فصل 5فصل: چرا میخوابیم / فصل 5
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Changes in Sleep Across the Life Span
SLEEP BEFORE BIRTH
Through speech or song, expecting parents will often thrill at their ability to elicit small kicks and movements from their in utero child. Though you should never tell them this, the baby is most likely fast asleep. Prior to birth, a human infant will spend almost all of its time in a sleep-like state, much of which resembles the REM-sleep state. The sleeping fetus is therefore unaware of its parents’ performative machinations. Any co-occurring arm flicks and leg bops that the mother feels from her baby are most likely to be the consequence of random bursts of brain activity that typify REM sleep.
Adults do not—or at least should not—throw out similar nighttime kicks and movements, since they are held back by the body-paralyzing mechanism of REM sleep. But in utero, the immature fetus’s brain has yet to construct the REM-sleep muscle-inhibiting system adults have in place. Other deep centers of the fetus brain have, however, already been glued in place, including those that generate sleep. Indeed, by the end of the second trimester of development (approximately week 23 of pregnancy), the vast majority of the neural dials and switches required to produce NREM and REM sleep have been sculpted out and wired up. As a result of this mismatch, the fetus brain still generates formidable motor commands during REM sleep, except there is no paralysis to hold them back. Without restraint, those commands are freely translated into frenetic body movements, felt by the mother as acrobatic kicks and featherweight punches.
At this stage of in utero development, most of the time is spent in sleep. The twenty-four-hour period contains a mishmash of approximately six hours of NREM sleep, six hours of REM sleep, and twelve hours of an intermediary sleep state that we cannot confidently say is REM or NREM sleep, but certainly is not full wakefulness. It is only when the fetus enters the final trimester that the glimmers of real wakefulness emerge. Far less than you would probably imagine, though—just two to three hours of each day are spent awake in the womb.
Even though total sleep time decreases in the last trimester, a paradoxical and quite ballistic increase in REM-sleep time occurs. In the last two weeks of pregnancy, the fetus will ramp up its consumption of REM sleep to almost nine hours a day. In the last week before birth, REM-sleep amount hits a lifetime high of twelve hours a day. With near insatiable appetite, the human fetus therefore doubles its hunger for REM sleep just before entering the world. There will be no other moment during the life of that individual—pre-natal, early post-natal, adolescence, adulthood, or old age—when they will undergo such a dramatic change in REM-sleep need, or feast so richly on the stuff.
Is the fetus actually dreaming when in REM sleep? Probably not in the way most of us conceptualize dreams. But we do know that REM sleep is vital for promoting brain maturation. The construction of a human being in the womb occurs in distinct, interdependent stages, a little bit like building a house. You cannot crown a house with a roof before there are supporting wall frames to rest it on, and you cannot put up walls without a foundation to seat them in. The brain, like the roof of a house, is one of the last items to be constructed during development. And like a roof, there are sub-stages to that process—you need a roof frame before you can start adding roof tiles, for instance.
Detailed creation of the brain and its component parts occurs at a rapid pace during the second and third trimesters of human development—precisely the time window when REM-sleep amounts skyrocket. This is no coincidence. REM sleep acts as an electrical fertilizer during this critical phase of early life. Dazzling bursts of electrical activity during REM sleep stimulate the lush growth of neural pathways all over the developing brain, and then furnish each with a healthy bouquet of connecting ends, or synaptic terminals. Think of REM sleep like an Internet service provider that populates new neighborhoods of the brain with vast networks of fiber-optic cables. Using these inaugural bolts of electricity, REM sleep then activates their high-speed functioning.
This phase of development, which infuses the brain with masses of neural connections, is called synaptogenesis, as it involves the creation of millions of wiring links, or synapses, between neurons. By deliberate design, it is an overenthusiastic first pass at setting up the mainframe of a brain. There is a great deal of redundancy, offering many, many possible circuit configurations to emerge within the infant’s brain once born. From the perspective of the Internet service provider analogy, all homes, across all neighborhoods, throughout all territories of the brain have been gifted a high degree of connectivity and bandwidth in this first phase of life.
Charged with such a herculean task of neuro-architecture—establishing the neural highways and side streets that will engender thoughts, memories, feelings, decisions, and actions—it’s no wonder REM sleep must dominate most, if not all, of early developmental life. In fact, this is true for all other mammals:I the time of life when REM sleep is greatest is the same stage when the brain is undergoing the greatest construction.
Worryingly, if you disturb or impair the REM sleep of a developing infant brain, pre- or early post-term, and there are consequences. In the 1990s, researchers began studying newly born rat pups. Simply by blocking REM sleep, their gestational progress was retarded, despite chronological time marching on. The two should, of course, progress in unison. Depriving the infant rats of REM sleep stalled construction of their neural rooftop—the cerebral cortex of the brain. Without REM sleep, assembly work on the brain ground to a halt, frozen in time by the experimental wedge of a lack of REM sleep. Day after day, the half-finished roofline of the sleep-starved cerebral cortex shows no growth change.
The very same effect has now been demonstrated in numerous other mammalian species, suggesting that the effect is probably common across mammals. When the infant rat pups were finally allowed to get some REM sleep, assembly of the cerebral rooftop did restart, but it didn’t accelerate, nor did it ever fully get back on track. An infant brain without sleep will be a brain ever underconstructed.
A more recent link with deficient REM sleep concerns autism spectrum disorder (ASD) (not to be confused with attention deficit hyperactivity disorder [ADHD], which we will discuss later in the book). Autism, of which there are several forms, is a neurological condition that emerges early in development, usually around two or three years of age. The core symptom of autism is a lack of social interaction. Individuals with autism do not communicate or engage with other people easily, or typically.
