Why We Sleep

by Matthew Walker

  The artificial light that bathes our modern indoor worlds will therefore halt the forward progress of biological time that is normally signaled by the evening surge in melatonin. Sleep in modern humans is delayed from taking off the evening runway, which would naturally occur somewhere between eight and ten p.m., just as we observe in hunter-gatherer tribes. Artificial light in modern societies thus tricks us into believing night is still day, and does so using a physiological lie.

  The degree to which evening electric light winds back your internal twenty-four-hour clock is important: usually two to three hours each evening, on average. To contextualize that, let’s say you are reading this book at eleven p.m. in New York City, having been surrounded by electric light all evening. Your bedside clock may be registering eleven p.m., but the omnipresence of artificial light has paused the internal tick-tocking of time by hindering the release of melatonin. Biologically speaking, you’ve been dragged westward across the continent to the internal equivalent of Chicago time (ten p.m.), or even San Francisco time (eight p.m.).

  Artificial evening and nighttime light can therefore masquerade as sleep-onset insomnia—the inability to begin sleeping soon after getting into bed. By delaying the release of melatonin, artificial evening light makes it considerably less likely that you’ll be able to fall asleep at a reasonable time. When you do finally turn out the bedside light, hoping that sleep will come quickly is made all the more difficult. It will be some time before the rising tide of melatonin is able to submerge your brain and body in peak concentrations, instructed by the darkness that only now has begun—in other words, before you are biologically capable of organizing the onset of robust, stable sleep.

  What of a petite bedside lamp? How much can that really influence your suprachiasmatic nucleus? A lot, it turns out. Even a hint of dim light—8 to 10 lux—has been shown to delay the release of nighttime melatonin in humans. The feeblest of bedside lamps pumps out twice as much: anywhere from 20 to 80 lux. A subtly lit living room, where most people reside in the hours before bed, will hum at around 200 lux. Despite being just 1 to 2 percent of the strength of daylight, this ambient level of incandescent home lighting can have 50 percent of the melatonin-suppressing influence within the brain.

  Just when things looked as bad as they could get for the suprachiasmatic nucleus with incandescent lamps, a new invention in 1997 made the situation far worse: blue light–emitting diodes, or blue LEDs. For this invention, Shuji Nakamura, Isamu Akasaki, and Hiroshi Amano won the Nobel Prize in physics in 2014. It was a remarkable achievement. Blue LED lights offer considerable advantages over incandescent lamps in terms of lower energy demands and, for the lights themselves, longer life spans. But they may be inadvertently shortening our own.

  The light receptors in the eye that communicate “daytime” to the suprachiasmatic nucleus are most sensitive to short-wavelength light within the blue spectrum—the exact sweet spot where blue LEDs are most powerful. As a consequence, evening blue LED light has twice the harmful impact on nighttime melatonin suppression than the warm, yellow light from old incandescent bulbs, even when their lux intensities are matched.

  Of course, few of us stare headlong into the glare of an LED lamp each evening. But we do stare at LED-powered laptop screens, smartphones, and tablets each night, sometimes for many hours, often with these devices just feet or even inches away from our retinas. A recent survey of over fifteen hundred American adults found that 90 percent of individuals regularly used some form of portable electronic device sixty minutes or less before bedtime. It has a very real impact on your melatonin release, and thus ability to time the onset of sleep.

  One of the earliest studies found that using an iPad—an electronic tablet enriched with blue LED light—for two hours prior to bed blocked the otherwise rising levels of melatonin by a significant 23 percent. A more recent report took the story several concerning steps further. Healthy adults lived for a two-week period in a tightly controlled laboratory environment. The two-week period was split in half, containing two different experimental arms that everyone passed through: (1) five nights of reading a book on an iPad for several hours before bed (no other iPad uses, such as email or Internet, were allowed), and (2) five nights of reading a printed paper book for several hours before bed, with the two conditions randomized in terms of which the participants experienced as first or second.

