✦ 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 towa
rd 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.
NARCOLEPSY
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 hav
ing 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.
Why We Sleep Page 27