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CHAPTER 7

Too Extreme for the Guinness Book of World Records

Sleep Deprivation and the Brain

Struck by the weight of damning scientific evidence, the Guinness Book of World Records has stopped recognizing attempts to break the sleep deprivation world record. Recall that Guinness deems it acceptable for a man (Felix Baumgartner) to ascend 128,000 feet into the outer reaches of our atmosphere in a hot-air balloon wearing a spacesuit, open the door of his capsule, stand atop a ladder suspended above the planet, and then free-fall back down to Earth at a top speed of 843 mph (1,358 kmh), passing through the sound barrier while creating a sonic boom with just his body. But the risks associated with sleep deprivation are considered to be far, far higher. Unacceptably high, in fact, based on the evidence.

What is that compelling evidence? In the following two chapters, we will learn precisely why and how sleep loss inflicts such devastating effects on the brain, linking it to numerous neurological and psychiatric conditions (e.g., Alzheimer’s disease, anxiety, depression, bipolar disorder, suicide, stroke, and chronic pain), and on every physiological system of the body, further contributing to countless disorders and disease (e.g., cancer, diabetes, heart attacks, infertility, weight gain, obesity, and immune deficiency). No facet of the human body is spared the crippling, noxious harm of sleep loss. We are, as you will see, socially, organizationally, economically, physically, behaviorally, nutritionally, linguistically, cognitively, and emotionally dependent upon sleep.

This chapter deals with the dire and sometimes deadly consequences of inadequate sleep on the brain. The chapter that follows will recount the diverse—though equally ruinous and similarly fatal—effects of short sleep on the body.

PAY ATTENTION

There are many ways in which a lack of sufficient sleep will kill you. Some take time; others are far more immediate. One brain function that buckles under even the smallest dose of sleep deprivation is concentration. The deadly societal consequences of these concentration failures play out most obviously and fatally in the form of drowsy driving. Every hour, someone dies in a traffic accident in the US due to a fatigue-related error.

There are two main culprits of drowsy-driving accidents. The first is people completely falling asleep at the wheel. This happens infrequently, however, and usually requires an individual to be acutely sleep-deprived (having gone without shut-eye for twenty-plus hours). The second, more common cause is a momentary lapse in concentration, called a microsleep. These last for just a few seconds, during which time the eyelid will either partially or fully close. They are usually suffered by individuals who are chronically sleep restricted, defined as getting less than seven hours of sleep a night on a routine basis.

During a microsleep, your brain becomes blind to the outside world for a brief moment—and not just the visual domain, but in all channels of perception. Most of the time you have no awareness of the event. More problematic is that your decisive control of motor actions, such as those necessary for operating a steering wheel or a brake pedal, will momentarily cease. As a result, you don’t need to fall asleep for ten to fifteen seconds to die while driving. Two seconds will do it. A two-second microsleep at 30 mph with a modest angle of drift can result in your vehicle transitioning entirely from one lane to the next. This includes into oncoming traffic. Should this happen at 60 mph, it may be the last microsleep you ever have.

David Dinges at the University of Pennsylvania, a titan in the field of sleep research and personal hero of mine, has done more than any scientist in history to answer the following fundamental question: What is the recycle rate of a human being? That is, how long can a human go without sleep before their performance is objectively impaired? How much sleep can a human lose each night, and over how many nights, before critical processes of the brain fail? Is that individual even aware of how impaired they are when sleep-deprived? How many nights of recovery sleep does it take to restore the stable performance of a human after sleep loss?

Dinges’s research employs a disarmingly simple attention test to measure concentration. You must press a button in response to a light that appears on a button box or computer screen within a set period of time. Your response, and the reaction time of that response, are both measured. Thereafter, another light comes on, and you do the same thing. The lights appear in an unpredictable manner, sometimes in quick succession, other times randomly separated by a pause lasting several seconds.

Sounds easy, right? Try doing it for ten minutes straight, every day, for fourteen days. That’s what Dinges and his research team did to a large number of subjects who were monitored under strict laboratory conditions. All of the subjects started off by getting a full eight-hour sleep opportunity the night before the test, allowing them to be assessed when fully rested. Then, the participants were divided into four different experimental groups. Rather like a drug study, each group was given a different “dose” of sleep deprivation. One group was kept up for seventy-two hours straight, going without sleep for three consecutive nights. The second group was allowed four hours of sleep each night. The third group was given six hours of sleep each night. The lucky fourth group was allowed to keep sleeping eight hours each night.

There were three key findings. First, although sleep deprivation of all these varied amounts caused a slowing in reaction time, there was something more telling: participants would, for brief moments, stop responding altogether. Slowness was not the most sensitive signature of sleepiness, entirely missed responses were. Dinges was capturing lapses, otherwise known as microsleeps: the real-life equivalent of which would be failing to react to a child who runs out in front of your car when chasing a ball.

When describing the findings, Dinges will often have you think of the repeating beep from a heart monitor in a hospital: beep, beep, beep. Now picture the dramatic sound effect you hear in emergency room television dramas when a patient starts to slip away as doctors frantically try to save their life. At first, the heartbeats are constant—beep, beep, beep—as are your responses on the visual attention task when you are well rested: stable, regular. Switch to your performance when sleep-deprived, and it is the aural equivalent of the patient in the hospital going into cardiac arrest: beep, beep, beep, beeeeeeeeeeeeeep. Your performance has flatlined. No conscious response, no motor response. A microsleep. And then the heartbeat comes back, as will your performance—beep, beep, beep—but only for a short while. Soon, you have another arrest: beep, beep, beeeeeeeeeeeeeep. More microsleeps.

