Insomnia

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 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.