiency. I believe we should recognize and treat sleep impairments in the elderly with a similar regard and compassion, recognizing that they do, in fact, need just as much sleep as other adults. Finally, the preliminary results of our brain stimulation studies suggest that older adults, may, in fact, need more sleep than they themselves can naturally generate, since they benefit from an improvement in sleep quality, albeit through artificial means. If older individuals did not need more deep sleep, then they should already be satiated, and not benefit from receiving more (artificially, in this case). Yet they do benefit from having their sleep enhanced, or perhaps worded correctly, restored. That is, older adults, and especially those with different forms of dementia, appear to suffer an unmet sleep need, which demands new treatment options: a topic that we shall soon return to.