Comparing the number of lapses, or microsleeps, day after day across the four different experimental groups gave Dinges a second key finding. Those individuals who slept eight hours every night maintained a stable, near-perfect performance across the two weeks. Those in the three-night total sleep deprivation group suffered catastrophic impairment, which was no real surprise. After the first night of no sleep at all, their lapses in concentration (missed responses) increased by over 400 percent. The surprise was that these impairments continued to escalate at the same ballistic rate after a second and third night of total sleep deprivation, as if they would continue to escalate in severity if more nights of sleep were lost, showing no signs of flattening out.

But it was the two partial sleep deprivation groups that brought the most concerning message of all. After four hours of sleep for six nights, participants’ performance was just as bad as those who had not slept for twenty-four hours straight—that is, a 400 percent increase in the number of microsleeps. By day 11 on this diet of four hours of sleep a night, participants’ performance had degraded even further, matching that of someone who had pulled two back-to-back all-nighters, going without sleep for forty-eight hours.

Most worrying from a societal perspective were the individuals in the group who obtained six hours of sleep a night—something that may sound familiar to many of you. Ten days of six hours of sleep a night was all it took to become as impaired in performance as going without sleep for twenty-four hours straight. And like the total sleep deprivation group, the accruing performance impairment in the four-hour and six-hour sleep groups showed no signs of leveling out. All signs suggested that if the experiment had continued, the performance deterioration would continue to build up over weeks or months.

Another research study, this one led by Dr. Gregory Belenky at Walter Reed Army Institute of Research, published almost identical results around the same time. They also tested four groups of participants, but they were given nine hours, seven hours, five hours, and three hours of sleep across seven days.

YOU DO NOT KNOW HOW SLEEP-DEPRIVED YOU ARE WHEN YOU ARE SLEEP-DEPRIVED

The third key finding, common to both of these studies, is the one I personally think is the most harmful of all. When participants were asked about their subjective sense of how impaired they were, they consistently underestimated their degree of performance disability. It was a miserable predictor of how bad their performance actually, objectively was. It is the equivalent of someone at a bar who has had far too many drinks picking up his car keys and confidently telling you, “I’m fine to drive home.”

Similarly problematic is baseline resetting. With chronic sleep restriction over months or years, an individual will actually acclimate to their impaired performance, lower alertness, and reduced energy levels. That low-level exhaustion becomes their accepted norm, or baseline. Individuals fail to recognize how their perennial state of sleep deficiency has come to compromise their mental aptitude and physical vitality, including the slow accumulation of ill health. A link between the former and latter is rarely made in their mind. Based on epidemiological studies of average sleep time, millions of individuals unwittingly spend years of their life in a sub-optimal state of psychological and physiological functioning, never maximizing their potential of mind or body due to their blind persistence in sleeping too little. Sixty years of scientific research prevent me from accepting anyone who tells me that he or she can “get by on just four or five hours of sleep a night just fine.”

Returning to Dinges’s study results, you may have predicted that optimal performance would return to all of the participants after a good long night of recovery sleep, similar to many people’s notion of “sleeping it off” on the weekends to pay off their weeknight sleep debt. However, even after three nights of ad lib recovery sleep, performance did not return to that observed at the original baseline assessment when those same individuals had been getting a full eight hours of sleep regularly. Nor did any group recover all the sleep hours they had lost in the days prior. As we have already learned, the brain is incapable of that.

In a disturbing later study, researchers in Australia took two groups of healthy adults, one of whom they got drunk to the legal driving limit (.08 percent blood alcohol), the other of whom they sleep-deprived for a single night. Both groups performed the concentration test to assess attention performance, specifically the number of lapses. After being awake for nineteen hours, people who were sleep-deprived were as cognitively impaired as those who were legally drunk. Said another way, if you wake up at seven a.m. and remain awake throughout the day, then go out socializing with friends until late that evening, yet drink no alcohol whatsoever, by the time you are driving home at two a.m. you are as cognitively impaired in your ability to attend to the road and what is around you as a legally drunk driver. In fact, participants in the above study started their nosedive in performance after just fifteen hours of being awake (ten p.m. in the above scenario).

Car crashes rank among the leading causes of death in most first-world nations. In 2016, the AAA Foundation in Washington, DC, released the results of an extensive study of over 7,000 drivers in the US, tracked in detail over a two-year period.I The key finding, shown in figure 12, reveals just how catastrophic drowsy driving is when it comes to car crashes. Operating on less than five hours of sleep, your risk of a car crash increases threefold. Get behind the wheel of a car when having slept just four hours or less the night before and you are 11.5 times more likely to be involved in a car accident. Note how the relationship between decreasing hours of sleep and increasing mortality risk of an accident is not linear, but instead exponentially mushrooms. Each hour of sleep lost vastly amplifies that crash likelihood, rather than incrementally nudging it up.

Figure 12: Sleep Loss and Car Crashes

Drunk driving and drowsy driving are deadly propositions in their own right, but what happens when someone combines them? It is a relevant question, since most individuals are driving drunk in the early-morning hours rather than in the middle of the day, meaning that most drunk drivers are also sleep-deprived.

We can now monitor driver error in a realistic but safe way using driving simulators. With such a virtual machine, a group of researchers examined the number of complete off-road deviations in participants placed under four different experimental conditions: (1) eight hours of sleep, (2) four hours of sleep, (3) eight hours of sleep plus alcohol to the point of being legally drunk, and (4) four hours of sleep plus alcohol to the point of being legally drunk.

Those in the eight-hour sleep group had few, if any, off-road errors. Those in the four-hour sleep condition (the second group) had six times more off-road deviations than the sober, well-rested individuals. The same degree of driving impairment was true of the third group, who had eight hours of sleep but were legally drunk. Driving drunk or driving drowsy were both dangerous, and equally dangerous.

A reasonable expectation was that performance in the fourth group of participants would reflect the additive impact of these two groups: four hours of sleep plus the effect of alcohol (i.e., twelve times more off-road deviations). It was far worse. This group of participants drove off the road almost thirty times more than the well-rested, sober group. The heady cocktail of sleep loss and alcohol was not additive, but instead multiplicative. They magnified each other, like two drugs whose effects are harmful by themselves but, when taken together, interact to produce truly dire consequences.

