Why We Sleep: The New Science of Sleep and Dreams

by Matthew Walker

If you really must keep going—and you have made that judgment in the life-threatening context it genuinely poses—then pull off the road into a safe layby for a short time. Take a brief nap (twenty to thirty minutes). When you wake up, do not start driving. You will be suffering from sleep inertia—the carryover effects of sleep into wakefulness. Wait for another twenty to thirty minutes, perhaps after having a cup of coffee if you really must, and only then start driving again.

When Dinges and Rosekind reported their findings to the FAA, they recommended that “prophylactic naps”—naps taken early during long-haul flights—should be instituted as policy among pilots, as many other aviation authorities around the world now permit.

The FAA, while believing the findings, was not convinced by the nomenclature. They believed the term “prophylactic” was ripe for many a snide joke among pilots. Dinges suggested the alternative of “planned napping.” The FAA didn’t like this, either, feeling it to be too “management-like.” Their suggestion was “power napping,” which they believed was more fitting with leadership- or dominance-based job positions, others being CEOs or military executives. And so the “power nap” was born.

The problem, however, is that people, especially those in such positions, came to erroneously believe that a twenty-minute power nap was all you needed to survive and fun...

No matter what you may have heard or read in the popular media, there is no scientific evidence we have suggesting that a drug, a device, or any amount of psychological willpower can replace sleep.

But in the subsequent studies that Dinges and many other researchers (myself included) have performed, neither naps nor caffeine can salvage more complex functions of the brain, including learning, memory, emotional stability, complex reasoning, or decision-making.

We have, however, discovered a very rare collection of individuals who appear to be able to survive on six hours of sleep, and show minimal impairment—a sleepless elite, as it were. Give them hours and hours of sleep opportunity in the laboratory, with no alarms or wake-up calls, and still they naturally sleep this short amount and no more.

There is but a fraction of 1 percent of the population who are truly resilient to the effects of chronic sleep restriction at all levels of brain function. It is far, far more likely that you will be struck by lightning (the lifetime odds being 1 in 12,000) than being truly capable of surviving on insufficient sleep thanks to a rare gene.

Many of us know that inadequate sleep plays havoc with our emotions.

A structure located in the left and right sides of the brain, called the amygdala—a key hot spot for triggering strong emotions such as anger and rage, and linked to the fight-or-flight response—showed well over a 60 percent amplification in emotional reactivity in the participants who were sleep-deprived.

It was as though, without sleep, our brain reverts to a primitive pattern of uncontrolled reactivity. We produce unmetered, inappropriate emotional reactions, and are unable to place events into a broader or considered context.

With a full night of plentiful sleep, we have a balanced mix between our emotional gas pedal (amygdala) and brake (prefrontal cortex). Without sleep, however, the strong coupling between these two brain regions is lost.

Insufficient sleep does not, therefore, push the brain into a negative mood state and hold it there. Rather, the under-slept brain swings excessively to both extremes of emotional valence, positive and negative.

Hypersensitivity to pleasurable experiences can lead to sensation-seeking, risk-taking, and addiction. Sleep disturbance is a recognized hallmark associated with addictive substance use.

Psychiatry has long been aware of the coincidence between sleep disturbance and mental illness. However, a prevailing view in psychiatry has been that mental disorders cause sleep disruption—a one-way street of influence. Instead, we have demonstrated that otherwise healthy people can experience a neurological pattern of brain activity similar to that observed in many of these psychiatric conditions simply by having their sleep disrupted or blocked.

Bipolar disorder should not be confused with major depression, in which individuals slide exclusively down into the negative end of the mood spectrum. Instead, patients with bipolar depression vacillate between both ends of the emotion spectrum, experiencing dangerous periods of mania (excessive, reward-driven emotional behavior) and also periods of deep depression (negative moods and emotions).

Depression is not, as you may think, just about the excess presence of negative feelings. Major depression has as much to do with absence of positive emotions, a feature described as anhedonia: the inability to gain pleasure from normally pleasurable experiences, such as food, socializing, or sex.

As the course continues throughout the semester, I return to the results of their sleep survey and link their own sleep habits with the science we are learning about. In this way, I try to point out the very personal dangers they face to their psychological and physical health due to their insufficient sleep, and the danger they themselves pose to society as a consequence.

Conducting a survey for understanding data behaviour.

However, when we looked at this same brain structure in the sleep-deprived participants, we could not find any significant learning activity whatsoever. It was as though sleep deprivation had shut down their memory in-box, and any new incoming information was simply being bounced.

