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From Sleeping Pills to Society Transformed
Things That Go Bump in the Night
Sleep Disorders and Death Caused by No Sleep
Few other areas of medicine offer a more disturbing or astonishing array of disorders than those concerning sleep. Considering how tragic and remarkable disorders in those other fields can be, this is quite a claim. Yet when you consider that oddities of slumber include daytime sleep attacks and body paralysis, homicidal sleepwalking, dream enactment, and perceived alien abductions, the assertion starts to sound more valid. Most astonishing of all, perhaps, is a rare form of insomnia that will kill you within months, supported by the life-extinguishing upshot of extreme total sleep deprivation in animal studies.
This chapter is by no means a comprehensive review of all sleep disorders, of which there are now over one hundred known. Nor is it meant to serve as a medical guide to any one disorder, since I am not a board certified doctor of sleep medicine, but rather a sleep scientist. For those seeking advice on sleep disorders, I recommend visiting the National Sleep Foundation website,I and there you will find resources on sleep centers near you.
Rather than attempting a quick-fire laundry list of the many tens of sleep disorders that exist, I have chosen to focus on a select few—namely somnambulism, insomnia, narcolepsy, and fatal familial insomnia—from the vantage point of science, and what the science of these disorders can meaningfully teach us about the mysteries of sleeping and dreaming.
The term “somnambulism” refers to sleep (somnus) disorders that involve some form of movement (ambulation). It encompasses conditions such as sleepwalking, sleep talking, sleep eating, sleep texting, sleep sex, and, very rarely, sleep homicide.
Understandably, most people believe these events happen during REM sleep as an individual is dreaming, and specifically acting out ongoing dreams. However, all these events arise from the deepest stage of non-dreaming (NREM) sleep, and not dream (REM) sleep. If you rouse an individual from a sleepwalking event and ask what was going through their mind, rarely will they report a thing—no dream scenario, no mental experience.
While we do not yet fully understand the cause of somnambulism episodes, the existing evidence suggests that an unexpected spike in nervous system activity during deep sleep is one trigger. This electrical jolt compels the brain to rocket from the basement of deep NREM sleep all the way to the penthouse of wakefulness, but it gets stuck somewhere in between (the thirteenth floor, if you will). Trapped between the two worlds of deep sleep and wakefulness, the individual is confined to a state of mixed consciousness—neither awake nor asleep. In this confused condition, the brain performs basic but well-rehearsed actions, such as walking over to a closet and opening it, placing a glass of water to the lips, or uttering a few words or sentences.
A full diagnosis of somnambulism can require the patient to spend a night or two in a clinical sleep laboratory. Electrodes are placed on the head and body to measure the stages of sleep, and an infrared video camera on the ceiling records the nighttime events, like a single night-vision goggle. At the moment when a sleepwalking event occurs, the video camera footage and the electrical brainwave readouts stop agreeing. One suggests that the other is lying. Watching the video, the patient is clearly “awake” and behaving. They may sit up on the edge of the bed and begin talking. Others may attempt to put on clothes and walk out of the room. But look at the brainwave activity and you realize that the patient, or at least their brain, is sound asleep. There are the clear and unmistakable slow electrical waves of deep NREM sleep, with no sign of fast, frenetic waking brainwave activity.
For the most part, there is nothing pathological about sleepwalking or sleep talking. They are common in the adult population, and even more common in children. It is not clear why children experience somnambulism more than adults, nor is it clear why some children grow out of having these nighttime events, while others will continue to do so throughout their lives. One explanation of the former is simply the fact that we have greater amounts of deep NREM sleep when we are young, and therefore the statistical likelihood of sleepwalking and sleep talking episodes occurring is higher.
Most episodes of the condition are harmless. Occasionally, however, adult somnambulism can result in a much more extreme set of behaviors, such as those performed by Kenneth Parks in 1987. Parks, who was twenty-three years old at the time, lived with his wife and five-month-old daughter in Toronto. He had been suffering from severe insomnia caused by the stress of joblessness and gambling debts. By all accounts, Parks was a nonviolent man. His mother-in-law—with whom he had a good relationship—called him a “gentle giant” on the basis of his placid nature yet considerable height and broad-shouldered form (he stood six foot four, and weighed 225 pounds). Then came May 23.
After falling asleep on the couch around 1:30 a.m. while watching television, Parks arose and got in his car, barefoot. Depending on the route, it is estimated that Parks drove approximately fourteen miles to his in-laws’ home. Upon entering the house, Parks made his way upstairs, stabbed his mother-in-law to death with a knife he had taken from their kitchen, and strangled his father-in-law unconscious after similarly attacking him with a cleaver (his father-in-law survived). Parks then got back in his car and, upon regaining full waking consciousness at some point, drove to a police station and said, “I think I have killed some people . . . my hands.” Only then did he realize the blood flowing down his arms as a result of severing his own flexor tendons with the knife.
Since he could remember only vague fragments of the murder (e.g., flashes of his mother-in-law’s face with a “help me” look on it), had no motive, and had a long history of sleepwalking (as did other members of his family), a team of defense experts concluded that Ken Parks was asleep when he committed the crime, suffering a severe episode of sleepwalking. They argued that he was unaware of his actions, and thus not culpable. On May 25, 1988, a jury rendered a verdict of not guilty. This defense has been attempted in a number of subsequent cases, most of which have been unsuccessful.
The story of Ken Parks is of the most tragic kind, and to this day Parks struggles with a guilt one suspects may never leave him. I offer the account not to scare the reader, nor to try to sensationalize the dire events of that late May night in 1987. Rather, I offer it to illustrate how non-volitional acts arising from sleep and its disorders can have very real legal, personal, and societal consequences, and demand the contribution of scientists and doctors in arriving at the appropriate legal justice.
I also want to note, for the concerned sleepwalkers reading this chapter, that most somnambulism episodes (e.g., sleep walking, talking) are considered benign and do not require intervention. Medicine will usually step in with treatment solutions only if the afflicted patient or his caretaker, partner, or parent (in the case of children) feels that the condition is compromising health or poses a risk. There are effective treatments, and it is a shame one never arrived in time for Ken Parks prior to that ill-fated evening in May.