After thirty years of intensive research, we can now answer many of the questions posed earlier. The recycle rate of a human being is around sixteen hours. After sixteen hours of being awake, the brain begins to fail. Humans need more than seven hours of sleep each night to maintain cognitive performance. After ten days of just seven hours of sleep, the brain is as dysfunctional as it would be after going without sleep for twenty-four hours. Three full nights of recovery sleep (i.e., more nights than a weekend) are insufficient to restore performance back to normal levels after a week of short sleeping. Finally, the human mind cannot accurately sense how sleep-deprived it is when sleep-deprived.

We shall return to the ramifications of these results in the remaining chapters, but the real-life consequences of drowsy driving deserve special mention. This coming week, more than 2 million people in the US will fall asleep while driving their motor vehicle. That’s more than 250,000 every day, with more such events during the week than weekends for obvious reasons. More than 56 million Americans admit to struggling to stay awake at the wheel of a car each month.

As a result, 1.2 million accidents are caused by sleepiness each year in the United States. Said another way: for every thirty seconds you’ve been reading this book, there has been a car accident somewhere in the US caused by sleeplessness. It is more than probable that someone has lost their life in a fatigue-related car accident during the time you have been reading this chapter.

You may find it surprising to learn that vehicle accidents caused by drowsy driving exceed those caused by alcohol and drugs combined. Drowsy driving alone is worse than driving drunk. That may seem like a controversial or irresponsible thing to say, and I do not wish to trivialize the lamentable act of drunk driving by any means. Yet my statement is true for the following simple reason: drunk drivers are often late in braking, and late in making evasive maneuvers. But when you fall asleep, or have a microsleep, you stop reacting altogether. A person who experiences a microsleep or who has fallen asleep at the wheel does not brake at all, nor do they make any attempt to avoid the accident. As a result, car crashes caused by drowsiness tend to be far more deadly than those caused by alcohol or drugs. Said crassly, when you fall asleep at the wheel of your car on a freeway, there is now a one-ton missile traveling at 65 miles per hour, and no one is in control.

Drivers of cars are not the only threats. More dangerous are drowsy truckers. Approximately 80 percent of truck drivers in the US are overweight, and 50 percent are clinically obese. This places truck drivers at a far, far higher risk of a disorder called sleep apnea, commonly associated with heavy snoring, which causes chronic, severe sleep deprivation. As a result, these truck drivers are 200 to 500 percent more likely to be involved in a traffic accident. And when a truck driver loses his or her life in a drowsy-driving crash, they will, on average, take 4.5 other lives with them.

In actual fact, I would like to argue that there are no accidents caused by fatigue, microsleeps, or falling asleep. None whatsoever. They are crashes. The Oxford English Dictionary defines accidents as unexpected events that happen by chance or without apparent cause. Drowsy-driving deaths are neither chance, nor without cause. They are predictable and the direct result of not obtaining sufficient sleep. As such, they are unnecessary and preventable. Shamefully, governments of most developed countries spend less than 1 percent of their budget educating the public on the dangers of drowsy driving relative to what they invest in combating drunk driving.

Even well-meaning public health messages can get lost in a barrage of statistics. It often takes the tragic recounting of personal stories to make the message real. There are thousands of such events that I could describe. Let me offer just one in the hopes of saving you from the harms of driving drowsy.

Union County, Florida, January 2006: a school bus transporting nine children came to a halt at a stop sign. A Pontiac Bonneville car carrying seven occupants pulled up behind the bus and also came to a stop. At this moment, an eighteen-wheel truck came barreling down the road behind both vehicles. It didn’t stop. The truck struck the Pontiac, riding up over it and, with the car concertinaed underneath, then hit the bus. All three vehicles traveled through a ditch and continued moving, at which point the imploded Pontiac became engulfed in flames. The school bus rotated counterclockwise and kept traveling, now on the opposite side of the road, back-to-front. It did so for 328 feet until it went off the road and collided with a thick grove of trees. Three of the nine children in the bus were ejected through the windows upon impact. All seven passengers in the Pontiac were killed, as was the bus driver. The truck driver and all nine children in the bus sustained serious injuries.

The trucker was a qualified and legally licensed driver. All toxicology tests performed on his blood were negative. However, it later emerged that he had been awake for thirty-four hours straight and had fallen asleep at the wheel. All of the Pontiac’s seven occupants who died were children or adolescents. Five of the seven were children in the Pontiac car were from a single family. The oldest occupant was a teenager, who had been legally driving the car. The youngest occupant was a baby of just twenty months old.

There are many things that I hope readers take away from this book. This is one of the most important: if you are drowsy while driving, please, please stop. It is lethal. To carry the burden of another’s death on your shoulders is a terrible thing. Don’t be misled by the many ineffective tactics people will tell you can battle back against drowsiness while driving.II Many of us think we can overcome drowsiness through sheer force of will, but, sadly, this is not true. To assume otherwise can jeopardize your life, the lives of your family or friends in the car with you, and the lives of other road users. Some people only get one chance to fall asleep at the wheel before losing their life.

If you notice yourself feeling drowsy while driving, or actually falling asleep at the wheel, stop for the night. 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. This, however, will only get you so far down the road before you need another such recharge, and the returns are diminishing. Ultimately, it is just not worth the (life) cost.

CAN NAPS HELP?

In the 1980s and ’90s, David Dinges, together with his astute collaborator (and recent administrator of the National Highway Traffic Safety Administration) Dr. Mark Rosekind, conducted another series of groundbreaking studies, this time examining the upsides and downsides of napping in the face of unavoidable sleep deprivation. They coined the term “power naps”—or, should I say, ceded to it. Much of their work was with the aviation industry, examining pilots on long-haul travel.