  Compared to reading a printed book, reading on an iPad suppressed melatonin release by over 50 percent at night. Indeed, iPad reading delayed the rise of melatonin by up to three hours, relative to the natural rise in these same individuals when reading a printed book. When reading on the iPad, their melatonin peak, and thus instruction to sleep, did not occur until the early-morning hours, rather than before midnight. Unsurprisingly, individuals took longer to fall asleep after iPad reading relative to print-copy reading.

  But did reading on the iPad actually change sleep quantity/quality above and beyond the timing of melatonin? It did, in three concerning ways. First, individuals lost significant amounts of REM sleep following iPad reading. Second, the research subjects felt less rested and sleepier throughout the day following iPad use at night. Third was a lingering aftereffect, with participants suffering a ninety-minute lag in their evening rising melatonin levels for several days after iPad use ceased—almost like a digital hangover effect.

  Using LED devices at night impacts our natural sleep rhythms, the quality of our sleep, and how alert we feel during the day. The societal and public health ramifications, discussed in the penultimate chapter, are not small. I, like many of you, have seen young children using electronic tablets at every opportunity throughout the day … and evening. The devices are a wonderful piece of technology. They enrich the lives and education of our youth. But such technology is also enriching their eyes and brains with powerful blue light that has a damaging effect on sleep—the sleep that young, developing brains so desperately need in order to flourish.fn1

  Due to its omnipresence, solutions for limiting exposure to artificial evening light are challenging. A good start is to create lowered, dim light in the rooms where you spend your evening hours. Avoid powerful overhead lights. Mood lighting is the order of the night. Some committed individuals will even wear yellow-tinted glasses indoors in the afternoon and evening to help filter out the most harmful blue light that suppresses melatonin.

  Maintaining complete darkness throughout the night is equally critical, the easiest fix for which comes from blackout curtains. Finally, you can install software on your computers, phones, and tablet devices that gradually de-saturate the harmful blue LED light as evening progresses.

  TURNING DOWN THE NIGHTCAP—ALCOHOL

  Short of prescription sleeping pills, the most misunderstood of all “sleep aids” is alcohol. Many individuals believe alcohol helps them to fall asleep more easily, or even offers sounder sleep throughout the night. Both are resolutely untrue.

  Alcohol is in a class of drugs called sedatives. It binds to receptors within the brain that prevent neurons from firing their electrical impulses. Saying that alcohol is a sedative often confuses people, as alcohol in moderate doses helps individuals liven up and become more social. How can a sedative enliven you? The answer comes down to the fact that your increased sociability is caused by sedation of one part of your brain, the prefrontal cortex, early in the timeline of alcohol’s creeping effects. As we have discussed, this frontal lobe region of the human brain helps control our impulses and restrains our behavior. Alcohol immobilizes that part of our brain first. As a result, we “loosen up,” becoming less controlled and more extroverted. But anatomically targeted brain sedation it still is.

  Give alcohol a little more time, and it begins to sedate other parts of the brain, dragging them down into a stupefied state, just like the prefrontal cortex. You begin to feel sluggish as the inebriated torpor sets in. This is your brain slipping into sedation. Your desire and ability to remain conscious are decreasing, and you can let go of consc
iousness more easily. I am very deliberately avoiding the term “sleep,” however, because sedation is not sleep. Alcohol sedates you out of wakefulness, but it does not induce natural sleep. The electrical brainwave state you enter via alcohol is not that of natural sleep; rather, it is akin to a light form of anesthesia.

  Yet this is not the worst of it when considering the effects of the evening nightcap on your slumber. More than its artificial sedating influence, alcohol dismantles an individual’s sleep in an additional two ways.

  First, alcohol fragments sleep, littering the night with brief awakenings. Alcohol-infused sleep is therefore not continuous and, as a result, not restorative. Unfortunately, most of these nighttime awakenings go unnoticed by the sleeper since they don’t remember them. Individuals therefore fail to link alcohol consumption the night before with feelings of next-day exhaustion caused by the undetected sleep disruption sandwiched in between. Keep an eye out for that coincidental relationship in yourself and/or others.