Simply disrupting the depth of an individual’s NREM sleep with infrequent sounds, preventing deep sleep and keeping the brain in shallow sleep, without waking the individual up will produce similar brain deficits and learning impairments.

You may have seen a movie called Memento, in which the lead character suffers brain damage and, from that point forward, can no longer make any new memories. In neurology, he is what we call “densely amnesic.” The part of his brain that was damaged was the hippocampus. It is the very same structure that...

Even the most elemental units of the learning process—the production of proteins that form the building blocks of memories within these synapses—are stunted by the state of sleep loss.

A lack of sleep therefore is a deeply penetrating and corrosive force that enfeebles the memory-making apparatus within your brain, preventing you from constructing lasting memory traces.

end-loading exams in the final days of the semester was an asinine decision. It forced a behavior in our students—that of short sleeping or pulling all-nighters leading up to the exam—that

it was long past the time for us to

Instead, I split my courses up into thirds so that students only have to study a handful of lectures at a time. Furthermore, none of the exams are cumulative. It’s a tried-and-true effect in the psychology of memory, described as mass versus spaced learning.

As with a fine-dining experience, it is far more preferable to separate the educational meal into smaller courses, with breaks in between to allow for digestion, rather than attempt to cram all of those informational calories down in one go.

In other words, if you don’t sleep the very first night after learning, you lose the chance to consolidate those memories, even if you get lots of “catch-up” sleep thereafter.

In terms of memory, then, sleep is not like the bank. You cannot accumulate a debt and hope to pay it off at a later point in time. Sleep for memory consolidation is an all-or-nothing event.

More than 40 million people suffer from the debilitating disease. That number has accelerated as the human life span has stretched, but also, importantly, as total sleep time has decreased.

While much remains to be understood, we now recognize that sleep disruption and Alzheimer’s disease interact in a self-fulfilling, negative spiral that can initiate and/or accelerate the condition.

Alzheimer’s disease is associated with the buildup of a toxic form of protein called beta-amyloid, which aggregates in sticky clumps, or plaques, within the brain. Amyloid plaques are poisonous to neurons, killing the surrounding brain cells.

And it was not just a general loss of deep sleep, which is common as we get older, but the very deepest of the powerful slow brainwaves of NREM sleep that the disease was ruthlessly eroding.

We are now examining whether this very particular “dent” in sleeping brainwave activity represents an early identifier of those who are at greatest risk of developing Alzheimer’s disease, years in advance.

Although the glymphatic system—the support team—is somewhat active during the day, Nedergaard and her team discovered that it is during sleep that this neural sanitization work kicks into high gear.

Phrased differently, and perhaps more simply, wakefulness is low-level brain damage, while sleep is neurological sanitation.

From this cascade comes a prediction: getting too little sleep across the adult life span will significantly raise your risk of developing Alzheimer’s disease.

But it is worth recalling that we already use this conceptual approach in medicine in the form of prescribing statins to higher-risk individuals in their forties and fifties to help prevent cardiovascular disease, rather than having to treat it decades later.

Chapter 8 Cancer, Heart Attacks, and a Shorter Life

Sleep is more than a pillar; it is the foundation on which the other two health bastions sit.

Widening the lens of focus, there are more than twenty large-scale epidemiological studies that have tracked millions of people over many decades, all of which report the same clear relationship: the shorter your sleep, the shorter your life.

Over

A lack of sleep more than accomplishes its own, independent attack on the heart.

Adults forty-five years or older who sleep fewer than six hours a night are 200 percent more likely to have a heart attack or stroke during their lifetime, as compared with those sleeping seven to eight hours a night.

Beyond accelerating your heart rate and increasing your blood pressure, a lack of sleep further erodes the fabric of those strained blood vessels, especially those that feed the heart itself, called the coronary arteries.

Although the mechanisms by which sleep deprivation degrades cardiovascular health are numerous, they all appear to cluster around a common culprit, called the sympathetic nervous system.

the evolutionarily ancient fight-or-flight stress response within the body,

For as long as the state of insufficient sleep lasts, and for some time thereafter, the body remains stuck in some degree of a fight-or-flight state.

As your sleep-deprived heart beats faster, the volumetric rate of blood pumped through your vasculature increases, and with that comes the hypertensive state of your blood pressure. Occurring at the same time is a chronic increase in a stress hormone called cortisol, which is triggered by the overactive sympathetic nervous system.

During deep NREM sleep specifically, the brain communicates a calming signal to the fight-or-flight sympathetic branch of the body’s nervous system, and does so for long durations of the night. As a result, deep sleep prevents an escalation of this physiological stress that is synonymous with increased blood pressure, heart attack, heart failure, and stroke.