The most dangerous time of flight is landing, which arrives at the end of a journey, when the greatest amount of sleep deprivation has often accrued. Recall how tired and sleepy you are at the end of an overnight, transatlantic flight, having been on the go for more than twenty-four hours. Would you feel at peak performance, ready to land a Boeing 747 with 467 passengers on board, should you have the skill to do so? It is during this end phase of flight, known in the aviation industry as “top of descent to landing,” that 68 percent of all hull losses—a euphemism for a catastrophic plane crash—occur.

The researchers set to work answering the following question, posed by the US Federal Aviation Authority (FAA): If a pilot can only obtain a short nap opportunity (40–120 minutes) within a thirty-six-hour period, when should it occur so as to minimize cognitive fatigue and attention lapses: at the start of the first evening, in the middle of the night, or late the following morning?

It first appeared to be counterintuitive, but Dinges and Rosekind made a clever, biology-based prediction. They believed that by inserting a nap at the front end of an incoming bout of sleep deprivation, you could insert a buffer, albeit temporary and partial, that would protect the brain from suffering catastrophic lapses in concentration. They were right. Pilots suffered fewer microsleeps at the end stages of the flight if the naps were taken early that prior evening, versus if those same nap periods were taken in the middle of the night or later that next morning, when the attack of sleep deprivation was already well under way.

They had discovered the sleep equivalent of the medical paradigm of prevention versus treatment. The former tries to avert an issue prior to occurrence, the latter tries to remedy the issue after it has happened. And so it was with naps. Indeed, these short sleep bouts, taken early, also reduced the number of times the pilots drifted into light sleep during the critical, final ninety minutes of flight. There were fewer of these sleep intrusions, measured with EEG electrodes on the head.

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 function with perfect, or even acceptable, acumen. Brief power naps have become synonymous with the inaccurate assumption that they allow an individual to forgo sufficient sleep, night after night, especially when combined with the liberal use of caffeine.

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. Power naps may momentarily increase basic concentration under conditions of sleep deprivation, as can caffeine up to a certain dose. 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.

One day we may discover such a counteractive method. Currently, however, there is no drug that has the proven ability to replace those benefits that a full night of sleep infuses into the brain and body. David Dinges has extended an open invitation to anyone suggesting that they can survive on short sleep to come to his lab for a ten-day stay. He will place that individual on their proclaimed regiment of short sleep and measure their cognitive function. Dinges is rightly confident he’ll show, categorically, a degradation of brain and body function. To date, no volunteers have matched up to their claim.

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. Part of the explanation appears to lie in their genetics, specifically a sub-variant of a gene called BHLHE41.III Scientists are now trying to understand what this gene does, and how it confers resilience to such little sleep.

Having learned this, I imagine that some readers now believe that they are one of these individuals. That is very, very unlikely. The gene is remarkably rare, with but a soupçon of individuals in the world estimated to carry this anomaly. To impress this fact further, I quote one of my research colleagues, Dr. Thomas Roth at the Henry Ford Hospital in Detroit, who once said, “The number of people who can survive on five hours of sleep or less without any impairment, expressed as a percent of the population, and rounded to a whole number, is zero.”

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.

EMOTIONAL IRRATIONALITY

“I just snapped, and . . .” Those words are often part of an unfolding tragedy as a soldier irrationally responds to a provocative civilian, a physician to an entitled patient, or a parent to a misbehaving child. All of these situations are ones in which inappropriate anger and hostility are dealt out by tired, sleep-deprived individuals.

Many of us know that inadequate sleep plays havoc with our emotions. We even recognize it in others. Consider another common scenario of a parent holding a young child who is screaming or crying and, in the midst of the turmoil, turns to you and says, “Well, Steven just didn’t get enough sleep last night.” Universal parental wisdom knows that bad sleep the night before leads to a bad mood and emotional reactivity the next day.

While the phenomenon of emotional irrationality following sleep loss is subjectively and anecdotally common, until recently we did not know how sleep deprivation influenced the emotional brain at a neural level, despite the professional, psychiatric, and societal ramifications. Several years ago, my team and I conducted a study using MRI brain scanning to address the question.

We studied two groups of healthy young adults. One group stayed awake all night, monitored under full supervision in my laboratory, while the other group slept normally that night. During the brain scanning session the next day, participants in both groups were shown the same one hundred pictures that ranged from neutral in emotional content (e.g., a basket, a piece of driftwood) to emotionally negative (e.g., a burning house, a venomous snake about to strike). Using this emotional gradient of pictures, we were able to compare the increase in brain response to the increasingly negative emotional triggers.

Analysis of the brain scans revealed the largest effects I have measured in my research to date. 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. In contrast, the brain scans of those individuals who were given a full night’s sleep evinced a controlled, modest degree of reactivity in the amygdala, despite viewing the very same images. 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.

This answer raised another question: Why were the emotion centers of the brain so excessively reactive without sleep? Further MRI studies using more refined analyses allowed us to identify the root cause. After a full night of sleep, the prefrontal cortex—the region of the brain that sits just above your eyeballs; is most developed in humans, relative to other primates; and is associated with rational, logical thought and decision-making—was strongly coupled to the amygdala, regulating this deep emotional brain center with inhibitory control. 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. We cannot rein in our atavistic impulses—too much emotional gas pedal (amygdala) and not enough regulatory brake (prefrontal cortex). Without the rational control given to us each night by sleep, we’re not on a neurological—and hence emotional—even keel.

Recent studies by a research team in Japan have now replicated our findings, but they’ve done so by restricting participants’ sleep to five hours for five nights. No matter how you take sleep from the brain—acutely, across an entire night, or chronically, by short sleeping for a handful of nights—the emotional brain consequences are the same.