For many individuals these days, shudder quotes have come home to roost around the phrase “a good night’s sleep,” as the writer Will Self has lamented. Insomnia, to which his grumblings owe their origin, is the most common sleep disorder. Many individuals suffer from insomnia, yet some believe they have the disorder when they do not. Before describing the features and causes of insomnia (and in the next chapter, potential treatment options), let me first describe what insomnia is not—and in doing so, reveal what it is.
Being sleep deprived is not insomnia. In the field of medicine, sleep deprivation is considered as (i) having the adequate ability to sleep; yet (ii) giving oneself an inadequate opportunity to sleep—that is, sleep-deprived individuals can sleep, if only they would take the appropriate time to do so. Insomnia is the opposite: (i) suffering from an inadequate ability to generate sleep, despite (ii) allowing oneself the adequate opportunity to get sleep. People suffering from insomnia therefore cannot produce sufficient sleep quantity/quality, even though they give themselves enough time to do so (seven to nine hours).
Before moving on, it is worth noting the condition of sleep-state misperception, also known as paradoxical insomnia. Here, patients will report having slept poorly throughout the night, or even not sleeping at all. However, when these individuals have their sleep monitored objectively using electrodes or other accurate sleep monitoring devices, there is a mismatch. The sleep recordings indicate that the patient has slept far better than they themselves believe, and sometimes indicate that a completely full and healthy night of sleep occurred. Patients suffering from paradoxical insomnia therefore have an illusion, or misperception, of poor sleep that is not actually poor. As a result, such patients are treated as hypochondriacal. Though the term may seem dismissive or condescending, it is taken very seriously by sleep medicine doctors, and there are psychological interventions that help after the diagnosis is made.
Returning to the condition of true insomnia, there are several different sub-types, in the same way that there are numerous different forms of cancer, for example. One distinction separates insomnia into two kinds. The first is sleep onset insomnia, which is difficulty falling asleep. The second is sleep maintenance insomnia, or difficulty staying asleep. As the actor and comedian Billy Crystal has said when describing his own battles with insomnia, “I sleep like a baby—I wake up every hour.” Sleep onset and sleep maintenance insomnia are not mutually exclusive: you can have one or the other, or both. No matter which of these kinds of sleep problems is occurring, sleep medicine has very specific clinical boxes that must be checked for a patient to receive a diagnosis of insomnia. For now, these are:
Dissatisfaction with sleep quantity or quality (e.g., difficulty falling asleep, staying sleep, early-morning awakening)
Suffering significant distress or daytime impairment
Has insomnia at least three nights each week for more than three months
Does not have any coexisting mental disorders or medical conditions that could otherwise cause what appears to be insomnia
What this really means in terms of boots-on-the-ground patient descriptions is the following chronic situation: difficulty falling asleep, waking up in the middle of the night, waking up too early in the morning, difficulty falling back to sleep after waking up, and feeling unrefreshed throughout the waking day. If any of the characteristics of insomnia feel familiar to you, and have been present for several months, I suggest you consider seeking out a sleep medicine doctor. I emphasize a sleep medicine doctor and not necessarily your GP, since GPs—superb as they often are—have surprisingly minimal sleep training during the entirety of medical school and residency. Some GPs are understandably apt to prescribe a sleeping pill, which is rarely the right answer, as we will see in the next chapter.
The emphasis on duration of the sleep problem (more than three nights a week, for more than three months) is important. All of us will experience difficulty sleeping every now and then, which may last just one night or several. That is normal. There is usually an obvious cause, such as work stress or a flare-up in a social or romantic relationship. Once these things subside, though, the sleep difficulty usually goes away. Such acute sleep problems are generally not recognized as chronic insomnia, since clinical insomnia requires an ongoing duration of sleep difficulty, week after week after week.
Even with this strict definition, chronic insomnia is disarmingly common. Approximately one out of every nine people you pass on the street will meet the strict clinical criteria for insomnia, which translates to more than 40 million Americans struggling to make it through their waking days due to wide-eyed nights. While the reasons remain unclear, insomnia is almost twice as common in women than in men, and it is unlikely that a simple unwillingness of men to admit sleep problems explains this very sizable difference between the two sexes. Race and ethnicity also make a significant difference, with African Americans and Hispanic Americans suffering higher rates of insomnia than Caucasian Americans—findings that have important implications for well-recognized health disparities in these communities, such as diabetes, obesity, and cardiovascular disease, which have known links to a lack of sleep.
In truth, insomnia is likely to be a more widespread and serious problem than even these sizable numbers suggest. Should you relax the stringent clinical criteria and just use epidemiological data as a guide, it is probable that two out of every three people reading this book will regularly have difficulty falling or staying asleep at least one night a week, every week.
Without belaboring the point, insomnia is one of the most pressing and prevalent medical issues facing modern society, yet few speak of it this way, recognize the burden, or feel there is a need to act. That the “sleep aid” industry, encompassing prescription sleeping medications and over-the-counter sleep remedies, is worth an astonishing $30 billion a year in the US is perhaps the only statistic one needs in order to realize how truly grave the problem is. Desperate millions of us are willing to pay a lot of money for a good night’s sleep.
But dollar values do not address the more important issue of what’s causing insomnia. Genetics plays a role, though it is not the full answer. Insomnia shows some degree of genetic heritability, with estimates of 28 to 45 percent transmission rates from parent to child. However, this still leaves the majority of insomnia being associated with non-genetic causes, or gene-environment (nature-nurture) interactions.
To date, we have discovered numerous triggers that cause sleep difficulties, including psychological, physical, medical, and environmental factors (with aging being another, as we have previously discussed). External factors that cause poor sleep, such as too much bright light at night, the wrong ambient room temperature, caffeine, tobacco, and alcohol consumption—all of which we’ll visit in more detail in the next chapter—can masquerade as insomnia. However, their origins are not from within you, and therefore not a disorder of you. Rather, they are influences from outside and, once they are addressed, individuals will get better sleep, without changing anything about themselves.
Other factors, however, come from within a person, and are innate biological causes of insomnia. Noted in the clinical criteria described above, these factors cannot be a symptom of a disease (e.g., Parkinson’s disease) or a side effect of a medication (e.g., asthma medication). Rather, the cause(s) of the sleep problem must stand alone in order for you to be primarily suffering from true insomnia.
