W HY W E S L E E P ー 2 9 human performance, many ofwhich have studied professional and elite athletes specifically. Obtain anything less than eight hours of sleep a night, and especially less than six hours a night, and the following hap- pens: time t0 physical exhaustion drops by 10 t0 30 percent, and aero- bic output is significantly reduced. Similar impairments are observed ⅲ limb extension force and vertical jump height, together with decreases in peak and sustained muscle strength. Add t0 this marked impairments in cardiovascular, metabolic, and respiratory capabilities that hamper an underslept body, including faster rates of lactic acid buildup, reductions in blOOd oxygen saturation, and converse increases in blOOd carbon diOX- ide, due ⅲ part tO a reduction in the amount Of air that the lungs can expire. Even the ability ofthe body to cool itself during physical exertion through sweating—a critical part ofpeak performance—is impaired by sleep loss. then there is inJury risk lt is the greatest fear of competi- tive athletes and their coaches. Concern 記 SO comes 仕 om the general managers 0f professional teams, wh0 consider their players as pnzed financial investments. ln the context Of injury, there is no better risk- mitigating insurance policy for these investments than sleep. Described in a research study Of competitive young athletes in 2014 , * you can see that a chronic lack Of sleep across the season predicted a massively higher risk ofinjury (figure 10 ). Figure 10 : Sleep し 055 and SPO 引可 u コ 0 80 70 60 50 40 30 20 10 0 6h 「 8h 「 7h 「 Average Sleep 9h 「 *M. D. Milewski et 記 . , "Chronic lack of sleep is associated with increased sports injuries in adolescent athletes : ル肝〃記可 2 市砒 c 0 なん 0 カ ae cs 34 , no. 2 ( 2014 ) : 129 ー 33.

W HY W E S L E E P 8 7 however, is a much more tumultuous power struggle between NREM and REM sleep. Although the amount of total sle ep gradually declines 仕 om birth onwards, the while becoming more stable and consoli- dated, the ratio 0f time spent in NREM sleep and REM sleep does not decline ⅲ 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, ⅶⅡ have a 70 / 30 split between NREM and REM sleep across the eleven hours oftotal daily slumber. ln 0ther words, the proportion 0f REM sleep decreasesin early childhood while the proportion 0f NREM sleep actually increases, even though t0tal sleep time decreases. The downgrading ofthe REM-sleep portion, and the upswmg ⅲ 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 through- out early and midadulthood. SLEEP AND ADOLESCENCE Why do we spend so much time in REM sleep in the womb and early ⅲ life, yet switch to a heavier dominance ofdeep NREM sleep in late child- hood 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 0f life, yet an exponential rise in deep NREM sleep intensity ⅲ mid- and late childhood, hitting a peak just before puberty, and then damping back down.What's so special about this り甲 e of deep sleep at this transitional time oflife? Prior to birth, and soon after, the challenge for development was t0 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 t0 populate brain neighborhoods with neural connectivity, and then activate those path- ways with a healthy dose ofinformational bandwidth. But since this first round ofbrain mring is purposefully overzealous, a second round ofremodeling must take place. lt does so during late child- hood and adolescence. Here, the architectural go is not to scale up, but

ー 4 8 MATHEW WALKER but now explore how the sleep-deprived brain responds t0 increasingly positive and rewarding experiences, such as exciting images ofextreme sports, or the chance ofwinmng increasing amounts ofmoney in fulfill- ing tasks. Ⅵ厄 discovered that different deep emotional centers ⅲ the brain just above and behind the amygdala, called the striatum—associated with impulsivity and reward, and bathed by the chemical dopamine— had become hyperactive in sleep-deprived individuals in response t0 the rewarding, pleasurable experiences. As with the amygdala, the heightened sensitivity 0f these hedonic reglons was linked t0 a loss 0f the rational control 仕 om the prefrontal cortex. lnsufficient sleep does not, therefore, push the brain into a negative mood state and h01d it there. Rather, the under-slept brain swings exces- sively tO bOth extremes ofemotional valence, positive and negative. You may think that the former counter-balances the latter, thereby neutralizing the problem. Sadly, emotions, and their guiding ofoptimal decision and actions, dO not work this way. Extremity is Often danger- OIIS. Depression and extreme negative I れ 00d can, for example, infuse an individual with a sense Of worthlessness, together with ideas Of questioning life's value. There iS now clearer evidence Of thiS concern. Studies of adolescents have identified a link between sleep disruption and suicidal thoughts, suicide attempts, and, traglcally, suicide com- pletion in the days after. One more reason for society and parents tO value plentiful sleep in teens rather than chastise it, especially consid- ering that suicide is the second-leading cause 0f death in young adults in developed nations after car accidents. lnsufficient sleep has also been linked to aggression, bullying, and behavioral problems in children across a range 0f ages. A similar rela- tionship between a lack 0f sleep and violence has been observed in adult prison populations; places that, I should add, are woefully poor at enabling good sleep that could reduce aggression, violence, psychiat- ric disturbance, and suicide, which, beyond the humanitarian concern, increases costs tO the taxpayer. Equally problematic issues arise from extreme swings in positive mood, though the consequences are different. Hypersensitivity tO pleasurable experiences can lead tO sensation-seeking, risk-taking,