When we conducted our original experiments, I was struck by the pendulum-like swings in the mood and emotions of our participants. In a flash, sleep-deprived subjects would go from being irritable and antsy to punch-drunk giddy, only to then swing right back to a state of vicious negativity. They were traversing enormous emotional distances, from negative to neutral to positive, and all the way back again, within a remarkably short period of time. It was clear that I had missed something. I needed to conduct a sister study to the one I described above, but now explore how the sleep-deprived brain responds to increasingly positive and rewarding experiences, such as exciting images of extreme sports, or the chance of winning increasing amounts of money in fulfilling tasks.

We discovered that different deep emotional centers in the brain just above and behind the amygdala, called the striatum—associated with impulsivity and reward, and bathed by the chemical dopamine—had become hyperactive in sleep-deprived individuals in response to the rewarding, pleasurable experiences. As with the amygdala, the heightened sensitivity of these hedonic regions was linked to a loss of the rational control from the prefrontal cortex.

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.

You may think that the former counter-balances the latter, thereby neutralizing the problem. Sadly, emotions, and their guiding of optimal decision and actions, do not work this way. Extremity is often dangerous. Depression and extreme negative mood can, for example, infuse an individual with a sense of worthlessness, together with ideas of questioning life’s value. There is now clearer evidence of this concern. Studies of adolescents have identified a link between sleep disruption and suicidal thoughts, suicide attempts, and, tragically, suicide completion in the days after. One more reason for society and parents to value plentiful sleep in teens rather than chastise it, especially considering that suicide is the second-leading cause of death in young adults in developed nations after car accidents.

Insufficient sleep has also been linked to aggression, bullying, and behavioral problems in children across a range of ages. A similar relationship between a lack of sleep and violence has been observed in adult prison populations; places that, I should add, are woefully poor at enabling good sleep that could reduce aggression, violence, psychiatric disturbance, and suicide, which, beyond the humanitarian concern, increases costs to the taxpayer.

Equally problematic issues arise from extreme swings in positive mood, though the consequences are different. Hypersensitivity to pleasurable experiences can lead to sensation-seeking, risk-taking, and addiction. Sleep disturbance is a recognized hallmark associated with addictive substance use.IV Insufficient sleep also determines relapse rates in numerous addiction disorders, associated with reward cravings that are unmetered, lacking control from the rational head office of the brain’s prefrontal cortex.V Relevant from a prevention standpoint, insufficient sleep during childhood significantly predicts early onset of drug and alcohol use in that same child during their later adolescent years, even when controlling for other high-risk traits, such as anxiety, attention deficits, and parental history of drug use.VI You can now appreciate why the bidirectional, pendulum-like emotional liability caused by sleep deprivation is so concerning, rather than counter-balancing.

Our brain scanning experiments in healthy individuals offered reflections on the relationship between sleep and psychiatric illnesses. There is no major psychiatric condition in which sleep is normal. This is true of depression, anxiety, post-traumatic stress disorder (PTSD), schizophrenia, and bipolar disorder (once known as manic depression).

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. Indeed, many of the brain regions commonly impacted by psychiatric mood disorders are the same regions that are involved in sleep regulation and impacted by sleep loss. Further, many of the genes that show abnormalities in psychiatric illnesses are the same genes that help control sleep and our circadian rhythms.

Had psychiatry got the causal direction wrong, and it was sleep disruption instigating mental illness, not the other way around? No, I believe that is equally inaccurate and reductionist to suggest. Instead, I firmly believe that sleep loss and mental illness is best described as a two-way street of interaction, with the flow of traffic being stronger in one direction or the other, depending on the disorder.

I am not suggesting that all psychiatric conditions are caused by absent sleep. However, I am suggesting that sleep disruption remains a neglected factor contributing to the instigation and/or maintenance of numerous psychiatric illnesses, and has powerful diagnostic and therapeutic potential that we are yet to fully understand or make use of.

Preliminary (but compelling) evidence is beginning to support this claim. One example involves bipolar disorder, which most people will recognize by the former name of manic depression. 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). These extremes are often separated by a time when the patients are in a stable emotional state, neither manic nor depressed.

A research team in Italy examined bipolar patients during the time when they were in this stable, inter-episode phase. Next, under careful clinical supervision, they sleep-deprived these individuals for one night. Almost immediately, a large proportion of the individuals either spiraled into a manic episode or became seriously depressed. I find it to be an ethically difficult experiment to appreciate, but the scientists had importantly demonstrated that a lack of sleep is a causal trigger of a psychiatric episode of mania or depression. The result supports a mechanism in which the sleep disruption—which almost always precedes the shift from a stable to an unstable manic or depressive state in bipolar patients—may well be a (the) trigger in the disorder, and not simply epiphenomenal.

Thankfully, the opposite is also true. Should you improve sleep quality in patients suffering from several psychiatric conditions using a technique we will discuss later, called cognitive behavioral therapy for insomnia (CBT-I), you can improve symptom severity and remission rates. My colleague at the University of California, Berkeley, Dr. Allison Harvey has been a pioneer in this regard.

By improving sleep quantity, quality, and regularity, Harvey and her team have systematically demonstrated the healing abilities of sleep for the minds of numerous psychiatric populations. She has intervened with the therapeutic tool of sleep in conditions as diverse as depression, bipolar disorder, anxiety, and suicide, all to great effect. By regularizing and enhancing sleep, Harvey has stepped these patients back from the edge of crippling mental illness. That, in my opinion, is a truly remarkable service to humanity.

The swings in emotional brain activity that we observed in healthy individuals who were sleep-deprived may also explain a finding that has perplexed psychiatry for decades. Patients suffering from major depression, in which they become exclusively locked into the negative end of the mood spectrum, show what at first appears to be a counterintuitive response to one night of sleep deprivation. Approximately 30 to 40 percent of these patients will feel better after a night without sleep. Their lack of slumber appears to be an antidepressant.