The two most common triggers of chronic insomnia are psychological: (1) emotional concerns, or worry, and (2) emotional distress, or anxiety. In this fast-paced, information-overloaded modern world, one of the few times that we stop our persistent informational consumption and inwardly reflect is when our heads hit the pillow. There is no worse time to consciously do this. Little wonder that sleep becomes nearly impossible to initiate or maintain when the spinning cogs of our emotional minds start churning, anxiously worrying about things we did today, things that we forgot to do, things that we must face in the coming days, and even those far in the future. That is no kind of invitation for beckoning the calm brainwaves of sleep into your brain, peacefully allowing you to drift off into a full night of restful slumber.
Since psychological distress is a principal instigator of insomnia, researchers have focused on examining the biological causes that underlie emotional turmoil. One common culprit has become clear: an overactive sympathetic nervous system, which, as we have discussed in previous chapters, is the body’s aggravating fight-or-flight mechanism. The sympathetic nervous system switches on in response to threat and acute stress that, in our evolutionary past, was required to mobilize a legitimate fight-or-flight response. The physiological consequences are increased heart rate, blood flow, metabolic rate, the release of stress-negotiating chemicals such as cortisol, and increased brain activation, all of which are beneficial in the acute moment of true threat or danger. However, the fight-or-flight response is not meant to be left in the “on” position for any prolonged period of time. As we have already touched upon in earlier chapters, chronic activation of the flight-or-flight nervous system causes myriad health problems, one of which is now recognized to be insomnia.
Why an overactive fight-or-flight nervous system prevents good sleep can be explained by several of the topics we have discussed so far, and some we have not. First, the raised metabolic rate triggered by fight-or-flight nervous system activity, which is common in insomnia patients, results in a higher core body temperature. You may remember from chapter 2 that we must drop core body temperature by a few degrees to initiate sleep, which becomes more difficult in insomnia patients suffering a raised metabolic rate and higher operating internal temperature, including in the brain.
Second are higher levels of the alertness-promoting hormone cortisol, and sister neurochemicals adrenaline and noradrenaline. All three of these chemicals raise heart rate. Normally, our cardiovascular system calms down as we make the transition into light and then deep sleep. Elevated cardiac activity makes that transition more difficult. All three of these chemicals increase metabolic rate, additionally increasing core body temperature, which further compounds the first problem outlined above.
Third, and related to these chemicals, are altered patterns of brain activity linked with the body’s sympathetic nervous system. Researchers have placed healthy sleepers and insomnia patients in a brain scanner and measured the changing patterns of activity as both groups try to fall asleep. In the good sleepers, the parts of the brain related to inciting emotions (the amygdala) and those linked to memory retrospection (the hippocampus) quickly ramped down in their levels of activity as they transitioned toward sleep, as did basic alertness regions in the brain stem. This was not the case for the insomnia patients. Their emotion-generating regions and memory-recollection centers all remained active. This was similarly true of the basic vigilance centers in the brain stem that stubbornly continued their wakeful watch. All the while the thalamus—the sensory gate of the brain that needs to close shut to allow sleep—remained active and open for business in insomnia patients.
Simply put, the insomnia patients could not disengage from a pattern of altering, worrisome, ruminative brain activity. Think of a time when you closed the lid of a laptop to put it to sleep, but came back later to find that the screen was still on, the cooling fans were still running, and the computer was still active, despite the closed lid. Normally this is because programs and routines are still running, and the computer cannot make the transition into sleep mode.
Based on the results of brain-imaging studies, an analogous problem is occurring in insomnia patients. Recursive loops of emotional programs, together with retrospective and prospective memory loops, keep playing in the mind, preventing the brain from shutting down and switching into sleep mode. It is telling that a direct and causal connection exists between the fight-or-flight branch of the nervous system and all of these emotion-, memory-, and alertness-related regions of the brain. The bidirectional line of communication between the body and brain amounts to a vicious, recurring cycle that fuels their thwarting of sleep.
The fourth and final set of identified changes has been observed in the quality of sleep of insomnia patients when they do finally drift off. Once again, these appear to have their origins in an overactive fight-or-flight nervous system. Patients with insomnia have a lower quality of sleep, reflected in shallower, less powerful electrical brainwaves during deep NREM. They also have more fragmented REM sleep, peppered by brief awakenings that they are not always aware of, yet still cause a degraded quality of dream sleep. All of which means that insomnia patients wake up not feeling refreshed. Consequentially, patients are unable to function well during the day, cognitively and/or emotionally. In this way, insomnia is really a 24/7 disorder: as much a disorder of the day as of the night.
You can now understand how physiologically complex the underlying condition is. No wonder the blunt instruments of sleeping pills, which simply and primitively sedate your higher brain, or cortex, are no longer recommended as the first-line treatment approach for insomnia by the American Medical Association. Fortunately, a non-pharmacological therapy, which we will discuss in detail in the next chapter, has been developed. It is more powerful in restoring naturalistic sleep in insomnia sufferers, and it elegantly targets each of the physiological components of insomnia described above. Real optimism is to be found in these new, non-drug therapies that I urge you to explore should you suffer from true insomnia.
I suspect that you cannot recall any truly significant action in your life that wasn’t governed by two very simple rules: staying away from something that would feel bad, or trying to accomplish something that would feel good. This law of approach and avoidance dictates most of human and animal behavior from a very early age.
The forces that implement this law are positive and negative emotions. Emotions make us do things, as the name suggests (remove the first letter from the word). They motivate our remarkable achievements, incite us to try again when we fail, keep us safe from potential harm, urge us to accomplish rewarding and beneficial outcomes, and compel us to cultivate social and romantic relationships. In short, emotions in appropriate amounts make life worth living. They offer a healthy and vital existence, psychologically and biologically speaking. Take them away, and you face a sterile existence with no highs or lows to speak of. Emotionless, you will simply exist, rather than live. Tragically, this is the very kind of reality many narcoleptic patients are forced to adopt for reasons we will now explore.
