Matthew Walker Rejects Quick Sleep Fixes as Science Points to Habits

Matthew Walker否定睡眠速效方案：科学表明习惯才是关键 作息不规律比睡眠时间短带来更高的心血管及死亡风险，而标准镁等常见补充剂无法穿透血脑屏障。 Matthew Walker博士深入剖析了睡眠卫生的核心支柱，强调睡眠质量与规律性往往比单纯的睡眠时长更为关键。他破除了关于蓝光以及镁、褪黑素等非处方助眠品的常见迷思，同时重点介绍了围绕DORA类药物和“睡眠储备”（sleep banking）的最新临床研究。此外，讨论还深入探讨了REM睡眠在处理心理创伤和维护情绪健康方面的神经学重要性，最后以关于人际关系、冲突与感恩的个人感悟收尾。 睡眠对人体细胞基因表达与全身机能至关重要，但全球医学教育平均仅分配1.2小时讲授睡眠科学；研究表明能在6小时或更少睡眠下免受身心损害的人口比例四舍五入实际为零。 (4:48) 周末补觉虽可使心血管疾病风险降低20%，但无法修复免疫力、血糖与认知损伤；而在面临高压或睡眠剥夺前提前进行“睡眠储备”（Sleep Banking），能将后续认知损伤减轻约40%。 (10:45) 晚间使用电子设备的主要危害来自内容对大脑的强烈精神刺激，而非蓝光本身；外源性褪黑素仅能发出黑暗信号而非制造睡眠，临床有效剂量建议在0.1毫克至3毫克之间。 (21:48) 优质睡眠由数量、质量、规律性与时机（QQRT）构成，其中规律就寝与作息对寿命的预测力甚至超过睡眠时长，高规律作息可使心血管代谢疾病风险降低57%。 (42:35) 绝大多数市售镁补充剂无法穿透血脑屏障，对脑驱动的睡眠机制收效甚微；若卧床约20分钟仍无法入睡应离开卧室，避免大脑形成将床与焦虑清醒绑定的条件性觉醒。 (55:31)

Dr. Matthew Walker argues that sleep regularity, biological timing, and physiological regulation outweigh popular supplement trends and rigid duration targets in dictating long-term cardiometabolic health, cognitive performance, and emotional resilience. Schedule Regularity and Banking Over Sleep Debt (42:35) Walker emphasizes a major shift in sleep epidemiology: consistency in sleep timing predicts lifespan more accurately than sleep duration alone. In a UK Biobank study of 60,000 individuals, highly regular sleepers—those adhering to bed and wake windows within a 30-minute range—showed a 49% reduction in all-cause mortality, a 39% decrease in cancer mortality, and a 57% lower risk of cardiometabolic disease compared to irregular sleepers varying by 90 to 120 minutes. While 7 to 9 hours remains the baseline to survive and thrive, regularity outperformed duration when placed head-to-head in predictive models. Addressing sleep debt, Walker qualifies his previous stance that sleep cannot be recovered. Analysis of over 90,000 UK Biobank participants revealed that weekend catch-up sleep reduced cardiovascular disease risk by 20% for chronically underslept workers, though it failed to restore immune, metabolic, or cognitive impairments. For predictable sleep deprivation, Walker cites research on sleep banking: deliberately increasing sleep to 8.5 or 9 hours per night before an anticipated stress period builds a safety buffer, reducing subsequent cognitive impairment under sleep loss challenges by roughly 40%. The Limits of Magnesium, Melatonin, and Sedatives (65:57) Walker challenges the efficacy of common over-the-counter sleep supplements, noting that most retail forms of magnesium, such as magnesium citrate and magnesium oxide, fail to cross the blood-brain barrier. While magnesium L-threonate shows modest promise and peripheral magnesium can induce skeletal muscle relaxation via vagal nerve signaling, supplementing individuals with normative magnesium levels yields minimal neurological change and mostly produces expensive urine. Similarly, melatonin acts merely as a circadian timing signal rather than a sleep generator. Meta-analyses show exogenous melatonin speeds sleep onset by an average of only 3.4 minutes and improves sleep efficiency by 2.2%. Doses exceeding 0.1 to 3 mg create lingering morning darkness signals that cause grogginess, while pediatric accidental overdoses have risen 503% over a decade. In pharmacotherapy, Walker distinguishes traditional sedatives from next-generation dual orexin receptor antagonists (DORAs). Benzodiazepines and Z-drugs (such as Ambien) stimulate neuroinhibitory GABA receptors, creating general sedation that actually reduces restorative glymphatic brain clearance by 30% to 40%. In contrast, DORAs selectively mute the wake-promoting neurotransmitter orexin. Clinical trials in adults aged 50 and older demonstrated that DORA-induced sleep actively facilitated glymphatic clearance of Alzheimer's-associated beta-amyloid and tau proteins in cerebrospinal fluid, though monthly costs near $400 and insurance hurdles limit widespread access. Environmental Triggers, Digital Habits, and Sleep Arousal (55:31) Modern sleep disruption stems less from blue light wavelengths and more from digital engagement and conditioned arousal. Subsequent replications have challenged earlier findings regarding blue light, demonstrating that interactive devices harm sleep primarily because they operate as engineered attention traps. Using phones in bed triggers sleep procrastination, while anticipating morning screen notifications causes anticipatory anxiety that reduces deep slow-wave sleep. To mitigate this without banning phones, Walker recommends Dr. Michael Grandner's rule of only using smartphones while standing up. Environmental modifications yield immediate, non-pharmacological improvements. Modern homes suffer from junk light; reducing evening ambient light below 30 to 50 lux and switching to warm wavelengths 90 minutes before bedtime increased REM sleep duration by 18% in experimental settings, while maintaining bedroom temperatures at 67–68°F (18°C) aids natural thermoregulation. When wakefulness persists in bed past roughly 20 minutes, Walker advises leaving the bedroom to dismantle conditioned arousal—the psychological association between the bed and active alertness—and warns against checking the clock during mid-night awakenings to prevent reinforcing wakefulness patterns. Neurological Recovery, Dreaming, and Metabolic Disruption (82:51) Sleep stages fulfill distinct, vital biological functions. Deep non-REM slow-wave sleep coordinates memory transfer from short-term holding sites to long-term storage like a long-wave radio transmitter. REM sleep acts as nocturnal emotional therapy: limbic structures such as the amygdala and hippocampus become up to 40% more active, while noradrenaline completely shuts down. This safe neurochemical state strips painful emotional charges from traumatic memories. When this mechanism fails, severe distress occurs; frequent nightmares correlate with an 800% increase in suicidal tendencies. Beyond emotional regulation, REM integrates new facts into a mind-wide web of distant associations, fostering creative problem-solving. Conversely, sleep loss exacts severe metabolic and cellular costs. A single night of sleep deprivation distorts the expression of 711 genes, upregulating pathways tied to chronic inflammation and cardiovascular stress while downregulating immune defense. Metabolically, deprivation elevates ghrelin and suppresses leptin, driving a 30% to 40% increase in hunger. When dieting while sleep-deprived, the body preferentially burns muscle, with 70% of lost weight coming from lean mass rather than fat. Caloric deficits also stimulate orexin release, an evolutionary mechanism designed to keep starving organisms awake to forage. Walker emphasizes that while emerging pharmacology like DORAs offers functional alternatives to blunt sedation, behavioral and environmental fundamentals remain the primary determinants of sleep architecture. Questions remain regarding the long-term safety of multi-year pediatric melatonin usage, the ethical risks of attempting to engineer genetic short sleep in work-driven societies, and how healthcare systems will integrate sleep education into standard medical training.

睡眠学者Dr. Matthew Walker指出，相较于单纯追求睡眠时长，维持稳定的入睡与唤醒作息规律性对降低全因死亡率与心血管疾病风险具有更为关键的预测效力；同时，大众普遍依赖的镁制剂与高剂量褪黑素多存在药理误区，改善睡眠应着眼于生物钟环境调控、神经压力管理及新型靶向干预。 睡眠规律性对寿命与心脑血管的决定作用 (42:35) Walker援引英国生物样本库（UK Biobank）针对6万名受试者的队列数据指出，在预测人类长寿方面，入睡与起床时间的规律性指标显著优于单纯的睡眠时长。将就寝和起床时间窗口严格控制在正负15分钟内的高规律作息群体，与作息波动达90至120分钟的低规律群体相比，全因死亡率下降了49%，癌症死亡率下降39%，心血管代谢疾病风险下降57%。尽管成年人维持机体生存仍需7至9小时的底线时长，但规律节律是决定生理能否处于良好运转状态的核心因素。 此外，针对9万人的研究显示，周末补觉可使平时严重睡眠不足者的心脑血管疾病发生率相对降低20%，但Walker强调这属于部分缓冲机制，无法逆转免疫功能、葡萄糖调节和认知敏锐度的损伤。针对明确可预见的高压或剥夺周期，在事前数天将睡眠主动拉长至8.5至9小时进行“睡眠储备”（Sleep Banking），可使随后的认知与心理功能损伤幅度降低约40%，为临床倒班、医护及竞技运动员提供了量化防护手段。 镁制剂与高剂量褪黑素的药理误区与风险 (21:48) 针对市面流行的补剂风潮，Walker澄清多数常见非处方镁制剂（如柠檬酸镁、氧化镁）无法通过血脑屏障，对脑部调控的睡眠结构几无直接作用，其多余剂量主要通过排泄流失或引起腹泻，仅有L-苏氨酸镁（Magnesium L-threonate）在文献中展现出部分中枢穿透能力。镁仅能通过外周骨骼肌放松间接经迷走神经向脑部回传平静信号，且补镁仅对原本存在血镁缺乏的患者有明确改善意义，对血镁正常人群的睡眠质量并无显著临床增益。 关于褪黑素，Walker强调其本质仅是向全身细胞通报进入黑夜的时间信号分子，并不参与实际生成或维持深度睡眠。临床荟萃分析显示，外源补充褪黑素使入睡时间平均仅缩短3.4分钟，睡眠效率提升仅2.2%，其幅度微弱且接近安慰剂效应。市售常见的10至20毫克大剂量远超人体生理分泌水平，不仅会在次日诱发持续性脑雾，且10年间美国儿童因误食褪黑素软糖导致的急诊住院激增503%；动物实验亦曾揭示超量褪黑素可能引起睾丸发育受阻。褪黑素的临床合理范畴应限定在0.1至3毫克内，且仅适用于跨时区时差及确诊的昼夜节律相位紊乱。 视丘感官闸门与夜间低照度光环境重构 (53:11) 人类入睡的神经机制依赖于视丘（Thalamus）作为感官闸门的物理闭合，以隔绝视、听等外界信号向大脑皮层的投递，而下丘脑的视交叉上核（SCN）则作为中央起搏器校准24小时生理节律。Walker指出，睡前使用手机的主要危害并非屏幕蓝光，而是互动内容诱发的高度精神警觉。晨起即看手机所激发的“预期性焦虑”会下调夜间深睡眠比例，可通过“仅限站立使用手机”的行为规范来弱化睡前拖延。 在物理环境干预上，晚间将室内照度降低至30勒克斯（lux）以下并滤除冷白光、改换暖黄光源，可使当晚快速眼动（REM）睡眠时长提升18%。针对夜间失眠或3点易醒的群体，Walker强调应避免因看时钟诱发皮质醇反常上升，并推行“20分钟法则”：若卧床约20分钟无法入眠必须离开卧室，防止大脑将床与清醒挫败建立病理性条件反射。 快速眼动睡眠的创伤修复与神经创造力 (82:51) 人脑在整夜约70至120分钟的离散睡眠周期中穿梭。阶段3慢波深睡眠通过巨幅低频脑波将海马体内脆弱的新记忆固化至新皮层；而REM做梦阶段则是全天24小时内唯一完全阻断去甲肾上腺素释放的时段。在此窗口内，杏仁核与海马体的神经代谢活跃度比清醒时高出多达40%，大脑得以在零压力生化环境下回放负面经历，剥离情绪创伤电荷。若此神经保护脱落则易发展为创伤后应激障碍（PTSD）。 临床高频噩梦是潜在自杀意念的重要警示指标。数据显示，总睡眠低于6小时与自杀倾向增加100%至150%相关，而严重的经常性噩梦障碍则与自杀意念激增800%高度关联。除情感疗愈外，REM睡眠还通过松散、跨领域的发散联想执行“记忆的团体治疗”，将日间信息碎块与既往认知网路交叉融合，为人类灵感与创造力构建神经计算底座。 睡眠代谢影响与新一代DORA靶向药物 (115:02) 急性睡眠剥夺在分子层面对代谢具备极强的破坏性：仅单夜失眠即会紊乱711个基因的表达活性，致使饱腹激素瘦素（Leptin）下降、饥饿激素脑肠肽（Ghrelin）骤增，引发30%至40%的食欲亢进；热量限制减重者若处于缺觉状态，其减去体重中高达70%来自骨骼肌肉而非体脂组织。此外，间歇性禁食和生酮饮食在早期会诱导食欲素（Orexin）代偿性分泌，激活进化层面的觅食唤醒驱动，进而暂时压缩睡眠时长。 在药理学迭代上，传统GABA类镇静安眠药（如唑吡坦/Ambien）实质是通过中枢抑制造成人工镇静，最新研究证实其会使大脑胶质淋巴系统（glymphatic system）夜间对代谢废物的清除率降低30%至40%。与之相对，第三代双食欲素受体拮抗剂（DORA）通过精准靶向阻断食欲素受体来关闭亢进的觉醒通路。脑脊液穿刺试验证明，50岁以上受试者服用DORA后，夜间有效排出了阿尔茨海默病致病性的β-淀粉样蛋白和tau蛋白，首度验证了药理性诱导睡眠同样具备生理性排毒功能。 Walker的研究体系表明，改善睡眠的基础在于尊重昼夜节律物理参数与行为定式，而非寄望于OTC补充剂。尽管DORA类新药在恢复天然睡眠架构与清除神经退行性病变蛋白方面展现出突破，但目前每月高达400美元的高昂自费成本与医保准入门槛仍限制其临床普及；同时，长期大剂量使用外源褪黑素对内分泌系统与生殖轴的远期安全性依然悬而未决，仍待大样本流行病学长期跟踪。

## Background 本期内容于 2025 年 11 月 17 日由知名商业访谈频道《The Diary Of A CEO》（主持人 Steven Bartlett）发布于 YouTube 平台。节目特邀加州大学伯克利分校神经科学与心理学教授、《我们为什么要睡觉》作者马修·沃克（Dr. Matthew Walker），深入探讨作息规律性与心血管疾病的关系、破除镁元素与褪黑素的助眠神话，并系统解析睡眠储备、快速眼动睡眠机制及新型处方药物对健康长寿的深远影响。 ## TL;DR 马修·沃克博士在对话中系统重构了现代睡眠科学认知，揭示出作息规律性在预测全因死亡率与心血管代谢疾病风险上比单纯睡眠时长更为关键。他提出了评估优质睡眠的“QQRT”（数量、质量、规律性、时型）四大基石，并澄清了市售多数形式的镁无法穿透血脑屏障、褪黑素仅是指示黑夜的“发令员”而非催眠药等常识盲区。访谈还详尽剖析了快速眼动（REM）睡眠通过关闭去甲肾上腺素来剥离创伤情绪的夜间疗愈机制，以及预先“睡眠储备”对抗急性缺觉的神经保护力。最后，沃克介绍了靶向食欲素系统的新一代 DORA 类药物如何促进类淋巴系统清除脑内致病蛋白，展示了睡眠医学的最新突破。 ## Atmosphere & style 整场访谈在硬核严谨的神经科学考据与温润深沉的人文关怀之间达成了绝佳平衡。沃克手持大脑解剖模型、以极具画面感的比喻抽丝剥茧时，展现出世界顶级学者的深厚底蕴；巴特利特则以敏锐的同理心和切身体会层层推进，让复杂的脑机制剖析极富生活启发性。随着话题从基因与睡眠效率延展至阿尔茨海默病、相濡以沫的爱情及向死而生的临终视角，节目氛围从充满求知欲的理性研讨升华为直击心灵的哲思对话，带给听众兼具智识洗礼与情感抚慰的沉浸体验。 ## Bulletin - [42:35](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=2555s) 作息规律性对寿命的预测力超越睡眠时长：UK Biobank 追踪超 6 万人数据表明，作息极不规律者过早死亡风险增加 49%、心血管代谢疾病风险增加 57%，固定就寝与起床时间的健康收益在正面统计竞争中击败了单纯的睡眠时长。 - [01:04:22](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=3862s) 大众助眠补剂机制澄清：绝大多数形式的镁补剂无法穿透血脑屏障，且正常血镁者无法通过超量补充获得额外催眠收益；褪黑素本质上只是提示黑夜降临的“发令枪”而非安眠药，元分析显示其平均仅缩短入睡时间 3.4 分钟，市面超生理剂量常引发严重晨间脑雾。 - [01:50:06](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=6606s) 睡眠剥夺对身体成分的破坏性打击：缺觉会导致饱腹激素（瘦素）骤降、饥饿激素（脑肠肽）激增，使食欲驱动力上升 30% 至 40%；在节食减重期间若处于睡眠匮乏状态，减掉的体重中多达 70% 来自宝贵的瘦肌肉组织，而非多余脂肪。 - [01:58:12](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=7092s) 失眠药物迎来 3.0 代际革新：新型双重食欲素受体拮抗剂（DORA）通过精准调低促醒神经递质来恢复自然睡眠，临床腰穿试验证明其能保留深度睡眠期脑部类淋巴系统对淀粉样蛋白和 Tau 蛋白的清除排毒功能，彻底颠覆了传统镇静剂（如 Ambien）抑制 30%–40% 脑部排毒的弊端。 ## Key takeaways - [42:35](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=2555s) 作息规律性（Regularity）在预测全因死亡率上明显击败睡眠时长，入睡和起床时间波动大的人群全因死亡风险高出 49%，癌症与心血管代谢疾病风险分别上升 39% 和 57%。 - [10:45](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=645s) 周末补觉仅能降低 20% 的心血管疾病风险，但无法逆转免疫缺陷、血糖紊乱与认知损伤；而在预见性缺觉前进行“睡眠储备”（Sleep Banking）可使随后的认知损伤降低约 40%。 - [19:42](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=1182s) 睡前电子屏幕破坏睡眠的核心元凶是交互内容引发的高唤醒度心理刺激，而非传统认为的屏幕蓝光抑制褪黑素；采用“站立使用手机”法则可打破床上刷屏的恶性循环。 - [21:48](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=1308s) 褪黑素不负责生成睡眠，其睡眠效率提升仅约 2.2%，市面 10–20 毫克的超生理剂量会导致清晨残留并引发脑雾；其临床有效场景仅限于跨时区时差调节与睡眠相位后移综合征。 - [35:12](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=2112s) 评估健康睡眠需依托 QQRT 框架（数量 Quantity、质量 Quality、规律性 Regularity、时型 Timing），其中 7 小时仅是不致过早死亡的生存底线，维持繁荣生活需 7–9 小时充足睡眠且睡眠效率应达到 85% 以上。 - [58:04](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=3484s) 长期在床上辗转反侧会建立“床 = 保持清醒”的条件性唤醒回路；失眠者应执行“20分钟法则”果断离床，并在夜醒后严格避免看表以防强化时间锚定与焦虑。 - [01:00:31](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=3631s) 睡前“数羊”会因计数挫败感加重失眠，应采用 4K 细节粒度的“心智漫步”（Mental Walk）构想熟悉路线，引导大脑从自我关注中抽离从而自然入睡。 - [01:04:22](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=3862s) 普通镁补剂无法穿透血脑屏障，且正常血镁人群额外补镁无助眠收益；对于处于“疲惫却亢奋”（tired but wired）的高压人群，南非醉茄与磷脂酰丝氨酸压低皮质醇与交感神经的效果更具循证支持。 - [01:18:20](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=4700s) 整夜后半程尤其是临醒前两小时富集了绝大部分快速眼动（REM）睡眠，提前 2 小时醒来虽然只减少 25% 的总时长，却会剥夺高达 50%–70% 的全部 REM 睡眠。 - [01:22:51](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=4971s) REM 睡眠是大脑 24 小时内完全关闭应激递质去甲肾上腺素的唯一时刻，它在神经化学安全环境中回放记忆，实现“将苦涩的情绪果皮从信息果肉上剥离”的夜间心理治疗功能。 - [01:31:00](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=5460s) 频繁发作的临床恶梦是自杀倾向暴增 800% 的极危哨兵生物标记物；通过意象重演疗法（IRT）利用记忆再巩固机制改写创伤剧本，可有效化解顽固性恶梦烈度。 - [01:36:54](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=5814s) 做梦是大脑内部的“信息炼金术”，在深睡眠完成独立碎片固化后，REM 睡眠如“记忆的团体心理治疗”般建立远距离非线性联想网络，是人类顿悟与创造力的生物学基石。 - [01:41:04](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=6064s) 携带 DEC2 或 ADRB1 突变的天然短睡眠者仅需约 6 小时睡眠且全天无倦意，但其突变概率（0.004）远低于一生中遭雷劈的概率（0.0064）；盲目通过基因编辑压缩睡眠会导致社会竞争性“睡眠货币贬值”。 - [01:53:00](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=6780s) 饥饿断食会触发下丘脑释放促醒物质食欲素（Orexin）以维持中枢兴奋驱动觅食；而嗜睡症与失眠症恰好构成食欲素系统缺乏与过度激活的镜像病理状态。 - [01:54:23](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=6863s) 以苏沃雷生等为代表的第三代失眠药物（DORAs）通过精准阻断食欲素受体关闭过度觉醒，诱导具有生理功能的自然睡眠并维持脑部排毒，显著优于传统 GABA 受体化学镇静剂。 ## Detailed walkthrough ### [00:00](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=0s) 睡眠科学新知与镁的真相：开场引言 节目开篇直指当下风靡全网的睡眠补剂——镁（Magnesium）。加州大学伯克利分校神经科学与心理学教授马修·沃克（Dr. Matthew Walker）一针见血地指出，市面上绝大多数形式的镁根本无法穿透血脑屏障（Blood-Brain Barrier），而睡眠本身是由大脑直接调控的。如果一种物质连大脑都进不去，又谈何从根本上改善脑部机制？盲目补充的结果往往只是在制造“昂贵的尿液（expensive urine）”。不过，沃克也透露目前确实有一种特定形式的镁具备相关科学证据支持，后续将详细展开。此外，他还抛出了一连串颠覆传统认知的研究：广为流传的“8小时睡眠神话”、给儿童服用褪黑素的潜在隐患、夜间频繁醒来的生理根源，以及一种极少数人知晓、但他本人真正看好的全新一类处方安眠药物。 在睡眠习惯方面，沃克特别警示了日常作息不规律的巨大健康代价。现实中很多人习惯今晚11点睡、明晚熬到凌晨1点、后晚又在10点半入睡。大规模统计数据显示，与入睡和起床时间高度规律的人群相比，作息混乱者过早死亡的风险显著增加49%，而罹患心血管与代谢疾病（cardiometabolic disease）的风险更是暴增57%。面对现代社会的睡眠危机，沃克总结出优质睡眠的四大支柱（Four Pillars of Good Sleep），并带来了关于“睡眠储备（Sleep Banking）”的前沿突破研究——这项策略能帮助面临高强度工作冲刺的职场人、即将面临连续40小时待命的急救医生以及新生儿父母抵御缺觉打击。 - 作息不规律（入睡和起床时间波动大）导致过早死亡风险增加 49%，心血管代谢疾病风险增加 57%。 - 睡眠四大支柱（涵盖数量、质量、规律性与时间点）构成了评估健康睡眠的全新基准框架。 - “睡眠储备（Sleep Banking）”最新实验表明，在预见性缺觉前主动储蓄睡眠，能显著提升随后的生理与认知韧性。 ```mermaid flowchart TD accTitle: 睡眠紊乱对健康风险的影响链 accDescr: 展示不规律睡眠作息如何引发心血管与代谢风险激增并导致过早死亡 subgraph Habit["作息模式"] A["作息严重不规律<br/>(入睡/起床时间大幅漂移)"] end subgraph Impact["病理与生理损伤"] B["心血管代谢疾病风险<br/>激增 57%"] C["整体生理机能<br/>与大脑修复受损"] end subgraph Outcome["远期预后"] D["过早死亡风险<br/>显著增加 49%"] end A --> B A --> C B --> D C --> D ``` ### [02:20](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=140s) 从“治愈困倦”到重塑DNA：马修·沃克的科学研究使命 在主持人史蒂芬·巴特利特（Steven Bartlett）的引介下，沃克系统梳理了自己的学术背景与科研历程。作为一名潜心研究睡眠二十余年的资深神经科学家，他的核心工作就是解开“人类究竟为何需要睡眠”这一未解之谜。半个世纪前，科学界对这一问题的回答简陋粗暴得令人发笑——“你睡觉是为了治愈困倦（You sleep to cure sleepiness）”。沃克打了个生动的比方：这就像说“你吃饭是为了消除饥饿”一样荒唐空洞，完全忽视了进食背后庞大复杂的生理系统支持。 如今，在几代顶尖学者的共同探索下，科学界彻底颠覆了这个问题的逻辑方向。沃克指出，我们现在要反过来问：“人体内是否存在任何一个关键生理系统，抑或大脑中是否存在任何一种认知运作，是在睡眠充足时没有得到极佳强化，或在睡眠匮乏时没有受到显著损伤的？”答案是斩钉截铁的：完全没有。睡眠的影响甚至深入到了基因层面，个人的睡眠状况会直接干预并重写脱氧核糖核酸（DNA）的核苷酸表达字母表，谱写出截然不同的日常健康轨迹。在更宏观的社会层面，缺觉还会系统性地改变社会关系结构、人际互动模式、价值信念系统，乃至决定一个人究竟是走向极端社交还是陷入深切孤独。 - 沃克专注神经科学与睡眠领域超过20年，研究范畴涵盖睡眠对大脑认知、神经回路及躯体健康的深远调控。 - 现代睡眠科学颠覆了传统认知：睡眠并非单纯缓解疲劳，而是全身器官修复、免疫维持与脑功能运作的绝对中枢。 - 睡眠剥夺会在分子层面上直接扰乱 DNA 基因表达网络，并在宏观层面加剧个体的孤独感与社交疏离。 ### [04:48](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=288s) 进化的大漏洞与社会污名：为什么我们总在牺牲睡眠？ 巴特利特分享了来自其受众的真实数据：在针对《The Diary Of A CEO》听众的千人问卷调查中，高达 75% 至 80% 的人正饱受各种睡眠问题的困扰。巴特利特坦言，自己在职业生涯初期乃至五年前，也曾把睡眠当作“可有可无、随时能省出来”的边角料时间。沃克对此表达了极大的理解，直言“这绝不是你的错”。在主观感受中，入睡后身体处于静止休眠，意识大部分处于空白离线状态，人们自然很难直观体会到损失一两小时睡眠究竟会引发多么灾难性的后果。 从纯粹的达尔文进化论视角来看，睡眠甚至像是一个极其愚蠢的生理设计：“当你陷入沉睡时，你无法寻找配偶、无法繁衍后代、无法照顾幼崽、无法采集觅食，最致命的是，你极易沦为掠食者的猎物。”进化史上任何一项具有如此多生存劣势的行为，理应在自然选择中被迅速淘汰。然而，睡眠在所有已知物种中均顽强保留了下来。学界名言一针见血：“如果睡眠没有承担极其关键的核心生理功能，那它绝对是自然进化史上犯下的最大错误（the biggest mistake the evolutionary process has ever made）。”现代科学证明，睡眠绝非消极被动的“关机”，而是大脑和身体高度活跃的系统性维护重组期。 公众对睡眠重要性的长期忽视，源于系统性的制度缺失与社会偏见。沃克列举了一项涵盖全球约11种医学课程体系的研究：医学生在漫长的受训生涯中，平均仅能接受约 1.2 个小时关于睡眠的专业教育，然而睡眠却占据了他们未来患者生命整整三分之一的时间。更严重的是社会文化对充足睡眠的污名化。现代人能极其自豪地宣称自己坚持健康饮食数月，或每周规律健身三次，却极少有人敢公开骄傲地表示自己每天雷打不动睡足 8.5 小时。因为一旦说出口，旁人往往会带着微妙的审视反问“真的吗？”——这种质疑背后的潜台词残酷而现实：“如果你有充裕的时间睡觉，说明你根本不够忙碌；而如果你不够忙，就代表你不是个重要的人物。” - 现代医学院课程严重边缘化睡眠科学，全球多项医学教育体系平均仅分配约 1.2 小时学习睡眠医学。 - 社会普遍存在推崇熬夜、贬抑睡眠的毒性文化，将睡眠充足错误地等同于“清闲”与“边缘化”。 - 进化生物学铁律：睡眠在所有高级物种中得以代代延续，恰恰确证了其维持生命运作不可替代的多重生理功能。 ### [08:29](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=509s) 被忽视的睡眠障碍群体：从失眠到不宁腿综合征 针对巴特利特关于受众群体的提问——从寻求微弱机能突破的精英，到饱受严重睡眠障碍折磨的患者，听众到底在寻找什么？沃克将关注点首先落在了饱受折磨的临床病患群体上。在这场睡眠危机的金字塔底端，首先是数量庞大的失眠（Insomnia）患者，以及罹患睡眠呼吸暂停（Sleep Apnea）等器质性病变的群体。 沃克特别强调了极具破坏性却常被社会忽视的不宁腿综合征（Restless Legs Syndrome, RLS）。