  Second, alcohol is one of the most powerful suppressors of REM sleep that we know of. When the body metabolizes alcohol it produces by-product chemicals called aldehydes and ketones. The aldehydes in particular will block the brain’s ability to generate REM sleep. It’s rather like the cerebral version of cardiac arrest, preventing the pulsating beat of brainwaves that otherwise power dream sleep. People consuming even moderate amounts of alcohol in the afternoon and/or evening are thus depriving themselves of dream sleep.

  There is a sad and extreme demonstration of this fact observed in alcoholics who, when drinking, can show little in the way of any identifiable REM sleep. Going for such long stretches of time without dream sleep produces a tremendous buildup in, and backlog of, pressure to obtain REM sleep. So great, in fact, that it inflicts a frightening consequence upon these individuals: aggressive intrusions of dreaming while they are wide awake. The pent-up REM-sleep pressure erupts forcefully into waking consciousness, causing hallucinations, delusions, and gross disorientation. The technical term for this terrifying psychotic state is “delirium tremens.”fn2

  Should the addict enter a rehabilitation program and abstain from alcohol, the brain will begin feasting on REM sleep, binging in a desperate effort to recover that which it has been long starved of—an effect called the REM-sleep rebound. We observe precisely the same consequences caused by excess REM-sleep pressure in individuals who have tried to break the sleep-deprivation world record (before this life-threatening feat was banned).

  You don’t have to be using alcohol to levels of abuse, however, to suffer its deleterious REM-sleep-disrupting consequences, as one study can attest. Recall that one function of REM sleep is to aid in memory integration and association: the type of information processing required for developing grammatical rules in new language learning, or in synthesizing large sets of related facts into an interconnected whole. To wit, researchers recruited a large group of college students for a seven-day study. The participants were assigned to one of three experimental conditions. On day 1, all the participants learned a novel, artificial grammar, rather like learning a new computer coding language or a new form of algebra. It was just the type of memory task that REM sleep is known to promote. Everyone learned the new material to a high degree of proficiency on that first day—around 90 percent accuracy. Then, a week later, the participants were tested to see how much of that information had been solidified by the six nights of intervening sleep.

  What distinguished the three groups was the type of sleep they had. In the first group—the control condition—participants were allowed to sleep naturally and fully for all intervening nights. In the second group, the experimenters got the students a little drunk just before bed on the first night after daytime learning. They loaded up the participants with two to three shots of vodka mixed with orange juice, standardizing the specific blood alcohol amount on the basis of gender and body weight. In the third group, they allowed the participants to sleep naturally on the first and even the second night after learning, and then got them similarly drunk before bed on night 3.

  Note that all three groups learned the material on day 1 while sober, and were tested while sober on day 7. This way, any difference in memory among the three groups could not be explained by the direct effects of alcohol on memory formation or later recall, but must be due to the disruption of the memory facilitation that occurred in between.

  On day 7, participants in the control condition remembered everything they had originally learned, even showing an enhancement of abstraction and retention of knowledge relative to initial levels of learning, just as we’d expect from good sleep. In contrast, those who had their sleep laced with alcohol on the first night after learning suffered what can conservatively be described as partial amnesia seven days later, forgetting more than 50 percent of all that original knowledge. This fits well with evidence we discussed earlier: that of the brain’s non-negotiable requirement for sleep the first night after learning for the purposes of memory processing.

  The real surprise came in the results of the third group of participants. Despite getting two full nights of natural sleep after initial learning, having their sleep doused with alcohol on the third night still resulted in almost the same degree of amnesia—40 percent of the knowledge they had worked so hard to establish on day 1 was forgotten.

  The overnight work of REM sleep, which normally assimilates complex memory knowledge, had been interfered with by the alcohol. More surprising, perhaps, was the realization that the brain is not done processing that knowledge after the first night of sleep. Memories remain perilously vulnerable to any disruption of sleep (including that from alcohol) even up to three nights after learning, despite two full nights of natural sleep prior.