ー N D EX 3 5 3 mammals, 56 ー 57 early developmental life ⅲ , 80 ー 81 narcolepsy ⅲ , 247 NREM sleep in, 61 , 63 , 65 REM sleep ⅲ , 60 ー 62 , 63 , 74 , 75 , 80 sleep amount needed by, 58 sleep cycles ⅲ , temperature range needed by, 258 Mansbach, Adam, 85 ー 86 McCartney, Paul, 221 melatonin, 22 ー 24 artificial light blocking, 267 , 268 autistic children's profile for, 81 blue LED light blocking, 269 ー 70 , 326 , 327 concentrations in over-the-counter brands, 23 daylight's impact on release 0f, 23 ー 24 , 100 , 267 , 275 , 277 generation 0f sleep and, 23 jet lag and, 26 ー 27 older adults' use of, 1 開 regulated environmental light for, 328 as sleeping aid, 23 timing Of sleep onset and, 22 ー 23 work schedules and release 矼 304 memones REM sleep and replaying of, 41 sleep cycles and updating 0 44 ー 46 sleep deprivation's blocking 0f, 154 ー 55 sleep for selective remembering and forgetting 矼 120 ー 23 memory alcohol-infused sleep affecting, 273 ー 74 amyloid plaques and decline of, 159 brain storage shifts and, 109 ー 11 , 114 ー 15 creativity and, 132 motor skill learning and, 123 ー 31 NREM sleep and, 113 ー 14 , 115 , 116 ー 17 , 118 , 119 ー 20 , 122 older adults' sleep disturbances and loss of, 102 sleep benefits for, 108 ー 9 , 115 ー 16 sleep consolidation Of, 112 ー 14 , 115 , 156 ー 57 sleeping pills and, 284 ー 85 targeted reactivation Of, 116 , 119 ー 20 time-of-night effect with, 127 ー 28 memory association network, 225 ー 26 Mendeleev, Dmitri, 220 ー 21 , 226 , 230 mental disorders, and sleep disruption, 149 ー 50 microsleep, 134 , 135 ー 36 , 140 ー 41 , 144 , 169 , 319 midlife, sleep ⅲ , 95 ー 104 migration 0f birds, and sleep deprivation ⅲ , 67 ー 68 monkeys, sleep ⅲ , 72 monophasic sleep pattern children's transition to, 86 health impact 0f changing to, 71 in modern adults, 68 timing of, with light availability, 68 ー 69 ⅲ winter months, 68 morning types ("morning larks"), 20 ー 22 circadian rhythm variations and, 20 ー 21 genetics and, 21 , 22 work schedules and, 21 ー 22 , 304 , 334 motor disorders, recovery 仕 om , 123 ー 24 motor skill memory, 123 ー 31 athletes andperformance and, 128 ー 31 motor skill memory and, 128 ー 31 practice and sleep and, 124 ー 28 stroke recovery and relearning 0 125 , 131 time-of-night effect with, 127 ー 28 muscle activity, ⅲ REM sleep, 53 ー 54 nap pods, 304 naps biphasic sleep pattern 0f continuous night sleep with, 69 ー 71 creativity in dreaming during, 232 drowsiness after sleep deprivation and, 142 ー 43 hunter-gatherer sleep patterns and, 68 memory consolidation during, 115 memory removal during, 123 motor skill improvement using 128 older adults' sleep problems related to, 99