患有该病的人在试图入睡时，双腿会产生一种极其难受的蚂蚁爬行或蠕动样感觉（creepy, crawly feeling），患者被迫不断按摩双腿、反复下床踱步来暂时缓解这种折磨。这种神经系统异常会彻底粉碎入睡流程，造成夜间极其严重的睡眠剥夺。沃克尤为痛心地指出，无论是严重的呼吸暂停还是不宁腿综合征，在当下现实中都存在极其惊人的“低诊断率（markedly undiagnosed）”，大量患者常年深陷痛苦，却从未意识到这是一种可以通过专业医学手段干预治疗的神经系统疾病。 - 不宁腿综合征（RLS）以夜间双腿蠕动、蚁走感及不可抑制的活动冲动为特征，严重破坏睡眠连续性。 - 包括阻塞性睡眠呼吸暂停与不宁腿综合征在内的多种典型睡眠障碍，在临床实践与公众认知中普遍处于严重未诊断状态。 ### [09:20](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=560s) 破坏睡眠的日常因素与追求极致的“优化者” 在探讨睡眠困境时，人群大致可以分为几个群体。首先是一类没有任何临床睡眠障碍的人，但他们平时的行为却在不自觉地瓦解自己的睡眠结构。这包括摄入一些看似有助于入睡、实则严重破坏睡眠质量的物质，例如酒精、咖啡因以及 THC（四氢大麻酚）。此外，还有许多内在心理因素在作祟，比如压力、焦虑，或者纯粹是生活琐事的重压让人无法安眠。 离开“无睡眠障碍却睡不好”的群体，光谱的另一端则是对睡眠近乎痴迷的“生物黑客”（bio-hackers）与生物优化者（bio-optimizers）。马修·沃克（Matthew Walker）提到，他经常与高绩效人群合作，包括顶级商业领袖和职业运动员。对于这些顶尖人士而言，哪怕仅仅提升 2% 到 3% 的表现，背后可能就意味着数千万美元的商业价值，或是能否站上奥运会领奖台的决定性差距。 --- ### [10:45](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=645s) 颠覆认知：周末补觉真的能保护心脏吗？ 过去，马修·沃克一直强调“睡眠不像银行，你无法欠债后再还款”。现场摆放了一个罐子道具作为比喻：当一个人睡眠充足时，罐子装满了睡眠积分；而在工作日连续每晚只睡 5 个小时，就是在持续积累债务、透支健康。过去科学家普遍认为，一旦欠下睡眠债，罐子的盖子就已经闭死，即便周末再怎么多睡，也无法弥补体内已经造成的损伤。 ```mermaid flowchart TD accTitle: 周末补觉与心血管风险研究对比 accDescr: 对比工作日睡眠不足时，周末补觉与不补觉对心血管疾病风险的影响差异 subgraph 平日短睡眠群体 A["工作日短睡眠（例如每晚 5 小时）"] --> B["周末继续短睡"] A --> C["周末长睡补觉（Catch-up Sleep）"] end subgraph 心血管健康结果 B --> D["心血管疾病风险基准线较高"] C --> E["心血管疾病风险相对降低 20%"] E -. 仍不及持续充足睡眠.- F["整周作息规律且充足者（风险最低）"] end ``` 然而，英国生物样本库（UK Biobank）一项涉及超过 9 万人的突破性大数据研究，让马修·沃克修正了自己的部分观点。研究人员将受试者细分为“工作日短睡且周末也短睡”与“工作日短睡但周末多睡补觉”两类人群： * **心血管风险显著降低**：数据显示，工作日睡眠不足但周末通过长睡补觉的人，其心血管疾病发病风险比周末继续短睡的人降低了整整 20%。 * **并非“免费的午餐”**：这两组睡眠不足人群的心血管疾病风险，仍然普遍高于整周都保持充足睡眠的人群。 * **其他器官系统并未恢复**：科罗拉多大学博尔德分校的肯尼斯·赖特（Kenneth Wright）等学者的研究证实，周末补觉并不能挽救受损的免疫系统、血糖调节机制以及认知能力。因此，“睡眠银行”概念仅在心脏与心血管系统这一个维度上显示出了部分代偿效应。 --- ### [14:35](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=875s) 睡眠储备机制：提前为熬夜存好“健康缓冲垫” 除了事后弥补债务，沃尔特·里德陆军研究所（Walter Reed Army Institute of Research）的托马斯·巴尔金（Thomas Balkin）换了一个思考方向：如果预先知道未来即将面临严重的睡眠剥夺，人类是否能提前进行“睡眠储备”（Sleep Banking）？ 马修·沃克用财务做了生动形象的比喻：就像每年年底临近圣诞节时，大家都知道接下来会有大笔开销送礼，因此聪明的做法是在 10 月和 11 月提前勒紧裤腰带存钱。这样一来，当真正进入高消费阶段时，银行账户才不至于瞬间跌入透支深渊。研究团队对陆军学员展开了实验验证： * **实验设计**：实验要求受试者面对连续 2 至 3 晚的极度睡眠剥夺或完全通宵；但在测试前的一周内，实验组被允许每晚躺在床上的时间从原本受限的 8 小时延长至 10 小时，实际平均睡眠时间从平时的 7 到 7.5 小时提升到了 8.5 到近 9 小时，往“罐子”里存入了超额的睡眠储备。 * **认知损伤降低 40%**：当两组人共同进入剥夺睡眠的测试时，虽然他们的认知水平均比休息充分时下降，但提前“存入睡眠”的实验组在心智与认知能力上的受损程度，比按常规睡眠的对照组轻了约 40%。 * **适用人群广泛**：这一机制为许多必须面临睡眠短缺的高压群体提供了关键策略，例如即将迎接连续 40 小时轮班的值班医生、执行高难度任务的军事飞行员、需要高强度冲刺的创业者、即将临产的新生儿父母，以及大赛前夕极易因紧张而失眠的职业运动员（正如迈克尔·格兰德纳 Michael Grandner 的研究所示，运动员在大赛前夜往往睡得极差，提前几天储备睡眠能有效保障赛场发挥）。 史蒂文·巴特利特（Steven Bartlett）感叹，正是由于马修·沃克当年登上乔·罗根（Joe Rogan）播客并推出畅销书，才成为主流社会开始真正重视睡眠科学的催化剂。但面对那些被日常生活、压力与心理创伤缠绕，没有器质性疾病却依然严重受睡眠折磨的普通人，现代科学又给出了哪些实用的应对良方？话题随即由此展开。 ### [19:42](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=1182s) 睡前数字排毒与“蓝光神话”的破灭 当被问及如果今晚只能做三件事来彻底改善睡眠、睡满8小时时，马修·沃克（Matthew Walker）给出的第一个建议是“数字排毒”（Digital Detox）。具体做法是在睡前一小时内，尽量减少使用那些会让人情绪激动的社交媒体、工作电子邮件以及容易引发焦虑的即时短信。沃克打趣道，睡前听听播客是完全没问题的，主持人史蒂文·巴特利特（Steven Bartlett）立刻心领神会地开玩笑接话，呼吁观众“一定要在这里点赞、订阅并打开小铃铛”，引得两人一阵欢笑。 随后，沃克澄清了一个长期存在的误区——睡前屏幕造成的睡眠障碍，罪魁祸首其实并不是大家熟知的“蓝光”。过去大约十年间，学界和公众都深受一项极具影响力的经典研究所影响：该研究指出，睡前使用 iPad 阅读一小时会严重抑制褪黑素分泌、扰乱深度睡眠并减少做梦睡眠（REM 睡眠）；甚至在停止使用 iPad 后，其对做梦睡眠的“爆炸冲击半径”和负面余波竟能持续整整一周，宛如某种药物需要漫长的时间才能从体内代谢清除。然而，澳大利亚杰出的睡眠研究学者迈克尔·格拉迪萨尔（Michael Gradisar）在反复尝试后发现该实验结果根本无法复现，从而单枪匹马打破了这一行业思维定势。后续研究证实，屏幕发出的蓝光并非核心问题所在，电子设备带来的高唤醒度心理刺激才是让人无法入睡的真正原因。 ```mermaid flowchart TD accTitle: 屏幕影响睡眠的真实机制对比 accDescr: 对比过去认为的蓝光破坏褪黑素与现代科学证实的心理刺激模型 subgraph OldMyth ["传统蓝光神话认知"] A["睡前使用电子屏幕"] --> B["蓝光直接抑制褪黑素"] B --> C["破坏深度与REM睡眠长达一周"] end subgraph ModernScience ["现代科学最新认知"] D["睡前使用电子屏幕"] --> E["互动内容引发心理唤醒与焦虑"] E --> F["阻碍大脑自主进入放松入睡状态"] end ``` --- ### [21:48](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=1308s) 褪黑素不是安眠药：被高估的催眠效果与“晨间脑雾” 针对大众广泛服用的褪黑素，沃克强调了人们对其生理机能的严重误解：褪黑素是一种向大脑和身体发出“黑夜已降临、该准备睡觉了”信号的激素，但它本身**完全不参与生成睡眠**。沃克用了一个形象的比喻：褪黑素就像百米赛跑的发令员，它负责召集所有选手走上起跑线并扣动发令枪宣布比赛开始，但它自己绝不会迈开腿替选手去跑这100米——真正驱动睡眠进程的是另一套完全不同的脑化学机制。多项汇总所有临床试验的元分析（Meta-analyses）显示，褪黑素在统计学上仅仅能让人提前大约 3.4 分钟入睡，睡眠效率的提升也仅有 2.2% 左右，其效果基本等同于安慰剂。 尽管安慰剂效应是整个药理学中最稳定可靠的效应之一，但沃克严正警告：服用褪黑素绝非“多多益善”。许多市售褪黑素产品的单粒剂量高达 10 毫克甚至 20 毫克，这在医学上被称为“超生理剂量”（Supraphysiological dose），即远远超出了人体自身所能分泌的生理数量级。正常情况下，人体内的天然褪黑素在清晨来临时早已停止分泌并回落至近乎零水平，使人神清气爽地醒来；然而，若前一晚摄入了超高剂量的褪黑素，即便它能凭借药力将人“强行放倒”，到了清晨醒来后的前三到四个小时里，血液中残留的过量褪黑素仍会不断向大脑发送“现在依然是伸手不见五指的深夜”的化学信号。这会导致极其厚重的“晨间脑雾”（Dense nighttime fog），让人昏昏沉沉，不得不猛灌两三杯咖啡来强行提神。 - **元分析核心数据**：褪黑素平均仅缩短入睡潜伏期约 3.4 分钟，睡眠效率仅提高约 2.2%。 - **科学推荐剂量**：如果确实需要补充，合理剂量应控制在 0.1 毫克至 3 毫克 之间，而非市面上常见的 10~20 毫克超大剂量。 --- ### [24:25](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=1465s) 褪黑素真正适用的两类特殊场景 沃克指出，褪黑素并非日常助眠的万灵丹，但在以下两种特定临床与生理情境下具有极佳的调理价值： 1. **跨时区时差反应（Jet lag）**：此时补充褪黑素的关键在于精确把握服用时间，人为建立起生物学上的黑夜信号。例如从洛杉矶直飞伦敦，两地存在 8 小时的时差；当抵达伦敦准备在午夜入睡时，体内由洛杉矶时钟主导的生物钟实际上才到下午 4 点，天然褪黑素还要再过六七个小时才会上升。此时按当地入睡时间摄入褪黑素，就能人为接管并欺骗大脑，促使其提前适应新时区的昼夜节律。 2. **睡眠相位后移综合征（Delayed Sleep Phase Syndrome）**：约占总人口 1% 到 2% 的人群患有严重的昼夜节律相位紊乱，他们往往直到凌晨 3 点或 4 点甚至更晚才会产生睡意，白昼则极度嗜睡，几乎过着完全昼夜颠倒的“夜行性”生活。这种节律紊乱很大程度上由基因决定，并非当事人主观意愿或生活懒散。在隔绝自然光线与时钟的严密睡眠实验室中，可以测定出他们体内的褪黑素分泌曲线与常人无异，但分泌高峰（Crescendo）在 24 小时表盘上比常人整整推迟了大约 5 个小时。通过在傍晚或夜间适时补充褪黑素，能够巧妙诱导其生物节律提前，帮助他们更顺畅地融入主流社会的作息步调。 --- ### [27:12](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=1632s) 儿童滥用危机与激素干预的潜在健康风险 巴特利特提到，随着褪黑素被包装成形形色色的日常助眠保健品推向大众，资本与初创企业对其趋之若鹜，这是否令人担忧？沃克坦言自己内心十分矛盾，并从两个严峻维度指出了滥用褪黑素的隐患： 其一是**儿科群体的滥用与误食中毒危机**。在美国，褪黑素在儿童群体中的使用量呈指数级暴增，超市保健品区甚至开辟了大片醒目的紫色专属货架，摆满了专门针对儿童的褪黑素软糖。三年前发表的一项权威研究揭示了一个触目惊心的事实：在过去十年中，全美因褪黑素过量中毒而被送入急诊救治的儿童案例激增了整整 503%。 其二是**内生激素平衡与生殖发育的潜在长远干扰**。褪黑素是一种具有强大生物活性的激素，深度参与机体的生长发育和生殖系统调控。早在 1970 年代的研究便发现，在青春期发育阶段的大鼠模型中，长期给予大剂量褪黑素会导致幼鼠睾丸发育迟缓并引起睾丸萎缩。虽然褪黑素本身具备良好的抗氧化特性且整体急性毒性较低，但“天然并不等于毫无节制地安全”。沃克以男性外源性注射睾酮为例警告道：长期依赖外源性激素会诱发身体内在反馈抑制——连续注射睾酮约 18 个月后，睾丸自身合成睾酮的功能便会停摆，甚至在停药后都难以自行复原；对待同属活性激素的褪黑素，同样必须保持敬畏与审慎。 ### [29:45](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=1785s) 褪黑素的长期隐忧与“生物学没有免费午餐” 关于长期补充褪黑素是否会抑制人体自身分泌的问题，马修·沃克（Dr. Matthew Walker）澄清，现有科学研究尚未证实“外源补充高剂量褪黑素会导致身体彻底关闭自身分泌系统”。在针对某些小群体的 6 个月甚至 12 个月的研究中，参与者在停用褪黑素后，自身自然的褪黑素分泌都能逐渐恢复正常。然而，潜藏的巨大未知在于：现代人往往不是断断续续吃几个月，而是年复一年、长期依赖它入睡。医学界至今完全不清楚连续服用数年之后，身体的生理机制会发生何种不可逆的改变。 主持人史蒂芬·巴特利特（Steven Bartlett）坦言，这正是他初次面对褪黑素时犹豫不决的原因。在与各领域专家的交谈中，他深刻认识到人体的负反馈调节法则——如果人体持续摄入某种外源性激素（例如男性注射睾酮），身体就会认为体内储备充足，进而关闭自身的生产腺体，导致个体终生依赖外源补充。沃克对此深表赞同，并给出了警示：“生物学里从来没有免费的午餐，而且如果你选择与生物学规律对抗，最终通常会输得一败涂地。”沃克幽默地提到，每当有朋友向他极力推销某些号称没有任何副作用的“奇迹神药”（比如莫达非尼 Modafinil）时，他反而最感到恐惧——因为“缺乏证据并不等于不存在风险”（Absence of evidence is not evidence of absence），很多时候我们只是尚未发现生理代价究竟隐藏在何处。 ### [31:25](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=1885s) 屏幕剥夺睡眠的真相：注意力捕获、情绪唤醒与“站立玩手机”法则 回到提升睡眠质量的具体策略，沃克强调大家首先要做好“数字排毒”（Digital Detox），但他纠正了一个常见误区：睡前真正摧毁睡眠的元凶并不是屏幕发出的蓝光，而是设备背后极具杀伤力的心理激活效应。亚利桑那大学的睡眠专家迈克尔·格兰德纳（Dr. Michael Grandner）的研究表明，手机等智能设备本质上是顶尖科技公司斥资数千万美元打造的“注意力掠夺机器”，旨在最大限度收割用户的注意力。当你在夜间使用它们时，大脑神经系统会被高度唤醒，这种刺激就像给你的困意按下了“静音键”。 现实中人们往往经历这样的恶性循环：晚上 11 点你躺在床上时明明困得不行（甚至刚才在沙发上看电视时还在打瞌睡），但一旦解锁手机开始刷社交媒体，陷入所谓的“末日刷屏”（doomscrolling）和“床上摆烂”（bed rotting）状态，回过神来时指针已经指向了凌晨 1 点，从而导致严重的“报复性睡前拖延”。格兰德纳的研究还指出，并不是每个人对这种干扰的易感性都一样，那些具有较高神经质（neuroticism）、高冲动性或高焦虑特质的人群，在卧室使用电子设备时遭受的睡眠剥夺最为严重。 谈及现代人晨起的第一件事，史蒂芬自嘲地承认，自己常常在眼睛还没完全睁开时就已经摸到了手机。沃克指出，屏幕亮起的那一刻，海量的外部信息与他人安排便如“焦虑海啸”般将人淹没，这是一种极度糟糕的唤醒方式。他将其比作第二天一大早要赶关键航班的经历：这种“预期性焦虑”（anticipatory anxiety）会让人整夜处于浅睡眠，深睡期比例大幅锐减；而每天明知醒来就要面对手机信息轰炸的人，夜间睡眠也会不自觉地陷入这种浅层防御状态。鉴于让现代人把手机扔出卧室极其不现实（“妖怪已经从瓶子里放出来了”），沃克分享了好友格兰德纳提出的绝妙折中法： ```mermaid flowchart TD accTitle: 卧室手机站立使用规则 accDescr: 展示如何在卧室中使用手机以避免沉迷拖延入睡的流程图 A["允许将手机带入卧室"] --> B["建立核心规矩：只能站立使用"] B --> C["站立刷手机 7~8 分钟"] C --> D{"身体产生疲劳感，想要坐下或躺平"} D -->|"顺应困意与身体疲劳"| E["主动放下手机并上床入睡"] ``` - **注意力捕获机制**：电子设备通过即时多巴胺刺激抑制困意中枢，造成生理性疲劳与中枢神经过度兴奋脱节。 - **高危性格特质**：高焦虑度、高冲动性与神经质个体，在睡前接触算法流媒体时失控概率显著偏高。 - **站立使用准则**：打破“舒适躺卧+无限滑动”的恶性关联，利用站立带来的身体疲劳，促使大脑在数分钟内主动放弃使用设备。 ### [35:12](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=2112s) 优质睡眠的四大基石“QQRT”与生存与繁荣的界限 如果一个人在睡眠改善上只能挑选一件事来做，沃克的答案极其坚定：“规律性（Regularity）至高无上”。无论是工作日还是周末，每天在完全相同的时间上床和起床，其健康收益胜过其他所有单一技巧。为了系统化评估睡眠，沃克基于多年科学研究构建了一套睡眠框架——“优质睡眠的四大宏观基石”（The 4 Macros of Good Sleep），简称 **QQRT**。就像营养学中蛋白质、脂肪与碳水化合物三大宏观营养素缺一不可一样，优质睡眠依赖于四根支柱构成的稳固系统： ```mermaid flowchart LR accTitle: 优质睡眠的四大宏观基石 QQRT accDescr: 解释睡眠四大要素（数量、质量、规律性、时型）构成的椅腿平衡模型 subgraph QQRT["优质睡眠四大宏观要素 (QQRT)"] direction TB Q1["数量 Quantity<br/>7至9小时健康区间"] Q2["质量 Quality<br/>深睡与快速眼动睡眠连续性"] R["规律性 Regularity<br/>核心基石：固定作息节律"] T["时型/时机 Timing<br/>匹配个体昼夜节律表型"] end QQRT --> OUT["稳固平衡的健康机体<br/>（任一椅腿受损均导致系统倾覆）"] ``` 在谈到第一个要素“数量”（Quantity）时，沃克明确纠正了大众的教条化思维：所谓的“每晚必须睡足 8 小时”是一个毫无科学依据的神话，真正的黄金区间是 **7 到 9 小时**。大规模流行病学数据表明，睡眠时间越短，全因死亡率（all-cause mortality）就越高，“睡得越少，命就越短”。 面对社交网络上部分人声称“从死亡率曲线来看，睡 6 小时与睡 7 小时差异极小，因此 6 小时完全够用”的论调，沃克进行了犀利的反驳。他指出这类言论混淆了两个完全不同的生理维度：**生存（Survive）**与**繁荣（Thrive）**。 - **7 小时是机体勉强维持生理机能、避免过早死亡的“生存底线”**； - 能够让你在白天保持敏锐心智、充沛体能、稳定情绪并预防慢性退行性疾病的睡眠量，则是支撑你“繁荣生活”的更高追求。用仅仅不死于心脏病或短命的生存底线，来定义白天的生命质量，是完全错误的逻辑。 ### [38:00](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=2280s) 进化的残酷算盘：为什么父母没有“少睡免疫卡”？ 针对许多新手父母即便每晚只有 4 到 5 小时破碎睡眠却依然显得精力过人的现象，史蒂芬好奇地发问：大自然在漫长的进化历程中，是否赋予了为人父母者某种独特的生理代偿机制或适应力，使他们的大脑能够在缺觉状态下免受损伤？ 沃克对此给出了明确的否定答案：从生理学和神经科学证据来看，成为父母并不会让人获得某种免受睡眠剥夺伤害的“魔法免疫针”。从进化生物学的残酷逻辑来剖析，人类远古祖先以部落为单位群居，抚养后代是由族群共同分担的集体任务。在大自然的演化算盘中，一旦个体完成交配繁衍并将自己的遗传基因成功传递下去，自然选择对该个体寿命和健康维护的资源倾斜就会骤降；进化的重心会毫不犹豫地转向带有新鲜基因的下一代。 正如大自然界中许多生物一样，父母的肉身在基因传递后往往会被无情“牺牲”。史蒂芬随即联想到一部著名的章鱼纪录片所展现的自然写照：雌性章鱼在洞穴深处产卵并完成孵化后，会耗尽所有生命力，甚至主动停止进食，最终在幼崽孵化后静静死在原地。大自然为了基因延续的使命，从来不会优先保障繁殖后个体的舒适与安康。人类父母在极端缺觉下的硬撑，并不是因为身体获得了进化的超能力，而只是在透支代偿生理机能，背后的健康代价并未被大自然免除。 ### [39:36](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=2376s) 睡眠神话破灭：不存在“睡得少却不受损”的特殊体质 对话承接了此前关于章鱼繁衍后便死去的单次繁殖（semelparity）现象——雌性章鱼倾其所有保护并为受精卵增氧，一旦小章鱼孵化便迅速走向死亡，这一过程由其眼腺（类似于哺乳动物的垂体）释放的激素变化引发，而雄性往往在交配后数月内死亡。Matthew Walker 笑着感叹幸好人类不是章鱼，但这引出了一个极为严肃的话题：人类在进入为人父母的阶段后，并不会被赐予任何抵抗睡眠剥夺的“隐形无敌斗篷”。 在科学界，经常有人宣称自己天生只需要极少的睡眠。然而 Matthew Walker 指出，人群中那些每晚睡眠时间不足 6 小时、且大脑和身体机能均未表现出任何实质性损伤的个体数量，如果四舍五入并以人口百分比来表示的话，“答案是整整 0%”。睡眠的“量”（Quantity）固然不可或缺，但在长久以来，公众乃至科学界都曾片面地将“睡眠时长”视作衡量睡眠是否健康的唯一标尺。 --- ### [40:48](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=2448s) QQRT 模型之“质”：睡眠效率与慢波脑电 不仅要看睡眠时长，还必须审视睡眠的“质”（Quality）。在睡眠科学的“QQRT 框架”（数量 Quantity、质量 Quality、规律性 Regularity、时型 Timing）中，睡眠质量被严格界定为两个核心维度： 1. **睡眠连续性（Continuity）与睡眠效率（Sleep Efficiency）**： - 良好的睡眠质量表现为整夜持续、完整的大段睡眠，而非被多次夜醒撕裂得支离破碎。 - 消费级睡眠手环或智能戒指通常能直接读取这一指标。其计算公式为：**在床上的实际入睡时间占在床总时间的百分比**。 - 科学健康的基准线是 **85% 或以上**。如果睡眠效率低于 85%，就说明睡眠质量已出现实质性缺陷，亟需调整或干预。 2. **深睡慢波脑电的能量（Slow-Wave Power）**： - 这是普通穿戴设备无法准确读取、必须在专业睡眠实验室中贴满电极（Matthew Walker 戏称这让人看起来像个“意大利面怪物”）才能测得的指标。 - 它衡量的是非快速眼动睡眠（NREM）深睡期那些宏大、缓慢的脑电波所具备的功率与能量。 最新研究数据表明，睡眠质量在预测全因死亡率方面的重要性丝毫不亚于睡眠时长。尤其在**心理与心理健康领域**，睡眠质量展现出的预测关联性甚至显著超越了单纯的睡眠时间长短。 ```mermaid flowchart TD accTitle: 睡眠健康 QQRT 评估框架 accDescr: 展示 QQRT 模型中的两大核心支柱：睡眠数量与睡眠质量的细分评估维度 subgraph S_QUAL ["睡眠质量 (Quality)"] A["睡眠连续性 / 睡眠效率"] --> B["合格标准：在床睡眠占比 ≥ 85%"] C["深睡慢波能量 (Slow Waves)"] --> D["实验室 EEG 监测非快速眼动深睡"] end subgraph S_OUT ["健康与寿命产出"] B --> E["全因死亡率显著下降"] D --> F["强力预测心理与精神健康状态"] end ``` --- ### [42:35](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=2555s) 规律性（Regularity）：比睡眠时长更能预测死亡风险的指标 除了时长与质量，Matthew Walker 坦言自己在近年来认知转变最大、愈发坚决推崇的要素是“规律性”（Regularity）。来自英国生物样本库（UK Biobank）的一项追踪了超过 60,000 名受试者的大型前瞻性研究，彻底改写了睡眠医学界对健康指标优先级的排序。 研究人员根据受试者就寝与起床的时间浮动，将其划分为四个四分位数组： - **高度规律组**：就寝与起床时间浮动在正负 15 分钟以内，即整个作息窗口的弹性仅有 30 分钟。 - **极不规律组**：入睡时间每天波动达 90 至 120 分钟（如一晚晚上 11:00 睡，下一晚凌晨 1:00，再下一晚晚上 10:30，作息完全混乱）。 将高度规律组与极不规律组对比，所呈现的健康差异极其震撼： - **全因死亡风险相对下降 49%**； - **癌症死亡风险相对下降 39%**； - **心血管代谢疾病（Cardiometabolic Disease）风险相对下降 57%**。 更具颠覆性的是，研究人员将“睡眠时长”与“睡眠规律性”放进同一个统计模型中进行正面竞争（Walker 将其形容为一场可口可乐对百事可乐式的硬碰硬较量）。包括 Walker 本人在内的多数科学家原本押注时长会胜出，然而最终数据证明：**作息的规律性在预测全因死亡率上以明显优势击败了睡眠时长**。这并不意味着人可以每天只睡 4 小时但只要固定作息就高枕无忧，它强调的是，规律作息释放出的生物学保护信号远超以往的想象。 --- ### [45:47](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=2747s) 摆脱“垃圾光线”：7天昏暗环境与降温实验 为了帮助人们建立更好的就寝节律，Matthew Walker 总结了三步落地策略：数字戒断、固定时间就寝与起床，以及控制**夜间光照**。Walker 直言，现代社会本质上是一个“严重匮乏黑暗的社会”（dark-deprived society）。 人类夜间接触大量有害的人造光照，Walker 称之为“垃圾光线”（Junk Light，类似于垃圾 DNA 的概念）。这些不必要的人造光照射入视网膜，欺骗大脑认为外界仍是白昼，从而直接扰乱退黑素分泌与褪黑生理机制。为此，Walker 提出了一个切实可行的 **“7天睡眠提升挑战”**： - **提前 1 小时闹钟与关灯**：在计划入睡前 1 小时设定闹钟。闹钟响起时，关闭家中绝大部分灯光。Walker 分享自己的生活习惯：他和妻子会在睡前 1 小时将电视背后的氛围灯调至仅仅 5% 的微弱亮度，其余全灭，既保留防跌倒的微光，又营造彻底的昏暗。 - **环境降温**：同步将卧室环境温度调低至约 67–68°F（约 18°C）。 - **执行双向 A/B 测试**：在坚持 7 天睡前 1 小时昏睡昏暗干预后，不仅要感受自己是否更容易产生困意（催眠效应），更要在第 8 天**主动恢复原来的全开灯模式**。通过对比“干预前后”与“停止干预后”的双向表现，排除安慰剂效应，真正用身体验证昏暗环境对自身睡眠驱动力的巨大改善。 --- ### [48:28](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=2908s) 探秘大脑中枢：生物钟与下丘脑的作用机制 当被问及“为什么大脑和激素系统会对固定的睡眠时间有着如此严苛的要求”时，Walker 强调：“人们往往不遵循空洞的规则，人们遵循的是规则背后的原因（Reasons not rules）。” 为了向受众形象展示睡眠的生物学硬件，Walker 在录制现场拿出了一个真实比例的人脑结构解剖模型。他卸下大脑皮层，露出皮层下结构（Subcortical sections）： - **丘脑（Thalamus）**：位于大脑核心区域，充当着整个大脑的感觉闸门（Sensory gate），处理视觉、听觉、触觉、味觉等几乎所有外部感官信号。 - **下丘脑（Hypothalamus）**：紧挨着丘脑下方，其中深藏着统领人体 24 小时昼夜节律（Circadian Rhythm）的总指挥官——视交叉上核（主生物钟）。人体几乎所有的细胞、器官与激素释放节律，都严重依赖该中枢对恒定节律的精准同步。 ### [49:42](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=2982s) 丘脑与视交叉上核：大脑的感觉闸门与主时钟 Matthew Walker 博士首先用解剖学机制阐明了大脑如何感知外界以及如何入睡。外界的所有感官信息——视觉、听觉、味觉等——都会先涌入一个被称为“丘脑”（thalamus）的结构。丘脑扮演着感觉闸门的角色，它决定是否将这些感官信号上传至大脑皮层（cortex）。一旦信号进入大脑皮层，人便开始处理这些信息，从而产生对外部世界的意识感知。 而在入睡过程中，有趣的事情发生了：丘脑这道感官闸门会自动关闭。此时，你的眼睛在解剖学层面依然能接收光线，耳朵依然能拾取震动，舌头依然有味觉能力；但由于丘脑的闸门紧紧闭合，这些进入大脑的信号无法被传递至大脑皮层，外部世界的知觉由此中断——用通俗的话说，你睡着了。 ```mermaid flowchart TD accTitle: 感官输入与丘脑的闸门调节机制 accDescr: 展示清醒状态与睡眠状态下丘脑如何阻断或上传感觉信息至大脑皮层 subgraph AwakeState ["清醒状态"] A1["外界感官刺激<br/>（视、听、味等）"] --> B1["丘脑闸门：开启"] B1 --> C1["大脑皮层处理"] C1 --> D1["产生清醒意识与知觉"] end subgraph SleepState ["入睡过程"] A2["外界感官刺激<br/>（眼/耳继续工作）"] --> B2["丘脑闸门：闭合"] B2 -.->|阻断上传| C2["大脑皮层无信号输入"] C2 --> D2["外界知觉中断：进入睡眠"] end ``` 在丘脑的正下方是下丘脑（hypothalamus，“hypo”代表在下方）。下丘脑内有一小团极关键的神经核团，称为视交叉上核（suprachiasmatic nucleus, SCN）。虽然人体内的每一个细胞都有自己的微型分子钟，但视交叉上核就像《指环王》中统领万物的“至尊魔戒”一样，是人体内统领所有节律的“主时钟”（master 24-hour clock）。它精准调控着清醒与睡眠周而复始的24小时循环。 为了维持像石英表一样的精准度，大脑必须依赖外部信号对视交叉上核进行校准，其中最强有力的信号就是光线： - **授时因子（Zeitgeber）机制**：视网膜捕捉到光子后，会向视交叉上核发送信号，提示白天已经到来，唤醒身体节律进入上升期。虽然体温与进食也是辅助信号，但光线才是主导开关。 - **光子校准（Photon Fingers）**：光线就像一只无形的手，每天把视交叉上核那只略有偏差的发条表精准拔回24小时刻度。 - **自由运行周期漂移**：洞穴隔离实验表明，如果完全剥离光线信号，人类内在的生物钟并不是精准的24小时，而是会缓慢漂移到大约24小时15分钟左右，每天都会延后一点点。 --- ### [52:31](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=3151s) 节律调控、灯光勒克斯值与快速眼动睡眠（REM） 除了光线，身体活动与运动也是极佳的昼夜节律校准器，但前提是必须在合适的时间进行。如果在凌晨3点或4点剧烈运动，活动信号就会向大脑传递错误的白天指令，从而扰乱昼夜节律。 同理，夜间的规律性同样依赖光线管理。现代人夜晚的人造光源会严重欺骗大脑，使其误以为天还没黑。主持人 Steven Bartlett 询问是否有夜间可以安全使用的光源，比如蜡烛。Walker 博士指出，关键在于光照强度（以勒克斯 Lux 为衡量单位）： - **安全阈值**：夜间环境光最好保持在 50 lux 以下，甚至降到 30 lux 以下，这不会对生物钟造成明显干扰。可以在应用商店下载免费的 Lux 计测仪（Lux Meter）在房间里检测是否有过亮的高光点。 - **提升 18% REM 睡眠的极简策略**：一项研究显示，受试者在睡前 90 分钟将环境光调暗至 30 lux 以下并过滤掉所有蓝光（使用温暖的黄光），其快速眼动睡眠（REM sleep）足足增加了 18%。这种效果甚至无需借助任何药物。 - **行为作为锚点**：固定的就寝和起床时间是大脑最强大的行为锚点。规律的作息就像电影场景的分镜转换一样明确，不断为视交叉上核提供确定性信号，从而全面提升睡眠的时长与质量。 --- ### [55:31](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=3331s) 条件性唤醒（Conditioned Arousal）与失眠的形成 当 Steven 提到如果在床上躺三小时看 Netflix 会让大脑混乱时，Walker 博士指出了一个重要的临床概念——**条件性唤醒**（conditioned arousal）。这听起来很惹火，但其实是睡眠医学中用来解释失眠形成的核心神经机制。 大脑是一个超级联想器官。Walker 打了个形象的比方：当你第一次看牙医坐上牙医椅时，可能觉得靠背很舒服甚至蛮新鲜；但如果连去了十四五次，每次都伴随着钻牙的痛苦，下一次只要走近那把椅子，你的身体就会瞬间紧绷抗拒。床也是同理：如果你在床上除了睡觉和性生活（sleep and sex）之外，还刷手机、办公、吃饭、聊天、看电视，大脑便无法建立“床 = 睡觉”的确定性预测关系。 ```mermaid flowchart LR accTitle: 失眠维持与条件性唤醒回路 accDescr: 解释急性应激诱发失眠后，大脑如何通过在床上的清醒时间建立错误的条件反射 A["初始诱因<br/>（如亲人离世/重大压力）"] --> B["短期失眠：<br/>在床上辗转反侧"] B --> C["大脑神经联想重塑：<br/>床 = 保持清醒的地方"] C --> D["条件性唤醒建立：<br/>看到床即神经紧张"] D --> E["慢性失眠长期维持<br/>（诱因消退后依然失眠）"] ``` - **失眠的诱发与维持不同源**：许多人最初是因为突发生活变故（例如痛失亲人、极度悲痛）而失眠；但一个月后，即便悲伤逐渐缓解，失眠却留了下来。这是因为患者每晚在床上辗转反侧数小时，大脑迅速习得了“床是保持清醒的战场”这一负面关联，床反而变成了患者的“宿敌”。 --- ### [58:04](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=3484s) 破除失眠魔咒：20分钟法则与不要看钟 针对这种恶性联想，Walker 博士给出了在认知行为疗法中极为关键的操作指南——**20分钟法则**（The 20-minute rule）： - **果断离开床铺**：如果在床上躺了大约 20 分钟仍然毫无睡意，不要焦虑，也不要躺在床上硬熬。告诉自己“今晚状态不好没关系”，然后起床走到另一个光线昏暗的房间，读读书、听听播客。 - **困了再回床**：没有硬性的时间限制，直到感到真正的困倦来袭，才允许自己重新上床。通过这种方式，逐渐洗掉“床 = 清醒”的负面联想，重新建立“床 = 快速入睡”的神经反射。 - **不要看时间**：很多人饱受“凌晨 3 点惊醒”的折磨。Walker 博士反问：“你怎么知道那是凌晨 3 点？”看钟表会带来两大致命危害：第一，立即引发对第二天状态的焦虑感；第二，大脑会强化时间锚定，主动形成“我每到 3 点就必须醒来”的神经习惯。 - **放下对睡眠的控制欲**：半夜强迫自己入睡，就像拼命想回忆起一个想不起来的名字一样——你越用力，目标跑得越远。Walker 总结道：“睡眠是自然降临到你身上的事，而不是你强行制造出来的事”（"Sleep is something that happens to you. It's not something that you make happen."）。 ### [59:49](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=3589s) 睡不着时不想起身的替代方案：冥想、箱式呼吸与身体扫描 如果半夜醒来或辗转反侧却实在不想爬出温暖的被窝，马修·沃克（Matthew Walker）建议尝试几种能够平复神经的具体练习。第一种是正念冥想，手机上有很多现成的冥想 App，直接跟着一段引导音频练习即可。第二种是呼吸调节，例如经典的“箱式呼吸法”（Box Breathing），比如吸气 5 秒、屏息 6 秒、再呼气 7 秒；具体的呼吸节律数字可以因人而异，核心在于通过有节奏的深长呼吸来安抚神经系统。 第三种极为有效的方法是“身体扫描”（Body Scan）。闭上双眼，将注意力从头顶开始逐渐向下移动：感受前额是否存在紧绷感，若有便主动让它舒展放松；接着感知颈部是否有僵硬压迫，随后顺着脊柱逐步向下游走；体会两片肩胛骨沉入床垫的重量感，再把意识引导至胸口、腹部，乃至双腿与脚趾。这种自上而下逐一排查并释放躯体张力的过程，能引导整个身心一步步陷入深沉的松弛状态。 - **箱式呼吸范例**：吸气 5 秒、憋气 6 秒、呼气 7 秒，借由控制呼吸比率快速降低心率与神经亢奋度。 - **身体扫描的核心动作**：从头顶、前额、颈部一路扫描至肩胛骨、胸腔与全身，逐块肌肉主动释放蓄积的压力。 --- ### [01:00:31](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=3631s) 为什么“数羊”只会让你更清醒？加州大学伯克利分校的“心智漫步”研究 许多人从小被告知睡不着就去“数羊”，但沃克指出，科学研究证实数羊实际上是个糟糕透顶的主意，反而会让你睡得更差。加州大学伯克利分校的艾莉森·哈维（Alison Harvey）教授曾对此展开深入研究。沃克幽默地调侃道，数羊时你脑海里浮现的无非是“一团团带着古怪表情、咩咩叫着跳过栅栏的羊毛球”；每一次计数，实际上都在无形中强化并提醒你“我又浪费了一分钟没睡着”，从而引发更强烈的挫败感与焦虑。 