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January 15 - February 23, 2025
Some may consider this informational daisy-chaining to be trivial, but it is one of the key operations differentiating your brain from your computer. Computers can store thousands of individual files with precision. But standard computers do not intelligently interlink those files in numerous and creative combinations. Instead, computer files sit like isolated islands. Our human memories are, on the other hand, richly interconnected in webs of associations that lead to flexible, predictive powers.
Like an insightful interviewer, dreaming takes the approach of interrogating our recent autobiographical experience and skillfully positioning it within the context of past experiences and accomplishments, building a rich tapestry of meaning.
The same regions of the brain that were active during physical right and left voluntary hand movements observed while the individuals were awake similarly lit up in corresponding ways during times when the lucid participants signaled that they were clenching their hands while dreaming!
Other studies using similar eye movement communication designs have further shown that individuals can deliberately bring themselves to timed orgasm during lucid dreaming, an outcome that, especially in males, can be objectively verified using physiological measures by (brave) scientists.
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.
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.
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 good sleep quality or quantity, 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
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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.
The two most common triggers of chronic insomnia are psychological: (1) emotional concerns, or worry, and (2) emotional distress, or anxiety.
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.
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.
Second are higher levels of the alertness-promoting hormone cortisol, and sister neurochemicals adrenaline and noradrenaline. All three of these chemicals raise heart rate.
Third, and related to these chemicals, are altered patterns of brain activity linked with the body’s sympathetic nervous system.
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
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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.
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.
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.
There are at least three core symptoms that make up the disorder: (1) excessive daytime sleepiness, (2) sleep paralysis, and (3) cataplexy.
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.
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.
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.
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.
Two additional results quickly followed. First, death ensued as quickly from total sleep deprivation as it did from total food deprivation. Second, rats selectively deprived of REM-sleep died within 27-54 days. A total absence of NREM sleep still proved fatal, it just took longer to inflict the same mortal consequence—within 28-66 days.
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.
The third, and perhaps most telling, consequence of sleep loss was skin deep. The privation of sleep had left these rats literally threadbare.
top-and-tail snipping of our sleep time and that of our children—five key factors have changed how much and how well we sleep: (1) constant electric light as well as LED light, (2) regularized temperature, (3) caffeine (discussed in chapter 2), (4) alcohol, and (5) a legacy of punching time cards.
More than a third of our brain is devoted to processing visual information, far exceeding that given over to sounds or smells, or those supporting language and movement.
The visible light spectrum—that which our eyes can see—runs the gamut from shorter wavelengths (approximately 380 nanometers) that we perceive as cooler violets and blues, to the longer wavelengths (around 700 nanometers) that we sense as warmer yellows and reds.
The loss of daylight informs our suprachiasmatic nucleus that nighttime is now in session; time to release the brake pedal on our pineal gland, allowing it to unleash vast quantities of melatonin that signal to our brains and bodies that darkness has arrived and it is time for bed.
Perhaps more than the blue light itself, research from Flinders University suggests that the harmful impact of evening smartphone and laptop use on sleep is due to a significant alerting effect. By artificially forcing us awake, thereby masking our natural tiredness at night, prebed technology keeps people awake for longer, and makes falling asleep more difficult.
Give alcohol a little more time, and it begins to sedate other parts of the brain, dragging them down into a stupefied state, just like the prefrontal cortex. You begin to feel sluggish as the inebriated torpor sets in. This is your brain slipping into sedation. Your desire and ability to remain conscious are decreasing, and you can let go of consciousness more easily. I am very deliberately avoiding the term “sleep,” however, because sedation is not sleep. Alcohol sedates you out of wakefulness, but it does not induce natural sleep. The electrical brainwave state you enter via alcohol is not
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First, alcohol fragments sleep, littering the night with brief awakenings. Alcohol-infused sleep is therefore not continuous and, as a result, not restorative.
Second, alcohol will often suppress REM sleep, especially during the first half or two-thirds of the night.
a tremendous buildup in, and backlog of, pressure to obtain REM sleep. So great, in fact, that it inflicts a frightening consequence upon these individuals: aggressive intrusions of dreaming while they are wide awake. The pent-up REM-sleep pressure erupts forcefully into waking consciousness, causing hallucinations, delusions, and gross disorientation. This process contributes to the psychotic state in alcoholics called, “delirium tremens.”
Nightly alcohol will likely disrupt your sleep, and the annoying advice of abstinence is the best, and most honest, I can offer.
You may think the feeling of being facially clean helps you sleep better, but facial cleanliness makes no difference to your slumber. The act itself does have sleep-inviting powers, however, as that water, warm or cold, helps dissipate heat from the surface of the skin as it evaporates, thereby cooling the inner body core.
Through climate-controlled homes with central heat and air-conditioning, and the use of bedcovers and pajamas, we have architected a minimally varying or even constant thermal tenor in our bedrooms. Bereft of the natural drop in evening temperature, our brains do not receive the cooling instruction within the hypothalamus that facilitates a naturally timed release of melatonin.
A bedroom temperature of around 65 degrees Fahrenheit (18.3°C) is a reasonable goal for the sleep of most people, assuming standard bedding and clothing.
Hot baths prior to bed can also induce 10 to 15 percent more deep NREM sleep in healthy adults.fn4
Waking up at the same time of day, every day, no matter if it is the week or weekend is a good recommendation for maintaining a stable sleep schedule if you are having difficulty with sleep.
Squeezed by the vise grips of an electrified night and early-morning start times, bereft of twenty-four-hour thermal cycles, and with caffeine and alcohol that some individuals may use in various quantities, many of us can feel understandably exhausted and crave that which seems always elusive: a full, restful night of natural deep sleep.
Sleeping pills, old and new, target the same system in the brain that alcohol does—the receptors that stop your brain cells from firing—and are thus part of the same general class of drugs: sedatives. Sleeping pills effectively knock out the higher regions of your brain’s cortex.
If you compare natural, deep-sleep brainwave activity to that induced by modern-day sleeping pills, such as zolpidem (brand name Ambien) or eszopiclone (brand name Lunesta), the electrical signature, or quality, is deficient. The electrical type of “sleep” these drugs produce is lacking in the largest, deepest brainwaves.fn1
The majority of prescription sleeping pills are, after all, in a class of physically addictive drugs. Dependency scales with continued use, and withdrawal ensues in abstinence.
Summarizing the findings, the committee stated that sleeping pills only produced “slight improvements in subjective and polysomnographic sleep latency”—that is, the time it takes to fall asleep. The committee concluded the report by stating that the effect of current sleeping medications was “rather small and of questionable clinical importance.”
As expected, natural sleep solidified memory connections within the brain in the placebo condition that had been formed during the initial learning phase. Ambien-induced sleep, however, not only failed to match these benefits (despite the animals sleeping just as long), but caused a 50 percent weakening (unwiring) of the brain-cell connections originally formed during learning. In doing so, Ambien-laced sleep became a memory eraser, rather than engraver.
Those taking sleeping pills were 4.6 times more likely to die over this short two-and-a-half-year period than those who were not using sleeping pills. Kripke further discovered that the risk of death scaled with the frequency of use. Those individuals classified as heavy users, defined as taking more than 132 pills per year, were 5.3 times more likely to die over the study period than matched control participants who were not using sleeping pills.
Even very occasional users—those defined as taking just eighteen pills per year—were still 3.6 times more likely to die at some point across the assessment window than non-users.
One frequent link with mortality appears to be higher-than-normal rates of infection.
Another possible concern of death linked to sleeping pill use is an increased risk for fatal car accidents.
