Pagina principale Why We Sleep: Unlocking the Power of Sleep and Dreams

Why We Sleep: Unlocking the Power of Sleep and Dreams

Categories: Biology
Anno: 2017
Editore: Scribner
Lingua: english
Pagine: 277
ISBN 10: 1501144316
ISBN 13: 9781501144318
File: PDF, 3.39 MB
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Contents

– Part 1 –
This Thing Called Sleep
Chapter 1

To Sleep . . .

Chapter 2

Caffeine, Jet Lag, and Melatonin: Losing and Gaining Control of Your Sleep Rhythm

Chapter 3 Defining and Generating Sleep: Time Dilation and What We Learned from a Baby in
1952
Chapter 4 Ape Beds, Dinosaurs, and Napping with Half a Brain: Who Sleeps, How Do We Sleep,
and How Much?
Chapter 5

Changes in Sleep Across the Life Span

– Part 2 –
Why Should You Sleep?
Chapter 6

Your Mother and Shakespeare Knew: The Benefits of Sleep for the Brain

Chapter 7

Too Extreme for the Guinness Book of World Records: Sleep Deprivation and the Brain

Chapter 8

Cancer, Heart Attacks, and a Shorter Life: Sleep Deprivation and the Body

– Part 3 –
How and Why We Dream
Chapter 9

Routinely Psychotic: REM-Sleep Dreaming

Chapter 10 Dreaming as Overnight Therapy
Chapter 11 Dream Creativity and Dream Control

– Part 4 –
From Sleeping Pills to Society Transformed
Chapter 12 Things That Go Bump in the Night: Sleep Disorders and Death Caused by No Sleep
Chapter 13 iPads, Factory Whistles, and Nightcaps: What’s Stopping You from Sleeping?
Chapter 14 Hurting and Helping Your Sleep: Pills vs. Therapy
Chapter 15 Sleep and Society: What Medicine and Education Are Doing Wrong; What Google
and NASA Are Doing Right

Chapter 16 A New Vision for Sleep in the Twenty-First Century
Conclusion: To Sleep or Not to Sleep
Acknowledgments
About the Author
Appendix: Twelve Tips for Healthy Sleep
Illustration Permissions

To Dacher Keltner, for inspiring me to write.

PART 1

This Thing Called Sleep

CH; APTER 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 Brontë’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
naïveté, 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-in-america/episode/sleepless-inamerica.
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
Jean-Jacques 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 twentyfour-hour 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
self-generated, 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 twenty-six 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 selfrespecting 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.

Figure 1: Typical Twenty-Four-Hour Circadian Rhythm (Core Body Temperature)

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.
Figure 2: The Cycle of Melatonin

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 timelagged 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 shortterm 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 sleep-inducing 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 sleep-disrupting 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.
Figure 3: Effects of Various Drugs on Spider Web Building

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.

Figure 4: The Two Factors Regulating Sleep and Wakefulness

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.

Figure 5: The Urge to Be Awake

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.
Figure 6: The Urge to 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 self-experiment, 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.
Figure 7: The Ebb and Flow of Sleep Deprivation

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 sleep-disordered 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 twenty-four 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
variability of 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 badquality 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, ovalshaped 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 non-conscious 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 goldstandard 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).
Figure 8: The Architecture of Sleep

Had I not added the vertical dashed lines demarcating each ninety-minute 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 early-morning
meeting or because you are an athlete whose coach demands early-morning 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)?

Figure 9: The Brainwaves of Wake and 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, slow-wave 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 deepsleep 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 slow-wave 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
breath-pause. 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 worl