哈维教授发现了一种行之有效的替代方案——“心智漫步”（Mental Walk）。其精髓在于在脑海中以极高的清晰度去构想一段自己无比熟悉的路线。沃克以自己带狗散步为例：在脑中具象化走到架子前、拉开门，仔细权衡“今天用红色的牵引绳还是蓝色的”，随后用右手扣上狗链，用左手推开大门，转身走下台阶……他强调，这种想象必须达到“4K 超高清的颗粒度”。 这些练习的底层共性在于“让大脑从自我关注中抽离出来”（get your mind off itself）。这就像努力回忆某个熟人的名字一样，你越是咬牙苦思越想不起来；可一旦你把注意力移开，名字瞬间就会从潜意识里蹦出来。入睡同样如此，当你全神贯注于一段逼真的虚拟漫步时，大脑不再焦虑于“怎么还没睡着”，接下来的记忆往往直接跳到了清晨闹钟响起的瞬间。 --- ### [01:02:23](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=3743s) 睡前听罪案纪录片 vs. 睡眠故事：Calm 应用的独角兽崛起之路 针对这种“转移大脑注意力”的机制，斯蒂芬·巴特利特（Steven Bartlett）打趣地承认，自己睡前喜欢听极其逼真的真实罪案（True Crime）或连环杀手纪录片。沃克忍俊不禁地提醒，如果纪录片的内容充斥着惨叫、肢体横飞和鲜血，听起来就像昆汀·塔伦蒂诺（Quentin Tarantino）的暴力美学电影，那极大概率会剧烈干扰深度睡眠；但如果听众主观上觉得这类叙事具有奇妙的安抚和催眠效果，倒也未尝不可。 这种将注意力引向外界的心理需求，直接催生了商业上的巨大奇迹。知名冥想软件 Calm 最初主打晨间冥想，业务发展平平。后来数据分析团队发现，大量用户并非在清晨使用，而是在深夜就寝前疯狂打开应用，以此来“自我治疗”失眠。团队顿悟了一个朴素的道理：人在童年时期最渴望听父母讲睡前故事入眠，成年人其实并没有什么不同。 Calm 顺势推出了“睡前故事”（Sleep Stories）功能，邀请了马修·麦康纳（Matthew McConaughey）、哈里·斯泰尔斯（Harry Styles）以及沃克等知名人士录制。这一举措让 Calm 一举扭亏为盈，成为全球首批估值突破 10 亿美元的数字健康“独角兽”企业。优美而缓慢的叙事之所以具备绝佳的催眠效果，本质上依然是成功转移了大脑内部的焦虑杂念。 --- ### [01:04:22](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=3862s) 镁元素真的能助眠吗？“捡了芝麻丢了西瓜”与血脑屏障的真相 谈及市面上炙手可热的睡眠补充剂（尤其是各种形式的镁），沃克的态度十分明确：失眠者如果把希望寄托在补充剂上，无异于“为了捡地上的几分硬币，而跨过了大把的钞票”（stepping over dollars to pick up pennies）。睡眠质量的大幅提升永远来自于底层生活方式的基石——保持作息规律、严格控制下午和晚间的咖啡因与酒精摄入、睡前调暗一半光源以及进行数码断联。 沃克从商业逻辑反推：如果世上真存在能解决所有睡眠问题的“灵丹妙药”，制药巨头早就将其收入囊中。乔治·卢卡斯（George Lucas）花了近 30 年才让《星球大战》IP 积累了约 40 亿美元收入，而处方安眠药安必恩（Ambien）仅仅用了 22 个月就达成了这一商业体量。 ```mermaid flowchart TD accTitle: 镁元素对睡眠的间接调节机制 accDescr: 展示镁元素如何通过外周肌肉松弛经迷走神经向中枢大脑传递平静信号 subgraph Peripheral["外周生理作用"] A["口服补充镁元素"] --> B["促进全身骨骼肌舒张"] end subgraph Pathway["神经通路"] B --> C["激活迷走神经 (Vagus Nerve)"] C --> D["向中枢脑干传递上行抑制信号"] end subgraph Central["中枢神经效应"] D --> E["诱导神经系统进入静止平静状态 (Quiescence)"] E --> F["间接辅助酝酿睡意"] end ``` 关于镁元素的医学证据，沃克指出了两大科学误区： 1. **血脑屏障穿透难题**：睡眠是由大脑主导的中枢活动，但市面上常见的氧化镁（Magnesium Oxide）或柠檬酸镁（Magnesium Citrate）根本无法穿透血脑屏障进入脑组织；唯一有微弱证据显示能够进入中枢的是 L-苏氨酸镁（Magnesium L-Threonate）。 2. **缺乏者获益 vs. 正常人无效**：30 年前的原始研究发现，睡眠障碍人群中部分存在严重的镁缺乏症，通过补镁恢复正常血镁水平后，其睡眠确实改善了。但这绝不意味着血镁正常的健康人超量补充会有额外的催眠收益。这如同给一个血氧饱和度已达到 98.6% 的健康人使用昂贵制氧机，无论机器多先进都不可能把血氧提到 100% 以上。盲目过量摄入，最终制造的往往只是“昂贵的尿液”。 当然，镁元素并非毫无用处，它能够促进肌肉组织放松。肌肉松弛产生的舒缓信号会通过迷走神经（Vagus Nerve）向上反馈给大脑，从而诱导中枢神经进入一种静止、平和的状态（Quiescence），由此产生间接的助眠效应。 --- ### [01:08:06](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=4086s) 应对“疲惫却亢奋”状态：南非醉茄与磷脂酰丝氨酸的作用机制 与效果被夸大的镁元素相比，沃克指出南非醉茄（Ashwagandha）与磷脂酰丝氨酸（Phosphatidylserine）在临床上有更加切实的研究数据支持。这两种成分的核心作用机理在于： - 有效抑制人体交感神经系统的过度激活（调低“战斗或逃跑”反应的亢奋阈值）； - 直接降低体内循环中的应激激素——皮质醇（Cortisol）的分泌水平。 沃克在睡眠中心频繁接诊处于“疲惫却亢奋”（tired but wired）状态的来访者。这种人虽然肉体精疲力竭，但神经系统却因高压或情绪激动而处于紧绷轰鸣状态。例如在大型舞台演讲或高强度商业谈判后，尽管已是夜里 11 点，身体极度渴求睡眠，但脑内高涨的神经兴奋性却彻底锁死了入睡通路。对于这种特定的交感神经过载状态，能够压低皮质醇与神经激惹度的补剂才能真正起到对症平抑的效果。 ### [01:09:07](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=4147s) 皮质醇节律与两类失眠的生理机制 当人体处于极度紧绷、神经紧绷（wired）而无法入睡的状态时，本质上是交感神经系统的“战斗或逃跑”（fight-or-flight）分支被过度激活。此时需要将神经系统推回平静状态，磷脂酰丝氨酸（Phosphatidylserine）与南非醉茄（Ashwagandha）等补剂能够促进副交感神经系统的恢复。然而，它们还会显著抑制皮质醇（Cortisol）。马修·沃克指出，皮质醇经常被妖魔化，但它实际上是一种至关重要的促醒激素。在健康机体中，皮质醇早在晨起前数小时便开始逐步攀升，帮助人们自然苏醒，并在上午中后段达到最高峰（crescendo），使人在不需要咖啡因的情况下保持清醒；随后其水平稳步下降，直到临睡前降至全天的最低谷（nadir）。 临床上通常将失眠划分为两种主要形式：入睡困难型失眠（Sleep Onset Insomnia，即躺下无法睡着）与睡眠维持困难型失眠（Sleep Maintenance Insomnia，即夜间频繁醒来）。对人体每 30 分钟连续监测皮质醇的研究揭示了失眠患者独特的内分泌异常： - **健康人群**：临睡前皮质醇降至最低谷，前半夜保持极低水平。 - **入睡困难患者**：上午的皮质醇分泌曲线正常，但在临睡前却反常地再度飙升，阻断了向睡眠状态的平稳过渡。 - **睡眠维持困难患者**：尽管前半夜皮质醇处于低位，但在半夜时分却出现异常的高尖峰，直接导致夜间惊醒且难以重返睡眠。 ### [01:11:39](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=4299s) 赞助商插播：LinkedIn 广告投放精准度 主持人史蒂芬·巴特利特分享了与诸多创业者交流时的痛点：很多广告投放效果不佳并非因为文案或创意不足，而是因为信息未触达目标受众。在 B2B 营销领域，触达精准人群尤为关键。LinkedIn 广告网络拥有超过 10 亿职场人士，其中涵盖约 1.3 亿核心决策者，支持根据职位头衔、资历级别、公司规模、行业乃至个人专业技能进行高精度定向投放，并带来了卓越的广告支出回报率（ROAS）。 ### [01:12:41](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=4361s) 睡眠的四大模块与睡眠脑电图（Hypnogram）的过山车机制 史蒂芬提到从马修·沃克的研究中得到启发，认识到早晨醒来前的“最后一个小时”可能是床上最具价值的一小时。他的伴侣过去习惯只睡 6 到 6.5 小时便早起，这在一定程度上源于贪睡引发的内疚感；但在了解睡眠后半程富含快速眼动睡眠（REM）后，他鼓励她睡满整整 8 小时。为了系统解释这一现象，沃克借助睡眠脑电图（Hypnogram）详细剖析了夜晚睡眠阶段的循环交替： ```mermaid flowchart TD accTitle: 睡眠周期的阶段流转图 accDescr: 展示从入睡到深度睡眠再上升至REM睡眠的过山车式交替循环 subgraph Wake_Trans["入睡阶段"] S1["非快速眼动1期 (NREM 1)<br/>过渡桥梁 (10-15分钟)"] end subgraph Deep_Descent["深层巩固阶段"] S2_Down["非快速眼动2期 (NREM 2)<br/>认知处理 (15-20分钟)"] S3["深度非快速眼动3期 (NREM 3)<br/>慢波深度睡眠 / 记忆固化与身体修复"] end subgraph Rise_REM["回升与做梦阶段"] S2_Up["非快速眼动2期 (NREM 2)<br/>上升过渡"] REM["快速眼动睡眠 (REM)<br/>情绪处理 / 梦境 (初次约10分钟)"] end S1 --> S2_Down S2_Down --> S3 S3 --> S2_Up S2_Up --> REM REM -.->|"开启下一周期 (平均90分钟)"| S2_Down ``` - **非快速眼动 1 期（NREM 1）**：这是清醒与真正睡眠之间的过渡阶段，被称为美妙的“阈限状态”（liminal state）。如果在此阶段被叫醒，人们通常会声称“我根本没睡着”。该阶段极其短暂，通常仅持续 10 到 15 分钟。 - **非快速眼动 2 期（NREM 2）**：沃克称之为“睡眠的主力军”（the workhorse of sleep），整夜大约有 50% 的时间处于此阶段。尽管常被称为浅睡期，但大脑在此期间进行着大量的认知信息加工，绝非只是通往深睡的垫脚石。 - **深度非快速眼动 3 期（NREM 3 / 慢波睡眠）**：进入睡眠后的前几个小时，脑电波显著变慢但振幅变得极其庞大。这种强有力的低频慢波就像长波无线电广播，能够在全脑大范围内高效传输信息。在此期间，大脑按下“保存键”，将新学到的脆弱记忆从短期存储库（海马体）永久转存至长期存储区（大脑皮层），实现对新知识的“未来防御”（future-proof），同时机体的大多数主要生理系统在此阶段完成深度修复与再生。 在完成深度慢波睡眠后，脑波并不会直接跳入 REM，而是像坐过山车一样重新升回非快速眼动 2 期，随后在入睡约 70 至 80 分钟时首次触发短暂的 REM 快速眼动睡眠（约 10 分钟）。 ### [01:17:26](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=4646s) 90分钟周期的个体差异与睡眠硬件误区 虽然大众科普常将睡眠周期简化为固定的“90 分钟非快速眼动与快速眼动循环”，但沃克直言这是一个被普遍误解的硬伤。90 分钟仅仅是整个人群的**平均数值**，在真实的个体之间，一个完整的睡眠周期跨度可以在 70 分钟至 120 分钟之间大幅波动。 因此，市面上许多声称能够通过算法在 90 分钟周期节点将人精准唤醒的床头智能硬件或闹钟，由于建立在刻板的平均假设之上，往往无法精准匹配个体每晚动态变化的神经电生理节奏。更关键的是，非快速眼动与快速眼动的比例在整夜进程中不断演变：前半夜绝大部分时间被深睡慢波占据，而快速眼动睡眠则绝大部分密集堆积在后半夜乃至清晨的最后一个周期中。 ### [01:18:20](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=4700s) 睡眠周期的动态变化与清晨 REM 睡眠的断崖式损失 许多睡眠监测应用声称能计算出唤醒用户的“完美时刻”，马修·沃克（Matthew Walker）直斥这种说法纯属“无稽之谈”（nonsense）。这类软件往往机械地套用固定的 90 分钟周期，但现实中每个人的周期差异极大——有的短至 75 分钟，有的则长达 105 分钟。虽然人类确实以大约 90 分钟为一个轮次在非快速眼动（NREM）睡眠与快速眼动（REM）睡眠之间循环往复，但这两种睡眠状态的比例在整晚并不是一成不变的，而是随着夜色深浅发生动态倾斜。在前半夜，睡眠周期几乎被大量深度的 NREM 慢波睡眠占据，REM 睡眠极少；而到了后半夜，天平彻底倒向另一侧，大脑将大部分时间投入到 REM 睡眠中，尤其是在苏醒前的最后两个小时达到顶峰。 这种倾斜机制带来了极具现实意义的后果。沃克举例说，假设一个人习惯于午夜 12 点入睡、早上 8 点起床，若第二天为了赶早班飞机提前两小时在 6 点起床，从绝对时间来看，他损失了 2 个小时，即总睡眠时长的 25%。然而在睡眠结构上，他可能直接被剥夺了整晚 50%、60% 甚至 70% 的全部 REM 睡眠。正因如此，了解睡眠周期不仅仅是学术探讨，更是极其实用的健康策略。如果有人想在日常生活中以最高效的方式增加 REM 睡眠，最简单的方法其实就是“比平时晚起 15 分钟”，这 15 分钟会以不成比例的高概率直接转化为纯粹的 REM 睡眠。 - **应用算法漏洞**：商用闹钟应用强行预设 90 分钟周期，无法适应人体 75 至 105 分钟的个体差异。 - **前半夜 vs 后半夜**：前半夜由深度 NREM 睡眠占主导，后半夜（尤其是临醒前的最后 2 小时）绝大部分为 REM 睡眠。 - **睡眠削减的不对称性**：提前 2 小时醒来虽然只减少了 25% 的睡眠总时长，但会损失高达 50%–70% 的 REM 睡眠。 --- ### [01:20:17](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=4817s) REM 睡眠的大脑活动与每晚必经的“精神病态” REM 睡眠并非大脑静止休息的状态，恰恰相反，此时大脑部分脑区处于极度活跃的狂暴放电中。沃克拿出一个可拆解的人脑模型形象地展示，位于大脑深层、紧挨着脑干上方的边缘系统（Limbic system）——包括掌管情绪的核心“杏仁核”（Amygdala，左右半球各一个）以及紧邻的记忆中枢“海马体”（Hippocampus）——在做梦时活跃度比清醒时还要高出整整 40%。虽然广义的梦境可以定义为“醒来时报告的任何思维活动”（在浅睡或深睡期被唤醒，人们可能只会报告“我刚才在想你下次什么时候来叫我”这种平淡想法），但大众真正认知的那种色彩斑斓、情节跌宕的故事性梦境，全部诞生于 REM 睡眠之中。 沃克半开玩笑地对史蒂文下了一个戏剧性的诊断：“昨晚入睡进入做梦阶段时，你其实陷入了极度严重的精神病态（incredibly psychotic）。”他列举了判断精神疾病的五大经典临床指标，证明每个人在做梦时都在经历这趟“疯狂之旅”： 1. **幻觉（Hallucinations）**：看到了根本不存在的事物； 2. **妄想（Delusions）**：深信某些完全不合常理、绝不可能发生的事情； 3. **定向障碍（Disorientation）**：在时间、地点和人物关系上彻底错乱混乱； 4. **情绪不稳（Emotional Lability）**：情绪呈现出剧烈、不可控的大起大落； 5. **遗忘症（Amnesia）**：早晨醒来时，几乎将昨晚经历的一切忘得一干二净。 如果在白天清醒时出现上述任何一种症状，任何人都必须立刻寻求精神科的心理援助；然而在夜间睡眠中，这种看似疯狂的状态却是维系心理健康至关重要的生理与神经机制。 --- ### [01:22:51](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=4971s) 夜间心理治疗机制：剥离痛苦记忆的情绪外皮 人类为何需要做梦？沃克指出，梦境的第一大核心功能是充当“情绪急救箱”与“夜间心理治疗”（overnight therapy）。梦境就像一层温和的夜间神经舒缓膏，抚平那些艰难、痛苦的情绪创伤，使其尖锐的棱角变得圆润。其最终目的在于，当第二天重新回想起这段负面经历时，大脑依然保留着关于事件本身的客观记忆，但不再伴随当初那种令人反胃、心悸的内脏生理情绪应激反应。用沃克的话来说，REM 睡眠负责“将苦涩的情绪果皮从信息的橙子肉上彻底剥离”（strip the bitter emotional rind from the informational orange）。 这一神奇疗愈过程背后的神经化学开关在于：REM 梦境睡眠是人类在整整 24 小时周期中，大脑完全关闭应激神经递质“去甲肾上腺素”（Noradrenaline）的唯一时刻。在人体内，肾上腺素负责引发心跳加速的“战斗或逃跑”应激；而在中枢大脑内部，与之对应的正是去甲肾上腺素。当进入 REM 睡眠时，大脑的情绪中枢杏仁核与记忆中枢海马体被重新激活，强行回放并再处理白天的情感经历。但极其关键的是，这一过程发生在一个去甲肾上腺素彻底归零的“绝对安全神经化学温室”中。大脑借此得以在一个没有恐慌与压力的环境下重塑突触连接，安全地将情绪毒素从记忆本体中洗脱。 ```mermaid flowchart TD accTitle: REM Sleep Overnight Therapy Mechanism accDescr: Flowchart contrasting healthy REM emotional processing with PTSD nightmare cycles. subgraph Healthy["健康 REM 睡眠：夜间情绪疗愈"] A["再激活边缘系统<br/>（杏仁核 + 海马体回放记忆）"] --> B["神经化学安全环境<br/>（去甲肾上腺素浓度降至 0）"] B --> C["情绪与事实记忆解耦<br/>（剥离苦涩的情绪果皮）"] C --> D["醒来保留客观记忆<br/>但消除内脏应激反应"] end subgraph PTSD["PTSD 创伤患者：机制崩溃"] E["夜间去甲肾上腺素浓度过高<br/>（应激系统无法关闭）"] --> F["创伤记忆高负荷回放<br/>未能实现情绪剥离"] F --> G["大脑次日再次请求修复<br/>但反复失败"] G --> H["形成'破唱片'效应：<br/>陷入顽固的重复性恶梦"] end ``` --- ### [01:24:46](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=5086s) PTSD 创伤梦魇的根源与降压药哌唑嗪的意外突破 这种夜间心理治疗机制一旦失效，其最典型的临床病症便是创伤后应激障碍（PTSD）。PTSD 患者不仅表现出严重的 REM 睡眠结构破坏，更陷入了一种“永远无法走出来”的痛苦循环中。例如退伍老兵走出超市停车场，听到汽车排气管回火的爆鸣声，便会瞬间产生极其强烈的创伤倒叙（flashback），仿佛重回战火纷飞的爆炸现场。这正是因为大脑未能剥离情绪与记忆的关联，导致每次提取记忆时都会全盘复发原始的生理惊恐。为此，大脑在每个夜晚尝试重新介入，试图在梦中修复创伤，但由于 PTSD 患者脑内的去甲肾上腺素基线浓度异常过高，梦境无法提供无毒的神经化学安全环境。修复再三失败，大脑只能夜复一夜地重复调用这段未解的创伤，最终表现为如同“磨损的破唱片”一般反复发作的恶梦。 多年前，沃克在学术会议上刚发表这一理论假说、正苦于寻找临床数据支撑时，遇到了一个让他“脊背发凉、汗毛直立”的惊人巧合。来自西雅图附近普吉特海湾退伍军人事务部（Puget Sound VA）的一位精神科医生在同一场会议上分享了他的临床困惑：该医生原本只是给患有 PTSD 的退伍老兵开具一种廉价且能穿透血脑屏障的常用降压药——哌唑嗪（Prazosin）。结果出人意料的是，老兵们的血压并没有太大改善，但几乎所有人都反馈他们长年遭受的创伤性恶梦开始成群消失，睡眠质量和精神状态均大幅好转。这名医生在无意中降解了患者脑内多余的去甲肾上腺素，打破了阻碍大脑正常进行夜间创伤疗愈的生化枷锁，从而以最富戏剧性的方式证实了沃克的睡眠理论。 - **PTSD 核心缺陷**：由于大脑去甲肾上腺素过高，无法在 REM 睡眠中剥离应激反应，形成重复性创伤恶梦。 - **降压药临床偶然**：退伍军人事务部医生使用降压药哌唑嗪（Prazosin），原本旨在治疗高血压，却因药物穿透血脑屏障降低脑内去甲肾上腺素，意外治愈了老兵的顽固性恶梦。 ### [01:27:19](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=5239s) 创伤后应激障碍与恶梦的药物救赎：去甲肾上腺素与哌唑嗪 在创伤后应激障碍（PTSD）患者的大脑中，快速眼动（REM）睡眠期间的去甲肾上腺素水平异常偏高，导致大脑无法剥离创伤记忆中的痛苦情绪。然而，一位研究人员在临床中使用一种降压药物（哌唑嗪，Prazosin）治疗患者时，无意中降低了他们 REM 睡眠时的去甲肾上腺素水平。这一偶然发现，使该药物最终成为了美国退伍军人事务部（VA）极少数获批用于治疗反复发作性恶梦的处方药之一。其核心机制在于：药物压低了过高的去甲肾上腺素，让大脑终于能够进入一个化学意义上的“安全状态”。 马修·沃克（Matthew Walker）博士回忆道，当时那位学者手里拥有寻找理论解释的临床数据，而沃克自己手里恰好有一套寻找临床证据的科学假说。沃克在对方做完演讲后立即冲上前去对他说：“我想我知道你为什么会看到这种结果了。”随后，沃克邀请他飞往加州大学伯克利分校，两人整整讨论了一天并共进晚餐，后来那位学者进一步开展了正规临床试验。不过沃克强调，这种药物绝非包治百病的灵丹妙药，并不是对所有人都起效。 --- ### [01:28:16](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=5296s) 意象重演疗法（IRT）与记忆再巩固机制 针对恶梦的治疗，如今有了比药物更强大、更有效的非药物手段——意象重演疗法（Image Rehearsal Therapy, 简称 IRT）。这项疗法依托于人类记忆科学在约二十年前的一项重大突破：记忆再巩固（Memory Reconsolidation）。沃克用文字处理软件打了生动的比方：如果每次你打开一个 Word 文档敲完字并点击保存，第二天再次双击该文档时却被系统锁死、无法编辑，那将是一个极度拙劣的信息储存系统。人类的记忆恰恰相反——第一次经历并入睡保存叫“记忆巩固”；当你清醒时重新调取该记忆，就如同“双击打开了文档”，记忆会重新回到脆弱、易塑的可编辑状态；随后你修改了内容，并在下一个夜晚的睡眠中将其重新保存，这就是“再巩固”。 在临床治疗由创伤引发的恶梦时，这一机制被发挥到了极致。例如，一位经历过惨烈车祸（刹车失灵、闯红灯被侧面撞击受重伤）的患者，每晚都会在恶梦中反复重现车祸全过程。在 IRT 疗法中，患者在治疗师的引导下，大声重述那个梦境，即“重新激活脆弱的创伤记忆”；紧接着，治疗师引导患者改写故事结局——比如在剧本中加入“你低头发现车里还有一个手动机械手刹”，于是患者在脑海中逐渐拉起手刹，将车稳稳停靠在路边，避免了车祸。通过白天不断调取并改写叙事，夜间睡眠就会以改写后的安全脚本重新巩固记忆，从而逐步化解恶梦的恐怖烈度。 ```mermaid flowchart TD accTitle: 意象重演疗法与记忆再巩固机制 accDescr: 展示从创伤记忆激活、治疗性改写叙事到夜间睡眠再巩固以化解恶梦的完整过程。 subgraph MemoryReactivation["记忆激活阶段"] A["固化创伤记忆<br/>（原初车祸惨剧）"] --> B["主动唤醒口述<br/>（双击打开Word文档）"] B --> C["记忆进入脆弱易塑状态"] end subgraph NarrativeRewriting["叙事重塑阶段"] C --> D["引入可控应对<br/>（拉起手刹平稳停车）"] D --> E["改写创伤剧本与情感关联"] end subgraph Reconsolidation["夜间再巩固"] E --> F["入睡经历 REM 睡眠"] F --> G["安全脚本重新储存<br/>（恶梦发生率与烈度消退）"] end ``` --- ### [01:31:00](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=5460s) 坏梦与恶梦障碍的区别：自杀倾向的“金丝雀”预警 沃克厘清了普通“坏梦”（Bad Dreams）与临床“恶梦障碍”（Nightmare Disorder）的界限。普通人都会做坏梦，但往往频率很低，可能一个月或几个月才偶发一次。然而，恶梦障碍有着极其严苛的医学定义：恶梦发作频繁（通常每周至少两次），会直接将人从熟睡中惊醒，醒来后具有极其生动的细节回忆，并且引发显著的日间痛苦，甚至让人产生绝望感或生命不值得活下去的念头。沃克郑重呼吁，一旦恶梦引发日间绝望，必须立即寻求专业医疗救助。 睡眠实验室的流行病学数据揭示了令人震惊的危险关联： - 睡眠时间严重不足（每晚少于 6 小时）会使自杀念头、自杀未遂乃至自杀身亡的风险上升 100% 至 150%。 - 相比之下，长期遭受频繁恶梦困扰的人群，其自杀倾向与行为的风险暴增了整整 800%。 沃克指出，研究界并不认为恶梦直接导致了自杀行为，恶梦更像是心理危机中“煤矿里的金丝雀”（canary in the coal mine）。它是夜间睡眠脑电杂音中泄漏出的最敏感的危险警报信号，是心理崩溃的极度危险的生物标记物（biomarker）。 - 坏梦与恶梦障碍的区别在于发生频率（恶梦至少每周 2 次）、强行惊醒、梦境清晰留存以及导致严重的日间功能受损与绝望。 - 短睡眠使自杀相关风险增加 1 至 1.5 倍，而频繁恶梦则将自杀风险直接推高 8 倍。 - 恶梦是监测重度抑郁与自杀危机的核心临床哨兵指标，具备可干预性，患者无需默默承受。 --- ### [01:33:23](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=5603s) 做梦的情绪疗愈价值：罗莎琳·卡特赖特的突破性研究 当被问及恶梦究竟是睡眠系统的功能障碍还是具有适应性价值的信号时，沃克解释称，反复发作的创伤恶梦确实是情绪脱敏系统崩溃的标志；事实上，反复性恶梦在 PTSD 中具有如此高度的一致性，以至于它本身就是确诊 PTSD 的核心诊断依据之一。然而，对于健康人群的常规做梦（甚至是轻度的不愉快梦境），现代脑科学证实它扮演着“情绪急救”（Emotional First Aid）的关键角色。 已故杰出睡眠科学家罗莎琳·卡特赖特（Rosalind Cartwright）曾进行过一项里程碑式的长期追踪研究。她招募了一批因经历丧亲之痛或经历痛苦离婚而罹患抑郁症的患者，记录他们每晚的梦境日记，并持续跟踪了一整年。12 个月后，结果出现了截然对立的两极分化：大约一半的患者彻底从抑郁症中康复，另一半则依然深陷抑郁泥潭。当卡特赖特回头对比这两组患者最初的梦境数据时，得出了一个惊人发现： - 能够摆脱抑郁并获得临床缓解的患者，在事发之初做梦时，**梦境内容直接围绕着那个痛苦的创伤事件本身**展开。 - 未能康复的患者虽然同样拥有充足的快速眼动睡眠（REM）并且也在做梦，但他们的梦境内容与现实中的创伤经历毫不相关。 这项试验证明，仅仅拥有 REM 睡眠是不够的；大脑必须在梦境中“亲自处理并直面那个痛苦事件”，才能实现情绪疗愈。面对主持人提出“遭遇人生变故时是否应该在睡前强迫自己思考这件事”的疑问，沃克笑着表示“是也不是”。人类经历了大约 340 万年的演化才形成了独一无二的睡眠与梦境机制，这套经历数百万年打磨的系统比任何人都更懂得如何安排夜间梦境的“播放列表”，人们无需刻意强求或干预。 --- ### [01:36:40](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=5800s) 做梦的第二大功能：信息炼金术与创造力 沃克总结道，做梦的第一项核心功能是经过扎实科学验证的“情绪急救箱”，帮助人类剥离痛苦经历的剧烈情绪外壳。紧接着，他引出了快速眼动睡眠完全独立但同样震撼的第二大核心功能：做梦是人类大脑内部的“信息炼金术”（Informational Alchemy），是创造力与顿悟思维的终极孵化器。深度非快速眼动睡眠（Non-REM）负责记忆的粗暴留存与整理，而快速眼动睡眠中的梦境，则开始将这些看似毫不相干的记忆碎片进行跨维度的重组与碰撞。 ### [01:36:54](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=5814s) 快速眼动睡眠（REM）：记忆的“团体心理治疗”与创造力之源 Matthew Walker 博士深入剖析了睡眠对记忆处理的双重阶段机制。在慢波深睡眠（Deep Sleep）阶段，大脑会将白天新学到的信息固定下来，如同“将化石封存在琥珀中”，妥善保存每一个独立的知识片段。紧接着到来的快速眼动睡眠（REM Sleep，即做梦睡眠）则开启了记忆处理的第二阶段：它将这些新获取的碎片，与我们脑海中既有的庞大信息“过往目录”（back catalog）彻底融为一体。醒来时，你的大脑已经建立起一个全面修订的“全脑联想网络”（mind-wide web of associations），使我们能够推导出之前看似无解难题的解决方案。 ```mermaid flowchart TD accTitle: 记忆巩固与整合的双阶段睡眠模型 accDescr: 展示从清醒学习、深睡眠化石般封存，到REM睡眠融会贯通产生创造力的过程。 subgraph S1["第一阶段：深睡眠 (Deep Sleep)"] A["白天获取的新记忆碎片"] --> B["如琥珀封存化石般固定记忆"] end subgraph S2["第二阶段：REM 睡眠 (做梦阶段)"] B --> C["记忆的'团体心理治疗'"] C --> D["远距离、非线性的联想碰撞"] D --> E["拼图完成：唤醒全新解题洞察"] end ``` Walker 将 REM 睡眠生动地比喻为“记忆的团体心理治疗”（group therapy for memories）——白天输入的所有信息都来到这里佩戴上姓名胸牌互相结识。然而，不同于清醒状态下的严谨逻辑关联，REM 睡眠更像是一场“跑偏的谷歌搜索”：你输入检索词“CEO的日记”（Diary of a CEO），它却直接把你带到了搜索结果第 20 页一条看似风马牛不相及的内容——犹他州的一场曲棍球比赛。当你困惑这两者有何关联时，细究才会发现原来是当地一位著名 CEO 拾获了一本遗失已久的日记，而他恰好正在现场观赛。梦境正是凭借这种跨越遥远距离、非显而易见的连接在运作。正如人们常带著零散的拼图碎片入睡，醒来时拼图却已完整拼就。 这种将原本不搭界的事物融合在一起的能力，偶尔会在进化适应度上带来显著飞跃，而这正是人类“创造力”（creativity）的生物学基石。Walker 指出，世界上没有任何一种文化或语言会劝你“在难题上死撑着别睡”，大家说的都是“睡一觉，明天再说”（Sleep on a problem）。从法语到斯瓦希里语，这一概念在各种语言中广泛存在，证明睡眠对创造力的赋能是超越文化边界的智人共通体验。 - **深睡眠与 REM 睡眠的分工**：深睡眠负责单个记忆片段的坚固固化；REM 睡眠负责跨时间跨度的网络联想与全局整合。 - **全脑联想网络**：REM 睡眠创造出的非显性认知桥梁，是解决棘手复杂问题的关键。 - **文化普适性**：跨越语种和地域，“睡上一觉再做决定”是人类对抗思维僵局的共有认知本能。 --- ### [01:39:10](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=5950s) 商业赞助环节：工作负载与个人创业平台 本段穿插了播客节目的赞助内容： - **Pipedrive**：针对中小型企业设计的客户关系管理（CRM）工具。Steven Bartlett 提到销售和商务人士背负着繁重杂乱的“隐形认知负担”（会议记录、时间节点管理等），团队引入 Pipedrive 旨在减少行政琐碎事务，让员工专注于客户沟通与业务推进。该工具已在全球 170 多个国家的 10 万多家企业中应用。 - **Stan Store**：由 Steven Bartlett 共同拥有的数字创作者与个人商业变现平台，支持创作者在几分钟内搭建销售数字产品、咨询、社群和会员资格的个人主页，无需处理复杂的建站技术问题。 --- ### [01:41:04](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=6064s) 反乌托邦未来：“短睡眠基因”携带者与基因工程的伦理隐忧 在探讨不同睡眠人群的诉求时，Steven Bartlett 询问在优化者、不良习惯者和睡眠障碍患者之外，还有什么至关重要却尚未涉及的话题。Matthew Walker 提出了一个极具颠覆性的命题——“反乌托邦式的未来”，其核心源自近年来睡眠科学界最轰动的发现：天然“基因型短睡眠者”（genetic short sleepers）。这类人群由于天生携带特定的基因突变，每晚仅需睡 6 小时 15 分钟（即 6.25 小时）甚至更少，其大脑和身体功能完全不受任何损害，且不会产生常规睡眠不足所带来的严重慢性病风险。 目前科学家已经确认了 4 个相关基因，其中包括最早发现的 **DEC2** 基因以及 **ADRB1** 基因（Walker 幽默地调侃 ADRB1 的名字听起来像 Radiohead 乐队的新专辑）。针对许多听众可能侥幸认为自己也是天选之人的心理，Walker 列举了极具冲击力的数据：普通人在一生中被雷劈中的概率约为 0.0064，而拥有 ADRB1 短睡眠基因的概率仅为 0.004。也就是说，一个人被雷劈中的概率在统计学上明显高于拥有该突变基因的概率。 ```mermaid flowchart LR accTitle: 普通人与短睡眠基因携带者的生理觉醒对比 accDescr: 比较普通人白天的疲惫波动和低效率睡眠，与基因携带者全天恒定高觉醒和极高深度的睡眠。 subgraph Normal["普通人群 (普通调光开关)"] N1["白天觉醒度波动 (80%至疲倦下滑)"] N2["夜间睡眠效率相对波动 (约85%)"] end subgraph Mutant["短睡眠基因人群 (全开/全关硬开关)"] M1["白天强力觉醒 (17-18小时保持100%清醒)"] M2["夜间极速进入深度沉睡 (超高睡眠效率)"] end ``` 通过基因编辑与机制研究，科学家揭开了这些“超人”背后的生理奥秘： 1. **日间觉醒驱动极强**：普通人的清醒状态像一个“调光开关”，白天觉醒度通常在 80% 左右波动，中途会出现明显的精力低谷与困顿；而短睡眠者的清醒状态如同一个“硬开关”，白天全天维持 100% 的极度明亮清醒，连续保持 17 至 18 小时的充沛活力毫无压力。 2. **夜间睡眠深度与效率极高**：进入睡眠后，他们的睡眠效率远超普通人推荐的 85% 基准线，几乎全部睡眠时间都是极其扎实、深沉的深睡眠与优质睡眠，睡眠浓缩且深度极大。 当探讨能否通过基因编辑将所有人类都改造成这种短睡眠体质时，Walker 表达了他深层的恐惧。尽管在资本主义社会框架下，少睡被视为终极梦想——因为人在睡眠时“既不生产也不消费”，消灭睡眠似乎能极大释放生产力并刺激消费——但 Walker 一针见血地指出这是一种危险的“睡眠货币贬值”（sleep currency inflation）。 他警告道，社会博弈是残酷的：“一旦 6 小时变成新的 8 小时标准，人们立刻就会开始只睡 4 小时；而当我找到让人只需睡 4 小时的基因突变时，大家又会以此类推压缩到 2 小时。”在竞争激烈的社会内卷中，人类只会把生理底线当成压榨自我的新跳板，使睡眠专家永远处于疲于奔命、被动防御的恶性循环之中。 - **基因发现**：已确认至少 4 个短睡眠基因，代表性基因包括 DEC2 和 ADRB1。 - **罕见程度**：携带 ADRB1 基因突变的概率（0.004）比一生中被雷电击中的概率（0.0064）还要低。 - **生理特质**：17-18 小时全功率清醒无波动、入睡极深、睡眠效率极高。 - **社会伦理风险**：基因改造无法终结睡眠剥夺，只会在全社会引发睡眠底线的内卷通胀，带来更加病态的过度压榨。 ### [01:48:42](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=6522s) 基因短睡眠者与检测方式 短睡眠基因携带者展现出惊人的睡眠密度与极强的清醒驱动力。他们是效率极高的睡眠者，普通人需要 8 小时才能完成的睡眠修复，他们仅需 6 小时就能全部搞定。 对于如何确定自己是否属于这种罕见体质，Dr. Matthew Walker 指出，用户并不一定非要走进专业的睡眠实验室。如果之前做过商业基因检测（如 23andMe 等），许多服务都支持下载原始数据（raw data）。用户可以将这些原始数据上传到名为 Promethease 的基因数据分析平台。尽管该平台界面老旧、略显极客且粗糙，输出的报告长达数十页且毫无商业修饰，但它能直接检索关键的短睡眠基因突变，例如 DEC2 基因或 ADRB1 基因的特定突变型，从而明确自己到底是不是天生的短睡眠者。 ### [01:50:06](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=6606s) 睡眠不足如何摧毁食欲控制与身体成分 当话题转向断食与生酮饮食（Ketosis）等饮食状态对睡眠的影响时，Dr. Matthew Walker 指出饮食与睡眠之间存在强烈的双向作用：你吃什么固然会改变你的睡眠，但更具决定性的是，你的睡眠状况会剧烈重塑你的进食冲动以及身体对热量的代谢处理方式。 人在缺觉时对高热量垃圾食品产生强烈渴望，这背后是由两种关键的食欲激素决定的——瘦素（Leptin）与脑肠肽（Ghrelin）。Dr. Matthew Walker 幽默地形容它们听起来就像《指环王》里的霍比特人： - **瘦素（Leptin）**：向大脑发送“饱腹、停止进食”的信号。缺觉状态下，瘦素分泌受损骤降，大脑失去了饱腹信号。 - **脑肠肽（Ghrelin）**：刺激胃部咕咕作响并发出“饥饿、需要继续吃”的信号。