Medically, narcolepsy is considered to be a neurological disorder, meaning that its origins are within the central nervous system, specifically the brain. The condition usually emerges between ages ten and twenty years. There is some genetic basis to narcolepsy, but it is not inherited. Instead, the genetic cause appears to be a mutation, so the disorder is not passed from parent to child. However, gene mutations, at least as we currently understand them in the context of this disorder, do not explain all incidences of narcolepsy. Other triggers remain to be identified. Narcolepsy is also not unique to humans, with numerous other mammals expressing the disorder.
There are at least three core symptoms that make up the disorder: (1) excessive daytime sleepiness, (2) sleep paralysis, and (3) cataplexy.
The first symptom of excessive daytime sleepiness is often the most disruptive and problematic to the quality of day-to-day life for narcoleptic patients. It involves daytime sleep attacks: overwhelming, utterly irresistible urges to sleep at times when you want to be awake, such as working at your desk, driving, or eating a meal with family or friends.
Having read that sentence, I suspect many of you are thinking, “Oh my goodness, I have narcolepsy!” That is unlikely. It is far more probable that you are suffering from chronic sleep deprivation. About one in every 2,000 people suffers from narcolepsy, making it about as common as multiple sclerosis. The sleep attacks that typify excessive daytime sleepiness are usually the first symptom to appear. Just to give you a sense of what that feeling is, relative to what you may be considering, it would be the sleepiness equivalent of staying awake for three to four days straight.
The second symptom of narcolepsy is sleep paralysis: the frightening loss of ability to talk or move when waking up from sleep. In essence, you become temporarily locked in your body.
Most of these events occur in REM sleep. You will remember that during REM sleep, the brain paralyzes the body to keep you from acting out your dreams. Normally, when we wake out of a dream, the brain releases the body from the paralysis in perfect synchrony, right at the moment when waking consciousness returns. However, there can be rare occasions when the paralysis of the REM state lingers on despite the brain having terminated sleep, rather like that last guest at a party who seems unwilling to recognize the event is over and it is time to leave the premises. As a result, you begin to wake up, but you are unable to lift your eyelids, turn over, cry out, or move any of the muscles that control your limbs. Gradually, the paralysis of REM sleep does wear off, and you regain control of your body, including your eyelids, arms, legs, and mouth.
Don’t worry if you have had an episode of sleep paralysis at some point in your life. It is not unique to narcolepsy. Around one in four healthy individuals will experience sleep paralysis, which is to say that it is as common as hiccups. I myself have experienced sleep paralysis several times, and I do not suffer from narcolepsy. Narcoleptic patients will, however, experience sleep paralysis far more frequently and severely than healthy individuals. This nevertheless means that sleep paralysis is a symptom associated with narcolepsy, but it is not unique to narcolepsy.
A brief detour of an otherworldly kind is in order at this moment. When individuals undergo a sleep paralysis episode, it is often associated with feelings of dread and a sense of an intruder being present in the room. The fear comes from an inability to act in response to the perceived threat, such as not being able to shout out, stand up and leave the room, or prepare to defend oneself. It is this set of features of sleep paralysis that we now believe explains a large majority of alien abduction claims. Rarely do you hear of aliens accosting an individual in the middle of the day with testimonial witnesses standing in plain sight, dumbstruck by the extraterrestrial kidnapping in progress. Instead, most alleged alien abductions take place at night; most classic alien visitations in Hollywood movies like Close Encounters of the Third Kind or E.T. also occur at night. Moreover, victims of claimed alien abductions frequently report the sense of, or real presence of, a being in the room (the alien). Finally—and this is the key giveaway—the alleged victim frequently describes having been injected with a “paralyzing agent.” Consequently, the victim will describe wanting to fight back, run away, or call out for help but being unable to do so. The offending force is, of course, not aliens, but the persistence of REM-sleep paralysis upon awakening.
The third and most astonishing core symptom of narcolepsy is called cataplexy. The word comes from the Greek kata, meaning down, and plexis, meaning a stroke or seizure—that is, a falling-down seizure. However, a cataplectic attack is not a seizure at all, but rather a sudden loss of muscle control. This can range from slight weakness wherein the head droops, the face sags, the jaw drops, and speech becomes slurred to a buckling of knees or a sudden and immediate loss of all muscle tone, resulting in total collapse on the spot.
You may be old enough to remember a child’s toy that involved an animal, often a donkey, standing on a small, palm-sized pedestal with a button underneath. It was similar to a puppet on strings, except that the strings were not attached to the outside limbs, but rather woven through the limbs on the inside, and connected to the button underneath. Depressing the button relaxed the inner string tension, and the donkey would collapse into a heap. Release the button, pulling the inner strings taut, and the donkey would snap back upright to firm attention. The demolition of muscle tone that occurs during a full-blown cataplectic attack, resulting in total body collapse, is very much like this toy, but the consequences are no laughing matter.
If this were not wicked enough, there is an extra layer of malevolence to the condition that truly devastates the patient’s quality of life. Cataplectic attacks are not random, but are triggered by moderate or strong emotions, positive or negative. Tell a funny joke to a narcoleptic patient, and they may literally collapse in front of you. Walk into a room and surprise a patient, perhaps while they are chopping food with a sharp knife, and they will collapse perilously. Even standing in a nice warm shower can be enough of a pleasurable experience to cause a patient’s legs to buckle and have a potentially dangerous fall caused by the cataplectic muscle loss.
Now extrapolate this, and consider the dangers of driving a car and being startled by a loud horn. Or playing an enjoyable game with your children, or having them jump on you and tickle you, or feeling strong, tear-welling joy at one of their musical school recitals. In a narcoleptic patient with cataplexy, any one of these may cause the sufferer to collapse into the immobilized prison of his or her own body. Consider, then, how difficult it is to have a loving, pleasurable sexual relationship with a narcoleptic partner. The list becomes endless, with predictable and heart-wrenching outcomes.
Unless patients are willing to accept these crumpling attacks, which is really no option of any kind, all hope of living an emotionally fulfilling life must be abandoned. A narcoleptic patient is banished to a monotonic existence of emotional neutrality. They must forfeit any semblance of succulent emotions that we are all nourished by on a moment-to-moment basis. It is the dietary equivalent of eating the same tepid bowl of unflavorful porridge day after day. You can well imagine the loss of appetite for such a life.