Our current understanding of what causes autism is incomplete, but central to the condition appears to be an inappropriate wiring up of the brain during early developmental life, specifically in the formation and number of synapses—that is, abnormal synaptogenesis. Imbalances in synaptic connections are common in autistic individuals: excess amounts of connectivity in some parts of the brain, deficiencies in others.
Realizing this, scientists have begun to examine whether the sleep of individuals with autism is atypical. It is. Infants and young children who show signs of autism, or who are diagnosed with autism, do not have normal sleep patterns or amounts. The circadian rhythms of autistic children are also weaker than their non-autistic counterparts, showing a flatter profile of melatonin across the twenty-four-hour period rather than a powerful rise in concentration at night and rapid fall throughout the day.II Biologically, it is as if the day and night are far less light and dark, respectively, for autistic individuals. As a consequence, there is a weaker signal for when stable wake and solid sleep should take place. Additionally, and perhaps related, the total amount of sleep that autistic children can generate is less than that of non-autistic children.
Most notable, however, is the significant shortage of REM sleep. Autistic individuals show a 30 to 50 percent deficit in the amount of REM sleep they obtain, relative to children without autism.III Considering the role of REM sleep in establishing the balanced mass of synaptic connections within the developing brain, there is now keen interest in discovering whether or not REM-sleep deficiency is a contributing factor to autism.
Existing evidence in humans is simply correlational, however. Just because autism and REM-sleep abnormalities go hand in hand does not mean that one causes the other. Nor does this association tell you the direction of causality even if it does exist: Is deficient REM sleep causing autism, or is it the other way around? It is curious to note, however, that selectively depriving an infant rat of REM sleep leads to aberrant patterns of neural connectivity, or synaptogenesis, in the brain.IV Moreover, rats deprived of REM sleep during infancy go on to become socially withdrawn and isolated as adolescents and adults.V Irrespective of causality issues, tracking sleep abnormalities represents a new diagnostic hope for the early detection of autism.
Of course, no expecting mother has to worry about scientists disrupting the REM sleep of their developing fetus. But alcohol can inflict that same selective removal of REM sleep. Alcohol is one of the most powerful suppressors of REM sleep that we know of. We will discuss the reason that alcohol blocks REM-sleep generation, and the consequences of that sleep disruption in adults, in later chapters. For now, however, we’ll focus on the impact of alcohol on the sleep of a developing fetus and newborn.
Alcohol consumed by a mother readily crosses the placental barrier, and therefore readily infuses her developing fetus. Knowing this, scientists first examined the extreme scenario: mothers who were alcoholics or heavy drinkers during pregnancy. Soon after birth, the sleep of these neonates was assessed using electrodes gently placed on the head. The newborns of heavy-drinking mothers spent far less time in the active state of REM sleep compared with infants of similar age but who were born of mothers who did not drink during pregnancy.
The recording electrodes went on to point out an even more concerning physiological story. Newborns of heavy-drinking mothers did not have the same electrical quality of REM sleep. You will remember from chapter 3 that REM sleep is exemplified by delightfully chaotic—or desynchronized—brainwaves: a vivacious and healthy form of electrical activity. However, the infants of heavy-drinking mothers showed a 200 percent reduction in this measure of vibrant electrical activity relative to the infants born of non-alcohol-consuming mothers. Instead, the infants of heavy-drinking mothers emitted a brainwave pattern that was far more sedentary in this regard.VI If you are now wondering whether or not epidemiological studies have linked alcohol use during pregnancy and an increased likelihood of neuropsychiatric illness in the mother’s child, including autism, the answer is yes.VII
Fortunately, most mothers these days do not drink heavily during pregnancy. But what about the more common situation of an expectant mom having an occasional glass or two of wine during pregnancy? Using noninvasive tracking of heart rate, together with ultrasound measures of body, eye, and breathing movement, we are now able to determine the basic stages of NREM sleep and REM sleep of a fetus when it is in the womb. Equipped with these methods, a group of researchers studied the sleep of babies who were just weeks away from being born. Their mothers were assessed on two successive days. On one of those days, the mothers drank non-alcoholic fluids. On the other day, they drank approximately two glasses of wine (the absolute amount was controlled on the basis of their body weight). Alcohol significantly reduced the amount of time that the unborn babies spent in REM sleep, relative to the non-alcohol condition.
That alcohol also dampened the intensity of REM sleep experienced by the fetus, defined by the standard measure of how many darting rapid eye movements adorn the REM-sleep cycle. Furthermore, these unborn infants suffered a marked depression in breathing during REM sleep, with breath rates dropping from a normal rate of 381 per hour during natural sleep to just 4 per hour when the fetus was awash with alcohol.VIII
Beyond alcohol abstinence during pregnancy, the time window of nursing also warrants mention. Almost half of all lactating women in Western countries consume alcohol in the months during breastfeeding. Alcohol is readily absorbed in a mother’s milk. Concentrations of alcohol in breast milk closely resemble those in a mother’s bloodstream: a 0.08 blood alcohol level in a mother will result in approximately a 0.08 alcohol level in breast milk.IX Recently we have discovered what alcohol in breast milk does to the sleep of an infant.
Newborns will normally transition straight into REM sleep after a feeding. Many mothers already know this: almost as soon as suckling stops, and sometimes even before, the infant’s eyelids will close, and underneath, the eyes will begin darting left-right, indicating that their baby is now being nourished by REM sleep. A once-common myth was that babies sleep better if the mother has had an alcoholic drink before a feeding—beer was the suggested choice of beverage in this old tale. For those of you who are beer lovers, unfortunately, it is just that—a myth. Several studies have fed infants breast milk containing either a non-alcoholic flavor, such as vanilla, or a controlled amount of alcohol (the equivalent of a mother having a drink or two). When babies consume alcohol-laced milk, their sleep is more fragmented, they spend more time awake, and they suffer a 20 to 30 percent suppression of REM sleep soon after.X Often, the babies will even try to get back some of that missing REM sleep once they have cleared it from their bloodstream, though it is not easy for their fledgling systems to do so.