9 8 MATTHEW WALKER sleep is chronically disrupted. The problem in agmg is that family mem- bers observe these daytime features in older relatives and jump to a diagnosis 0f dementia, overlooking the possibility that bad sleep is an equally likely cause. N0t 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 offrag- mented 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 cogni- tive haze the fact that it is dark. Furthermore, having been recumbent in bed means that when you stand and start moving, blood can race 仕 om your head, encouraged by gravity, down toward your legs. You feel light-headed and unsteady on your feet as a consequence. The lat- ter is especially true in Older adults whose control Of blOOd pressure is itself often impaired. All Of these issues mean that an older indi- vidual is at a far higher risk of stumbling, falling, and breaking bones during nighttime visits t0 the bathroom. Falls and fractures markedly increase morbidity and significantly hasten the end of life 0f an older adult. ln the footnotes, I offer a list of tips for safer nighttime sleep in the elderly. * The third sleep change with advanced age is that of c か ca 市 4 〃 〃襯 / 〃 g. ln sharp contrast tO adolescents, seniors C01 1 only experience a regression ⅲ sleep timing, leading tO earlier and earlier bedtimes. The cause iS an earlier evening release and peak 0f 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 *Tips for safe sleep ⅲ the elderly: ( 1 ) have a side lamp within reach that you can switch on easily, ( 2 ) use dim or motion-activated night-lights in the bathrooms and hallways to illuminate your path, ( 3 ) remove obstacles or rugs en route tO the bathroom to prevent stumbles or trips, and ( 4 ) keep a telephone by your bed with emergency phone numbers programmed on speed dial.

CHAPTER 14 Hurting and Helping Your Sleep 乃広既励 erap. ⅲ the past month, almost 10 million people in America ⅶⅡ have swal- lowed some kind ofa sleeping aid. Most relevant, and a key focus ofthis ch 叩 ter, is the (ab)use 0f prescription sleeping pills. Sleeping pills d0 not provide natural sleep, can damage health, and increase the risk 0f life-threatening diseases. Ⅵ厄 will explore the alternatives that exist for improving sleep and combating insipid insomnia. SHOULD YOIJ TAKE ′ 0 OFTHESE BEFORE BED? NO past or current sleeping medications on the legal ()r illegal) market induce natural sleep. Don't get me wrong—no one would claim that you are awake after taking prescription sleeping pills. But t0 suggest that you are experiencing natural sleep would be an equally false assertion. The older sleep medications—termed "sedative hypnotics," such as diazepam—were blunt instruments. They sedated you rather than assisting you int0 sleep. Understandably, many people mistake the former for the latter. Most 0f the newer sleeping pills on the market present a similar situation, though they are slightly less heavy in their sedating effects. Sleeping pills, 01d and new, target the same system in the brain that alC0h01 does—the receptors that stop your brain cells 仕 om firing—and are thus part 0f the same general class 0f drugs: sed- atives. Sleeping pills effectively knock out the higher regions 0f your brains cortex. lfyou compare natural, deep-sleep brainwave activity t0 that induced by modern-day sleeping pills, such as zolpidem (brand name Ambien)