缺觉状态下，脑肠肽水平显著飙升。 两者的反向变动使缺觉者的饥饿感暴增 30% 到 40%。雪上加霜的是，睡眠剥夺还会改变热量的分配去向：摄入的卡路里更倾向于以脂肪的形式堆积（尤其是腹部脂肪），而不是作为糖原储存在肌肉中。一项针对节食减肥人群的对比研究显示，无论睡眠充足与否，两组人减轻的总体重几乎完全相同；然而，睡眠不足的节食者所减轻的体重中，有高达 70% 来自于瘦肌肉组织，而非多余的脂肪。换句话说，缺觉减脂的结局是“留下了你想减掉的脂肪，丢掉了你想保留的肌肉”。 ```mermaid flowchart TD accTitle: 睡眠不足对食欲与身体成分的影响机制 accDescr: 展示睡眠剥夺如何通过激素失调与能量储存偏向导致肌肉流失和脂肪堆积 subgraph Hormones["激素失衡"] A["睡眠剥夺 / 缺觉"] --> B["瘦素 (Leptin) 下降<br/>失去饱腹信号"] A --> C["脑肠肽 (Ghrelin) 上升<br/>饥饿信号暴增"] B & C --> D["饥饿驱动力上升 30% - 40%"] end subgraph BodyComp["热量代谢与身体成分"] D --> E["热量摄入增加"] A --> F["热量代谢偏向改变"] F --> G["偏好转化为脂肪储存 (如腹部脂肪)"] F --> H["减重时 70% 减掉的是瘦肌肉"] end ``` ### [01:53:00](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=6780s) 断食、生酮与食欲素的觉醒机制 在谈及生酮与断食对睡眠的影响时，主持人分享了自己进入生酮状态时睡眠时长会骤降到 5 至 6 小时、Whoop 睡眠评分大幅暴跌的生理冲击。Dr. Matthew Walker 解释，这与一种名为食欲素（Orexin，又称下丘脑泌素）的促清醒神经化学物质直接相关。 从进化生物学角度来看，人类在远古时期唯一被迫缩短睡眠的场景就是面临热量匮乏。当身体处于断食或热量赤字时，大脑会误以为个体正陷入饥荒困境。为了确保生存，大脑不会允许机体安心入睡，而是大量释放食欲素，强制维持中枢神经系统的亢奋清醒，以此驱动生物体保持更长时间的觉醒状态去寻找食物。虽然现代人断食是一种主动健康选择，但大脑的进化机制并不能区分主动节食与被动挨饿。 这种生理机制在嗜睡症（Narcolepsy）患者身上体现得尤为透彻。与断食者体内食欲素过量导致的过度清醒恰好相反，嗜睡症患者是因为大脑中缺乏食欲素，导致他们无法维持稳定的日间清醒状态，会在白天不受控制地突然陷入沉睡。 ### [01:54:23](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=6863s) 从镇静剂到食欲素受体拮抗剂（DORAs）：睡眠药物的代际革新 失眠症的本质恰好与嗜睡症互为镜像：嗜睡症是患者在想要清醒的白天被迫入睡，而失眠症则是患者在渴望入睡的夜晚被迫清醒。这一认知催生了睡眠医学领域的革命性突破，Dr. Matthew Walker 将睡眠药物的发展形象地划分为三个代际： 1. **睡眠药物 1.0 时代（苯二氮䓬类）**：如安定（Valium）、阿普唑仑（Xanax）等，对于修复睡眠结构并不理想。 2. **睡眠药物 2.0 时代（非苯二氮䓬类 Z-drugs）**：如安必恩（Ambien）、鲁奈斯塔（Lunesta）、索纳塔（Sonata）等。1.0 与 2.0 代药物的作用路径相似，它们作用于大脑皮层的 GABA 受体（大脑主要的中枢抑制性神经递质受体），通过强行按死皮层神经元电活动的“红灯”来麻醉大脑。这种状态在医学上属于化学镇静（sedation），而“镇静绝非自然的睡眠”，许多服药者只是将失去意识的镇静状态误认为了睡眠。 3. **睡眠药物 3.0 时代（双重食欲素受体拮抗剂，DORAs）**：这是 Dr. Matthew Walker 明确表态认可并看好的全新一代失眠治疗药物。目前已有三种获得 FDA 批准的代表性药物： - 苏沃雷生（Suvorexant） - 莱姆博雷生（Lemborexant） - 达利雷生（Daridorexant） 与传统药物简单粗暴地用化学手段镇静大脑皮层截然不同，DORAs 类药物犹如一双灵巧的“生化手指”，直接深入脑干部位的食欲素中枢。它们并不强加睡意，而是精准调低促使大脑清醒的“音量旋钮”，在消除过度觉醒驱动力之后抽身退场，让机体自身的“天然真实睡眠”（Naturalistic Sleep）自然而然地接管大脑。临床数据已充分证实这类药物在延长睡眠时间方面的卓越有效性。 ### [01:58:12](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=7092s) DORA类新药与脑部排毒：摆脱“垃圾睡眠” 马修·沃克（Matthew Walker）从科学家的严谨甚至挑剔的视角指出，评价一种新型助眠药物绝不能仅看它是否延长了总睡眠时间或提高了睡眠效率。他提出了犀利的质疑：“那又怎样？就算它给你的夜晚增加了睡眠时间，我们怎么知道那是具有生理功能的睡眠，而不是像无效基因一样的‘垃圾睡眠’（junk sleep）？”为了验证新型DORA药物（双食欲素受体拮抗剂）带来的睡眠是否真正具有生理效益，科研人员开展了一项极具开创性的临床试验。人体大脑在深度非快速眼动睡眠（deep non-REM sleep）期间，其独有的脑部“类淋巴系统”（glymphatic system）会全功率启动，如同一场夜间强力大扫除，泵送脑脊液冲洗掉白天积累的代谢废物，其中最关键的两种就是导致阿尔茨海默病的罪魁祸首——淀粉样蛋白（beta-amyloid）和Tau蛋白。 在这项极具挑战性的研究中，研究人员招募了50岁以上的受试者，在睡前和次日清晨分别对其进行腰椎穿刺（lumbar puncture），抽取脑脊液来定量检测脑内代谢废物的浓度。结果显示，与安慰剂组相比，服用DORA类药物的受试者不仅睡眠连续性显著改善、夜间清醒时间大幅减少，而且次日清晨清除的淀粉样蛋白和Tau蛋白水平明显更高。这一发现并在动物实验中得到了成功复现，有力证明了DORA药物诱导的睡眠绝非无意义的表象，而是具备实质性生理修复价值的自适应睡眠。这与传统安眠药形成了鲜明对比——最新研究发现，像安必恩（Ambien）这类传统镇静催眠药实际上会将夜间脑部脉冲清洗液的活动抑制约30%至40%。不过，沃克也无奈地指出了现实阻碍：DORA类药物目前价格极其昂贵，在美国自费价格可高达每月400美元，许多医疗保险尚不报销，在英国和欧洲其他地区的获取也受到严格限制。尽管饱受失眠折磨的患者往往甘愿“哪怕掏400美元也想抹去整整一个月的糟糕失眠”，但高昂的药价依然将多数人拒之门外。 - **脑部类淋巴系统运作机制**：深度非快速眼动睡眠期间高强度启动，通过脑脊液清除阿尔茨海默病毒性蛋白（淀粉样蛋白与Tau蛋白）。 - **传统安眠药的副作用**：最新数据表明，安必恩（Ambien）会使脑部排毒清洗液的脉冲流动减少30%到40%。 - **DORA药物现状**：经腰穿脑脊液临床试验证明其睡眠具有功能性排毒效益；目前自费价格约400美元/月，美欧多地医保覆盖仍有限。 ### [02:01:37](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=7297s) 睡眠的下游连锁反应与基因层面的破坏 听完最新的睡眠医学突破，主持人史蒂芬·巴特利特（Steven Bartlett）大受震撼，直言自己此前从未意识到睡眠科学已经发展出如此深奥的前沿发现，也意识到不良生活方式如何严重破坏了现代人的入睡机制。史蒂芬破例在节目中发起了一项听众推荐机制，鼓励大家将这期充满干货的对话分享给饱受睡眠障碍折磨或渴望优化睡眠的亲友。他动情地回忆起上一期与沃克录制节目后，走在街上经常有路人上前倾诉：正是因为把那期播客转发给了饱受失眠困扰的家人，对方彻底调整了生活习惯，睡眠恢复后，生活状态发生了翻天覆地的转变。 史蒂芬强调，睡眠问题处于生命状态的最上游，我们日常遭遇的亲密关系破裂、性欲减退、创造力枯竭等种种困扰，追根溯源往往都是睡眠不足在下游引发的恶果。沃克对此表示高度赞同，并援引了他此前在乔·罗根（Joe Rogan）节目中探讨的基因研究：仅仅是一段时期的严重睡眠不足，就会导致人体内多达711个基因的表达发生异常扭曲。在这些受损的基因中，与心血管疾病、慢性压力和炎症反应相关的基因被异常过度激活，而负责免疫防御机制的基因表达则被显著抑制，导致机体陷入免疫功能缺陷状态。这种由睡眠债务引发的基因表达紊乱会形成恶性循环，给长期缺觉者的身心健康带来滚雪球式的灾难性打击。 - **基因表达畸变**：缺乏睡眠会导致人体内711个基因的活性发生扭曲。 - **健康失衡机制**：心血管风险、应激反应与炎症相关基因表达过量上调；免疫防御相关基因显著下调，造成机体免疫缺陷。 - **身心连锁效应**：睡眠处于情绪调控、性欲、创造力和人际关系等核心生命功能的决定性“上游”。 ### [02:03:48](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=7428s) 成功的两面性：使命感与公众审视下的脆弱 在探讨完睡眠科学后，对话转入了播客的经典保留环节——由上一位受访嘉宾向沃克提问：“成功带给了你什么你此前做梦都想不到的东西？”面对这个问题，沃克沉思片刻后给出了极为真诚的剖析。他表示成功赋予了自己两样东西：一样是莫大的恩赐，另一样则是沉重的负担。积极的一面在于，畅销书《我们为什么要睡觉》（*Why We Sleep*）的轰动彻底改变了他的人生轨迹，赋予了他奔赴世界各地、向大众传播睡眠科学的珍贵舞台与话语权。沃克坦言自己曾长期深陷“冒名顶替综合征”（imposter syndrome），时常自怨自艾地想“为什么是我？世界上明明有那么多比我优秀的睡眠科学家”。直到一位好友严厉地训诫他“闭嘴吧，赶紧接受现实，好好想想你能用这个平台做些什么”，他才真正摆脱内耗，全力拥抱向世界普及睡眠生理学的使命。 然而，站上万众瞩目的舞台也伴随着意想不到的代价。沃克生动地形容道：“当你把头探出公众的城垛之上时，千万不要对迎面而来的冷枪暗箭感到意外。”他坦白，只要一个人内心深处还存有一丝一毫的缺乏安全感，网络上的非议与恶评就会狠狠击中要害。聚光灯的审视迫使他滋生出前所未有的脆弱与自卑——倘若未曾成名，他绝不会对自己的智识表达、声线嗓音、乃至被嘲讽为“灾难般的男团发型”而感到如此敏感和局促。但沃克随即释怀地表示，这仅仅是微不足道的代价；回望投身睡眠研究近25年的漫长岁月，他依然觉得自己是这颗星球上最幸运的人，这项被他誉为“全科学界最迷人的课题”给予了他无与伦比的慷慨回馈。 ```mermaid flowchart TD accTitle: 成功的两面性模型 accDescr: 马修·沃克对名望与科学成功带来的正负面影响的心理认知流向 subgraph Positive["正面馈赠：传播使命"] A["《我们为什么要睡觉》全球成功"] --> B["克服冒名顶替综合征"] B --> C["获得全球讲台与影响力"] C --> D["为沉默的睡眠生理学发声"] end subgraph Negative["负面代价：暴露脆弱"] E["探头置身公众舆论城垛"] --> F["承受网络非议与苛责"] F --> G["放大内在不安全感"] G --> H["对容貌/智力/嗓音产生容貌与自我焦虑"] end ``` ### [02:06:15](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=7575s) 科学家的感性转变：找到命中注定的另一半 当史蒂芬顺着话题关切地询问“你现在快乐吗？”时，沃克毫无迟疑地给出了令人动容的回答：“比你能想象的还要快乐，此刻正是我人生中最快乐的阶段。”在史蒂芬的鼓励下，这位一向以严谨理性著称的脑科学家，罕见地向听众敞开了自己最私密的内心世界。沃克动情地透露，自己终于找到了生命中属于他的那个人（"I found my person"）。 “她就像晴朗蓝天中突然劈下的一道闪电，我从未预料到她的出现，”沃克在分享这段伴侣关系时显得动情而平静。他坦言，在这位伴侣身边，他体验到了前所未有的自在与笃定，甚至比独自独处时更能坦然做真实的自己；而对方的存在，每天都在激励他成为一个更好的人。这种前所未有的深层宁静，彻底打破了他长久以来的认知框架。沃克承认，作为一名习惯凡事讲求实证、信奉硬核科学数据的学者，他在过去的人生中从不相信世上存在所谓的“真命天子/天女（the one）”；若是两年前有人告诉他会体会到这种宿命般的宁静与圆满，他一定会嗤之以鼻。然而生活给予他的这份意外馈赠，让这位理性至上的科学家彻底臣服于爱与平和的力量。 ### [02:07:48](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=7668s) 克莱夫·韦尔林的故事：永远不把伴侣视为理所当然 马修·沃克（Matthew Walker）坦言，如果过去有人跟他谈论对爱情的笃定与“真命天子”的信念，他一定会觉得对方误入歧途、脑子糊涂，甚至该把嗑的药扔掉，因为世上根本不存在这种绝对的笃定。然而如今，他深情地形容自己的妻子是一份“天赐的礼物（a gift）”，并祈祷自己永远不要把她视为理所当然。 谈到珍惜伴侣，沃克分享了神经科学界极其著名且令人动容的克莱夫·韦尔林（Clive Wearing）的故事——经典悬疑电影《记忆碎片》（*Memento*）中严重健忘症角色的灵感原型。克莱夫因脑部感染病毒彻底摧毁了记忆中枢，患上了重度顺行性遗忘症（dense amnesia）。他只能生活在两到三秒的狭窄时间切片里，意识的聚光灯在时间中盲目滑移：他没有过去的记忆，也没有对未来的期待。然而，在整个人类世界中，他唯一记得、唯一能认出的人，就是他的妻子。即便别人陪他聊了整整三个小时，一旦那人走出房间五分钟再回来打招呼，克莱夫就会完全像陌生人一样问对方名字；唯独面对妻子，每次她离开房间仅仅五分钟再推门而入，克莱夫都会像阔别数年般从椅子上一跃而起，脸上洋溢着无与伦比的狂喜，飞奔过去将她紧紧拥入怀中亲吻。 沃克指出，现代人在亲密关系中常常陷入“自满与习以为常（complacency）”的消极力量，往往只有失去对方时才幡然醒悟伴侣有多么珍贵。因此，即使在自己心情糟糕、疲惫沮丧、被消极压力笼罩而不想理会任何人的日子里，只要妻子下班推门而入，沃克都会在心中唤醒克莱夫·韦尔林那种毫无保留的热烈反应，以此冲破负面情绪的阴霾，提醒自己眼前的人有多么难能可贵。 ```mermaid flowchart TD accTitle: 克莱夫·韦尔林的记忆与情感机制 accDescr: 展示克莱夫·韦尔林因病毒受损的短暂记忆机制，以及对妻子永恒情感的特例对比 subgraph MemoryLoss["受损的认知状态"] A["病毒摧毁记忆中枢"] --> B["仅存 2-3 秒意识窗口"] B --> C["无法形成任何新记忆"] C --> D["无过去回忆 / 无未来预期"] end subgraph EmotionalCore["唯一保留的情感锚点"] E["辨认并深爱妻子"] --> F["离开房间 5 分钟重逢"] F --> G["爆发出极度狂喜与热烈拥抱"] end MemoryLoss -.->|"打破记忆阻隔"| EmotionalCore ``` --- ### [02:10:31](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=7831s) 直面死亡与争吵的艺术：你我携手对抗问题 史蒂文·巴特利特（Steven Bartlett）对此深有共鸣。他透露自己现在每周都会频繁省思：当生命走到终点时，自己究竟会如何看待这段亲密关系。几天前他和伴侣发生争执时，他突然在争辩中途停下来对她说：“我们一定会为现在的争吵感到无比后悔。”因为一旦未来的某一天接到那个噩耗电话，得知彼此之一即将离开人世，回头看这白白浪费在争吵上的三十分钟，即便倾尽所有也换不回来。 史蒂文反思道，情侣间常常会为了“一块巧克力”之类极其琐碎可笑的小事大动干戈，而死亡的必然性恰好能让人从这种“自以为永生不死”的狭隘琐碎中解脱出来，粉碎把伴侣视作理所当然的自满。但两人也一致强调，这并不意味着遇到问题要刻意回避冲突： - **关键不是回避争吵，而是学会如何建设性地争执**：争吵时必须牢记是“你和我一起对抗问题（me and you versus the problem）”，而不是“我对抗你”。 - **为了彼此而战，而非与彼此为敌**："You have to be fighting for each other, not fighting against each other." --- ### [02:12:09](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=7929s) 走出胜负欲与怨恨：人生终局视角的释怀 沃克将高质量的冲突比作去健身房锻炼：在走向健身房的那一刻，你可能百般不情愿、浑身难受，但只要科学地完成了训练，走出来时整个人必定比进去之前感觉更好。夫妻争吵也是如此，虽然在争吵刚结束的一小时或一天内可能依然不好受，但只要处理得当，这段关系在冲突过后往往能变得比从前更加坚固。 克莱夫·韦尔林的故事教会沃克的另一核心要义是**摒弃怨恨（resentment）**。沃克指出： - 怨恨是阻碍情感修复与内心平静的最大障碍；怨恨意味着创伤未被消化、关系未能翻篇。 - 怨恨往往源自幼稚的胜负欲——“这场争论到底是我赢了还是你赢了？”但亲密关系从来不是争夺分数的赛场。 - 在发生分歧之后，始终要将深爱的这个人置于冲突本身之上，主动递出橄榄枝。 沃克进一步将这种临终视角扩展到日常琐事中。例如车子停在路边被人追尾，或者飞往洛杉矶时在停机坪上延误四个小时，周围乘客暴躁地对地勤人员恶语相向。沃克心想，当你躺在临终病床上回顾一生时，难道会遗憾“天哪，我真忘不了飞往洛杉矶延误四小时的那天”吗？显然不会。既然在临死前根本不会为此焦虑，那现在又何必为它耗费心神？放平心态，好好活着才是真谛。 --- ### [02:14:44](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=8084s) 致谢科学引路人与 DOAC Circle 独家社区 史蒂文向马修·沃克表达了由衷的敬意与感谢，盛赞他作为当代睡眠科学的“首席火炬手（chief torchbearer）”，不仅掀起了一场全球性的睡眠健康浪潮，还让数以百万计的人深刻审视自身的挣扎与生活方式。史蒂文动情地表示，尽管沃克可能永远无法亲面所有受惠之人，但那些改变就像投入海洋的涟漪，不仅改善了无数普通人的睡眠与幸福，更将惠及他们的子孙后代。 沃克则极为谦逊地谢绝了这些赞誉，坦言自己不过是“站在巨人的肩膀上”： - 他只是在忠实转述同行学者以及前代先驱科学家们辛勤耕耘的杰出成果。 - 他幽默地自嘲称自己只是个“发声的传声筒，而且算不上多优秀的那种”，所有的掌声与感激应属于整个睡眠科学研究领域的学者们。 访谈结束后，史蒂文宣布启动全新的全球私人会员社区“DOAC Circle”。该社区首期仅限前 10,000 名用户加入，旨在为核心听众提供更深度的幕后互动，权益包括查看史蒂文录制访谈时 iPad 上的专属提纲简报、未公开的花絮与禁播片段、与嘉宾的私下交流，并能直接参与选题策划与嘉宾推荐。 ### [02:16:56](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=8216s) 结语与节目尾声 在整场深入探讨睡眠科学、神经机制以及现代生活干预策略的长谈接近尾声之际，主持人 Steven Bartlett 向听众致以简短而亲切的道别。他留下一句 "I will speak to you there"，邀请大家在评论区及社群互动中继续展开交流，为 Dr. Matthew Walker 这场干货满满且极具启发性的深度对话画上了圆满句号。 随后，节目在标志性的片尾音乐与空灵歌声中缓缓淡出收尾。 ## Notable quotes > [04:48](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=288s) 如果睡眠没有承担极其关键的核心生理功能，那它绝对是自然进化史上犯下的最大错误（the biggest mistake the evolutionary process has ever made）。 — Dr. Matthew Walker > [29:45](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=1785s) 生物学里从来没有免费的午餐，而且如果你选择与生物学规律对抗，最终通常会输得一败涂地。 — Dr. Matthew Walker > [58:04](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=3484s) 睡眠是自然降临到你身上的事，而不是你强行制造出来的事（Sleep is something that happens to you. It's not something that you make happen.）。 — Dr. Matthew Walker > [01:04:22](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=3862s) 失眠者如果把希望寄托在补充剂上，无异于为了捡地上的几分硬币，而跨过了大把的钞票（stepping over dollars to pick up pennies）。 — Dr. Matthew Walker > [01:22:51](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=4971s) REM 睡眠负责将苦涩的情绪果皮从信息的橙子肉上彻底剥离（strip the bitter emotional rind from the informational orange）。 — Dr. Matthew Walker > [02:03:48](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=7428s) 当你把头探出公众的城垛之上时，千万不要对迎面而来的冷枪暗箭感到意外。 — Dr. Matthew Walker > [02:06:15](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=7575s) 她就像晴朗蓝天中突然劈下的一道闪电，我从未预料到她的出现。 — Dr. Matthew Walker > [02:10:31](https://www.youtube.com/watch?v=qxxnRMT9C-8&t=7831s) You have to be fighting for each other, not fighting against each other. — Steven Bartlett ## Mentioned Dr. Matthew Walker, Steven Bartlett, The Diary Of A CEO, Why We Sleep, UK Biobank, Kenneth Wright, Walter Reed Army Institute of Research, Thomas Balkin, Michael Grandner, Joe Rogan, Michael Gradisar, Alison Harvey, Calm, George Lucas, Ambien, Rosalind Cartwright, Pipedrive, Stan Store, 23andMe, Promethease, Suvorexant, Lemborexant, Daridorexant, Prazosin, Clive Wearing, Memento, DOAC Circle ## Video description Dr Matthew Walker is a Professor of Neuroscience and Psychology at the University of California, Berkeley, and one of the world’s leading experts on sleep science, with over 20 years of research. He is host of The Matt Walker Podcast and bestselling author of ‘Why We Sleep: The New Science of Sleep and Dreams’. He explains: ◼️The shocking link between poor sleep timing and increased cancer risk ◼️How alcohol and caffeine silently sabotage deep sleep and mental performance ◼️Why screen time and light exposure before bed are secretly rewiring your brain ◼️How “sleep banking” before stress, travel, or work sprints can boost resilience ◼️Why parents, professionals, and athletes all need radically different sleep strategies Enjoyed the episode? Share it using this link and get points for every referral: https://doac-perks.com 00:00 Intro 02:20 Sleep Changes Your DNA 04:48 The Stigma Around Sleep and Laziness 08:29 What's Stopping People From Sleeping? 10:45 The Shocking Link Between Weekend Sleep-Ins and Heart Disease 14:35 New Research: Sleep Banking for Low-Sleep Periods 16:11 Boost Cognitive Performance With This Sleep Hack 19:01 3 Ways to Instantly Improve Sleep Quality 20:29 It's Not Blue Light That's Keeping You Awake 21:48 Melatonin Doesn’t Make You Sleep – Here's What It Does 24:15 How Much Melatonin Is Right? 25:41 The 1% With a Nocturnal Clock Who Can't Sleep Until 3 AM 27:12 Is Melatonin Really the Magic Sleep Pill? 30:19 The Trade-Offs of Sleep Medication 34:51 The Key to a Digital Detox 35:32 The 4 Macros of Good Sleep: QQRT 36:49 The Minimum Sleep Needed to Stay Alive 42:35 How Sleep Regularity Predicts Life Expectancy 46:37 Try This 7-Day Sleep Enhancer Challenge 53:11 How to Tell If Your Room Is Dark Enough for Sleep 01:00:50 Why Counting Sheep Doesn’t Work 01:02:44 The Better Alternative to Counting Sheep 01:04:23 Magnesium for Sleep: Does It Really Work? 01:11:34 Ads 01:13:20 How REM Sleep Works and How to Maximize It 01:20:17 Why REM Sleep Is Important 01:21:54 Entering a 'Psychosis' State During Dreams 01:24:51 Rewriting Trauma Through Dream Healing 01:30:58 Nightmares as a Warning Sign for Mental Health 01:35:55 REM Sleep Is Like Group Therapy for Memories 01:39:17 Ads 01:41:04 The Dystopian Future: Superhumans Who Sleep Only 6 Hours 01:45:04 Could Humans Be Engineered to Sleep Less? 01:50:06 Why You Crave Junk Food When Underslept 01:54:23 A New Drug That Could Help With Insomnia 02:03:37 What Did Success Bring You? 02:07:20 I Didn’t Believe in Finding “The One” 02:28:54 The Future of AI and Sleep Follow Dr Matthew: X - https://bit.ly/4oIRpAY Instagram - https://bit.ly/49OgFB4 Podcast - https://bit.ly/489MJhA You can purchase Dr Matthew’s book, ‘Why We Sleep’, here: https://amzn.to/4pbpp8n The Diary Of A CEO: ◼️Join DOAC circle here - https://doaccircle.com/ ◼️Be the first to hear about Steven's new book - https://bit.ly/jfdi-doac ◼️Shop the 1% Diary - https://bit.ly/3YFbJbt ◼️The Diary Of A CEO Conversation Cards (Third Edition) - https://g2ul0.app.link/f31dsUttKKb ◼️Get email updates - https://bit.ly/diary-of-a-ceo-yt ◼️Follow Steven - https://g2ul0.app.link/gnGqL4IsKKb Independent Research: https://stevenbartlett.com/wp-content/uploads/2025/11/DOAC-Matthew-Walker-2-Independent-Research-further-reading.pdf Sponsors: Linkedin Ads - https://www.linkedin.com/DIARY Pipedrive - http://pipedrive.com/CEO Stan Store - https://stevenbartlett.stan.store for your 14-Day free trial Last chance to join the waitlist for the limited edition Diary Of A CEO Conversation Cards here: https://bit.ly/cardswaitlist [Source](https://www.youtube.com/watch?v=qxxnRMT9C-8)

[4:48] Dr. Matthew Walker: 如果睡眠没有承担极其关键的核心生理功能，那它绝对是自然进化史上犯下的最大错误（the biggest mistake the evolutionary process has ever made）。 [29:45] Dr. Matthew Walker: 生物学里从来没有免费的午餐，而且如果你选择与生物学规律对抗，最终通常会输得一败涂地。 [58:04] Dr. Matthew Walker: 睡眠是自然降临到你身上的事，而不是你强行制造出来的事（Sleep is something that happens to you. It's not something that you make happen.）。 [64:22] Dr. Matthew Walker: 失眠者如果把希望寄托在补充剂上，无异于为了捡地上的几分硬币，而跨过了大把的钞票（stepping over dollars to pick up pennies）。 [82:51] Dr. Matthew Walker: REM 睡眠负责将苦涩的情绪果皮从信息的橙子肉上彻底剥离（strip the bitter emotional rind from the informational orange）。 [123:48] Dr. Matthew Walker: 当你把头探出公众的城垛之上时，千万不要对迎面而来的冷枪暗箭感到意外。 [126:15] Dr. Matthew Walker: 她就像晴朗蓝天中突然劈下的一道闪电，我从未预料到她的出现。 [130:31] Steven Bartlett: You have to be fighting for each other, not fighting against each other.

[2:20] Dr. Matthew Walker: Your sleep and how you are sleeping or not sleeping will change the very DNA nucleic alphabet that spells out your daily health narrative. [19:01] Dr. Matthew Walker: Melatonin is like the starting official at the 100-meter race. It brings all of the racers to the line and it begins the timing of the race, but it doesn't participate in the creation of the race itself. [36:49] Dr. Matthew Walker: 7 hours is the minimum amount of sleep that you need to survive, because the way that we quantify what minimum is is based on whether you die or you don't prematurely. The amount of sleep that you need to survive is different than the amount of sleep that you need to thrive. [55:31] Dr. Matthew Walker: Only return to bed when you are sleepy. There's no time limit. And that way, you gradually relearn the association that my bed is the place where I always get consistent sleep—because otherwise, it's the dentist's chair. [59:53] Dr. Matthew Walker: I want you in 4K detail in terms of granularity. What's common about every method I've just described... is that you get your mind off itself. [73:20] Matthew Walker: long wave radio station [82:51] Matthew Walker: emotional first aid [82:51] Matthew Walker: overnight therapy [90:58] Matthew Walker: canary in the coal mine [97:01] Matthew Walker: group therapy for memories [103:18] Matthew Walker: sleep currency inflation [126:00] Dr. Matthew Walker: when you raise your head above the public parapet, don't be surprised if shots are fired. [126:18] Dr. Matthew Walker: She appeared like lightning from a clear blue sky... I've never been able to be more myself, even with myself, than I have with her. [126:18] Steven Bartlett: We're going to regret this so much when our time is up. [131:15] Dr. Matthew Walker: If you're not stressing about it when you're dying, why are you stressing about it now? Live. [134:44] Dr. Matthew Walker: I stand on the shoulders of giants... I am simply relaying all of the incredible work of all of my colleagues in the field and all of those who came before me. I'm just the mouthpiece...