What emerges from all of these studies is that REM sleep is not optional during early human life, but obligatory. Every hour of REM sleep appears to count, as evidenced by the desperate attempt by a fetus or newborn to regain any REM sleep when it is lost.XI Sadly, we do not yet fully understand what the long-term effects are of fetal or neonate REM-sleep disruption, alcohol-triggered or otherwise. Only that blocking or reducing REM sleep in newborn animals hinders and distorts brain development, leading to an adult that is socially abnormal.
Perhaps the most obvious and tormenting (for new parents) difference between the sleep of infants and young children and that of adults is the number of slumber phases. In contrast to the single, monophasic sleep pattern observed in adults of industrialized nations, infants and young kids display polyphasic sleep: many short snippets of sleep through the day and night, punctuated by numerous awakenings, often vocal.
There is no better or more humorous affirmation of this fact than the short book of lullabies, written by Adam Mansbach, entitled Go the F**k to Sleep. Obviously, it’s an adult book. At the time of writing, Mansbach was a new father. And like many a new parent, he was run ragged by the constant awakenings of his child: the polyphasic profile of infant sleep. The incessant need to attend to his young daughter, helping her fall back to sleep time and time and time again, night after night after night, left him utterly exasperated. It got to the point where Mansbach just had to vent all the loving rage he had pent up. What came spilling out onto the page was a comedic splash of rhymes he would fictitiously read to his daughter, the themes of which will immediately resonate with many new parents. “I’ll read you one very last book if you swear,/You’ll go the fuck to sleep.” (I implore you to listen to the audiobook version of the work, narrated to perfection by the sensational actor Samuel L. Jackson.)
Fortunately, for all new parents (Mansbach included), the older a child gets, the fewer, longer, and more stable their sleep bouts become.XII Explaining this change is the circadian rhythm. While the brain areas that generate sleep are molded in place well before birth, the master twenty-four-hour clock that controls the circadian rhythm—the suprachiasmatic nucleus—takes considerable time to develop. Not until age three or four months will a newborn show modest signs of being governed by a daily rhythm. Slowly, the suprachiasmatic nucleus begins to latch on to repeating signals, such as daylight, temperature change, and feedings (so long as those feedings are highly structured), establishing a stronger twenty-four-hour rhythm.
By the one-year milestone of development, the suprachiasmatic nucleus clock of an infant has gripped the steering reins of the circadian rhythm. This means that the child now spends more of the day awake, interspersed with several naps and, mercifully, more of the night asleep. Mostly gone are the indiscriminate bouts of sleep and wake that once peppered the day and night. By four years of age, the circadian rhythm is in dominant command of a child’s sleep behavior, with a lengthy slab of nighttime sleep, usually supplemented by just a single daytime nap. At this stage, the child has transitioned from a polyphasic sleep pattern to a biphasic sleep pattern. Come late childhood, the modern, monophasic pattern of sleep is finally made real.
What this progressive establishment of stable rhythmicity hides, however, is a much more tumultuous power struggle between NREM and REM sleep. Although the amount of total sleep gradually declines from birth onwards, all the while becoming more stable and consolidated, the ratio of time spent in NREM sleep and REM sleep does not decline in a similarly stable manner.
During the fourteen hours of total shut-eye per day that a six-month-old infant obtains, there is a 50/50 timeshare between NREM and REM sleep. A five-year-old, however, will have a 70/30 split between NREM and REM sleep across the eleven hours of total daily slumber. In other words, the proportion of REM sleep decreases in early childhood while the proportion of NREM sleep actually increases, even though total sleep time decreases. The downgrading of the REM-sleep portion, and the upswing in NREM-sleep dominance, continues, throughout early and midchildhood. That balance will finally stabilize to an 80/20 NREM/REM sleep split by the late teen years, and remain so throughout early and midadulthood.
SLEEP AND ADOLESCENCE
Why do we spend so much time in REM sleep in the womb and early in life, yet switch to a heavier dominance of deep NREM sleep in late childhood and early adolescence? If we quantify the intensity of the deep-sleep brainwaves, we see the very same pattern: a decline in REM-sleep intensity in the first year of life, yet an exponential rise in deep NREM sleep intensity in mid- and late childhood, hitting a peak just before puberty, and then damping back down. What’s so special about this type of deep sleep at this transitional time of life?
Prior to birth, and soon after, the challenge for development was to build and add vast numbers of neural highways and interconnections that become a fledgling brain. As we have discussed, REM sleep plays an essential role in this proliferation process, helping to populate brain neighborhoods with neural connectivity, and then activate those pathways with a healthy dose of informational bandwidth.
But since this first round of brain wiring is purposefully overzealous, a second round of remodeling must take place. It does so during late childhood and adolescence. Here, the architectural goal is not to scale up, but to scale back for the goal of efficiency and effectiveness. The time of adding brain connections with the help of REM sleep is over. Instead, pruning of connections becomes the order of the day or, should I say, night. Enter the sculpting hand of deep NREM sleep.