The reason sleep deprivation is not a commonly used treatment, however, is twofold. First, as soon as these individuals do sleep, the antidepressant benefit goes away. Second, the 60 to 70 percent of patients who do not respond to the sleep deprivation will actually feel worse, deepening their depression. As a result, sleep deprivation is not a realistic or comprehensive therapy option. Still, it has posed an interesting question: How could sleep deprivation prove helpful for some of these individuals, yet detrimental to others?

I believe that the explanation resides in the bidirectional changes in emotional brain activity that we observed. 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.

The one-third of depressed individuals who respond to sleep deprivation may therefore be those who experience the greater amplification within reward circuits of the brain that I described earlier, resulting in far stronger sensitivity to, and experiencing of, positive rewarding triggers following sleep deprivation. Their anhedonia is therefore lessened, and now they can begin to experience a greater degree of pleasure from pleasurable life experiences. In contrast, the other two-thirds of depressed patients may suffer the opposite negative emotional consequences of sleep deprivation more dominantly: a worsening, rather than alleviation, of their depression. If we can identify what determines those who will be responders and those who will not, my hope is that we can create better, more tailored sleep-intervention methods for combating depression.

We will revisit the effects of sleep loss on emotional stability and other brain functions in later chapters when we discuss the real-life consequences of sleep loss in society, education, and the workplace. The findings justify our questioning of whether or not sleep-deprived doctors can make emotionally rational decisions and judgments; under-slept military personnel should have their fingers on the triggers of weaponry; overworked bankers and stock traders can make rational, non-risky financial decisions when investing the public’s hard-earned retirement funds; and if teenagers should be battling against impossibly early start times during a developmental phase of life when they are most vulnerable to developing psychiatric disorders. For now, however, I will summarize this section by offering a discerning quote on the topic of sleep and emotion by the American entrepreneur E. Joseph Cossman: “The best bridge between despair and hope is a good night’s sleep.”VII

TIRED AND FORGETFUL?

Have you ever pulled an “all-nighter,” deliberately staying awake all night? One of my true loves is teaching a large undergraduate class on the science of sleep at the University of California, Berkeley. I taught a similar sleep course while I was at Harvard University. At the start of the course, I conduct a sleep survey, inquiring about my students’ sleep habits, such as the times they go to bed and wake up during the week and weekend, how much sleep they get, if they think their academic performance is related to their sleep.

Inasmuch as they are telling me the truth (they fill the survey out anonymously online, not in class), the answer I routinely get is saddening. More than 85 percent of them pull all-nighters. Especially concerning is the fact that of those who said “yes” to pulling all-nighters, almost a third will do so monthly, weekly, or even several times a week. 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.

The most common reason my students give for pulling all-nighters is to cram for an exam. In 2006, I decided to conduct an MRI study to investigate whether they were right or wrong to do so. Was pulling an all-nighter a wise idea for learning? We took a large group of individuals and assigned them to either a sleep group or a sleep deprivation group. Both groups remained awake normally across the first day. Across the following night, those in the sleep group obtained a full night of shut-eye, while those in the sleep deprivation group were kept awake all night under the watchful eye of trained staff in my lab. Both groups were then awake across the following morning. Around midday, we placed participants inside an MRI scanner and had them try to learn a list of facts, one at a time, as we took snapshots of their brain activity. Then we tested them to see how effective that learning had been. However, instead of testing them immediately after learning, we waited until they had had two nights of recovery sleep. We did this to make sure that any impairments we observed in the sleep-deprived group were not confounded by them being too sleepy or inattentive to recollect what they may very well have learned. Therefore, the sleep-deprivation manipulation was only in effect during the act of learning, and not during the later act of recall.

When we compared the effectiveness of learning between the two groups, the result was clear: there was a 40 percent deficit in the ability of the sleep-deprived group to cram new facts into the brain (i.e., to make new memories), relative to the group that obtained a full night of sleep. To put that in context, it would be the difference between acing an exam and failing it miserably!

What was going wrong within the brain to produce these deficits? We compared the patterns of brain activity during attempted learning between the two groups, and focused our analysis on the brain region that we spoke about in chapter 6, the hippocampus—the information “in-box” of the brain that acquires new facts. There was lots of healthy, learning-related activity in the hippocampus in the participants who had slept the night before. 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. You don’t even need the blunt force of a whole night of sleep deprivation. 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 sleep deprivation will attack, blocking your brain’s capacity for new learning.

I cannot tell you how many of my students have come up to me at the end of the lecture in which I describe these studies and said, “I know that exact feeling. It seems as though I’m staring at the page of the textbook but nothing is going in. I may be able to hold on to some facts the following day for the exam, but if you were to ask me to take that same test a month later, I think I’d hardly remember a thing.”

The latter description has scientific backing. Those few memories you are able to learn while sleep-deprived are forgotten far more quickly in the hours and days thereafter. Memories formed without sleep are weaker memories, evaporating rapidly. Studies in rats have found that it is almost impossible to strengthen the synaptic connections between individual neurons that normally forge a new memory circuit in the animals that have been sleep-deprived. Imprinting lasting memories into the architecture of the brain becomes nearly impossible. This is true whether the researchers sleep-deprived the rats for a full twenty-four hours, or just a little, for two or three hours. 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.

The very latest work in this area has revealed that sleep deprivation even impacts the DNA and the learning-related genes in the brain cells of the hippocampus itself. 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. It is rather like building a sand castle too close to the tide line—the consequences are inevitable.

While at Harvard University, I was invited to write my first op-ed piece for their newspaper, the Crimson. The topic was sleep loss, learning, and memory. It was also the last piece I was invited to write.