WHY WE SLEEP acquiring new skills. M0tor learning and general physicality remain part of our lives, from the banal (learning t0 type on a slightly new laptop or text on a different-size smartphone) tO the essential, such as experienced surgeons learning a endoscopic procedure or pilots learning t0 fly different or new aircraft. And so, therefore, we continue t0 need and rely upon our NREM sleep for refining and maintaining those motor movements. Of interest tO parents, the most dramatic time Of skilled motor learning in any human's life occurs in the first years after birth, as we start tO stand and walk. lt is 0f little surprise that we see a spike ⅲ stage 2 NREM sleep, includ- ing sleep spindles, right around the infant's time 0f transition from crawling to walking. Returning んⅡ circle to that which I had learned years ago at the Queen's Medical Center regarding brain damage, we have now dis- covered that the slow, day-by-day return 0f motor function in stroke patients is due, ⅲ part, t0 the hard night-by-night work 0f sleep. FO ト lowing a stroke, the brain begins tO reconfigure those neural connec- tions that remain, and sprout new connections around the damaged zone. ThiS plastic reorganization and the genesis Of new connections underlie the return Of some degree Of motor function. We now have preliminary evidence that sleep is one critical ingredient assisting in this neural recovery effort. Ongoing sleep quality predicts the grad- ual return Of motor function, and further determines the relearning of numerous movement skills. * Should more such findings emerge, then a more concerted effort tO prioritize sleep as a therapeutic aid in patients whO have suffered brain damage may be warranted, or even the implementation Of sleep-stimulation methods like those described earlier. There is much that sleep can d0 that we in medi- cine currently cannot. SO long as the scientific evidence justifies it, we should make use of the powerful health tool that sleep represents in making our patients well. 物に Herron, D. Dijk, J. EIlis, J. Sanders, and A. M. Sterr,"Sleep correlates 0f motor recovery ⅲ chronic stroke: a pilot study using sleep diaries and actigr 叩 hfJournal ツ & e Research 17 ( 2 開 8 ) : 103 ; and C. Siengsukon and L. A. Boyd,"SIeep enhances off-line spatial and temporal motor learning after stroke," Ⅳ ro 尾んわ〃 0 〃 & ル″ ra / 召印 r4 , no. 23 ( 2009 ) : 327 ー 35.

WHY WE SLEEP ー 7 9 at the University 0f Chicago. Sample the hormone levels circulating in the blood ofthese tired participants and you will find a marked drop in testosterone relative tO their own baseline levels Of testosterone when fully rested. The size of the hormonal blunting effect is so large that it effectively "ages a man by ten tO fifteen years ⅲ terms Of testosterone virility. The experimental results support the finding that men suffering 仕 om sleep disorders, especially sleep apnea associated with snoring, have significantly lower levels Of testosterone than those Of similar age and backgrounds but wh0 d0 not suffer 仕 om a sleep condition. Uttering the results of such studies ⅶⅡ often quell any vocal (alpha) males that I occasionally come across when giung public lectures. As you may imagine, their ardent, antisleep stance becomes a little wobbly upon receivmg such information.With a genume lack 0f malice, I pro- ceed t0 inform them that men wh0 report sleeping t00 liffle—or having poor-quality sleep—have a 29 percent lower sperm count than those obtaining a Ⅱ and restful night 0f sleep, and the sperm themselves have more deformities. I usually conclude my response with a paren- theticallow blow, noting that these under-slept men 引 so have signifi- cantly smaller testicle s than well-rested counterparts. Rare podium fracases aside, IOW testosterone iS a clinically con- cerning and life-impacting matter. Males with IOW testosterone Often feel tired and fatigued throughout the day. They find it difficult t0 con- centrate on work tasks, as testosterone has a sharpening effect on the brain's ability to focus. And 0f course, they have a dulled libido, making an active, fulfilling, and healthy sex life more challenging. lndeed, the self-reported mood and vigor ofthe young men described in the above study progressively decreased ⅲ lockstep with their increasing state Of sleep deprivation and their declining levels 0f testosterone. Add t0 this the fact that testosterone maintains bone density, and plays a causal role ⅲ building muscle mass and therefore strength, and you can begin t0 get a sense 0f why a んⅡ night 0f sleep—and the natural hormonal replacement therapy it provides—is SO essential t0 this aspect ofhealth and an active life for men 0f all ages. Men are not the only ones whO become reproductively compromised by a lack 0f sleep. Routinely sleeping less than six hours a night re sults in a 20 percent drop ⅲ follicular-releasing hormone ⅲ women—a criti-