Our analogy of the Internet service provider is a helpful one to return to. When first setting up the network, each home in the newly built neighborhood was given an equal amount of connectivity bandwidth and thus potential for use. However, that’s an inefficient solution for the long term, since some of these homes will become heavy bandwidth users over time, while other homes will consume very little. Some homes may even remain vacant and never use any bandwidth. To reliably estimate what pattern of demand exists, the Internet service provider needs time to gather usage statistics. Only after a period of experience can the provider make an informed decision on how to refine the original network structure it put in place, dialing back connectivity to low-use homes, while increasing connectivity to other homes with high bandwidth demand. It is not a complete redo of the network, and much of the original structure will remain in place. After all, the Internet service provider has done this many times before, and they have a reasonable estimate of how to build a first pass of the network. But a use-dependent reshaping and downsizing must still occur if maximum network efficiency is to be achieved.
The human brain undergoes a similar, use-determined transformation during late childhood and adolescence. Much of the original structure laid down early in life will persist, since Mother Nature has, by now, learned to create a quite accurate first-pass wiring of a brain after billions of attempts over many thousands of years of evolution. But she wisely leaves something on the table in her generic brain sculpture, that of individualized refinement. The unique experiences of a child during their formative years translate to a set of personal usage statistics. Those experiences, or those statistics, provide the bespoke blueprint for a last round of brain refinement,XIII capitalizing on the opportunity left open by nature. A (somewhat) generic brain becomes ever more individualized, based on the personalized use of the owner.
To help with the job of refinement and downscaling of connectivity, the brain employs the services of deep NREM sleep. Of the many functions carried out by deep NREM sleep—the full roster of which we will discuss in the next chapter—it is that of synaptic pruning that features prominently during adolescence. In a remarkable series of experiments, the pioneering sleep researcher Irwin Feinberg discovered something fascinating about how this operation of downscaling takes place within the adolescent brain. His findings help justify an opinion you may also hold: adolescents have a less rational version of an adult brain, one that takes more risks and has relatively poor decision-making skills.
Using electrodes placed all over the head—front and back, left side and right, Feinberg began recording the sleep of a large group of kids starting at age six to eight years old. Every six to twelve months, he would bring these individuals back to his laboratory and perform another sleep measurement. He didn’t stop for ten years. He amassed more than 3,500 all-night assessments: a scarcely believable 320,000 hours of sleep recordings! From these, Feinberg created a series of snapshots, depicting how deep-sleep intensity changed with the stages of brain development as the children made their often awkward transition through adolescence into adulthood. It was the neuroscience equivalent of time-lapse photography in nature: taking repeat pictures of a tree as it first comes into bud in the spring (babyhood), then bursts into leaf during the summer (late childhood), then matures in color come the fall (early adolescence), and finally sheds its leaves in the winter (late adolescence and early adulthood).
During mid- and late childhood, Feinberg observed moderate deep-sleep amounts as the last neural growth spurts inside the brain were being completed, analogous to late spring and early summer. Then Feinberg began seeing a sharp rise in deep-sleep intensity in his electrical recordings, right at the time when the developmental needs of brain connectivity switch from growing connections to shedding them; the tree’s equivalent of fall. Just as maturational fall was about to turn to winter, and the shedding was nearly complete, Feinberg’s recordings showed a clear ramping back down in deep NREM-sleep intensity to lower intensity once more. The life cycle of childhood was over, and as the last leaves dropped, the onward neural passage of these teenagers had been secured. Deep NREM sleep had aided their transition into early adulthood.
Feinberg proposed that the rise and fall of deep-sleep intensity were helping lead the maturational journey through the precarious heights of adolescence, followed by safe onward passage into adulthood. Recent findings have supported his theory. As deep NREM sleep performs its final overhaul and refinement of the brain during adolescence, cognitive skills, reasoning, and critical thinking start to improve, and do so in a proportional manner with that NREM sleep change. Taking a closer look at the timing of this relationship, you see something even more interesting. The changes in deep NREM sleep always precede the cognitive and developmental milestones within the brain by several weeks or months, implying a direction of influence: deep sleep may be a driving force of brain maturation, not the other way around.
Feinberg made a second seminal discovery. When he examined the timeline of changing deep-sleep intensity at each different electrode spot on the head, it was not the same. Instead, the rise-and-fall pattern of maturation always began at the back of the brain, which performs the functions of visual and spatial perception, and then progressed steadily forward as adolescence progressed. Most striking, the very last stop on the maturational journey was the tip of the frontal lobe, which enables rational thinking and critical decision-making. Therefore, the back of the brain of an adolescent was more adult-like, while the front of the brain remained more child-like at any one moment during this developmental window of time.XIV
His findings helped explain why rationality is one of the last things to flourish in teenagers, as it is the last brain territory to receive sleep’s maturational treatment. Certainly sleep is not the only factor in the ripening of the brain, but it appears to be a significant one that paves the way to mature thinking and reasoning ability. Feinberg’s study reminds me of a billboard advertisement I once saw from a large insurance firm, which read: “Why do most 16-year-olds drive like they’re missing part of their brain? Because they are.” It takes deep sleep, and developmental time, to accomplish the neural maturation that plugs this brain “gap” within the frontal lobe. When your children finally reach their mid-twenties and your car insurance premium drops, you can thank sleep for the savings.
The relationship between deep-sleep intensity and brain maturation that Feinberg described has now been observed in many different populations of children and adolescents around the world. But how can we be sure that deep sleep truly offers a neural pruning service necessary for brain maturation? Perhaps changes in sleep and brain maturation simply occur at roughly the same time but are independent of each other?
The answer is found in studies of juvenile rats and cats at the equivalent stage to human adolescence. Scientists deprived these animals of deep sleep. In doing so, they halted the maturational refinement of brain connectivity, demonstrating a causal role for deep NREM sleep in propelling the brain into healthy adulthood.XV Of concern is that administering caffeine to juvenile rats will also disrupt deep NREM sleep and, as a consequence, delay numerous measures of brain maturation and the development of social activity, independent grooming, and the exploration of the environment—measures of self-motivated learning.XVI
Recognizing the importance of deep NREM sleep in teenagers has been instrumental to our understanding of healthy development, but it has also offered clues as to what happens when things go wrong in the context of abnormal development. Many of the major psychiatric disorders, such as schizophrenia, bipolar disorder, major depression, and ADHD are now considered disorders of abnormal development, since they commonly emerge during childhood and adolescence.