In the article, I described the above studies and their relevance, returning time and again to the pandemic of sleep deprivation that was sweeping through the student body. However, rather than lambaste the students for these practices, I pointed a scolding finger directly at the faculty, myself included. I suggested that if we, as teachers, strive to accomplish just that purpose—to teach—then 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 was in direct opposition to the goals of nurturing young scholarly minds. I argued that logic, backed by scientific fact, must prevail, and that it was long past the time for us to rethink our evaluation methods, their contra-educational impact, and the unhealthy behavior it coerced from our students.

To suggest that the reaction from the faculty was icy would be a thermal compliment. “It was the students’ choice,” I was told in adamant response emails. “A lack of planned study by irresponsible undergraduates” was another common rebuttal from faculty and administrators attempting to sidestep responsibility. In truth, I never believed that one op-ed column would trigger a U-turn in poor educational examination methods at that or any other higher institute of learning. As many have said about such stoic institutions: theories, beliefs, and practices die one generation at a time. But the conversation and battle must start somewhere.

You may ask whether I have changed my own educational practice and assessment. I have. There are no “final” exams at the end of the semester in my classes. 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 chapter 6 I described the crucial role for sleep after learning in the offline cementing, or consolidating, of recently learned memories. My friend and longtime collaborator at Harvard Medical School, Dr. Robert Stickgold, conducted a clever study with wide-reaching implications. He had a total of 133 undergraduates learn a visual memory task through repetition. Participants then returned to his laboratory and were tested to see how much they had retained. Some subjects returned the next day after a full night of sleep. Others returned two days later after two full nights of sleep, and still others after three days with three nights of sleep in between.

As you would predict by now, a night of sleep strengthened the newly learned memories, boosting their retention. Additionally, the more nights of sleep participants had before they were tested, the better their memory was. All except another sub-group of participants. Like the subjects in the third group, these participants learned the task on the first day, and learned it just as well. They were then tested three nights later, just like the third group above. The difference was that they were deprived of sleep the first night after learning and were not tested the following day. Instead, Stickgold gave them two full recovery nights of sleep before testing them. They showed absolutely no evidence of a memory consolidation improvement. 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. It is a concerning result in our 24/7, hurry-up, don’t-wait society. I feel another op-ed coming on . . .

SLEEP AND ALZHEIMER’S DISEASE

The two most feared diseases throughout developed nations are dementia and cancer. Both are related to inadequate sleep. We will address the latter in the next chapter regarding sleep deprivation and the body. Regarding the former, which centers on the brain, a lack of sleep is fast becoming recognized as a key lifestyle factor determining whether or not you will develop Alzheimer’s disease.

The condition, originally identified in 1901 by German physician Dr. Aloysius Alzheimer, has become one of the largest public health and economic challenges of the twenty-first century. 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. One in ten adults over the age of sixty-five now suffers from Alzheimer’s disease. Without advances in diagnosis, prevention, and therapeutics, the escalation will continue.

Sleep represents a new candidate for hope on all three of these fronts: diagnosis, prevention, and therapeutics. Before discussing why, let me first describe how sleep disruption and Alzheimer’s disease are causally linked.

As we learned in chapter 5, sleep quality—especially that of deep NREM sleep—deteriorates as we age. This is linked to a decline in memory. However, if you assess a patient with Alzheimer’s disease, the disruption of deep sleep is far more exaggerated. More telling, perhaps, is the fact that sleep disturbance precedes the onset of Alzheimer’s disease by several years, suggesting that it may be an early-warning sign of the condition, or even a contributor to it. Following diagnosis, the magnitude of sleep disruption will then progress in unison with the symptom severity of the Alzheimer’s patient, further suggesting a link between the two. Making matters worse, over 60 percent of patients with Alzheimer’s disease have at least one clinical sleep disorder. Insomnia is especially common, as caregivers of a loved one with Alzheimer’s disease will know all too well.

It was not until relatively recently, however, that the association between disturbed sleep and Alzheimer’s disease was realized to be more than just an association. 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. What is strange, however, is that amyloid plaques only affect some parts of the brain and not others, the reasons for which remain unclear.

What struck me about this unexplained pattern was the location in the brain where amyloid accumulates early in the course of Alzheimer’s disease, and most severely in the late stages of the condition. That area is the middle part of the frontal lobe—which, as you will remember, is the same brain region essential for the electrical generation of deep NREM sleep in healthy young individuals. At that time, we did not understand if or why Alzheimer’s disease caused sleep disruption, but simply knew that they always co-occurred. I wondered whether the reason patients with Alzheimer’s disease have such impaired deep NREM sleep was, in part, because the disease erodes the very region of the brain that normally generates this key stage of slumber.

I joined forces with Dr. William Jagust, a leading authority on Alzheimer’s disease, at the University of California, Berkeley. Together, our research teams set about testing this hypothesis. Several years later, having assessed the sleep of many older adults with varying degrees of amyloid buildup in the brain that we quantified with a special type of PET scan, we arrived at the answer. The more amyloid deposits there were in the middle regions of the frontal lobe, the more impaired the deep-sleep quality was in that older individual. 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. This distinction was important, since it meant that the sleep impairment caused by amyloid buildup in the brain was more than just “normal aging.” It was unique—a departure from what is otherwise the signature of sleep decline as we get older.

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. If sleep does prove to be an early diagnostic measure—especially one that is relatively cheap, noninvasive, and can be easily obtained in a large number of individuals, unlike costly MRI or PET scans—then early intervention becomes possible.

Building on these findings, our recent work has added a key piece in the jigsaw puzzle of Alzheimer’s disease. We have discovered a new pathway through which amyloid plaques may contribute to memory decline later in life: something that has been largely missing in our understanding of how Alzheimer’s disease works. I mentioned that the toxic amyloid deposits only accumulate in some parts of the brain and not others. Despite Alzheimer’s disease being typified by memory loss, the hippocampus—that key memory reservoir in the brain—is mysteriously unaffected by amyloid protein. This question has so far baffled scientists: How does amyloid cause memory loss in Alzheimer’s disease patients when amyloid itself does not affect memory areas of the brain? While other aspects of the disease may be at play, it seemed plausible to me that there was a missing intermediary factor—one that was transacting the influence of amyloid in one part of the brain on memory, which depended on a different region of the brain. Was sleep disruption the missing factor?