[0:00] Here's the problem with magnesium [0:01] supplementation [music] [0:02] when it comes to sleep. The first thing [0:04] to note is that most forms of magnesium [0:05] don't cross the blood brain barrier and [0:07] sleep [music] is produced by your brain. [0:10] So, how can something that doesn't get [0:11] into your brain affect brain process? [0:14] All you're doing is creating probably [0:15] expensive urine. [0:18] However, there is one form of magnesium [0:20] that seems to have some evidence in [0:22] favor of [music] it, which we can speak [0:23] about, but it doesn't stop there. [0:25] There's so much new evidence that we [0:27] have, including this myth of 8 [music] [0:29] hours, my fear about giving melatonin to [0:31] kids, why you keep waking up in the [0:33] middle of the night, and the invention [0:35] of the first new class of sleeping [0:37] [music] medication that I actually [0:38] favor, and most people are not aware of [0:40] it. Okay, let me write this down. [0:42] Matthew Walker [music] is back. And the [0:44] world-renowned sleep expert and [0:46] neuroscience professor is sharing brand [0:48] new research to combat [music] the sleep [0:49] loss epidemic and help you get the [0:51] perfect night's sleep. As a society, we [0:54] have struggles with sleep at night due [0:55] to many reasons, but no one teaches us [0:58] this stuff, and it's things like, say [1:00] you go to bed at 11:00 one night, 1:00 [1:02] a.m. the next night, then 10:30 p.m. the [1:05] next night, and it's remarkable how many [1:06] people do this. But studies have shown [1:08] that you are statistically 49% more [1:11] likely to prematurely die versus those [1:13] people who were most regular in terms of [1:15] going to bed and waking up at the same [1:16] time. And worse, they had a 57% [1:19] cardiometabolic disease [music] risk [1:22] increase. What the Science really [1:24] teaches us that there are four pillars [1:25] of good sleep. And [music] then there's [1:26] this incredible new study looking at [1:28] sleep banking. And this is remarkable [1:30] for people who are facing a sprint at [1:32] work or a medical doctor about to go on [1:34] call for the next 40 hours, new parents, [1:36] and we can go through all of that. But [1:38] if you were to push me to say the three [1:39] [music] most impactful things that you [1:41] can start doing tonight to start [1:42] sleeping better, it would be [1:49] I see messages all the time in the [1:50] comment section that some of you didn't [1:52] realize you didn't subscribe. So, [1:53] >> [snorts] [1:54] >> if you could do me a favor and [1:55] double-check if you're a subscriber to [1:56] this channel, that would be tremendously [1:57] appreciated. It's the simple, it's the [1:59] free thing that anybody can do to help [2:01] us here to keep everything going in this [2:04] show in the trajectory it's on. So, [2:06] please do double-check if you subscribed [2:08] and thank you so much because in a [2:10] strange way, you are you're part of our [2:12] history and you're on this journey with [2:14] us and I appreciate you for that. So, [2:15] thank you. [2:18] >> [music] [2:18] [singing] [2:20] >> Dr. Matthew Walker. [2:21] Here in front of me, I have these cards [2:24] which I'm going to reveal a bit later, [2:26] but these kind of hold what you consider [2:27] to be the four pillars of great sleep. [2:31] But you also spend much of your [2:33] professional career just studying the [2:35] brain generally to understand human [2:36] performance and how we can [2:39] change our lifestyles and also introduce [2:41] some of these new sort of treatments to [2:43] improve how our brain performs. I want [2:44] to talk about all of that as well. But [2:46] to start, for anyone that is unfamiliar [2:48] with you and has been hiding under a [2:50] rock, [2:51] how do you summarize who you are [2:53] professionally, [2:55] the sort of academic references you're [2:57] drawing on, and the experiences and [2:59] research you've done so that the viewer [3:01] listening at home [3:03] understands the full world that you [3:05] operate in, study, and have experienced. [3:08] I am a neuroscientist by trade, but my [3:10] specialty is sleep, the effects of sleep [3:13] on the brain and the body, and I've [3:15] probably spent about the past two [3:16] decades trying to understand exactly [3:19] why do we sleep? [3:22] Because 50 years ago, [3:24] the crass answer to the question, why do [3:26] you sleep? was the following. You sleep [3:29] to cure sleepiness. [3:32] Which is the factuous equivalent of [3:33] saying, well, you eat to cure hunger. [3:35] No, you don't eat to cure cure hunger, [3:37] you eat to support all sorts of [3:40] physiological and biological benefits. [3:42] But now, and this is not due to my [3:44] research, this is all of the incredible [3:46] colleagues whose sort of shoulders that [3:48] I stand on, [3:49] we've now had to upend the question. [3:51] We now have to ask, is there any major [3:53] physiological system in your body, or is [3:56] there any operation of your mind that [3:58] isn't wonderfully enhanced by sleep when [4:00] you get it, or demonstrably impaired [4:02] when you don't get enough? And the [4:04] answer now seems to be, no, we there is [4:07] no such system, even down to the level [4:10] of your DNA. [4:12] Your sleep and how you are sleeping or [4:15] not sleeping will change the very DNA [4:18] nucleic alphabet that spells out your [4:21] daily health narrative. [4:23] And we can see it all the way up to [4:25] society. Sleep can change the fabric of [4:28] society, can change how we interact with [4:30] other people, it can change our belief [4:33] systems, it can change how lonely or [4:35] sort of hyper-social we are. So, to your [4:38] question, I'm a sleep scientist by [4:40] trade, and I suppose my mission has been [4:43] trying to reunite humanity with the [4:45] sleep that it seems to be so bereft of. [4:48] We had a fantastic conversation last [4:50] time and my audience [4:52] valued it tremendously. I know that cuz [4:53] we we often survey our audience and we [4:55] we get to see some of the the back-end [4:56] stats. And this conversation about sleep [4:59] is particularly personal to everybody [5:00] listening because when we surveyed our [5:02] audience ahead of this conversation [5:03] today, about 75 or 80% of the Diary of a [5:07] CEO audience struggle with sleep for a [5:10] variety of different reasons. So, we [5:11] actually asked them, a thousand of them, [5:13] their questions to ask you today. But [5:15] also, the other reason I really wanted [5:17] to chat to you is the science of sleep. [5:19] I mean, as is the way of science, is [5:20] always evolving. We're learning new [5:22] things and even since we spoke last [5:24] time, there is new sleep science which [5:26] we're going to talk about today. And one [5:27] of those particular things we're going [5:28] to talk about is going to be [5:29] demonstrated using [5:31] this jar. [5:32] >> [laughter] [5:32] >> Because I always want to know what the [5:34] updated sleep science is so that I can [5:36] be a better sleeper because I agree with [5:38] everything you said about how [5:39] foundational sleep is in my life. [5:44] I and um I didn't know this at the start [5:46] of my career. I didn't know this even a [5:48] couple of years ago, 5 years ago, I [5:49] didn't know. I thought sleep was one of [5:51] those things you could just [5:52] take it or leave. Yeah. I mean, and it's [5:55] not your fault in so many ways because [5:58] if you didn't know what I know, you [6:00] would just think, well, when I sleep, my [6:02] body is dormant and my mind for the most [6:04] part is blank. So, is it so catastrophic [6:08] to lose, you know, an hour or two of [6:11] sleep? And you know, you have to then [6:13] think about from an evolutionary [6:15] perspective, [6:16] it is such an idiotic idea [6:19] to sleep because when you're sleeping, [6:21] you're not finding a mate, you're not [6:23] reproducing, you're not caring for your [6:24] young, you're not foraging for food, and [6:26] worst of all, you're vulnerable to [6:27] predation. [6:29] So, on any one of those grounds, and [6:31] especially all of them as a collective, [6:32] sleep should have been strongly selected [6:34] against in the course of evolution. [6:38] And my point is that, and it's often [6:39] been said that if sleep doesn't serve an [6:41] absolutely vital set of functions, [6:43] plural, then it's the biggest mistake [6:45] the evolutionary process has ever made. [6:47] And we now realize it didn't make a [6:48] spectacular blunder. But really, I guess [6:51] to the point of it is [6:53] sleep is not a passive state. It's an [6:56] incredibly active state both in the [6:58] terms of the brain and the body. And so, [7:01] you uh should not feel sort of, you [7:04] know, remiss or ashamed that you didn't [7:06] value the importance of sleep because [7:08] firstly, as a subjective sense, you just [7:10] think, well, my mind was offline for a [7:12] while. [7:14] Second, we also know that we don't teach [7:16] the importance of sleep in education. [7:18] And doctors themselves, you know, [7:19] there's a great study and they what they [7:20] found is that medical doctors across, I [7:23] think it was about 11 different [7:24] curricula around the world, they will [7:27] only receive about 1.2 hours of [7:30] education on sleep. But it's a third of [7:33] their patients' lives. [7:35] So, there's [7:36] a collection of sort of almost perfect [7:39] storms that have happened to keep [7:42] society ignorant of the importance and [7:45] the value of sleep. I think that's why [7:48] we often so shortchange it, together [7:51] with also something terrible, which is [7:53] stigma. [7:54] That people are so proud to say, well, [7:58] I've been eating really healthy the past [8:00] couple of months or, you know, I've been [8:01] going to the gym, you know, three times [8:03] a week consistently for the past year. [8:06] No one is ever going out into society [8:09] and saying, you know, I I've been [8:11] getting 8 and 1/2 hours of sleep [8:13] consistently every night. Because if you [8:15] did, people would say, really? [8:17] And there's a there's a slight edge to [8:19] the really, which is that if you have [8:22] time to sleep, [8:24] then you must not be busy. And if you're [8:26] not busy, you must not be important. [8:30] So, can you do me a favor and for the [8:32] listener at home, can you tell me [8:35] what the different groups of people [8:38] that are listening to this conversation [8:39] right now are seeking? From the extreme [8:41] end being [8:43] sleep apnea, I get no sleep, I'm an [8:45] insomniac, to the other end where maybe [8:47] they're looking for marginal performance [8:49] gains. Like, what are the what are the [8:50] cohorts of people you see and the [8:51] reasons why they're so interested in [8:53] your work? They listen to your podcast, [8:54] they read your books. What are the [8:55] cohorts? Firstly, we have the collection [8:58] of people who have insomnia. [9:00] Those people who have other sleep [9:01] disorders like sleep apnea, which we can [9:03] speak about. There's another disorder [9:05] called restless leg syndrome. It's a [9:06] terrible disorder where your legs start [9:09] to feel as though they've got this sort [9:10] of creepy, crawly feeling and you've [9:11] constantly got to massage them and move [9:13] them. It's a terrible disruptor of your [9:15] sleep. All of these disorders are [9:17] markedly undiagnosed, by the way. And [9:20] then you've got another collection of [9:23] individuals who they don't have any [9:26] sleep disorders, but they are either [9:29] doing things that will dismantle our [9:31] sleep. So, either they're taking on [9:34] things into themselves like alcohol, [9:36] caffeine, THC that aren't the sleep [9:40] helpers, even though sometimes they [9:42] think they are. [9:43] And then you've got perhaps the internal [9:46] things that will prevent you from [9:47] sleeping well, things like stress and [9:49] anxiety. And then you've also just got [9:52] life itself that can get in the way. [9:55] And then moving from the sleep disorders [9:58] realm to the uh I don't have a sleep [10:00] disorder, but I'm probably not doing it [10:02] right, {quote} {unquote}, when it comes [10:04] to sleep. Then you've got the people who [10:06] are obsessed about getting it right, and [10:09] they are the bio-optimizers, [10:12] this sort of the, you know, the [10:14] bio-hackers. And then you've also got, I [10:16] work with a lot of high-performance [10:18] individuals who are really trying to [10:21] just scratch out those last couple of [10:23] percentages, either at in business or [10:26] often we're working with professional [10:27] athletes. These are the people for whom [10:30] two or three percentage point changes [10:33] can be [10:34] tens of millions of dollars, or they can [10:36] be the difference between standing on a [10:38] podium at the Olympics or not. And so, [10:42] this is is a broad collection of [10:43] wonderful characters. [10:45] And since we last spoke, is there now a [10:47] lot of new sleep science and [10:48] understanding as it relates to sleep [10:51] performance and these three categories [10:53] of sleep deficient, sleep disorders, [10:55] lifestyle factors, and then the [10:57] optimizers? [10:58] Yeah, I think there's there's a broad [11:00] collection of new evidence that we have, [11:03] but maybe let me come on to the middle [11:06] group. You know, I used to say that for [11:07] people who were deficient in their [11:10] sleep, that sleep wasn't like the bank. [11:13] That you can't accumulate a debt. Oh, [11:17] here we go. Okay. [11:19] So, what we can see here is that the jar [11:21] used to be full. [11:22] Full of sleep credit when you're [11:23] sleeping well. [11:25] And then during the week, I'm short [11:27] sleeping. So, maybe I'm only getting 5 [11:29] hours a night. So, I'm constantly going [11:32] into debt. So, I'm losing all of this [11:34] wonderful sleep credit, and my system is [11:37] building up this collateral debt. [11:39] And then we used to think that sleep was [11:42] not like the bank, that once you've gone [11:44] into debt, unfortunately, [11:49] the lid is closed, and even at the [11:51] weekend, if you try to pay it back, [11:54] you can't put back credit into the [11:57] system. [11:58] However, there was a study published [12:00] from what's called the UK Biobank, which [12:02] is this incredible data set. It's [12:04] revolutionary. And they studied in this [12:07] particular research paper over 90,000 [12:10] individuals. [12:11] And what they did was they essentially [12:13] split them down into those individuals [12:16] who were short sleeping during the week, [12:18] and then short sleeping at the weekend. [12:21] And they compared them to those [12:22] individuals who were short sleeping [12:23] during the week, but then long sleeping [12:26] at the weekend. They were doing catch-up [12:27] sleep. That's me. And that's so many [12:29] individuals, it turns out. If you look [12:31] at the data, it's it's remarkable how [12:33] many people do this this catch-up sleep [12:35] behavior. [12:36] But what was amazing is that in the [12:38] people who were short sleeping during [12:39] the week, but long sleeping at the [12:41] weekend, they had a 20% [12:44] reduced cardiovascular disease risk [12:46] relative to the people who were short [12:49] sleeping during the week, but also short [12:51] sleeping at the weekend. Now, to be [12:53] clear, both of those groups had a higher [12:57] cardiovascular disease risk than people [12:59] who were sleeping sufficiently during [13:01] the week and sleeping sufficiently [13:03] during the weekend. So, I'm not saying [13:04] that it's a completely free lunch, but [13:07] for the first time, we realized that at [13:10] least one system, major organ system in [13:12] your body, is like the bank, which is [13:15] that if your heart [13:18] at the weekend, [13:23] you can [13:25] just keep [13:26] putting credit back, [13:28] and your system doesn't suffer as much. [13:30] For your heart? For your heart. Okay. [13:33] But again, many of the other major [13:35] physiological systems don't show that. [13:37] So, work by people like Kenneth Wright [13:39] at the University of Boulder, Colorado, [13:40] he's shown that your immune system [13:42] doesn't rebound after long sleep at the [13:44] weekend, your regulation of blood sugar, [13:47] your cognitive ability. So, that's [13:49] one way in which I've changed my mind [13:51] regarding sleep and the bank. [13:53] But there's a very different new set of [13:55] data that has changed my mind completely [13:58] about this idea of sleep and the bank. [14:01] Now, what we've just discussed here is [14:03] to say, I went into debt, [14:06] and then I was hoping to try and pay it [14:08] off with credit at the weekend. So, the [14:11] jar represents the debt that you have, [14:13] the sleep direct. Yeah. And what I'm [14:15] trying to do is force more coinage [14:21] in at the weekend [14:22] to see [14:24] if I can offset the debt that I created [14:26] and get back to net net neutral by the [14:29] end of the weekend. Now, it turns out [14:30] you can't do that. Even if you sleep for [14:33] as long as you want, but here's this new [14:36] remarkable data. It came from Walter [14:38] Reed Medical Army Institute, a [14:41] researcher called Thomas Balkin. And [14:42] what he was interested in was flipping [14:45] the direction of the question. [14:47] Not if I go into debt, can I pay back [14:50] with credit, [14:51] but what if I know in future I'm going [14:54] to face a debt, an upcoming debt, [14:57] can I do sleep banking? Oh, so if I've [15:00] got a big thing coming up where I'm [15:01] traveling across the world and I know [15:03] I'm going to be sleep deficient, can I [15:05] sleep a lot before it to create a [15:08] What would the financial analogy be? [15:10] >> the financial analogy would be, let's [15:12] say that we're coming up to Christmas. [15:15] Yeah. And you're going to spend lots on, [15:17] you know, presents and all sorts of [15:19] stuff. So, I know that in October and [15:22] November, I'm going to tighten my [15:24] financial belt. I see. [15:26] >> So, that when I go into the sort of [15:28] Christmas period and I'm spending a lot [15:30] more money, my bank account isn't hit as [15:33] hard. I don't go into as much of a sort [15:36] of a debt situation because I've built [15:38] up credit. [15:39] >> So, you can create sleep savings. [15:41] Correct. It's a sleep saving system. So, [15:43] essentially, you know, [15:45] what he was able to do, [15:48] not [15:49] just put [15:50] the jar to full, [15:52] but he was actually packing in [15:55] even more [15:57] so that you almost got this wonderful [16:04] overflow of sleep. How did he know? [16:07] He didn't. It was the experimental [16:09] hypothesis. [16:10] And And but how did they prove it? So, [16:12] what they did is that they woke you up [16:14] to a period when you're going to have [16:16] two or three nights of either no sleep [16:19] or marked sleep reduction. [16:21] And in the week beforehand, with these [16:24] army cadets, instead of being limited to [16:27] 8 hours of time in bed, they were able [16:29] to get 10 hours of time in bed. [16:31] And they could sleep all that they want. [16:34] And so, they went from probably an [16:36] average of about 7, 7 and 1/2 hours of [16:38] sleep to about 8 and 1/2, [16:41] almost 9 hours of sleep. So, they were [16:43] extending their sleep duration. [16:47] And so that they had built up this [16:49] buffer. It's almost like a sort of a a [16:51] sleep safety net that's in place, so [16:54] that when you go into the tumble of [16:57] sleep deprivation, [16:59] you're sort of almost bolstered and [17:01] you're lifted higher, and therefore your [17:04] degree of impairment that you suffer [17:06] under conditions of sleep deprivation is [17:08] significantly less if you banked sleep [17:11] beforehand versus those people who were [17:13] just sleeping normally [17:15] and then face the deprivation. They went [17:17] down much further in terms of their [17:19] cognitive and mental performance. So, he [17:22] gave them challenges and tasks to do [17:23] Correct. [17:24] >> in two different groups. One group had [17:25] sleep savings saved up from sleeping [17:27] well the previous week, one group [17:28] didn't. That's right. [17:29] >> And they performed remarkably different. [17:32] So, both of them were impaired relative [17:34] to a sleep rested person. Okay. However, [17:37] the people, it's sort of, you know, how [17:39] how much of a drop in your cognitive [17:41] performance do you suffer? And what he [17:43] found was that people who had built up [17:46] this credit, this savings account of [17:48] sleep in the days in the week [17:50] beforehand, they suffered about 40% less [17:55] of an impairment relative to the people [17:58] who had not created any savings plan. [18:02] Now, they weren't in debt, they were [18:04] just net neutral. But boy, did they drop [18:06] quickly. [18:08] Whereas those people who'd had some [18:10] cash in their sleep credit system, [18:13] they didn't fall anywhere near as far. [18:15] But this is remarkable for people, like [18:17] you were saying, who are facing, let's [18:18] say, if I've got a sprint at work, or [18:21] I'm a medical doctor, and I know I'm [18:23] about to go on call for the next 40 [18:25] hours, you're in military aviation, all [18:27] of the new parents, all of these [18:29] circumstances are places where now we [18:31] know, athletes are a great example, when [18:34] we work with athletes, people like [18:36] Michael Grandner have demonstrated that [18:38] athletes sleep terribly, typically, the [18:41] night before a huge performance. No [18:42] matter, you know, of course, they're [18:44] nervous. Mhm. But what you can do is you [18:46] can have them bank sleep in the days [18:48] before when they're not as nervous, and [18:50] therefore their performance doesn't [18:52] suffer as much, even though they know [18:54] they're going to be deprived. Sleep is [18:56] so important, isn't it? And I think [18:58] everybody now knows that because of [18:59] people like yourself, or really, you [19:01] know, you were the real pioneer in [19:02] pushing this subject into the world. I [19:03] remember when you first went on Joe [19:05] Rogan's show, the amount of my friends [19:06] that sent me that episode and then sent [19:08] me your book was just staggering. It was [19:10] like that was the catalyst moment, I [19:11] think, in society for the mainstream to [19:14] really start talking and caring about [19:15] sleep. However, [19:17] there's still so many people struggling [19:19] um [19:21] because of all the factors that you [19:22] talked about when we were talking about [19:23] group two, who have those lifestyle [19:24] factors, the stress, the psychological [19:26] factors, the trauma, etc., etc. [19:29] What can we give them, [19:32] those people, the people that really, [19:33] really struggle? Maybe they haven't got [19:35] a disorder, we'll come to the people [19:36] with sort of sleep disorders later, and [19:37] we'll talk about optimizers. But what [19:39] what is the new information or advice [19:42] that we can give them [19:44] that will help them once and for all [19:47] sleep 8 hours a night and get their life [19:49] back? [19:51] If you were to push me to say what are [19:52] the three most [19:55] impactful things that you can start [19:57] doing tonight to start sleeping better, [20:00] it would be the following. [20:03] Digital detox. Okay, let me write this [20:05] down. Digital detox, okay. And what does [20:07] that mean? One hour before bed, [20:11] try to limit [20:13] activating social media engagement, [20:17] email, [20:18] and text messages that are going to [20:21] trigger you. It's fine to listen to a [20:23] podcast, you know, [20:26] >> [laughter] [20:26] >> You heard it here, folks. [20:28] Right from my mouth. But it's also good [20:30] to like and subscribe, would you say? I [20:31] would say that, you know, like and [20:33] subscribe and then just click here so [20:35] that you get the latest notification. [20:37] You get that bell, just click on the [20:39] bell icon so that you [20:41] >> [laughter] [20:42] >> So, it's not a problem of blue light. A [20:46] quick aside, we've been taught this myth [20:48] of the blue light effect. Yeah. From [20:51] devices and it really is a myth because [20:53] an incredible Australian researcher, a [20:55] guy called Michael Gradisar, has almost [20:57] single-handedly [20:58] changed the the what I think of as being [21:02] the zeitgeist for a while after a very [21:04] influential paper, which is a great [21:05] paper. And what they showed was that one [21:07] hour of iPad reading before bed [21:10] ended up impairing your melatonin. It [21:12] disrupted sleep. It reduced the amount [21:14] of dream sleep and even after they [21:16] stopped reading the iPad, the blast [21:19] radius impact on your dream sleep lasted [21:21] a week. It's almost like the drug needed [21:23] to get washed out the system. That even [21:25] when you you'd stop using technology for [21:27] an hour before bed, [21:29] the impact of that technology, even [21:31] though you'd stop using it, could still [21:33] be seen in the echo of sleep disruption [21:35] for a week later. It was a very [21:37] influential study in a very prestigious [21:39] channel. When was that? A while ago? [21:41] That was probably about 10 years ago. [21:42] But then Michael Gradisar, this [21:44] incredible Australian researcher, [21:45] started to say, "Well, I can't replicate [21:47] these findings." [21:49] And what he was discovering is that it's [21:51] not the blue light that's the problem. [21:53] Now, the blue light will change aspects [21:55] of your melatonin and melatonin is a [21:56] hormone. [21:58] It simply tells your brain and your body [21:59] when it's night time, when it's time to [22:02] fall asleep. It doesn't participate in [22:03] the generation of sleep. Melatonin is [22:05] like the starting official at the 100-m [22:07] race. It brings all of the racers to the [22:09] line and it begins the timing of the [22:11] race, but it doesn't participate in the [22:13] creation of the race itself. That's a [22:15] different set of chemicals. [22:16] >> It doesn't make you go to sleep. [22:17] >> It doesn't make you And if you look at [22:19] what we call meta-analyses, where we [22:21] gather together all of the individual [22:23] studies on a topic and we put them in a [22:24] big statistical bucket, what they found [22:26] is that melatonin will only improve the [22:28] speed with which you fall asleep by [22:31] about um 3.4 minutes and it will only [22:34] increase the efficiency of your sleep by [22:37] about 2.2%. So, not much more than [22:40] placebo. [22:41] Um so, melatonin is [22:44] it it's Now, the placebo effect is the [22:46] most reliable effect in all of [22:47] pharmacology. So, you know, maybe no [22:50] harm, no foul. I would say, and don't [22:53] forget I will come back to the three, [22:54] but when it comes to melatonin, be [22:56] careful. More isn't always better. [22:59] And you run the risk of [23:02] confusing your morning brain [23:05] into a dense nighttime fog. And what I [23:08] mean by that is [23:10] 10 mg or 20 mg of melatonin is what we [23:14] call a supraphysiological dose, which [23:16] again is just a fancy medical term to [23:18] say it's a size of magnitude of [23:20] melatonin that your body would never [23:22] naturally release. It's far greater. [23:25] So, melatonin is the signal of darkness [23:28] and normally by the morning hours, our [23:30] natural release of melatonin has stopped [23:33] and you're down to zero levels again. In [23:35] the morning? In the morning. So, you [23:36] wake [clears throat] up and your body no [23:38] longer has the signal of melatonin [23:40] saying it's night, it's night, it's [23:41] night. But if you've dosed yourself with [23:43] 10 mg or 20 mg of melatonin, [23:47] you run the risk of saying, "Well, yes, [23:48] I know it [23:50] quote unquote knocks me out." But the [23:52] problem is in the first, you know, three [23:54] or four hours of the waking morning, [23:56] you're struggling because you're in this [23:57] fog of a hormonal melatonin, a hormonal [24:01] signal saying it's still pitch black. [24:04] Now, it's not. It's bright light [24:06] outside, but your body is fooled into [24:07] thinking it's pitch black because you've [24:09] dosed yourself too high and no wonder [24:12] you're reaching for two or three cups of [24:13] coffee in the morning. [24:15] So, what what dose of melatonin should I [24:16] be taking? Somewhere between probably [24:18] about 0.1 [24:21] to 3 mg. And do you advise melatonin for [24:24] people? [24:25] Yes, in two conditions. The first, or [24:27] circumstances I should say. The first is [24:30] when you're going through jet lag. [24:31] Wonderfully helpful, but timing is [24:35] critical. You need to create that sort [24:37] of that artificial signal of night [24:39] because let's say that you and I here in [24:41] Los Angeles, we're both going to fly [24:43] back to London tomorrow. And London is [24:46] eight hours ahead. So, we fly overnight, [24:50] we arrive in London and then that first [24:52] night, let's say we decide to go to bed [24:55] or I decide to go to bed in the hotel at [24:57] midnight. The problem is here in Los [25:00] Angeles, on my body clock, it's still [25:02] 4:00 p.m. cuz London's eight hours [25:04] ahead. So, my melatonin is not going to [25:07] rise for probably another six or seven [25:09] hours. So, I need to artificially hijack [25:13] my melatonin system and tell my brain, [25:15] "Oh, no, it's not 4:00 p.m. [25:18] It's instead, it's midnight." And so [25:20] there, under conditions of jet lag, very [25:23] helpful. The second is if you have a [25:25] circadian rhythm disorder. Let's say [25:27] that you're someone who has a an [25:30] advanced circadian phase. What that [25:32] means is you're someone who really can't [25:34] get sleepy until 3:00 or 4:00 in the [25:36] morning and you would prefer to be [25:38] sleeping throughout most of the day. So, [25:39] you you're almost nocturnal. Is that a [25:42] genetic disorder? And yes, it's a [25:43] genetic disorder in part. [25:45] >> How many people have that? [25:47] Probably 1 to 2% of the population have [25:49] a very severe [25:51] advanced circadian phase disorder. [25:54] But there, melatonin can also be helpful [25:56] because once again, their melatonin part [25:58] of their problem is that their melatonin [26:00] is very delayed. So, they don't get the [26:02] signal of "Oh, it's night" until maybe [26:05] 4:00 in the morning. You and I, we start [26:08] to get our signal of melatonin, [26:10] depending on our chronotype, by [26:12] somewhere between about 9:00, 10:00, or [26:14] 11:00 p.m. [26:15] They may be delayed by five hours. So, [26:17] if we can give them melatonin, we can [26:19] artificially try to fool their brain [26:21] into thinking it's actually earlier in [26:23] their biological rhythm. So, they sleep [26:25] earlier and they're more in sync with [26:28] the rest of society. How does someone [26:29] know if they're that type of person, if [26:31] they have that disorder? Is there [26:32] There's not a way to test, is there? [26:34] Well, what we typically do is we will [26:35] bring you into a laboratory and we will [26:37] measure your innate levels. So, we will [26:40] shut out sort of all windows, all clock [26:42] faces are gone, and we just let you run [26:44] your natural rhythm. Mhm. And they have [26:48] the same rise and fall in melatonin, [26:50] just like you and I do. Except where [26:52] it's doing that rise and fall of [26:54] melatonin on the 24-hour clock face is [26:57] radically different. Okay. For you and [26:59] I, it's, you know, 9:00, 10:00 p.m., [27:01] 11:00 p.m. at night when we're starting [27:03] that melatonin crescendo. For them, it's [27:05] 4:00 in the morning. So, we can measure [27:07] it. It's not in their minds, it's not [27:09] their choice. It's a biological edict. [27:12] Are you concerned that melatonin is [27:14] becoming more and more popular as a way [27:17] to solve [27:18] lifestyle issues [27:21] that have caused sleep impairment? [27:22] Because I'm seeing loads of You know, [27:24] I'm an investor, so I see lots of [27:25] companies now pitching me different [27:27] products that have melatonin in them as [27:30] a sort of day-to-day sleeping [27:32] supplement. I think I'm really torn. [27:35] I've been on both sides of this argument [27:37] and [27:38] I'm cautious about it for two reasons. [27:41] The first is in pediatric populations [27:43] here in the United States. Pediatric? [27:45] >> Yeah, so the people's use of melatonin [27:49] in kids is increasing. So, in pediatric [27:52] populations, it's [27:54] increasing exponentially. And in fact, [27:56] if you go down the sort of the [27:58] supermarket aisles here in America, [28:00] often if you go into sort of the the [28:02] health sort of food section, there's [28:04] this big purple section. That's the [28:06] melatonin section. And a large [28:08] proportion of that is there dedicated to [28:11] gummies for your children with [28:13] melatonin. [28:15] And [28:16] there was a study that was published [28:17] about three years ago that showed here [28:20] in America, over the past 10 years, [28:22] there has been a 503% [clears throat] [28:25] increase [28:26] in poisonous overdose admissions to [28:29] hospitals of melatonin in the past 10 [28:31] years. 503% [28:33] increase. [28:35] So, firstly, we've got to be a bit [28:36] careful. The second reason is that [28:39] melatonin is a bioactive hormone and [28:42] it's also involved in reproductive [28:44] development. And there were studies done [28:45] back in the 1970s, I think, where they [28:48] were looking at juvenile male rats, [28:50] which is to say male rats who were going [28:51] through adolescence. [28:53] And they were dosing them with high [28:54] amounts of melatonin. And what they [28:56] found is that that stunted the [28:59] development of the testes, of the [29:01] testicles, and it caused testicular [29:04] atrophy. Now, these were very high [29:05] doses, but we've got to be a little bit [29:08] careful. We think We say, "Well, [29:09] melatonin's a natural hormone, so [29:12] anything natural is safe." Melatonin [29:14] overall, in terms of its safety profile, [29:16] is very safe. It's actually a very good [29:18] antioxidant. [29:19] But you've got to be careful because [29:22] things like, for example, testosterone [29:23] supplementation in males, what we know [29:25] is that if you're injecting [29:27] testosterone, [29:29] after a while, after maybe 18 months or [29:31] so, the testes themselves will stop [29:34] producing their own testosterone. And [29:37] even if you stop the administration of [29:39] the exogenous testosterone, the [29:42] injection, the testes never return their [29:45] function of producing testosterone. [29:48] Now, we don't have any evidence yet that [29:50] that's the case that if you keep taking [29:51] melatonin at high dose, your body, the [29:53] fear would be, shuts down its own [29:55] natural production of melatonin. I've [29:57] seen no evidence of that. In fact, I've [29:59] seen evidence to the contrary that even [30:01] after about 6 months or even 12 months [30:03] in certain small cities, when you stop [30:06] melatonin, the production starts again [30:08] naturally. It seems fine. Problem is, [30:11] people haven't been taking melatonin for [30:13] just 12 months. They've been taking it [30:15] for years. [30:17] We've got no idea what happens after [30:18] years. That was my hesitation when the [30:21] first time someone offered me melatonin [30:23] is from doing this podcast and speaking [30:24] to smart people like yourself, I've come [30:26] to learn this sort of principle that if [30:29] you start making something for your body [30:30] in terms of a hormone, if you start sort [30:32] of [30:33] consuming something externally, like [30:35] testosterone, your body will say, "Fine, [30:37] I don't need to do this." It will try [30:38] and return to that level of balance [30:40] where the quantities in your system are [30:42] maintained, which means it kind of [30:43] learns to shut down. And I always think [30:45] about the case of testosterone cuz men [30:47] know that if we start injecting [30:48] testosterone, then we're going to have [30:49] to pretty much do it forever. Yeah. Um [30:51] if we want the those levels to be the [30:52] same. Yeah, that's the worry is that [30:54] there are no free lunches in biology and [30:56] usually if you fight biology, you [30:59] typically lose. There's always a [31:00] trade-off. And so when my friends often [31:02] like talk to me about like these miracle [31:04] things or this thing or take modafinil [31:06] and everything will be fine and da da da [31:07] da da. I go, "Yeah, but what's the [31:08] trade-off?" And I get most concerned [31:10] when they say there isn't one. Cuz then [31:12] I go, "Shit, we don't know it." [31:13] >> [laughter] [31:14] >> Yeah. You've got to be careful because [31:16] absence of evidence is not evidence of [31:19] absence. Mhm. [31:22] Be very careful when you're [31:24] doing that deal with with your [31:25] physiology. So, to come back to the sort [31:29] of the three things, the first thing we [31:30] were mentioning is digital detox and [31:33] don't worry about the blue light. [31:35] Worry about light in general. I'll come [31:37] on to that cuz that's the second. But, [31:38] Michael Grandner, as I was saying, what [31:40] he found is that the blue light doesn't [31:41] really disrupt your sleep. [31:43] It's a combination of first, these that [31:46] we use are attention capture devices and [31:50] they are designed to fleece you of your [31:53] attention economy and they do it [31:55] ruthlessly well. They've spent tens of [31:57] millions of dollars designing these [31:59] products to do that. [32:01] So, what happens is that these devices [32:03] become hugely activating. [32:06] And as a result, they essentially will [32:08] be a mute button on your sleepiness. So, [32:10] you could be there, you get into bed, [32:12] it's 11:00 p.m. You think, "I am so [32:14] tired. I was falling asleep on the the [32:16] the couch watching television." And then [32:17] you get to bed, you start going on to [32:19] social media, and then you start [32:20] doomscrolling, and then you get into [32:22] this what we call bed rotting, where you [32:24] just sit there. And now you look at the [32:25] clock and it's no longer 11:00 p.m. It's [32:28] 1:00 a.m. And you've just done sleep [32:30] procrastination. Now, it turns out that [32:32] it's yes that that these are attention [32:36] grabbing devices that will mute your [32:38] sleepiness. [32:39] But, you have to be of a certain [32:40] personality type, he found. Not all of [32:43] us are vulnerable to this sleep [32:45] disruption of devices. You have to be [32:47] someone who is perhaps neurotic, someone [32:50] who has high impulsivity, or someone who [32:52] is perhaps high anxious. If you are of [32:55] any of those kinds, you should be really [32:58] careful about your use of technology in [33:00] the bedroom. Now, for me to, you know, [33:02] sit here and say, "Look, [33:05] put your phone in the car in the garage [33:07] and that way, you know, that's what I [33:08] would love because [33:11] what we've learned to do in this modern [33:13] era is the first thing when you wake up. [33:16] What is it that you do? [33:18] No no comment. [33:19] >> [laughter] [33:21] >> What about you? [33:24] It's just you and I, Stephen. [33:26] Um I grab my phone before my eyes are [33:27] even open. And what happens is this sort [33:30] of small tsunami of anxiety washes over [33:33] you because as soon as you unlock the [33:35] phone, it's everyone else's agenda for [33:37] your day but your own. And it's a [33:39] terrible way to wake up. Have you ever [33:40] had the experience where you've got to [33:42] wake up for an early morning flight and [33:44] it's a critical flight? You know that [33:46] that night is not going to be a good [33:48] night of sleep. It's going to be a [33:50] shallow kind of sleep. It's what we call [33:52] anticipatory anxiety. You are [33:55] anticipating an anxious event in the [33:57] morning. [33:58] And studies have shown that when we [34:00] create this anticipatory anxiety, the [34:03] amount of deep sleep that you have drops [34:06] significantly. You don't sleep as well. [34:09] And therefore, if we just do this little [34:11] sort of version, this LITE version of [34:15] the morning flight, which is we know [34:17] that when we go to bed and we put our [34:18] phone down, we know that when we wake up [34:20] every morning, we're just going to open [34:22] it up to that hit of anxiety every [34:25] morning. No wonder our sleep can start [34:27] to get shallow. [34:29] Now, I'm not going to sit here and say, [34:31] "Well, don't take your phone into the [34:33] bedroom because the genie is out the [34:34] bottle and no matter what I say, it's [34:36] not going back in anytime soon." And a [34:38] friend of mine, Michael Grandner, has [34:40] got this beautiful [34:41] uh framework where he says, "You can [34:43] take your phone into your bedroom. It's [34:45] fine. [34:46] But, you can only use your phone [34:50] standing up. Oh. [34:53] >> [laughter] [34:53] >> What's his name? Um Michael Grandner. [34:55] He's from Brooklyn. [34:56] >> his own business. [34:58] And and what happens is that you you're [35:00] there and you think after about 7 or 8 [35:01] minutes, "Oh, I'm just I'm just going to [35:03] have a bit of a sit down here." As soon [35:04] as that phone goes away. So, I would say [35:07] that digital detox is the first friend [35:11] that will really help your sleep. The [35:13] the second is regularity and we'll come [35:16] on to regularity when we speak about, [35:18] you know, what really makes for good [35:19] sleep. [35:21] If you were to only do one thing, [35:23] not three things, but just one thing, go [35:25] to bed and wake up at the same time no [35:27] matter whether it's the weekday or the [35:29] weekend, regularity is king. Okay, so [35:32] that's the third pillar. That's correct. [35:34] Regularity. Okay. [35:37] And then I have [35:40] the T for timing. Correct. [35:42] Which we'll go through these. [35:44] Quantity, which we've talked a little [35:45] bit about already, and quality. [35:47] Correct. So, when I looked at the [35:50] science, for me, I created this [35:52] framework of the four macros of good [35:54] sleep. You've heard of the three macros [35:55] of food, macronutrients, fat, protein, [35:58] carbohydrate. To me, there are four [36:00] macros of good sleep and it's QQRT. [36:03] QQRT. And it stands for [36:06] quantity, [36:13] quality, [36:15] regularity, [36:18] and timing. And think of it less like [36:21] pillars, but the four legs of a chair. [36:24] And if any one of these becomes [36:25] unstable, the chair will topple over. [36:28] So, I'll probably start with the one [36:30] that people have heard me bang on about, [36:32] which is quantity. 