We will return to the issue of sleep and psychiatric illness several times in the course of this book, but schizophrenia deserves special mention at this juncture. Several studies have tracked neural development using brain scans every couple of months in hundreds of young teenagers as they make their way through adolescence. A proportion of these individuals went on to develop schizophrenia in their late teenage years and early adulthood. Those individuals who developed schizophrenia had an abnormal pattern of brain maturation that was associated with synaptic pruning, especially in the frontal lobe regions where rational, logical thoughts are controlled—the inability to do so being a major symptom of schizophrenia. In a separate series of studies, we have also observed that in young individuals who are at high risk of developing schizophrenia, and in teenagers and young adults with schizophrenia, there is a two- to threefold reduction in deep NREM sleep.XVII Furthermore, the electrical brainwaves of NREM sleep are not normal in their shape or number in the affected individuals. Faulty pruning of brain connections in schizophrenia caused by sleep abnormalities is now one of the most active and exciting areas of investigation in psychiatric illness.XVIII
Adolescents face two other harmful challenges in their struggle to obtain sufficient sleep as their brains continue to develop. The first is a change in their circadian rhythm. The second is early school start times. I will address the harmful and life-threatening effects of the latter in a later chapter; however, the complications of early school start times are inextricably linked with the first issue—a shift in circadian rhythm. As young children, we often wished to stay up late so we could watch television, or engage with parents and older siblings in whatever it was that they were doing at night. But when given that chance, sleep would usually get the better of us, on the couch, in a chair, or sometimes flat out on the floor. We’d be carried to bed, slumbering and unaware, by those older siblings or parents who could stay awake. The reason is not simply that children need more sleep than their older siblings or parents, but also that the circadian rhythm of a young child runs on an earlier schedule. Children therefore become sleepy earlier and wake up earlier than their adult parents.
Adolescent teenagers, however, have a different circadian rhythm from their young siblings. During puberty, the timing of the suprachiasmatic nucleus is shifted progressively forward: a change that is common across all adolescents, irrespective of culture or geography. So far forward, in fact, it passes even the timing of their adult parents.
As a nine-year-old, the circadian rhythm would have the child asleep by around nine p.m., driven in part by the rising tide of melatonin at this time in children. By the time that same individual has reached sixteen years of age, their circadian rhythm has undergone a dramatic shift forward in its cycling phase. The rising tide of melatonin, and the instruction of darkness and sleep, is many hours away. As a consequence, the sixteen-year-old will usually have no interest in sleeping at nine p.m. Instead, peak wakefulness is usually still in play at that hour. By the time the parents are getting tired, as their circadian rhythms take a downturn and melatonin release instructs sleep—perhaps around ten or eleven p.m., their teenager can still be wide awake. A few more hours must pass before the circadian rhythm of a teenage brain begins to shut down alertness and allow for easy, sound sleep to begin.
This, of course, leads to much angst and frustration for all parties involved on the back end of sleep. Parents want their teenager to be awake at a “reasonable” hour of the morning. Teenagers, on the other hand, having only been capable of initiating sleep some hours after their parents, can still be in their trough of the circadian downswing. Like an animal prematurely wrenched out of hibernation too early, the adolescent brain still needs more sleep and more time to complete the circadian cycle before it can operate efficiently, without grogginess.
If this remains perplexing to parents, a different way to frame and perhaps appreciate the mismatch is this: asking your teenage son or daughter to go to bed and fall asleep at ten p.m. is the circadian equivalent of asking you, their parent, to go to sleep at seven or eight p.m. No matter how loud you enunciate the order, no matter how much that teenager truly wishes to obey your instruction, and no matter what amount of willed effort is applied by either of the two parties, the circadian rhythm of a teenager will not be miraculously coaxed into a change. Furthermore, asking that same teenager to wake up at seven the next morning and function with intellect, grace, and good mood is the equivalent of asking you, their parent, to do the same at four or five a.m.
Sadly, neither society nor our parental attitudes are well designed to appreciate or accept that teenagers need more sleep than adults, and that they are biologically wired to obtain that sleep at a different time from their parents. It’s very understandable for parents to feel frustrated in this way, since they believe that their teenager’s sleep patterns reflect a conscious choice and not a biological edict. But non-volitional, non-negotiable, and strongly biological they are. We parents would be wise to accept this fact, and to embrace it, encourage it, and praise it, lest we wish our own children to suffer developmental brain abnormalities or force a raised risk of mental illness upon them.
It will not always be this way for the teenager. As they age into young and middle adulthood, their circadian schedule will gradually slide back in time. Not all the way back to the timing present in childhood, but back to an earlier schedule: one that, ironically, will lead those same (now) adults to have the same frustrations and annoyances with their own sons or daughters. By that stage, those parents have forgotten (or have chosen to forget) that they, too, were once adolescents who desired a much later bedtime than their own parents.
You may wonder why the adolescent brain first overshoots in their advancing circadian rhythm, staying up late and not wanting to wake up until late, yet will ultimately return to an earlier timed rhythm of sleep and wake in later adulthood. Though we continue to examine this question, the explanation I propose is a socio-evolutionary one.