To test this theory, we had elderly patients with varying levels of amyloid—low to high—in their brains learn a list of new facts in the evening. The next morning, after recording their sleep in the laboratory that night, we tested them to see how effective their sleep had been at cementing and thus holding on to those new memories. We discovered a chain-reaction effect. Those individuals with the highest levels of amyloid deposits in the frontal regions of the brain had the most severe loss of deep sleep and, as a knock-on consequence, failed to successfully consolidate those new memories. Overnight forgetting, rather than remembering, had taken place. The disruption of deep NREM sleep was therefore a hidden middleman brokering the bad deal between amyloid and memory impairment in Alzheimer’s disease. A missing link.

These findings, however, were only half of the story, and admittedly the less important half. Our work had shown that the amyloid plaques of Alzheimer’s disease may be associated with the loss of deep sleep, but does it work both ways? Can a lack of sleep actually cause amyloid to build up in your brain to begin with? If so, insufficient sleep across an individual’s life would significantly raise their risk of developing Alzheimer’s disease.

Around the same time that we were conducting our studies, Dr. Maiken Nedergaard at the University of Rochester made one of the most spectacular discoveries in the field of sleep research in recent decades. Working with mice, Nedergaard found that a kind of sewage network called the glymphatic system exists within the brain. Its name is derived from the body’s equivalent lymphatic system, but it’s composed of cells called glia (from the Greek root word for “glue”).

Glial cells are distributed throughout your entire brain, situated side by side with the neurons that generate the electrical impulses of your brain. Just as the lymphatic system drains contaminants from your body, the glymphatic system collects and removes dangerous metabolic contaminants generated by the hard work performed by neurons in your brain, rather like a support team surrounding an elite athlete.

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. Associated with the pulsing rhythm of deep NREM sleep comes a ten- to twentyfold increase in effluent expulsion from the brain. In what can be described as a nighttime power cleanse, the purifying work of the glymphatic system is accomplished by cerebrospinal fluid that bathes the brain.

Nedergaard made a second astonishing discovery, which explained why the cerebrospinal fluid is so effective in flushing out metabolic debris at night. The glial cells of the brain were shrinking in size by up to 60 percent during NREM sleep, enlarging the space around the neurons and allowing the cerebrospinal fluid to proficiently clean out the metabolic refuse left by the day’s neural activity. Think of the buildings of a large metropolitan city physically shrinking at night, allowing municipal cleaning crews easy access to pick up garbage strewn in the streets, followed by a good pressure-jet treatment of every nook and cranny. When we wake each morning, our brains can once again function efficiently thanks to this deep cleansing.

So what does this have to do with Alzheimer’s disease? One piece of toxic debris evacuated by the glymphatic system during sleep is amyloid protein—the poisonous element associated with Alzheimer’s disease. Other dangerous metabolic waste elements that have links to Alzheimer’s disease are also removed by the cleaning process during sleep, including a protein called tau, as well as stress molecules produced by neurons when they combust energy and oxygen during the day. Should you experimentally prevent a mouse from getting NREM sleep, keeping it awake instead, there is an immediate increase in amyloid deposits within the brain. Without sleep, an escalation of poisonous Alzheimer’s-related protein accumulated in the brains of the mice, together with several other toxic metabolites. Phrased differently, and perhaps more simply, wakefulness is low-level brain damage, while sleep is neurological sanitation.

Nedergaard’s findings completed the circle of knowledge that our findings had left unanswered. Inadequate sleep and the pathology of Alzheimer’s disease interact in a vicious cycle. Without sufficient sleep, amyloid plaques build up in the brain, especially in deep-sleep-generating regions, attacking and degrading them. The loss of deep NREM sleep caused by this assault therefore lessens the ability to remove amyloid from the brain at night, resulting in greater amyloid deposition. More amyloid, less deep sleep, less deep sleep, more amyloid, and so on and so forth.

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. Precisely this relationship has now been reported in numerous epidemiological studies, including those individuals suffering from sleep disorders such as insomnia and sleep apnea.VIII Parenthetically, and unscientifically, I have always found it curious that Margaret Thatcher and Ronald Reagan—two heads of state that were very vocal, if not proud, about sleeping only four to five hours a night—both went on to develop the ruthless disease. The current US president, Donald Trump—also a vociferous proclaimer of sleeping just a few hours each night—may want to take note.

A more radical and converse prediction that emerges from these findings is that, by improving someone’s sleep, we should be able to reduce their risk of developing Alzheimer’s disease—or at least delay its onset. Tentative support has emerged from clinical studies in which middle- and older-age adults have had their sleep disorders successfully treated. As a consequence, their rate of cognitive decline slowed significantly, and further delayed the onset of Alzheimer’s disease by five to ten years.IX

My own research group is now trying to develop a number of viable methods for artificially increasing deep NREM sleep that could restore some degree of the memory consolidation function that is absent in older individuals with high amounts of amyloid in the brain. If we can find a method that is cost effective and can be scaled up to the population level for repeat use, my goal is prevention. Can we begin supplementing the declining deep sleep of vulnerable members of society during midlife, many decades before the tipping point of Alzheimer’s disease is reached, aiming to avert dementia risk later in life? It is an admittedly lofty ambition, and some would argue a moon shot research goal. 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.

Insufficient sleep is only one among several risk factors associated with Alzheimer’s disease. Sleep alone will not be the magic bullet that eradicates dementia. Nevertheless, prioritizing sleep across the life span is clearly becoming a significant factor for lowering Alzheimer’s disease risk.

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