  Framed practically, let’s say that you are a student cramming for an exam on Monday. Diligently, you study all of the previous Wednesday. Your friends beckon you to come out that night for drinks, but you know how important sleep is, so you decline. On Thursday, friends again ask you to grab a few drinks in the evening, but to be safe, you turn them down and sleep soundly a second night. Finally, Friday rolls around—now three nights after your learning session—and everyone is heading out for a party and drinks. Surely, after being so dedicated to slumber across the first two nights after learning, you can now cut loose, knowing those memories have been safely secured and fully processed within your memory banks. Sadly, not so. Even now, alcohol consumption will wash away much of that which you learned and can abstract by blocking your REM sleep.

  How long is it before those new memories are finally safe? We actually do not yet know, though we have studies under way that span many weeks. What we do know is that sleep has not finished tending to those newly planted memories by night 3. I elicit audible groans when I present these findings to my undergraduates in lectures. The politically incorrect advice I would (of course never) give is this: go to the pub for a drink in the morning. That way, the alcohol will be out of your system before sleep.

  Glib advice aside, what is the recommendation when it comes to sleep and alcohol? It is hard not to sound puritanical, but the evidence is so strong regarding alcohol’s harmful effects on sleep that to do otherwise would be doing you, and the science, a disservice. Many people enjoy a glass of wine with dinner, even an aperitif thereafter. But it takes your liver and kidneys many hours to degrade and excrete that alcohol, even if you are an individual with fast-acting enzymes for ethanol decomposition. Nightly alcohol will disrupt your sleep, and the annoying advice of abstinence is the best, and most honest, I can offer.

  GET THE NIGHTTIME CHILLS

  Thermal environment, specifically the proximal temperature around your body and brain, is perhaps the most underappreciated factor determining the ease with which you will fall asleep tonight, and the quality of sleep you will obtain. Ambient room temperature, bedding, and nightclothes dictate the thermal envelope that wraps around your body at night. It is ambient room temperature that has suffered a dramatic assault
from modernity. This change sharply differentiates the sleeping practices of modern humans from those of pre-industrial cultures, and from animals.

  To successfully initiate sleep, as described in chapter 2, your core temperature needs to decrease by 2 to 3 degrees Fahrenheit, or about 1 degree Celsius. For this reason, you will always find it easier to fall asleep in a room that is too cold than too hot, since a room that is too cold is at least dragging your brain and body in the correct (downward) temperature direction for sleep.

  The decrease in core temperature is detected by a group of thermosensitive cells situated in the center of your brain within the hypothalamus. Those cells live right next door to the twenty-four-hour clock of the suprachiasmatic nucleus in the brain, and for good reason. Once core temperature dips below a threshold in the evening, the thermosensitive cells quickly deliver a neighborly message to the suprachiasmatic nucleus. The memo adds to that of naturally fading light, informing the suprachiasmatic nucleus to initiate the evening surge in melatonin, and with it, the timed ordering of sleep. Your nocturnal melatonin levels are therefore controlled not only by the loss of daylight at dusk, but also the drop in temperature that coincides with the setting sun. Environmental light and temperature therefore synergistically, though independently, dictate nightly melatonin levels and sculpt the ideal timing of sleep.

  Your body is not passive in letting the cool of night lull it into sleep, but actively participates. One way you control your core body temperature is using the surface of your skin. Most of the thermic work is performed by three parts of your body in particular: your hands, your feet, and your head. All three areas are rich in crisscrossing blood vessels, known as the arteriovenous anastomoses, that lie close to the skin’s surface. Like stretching clothes over a drying line, this mass of vessels will allow blood to be spread across a large surface area of skin and come in close contact with the air that surrounds it. The hands, feet, and head are therefore remarkably efficient radiating devices that, just prior to sleep onset, jettison body heat in a massive thermal venting session so as to drop your core body temperature. Warm hands and feet help your body’s core cool, inducing inviting sleep quickly and efficiently.