7 to 9 hours. This [36:35] myth of 8 hours is nonsense. It's a [36:37] wonderful range, 7 to 9 hours. [36:41] And what we know is that using that [36:43] sweet spot of 7 to 9 hours, when you get [36:45] less than that, the shorter your sleep, [36:48] the shorter your life. [ __ ] Short sleep [36:51] predicts all-cause mortality. Now, we [36:53] say that this is the minimum of 7 hours [36:56] of sleep and some people have argued, [36:57] perhaps correctly, that look, if you [36:59] look at these mortality curves, there's [37:01] not much of a percentage difference [37:03] between sleeping 6 hours versus the 7 [37:06] that you're telling me is minimum. So, 6 [37:09] hours is just fine. So, all of this [37:10] nonsense and rhetoric is is is silly [37:13] from you. [37:14] And I think they made a conflation [37:16] because [37:18] 7 hours [37:20] is the minimum amount of sleep that you [37:22] need to survive [37:25] because the way that we quantify what [37:27] minimum is is based on whether you die [37:29] or you don't prematurely. [37:33] The amount of sleep that you need to [37:35] survive is different than the amount of [37:38] sleep that you need to thrive. [37:41] And people will conflate the former with [37:43] the latter. So, you've got to be careful [37:45] when people are sort of touting on [37:46] social media that say, "Well, no, but [37:48] look, you there's not much difference [37:49] between my sort of survival rate on 6 [37:51] hours versus 7 hours." [37:53] You may have a just as much of a long [37:55] life, but the quality of your life will [37:58] be very different. So, that's quantity, [38:00] 7 to 9 hours. And is that does it change [38:03] for parents, by the way, because I've [38:05] met so many parents that seem to be [38:06] functioning better than me and they've [38:07] got four they're having like four or [38:08] five hours sleep. Did evolution not give [38:11] parents any leeway or anything when they [38:13] have kids that suddenly their brain [38:14] changes and now they can survive with [38:16] less sleep? The evidence doesn't suggest [38:18] that once you go through parenthood, you [38:21] get some magic sort of, you know, [38:23] immunity shot that makes you, you know, [38:26] resilient and not vulnerable to a lack [38:29] of sleep. And in some ways, you could [38:31] argue because we used to, you know, live [38:34] as a collective tribe and we would share [38:36] duties, at that point, you know, mother [38:40] nature doesn't really worry too much [38:41] about you now [38:43] because you've already procreated and [38:46] you've passed on your genetic code. So, [38:48] you are now the the sort of the, you [38:51] know, the not particularly well, you [38:53] know, cared for individual through [38:55] evolution. It's your offspring that gets [38:59] So, it sacrifices you [39:00] in a way. I mean, that's what we see in [39:02] the animal kingdom. Did you see that [39:03] documentary about the octopus? Yeah. It [39:06] it was just I mean, I thought it was [39:07] beautiful documentary, but um The TLDR [39:10] for anyone that hasn't seen it is once [39:11] the octopus and I'm going to completely [39:12] butcher this, so please ignore. [39:14] Um once the octopus has given birth, [39:17] it dies. Basically, it doesn't move out [39:20] of that hole and it dies. Is that rough? [39:23] Well, I don't know if if it dies, but [39:25] its level of of active life I searched, [39:28] "Does the octopus die after [39:29] reproduction?" And it says, "Yes. Female [39:31] octopuses die after their eggs hatch. [39:33] After laying eggs, a female stops eating [39:36] and devotes all of her her energy to [39:38] protecting and oxygenating them until [39:40] they hatch. Once they do, she dies [39:43] shortly after. A process called [39:45] semelparity, [39:47] meaning they reproduce only once. This [39:50] death is triggered by hormone changes [39:53] from the optic gland similar to [39:55] mammalian pituitary glands. [39:57] And males die shortly after mating as [40:00] well, usually within a few months. [40:04] That is wild. In some ways it [40:06] it's tragic and it reminds me I'm so [40:08] glad that I'm not an [40:11] >> [laughter] [40:12] >> But but coming back to it. So, for [40:16] there doesn't seem to be some, you know, [40:18] magic cloak of invincibility that you [40:21] put on when you go through parenthood. [40:24] Certainly what we know is that the [40:26] number of individuals who can survive on [40:29] 6 hours of sleep or less and show no [40:31] impairment in either their brain or [40:33] their body, rounded to a whole number [40:35] and expressed as a percent of the [40:37] population, is zero. [40:40] So, quantity matters, but it turns out [40:43] that we got it wrong in thinking that [40:45] was the only thing because [40:48] then came quality. So, QQRt. Quality is [40:52] defined in sleep science as two things. [40:55] The first is something that your sleep [40:57] tracker will measure, which is the [40:58] continuity of your sleep, meaning do you [41:01] sleep in one or two nice long bouts [41:03] throughout the night? That's good [41:05] quality of sleep, nice continuous bouts. [41:08] Versus your sort of sleep is very [41:10] fragmented by all of these awakenings, [41:12] that's very poor quality of sleep. And [41:14] the way that you can measure it in your [41:15] sleep tracker is just by looking at the [41:18] app and there'll be something called [41:19] sleep efficiency. Sleep efficiency is [41:22] defined as the following: of the time [41:24] that you're in bed, what percent of that [41:26] time is spent asleep? And what we like [41:29] to see is you north of 85% or above. So, [41:32] this is kind of like the users guide to [41:33] sleep trackers. [41:35] What I want to see is 85% or more. If [41:38] you're less than that, we need to have a [41:39] conversation. That's number one good [41:42] quality of sleep. The second, which is [41:44] what sort of what these trackers can't [41:46] really do, but I can do in the sleep [41:48] laboratory when you look like a [41:49] spaghetti monster cuz I put electrodes [41:51] all over your head, [41:52] >> [snorts] [41:52] >> I can measure the quality of your big [41:54] deep slow brain waves of deep non-REM [41:57] sleep. [41:58] And that is a second measure, the power [42:00] of those big slow brain waves. That's a [42:03] second measure. And quality seems to be [42:06] as predictive as quantity [42:09] in making a difference not just to your [42:11] all-cause mortality, but quality even [42:14] more than quantity when it comes to [42:17] mental health has been showing the [42:19] biggest signal. [42:21] So, again, it's not that quantity [42:23] doesn't matter. You do have to get [42:25] sufficient amounts of sleep. But [42:26] quality, as much as quantity, should be [42:30] paid attention to and I haven't said [42:32] that enough. [42:34] The next is where we came to in our sort [42:36] of three things that I was saying. The [42:37] first is digital detox. Then the next [42:39] thing I said is regularity. [42:42] This is somewhere where I've also [42:43] changed my mind on. I've doubled down on [42:45] regularity. There was a study that also [42:48] came out of that same data set that I [42:49] described. It's called the UK Biobank [42:52] data. And now they didn't look at 90,000 [42:54] individuals, but they looked at 60,000 [42:56] individuals. [42:58] And they decided that they were going to [43:00] compare and split them into quartiles. [43:03] So, the most regular [43:05] to the second most regular [43:07] to then sort of the third most regular [43:10] and then the final was those who were [43:12] the least regular. And what does regular [43:14] mean in this context? [43:15] >> Good question. Highly regular [43:17] individuals plus or minus 15 minutes in [43:20] terms of going to bed and waking up at [43:22] the same time. In other words, a total [43:23] wiggle room of 30 minutes. Oh, okay. So, [43:25] if I'm always going to bed at 9:00 p.m. [43:27] and I do that 5 days in a row, I'm [43:28] regular timing really. [43:29] >> So so it's it's regularity in terms of [43:32] when you're going to bed and waking up. [43:35] So, it's you're right, it's timing in a [43:37] way, but I'll come on to why there is a [43:39] separate key for timing in just a [43:40] second, but regularity here was okay, [43:43] plus or minus. So, let's say you go to [43:45] bed at 8:45 p.m. one night and then 9:00 [43:48] and then 9:10 p.m. and then you're back [43:50] to 8:00. That's beautiful tight timing. [43:53] I like that. Whereas the those people [43:55] who were least regular, they were 90 to [43:58] 120 minutes disparate. They were going [44:00] to bed, let's say, at 11:00 one night [44:02] then 1:00 a.m. the next night then they [44:05] were going to bed at 10:30 p.m. and then [44:07] they were going to bed at 12:30. They [44:09] were all over the map. So, what they [44:11] found was that those people who were [44:13] most regular versus least regular, they [44:16] sort of compared the extremes of these [44:18] two, [44:19] those people who were most regular had a [44:21] 49% [44:24] relative decrease in all-cause [44:26] mortality. So, they were 49% less likely [44:29] to prematurely die than those people who [44:31] were least likely to die. They had a 39% [44:35] cancer mortality risk reduction. [44:38] Great. They had a 57% [44:41] cardiometabolic [44:43] disease risk reduction. [44:46] So, that was stunning that regularity [44:48] was incredibly powerful as a predictive [44:51] signal of your different forms of [44:53] mortality. [44:54] That wasn't the best part of the paper, [44:56] though. [44:57] They'd also measured quantity as well as [44:59] regularity in these same individuals. [45:02] So, then they decided to say, "Well, I'm [45:05] going to take our measure of quantity [45:06] and regularity and we're going to put [45:08] them both in the same statistical bucket [45:10] and do a Coke-Pepsi challenge to see [45:12] which one wins out in terms of [45:14] predicting all-cause mortality." We all [45:17] bet in the sleep field, at least I did, [45:18] it was going to be quantity. I was [45:20] wrong. [45:21] Regularity beat out quantity in [45:24] predicting all-cause mortality and by [45:26] quite some margin. Now, that doesn't [45:28] mean that you can now go away and say, [45:30] "I'm going to start sleeping 4 hours, [45:32] but incredibly consistent 4 hours." You [45:35] need both quantity and quality, but [45:37] goodness does regularity seem to carry a [45:40] massive signal. So, the coming back to [45:42] those three things, I would say digital [45:44] detox, just go to bed and wake up at the [45:46] same time. [45:47] And the final thing is light. In this [45:49] modern world, we are a dark-deprived [45:52] society. [45:54] We get what I call junk light at night. [45:57] So, you've heard of junk DNA? Well, we [45:59] get junk light at night. [46:01] We don't need all of this light and it [46:03] fools our brain into thinking it's still [46:05] daytime outside. So, no wonder as a [46:07] society, we have some struggles with [46:09] sleep at night. Now, that's due to many [46:11] reasons, stress, too much caffeine, [46:14] alcohol, THC, but excessive light is one [46:17] of the easiest things that you can do. [46:20] So, for the next 7 days, [46:22] just do me this experiment, [46:24] if you can, [46:26] set an alarm 1 hour before your normal [46:28] bedtime. When that alarm goes off, turn [46:31] off and I I do this myself, turn off [46:34] almost all of the lights in your house. [46:37] When you say all of the lights, do you [46:38] mean the little red light on my smoke [46:40] alarm or No, that's fine. But, you know, [46:43] so my wife and I, 1 hour before bed, [46:45] almost all the lights. We've got sort of [46:47] this little set of this sort of light [46:49] that goes around the television, the [46:50] back of the television, so it kind of [46:51] looks like the television's cool and [46:52] illuminated. [46:54] I will set that down to about 5% [46:57] of brightness [46:58] and all of the rest of the lights out. [47:00] So, you can kind of just still see some [47:02] illumination, so I'm not sort of, you [47:04] know, looking desperately uncool in [47:07] in front of it when I'm tripping over [47:08] things cuz it's complete black, you [47:10] know. Then start cooling the house or [47:12] the room as best you can to around about [47:14] 67-68° [47:16] Fahrenheit or about 18° Celsius. We can [47:18] speak about temperature, but just do [47:20] this experiment for the next 7 days. 1 [47:22] hour before bed, the alarm goes off, you [47:25] switch off all of the lights [47:27] and ask the following question, do you [47:29] feel sleepier? Is it soporific? Does it [47:32] make you feel more sleepy [47:34] as a result? But don't stop there. What [47:37] you've gone and done is the first [47:39] positive experiment, which is you've [47:41] gone from the no intervention, lights [47:44] are on, to then the Matt's intervention, [47:47] which is now the lights are off for 1 [47:48] hour before bed. Don't just ask, "Is my [47:51] sleep better when the lights were out [47:53] for 1 hour before bed?" Once that 7-day [47:56] period has finished, go back to doing [47:59] what you were doing before, which is [48:00] keep all of the lights on and ask [48:03] yourself, "Did my sleep get better when [48:05] I did the intervention and did my sleep [48:07] go back to being worse when I stopped?" [48:09] Because I'm trying to teach you [48:10] bidirectionality in the experiment. Does [48:12] that make some sense? Yeah, so you get [48:14] to [48:15] get to basically do an AB test. Correct. [48:17] You get to see both sides of the [48:19] equation and with that, it's more proof [48:21] positive than just one direction alone [48:23] cuz who knows, it could just be a [48:24] placebo effect. [48:25] So, regularity, coming back to it, is [48:28] critical. So, we've talked spoken about [48:30] QQR, quantity, quality, regularity. On [48:33] the [48:34] um [48:35] regularity [48:36] >> regularity point, why? What's going on [48:39] in our brain that's making it from a [48:41] hormonal perspective or other that's [48:43] making it important for us to sleep at [48:45] the same time? It's a bloody great [48:47] question. People don't respond to rules, [48:50] they respond to reasons not rules. So, [48:52] let me try and explain the reason behind [48:54] the sort of the rule. When it comes to [48:56] regularity, we have something called a [48:58] circadian rhythm that we've spoken [49:00] about. And there's a clock that sits [49:03] inside of your brain, deep in the middle [49:05] of the brain. So, [49:07] we have, it just turns out, [49:09] a brain here. [49:11] Lovely. Okay. So, [49:13] we've got one of these hemispheres here [49:15] and then I'm just going to take out what [49:17] we call the subcortical sections. So, [49:20] these are the areas that are below the [49:21] subcortex. So, here is the brain. So, [49:24] this is the front of the brain, the back [49:25] of the brain, top of the brain, and [49:26] here's the brain stem. And it turns out [49:28] that right in the middle of the brain, [49:30] right here, is an area called the [49:32] hypothalamus. [49:34] Now, here, this structure here, this is [49:36] the thalamus. This is the sensory gate [49:38] of your brain. So, all of your five [49:40] senses, sound, touch, taste, smell, they [49:42] all flood into this gate called the [49:45] thalamus. And then the thalamus will [49:47] decide whether it sends those sensory [49:49] signals up to your cortex. And when it [49:51] sends the signals up to your cortex, you [49:54] start processing them and you become [49:56] consciously aware of the external world. [49:59] Now, as we're falling asleep, just as an [50:00] aside, what's interesting is that this [50:02] gate, the sensory gate, the thalamus, [50:05] once we start to fall asleep, the gate [50:07] will close shut. [50:09] Now, your eyes are technically still [50:11] seeing, your ears are still hearing, [50:13] your tongue is still tasting. [50:15] But because the gate of the thalamus, [50:17] the sensory gate, closes shut, those [50:20] signals that are coming into your brain [50:22] are no longer sent up to your cortex, so [50:25] you stop perceiving the outside world, [50:27] which is just simply a different way of [50:29] saying you've fallen asleep. [50:31] Now, the hypothalamus, you've heard of [50:34] hypo sort of hypertension or sort of, [50:36] you know, hypothermia, that means lower. [50:40] So, here's the thalamus. This area here [50:42] is called the hypothalamus. [50:44] And it's a tiny structure, but within [50:46] that structure contains a nucleus. And [50:49] that group of cells, the nucleus, has a [50:52] fancy term and it's called the [50:53] suprachiasmatic nucleus. But the [50:56] suprachiasmatic nucleus is your master [50:58] 24-hour clock. [51:00] Every cell in your body has a clock [51:04] inside of it. [51:05] But this is the master clock. It's like [51:08] Lord of the Rings, there's one ring to [51:10] rule them all. Well, there's one clock [51:12] to rule them all. [51:13] And here, in the suprachiasmatic [51:15] nucleus, you get the 24-hour rhythm of [51:18] being awake and being asleep, being [51:20] awake and being asleep. How does your [51:22] brain keep quartz-like precision 24-hour [51:26] clock time? How does it do that? [51:30] The way it does that is that it uses [51:32] signals such as light and dark. [51:35] >> From your eyes? From your eye. [51:37] And so, when light comes through the [51:39] retina, [51:40] it tells the hypothalamus it's daytime [51:44] and therefore you should be awake. And [51:46] its rhythm starts its awesome sort of [51:48] upswing. And temperature can do this, [51:50] and feeding can do this, all sorts of [51:51] different things. But for the most part, [51:53] light is the principal governor that [51:57] essentially acts like electrical, I [51:59] should say, photon fingers that pops the [52:01] wristwatch dial out and resets it [52:03] precisely to 24 hours every single day. [52:06] Because if you're left in the dark with [52:08] no signals of light, your clock isn't [52:11] precise. It drifts to about 24 hours and [52:14] 15 minutes, so you start going forward a [52:16] little bit every single day. If you go [52:17] into a cave, and people have done this [52:19] experiment. The thing that keeps it [52:20] precise is light. [52:22] So, you need light to keep a beautiful [52:25] 24-hour rhythm. [52:27] One of those things that's under the [52:28] control of your 24-hour rhythm is your [52:31] sleep-wake cycle. What if I'm doing [52:33] exercise? Exercise is a wonderful [52:36] entrainer of your circadian rhythm, as [52:38] long as you're doing it at the right [52:40] time. [52:41] So, if you're starting to exercise at [52:43] 3:00 or 4:00 in the morning, [52:45] that's not good, because that's an [52:46] activity signal that's going to confuse [52:49] the brain into thinking it's the active [52:51] period, which is normally, because we're [52:52] a diurnal species, the day. [52:54] And it's the same thing, coming back to [52:56] my point of regularity, [52:58] using light as the best way to help with [53:02] that regularity, because light, [53:04] if it's artificial at night, fools your [53:07] brain into thinking that it's daytime [53:10] still outside. I mean, is there any such [53:11] thing as non-artificial light? I mean, I [53:13] guess with the sun, but I mean, is there [53:15] a type of light that I could use at [53:17] night, like candles or something? Or [53:18] Yes, below 30 lux Right. [53:22] >> is not going to necessarily do you a [53:24] disservice. Probably below 50 lux. Now, [53:26] lux, l u x, is just a measure of light [53:29] intensity. And you can download on the [53:31] App Store a free lux meter. And if [53:33] you're an idiot nerd like me, you're [53:35] going all over the house at night and [53:37] you're sort of putting it in different [53:38] locations. You're seeing, "God, God, is [53:40] there any kind of white spots here [53:41] where, you know, the lux is too high?" [53:44] But you need to drop that that lux. By [53:46] the way, it's a great way, if people [53:48] want to say, "Look, my REM sleep is [53:49] deficient. How can I get more REM [53:51] sleep?" There was a great study where [53:53] they did something similar to what I'm [53:54] telling you now. [53:56] 90 minutes before bed, they turned down [53:59] the lights to below 30 lux and they [54:02] pulled out all of the blue light. [54:04] And just that trick of dropping the [54:06] lights down 90 minutes before bed, below [54:09] 30 lux, making it warm, yellow light, [54:13] increased their REM sleep by 18%. Wow. [54:16] It's a huge margin. So, no need for [54:18] pharmacology. But to your question, why [54:21] is regularity [54:23] important? Well, I told you that light [54:25] is one of the signals that can create [54:28] regularity. It turns out that your [54:30] behavior [54:32] is another thing that will tell your [54:34] brain. So, meaning, when you go to bed [54:37] and wake up at the same time, [54:39] it acts like an anchor. It anchors your [54:42] circadian rhythm and it tells you, [54:45] almost like a scene in a movie, this [54:48] scene is now complete, a new scene [54:50] starts. This scene is complete, a new [54:52] scene starts. So, every time that you're [54:54] going to bed at the same time and waking [54:56] up at the same time, you are feeding the [54:58] suprachiasmatic nucleus, the master [55:00] 24-hour clock in your brain. You're [55:02] feeding it signals of regularity. [55:06] And when it feeds on signals of [55:08] regularity, it improves the quantity and [55:12] the quality of your sleep. [55:15] Your circadian rhythm likes consistency. [55:18] It likes regular signals. When you feed [55:20] it signals of light, of activity, of [55:23] waking up, going to bed, [55:25] you improve the quantity and the quality [55:27] of your sleep. That's the reason behind [55:29] the underlying rule. So, having a TV in [55:31] your bedroom is a terrible idea then, [55:33] because if [55:34] on that behavioral point, if I'm getting [55:36] in bed, but then I'm staying up for 3 [55:38] hours watching Netflix, my brain is [55:40] going to be quite confused about like [55:42] the behavioral pattern of what what I'm [55:44] doing in my life. [55:45] It's not going to associate the bed with [55:46] sleep, it's going to associate the bed [55:48] with movies. That's one of the problems [55:50] that we call it's called conditioned [55:52] arousal, which sounds a lot more [55:54] salacious than it actually is. It's a [55:56] term that we use in sleep medicine, [55:59] which may explain insomnia. So, with [56:03] insomnia, let's say that the first time [56:05] you go to this thing called the dentist [56:06] and you get in the chair and it's kind [56:08] of cool, you're reclined back and, you [56:10] know, you think this is fine. But then, [56:12] after about 14 or 15 visits, [56:15] when you get into that chair, you are no [56:17] longer looking forward to getting into [56:19] that chair, are you? Why? Because you've [56:21] learned the association that being in [56:23] that chair typically leads to a bad [56:26] outcome. [56:27] >> [laughter] [56:27] >> Now, the same thing is true with the [56:30] bed. If you start associating the bed [56:33] with anything other than sleep, and we [56:35] give you a pass in terms of sex, [56:38] sleep and sex, anything other than that, [56:40] you start to learn that this thing [56:42] called my bed is this place where I'm [56:45] awake, where I work, where I eat, where [56:48] we have conversations, where I watch [56:50] television. And so, you know, if I were [56:52] to and I'm going to I'm stealing Michael [56:54] Grandner's point, but if I were to say [56:56] to you, "Bed, sleep, bed, sleep, bed, [56:58] sleep, bed, sleep, bed, [57:00] sleep." Okay, if I were to say, "Bed, [57:03] scroll, bed, eat, bed, work, bed, sleep, [57:06] bed, TV, bed." [57:10] You've confused. Yeah. Because there's [57:13] no predictive signal. You've never bound [57:15] an association. Now, the way this works [57:17] to your disadvantage in insomnia is the [57:21] following. [57:22] The insomnia event that begins the [57:24] insomnia is typically not the thing that [57:26] maintains the insomnia. So, let's say [57:28] that I [57:30] um had I experienced a really difficult [57:32] bereavement [57:34] and that triggered a form of insomnia [57:36] where I couldn't sleep because of the [57:37] bereavement. [57:39] Gradually, the bereavement [57:42] is not the thing that's going to [57:43] maintain my insomnia. It's because every [57:46] time I have been going to bed over the [57:48] past month, [57:50] I have not been sleeping. I've been wide [57:53] awake in my bed. So, now, because your [57:55] brain is such an incredibly associative [57:57] device, it learns the association that [57:59] my bed is the place where I'm always [58:01] awake. [58:02] And what do we then do? We need to break [58:04] that association in insomnia. So, what [58:06] we do is we say the 20-minute rule. If [58:09] you've been in bed for about 20 minutes [58:10] and it's just not happening for you, [58:12] don't worry. Don't listen to idiots like [58:14] me that doom and gloom and disease and [58:15] sickness and one bad night is not going [58:18] to be a problem. It's just not. So, just [58:20] say, "Look, tonight is not my night. I [58:22] am not, however, going to lie in bed [58:26] awake, because very quickly my brain [58:28] starts to learn the association that my [58:29] bed is the place where I'm wide awake." [58:31] And you need to break that association, [58:32] so go to a different room in dim light, [58:35] just read a book, listen to a podcast, [58:38] whatever it is. And the rule of thumb is [58:40] the following. Only return to bed when [58:42] you are sleepy. [58:44] And so, there's no time limit. And that [58:46] way, you gradually relearn the [58:47] association that my bed is the place [58:49] where I always get consistent sleep, [58:51] because otherwise, it's the dentist's [58:53] chair. You walk into your bedroom [58:56] and you look at your bed and it's your [58:57] nemesis. And you convince yourself, even [59:00] before you get into bed, "I'm not going [59:02] to sleep, because that's the place where [59:03] I always don't sleep." And by the way, [59:06] if you suffer from the 3:00 a.m. [59:08] awakenings, my first question is, "How [59:10] do you know it's 3:00 a.m.?" [59:12] And that's your first problem. Looking [59:14] at the clock does two things. It makes [59:17] you more anxious. Yeah. And second, [59:20] because your brain is such an incredibly [59:21] associative device, [59:23] you start to then decide that 3:00 a.m. [59:26] is the time when I need to wake up. If [59:29] you keep looking at the clock, you keep [59:31] reinforcing that 3:00 or 4:00. And sleep [59:34] at 3:00 in the morning is like trying to [59:36] remember someone's name. The harder you [59:38] try, [59:39] the further you push sleep away. Sleep [59:41] is something that happens to you. It's [59:43] not something that you make happen. [59:47] And so, at that moment, the best advice, [59:49] if you don't want to get out of bed, is [59:51] do any one of the following. [59:53] Meditation. [59:54] Just do a guided meditation. You can [59:56] download apps. Next, if it that's not [59:58] your thing, that's okay. Do box [60:00] breathing. You know, you can sort of [60:02] inhale for five, hold for six, exhale [60:06] for seven. There's all sorts of [60:07] different numbers, but you can do [60:08] breathing exercises. The third, if you [60:10] don't like that, is a body scan. So, [60:12] close your eyes, start at the top of [60:14] your head, feel as you know, do I have [60:16] tension in my forehead? Do I need to [60:17] relax it? What about my neck? Do I need [60:19] to move through your body and gradually [60:21] go down? How are my shoulder blades [60:23] feeling? I just relax down into the bed. [60:25] And gradually down into the chest, into [60:27] the [60:28] move through and just relax. [60:31] If none of those things feel fun, the [60:33] next thing you can do is take yourself [60:35] on a mental walk. There's a great study [60:37] from my university at the University of [60:39] Berkeley, California. [60:41] And we didn't do the study, Alison [60:42] Harvey did it. By the way, counting [60:44] sheep, [60:45] bad idea. Makes your sleep worse. It [60:48] turns out. Why is that? Because well, [60:50] with every kind of little bleating [60:52] cotton wool ball with a strange look on [60:54] its face that leaps over the fence that [60:56] you're counting, you're reinforcing [60:58] every minute of sleep that you're not [61:00] getting, and it seems to make matters [61:02] worse. But what she found was that [61:04] there's an alternative. If you think [61:06] about a walk that you know in great [61:08] vivid detail. So, for me, it's going to [61:10] be walking the dog. So, I go over to the [61:13] shelf, I open the door, is it the red [61:14] lead or the I'm going to go with the [61:16] blue lead today. So, I clip the dog in [61:17] with my right hand, I open the door with [61:19] my left hand, I take a left down the [61:20] stairs, I look It's that level of I want [61:23] you 4K detail [61:25] in terms of granularity. [61:27] And what's common about every method [61:29] I've just described, meditation, box [61:32] breathing, [61:33] sort of body scan, going on a mental [61:36] walk, all of these things have in common [61:39] that you get your mind off itself. [61:43] In that particular example, where she [61:45] asks you to vividly think about a [61:47] journey that you know, what did she find [61:49] in the study? What she found is that [61:51] that increases the speed with which you [61:53] fall back asleep Uh-huh. significantly. [61:57] Because, as I said, it it's so, you [61:59] know, her work to me demonstrated that [62:02] it it is so like that name, because [62:05] the moment I stop trying to remember [62:08] someone's name, [62:09] what happens? [62:11] You remember. I remember it. [62:13] And so, when you do these types of [62:14] exercises where you're getting the mind [62:16] off itself, [62:18] the next thing that you typically [62:19] remember [62:20] is your alarm clock going off in the [62:22] morning. [62:23] Is this why people listen to very vivid [62:26] sleep stories, and why I listen to [62:29] serial killer documentaries? [62:31] Serial killer documentaries, [62:34] true crime documentaries, I should say. [62:35] That's a bit more [62:37] uh nice to palate. [62:39] I don't know of them. My suspicion is [62:41] that they may be doing your deep sleep a [62:44] disservice. Anything Stick up for me in [62:46] the comments. [62:47] >> [laughter] [62:48] >> If you listen to true crime to fall [62:49] asleep, please write it below in the [62:51] comment section. If you find it [62:53] subjectively wonderfully pacifying [62:57] and calming, [62:58] and there is not death, I know I'm being [63:00] >> maiming, blood, and limbs being [63:03] distributed at high velocity all over [63:05] the scene, I would say it's great. But [63:08] if it looks like a Quentin Tarantino [63:09] movie or sounds like one, [63:11] may be harm and foul, rather than [63:13] helpful. [63:14] >> just in my ears. [63:14] >> But yes, so, [63:16] you know, [63:17] we forget that, to the best of my [63:19] knowledge, the meditation company called [63:23] Calm, now I have no affiliation with [63:24] them. They were doing somewhat well, [63:27] but what they realized is that they [63:28] wanted people to sort of meditate in the [63:30] morning. When they used looked at their [63:31] usage statistics, people were meditating [63:33] in the morning, but then there was a [63:34] huge swath of usage right before bed. [63:37] People were self-medicating their state [63:39] of insomnia. And then, through a stroke [63:41] of genius, they realized, [63:43] when we were young, we used to love [63:45] falling asleep to our parents reading us [63:48] a story. [63:50] Why is that any different when we become [63:51] adults? So, they created sleep stories, [63:54] and they went from struggling as a [63:56] company, I think, to becoming the first, [63:58] or one of the first, billion-dollar [64:00] valuation health companies out there. [64:03] They became a unicorn. [64:04] And now they can they've got, you know, [64:06] people like, you know, Matthew [64:08] McConaughey, they've got Harry Styles, [64:10] and then occasionally they've got a [64:12] you know, an unfortunate British sleep [64:13] scientist with a bad voice, but you can [64:16] listen to these sleep stories, and they [64:18] are wonderfully soporific. Why? Because [64:20] they get your mind off itself. [64:22] We we talked earlier on about melatonin, [64:25] and there are other supplements which [64:27] people talk a lot about. One of the ones [64:29] that's become really popular [64:30] is magnesium. I've heard ashwagandha, [64:33] and I've heard magnesium a lot. Yeah. Is [64:35] there any efficacy to these? Are these [64:37] Are these useful? [64:38] The first thing I would say is that if [64:40] you're suffering from sleep problems, [64:41] and you're looking to supplements, [64:43] you're stepping over dollars to pick up [64:45] pennies. Okay. [64:47] What you need to do is think about the [64:49] fundamentals. [64:50] Regularity. [64:52] Watch your caffeine intake. [64:54] Make sure you're not drinking too much [64:55] alcohol. [64:56] Get regular, dim down half the lights, [64:59] digital detox. Any one of those, but [65:01] especially all of them combined, are [65:03] going to get you log orders of better [65:05] sleep than reaching for the [65:08] latest supplement bottle of whatever it [65:11] is. The second thing to say is, think [65:13] about it from a logical standpoint. If [65:16] there were really some supplement that [65:18] promises to be the Shangri-La of all [65:20] resplendent sleep at night, the drug [65:23] companies would have been all over it [65:25] decades ago. [65:26] To put in context, it took George Lucas, [65:29] I think, about 30 years to amass [65:31] something like 4 billion in revenue from [65:33] the Star Wars franchise. It took Ambien [65:35] 22 months. [65:38] That's how big a business sleep pharma [65:40] is. Ambien's what? A sleep pill? Ambien [65:42] is a sleep pill. [65:44] Magnesium, if you dig into it, and I I [65:47] did a deep dive about 3 years ago, [65:48] because I I kept hearing it, too, this [65:50] magnesium, magnesium. The first thing to [65:52] note is that most forms of magnesium, [65:54] magnesium oxy oxide or magnesium [65:57] citrate, most of these forms of [65:59] magnesium [66:01] don't cross the blood-brain barrier. [66:04] And sleep is produced by your brain. So, [66:07] how can something that doesn't get into [66:09] your brain affect [66:11] brain process number one? There is one [66:14] form of magnesium that seems to have [66:15] some evidence in favor of it. It's [66:17] called magnesium L- threo nate. But if [66:21] you look at the literature, where did [66:22] this story come from? [66:24] It turns out that about 30 years ago, [66:26] they started looking at people who had [66:28] disrupted sleep, and they would assess [66:29] their blood work. And what they found is [66:31] that some of those people were magnesium [66:33] deficient. [66:35] And when they supplemented them with [66:36] magnesium, and they became magnesium [66:39] normative, their sleep got better. [66:42] But that's very different than saying, [66:44] look, you and I were currently magnesium [66:47] normative, [66:48] and then dosing myself with high volumes [66:51] of magnesium, am I imagining that that's [66:54] going to make my sleep better? The The [66:55] analogy would be, let's say I develop [66:57] this incredible new oxygen saturation [67:00] machine, [67:01] and you say to me, well, but Matt, my [67:03] blood oxygen saturation right now, [67:05] looking at my device, tells me it's [67:07] 98.6%. [67:10] It doesn't matter how fancy or good my [67:11] machine is, I'm not going to get you [67:13] past 100%. You're already at ceiling [67:16] level. Mhm. And that's the problem with [67:18] magnesium supplementation. If you're [67:20] magnesium normative, all you're doing is [67:22] creating probably expensive urine [67:25] at that moment in time. [67:27] Now, there may be an indirect benefit of [67:29] magnesium [67:31] in that it does seem to relax muscles. [67:33] And when the body is in a state of [67:36] relaxation, it sends a signal of [67:38] relaxation back up a branch of nerves [67:41] called the vagus nerve that goes up to [67:43] the brain and signals to your brain [67:46] you're starting to relax down, and you [67:47] get the state of quiescence. And that's [67:50] very helpful for sleep. So, magnesium [67:52] may still have an indirect benefit on [67:54] sleep through its relaxation kind of [67:57] policy that it instantiates in the body. [68:00] But overall, magnesium [68:02] is not really moving the needle, if you [68:04] look at the studies. [68:06] Ashwagandha [68:08] is different. Ashwagandha and another [68:10] compound called phosphatidylserine. [68:14] Phosphatidylserine [68:15] and ashwagandha, both of these [68:17] supplements seem to help do one of two [68:21] things. They either ratchet down the [68:23] fight-or-flight branch of your nervous [68:25] system, and they can also reduce the [68:28] amount of cortisol that the body is [68:30] releasing. [68:32] That's important, because [68:34] I see a lot of people coming to the [68:35] sleep center where I'm at, and they have [68:37] what I call the tired but wired [68:39] phenomenon, where they come to me and [68:41] they say, I am so tired. I am so so [68:44] tired, but I'm just so wired emotionally [68:47] and from a nervous perspective that I [68:49] can't fall asleep. And let's say that [68:51] you've done let's say, you know, an [68:52] on-stage event, and it's incredible. [68:55] You've got that on-stage buzz, you come [68:57] off stage at 11:00 p.m., and normally [68:59] you'd be fast asleep, but you know you [69:01] are so wired, it doesn't matter. You are [69:04] tired as tired as can be, but you're so [69:07] wired, you can't fall asleep. That's the [69:09] fight-or-flight branch being switched [69:10] on, and you just can't fall asleep. You [69:12] need to push it back off. [69:13] Phosphatidylserine and ashwagandha will [69:16] both push you back over into the more [69:19] quiescent, what we call parasympathetic [69:21] nervous system branch. That's good. [69:24] However, [69:25] they also will reduce cortisol, and [69:27] cortisol is a wake promoting hormone. [69:30] Cortisol is fine. We it gets a bad rap. [69:33] You need to have your cortisol start to [69:35] spike a few hours before bed and it [69:37] helps with the waking up process. It's [69:40] wonderful. Every day we have a cortisol [69:42] spike that starts happening before we [69:44] wake up. It's one of the things that [69:46] helps us wake up and then it builds us [69:49] to this beautiful crescendo mid morning. [69:52] Where you should be awakened [69:54] not needing caffeine. And it drops [69:56] before bed. And then it starts to peak [69:59] in a sort of middle early afternoon and [70:02] in fact usually peaks at late morning [70:03] hours I should say and then it will [70:05] start its awesome sort of down swing. [70:07] And what you see is that right before [70:09] you go to bed cortisol should hit its [70:12] lowest point, what we call its nadir, [70:15] its lowest trough. Mhm. What's [70:17] [clears throat] interesting by the way [70:18] just as an aside is that insomnia we can [70:22] classify usually as at least one of two [70:24] different types. There's actually [70:25] multiple but let's just say there are [70:27] of those multiple there are two types. [70:29] One is called sleep onset insomnia, I [70:32] can't fall asleep. The other is sleep [70:34] maintenance insomnia, I can't stay [70:36] asleep. [70:37] When they've looked at people's cortisol [70:40] on a 30 minute by 30 minute basis on the [70:42] 24 hour clock face, we go through just [70:45] what we described. Just before we wake [70:47] up we get this rising cortisol, it peaks [70:49] late morning and then it drops down and [70:52] right before bed our cortisol is almost [70:54] at its lowest point. [70:56] With insomnia patients they show exactly [70:58] the same thing, a beautiful rise [71:01] in the late morning hours. It starts to [71:03] come down but then you see two [71:05] anomalies. [71:07] Right before bed it goes back up. [71:10] And then in the middle of the night even [71:13] when it's starting to rise it will have [71:14] this abnormal spike right in the middle [71:16] of the night too. [71:18] And what we believe is that that may in [71:20] part explain sleep onset insomnia. [71:23] Cortisol should be coming down and [71:24] should stay low right before we go to [71:26] bed but then it jumps back up in [71:27] insomnia patients. I can't fall asleep. [71:30] And then it continues to stay low [71:33] throughout the first half of the night [71:34] but then it also spikes in insomnia [71:36] patients. I can't stay asleep. [71:39] I've had so many founders speak to me [71:41] and say, "Why didn't this particular ad [71:43] that I ran on this platform work for [71:45] me?" Maybe the copy wasn't good, the [71:46] creative wasn't strong but usually the [71:48] problem is they're not having the right [71:49] conversation because that ad never [71:51] reached the right person. And if you're [71:52] in B2B marketing, that is much of the [71:55] game and this is where LinkedIn ads [71:57] solves that problem for you. Their [71:59] targeting is ridiculously specific. You [72:01] can target by job title, seniority, [72:03] company size, industry and even [72:05] someone's skill set. And then network [72:08] includes over a billion professionals. [72:10] About 130 million of them are decision [72:13] makers. So when you use LinkedIn ads [72:15] you're putting your brand in front of [72:16] the right people. And LinkedIn ads also [72:18] drive the highest B2B return on ad spend [72:20] across all ad networks in my experience. [72:23] If you want to give them a try head over [72:25] to linkedin.com/diary [72:28] and when you spend $250 on your first [72:30] LinkedIn ads campaign you'll get an [72:32] extra $250 credit from me for the next [72:36] one. That's linkedin.com/diary. [72:39] Terms and conditions apply. [72:41] We were talking about regularity, timing [72:43] and all these things and quality and [72:44] quantity. [72:45] But one of the things I learned from [72:46] your work is that that last hour is [72:50] potentially the most important hour of [72:52] me being in bed. And I I say this in [72:54] part because my my girlfriend she would [72:56] wake she'd have about six six hours six [72:58] and a half hours sleep. She sleeps very [73:00] very well, perfect sleeper. But she'd [73:01] always get up really really really [73:03] early. And [73:05] in part that was because of the the [73:06] guilt that I talked about. But I had a [73:08] conversation with her about the guilt [73:09] and I said, "Just stay in bed as long as [73:10] you need to stay in bed. Like just have [73:12] that extra eighth hour." And in part [73:14] that's because I learned that [73:16] the further we go in sleep, the more REM [73:19] we're getting. Yeah. Okay, can you [73:21] explain that to me with these four [73:22] blocks? Why that last hour is [73:25] particularly important and why we [73:26] shouldn't be jumping out of bed or why [73:28] we should be using certain sleep devices [73:30] to wake us up when we're at the end of [73:31] that last hour of REM. Absolutely. So [73:34] here we have the four blocks of sleep. [73:37] So when we first fall asleep we go into [73:40] light non rapid eye movement sleep stage [73:42] one. This is the stage of sleep that if [73:45] I wake you up out of it you say, "I [73:48] wasn't sleeping." Mhm. Now you it's just [73:50] that you're just in that transitional [73:52] phase, this beautiful liminal state [73:55] between the windows of wakefulness and [73:57] true sleep. So this is your bridge [74:00] between the waking world and the sleep [74:01] world and it doesn't last for very long, [74:03] maybe just 10 or 15 minutes at tops. [74:06] Then you get into the workhorse of [74:08] sleep. This is stage two non REM sleep. [74:11] 50% of your night is spent in stage two [74:14] non REM sleep. I don't like the word [74:16] light non REM sleep. I've often used it [74:19] but it's not really it's we do a lot of [74:22] cognitive processing in stage two non [74:23] REM sleep. It's good stuff. It's not [74:26] just the stage that you have to go [74:27] through from sort of you know deep non [74:30] REM sleep to go back to stage two in [74:32] order for you to get to REM but I'll [74:34] come to that. So we have fallen asleep [74:37] 10 minutes. [74:38] >> Yeah. [74:39] Now we're in stage two non REM sleep. [74:40] We'll stay there for about 15 or 20 [74:42] minutes. Then if it's [clears throat] in [74:45] the first couple of hours of the night [74:46] we go down into the very deepest stages [74:49] of deep non REM sleep. This is where the [74:51] brain wave patterns slow down [74:54] but the brain waves become incredibly [74:56] big. Huge big powerful slow brain waves. [75:00] This is where you get an enormous amount [75:02] of restoration recovery of many of your [75:05] major physiological systems. [75:08] So physical recovery. Physical recovery [75:10] but mental too. Yeah. [75:12] It's during deep sleep that you take [75:14] newly minted memories that you've [75:16] learned and you hit the save button on [75:18] those memories so that you don't forget. [75:20] Deep sleep essentially is going to [75:22] future proof the information that you [75:25] just learned today. [75:27] It transfers information from a short [75:30] term storage vulnerable reservoir to a [75:32] more permanent long term storage site. [75:35] It's during deep non REM sleep when we [75:36] have this communication. So think of [75:39] those deep powerful slow brain waves [75:41] like long wave radio station when you [75:43] used to tune into a radio station in the [75:45] car. [75:46] You get huge ability for information [75:48] transfer across long distances across [75:51] huge paths in the brain. It's amazing. [75:54] So we've gone from light non REM. Then [75:57] we go down into deep non REM. We'll stay [75:58] there for about 15 or 20 minutes. Then [76:01] we'll start to rise back up again. We'll [76:03] go back into stage two non REM sleep. [76:05] Wait, we've gone from one two three to [76:07] two. Yes. So we've gone Think about it [76:10] more [76:13] almost like a roller coaster ride. So we [76:15] go from light non REM [76:17] and then we go down into stage two non [76:19] REM. Then we go down into deep sleep and [76:22] then we're going to rise back up into [76:24] light stage two non REM sleep. We're [76:27] going to stay there and after about 70 [76:29] 80 minutes you're going to pop up [76:32] and you'll have a short REM sleep [76:33] period. Oh okay, like this. [76:35] >> And this is beautiful. So this is what [76:37] we call a hypnogram. I'll put this on [76:40] the screen for anyone. Lovely. So what [76:42] I'm describing here is this roller [76:44] coaster ride. So we've fallen asleep, [76:45] light stage one non REM. Go down into [76:48] stage two. Then you go down and you have [76:51] a heavy period of deep non REM slow wave [76:53] sleep stage three. [76:55] And then and that's what you see on your [76:57] sleep tracker is deep sleep. This is [76:58] light sleep. This is deep sleep. Stage [77:00] two non REM sleep, light sleep, stage [77:02] three non REM sleep, deep sleep. But [77:05] then you'll start to climb back up and [77:08] then [clears throat] you may pop up and [77:09] you'll have a short REM sleep period [77:10] here after about 70 or 80 minutes. So [77:13] you'll have about 10 minutes of REM [77:14] sleep [77:15] and then back down you go again. You go [77:17] down into non REM sleep and then up into [77:20] REM. Down into non REM sleep and you'll [77:22] go up into REM. Down into non REM sleep [77:24] and up into REM. [77:26] So what's interesting however is that [77:28] the ratio of non REM to REM changes. Now [77:33] there's a myth out there and it's a bit [77:35] of a problem. [77:37] We humans have a 90 minute average non [77:41] REM to REM cycle. So we go down into non [77:43] REM sleep and then up into REM sleep [77:45] every 90 minutes. Then we go back down [77:47] into non REM sleep and then up into REM [77:48] sleep. So we go down into non REM sleep [77:51] and then up into REM in this 90 minute [77:53] cycle. [77:55] The problem is that [77:57] it's on average 90 minutes. It ranges [77:59] from 70 minutes to up to 120 minutes [78:02] from one individual to the next. So you [78:04] know these devices that you may have [78:06] seen tried to sort of you know [78:07] entrepreneurship, they say, "I'm going [78:09] to wake you up at the ideal moment in [78:12] your 90 minute cycle so that this thing [78:15] that sits on my bedside I tap it when [78:17] I'm the lights go out and then it's [78:18] going to go on its 90 minute cycle and [78:20] it's going to figure out the perfect [78:21] moment to wake you up." It's nonsense. [78:24] Because my sleep cycle may be 75 [78:27] minutes, yours may be 105 minutes. It's [78:29] got no idea cuz it's using a hard coded [78:31] 90 minute cycle. It's it's in some ways [78:34] nonsense. [78:35] But we go down into non REM sleep and up [78:38] into REM sleep every 90 minutes. What [78:39] changes however is the ratio of non REM [78:43] to REM within those 90 minute cycles as [78:46] you move across the night such that in [78:48] the first half of the night the majority [78:51] of those 90 minute cycles are comprised [78:53] of lots of deep non REM sleep and very [78:56] little REM sleep. But as you push [78:58] through to the second half of the night, [79:00] now that seesaw balance shifts over and [79:03] you spend much more of your time in REM [79:05] sleep in the second half of the night [79:07] and particularly just as you said in the [79:09] last two hours of the night. Why is this [79:11] consequential? Well, just as you said [79:13] and you spoke about for your girlfriend, [79:15] let's say that you know I normally go to [79:17] bed for argument's sake and I'm not [79:19] saying this is the ideal time but I go [79:20] to bed at midnight to make the math [79:22] easy, and I wake up at 8:00. But [79:24] tomorrow, I've got to catch my flight [79:25] back home. So, I'm going to wake up 2 [79:28] hours early. So, I'm going to wake up at [79:29] 6:00 rather than 8:00. I've lost 2 hours [79:32] of sleep. So, how much total sleep have [79:34] I lost? Well, I've lost 25% of my total [79:36] sleep, 2 hours of my 8 hours, 25%. Well, [79:40] yes and no. I've lost 25% of my total [79:43] sleep, [79:44] but I may have lost [79:46] 50, 60, 70% of all of my REM sleep. Why? [79:49] Because REM sleep comes in the second [79:51] half of the particularly those last [79:53] couple of hours of sleep. So, that's why [79:54] it's not just academic that you [79:56] understand the sleep cycle relationship, [79:58] but it's also pragmatic because it can [80:00] impact the amount In fact, the easiest [80:02] way, if people said, "How can I get more [80:04] REM sleep?" [80:05] I would say, "Just sleep 15 minutes [80:08] later into the day than you normally [80:10] would do, and you will [80:11] disproportionately bias yourself towards [80:14] getting significantly more REM sleep." [80:17] And why does REM sleep matter? [80:19] REM sleep is a brain state, firstly, [80:21] that is incredibly active. In some In [80:23] fact, some parts of the brain, [80:24] particularly if I were to show you these [80:27] deep emotional centers of the brain, as [80:29] I pull this brain apart, [80:32] so, we've got these sort of deep [80:34] emotional centers in the brain that sit [80:37] and in fact, they sort of they're more [80:38] just underneath in here tucked in inside [80:41] just next to your brain stem at the top [80:43] of it. And these emotional centers are [80:45] called the amygdala, and you have one on [80:47] the left and one on the right side of [80:49] your brain. That part of the brain, [80:51] together with a memory structure that [80:52] runs alongside it called the [80:54] hippocampus, those two parts of the [80:56] brain form what we call the limbic [80:58] system. And you may have heard of the [80:59] limbic system, so the emotional centers [81:01] of the brain. Those can be up to 40% [81:03] more active when you're in dream sleep [81:05] than when you're awake. Dream sleep? [81:08] Dream sleep is rapid eye movement sleep. [81:10] >> REM sleep? So, REM sleep is the stage [81:12] now It depends on how you define [81:14] dreaming. [81:15] If you define dreaming as any mental [81:17] activity reported upon awakening, then [81:19] you dream in all stages of sleep, light [81:21] non-REM sleep, deep REM sleep. So, what [81:22] would What would that sound like? Well, [81:24] if I woke you up and said, "Steven, just [81:26] tell me what was going through your [81:27] head?" And you said, "Well, I was just [81:28] thinking about the next time you're [81:29] going to come in and wake me up." That's [81:31] just a dream thought. [81:33] What Most people think of dreams as the [81:36] dreams that we have from REM sleep, from [81:39] rapid eye movement sleep. That's why we [81:41] call it dream sleep. Dreams from rapid [81:43] eye movement sleep are florid, they're [81:45] narrative. In fact, last night when you [81:48] fell asleep and you went into dream [81:49] sleep, you became [81:52] incredibly psychotic. [81:54] Excuse me. [81:55] Now, before you reject my diagnosis of [81:57] your nighttime psychosis, let me give [81:59] you five good reasons. When you went [82:01] into dream sleep last night, you started [82:03] to see things which were not there. So, [82:05] you were hallucinating. Second, you [82:07] believed things that couldn't possibly [82:09] be true. So, you were delusional. [82:12] Third, you became confused about time, [82:14] place, and person. So, in psychiatry, we [82:16] call that being disorientated. [82:19] Fourth, you had wildly fluctuating [82:22] emotions. [82:23] Something that we call being emotionally [82:25] labile. You're all over the place. [82:27] And then, how wonderful, you and I, cuz [82:30] I'll include myself now as being [82:31] psychotic, you and I, we both woke up [82:34] this morning and we forgot most if not [82:36] all of that dream experience. So, we're [82:37] suffering from amnesia. [82:39] If you were to experience any one of [82:40] those five symptoms whilst you're awake, [82:42] you'd be seeking some degree of [82:44] psychological help. But for reasons that [82:46] we're only now understanding, it seems [82:48] to be a normal biological and [82:49] psychological process. So, what are the [82:51] reasons? Why do we dream? We dream for [82:54] at least two different reasons. The [82:56] first reason is emotional first aid. [83:01] REM sleep is what I've defined as [83:03] overnight therapy. [83:05] And it's during dream sleep where your [83:07] brain takes difficult, painful emotional [83:09] experiences, [83:11] and it acts like a nocturnal soothing [83:12] balm, and it just takes the sharp edges [83:15] off those difficult, painful [83:16] experiences, so that you come back the [83:18] next day and you have a memory of an [83:22] emotional event, but it's no longer [83:24] emotion You don't have that same [83:25] visceral regurgitation of of that same [83:29] emotional charge. [83:31] Why is REM sleep able to do this [83:34] overnight therapy, this deep [83:35] potentiation? Why is REM sleep able to [83:38] sort of strip the bitter emotional rind [83:41] from the informational orange, as it [83:43] were? [83:44] The reason is the following. [83:46] Dream sleep, REM sleep, is the only time [83:49] during the 24-hour period where the [83:51] brain shuts off a stress-related [83:54] neurochemical called noradrenaline. [83:56] Now, you've heard of the cystic chemical [83:58] downstairs in your body called [84:00] adrenaline. Well, upstairs in the brain, [84:02] we don't have adrenaline, we have [84:03] noradrenaline. [84:04] REM sleep is the only time [84:06] where it's completely shut off. [84:09] And what we put forward as a theory [84:10] called overnight therapy where your [84:12] brain [84:14] has, as I told you, these emotional [84:16] centers and these memory centers, the [84:17] emotional centers, the amygdala, the [84:19] memory centers, the hippocampus. [84:21] You reactivate those structures when you [84:23] go into dream sleep. [84:25] So, your brain gets the chance to [84:26] reactivate and replay and reprocess [84:29] emotional experiences. However, [84:31] it's doing it in a {quote} and {quote} [84:33] safe neurochemical environment because [84:36] that stress chemical of noradrenaline is [84:38] completely shut off. So, it's the ideal [84:41] neurochemical therapy [84:43] for stripping the emotion from the [84:45] memory. [84:46] And we put forward a theory that perhaps [84:48] the quintessential disorder where this [84:50] fails [84:51] is PTSD. [84:53] Because when you speak to those [84:54] patients, not only do we see that their [84:56] REM sleep is disrupted, [84:59] when you speak to those patients, they [85:01] will say, "Look, I just can't {quote} [85:02] and {quote} get over the event." What [85:05] they mean by that is [85:07] the war veteran who's now going to the [85:09] supermarket and they come outside and [85:12] they're in the car park and the car [85:13] backfires and they instantly have the [85:15] flashback to the the sort of detonation [85:19] on the military field. [85:21] And what's happening there is that the [85:22] brain has not stripped the emotion from [85:25] the memory. So, every time they relive [85:27] the memory, they regurgitate that same [85:30] emotional reaction. Mhm. So, no wonder [85:33] we proposed that the brain then comes [85:35] back the following night and says, [85:36] "Look, I'm sorry, sleep. I still got [85:39] this trauma memory. Can you do your [85:41] trick of stripping the emotion from the [85:43] memory?" And it fails again. So, in the [85:45] next night, it comes back and says, "I'm [85:47] sorry [85:48] to bother you, but I've still got this [85:49] emotionally charged memory. Please do [85:51] your trick of stripping the emotion from [85:52] memory." It fails again. This sounds [85:55] like the broken record of repetitive [85:57] nightmares that we see in PTSD. [86:00] Why could this be happening? Levels of [86:03] noradrenaline in the brain in patients [86:06] with PTSD are too high. [86:08] And I was at a conference some years ago [86:10] where I was presenting this theory. We [86:12] just presented this theory. It was a [86:13] theory, and it was in search of data. [86:16] And it turns out at the same conference, [86:17] it was one of those incredible moments [86:19] you get hairs on the back of your neck. [86:21] There was a psychiatrist from Puget [86:23] Sound, which is just outside of Seattle [86:25] on the West Coast of America, [86:27] and he had been treating his war [86:29] veterans in the Veterans Administration [86:31] with a blood pressure medication called [86:34] prazosin. [86:35] Now, it turns out that prazosin, it's a [86:37] generic drug because it's the Veterans [86:39] Administration, so it's cheap, and it [86:41] crosses the blood-brain barrier. [86:43] When prazosin gets into the brain, one [86:45] of the things that it does is shut down [86:48] levels of noradrenaline. Why was this [86:51] interesting? What he was perplexed by is [86:53] that he was saying, "I'm giving this [86:55] blood pressure medication to my war [86:56] veterans with PTSD. [86:58] It's not helping too much with their [86:59] blood pressure, but they're all coming [87:01] back saying, 'All of those repetitive [87:03] nightmares, they're starting to go away, [87:05] and I'm sleeping better and I'm feeling [87:07] better.'" [87:09] What he had done was inadvertently [87:11] treated their high levels of [87:13] noradrenaline, which were preventing the [87:16] brain from kind of stop dropping those [87:19] levels of noradrenaline down and [87:20] processing the emotion from the memory. [87:23] It was too high in those PTSD PTSD [87:25] patients, but by treating them with this [87:26] drug, he'd inadvertently brought the [87:28] levels of noradrenaline down during REM [87:31] sleep. [87:32] And then, it ultimately became one of [87:34] the only prescribed medications in the [87:36] Veterans Administration for repetitive [87:38] nightmares. [87:39] Because why? The brain had finally got [87:42] down into a {quote} and {quote} safe [87:44] chemical state because noradrenaline was [87:46] too high, but he treated them with this [87:48] drug. So, he had data that was in search [87:53] of a theory. I had a theory that was in [87:56] search of clinical data, and so, I raced [87:59] to him after he gave his presentation. I [88:00] said, "I think I know why you're finding [88:03] what you're finding." I flew him down to [88:05] Berkeley. We spent all day together, [88:07] went out for dinner together, and as I [88:08] said, ultimately, he went on to do [88:10] clinical trials in it. It's not a [88:11] cure-all for everyone, by the way. It [88:14] doesn't work for everyone. [88:16] But And I would say that there is now a [88:18] better treatment for nightmares if [88:20] you're suffering from nightmares, [88:22] and it's called image rehearsal therapy, [88:24] or IRT. [88:27] And it works through an incredible [88:28] mechanism of memory that we actually had [88:31] discovered about, gosh, 20 years ago [88:33] now, called memory reconsolidation. [88:36] So, when you learn information, it would [88:39] be Oh, let's take a Word document. [88:42] Wouldn't it be staffed if you opened up [88:44] a Word document, you started typing in, [88:46] you know, all this information, you hit [88:47] save, and then you come back tomorrow, [88:50] and you double-click on the document, [88:52] and Word has shut you out. You can't [88:53] edit the document. That's a really bad [88:55] information storage system. It's a bad [88:57] idea. [88:58] Your human memories are just like this. [89:01] You form new memories, then you sleep [89:04] and you save them. [89:05] But when you come back and you [89:07] reactivate that memory, when you recall [89:10] a memory, [89:11] you bring it back into this opened-up [89:14] state. It's like double-clicking on the [89:15] memory, and the memory becomes fragile [89:17] and malleable once again, so you can [89:20] update and edit that memory. And then [89:22] the next night you resave it. It's [89:23] called reconsolidation. So, the first [89:25] night I save it, that's consolidation. [89:27] Then I reactivate it, I modify it, and [89:30] then the next night I reconsolidate it. [89:33] So, coming back to nightmares, it turns [89:36] out that you can do this with trauma [89:38] patients who have nightmares caused by [89:41] trauma. For example, let's say that you [89:42] got into a horrific road accident, [89:45] and you went through your brakes failed, [89:46] you went through the red light, you got [89:48] T-boned. It was just traumatic. It's all [89:51] traumatic. [89:53] And what you do with the therapist, [89:54] because you're having these repetitive [89:56] nightmares of reliving that same car [89:58] crash every night, [90:00] you work with them and you tell them the [90:03] dream. You recall the dream actively out [90:06] loud. But then, working with a [90:07] therapist, what you do is you modify the [90:10] outcome. So, instead of me saying the [90:12] brakes failed, now in the new scenario [90:15] with your therapist, you say, "Well, you [90:16] look down and there's a manual handbrake [90:18] in the car." So, you realize that you [90:20] can actually just gradually start [90:21] applying the handbrake, and you bring [90:23] the car to a safe halt, and you go to [90:25] the side of the road, and there's no [90:27] accident. And what you're doing is [90:29] you're reopening back up that trauma [90:31] memory, and you're rewriting [90:34] the narrative. [90:35] And then you sleep, and you update that [90:38] memory. And by recalling and rewriting [90:41] the memory each and every waking day, [90:44] you end up dissipating the severity of [90:47] your trauma nightmare every single [90:49] night. And it's called image rehearsal [90:52] therapy for nightmares. It's incredibly [90:54] powerful. It's probably more powerful [90:56] than the prazosin drug that I spoke [90:57] about. [90:58] And I'm guessing [91:00] people don't sleep and also have [91:01] nightmares for a variety of reasons [91:03] relating to trauma generally. Ah, it's a [91:05] good question perhaps, which is in some [91:07] ways [91:08] what's the difference between a bad [91:10] dream and a nightmare? Mhm. [91:12] >> [clears throat] [91:12] >> Because all of us will have bad dreams. [91:15] Bad dreams are usually things that [91:17] happen infrequently. Maybe you have them [91:19] once every month, every couple of [91:21] months. [91:21] >> Yeah. The definition of nightmare [91:23] disorder is that you have to have these [91:25] dreams frequently, maybe at least twice [91:27] a week. [91:28] They have to wake you up [91:31] out of your sleep, and you have vivid [91:34] recall. [91:35] Plus, it has to cause you some kind of [91:38] daytime distress, where you're not [91:40] feeling good about the day. It's causing [91:43] you mental anguish. And furthermore, if [91:46] it starts to lead to hopelessness [91:49] or a sense that your life is not worth [91:52] living, you absolutely need to go and [91:54] see someone. And here's what we've [91:56] discovered about nightmares. [92:00] Short sleep duration, not getting enough [92:02] sleep, sleeping less than 6 hours, [92:04] predicts by about 100 to 150% higher [92:08] percentage chance of you having suicidal [92:11] thoughts, [92:12] attempting suicide, or tragically [92:15] suicide completion. That's bad sleep. [92:19] It turns out that nightmares, [92:21] so if short sleep has a 150% higher [92:25] likelihood of suicidality, [92:29] having nightmares has an 800% [92:33] higher likelihood of suicidal tendencies [92:36] associated with it. Now, we don't think [92:38] that nightmares are causing suicidal [92:41] tendencies. [92:42] That's not what we believe. We believe, [92:44] however, that nightmares, much more than [92:46] disrupted sleep, nightmares seem to be [92:49] the canary in the coal mine. Nightmares [92:52] are this distress beacon that leaks from [92:55] our electrical static of sleep at night, [92:58] and it is incredibly sensitive to your [93:01] suicidal tendencies, your suicidal [93:04] attempts, and as I said, suicide [93:05] completion as well. [93:07] Nightmares are a biomarker. If you are [93:10] having distressing nightmares that are [93:12] waking you up, [93:14] you need to go and speak to someone [93:15] about it. It's absolutely paramount, [93:18] because there are good, effective ways [93:20] that you can dissipate those nightmares. [93:23] I'm trying to understand whether it's a [93:24] a malfunction or it's a signal. I guess [93:27] it might be both. It's a very good [93:29] question, which is is it adaptive or is [93:32] it maladaptive? Is it a good thing to [93:35] have a nightmare, or is it a bad thing [93:37] to have a nightmare? [93:39] We don't quite have the answer to that. [93:41] But let me come back to I told you there [93:43] were two functions of dream sleep, and [93:45] we're still in the first one, which is [93:47] emotional first aid. And it turns out [93:49] that your thinking is incredibly astute. [93:52] We believe that at least normative [93:54] dreams, not nightmares. Nightmares may [93:57] be the system failing, just as I spoke [93:59] about in PTSD with repetitive [94:01] nightmares. [94:02] In fact, repetitive nightmares are so [94:04] consistent in PTSD that you can't [94:06] receive a diagnosis of PTSD without [94:08] having repetitive nightmares. That's how [94:10] sort of diagnostic they are. But [94:12] dreaming, normative dreaming, even if [94:15] they're bad dreams, is beneficial. How [94:18] can I make that claim? There was a study [94:20] done by a late sleep scientist, a woman [94:22] called Rosalind Cartwright, [94:24] and she was studying people who'd gone [94:26] through a difficult period, let's say [94:28] bereavement or a very bitter divorce, [94:30] and they had become depressed because of [94:33] that experience. [94:34] And around the time of the experience, [94:36] she was seeing them as a therapist, and [94:38] she was having them do dream recall. So, [94:41] she was having them create dream diaries [94:43] every single night. And then she tracked [94:46] these patients for a year. And it turned [94:48] out that about roughly half of them, by [94:50] 12 months later, had remitted from their [94:52] depression. They got better. They'd got [94:54] past their depression. The other half [94:57] were still depressed. So then, she took [95:00] that data, and she went back with those [95:02] two groups, and she said, "Is there [95:04] anything different about their dreams?" [95:07] And it turned out that there was. Both [95:09] of those groups of people, whether they [95:12] could free of their depression or they [95:13] stayed in their depression, both of them [95:15] were dreaming at the time. Both of them [95:17] were having REM sleep. Both of them were [95:18] dreaming. What was the difference then? [95:21] Those individuals that went on to gain [95:23] remission [95:24] to their depression and get get better, [95:27] those people were dreaming of the events [95:30] itself at the time that they were [95:32] happening. Whereas those other people [95:34] who didn't go on to gain clinical [95:35] remission, they were dreaming. [95:38] They just weren't dreaming of the [95:39] experience itself. In other words, it's [95:42] not just sufficient to have REM sleep. [95:45] It's not just sufficient to have REM [95:47] sleep and be dreaming. You need to be [95:49] dreaming of the difficult, painful [95:51] experience that you're going through to [95:53] gain that clinical resolution. Damn. So, [95:56] if I have something going on in my life, [95:57] I need to think about it before I go to [95:58] bed. [95:59] Yes and no. [laughter] [96:02] What you have to realize is that [96:04] it's taken us, [96:06] depending on who you believe, 3.4 [96:08] million years of evolution to develop [96:10] this thing called hominid sleep and [96:13] dreaming and REM sleep. [96:15] I think that [96:17] that evolutionary millions of years [96:20] probably understands what the correct [96:22] blueprint playlist of dream experience [96:26] is and should be for me at night. And [96:29] therefore, I don't need to worry about [96:31] it. I shouldn't try to force anything. [96:33] That's the first function of dream [96:35] sleep. Is that it's emotional first aid, [96:38] and we've got good data for that. [96:40] But there's a second, completely [96:41] independent benefit of dreaming. [96:44] Dreaming is a form of informational [96:47] alchemy. [96:49] Dreaming is creativity. [96:52] Now, I told you that during deep non-REM [96:54] sleep, we take new memories that we've [96:56] learned, and we fixate them like amber, [96:58] sort of setting a fossil in. And we do [97:01] that during deep sleep. [97:03] That saves the individual pieces of the [97:05] new stuff. Then comes along REM sleep, [97:07] which happens after deep sleep, [97:10] and the second phase of memory [97:11] processing happens. That's where REM [97:13] sleep starts to fuse all of the things [97:15] that you've recently been learning with [97:17] this entire back catalog of information. [97:20] And so, you wake up with a revised [97:22] mind-wide web of associations that is [97:25] capable of divining solutions to [97:28] previously impenetrable problems. [97:31] So, you know, it's almost [97:33] it's like group therapy for memories. [97:35] That REM sleep gathers in all of the [97:36] information that you've learned during [97:37] the day, and everyone gets a name badge. [97:39] But unlike the waking, logical [97:42] connections that you make already, REM [97:44] sleep is like a Google search gone [97:46] wrong. That you insert, let's say, diary [97:49] of a CEO, and it takes you to page 20. [97:53] This is dream sleep. Mhm. And it's about [97:55] some field hockey game in Utah, and you [97:57] think, "Hang on a second, but how on [97:59] earth is that?" Well, there was someone [98:02] who had, you know, they'd found a diary [98:04] that'd been lost, you know, a long time [98:06] ago, and the guy who'd found it was a [98:08] famous CEO in the town of this sort of, [98:10] you know, Utah as he was watching. So, [98:13] it's a distant, non-obvious connection. [98:15] But it turns out that that's what [98:17] dreaming is all about. It's [snorts] [98:19] almost as though we go to sleep with the [98:21] pieces of the jigsaw, but by way of [98:23] dreaming, we wake up with the puzzle [98:25] complete. [98:27] And when you start to fuse things that [98:28] shouldn't should not normally go [98:30] together, but when they do, every now [98:33] and again, cause a marked advance in [98:35] evolutionary fitness, that is the [98:37] biological basis of creativity. It's the [98:40] reason that no one has ever told you, [98:42] "Look, Steven, you should stay awake on [98:44] a problem." [98:46] They don't. They tell you to sleep on a [98:48] problem. [98:49] And in every language that I've inquired [98:51] about to date from, [98:53] you know, from French to Swahili, that [98:57] term, sleeping on a problem or something [98:59] like it, exists. My point being is [99:02] the benefit, the creative benefit of [99:04] sleep transcends cultural boundaries. [99:07] It's a common experience of Homo [99:08] sapiens. [99:10] There is an invisible tax on self people [99:12] that no one really talks about enough. [99:14] The mental load of remembering [99:15] everything, like meeting notes, [99:17] timelines, and everything in between. [99:19] Until we started using our sponsor's [99:21] product called Pipedrive, one of the [99:23] best CRM tools for small and [99:24] medium-sized business owners. 