If you saw a patient collapse under the influence of cataplexy, you would be convinced that they had fallen completely unconscious or into a powerful sleep. This is untrue. Patients are awake and continue to perceive the outside world around them. Instead, what the strong emotion has triggered is the total (or sometimes partial) body paralysis of REM sleep without the sleep of the REM state itself. Cataplexy is therefore an abnormal functioning of the REM-sleep circuitry within the brain, wherein one of its features—muscle atonia—is inappropriately deployed while the individual is awake and behaving, rather than asleep and dreaming.
We can of course explain this to an adult patient, lowering their anxiety during the event through comprehension of what is happening, and help them rein in or avoid emotional highs and lows to reduce cataplectic occurrences. However, this is much more difficult in a ten-year-old youngster. How can you explain such a villainous symptom and disorder to a child with narcolepsy? And how do you prevent a child from enjoying the normal roller coaster of emotional existence that is a natural and integral part of a growing life and developing brain? Which is to say, how do you prevent a child from being a child? There are no easy answers to these questions.
We are, however, beginning to discover the neurological basis of narcolepsy and, in conjunction, more about healthy sleep itself. In chapter 3, I described the parts of the brain involved in the maintenance of normal wakefulness: the alerting, activating regions of the brain stem and the sensory gate of the thalamus that sits on top, a setup that looks almost like a scoop of ice cream (thalamus) on a cone (brain stem). As the brain stem powers down at night, it removes its stimulating influence to the sensory gate of the thalamus. With the closing of the sensory gate, we stop perceiving the outside world, and thus we fall asleep.
What I did not tell you, however, was how the brain stem knows that it’s time to turn off the lights, so to speak, and power down wakefulness to begin sleep. Something has to switch the activating influence of the brain stem off, and in doing so, allow sleep to be switched on. That switch—the sleep-wake switch—is located just below the thalamus in the center of the brain, in a region called the hypothalamus. It is the same neighborhood that houses the twenty-four-hour master biological clock, perhaps unsurprisingly.
The sleep-wake switch within the hypothalamus has a direct line of communication to the power station regions of the brain stem. Like an electrical light switch, it can flip the power on (wake) or off (sleep). To do this, the sleep-wake switch in the hypothalamus releases a neurotransmitter called orexin. You can think of orexin as the chemical finger that flips the switch to the “on,” wakefulness, position. When orexin is released down onto your brain stem, the switch has been unambiguously flipped, powering up the wakefulness-generating centers of the brain stem. Once activated by the switch, the brain stem pushes open the sensory gate of the thalamus, allowing the perceptual world to flood into your brain, transitioning you to full, stable wakefulness.
At night, the opposite happens. The sleep-wake switch stops releasing orexin onto the brain stem. The chemical finger has now flipped the switch to the “off” position, shutting down the rousing influence from the power station of the brain stem. The sensory business being conducted within the thalamus is closed down by a sealing of the sensory gate. We lose perceptual contact with the outside world, and now sleep. Lights off, lights on, lights off, lights on—this is the neurobiological job of the sleep-wake switch in the hypothalamus, controlled by orexin.
Ask an engineer what the essential properties of a basic electrical switch are, and they will inform you of an imperative: the switch must be definitive. It must either be fully on or fully off—a binary state. It must not float in a wishy-washy manner between the “on” and “off” positions. Otherwise, the electrical system will not be stable or predictable. Unfortunately, this is exactly what happens to the sleep-wake switch in the disorder of narcolepsy, caused by marked abnormalities of orexin.
Scientists have examined the brains of narcoleptic patients in painstaking detail after they have passed away. During these postmortem investigations, they discovered a loss of almost 90 percent of all the cells that produce orexin. Worse still, the welcome sites, or receptors, of orexin that cover the surface of the power station of the brain stem were significantly reduced in number in narcoleptic patients, relative to normal individuals.
Because of this lack of orexin, made worse by the reduced number of receptor sites to receive what little orexin does drip down, the sleep-wake state of the narcoleptic brain is unstable, like a faulty flip-flop switch. Never definitively on or off, the brain of a narcoleptic patient wobbles precariously around a middle point, teeter-tottering between sleep and wakefulness.
The orexin-deficient state of this sleep-wake system is the main cause of the first and primary symptom of narcolepsy, which is excessive daytime sleepiness and the surprise attacks of sleep that can happen at any moment. Without the strong finger of orexin pushing the sleep-wake switch all the way over into a definitive “on” position, narcoleptic patients cannot sustain resolute wakefulness throughout the day. For the same reasons, narcoleptic patients have terrible sleep at night, dipping into and out of slumber in choppy fashion. Like a faulty light switch that endlessly flickers on and off, day and night, so goes the erratic sleep and wake experience suffered by a narcoleptic patient across each and every twenty-four-hour period.
Despite wonderful work by many of my colleagues, narcolepsy currently represents a failure of sleep research at the level of effective treatments. While we have effective interventions for other sleep disorders, such as insomnia and sleep apnea, we lag far behind the curve for treating narcolepsy. This is in part due to the rarity of the condition, making it unprofitable for drug companies to invest their research effort, which is often a driver of fast treatment progress in medicine.
For the first symptom of narcolepsy—daytime sleep attacks—the only treatment used to be high doses of the wake-promoting drug amphetamine. But amphetamine is powerfully addictive. It is also a “dirty” drug, meaning that it is promiscuous and affects many different chemical systems in the brain and body, leading to terrible side effects. A newer, “cleaner” drug, called Provigil, is now used to help narcoleptic patients stay more stably awake during the day and has fewer downsides. Yet it is marginally effective.
Antidepressants are often prescribed to help with the second and third symptoms of narcolepsy—sleep paralysis and cataplexy—as they suppress REM sleep, and it is REM-sleep paralysis that is integral to these two symptoms. Nevertheless, antidepressants simply lower the incidence of both; they do not eradicate them.
Overall, the treatment outlook for narcoleptic patients is bleak at present, and there is no cure in sight. Much of the treatment fate of narcolepsy sufferers and their families resides in the slower-progressing hands of academic research, rather than the more rapid progression of big pharmaceutical companies. For now, patients simply must try to manage life with the disorder, living as best they can.