Central to the goal of adolescent development is the transition from parental dependence to independence, all the while learning to navigate the complexities of peer-group relationships and interactions. One way in which Mother Nature has perhaps helped adolescents unbuckle themselves from their parents is to march their circadian rhythms forward in time, past that of their adult mothers and fathers. This ingenious biological solution selectively shifts teenagers to a later phase when they can, for several hours, operate independently—and do so as a peer-group collective. It is not a permanent or full dislocation from parental care, but as safe an attempt at partially separating soon-to-be adults from the eyes of Mother and Father. There is risk, of course. But the transition must happen. And the time of day when those independent adolescent wings unfold, and the first solo flights from the parental nest occur, is not a time of day at all, but rather a time of night, thanks to a forward-shifted circadian rhythm.
We are still learning more about the role of sleep in development. However, a strong case can already be made for defending sleep time in our adolescent youth, rather than denigrating sleep as a sign of laziness. As parents, we are often too focused on what sleep is taking away from our teenagers, without stopping to think about what it may be adding. Caffeine also comes into question. There was once an education policy in the US known as “No child left behind.” Based on scientific evidence, a new policy has rightly been suggested by my colleague Dr. Mary Carskadon: “No child needs caffeine.”
SLEEP IN MIDLIFE AND OLD AGE
As you, the reader, may painfully know; sleep is more problematic and disordered in older adults. The effects of certain medications more commonly taken by older adults, together with coexisting medical conditions, result in older adults being less able, on average, to obtain as much sleep, or as restorative a sleep, as young adults.
That older adults simply need less sleep is a myth. Older adults appear to need just as much sleep as they do in midlife, but are simply less able to generate that (still necessary) sleep. Affirming this, large surveys demonstrate that despite getting less sleep, older adults reported needing, and indeed trying, to obtain just as much sleep as younger adults.
There are additional scientific findings supporting the fact that older adults still need a full night of sleep, just like young adults, and I will address those shortly. Before I do, let me first explain the core impairments of sleep that occur with aging, and why those findings help falsify the argument that older adults don’t need to sleep as much. These three key changes are: (1) reduced quantity/quality, (2) reduced sleep efficiency, and (3) disrupted timing of sleep.
The postadolescent stabilization of deep-NREM sleep in your early twenties does not remain very stable for very long. Soon—sooner than you may imagine or wish—comes a great sleep recession, with deep sleep being hit especially hard. In contrast to REM sleep, which remains largely stable in midlife, the decline of deep NREM sleep is already under way by your late twenties and early thirties.
As you enter your fourth decade of life, there is a palpable reduction in the electrical quantity and quality of that deep NREM sleep. You obtain fewer hours of deep sleep, and those deep NREM brainwaves become smaller, less powerful, and fewer in number. Passing into your mid- and late forties, age will have stripped you of 60 to 70 percent of the deep sleep you were enjoying as a young teenager. By the time you reach seventy years old, you will have lost 80 to 90 percent of your youthful deep sleep.
Certainly, when we sleep at night, and even when we wake in the morning, most of us do not have a good sense of our electrical sleep quality. Frequently this means that many seniors progress through their later years not fully realizing how degraded their deep-sleep quantity and quality have become. This is an important point: it means that elderly individuals fail to connect their deterioration in health with their deterioration in sleep, despite causal links between the two having been known to scientists for many decades. Seniors therefore complain about and seek treatment for their health issues when visiting their GP, but rarely ask for help with their equally problematic sleep issues. As a result, GPs are rarely motivated to address the problematic sleep in addition to the problematic health concerns of the older adult.
To be clear, not all medical problems of aging are attributable to poor sleep. But far more of our age-related physical and mental health ailments are related to sleep impairment than either we, or many doctors, truly realize or treat seriously. Once again, I urge an elderly individual who may be concerned about their sleep not to seek a sleeping pill prescription. Instead, I recommend you first explore the effective and scientifically proven non-pharmacological interventions that a doctor who is board certified in sleep medicine can provide.
The second hallmark of altered sleep as we age, and one that older adults are more conscious of, is fragmentation. The older we get, the more frequently we wake up throughout the night. There are many causes, including interacting medications and diseases, but chief among them is a weakened bladder. Older adults therefore visit the bathroom more frequently at night. Reducing fluid intake in the mid- and late evening can help, but it is not a cure-all.
Due to sleep fragmentation, older individuals will suffer a reduction in sleep efficiency, defined as the percent of time you were asleep while in bed. If you spent eight hours in bed, and slept for all eight of those hours, your sleep efficiency would be 100 percent. If you slept just four of those eight hours, your sleep efficiency would be 50 percent.
As healthy teenagers, we enjoyed a sleep efficiency of about 95 percent. As a reference anchor, most sleep doctors consider good-quality sleep to involve a sleep efficiency of 90 percent or above. By the time we reach our eighties, sleep efficiency has often dropped below 70 or 80 percent; 70 to 80 percent may sound reasonable until you realize that, within an eight-hour period in bed, it means you will spend as much as one to one and a half hours awake.
Inefficient sleep is no small thing, as studies assessing tens of thousands of older adults show. Even when controlling for factors such as body mass index, gender, race, history of smoking, frequency of exercise, and medications, the lower an older individual’s sleep efficiency score, the higher their mortality risk, the worse their physical health, the more likely they are to suffer from depression, the less energy they report, and the lower their cognitive function, typified by forgetfulness.XIX Any individual, no matter what age, will exhibit physical ailments, mental health instability, reduced alertness, and impaired memory if their sleep is chronically disrupted. The problem in aging is that family members observe these daytime features in older relatives and jump to a diagnosis of dementia, overlooking the possibility that bad sleep is an equally likely cause. Not all old adults with sleep issues have dementia. But I will describe evidence in chapter 7 that clearly shows how and why sleep disruption is a causal factor contributing to dementia in mid- and later life.