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If [100:54] you're ready to start building, join us. [100:57] Launch your business today with a free [100:58] 14-day trial at [101:00] stevenbartlett.stan.store. [101:04] What is the uh most important thing we [101:06] haven't talked about as it relates to [101:08] the personas of those people that are [101:09] probably listening right now, and for [101:11] the reasons why they might have clicked, [101:12] you know? [101:13] They're probably looking Again, we have [101:15] the optimizers, we have those that have [101:16] bad sleep habits, and then we have those [101:18] that have real sleep disorders. What is [101:20] the most important thing we haven't [101:21] talked about that we should have talked [101:22] about for them? [101:23] It may be the dystopian future. Let's [101:26] talk about the dystopian future, then. [101:27] >> [laughter] [101:28] >> What is a podcast if it does not [101:30] contain, at least in this day and age, a [101:32] dystopian future? What is the dystopian [101:34] future? [101:35] Probably the most spectacular discovery [101:38] that has happened since you and I last [101:39] spoke, [101:41] is the discovery of what we call the [101:42] genetic short sleepers. [101:46] These are individuals who, by way of a [101:48] genetic mutation, can survive on as [101:51] little as 6.25 hours of sleep, in other [101:54] words, 6 hours and 50 minutes of sleep, [101:57] and they show zero impairment in the [102:00] brain or their body. They can do just [102:03] fine on 6 hours of sleep. I know where [102:06] this is going. And we have four genes [102:09] that we've identified now. The first two [102:10] genes, the first one identified was [102:12] called the DEC2 gene, DEC2 gene. The [102:15] second was called the ADRB1 gene, which [102:19] I granted, I know it sounds like the [102:20] next Radiohead album, but it's it's not [102:22] the next Radiohead album. [102:25] And these genes allow these individuals [102:29] to get away with an amount of sleep that [102:31] normally would cause predictive disease [102:33] and sickness, just as we've spoken [102:35] about. So, at this point, probably some [102:38] people listening are thinking, [102:41] I think I'm one of those people. [102:44] Just to put it in context, [102:46] your the probability that you will be [102:49] struck by lightning in your lifetime is [102:52] 0.0064. [102:55] Highly unlikely. The chances of you [102:58] having the ADRB1 gene is 0.004. [103:03] And the AD BR1 gene is the short sleeper [103:05] gene? It's one of the short sleeping [103:07] genes. So, in other words, you are [103:08] statistically more likely to be struck [103:11] by lightning in your lifetime than you [103:13] are to have that short sleeping gene. [103:15] So, the probability is is is low. By the [103:18] way, [103:19] why is this the case? Why do they get [103:21] away with this? And we've discovered [103:23] now, by using sort of genetic [103:25] manipulations, we understand why. First [103:28] thing is that they have a much stronger [103:29] wake drive during the day. So, you and I [103:32] and all the rest of our mere mortals [103:34] will have these kind of like [103:36] oscillations in our consciousness [103:38] throughout the day, where we'll have [103:39] dips, where we feel a bit sleepy and [103:40] we're dragging, and then we'll kind of [103:42] get They don't have that. They have It's [103:45] like a light switch, like a dimmer [103:46] switch. You and I, we may sort of go up [103:49] to like 80% brightness when we're awake, [103:52] and then sometimes we'll flicker, and [103:53] then we'll go down, and we'll have [103:55] pretty solid sleep, maybe sort of, you [103:57] know, down to 20%, but the lights are [103:59] not quite off, you know? Our sleep is is [104:02] good, but not amazing. These people have [104:05] an all or nothing phenomena. They are [104:08] all 100% bright light throughout the [104:10] day. [104:11] And then, and they can maintain 17, 18 [104:14] hours of wakefulness, no problem. [104:17] And then, when they sleep, they sleep [104:19] hard. They have much more efficient [104:22] sleep. Remember we spoke about sleep [104:23] efficiency, and I wanted 85% or above. [104:26] Almost all of their time at night is [104:27] spent in solid, stable, sound [107:14] sleep. And the depth of their sleep they [107:16] have is greater. So, they're awake more [107:18] throughout the day. They build up a [107:20] stronger wakefulness [107:21] >> happens. It's not that I'm against that [107:23] idea. [107:24] I would love for the burden of disease [107:26] and sickness to be reduced, and people [107:27] not to suffer from that. And if I could [107:29] find a way to do it genetically, I [107:30] would. [107:31] And you could think about people [107:33] arguing, "Well, imagine the productivity [107:34] benefits." I mean, huge upside of that. [107:38] You know, people are being more [107:40] productive, and they're probably [107:41] spending more. So, from a capitalistic [107:42] society, it's the perfect It's the ad [107:44] man's dream. Because when when you're [107:45] asleep, it's antithetical to a [107:47] capitalistic society. Why? Because [107:49] you're neither producing nor consuming. [107:51] That's very cynical, and I don't buy [107:52] into that, but nevertheless. [107:54] So, all of these things would be [107:55] markedly better, would they not be, if [107:57] we genetically engineered this way? Why [107:59] do I fear it? [108:01] I know for a fact that as soon as six [108:04] becomes the new eight, [108:06] everyone starts sleeping four. [108:09] And now I'm just in back into the same [108:11] battle again. Because six is the minimum [108:13] that you need, and they say, "Well, if [108:14] that's the minimum, then I'll sleep [108:16] four." And when I find the next gene [108:17] that allows you to get away with 4 hours [108:19] of sleep, then they say, "Well, that's [108:20] great, so then I can go down to two." [108:22] And it's a form of almost this sleep [108:24] currency, you know, [108:26] inflation that I'm always fighting a [108:28] battle, and at some point, I'll always [108:31] be on the wrong side of that battle. [108:34] Crazy. These people with this gene [108:37] can thrive on 4 to 6 hours sleep without [108:40] any negative effects [108:42] that most of us would experience. [108:44] >> [clears throat and cough] [108:44] >> Correct. It's I'm So, you know, [108:47] what is going on there? And what we're [108:49] seeing is this this incredible density [108:52] of sleep, and this [108:54] epic drive for wakefulness. They are [108:56] more efficient sleepers. They can get [108:58] done what you and I take 8 hours to do. [109:02] They can do it in six. And I guess you [109:03] Is there a way to easily test this? I [109:05] guess go to a lab and get [109:06] >> Yeah. So, if you've ever done, you know, [109:08] I think um you know, all of those [109:10] genetic testing kits out there where you [109:12] and a lot of them will allow you to [109:13] download your raw data. All you need to [109:15] do is download your raw raw data and [109:17] then there's a company, I think it's [109:19] called Prometheus. Again, I have no [109:20] affiliation with them. I don't know how [109:22] valid they are. But then you upload your [109:25] raw genetic data into their model and [109:27] then it will list and it will rip it [109:30] apart. So normally those genetic [109:31] services, they give you a nice PDF and [109:33] it's kind of like maybe 15 pages of all [109:35] of the the main stuff and it's This [109:37] Prometheus is kind of like the, you [109:39] know, the old-school kind of scientist [109:42] nerdy. They will just give you this kind [109:44] of raw just kind of janky, you know, [109:48] 50-page report. [109:50] The interface is terrible, but you can [109:51] go in there and you can search to see [109:54] you know, what form of the DEC2 gene do [109:57] I have or what form of the ADRB1 gene do [110:00] I have and it will tell you are you a [110:02] genetic short sleeper or are you not? [110:05] And you can find out. I've been thinking [110:07] a lot lately about [110:08] about certain diet states as well and [110:10] whether that they have an impact on [110:11] sleep. We're talking about circadian [110:12] rhythms. So I was thinking about fasting [110:13] a lot and also think me myself and Jack [110:17] over there are [110:18] in ketosis right now. I was wondering if [110:20] you [110:21] when you think about brain performance [110:22] and sleep and different sort of states, [110:24] do you think much about fasting or [110:27] about ketosis or [110:29] Yeah, it's it's a mixed bag if you look [110:31] at it. Certainly what you eat will [110:34] change how you sleep. [110:36] But perhaps more powerfully is how you [110:39] sleep [110:40] dramatically changes how you eat and how [110:43] you dispose of those calories and what [110:45] happens inside of your body when you are [110:48] underslept. [110:49] But So I have lots of cravings when I've [110:51] short slept. Yes, you have and there's a [110:53] reason why [110:55] is firstly two appetite hormones called [110:58] leptin and ghrelin will go in opposite [111:00] directions. So [111:02] they sound like hobbits, I know, and [111:03] I've got some Lord of the Rings thing [111:04] here, but [111:06] leptin is the signal that says to your [111:08] brain you're full. Yeah. You're you're [111:10] satiated. Don't eat anymore. Ghrelin is [111:13] the opposite. It kind of makes your [111:15] stomach tummy growl and it says you're [111:17] hungry. You're not full. You need to eat [111:19] more. When you are underslept, leptin, [111:23] which says you're full, stop eating, [111:25] that hormone is impaired. It drops away. [111:28] So you lose the I'm full signal and [111:30] worse still, the ghrelin signal, which [111:33] says I'm hungry, that increases. [111:36] And so now you have about a 30 to 40% [111:39] increased hunger drive. And the final [111:42] part of this is that when you are [111:44] underslept and taking on board calories, [111:46] the way that you dispose of that energy [111:49] is different. [111:50] Your body has a higher predilection when [111:54] you are sleep deprived to disposing of [111:56] calories as fat rather than storing it, [111:59] for example, as glycogen in the muscles. [112:03] Oh, so when I'm underslept, I'm That's [112:05] why, you know, you're more likely to get [112:06] belly fat. Correct. And what's worse is [112:09] that there was a great study where they [112:11] looked at people who were dieting [112:13] and either getting sufficient sleep or [112:15] not getting sufficient sleep. What was [112:17] fascinating is that both of those [112:19] groups, whether you are well slept or [112:21] not well slept, you both lost weight. In [112:23] fact, you lost about the same amount of [112:25] weight. So you think, okay, so that's [112:27] fine. The problem was if you looked at [112:30] what you were losing, there was an [112:31] issue. [112:32] Those people who were dieting but not [112:34] getting sufficient sleep, 70% of all of [112:38] the weight that they lost came from lean [112:41] muscle mass [112:42] and not fat. In other words, when you're [112:44] not getting sufficient sleep, you keep [112:48] what you want to lose, which is fat, and [112:51] you lose what you want to keep, [112:54] which is muscle. [112:55] >> Oh gosh. [112:57] Damn, it's important, isn't it, this [112:58] sleep stuff? But coming back to ketosis, [113:00] by the way, I would say when people go [113:01] into a fasted state, usually what we see [113:05] is that the sleep gets shorter. [113:08] Mhm. And they'll say, I sleep almost [113:10] more efficiently. I'll sleep for maybe [113:12] just 4 or 5 hours, but I feel more alert [113:15] and more awake. [113:17] Now, some of that has to do with the [113:19] ketosis. When you are calorically [113:22] deprived, [113:23] the brain starts to realize that [113:26] something is wrong because you are [113:27] lacking calories. You're going into [113:29] starvation. So it drives on a chemical [113:32] called orexin. Orexin is a [113:34] wake-promoting chemical and it forces [113:37] your brain to release much more of this [113:39] wakefulness chemical called orexin. So [113:42] now when you're fasting, it's easier to [113:45] stay awake for longer and your brain [113:47] will deliberately stop you from sleeping [113:49] as much. Oh. It's not because it wants [113:53] you to sleep less. It's because the only [113:55] time during our evolutionary past that [113:58] we experienced short sleep was when we [114:02] were in a caloric deficit and the reason [114:03] came comes back again to this idea that [114:05] you have to stay awake longer cuz you're [114:08] not finding food. Now, your brain [114:10] doesn't know you've deliberately decided [114:12] to fast, which is a good thing in lots [114:14] of ways. [114:15] But that's one of the reasons that when [114:16] people are fasting, they'll say my sleep [114:19] goes to Yeah, mine [114:20] >> heck in a handbasket, you know, it's [114:22] >> really, really short. So when I'm I'm in [114:23] ketosis now and I'm like in on my way in [114:26] and my sleep will reduce to about five [114:28] five, six hours. My Whoop scores plummet [114:31] Yeah. until I kind of come out the other [114:33] end, which might take a couple of weeks [114:35] and then my sleep scores seem to [114:37] stabilize again. But that initial [114:38] transition period, it looks like it's [114:40] having a physiological shock. [114:41] >> It is and it the shock is this chemical [114:43] orexin, which is this wake-promoting [114:45] chemical, which will force you to stay [114:47] awake in a very solid fashion. By the [114:49] way, case in point, people with [114:51] narcolepsy, [114:52] this sleep disorder where they [114:54] inadvertently and uncontrollably fall [114:56] asleep during the day, they have the [114:58] opposite. I'm just telling I was just [115:00] telling you that when you are fasting, [115:02] your brain dumps out this chemical [115:04] orexin to force you awake and you're [115:06] wide awake. [115:07] People with narcolepsy, when we've [115:08] studied their brains, they have a [115:10] deficiency of this brain chemical [115:12] orexin. So they can't stay awake in a [115:16] stable fashion. They have the opposite [115:18] of your fasting problem. You're wide [115:20] awake because you've got too much [115:21] orexin. They've got too little orexin [115:24] and they therefore they can't sustain [115:27] stable wakefulness during the day. So [115:28] they're constantly falling asleep. Mhm. [115:30] This story of orexin has led to the [115:34] invention of the first new class of [115:36] sleeping medication that I actually [115:37] favor and most people are not aware of [115:40] it. It's a new class of We're on to [115:42] essentially web 3.0 of sleep medication. [115:45] Web 1.0 were the benzodiazepines, things [115:48] like Xanax and Valium. Not great for [115:51] sleep. [115:52] The second wave, the web 2.0, those were [115:54] things like Ambien, Lunesta, Sonata. [115:58] Both of those drugs worked in a very [116:00] similar way where they go up to your [116:02] cortex and they tickle a a receptor [116:05] called the GABA receptor, GABA, g a b a, [116:09] and it's the major neuroinhibitory [116:11] transmitter of the brain. So when these [116:13] drugs flood your brain, they just hit [116:15] the red light and they stop neural [116:17] firing of the cortex. Essentially, they [116:20] sedate you. And sedation is not sleep. [116:23] But when you take an Ambien, [116:25] you mistake sedation for sleep. It's not [116:29] quite the same. It's not naturalistic [116:30] sleep. [116:31] But after we [116:33] realized by way of the story of [116:35] narcolepsy that narcolepsy patients, [116:37] they don't have this chemical orexin and [116:40] they're falling asleep inappropriately [116:41] during the day. [116:43] Well, think about what insomnia is at [116:45] night. Insomnia is almost the opposite [116:48] of narcolepsy, which is that narcolepsy [116:52] patients, they're falling asleep during [116:54] the day when they want to be awake. [116:57] Insomnia patients are awake at night [116:59] when they want to be asleep. [117:01] So what they realized is that what we [117:03] can do if this chemical orexin, this [117:05] wakefulness volume button in the brain, [117:09] is a problem in insomnia patients, what [117:12] if we were to just develop a drug that [117:14] doesn't sedate the cortex like Ambien? [117:17] Instead, it goes down into the brainstem [117:19] where the center for orexin is. And [117:21] these new drugs, and they're called the [117:23] DORAs drugs, d o r a small s. And [117:28] they're a class of drugs. There are [117:29] three FDA-approved. [117:31] I'll try and spell them out for you. [117:33] They're called suvorexant, lemborexant, [117:36] and daridorexant. [117:38] Exact [117:39] Why am I synapses are filled with things [117:41] like those names, but there you go. [117:42] They're three FDA-approved drugs. [117:45] And what they do is they act like a [117:47] clever set of chemical fingers. They go [117:49] down into the brainstem where this sort [117:51] of orexin is being released and they [117:53] just dial down the volume on wakefulness [117:56] and then they take a step back and they [117:58] allow the antithesis of wakefulness to [118:00] come in its place, which is this thing [118:02] called naturalistic sleep. [118:04] Now, [118:06] if you look at that there's clinical [118:08] data, they absolutely make you sleep for [118:12] uh not necessarily a longer period of [118:13] time, but you're awake a lot less. So [118:15] you've got nice sleep efficiency, more [118:18] continuity. [118:19] But I as a scientist could be very [118:21] skeptical and I could come along and [118:23] say, okay, so this new drug, it [118:26] increases your total sleep time, [118:27] improves your sleep efficiency, but I [118:30] have four words, yes and so what? Just [118:33] because I've added sleep to your night, [118:37] how do I know that that's functional [118:39] sleep? How do I know that that's useful [118:40] sleep? Couldn't it just be like junk [118:42] DNA? It could be just junk sleep. [118:45] Well, they did a study where they looked [118:47] at what we call the glymphatic system in [118:49] your brain. There's a cleansing system [118:51] in your brain that kicks into high gear [118:53] during deep non-REM sleep and it flushes [118:56] the brain of all of the metabolic [118:58] toxins, two of which are things called [119:01] beta amyloid and tau protein, which are [119:03] the culprits of Alzheimer's and that's [119:04] why we know that sleep is so important [119:06] because at night it's a good night's [119:08] sleep clean. It's a power cleanse that [119:10] washes away the Alzheimer's toxins. [119:12] So, they did a study. [119:14] Heavens knows how they got these people [119:16] to participate. But, they brought them [119:18] in. They were 50 years or older. [119:21] And in the morning and the night before, [119:23] they had a lumbar spinal puncture and [119:25] they siphoned off cerebrospinal fluid so [119:29] they could measure how much of the [119:31] metabolic detritus was in the brain [119:33] before sleep and in the brain after [119:35] sleep, including [119:37] the metabolic waste products sort of [119:39] including beta amyloid and and tau [119:41] protein. [119:42] And they either had one of these drugs, [119:45] the doras drugs, [119:47] or they had a placebo. And fair enough, [119:50] when they took the the this new class of [119:51] medication, the web 3.0, the dora drug, [119:54] their sleep got better. [119:56] But, what they also found is that not [119:58] only did their sleep get better, but [120:00] they had cleansed the brain the next [120:02] morning of more beta amyloid and tau [120:06] protein than the placebo group. In other [120:08] words, it wasn't just epiphenomenal junk [120:11] sleep. It was beneficial sleep. It was [120:14] adaptive useful sleep because that [120:16] drug-induced sleep had washed away more [120:19] of the Alzheimer's proteins. And it was [120:21] the first demonstration and they've now [120:23] replicated it in animal models [120:25] that this is a sleeping pill that isn't [120:29] disadvantageous, [120:31] which we know to be the case for things [120:33] like Ambien. In fact, Ambien there's a [120:35] recent study that showed that it [120:36] decreases the cleansing pulsing fluid by [120:39] about 30 to 40% at night. [120:42] But, this is a new class of medications [120:44] that does the opposite. And this is new. [120:46] And this is new. The doras drugs, d o r [120:49] a small s. The problem is that a lot of [120:51] insurance companies here in the United [120:52] States currently do not reimburse. Some [120:55] do. [120:56] And I believe that it's some of these of [120:59] the three doras drugs, not all of them [121:00] are available in Europe or in the UK. [121:03] And because they're just so expensive. [121:05] And if you pay out of pocket, it can be [121:07] up to $400 a month [121:10] for these medications. Now, some [121:12] insomnia patients, when I go to them and [121:13] say at the end of a shockingly bad month [121:16] of sleep, if I went to them and said, [121:17] "Look, if you gave me $400 now, could I [121:20] I could wave a magic wand and eradicate [121:23] all of that bad sleep over the previous [121:24] month?" Would you like to give me $400? [121:26] Most of them would say, "Absolutely. [121:28] Take my money." But, still people are [121:30] being priced out at this stage. But, the [121:32] doras drugs, please look into them if [121:34] you're struggling with insomnia as well [121:35] as CBT-I. I didn't realize there was so [121:38] much new science and research that had [121:40] been discovered on how to sleep well, [121:43] what's going on in the brain, and also [121:45] some of the lifestyle factors that have [121:47] made sleeping so hard for so many [121:49] people. [121:50] And with that in mind, I want to do [121:51] something that I've never done before, [121:52] which is a world first for the Diary of [121:54] a CEO. Is I'm going to put a link below [121:57] because I think this is what a [121:58] particular episode where if you share [122:00] this conversation with some of your [122:02] friends who particularly struggle with [122:04] sleep or are sleep optimizers or who [122:05] have sleep disorders, they'll get a ton [122:07] of benefit from it. So, what I'm going [122:09] to do is in the description of wherever [122:11] you're listening to this podcast right [122:12] now, there is a link. And if you click [122:14] on that link, um you'll see that you've [122:16] got your own personalized link to share [122:18] this episode. And those of you that [122:20] share this episode, whether it's on your [122:21] story on social media or in a WhatsApp [122:23] group or wherever, on email, with your [122:25] friends, [122:26] you will collect points for every person [122:28] that listens. And I will reward [122:31] um you'll see as you click on the link [122:33] who have shared it the most. I in part I [122:34] say this because so many people come up [122:36] to me in the street and they came up to [122:37] me after our last conversation and they [122:39] said, um [122:40] "That conversation you did with Matt [122:41] Walker was so amazing. I sent it to my [122:43] aunt and she now she did this and she's [122:45] changed this and blah blah blah blah and [122:46] she's now sleeping well." And then all [122:48] the downstream impacts of that have been [122:49] profound. So, [122:51] I'm going to create this little system [122:53] to encourage all of you to share it with [122:54] someone that is struggling at the moment [122:56] with sleep because I do believe I do [122:57] believe that sleep is upstream from so [123:00] many of the downstream symptoms that [123:03] ruin our lives, whether it's [123:04] relationship issues, whether it's libido [123:06] issues, or whether it's creativity [123:08] issues. I mean, I was reading through [123:09] your work and I saw your conversation [123:11] with Rogan not so long ago where you [123:12] talked about the fact that a [123:14] sleep-deprived person has their genes [123:17] fundamentally working differently. You [123:18] talked about 700 genes working [123:20] differently. [123:20] >> Yeah, 711 genes are distorted in their [123:23] activity caused by a lack of sleep. Some [123:25] genes that are overexpressed that are [123:27] related to cardiovascular disease or [123:29] stress or inflammation and other genes [123:31] that are impaired, which are associated [123:34] with your immune system so you become [123:36] immune deficient. And it can be a [123:37] downward compounding spiral if you're [123:39] such a person that's really continually [123:41] struggling struggling with sleep and [123:42] building up some of that sleep debt. So, [123:44] that link is below. Check it out. And we [123:46] have a closing tradition on this podcast [123:48] where the last guest leaves a question [123:49] for the next. The question left for you [123:50] is, "What did success bring you that you [123:53] never could have dreamed of?" [123:58] It brought me two things. [124:01] One [124:03] beneficial, one lesser. [124:06] Beneficial is that [124:08] I have now the chance and have gifted [124:10] the chance to [124:14] fly around the world and [124:16] try to speak the word of sleep [124:19] because the physiology of it is so [124:21] silent. [124:22] And I used to lament, "Why me?" Because [124:25] there's so many other much better sleep [124:27] scientists in the world than me. [124:29] And a friend after I was saying like, "I [124:31] don't understand why me? I have imposter [124:33] syndrome." And he just told me to [124:35] shut [124:36] up [124:38] and accept that it's you and instead ask [124:40] the question, "What are you going to do [124:41] with it?" [124:43] And I changed how I embraced that. So, [124:45] I've been so fortunate that my life [124:47] after publishing the book that you're [124:48] holding [124:50] changed forever [124:52] and almost all for the better. And I'm [124:54] so fortunate. I've lived a life of such [124:58] fortune by way of the sleep mission. [125:01] I would say though that there is [125:05] also, and I suspect you may experience [125:08] some of this too, [125:10] when you raise your head above the [125:11] public parapet, [125:14] don't be surprised if shots are fired. [125:17] And [125:18] if you're someone who has even the [125:20] vaguest [125:24] hint of insecurity, [125:26] >> [laughter] [125:28] >> comments will do you lovely disservice. [125:30] And so, I think there's a degree of kind [125:33] of vulnerability and insecurity that you [125:36] can develop by way of becoming someone [125:39] who is in the eye of the public that had [125:41] I not been in the eye of the public, I [125:43] probably wouldn't have been, you know, [125:45] as self-conscious about whether it's, [125:47] you know, your intellect or your voice [125:50] or your [125:51] you know, disastrous, you know, boy band [125:53] haircut, whatever it is. [125:55] Um I would say that's the only slight [125:56] downside. Overall, I am the most [126:00] fortunate human that I know. [126:02] I'm so gifted by way of this thing [126:04] called sleep. It's a love affair that's [126:06] lasted me almost 25 years. [126:08] And I believe it's the most beguiling [126:11] topic in all of science. And it has [126:13] treated me so well. [126:15] You happy? [126:18] More than you could imagine. [126:20] At this moment in my life, [126:22] I am [126:23] the happiest I've been. [126:26] Why? [126:27] I have a [126:28] a peace that I found in life [126:32] for reasons that I can share or not [126:33] share. And Go ahead and share them. I'd [126:35] love to hear about this in my life. You [126:37] know, I found my person. Okay. And [126:40] and she is she [126:43] appeared like lightning from a clear [126:45] blue sky. [126:46] Never saw her coming. [126:48] And [126:52] it's interesting that [126:57] I've never been able to be more myself [127:01] even with myself [127:03] than I have with her. [127:06] Every day she makes me want to be a [127:08] better person. [127:10] And [127:14] I found peace [127:15] that I've never had before. [127:18] That you've never had before? [127:20] No. [127:21] Did you have peace last time we spoke? [127:24] I wouldn't say I was [127:26] without peace. [127:28] I didn't know this type of peace. [127:31] And I never believed in this notion of [127:33] the one. You know, I was a scientist, [127:34] I'm a hard-nosed empirical kind of guy. [127:37] And I just did not imagine it would be [127:40] such [127:42] uh I didn't think there was such a one. [127:45] I would have told you if you'd told me [127:46] that 2 years ago [127:48] you'd give me your love story of [127:50] certainty, I would have thought you were [127:52] misguided and that, [127:55] you know, [127:56] you just need to put down whatever [127:59] substances you're using cuz you're [128:00] delusional cuz there isn't such a thing. [128:03] Um [128:07] she's a gift. [128:09] And I hope I never take her for granted. [128:12] I doubt it. There's also an incredibly [128:14] sad story [128:16] of a gentleman called Clive Wearing. [128:20] And Clive is a famous individual in the [128:22] neuroscience world. [128:24] And Clive was the man who the movie [128:28] Memento [128:30] was based on, which is a movie where a [128:32] man has [128:34] brain damage and he has profound [128:35] amnesia. And from that moment forward, [128:37] he can never make any new memories [128:39] whatsoever. He's densely amnesic. [128:42] And he was a real-life individual. He [128:45] contracted a virus that destroyed his [128:48] memory centers. And from that point [128:50] forward, he could no longer make any new [128:51] memories. [128:52] And he lived in just two or three [128:54] seconds of time. And that spotlight of [128:57] consciousness just moved forward in [128:58] time. He had no recollection of the [129:00] past. He had no anticipation of the [129:02] future. And the only thing the only [129:04] person that he remembered and he would [129:07] recognize is his wife. So, he could have [129:09] spent this whole 3 hours speaking to [129:11] you. [129:12] And then you would walk out the room for [129:13] 5 minutes and you would walk back in and [129:15] you'd say, "Hi Clive. Nice to meet you." [129:17] And he'd say, "Hi, what's your name?" [129:19] Had no recollection. The only person [129:21] that he remembered was his wife. [129:23] But the problem was he never remembered [129:26] how long it's been since he last saw his [129:28] wife. [129:29] And so every time that she would walk [129:32] into the room after being out of it for [129:34] 5 minutes, he would jump out of his [129:36] chair and he had this incredible [129:39] elation. [129:41] And he would run and he would hug her [129:42] and kiss her. [129:44] And I think sometimes we take our [129:45] partners for granted. [129:48] And the only time we realize how [129:49] precious they are is when they're gone. [129:53] And I often think about that that [129:55] complacency [129:57] can be one of the greatest negative [129:58] forces in a relationship. And I always [130:00] think about Clive Wearing [130:02] even on the days where I'm having a bad [130:04] day or I'm in a bad mood and I knock [130:07] myself or I just don't want to be around [130:08] someone, I always try to remember his [130:10] reaction. [130:11] And when my wife walks back in from work [130:14] or I see her, you know, first thing [130:17] I try to remember how his reaction was [130:20] and [130:21] how I truly feel at the time despite the [130:23] blanket of negative [130:25] stress [130:26] trying to drown that feeling out. [130:31] It's a beautiful thing. I think about [130:33] that a lot as well. [130:34] In what way? Just the part of I'm way [130:37] more cognizant now [130:39] on a frequent basis, almost on a weekly [130:41] basis, of how I'm going to feel [130:45] when my time is up as it relates to my [130:48] romantic relationship. Like I think even [130:50] like mid-argument I will now think and I [130:53] mean this actually happened like a [130:54] couple of days ago. It wasn't really an [130:55] argument, we were just disagreeing about [130:56] something. I literally said mid mid uh [130:59] dispute that we were having, I said, [131:01] "We're going to regret this so much." [131:02] And what I meant was when I when that [131:04] day when that phone call rings and [131:06] someone gives me bad news that either [131:07] I'm going or you're going I'm going to [131:09] regret that this 30 minutes was wasted [131:11] doing this. Yeah. I'm really going to [131:13] regret it. How much would you give to [131:15] have that 30 minutes back? [131:16] >> Exactly. And it's like, you know, we're [131:17] [ __ ] arguing about I don't know, some [131:19] chocolate, whatever it might be, some [131:20] trivial thing. It's actually really [131:21] helped me because in the midst of those [131:23] storms I'm thinking through to that [131:26] moment when you get that phone call and [131:27] like you're ill or I'm ill and some [131:29] we're not going to be around much [131:30] longer. [131:31] Um it liberates you from [131:34] the pettiness that a sense of [131:35] immortality can create and that [131:38] pettiness results in the complacency [131:40] that you're describing that like [131:42] I did I took you for granted. Yeah. So, [131:44] it's a nice little mechanism now for me [131:46] to go, "Is this an important thing? Is [131:48] this really important?" And I have to [131:50] provide nuance there which is this [131:52] doesn't mean don't address things. [131:53] >> Correct. Yeah, I was just about to say [131:55] conflict is critical. You've got to [131:57] fight well. But let it be me and versus [132:00] you and the problem. Like me and you [132:01] versus the problem versus me just going [132:03] at you. Yes. You [132:04] >> You have to be fighting for each other, [132:07] not fighting against each other. [132:09] >> Yeah, exactly. And then you have to try [132:11] to then in that context of Clive Wearing [132:15] don't shy away from conflict if you need [132:17] to have the conversation. [132:19] Often it's like the gym. If you do it [132:21] well [132:22] you even on the days when you kind of go [132:25] into the gym, you think, "I I don't want [132:26] to do this or I just I don't feel good." [132:29] You always come out feeling better than [132:31] you did before. [132:32] And with conflict, if you do it well [132:35] you typically it may not be the hour [132:36] after or even the day after, but if you [132:38] do it well, you typically are better as [132:40] a couple [132:42] after than you were before the conflict [132:44] as long as you do it well. So, I'm not [132:46] saying don't have conflict. What I'm [132:48] saying is [132:50] Clive Wearing's story to me [132:52] of how he loved his wife with an intent [132:55] that I'd never experienced before until [132:57] I met my much better half [133:01] prevented me from resentment. [133:04] Resentment is the barrier that will keep [133:06] you from reparation [133:08] and a future of I think equanimity. [133:11] Because when you resent someone it means [133:14] that you haven't processed, you haven't [133:16] moved forward. And resentment usually [133:18] comes by way of I think a poor choice of [133:21] things such as, "Did I win the argument? [133:23] Did you win the argument?" It's not [133:26] about point scoring at least. And I've [133:28] done that before. I've been guilty of [133:30] all of that behavior. [133:31] But now with this person that I cherish [133:34] most [133:35] you know, I think of his lessons. It's [133:38] not that we don't have conflict, we do. [133:40] It's just that I value the person far [133:42] beyond the conflict afterwards. And I'll [133:46] always want to reach out with an olive [133:47] branch. [133:49] Because it's not worth it just as you [133:50] said when that call comes [133:53] you know, I I think of that sometimes [133:55] when I have a bad day. Let's say [133:56] someone, you know, I come back to my car [133:59] and my car has been rear-ended when it's [134:01] been parked. [134:03] Or, you know, I was coming here to fly [134:05] out and we were [134:07] 4 hours on the [134:09] tarmac waiting [134:10] and there's a guy in front of me who's [134:12] getting all agitated and giving the the [134:14] ground staff all sorts of vitriol. [134:18] And I was thinking, "Look, when you're [134:20] on your deathbed, my good fellow [134:22] are you going to look back at this day [134:25] and think, 'Gosh, you know, I remember [134:26] that one day when I was on that flight [134:29] coming out to LA and it was 4 hours [134:31] delayed.'" No, of course you're not. [134:34] So, if you're not stressing about it [134:36] when you're dying, why are you stressing [134:37] about it now? Mhm. [134:39] It's just not worth it. Mhm. [134:42] Live. [134:43] Thank you. [134:44] Thank you so much. I mean, I can't thank [134:45] you enough for the profound impact [134:47] you've had on so many millions of people [134:49] um being the [134:52] the chief torchbearer of the subject of [134:54] sleep and creating a movement around [134:57] sleep, but also a heightened awareness [134:59] of ourselves and our struggles. And that [135:00] is something that you'll never [135:01] understand. Like you'll never understand [135:03] the full magnitude of the many millions [135:05] of people you've positively impacted. Um [135:07] but I mean, even though you'll never get [135:09] to meet them all and you'll never get to [135:11] hear all of their thank yous [135:13] they are very very real people and they [135:14] are they you they them themselves are [135:17] these little ripples through the ocean [135:18] where their children and then the [135:20] generations to come get to sleep better [135:22] and enjoy their lives and live a [135:23] happier, healthier life because of the [135:25] work that you do. So, it's um incredibly [135:27] important work, Matthew. And I hope you [135:29] long continue it and a long a long [135:31] continue being the conduit of this very [135:32] important information to people like me [135:34] and my audience. Can't appreciate you [135:35] more. Thank you so much for saying that. [135:37] I [135:38] can't lay claim to any such um [135:41] uh [135:41] affirmations, but I would say that I [135:43] stand on the shoulders of giants and [135:45] that um I am simply relaying all of the [135:48] incredible work of all of my colleagues [135:50] in the field and all of those who came [135:51] before me. Um I'm just the mouthpiece [135:54] and not a particularly good one at that. [135:55] And for all of their work, it's really [135:57] the appreciation that I give to them. [135:59] So, thank you for giving me the [136:00] opportunity to say that. [136:03] >> [music] [136:06] >> Make sure you keep what I'm about to say [136:07] to yourself. I'm inviting 10,000 of you [136:10] to come even deeper into the Diary of a [136:11] CEO. Welcome to my inner circle. This is [136:15] a brand new private community that I'm [136:17] launching to the world. We have so many [136:18] incredible things that happen that you [136:20] are never shown. We have the briefs that [136:23] are on my iPad when I'm recording the [136:24] conversation. We have clips we've never [136:26] released. We have behind the scenes [136:28] conversations with the guest and also [136:29] the episodes that we've never ever [136:32] released and so much more. In the [136:35] circle, you'll have direct access to me. [136:37] You can tell us what you want this show [136:38] to be, who you want us to interview, and [136:40] the types of conversations you would [136:41] love us to have. But remember for now, [136:44] we're only inviting the first 10,000 [136:46] people that join before it closes. So, [136:48] if you want to join our private closed [136:50] community, head to the link in the [136:51] description below or go to the [136:52] DOACcircle.com. [136:56] I will speak to you there. [137:02] >> [music] [137:09] [music] [137:17] [music] [137:22] [singing]