Some of you may have had the same realization that several drug companies did when we learned about the role of orexin and the sleep-wake switch in narcolepsy: could we reverse-engineer the knowledge and, rather than enhance orexin to give narcoleptic patients more stable wakefulness during the day, try and shut it off at night, thereby offering a novel way of inducing sleep in insomnia patients? Pharmaceutical companies are indeed trying to develop compounds that can block orexin at night, forcing it to flip the switch to the “off” position, potentially inducing more naturalistic sleep than the problematic and sedating sleep drugs we currently have.
Unfortunately, the first of these drugs, suvorexant (brand name Belsomra), has not proved to be the magic bullet many hoped. Patients in the FDA-mandated clinical trials fell asleep just six minutes faster than those taking a placebo. While future formulations may prove more efficacious, non-pharmacological methods for the treatment of insomnia, outlined in the next chapter, remain a far superior option for insomnia sufferers.
FATAL FAMILIAL INSOMNIA
Michael Corke became the man who could not sleep—and paid for it with his life. Before the insomnia took hold, Corke was a high-functioning, active individual, a devoted husband, and a teacher of music at a high school in New Lexon, just south of Chicago. At age forty he began having trouble sleeping. At first, Corke felt that his wife’s snoring was to blame. In response to this suggestion, Penny Corke decided to sleep on the couch for the next ten nights. Corke’s insomnia did not abate, and only became worse. After months of poor sleep, and realizing the cause lay elsewhere, Corke decided to seek medical help. None of the doctors who first examined Corke could identify the trigger of his insomnia, and some diagnosed him with sleep-unrelated disorders, such as multiple sclerosis.
Corke’s insomnia eventually progressed to the point where he was completely unable to sleep. Not a wink. No mild sleep medications or even heavy sedatives could wrestle his brain from the grip of permanent wakefulness. Should you have observed Corke at this time, it would be clear how desperate he was for sleep. His eyes would make your own feel tired. His blinks were achingly slow, as if the eyelids wanted to stay shut, mid-blink, and not reopen for days. They telegraphed the most despairing hunger for sleep you could imagine.
After eight straight weeks of no sleep, Corke’s mental faculties were quickly fading. This cognitive decline was matched in speed by the rapid deterioration of his body. So compromised were his motor skills that even coordinated walking became difficult. One evening Corke was to conduct a school orchestral performance. It took several painful (though heroic) minutes for him to complete the short walk through the orchestra and climb atop the conductor’s rostrum, all cane-assisted.
As Corke approached the six-month mark of no sleep, he was bedridden and approaching death. Despite his young age, Corke’s neurological condition resembled that of an elderly individual in the end stages of dementia. He could not bathe or clothe himself. Hallucinations and delusions were rife. His ability to generate language was all but gone, and he was resigned to communicating through rudimentary head movements and rare inarticulate utterances whenever he could muster the energy. Several more months of no sleep and Corke’s body and mental faculties shut down completely. Soon after turning forty-two years old, Michael Corke died of a rare, genetically inherited disorder called fatal familial insomnia (FFI). There are no treatments for this disorder, and there are no cures. Every patient diagnosed with the disorder has died within ten months, some sooner. It is one of the most mysterious conditions in the annals of medicine, and it has taught us a shocking lesson: a lack of sleep will kill a human being.
The underlying cause of FFI is increasingly well understood, and builds on much of what we have discussed regarding the normal mechanisms of sleep generation. The culprit is an anomaly of a gene called PrNP, which stands for prion protein. All of us have prion proteins in our brain, and they perform useful functions. However, a rogue version of the protein is triggered by this genetic defect, resulting in a mutated version that spreads like a virus.II In this genetically crooked form, the protein begins targeting and destroying certain parts of the brain, resulting in a rapidly accelerating form of brain degeneration as the protein spreads.
One region that this malfeasant protein attacks, and attacks comprehensively, is the thalamus—that sensory gate within the brain that must close shut for wakefulness to end and sleep to begin. When scientists performed postmortem examinations of the brains of early sufferers of FFI, they discovered a thalamus that was peppered with holes, almost like a block of Swiss cheese. The prion proteins had burrowed throughout the thalamus, utterly degrading its structural integrity. This was especially true of the outer layers of the thalamus, which form the sensory doors that should close shut each night.
Due to this puncturing attack by the prion proteins, the sensory gate of the thalamus was effectively stuck in a permanent “open” position. Patients could never switch off their conscious perception of the outside world and, as a result, could never drift off into the merciful sleep that they so desperately needed. No amount of sleeping pills or other drugs could push the sensory gate closed. In addition, the signals sent from the brain down into the body that prepare us for sleep—the reduction of heart rate, blood pressure, and metabolism, and the lowering of core body temperature—all must pass through the thalamus on their way down the spinal cord, and are then mailed out to the different tissues and organs of the body. But those signals were thwarted by the damage to the thalamus, adding to the impossibility of sleep in the patients.
Current treatment prospects are few. There has been some interest in an antibiotic called doxycycline, which seems to slow the rate of the rogue protein accumulation in other prion disorders, such as Creutzfeldt-Jakob disease, or so-called mad cow disease. Clinical trials for this potential therapy are now getting under way.
Beyond the race for a treatment and cure, an ethical issue emerges in the context of the disease. Since FFI is genetically inherited, we have been able to retrospectively trace some of its legacy through generations. That genetic lineage runs all the way back into Europe, and specifically Italy, where a number of afflicted families live. Careful detective work has rolled the genetic timeline back further, to a Venetian doctor in the late eighteenth century who appeared to have a clear case of the disorder. Undoubtedly, the gene goes back even further than this individual. More important than tracing the disease’s past, however, is predicting its future. The genetic certainty raises a eugenically fraught question: If your family’s genes mean that you could one day be struck down by the fatal inability to sleep, would you want to be told your fate? Furthermore, if you know that fate and have not yet had children, would that change your decision to do so, knowing you are a gene carrier and that you have the potential to prevent a next-step transmission of the disease? There are no simple answers, certainly none that science can (or perhaps should) offer—an additionally cruel tendril of an already heinous condition.