ー 0 8 MATTHEW WALKER lic health message. We ⅷⅡ come to learn that sleep is the universal health care provider: whatever the physical or mental ailment, sleep has a prescription it can dispense. Upon completion Of these chapters, I hope even the most ardent 0f short-sleepers will be swayed, having a reformed deference. Earlier, I described the component stages of sleep. Here, I reveal the attendant virtues Of each. lronically, most all Of the "new," twenty-first- century discoveries regarding sleep were delightfully summarized in 1611 in Macbeth, act vo , scene れ vo , where Shakespeare prophetically states that sleep is "the chief nourisher in life's feast."* Perhaps, with less highfalutin language, your mother offered similar advice, extolling the benefits of sleep in healing emotional wounds, helping you learn and remember, gifting you with solutions to challenging problems, and preventing sickness and infection. Science, it seems, has simply been evidential, providing pro of of everything your mother, and 叩 p arently Shakespeare, knew about the wonders ofsleep. SLEEP FOR THE BRAIN Sleep is not the absence Of wakefulness. lt is far more than that. Described earlier, our nighttime sleep is an exquisitely complex, met- abolically active, and deliberately ordered series ofunique stages. Numerous functions 0f the brain are restored by, and depend upon, sleep. No one type of sleep accomplishes all. Each stage of sleep—light NREM sleep, deep NREM sleep, and REM sleep—offer different brain benefits at different times of night. Thus, no one 与甲 e of sleep is more essential than another. LOSing out on any one ofthese types ofsleep will cause brain impalrment. Of the many advantages conferred by sleep on the brain, that of memory is especially impressive, and particularly well understood. Sleep has proven itself time and again as a memory aid: both before *"Sleep that knits up the ravelld sleeve ofcare, The death ofeach day's life, sore labour's bath, Balm of hurt minds, great nature's second course, Chief nourisher ⅲ life's feast,— William Shakespeare, Macbeth, Folger Shakespeare Library (NewYork: Simon & Schuster; first edition, 2 開 3 ).

ー 6 2 MATTHEW WALKER fering 伝 om sleep disorders such as insomnia and sleep apnea. * Par- enthetically, and unscientifically, I have always found it curious that Margaret Thatcher and Ronald Reagan—two heads 0f state that were very vocal, ifnot proud, about sleeping only four to five hours a night— both went on t0 develop the ruthless disease. The current US president, Donald Trump—also a vociferous proclaimer 0f sleeping just a few hours each night—may want tO take note. A more radical and converse predlction that emerges 仕 om these findings is that, by improvmg someone's sleep, we should be able t0 reduce their risk 0f developing Alzheimer's disease—or at least delay its onset. Tentative support has emerged 仕 om clinical studies in which middle- and older-age adults have had their sleep disorders successfully treated. As a consequence, their rate ofcognitive decline slowed signifi- cantly, and further delayed the onset 0f Alzheimer's disease by five t0 ten years. My own research group is now trying to develop a number ofviable methods for artificially increasing deep NREM sleep that could restore some degree Of the memory consolidation function that is absent in older individuals with high amounts of amyloid in the brain. lfwe can find a method that is cost effective and can be scaled up t0 the popu- lation level for repeat use, my go 記 is prevention. Can we begin sup- plementing the declining deep sleep 0f vulnerable members 0f society during midlife, many decades before the tipping point 0f Alzheimer s disease is reached, aiming tO avert dementia risk later ⅲ life? lt is an admittedly lOfty ambition, and some would argue a moon shOt research go 矼 But it is worth recalling that we already use this conceptual *A. S. Lim et , "SIeep Fragmentation and the Risk Of lncident Alzheimer's Disease and Cognitive Decline in Older persons," Sleep 36 ( 2013 ) : 1027 ー 32 ; A. S. Lim et al„"M0difica- tion of the relationship of the apolipoprotein E epsilon4 allele t0 the risk Of Alzheimer s disease and neurofibrillary tangle density by sleep,"JAMA Ⅳ ro あ 70 ( 2013 ) : 1544 ー 51 ; R. S. O SO ⅱ 0 et al.,"Greater risk Of Alzheimer's disease ⅲ older adults with insomnia," / 0 ″記 e 月襯 e ca 〃 Geriatric Society 59 ( 2011 ) : 559 ー 62 ; and K. Yaffe et 矼 , "Sleep-disordered breathing, hypoxia, and risk 0f mild cognitive impairment and dementia ⅲ 01der women, / スれの 4 3 % ( 2011 ) : 613 ー 19. S. Anc01i-IsraeI et . ,"Cognitive effects of treating obstructive sleep apnea in Alzheimer s disease: a randomized controlled studfJournal e ス襯 e 厖 ca 〃 Geriatric SOC 56 ( 288 ) : 2076 ー 81 ; and W.d. S. Moraes et , "The effect of donepezil on sleep and REM sleep EEG in patients with Alzheimer's disease: a double-blind placebo-controlled study," Sleep 29 ( 2 開 6 ) : 199 ー 205.