A more immediate, though equally dangerous, consequence of fragmented sleep in the elderly warrants brief discussion: the nighttime bathroom visits and associated risk of falls and thus fractures. We are often groggy when we wake up during the night. Add to this cognitive haze the fact that it is dark. Furthermore, having been recumbent in bed means that when you stand and start moving, blood can race from your head, encouraged by gravity, down toward your legs. You feel light-headed and unsteady on your feet as a consequence. The latter is especially true in older adults whose control of blood pressure is itself often impaired. All of these issues mean that an older individual is at a far higher risk of stumbling, falling, and breaking bones during nighttime visits to the bathroom. Falls and fractures markedly increase morbidity and significantly hasten the end of life of an older adult. In the footnotes, I offer a list of tips for safer nighttime sleep in the elderly.XX
The third sleep change with advanced age is that of circadian timing. In sharp contrast to adolescents, seniors commonly experience a regression in sleep timing, leading to earlier and earlier bedtimes. The cause is an earlier evening release and peak of melatonin as we get older, instructing an earlier start time for sleep. Restaurants in retirement communities have long known of this age-related shift in bedtime preference, epitomized (and accommodated) by the “early-bird special.”
Changes in circadian rhythms with advancing age may appear harmless, but they can be the cause of numerous sleep (and wake) problems in the elderly. Older adults often want to stay awake later into the evening so that they can go to theater or the movies, socialize, read, or watch television. But in doing so, they find themselves waking up on the couch, in a movie theater seat, or in a reclining chair, having inadvertently fallen asleep mid-evening. Their regressed circadian rhythm, instructed by an earlier release of melatonin, left them no choice.
But what seems like an innocent doze has a damaging consequence. The early-evening snooze will jettison precious sleep pressure, clearing away the sleepiness power of adenosine that had been steadily building throughout the day. Several hours later, when that older individual gets into bed and tries to fall asleep, they may not have enough sleep pressure to fall asleep quickly, or stay asleep as easily. An erroneous conclusion follows: “I have insomnia.” Instead, dozing off in the evening, which most older adults do not realize is classified as napping, can be the source of sleep difficulty, not true insomnia.
A compounding problem arrives in the morning. Despite having had trouble falling asleep that night and already running a sleep debt, the circadian rhythm—which, as you’ll remember from chapter 2, operates independently of the sleep-pressure system—will start to rise around four or five a.m. in many elderly individuals, enacting its classic earlier schedule in seniors. Older adults are therefore prone to wake up early in the morning as the alerting drumbeat of the circadian rhythm grows louder, and corresponding hopes of returning back to sleep diminish in tandem.
Making matters worse, the strengths of the circadian rhythm and amount of nighttime melatonin released also decrease the older we get. Add these things up, and a self-perpetuating cycle ensues wherein many seniors are battling a sleep debt, trying to stay awake later in the evening, inadvertently dozing off earlier, finding it hard to fall or stay asleep at night, only to be woken up earlier than they wish because of a regressed circadian rhythm.
There are methods that can help push the circadian rhythm in older adults somewhat later, and also strengthen the rhythm. Here again, they are not a complete or perfect solution, I’m sad to say. Later chapters will describe the damaging influence of artificial light on the circadian twenty-four-hour rhythm (bright light at night). Evening light suppresses the normal rise in melatonin, pushing an average adult’s sleep onset time into the early-morning hours, preventing sleep at a reasonable hour. However, this same sleep-delaying effect can be put to good use in older adults, if timed correctly. Having woken up early, many older adults are physically active during the morning hours, and therefore obtain much of their bright-light exposure in the first half of the day. This is not optimal, as it reinforces the early-to-rise, early-to-decline cycle of the twenty-four-hour internal clock. Instead, older adults who want to shift their bedtimes to a later hour should get bright-light exposure in the late-afternoon hours.
I am not, however, suggesting that older adults stop exercising in the morning. Exercise can help solidify good sleep, especially in the elderly. Instead, I advise two modifications for seniors. First, wear sunglasses during morning exercise outdoors. This will reduce the influence of morning light being sent to your suprachiasmatic clock that would otherwise keep you on an early-to-rise schedule. Second, go back outside in the late afternoon for sunlight exposure, but this time do not wear sunglasses. Make sure to wear sun protection of some sort, such as a hat, but leave the sunglasses at home. Plentiful later-afternoon daylight will help delay the evening release of melatonin, helping push the timing of sleep to a later hour.
Older adults may also wish to consult with their doctor about taking melatonin in the evening. Unlike young or middle-age adults, where melatonin has not proved efficacious for helping sleep beyond the circumstance of jet lag, prescription melatonin has been shown to help boost the otherwise blunted circadian and associated melatonin rhythm in the elderly, reducing the time taken to fall asleep and improving self-reported sleep quality and morning alertness.XXI
The change in circadian rhythm as we get older, together with more frequent trips to the bathroom, help to explain two of the three key nighttime issues in the elderly: early sleep onset/offset and sleep fragmentation. They do not, however, explain the first key change in sleep with advancing age: the loss of deep-sleep quantity and quality. Although scientists have known about the pernicious loss of deep sleep with advancing age for many decades, the cause has remained elusive: What is it about the aging process that so thoroughly robs the brain of this essential state of slumber? Beyond scientific curiosity, it is also a pressing clinical issue for the elderly, considering the importance of deep sleep for learning and memory, not to mention all branches of bodily health, from cardiovascular and respiratory, to metabolic, energy balance, and immune function.