SLEEP DEPRIVATION VS. FOOD DEPRIVATION
FFI is still the strongest evidence we have that a lack of sleep will kill a human being. Scientifically, however, it remains arguably inconclusive, as there may be other disease-related processes that could contribute to death, and they are hard to distinguish from those of a lack of sleep. There have been individual case reports of humans dying as a result of prolonged total sleep deprivation, such as Jiang Xiaoshan. He was alleged to have stayed awake for eleven days straight to watch all the games of the 2012 European soccer championships, all the while working at his job each day. On day 12, Xiaoshan was found dead in his apartment by his mother from an apparent lack of sleep. Then there was the tragic death of a Bank of America intern, Moritz Erhardt, who suffered a life-ending epileptic seizure after acute sleep deprivation from the work overload that is so endemic and expected in that profession, especially from the juniors in such organizations. Nevertheless, these are simply case studies, and they are hard to validate and scientifically verify after the fact.
Research studies in animals have, however, provided definitive evidence of the deadly nature of total sleep deprivation, free of any comorbid disease. The most dramatic, disturbing, and ethically provoking of these studies was published in 1983 by a research team at the University of Chicago. Their experimental question was simple: Is sleep necessary for life? By preventing rats from sleeping for weeks on end in a gruesome ordeal, they came up with an unequivocal answer: rats will die after fifteen days without sleep, on average.
Two additional results quickly followed. First, death ensued as quickly from total sleep deprivation as it did from total food deprivation. Second, rats lost their lives almost as quickly from selective REM-sleep deprivation as they did following total sleep deprivation. A total absence of NREM sleep still proved fatal, it just took longer to inflict the same mortal consequence—forty-five days, on average.
There was, however, an issue. Unlike starvation, where the cause of death is easily identified, the researchers could not determine why the rats had died following sleep’s absence, despite how quickly death had arrived. Some hints emerged from assessments made during the experiment, as well as the later postmortems.
First, despite eating far more than their sleep-rested counterparts, the sleep-deprived rats rapidly began losing body mass during the study. Second, they could no longer regulate their core body temperature. The more sleep-deprived the rats were, the colder they became, regressing toward ambient room temperature. This was a perilous state to be in. All mammals, humans included, live on the edge of a thermal cliff. Physiological processes within the mammalian body can only operate within a remarkably narrow temperature range. Dropping below or above these life-defining thermal thresholds is a fast track to death.
It was no coincidence that these metabolic and thermal consequences were jointly occurring. When core body temperature drops, mammals respond by increasing their metabolic rate. Burning energy releases heat to warm the brain and body to get them back above the critical thermal threshold so as to avert death. But it was a futile effort in the rats lacking sleep. Like an old wood-burning stove whose top vent has been left open, no matter how much fuel was being added to the fire, the heat simply flew out the top. The rats were effectively metabolizing themselves from the inside out in response to hypothermia.
The third, and perhaps most telling, consequence of sleep loss was skin deep. The privation of sleep had left these rats literally threadbare. Sores had appeared across the rats’ skin, together with wounds on their paws and tails. Not only was the metabolic system of the rats starting to implode, but so, too, was their immune system.III They could not fend off even the most basic of infections at their epidermis—or below it, as we shall see.
If these outward signs of degrading health were not shocking enough, the internal damage revealed by the final postmortem was equally ghastly. A landscape of utter physiological distress awaited the pathologist. Complications ranged from fluid in the lungs and internal hemorrhaging to ulcers puncturing the stomach lining. Some organs, such as the liver, spleen, and kidneys, had physically decreased in size and weight. Others, like the adrenal glands that respond to infection and stress, were markedly enlarged. Circulating levels of the anxiety-related hormone corticosterone, released by the adrenal glands, had spiked in the sleepless rats.
What, then, was the cause of death? Therein lay the issue: the scientists had no idea. Not all the rats suffered the same pathological signature of demise. The only commonality across the rats was death itself (or the high likelihood of it, at which point the researchers euthanized the animals).
In the years that followed, further experiments—the last of their kind, as scientists felt (rightly, in my personal view) uneasy about the ethics of such experiments based on the outcome—finally resolved the mystery. The fatal final straw turned out to be septicemia—a toxic and systemic (whole organism) bacterial infection that coursed through the rats’ bloodstream and ravaged the entire body until death. Far from a vicious infection that came from the outside, however, it was simple bacteria from the rats’ very own gut that inflicted the mortal blow—one that an otherwise healthy immune system would have easily quelled when fortified by sleep.
The Russian scientist Marie de Manacéïne had in fact reported the same mortal consequences of continuous sleep deprivation in the medical literature a century earlier. She noted that young dogs died within several days if prevented from sleeping (which are difficult studies for me to read, I must confess). Several years after de Manacéïne’s studies, Italian researchers described equally lethal effects of total sleep deprivation in dogs, adding the observation of neural degeneration in the brain and spinal cord at postmortem.
It took another hundred years after the experiments of de Manacéïne, and the advancements in precise experimental laboratory assessments, before the scientists at the University of Chicago finally uncovered why life ends so quickly in the absence of sleep. Perhaps you have seen that small plastic red box on the walls of extremely hazardous work environments that has the following words written on the front: “Break glass in case of emergency.” If you impose a total absence of sleep on an organism, rat or human, it indeed becomes an emergency, and you will find the biological equivalent of this shattered glass strewn throughout the brain and the body, to fatal effect. This we finally understand.
NO, WAIT—YOU ONLY NEED 6.75 HOURS OF SLEEP!
Reflecting on these deathly consequences of long-term/chronic and short-term/acute sleep deprivation allows us to address a recent controversy in the field of sleep research—one that many a newspaper, not to mention some scientists, apprehended incorrectly. The study in question was conducted by researchers at the University of California, Los Angeles, on the sleep habits of specific pre-industrial tribes. Using wristwatch activity devices, the researchers tracked the sleep of three hunter-gatherer tribes that are largely untouched by the ways of industrial modernity: the Tsimané people in South America, and the San and Hadza tribes in Africa, which we have previously discussed. Assessing sleep and wake times day after day across many months, the findings were thus: tribespeople averaged just 6 hours of sleep in the summer, and about 7.2 hours of sleep in the winter.
Well-respected media outlets touted the findings as proof that human beings do not, after all, need a full eight hours of sleep, some suggesting we can survive just fine on six hours or less. For example, the headline of one prominent US newspaper read:
“Sleep Study on Modern-Day Hunter-Gatherers Dispels Notion That We’re Wired to Need 8 Hours a Day.”