Working with an incredibly gifted team of young researchers, I set out to try and answer this question several years ago. I wondered whether the cause of this sleep decline was to be found in the intricate pattern of structural brain deterioration that occurs as we age. You will recall from chapter 3 that the powerful brainwaves of deep NREM sleep are generated in the middle-frontal regions of the brain, several inches above the bridge of your nose. We already knew that as individuals get older, their brains do not deteriorate uniformly. Instead, some parts of the brain start losing neurons much earlier and far faster than other parts of the brain—a process called atrophy. After performing hundreds of brain scans, and amassing almost a thousand hours of overnight sleep recordings, we discovered a clear answer, unfolding in a three-part story.
First, the areas of the brain that suffer the most dramatic deterioration with aging are, unfortunately, the very same deep-sleep-generating regions—the middle-frontal regions seated above the bridge of the nose. When we overlaid the map of brain degeneration hot spots in the elderly on the brain map that highlighted the deep-sleep-generating regions in young adults, there was a near-perfect match. Second, and unsurprisingly, older adults suffered a 70 percent loss of deep sleep, compared with matched young individuals. Third, and most critical, we discovered that these changes were not independent, but instead significantly connected with one another: the more severe the deterioration that an older adult suffers within this specific mid-frontal region of their brain, the more dramatic their loss of deep NREM sleep. It was a saddening confirmation of my theory: the parts of our brain that ignite healthy deep sleep at night are the very same areas that degenerate, or atrophy, earliest and most severely as we age.
In the years leading up to these investigations, my research team and several others around the world had demonstrated how critical deep sleep was for cementing new memories and retaining new facts in young adults. Knowing this, we had included a twist to our experiment in older adults. Several hours before going to sleep, all of these seniors learned a list of new facts (word associations), quickly followed by an immediate memory test to see how much information they had retained. The next morning, following the night of sleep recording, we tested them a second time. We could therefore determine the amount of memory savings that had occurred for any one individual across the night of sleep.
The older adults forgot far more of the facts by the following morning than the young adults—a difference of almost 50 percent. Furthermore, those older adults with the greatest loss of deep sleep showed the most catastrophic overnight forgetting. Poor memory and poor sleep in old age are therefore not coincidental, but rather significantly interrelated. The findings helped us shed new light on the forgetfulness that is all too common in the elderly, such as difficulty remembering people’s names or memorizing upcoming hospital appointments.
It is important to note that the extent of brain deterioration in older adults explained 60 percent of their inability to generate deep sleep. This was a helpful finding. But the more important lesson to be gleaned from this discovery for me was that 40 percent of the explanation for the loss of deep sleep in the elderly remained unaccounted for by our discovery. We are now hard at work trying to discover what that is. Recently, we identified one factor—a sticky, toxic protein that builds up in the brain called beta-amyloid that is a key cause of Alzheimer’s disease: a discovery discussed in the next several chapters.
More generally, these and similar studies have confirmed that poor sleep is one of the most underappreciated factors contributing to cognitive and medical ill health in the elderly, including issues of diabetes, depression, chronic pain, stroke, cardiovascular disease, and Alzheimer’s disease.
An urgent need therefore exists for us to develop new methods that restore some quality of deep, stable sleep in the elderly. One promising example that we have been developing involves brain stimulation methods, including controlled electrical stimulation pulsed into the brain at night. Like a supporting choir to a flagging lead vocalist, our goal is to electrically sing (stimulate) in time with the ailing brainwaves of older adults, amplifying the quality of their deep brainwaves and salvaging the health- and memory-promoting benefits of sleep.
Our early results look cautiously promising, though much, much more work is required. With replication, our findings can further debunk the long-held belief that we touched on earlier: older adults need less sleep. This myth has stemmed from certain observations that, to some scientists, suggest that an eighty-year-old, say, simply needs less sleep than a fifty-year-old. Their arguments are as follows. First, if you deprive older adults of sleep, they do not show as dramatic an impairment in performance on a basic response-time task as a younger adult. Therefore, older adults must need sleep less than younger adults. Second, older adults generate less sleep than young adults, so by inference, older adults must simply need sleep less. Third, older adults do not show as strong a sleep rebound after a night of deprivation compared with young adults. The conclusion was that seniors therefore have less need for sleep if they have less of a recovery rebound.
There are, however, alternative explanations. Using performance as a measure of sleep need is perilous in older adults, since older adults are already impaired in their reaction times to begin with. Said unkindly, older adults don’t have much further to fall in terms of getting worse, sometimes called a “floor effect,” making it difficult to estimate the real performance impact of sleep deprivation.
Next, just because an older individual obtains less sleep, or does not obtain as much recovery sleep after sleep deprivation, does not necessarily mean that their need for sleep is less. It may just as easily indicate that they cannot physiologically generate the sleep they still nevertheless need. Take the alternative example of bone density, which is lower in older compared with younger adults. We do not assume that older individuals need weaker bones just because they have reduced bone density. Nor do we believe that older adults have bones that are weaker simply because they don’t recover bone density and heal as quickly as young adults after suffering a fracture or break. Instead, we realize that their bones, like the centers of the brain that produce sleep, deteriorate with age, and we accept this degeneration as the cause of numerous health issues. We consequently provide dietary supplements, physical therapy, and medications to try to offset bone deficiency. I believe we should recognize and treat sleep impairments in the elderly with a similar regard and compassion, recognizing that they do, in fact, need just as much sleep as other adults.
Finally, the preliminary results of our brain stimulation studies suggest that older adults, may, in fact, need more sleep than they themselves can naturally generate, since they benefit from an improvement in sleep quality, albeit through artificial means. If older individuals did not need more deep sleep, then they should already be satiated, and not benefit from receiving more (artificially, in this case). Yet they do benefit from having their sleep enhanced, or perhaps worded correctly, restored. That is, older adults, and especially those with different forms of dementia, appear to suffer an unmet sleep need, which demands new treatment options: a topic that we shall soon return to.
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