Others started out with the already incorrect assumption that modern societies need only seven hours of sleep, and then questioned whether we even need that much: “Do We Really Need to Sleep 7 Hours a Night?”
How can such prestigious and well-respected entities reach these conclusions, especially after the science that I have presented in this chapter? Let us carefully reevaluate the findings, and see if we still arrive at the same conclusion.
First, when you read the paper, you will learn that the tribespeople were actually giving themselves a 7- to 8.5-hour sleep opportunity each night. Moreover, the wristwatch device, which is neither a precise nor gold standard measure of sleep, estimated a range of 6 to 7.5 hours of this time was spent asleep. The sleep opportunity that these tribespeople provide themselves is therefore almost identical to what the National Sleep Foundation and the Centers for Disease Control and Prevention recommend for all adult humans: 7 to 9 hours of time in bed.
The problem is that some people confuse time slept with sleep opportunity time. We know that many individuals in the modern world only give themselves 5 to 6.5 hours of sleep opportunity, which normally means they will only obtain around 4.5 to 6 hours of actual sleep. So no, the finding does not prove that the sleep of hunter-gatherer tribes is similar to ours in the post-industrial era. They, unlike us, give themselves more sleep opportunity than we do.
Second, let us assume that the wristwatch measurements are perfectly accurate, and that these tribes obtain an annual average of just 6.75 hours of sleep. The next erroneous conclusion drawn from the findings was that humans must, therefore, naturally need a mere 6.75 hours of sleep, and no more. Therein lies the rub.
If you refer back to the two newspaper headlines I quoted, you’ll notice they both use the word “need.” But what need are we talking about? The (incorrect) presupposition made was this: whatever sleep the tribespeople were obtaining is all that a human needs. It is flawed reasoning on two counts. Need is not defined by that which is obtained (as the disorder of insomnia teaches us), but rather whether or not that amount of sleep is sufficient to accomplish all that sleep does. The most obvious need, then, would be for life—and healthy life. Now we discover that the average life span of these hunter-gatherers is just fifty-eight years, even though they are far more physically active than we are, rarely obese, and are not plagued by the assault of processed foods that erode our health. Of course, they do not have access to modern medicine and sanitation, both of which are reasons that many of us in industrialized, first-world nations have an expected life span that exceeds theirs by over a decade. But it is telling that, based on epidemiological data, any adult sleeping an average of 6.75 hours a night would be predicted to live only into their early sixties: very close to the median life span of these tribespeople.
More prescient, however, is what normally kills people in these tribes. So long as they survive high rates of infant mortality and make it through adolescence, a common cause of death in adulthood is infection. Weak immune systems are a known consequence of insufficient sleep, as we have discussed in great detail. I should also note that one of the most common immune system failures that kills individuals in hunter-gatherer clans are intestinal infections—something that shares an intriguing overlap with the deadly intestinal tract infections that killed the sleep-deprived rats in the above studies.
Recognizing this shorter life span, which fits well with the acclaimed shorter sleep amounts the researchers measured, the next error in logic many made is exposed by asking why these tribes would sleep what appears to be too little, based on all that we know from thousands of research studies.
We do not yet know of all the reasons, but a likely contributing factor lies in the title we apply to these tribes: hunter-gatherers. One of the few universal ways of forcing animals of all kinds to sleep less than normal amounts is to limit food, applying a degree of starvation. When food becomes scarce, sleep becomes scarce, as animals try to stay awake longer to forage. Part of the reason that these hunter-gatherer tribes are not obese is because they are constantly searching for food, which is never abundant for long stretches. They spend much of their waking lives in pursuit and preparation of nutrition. For example, the Hadza will face days where they obtain 1,400 calories or less, and routinely eat 300 to 600 fewer daily calories than those of us in modern Western cultures. A large proportion of their year is therefore spent in a state of lower-level starvation, one that can trigger well-characterized biological pathways that reduce sleep time, even though sleep need remains higher than that obtained if food were abundant. Concluding that humans, modern-living or pre-industrial, need less than seven hours of sleep therefore appears to be a wishful conceit, and a tabloid myth.
IS SLEEPING NINE HOURS A NIGHT TOO MUCH?
Epidemiological evidence suggests that the relationship between sleep and mortality risk is not linear, such that the more and more sleep you get, the lower and lower your death risk (and vice versa). Rather, there is an upward hook in death risk once the average sleep amount passes nine hours, resulting in a tilted backward J shape:
Two points are worthy of mention in this regard. First, should you explore those studies in detail, you learn that the causes of death in individuals sleeping nine hours or longer include infection (e.g., pneumonia) and immune-activating cancers. We know from evidence discussed earlier in the book that sickness, especially sickness that activates a powerful immune response, activates more sleep. Ergo, the sickest individuals should be sleeping longer to battle back against illness using the suite of health tools sleep has on offer. It is simply that some illnesses, such as cancer, can be too powerful even for the mighty force of sleep to overcome, no matter how much sleep is obtained. The illusion created is that too much sleep leads to an early death, rather than the more tenable conclusion that the sickness was just too much despite all efforts to the contrary from the beneficial sleep extension. I say more tenable, rather than equally tenable, because no biological mechanisms that show sleep to be in any way harmful have been discovered.
Second, it is important not to overextend my point. I am not suggesting that sleeping eighteen or twenty-two hours each and every day, should that be physiologically possible, is more optimal than sleeping nine hours a day. Sleep is unlikely to operate in such a linear manner. Keep in mind that food, oxygen, and water are no different, and they, too, have a reverse-J-shape relationship with mortality risk. Eating to excess shortens life. Extreme hydration can lead to fatal increases in blood pressure associated with stroke or heart attack. Too much oxygen in the blood, known as hyperoxia, is toxic to cells, especially those of the brain.
Sleep, like food, water, and oxygen, may share this relationship with mortality risk when taken to extremes. After all, wakefulness in the correct amount is evolutionarily adaptive, as is sleep. Both sleep and wake provide synergistic and critical, though often different, survival advantages. There is an adaptive balance to be struck between wakefulness and sleep. In humans, that appears to be around sixteen hours of total wakefulness, and around eight hours of total sleep, for an average adult.
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