Romosozumab-AQQG

☝关注弘小爱，多点健康多点爱~ 77岁的何奶奶，腰背酸痛整整3年。渐渐地，她的背越来越驼，人也越来越矮。 CT检查发现：L2、4、5椎体陈旧性骨折——骨头早就悄悄断过好几次了，她甚至都不知道，还以为只是“老年病”。   骨密度T值低至-4.9，属于重度骨质疏松，再骨折风险极高。加上她还有肾切除手术史，常规抗骨质疏松药用了一圈，效果都不理想。 家人天天揪着心：“万一摔一跤，那该怎么办？” 这样的困境，并不是个例。 在中国，50岁以上女性骨质疏松患病率高达32.1%，65岁以上女性超过一半“中招”。更残酷的是，髋部骨折后一年内，每5个人里就可能有一个去世。 这个病被称为“沉默的杀手”——它不疼不痒，却容易在某次弯腰、打个喷嚏或者不注意轻轻一绊时，突然以一场骨折“现身”。而很多老人骨折后卧床不起，生活质量断崖式下降，甚至再也没有站起来。 许多极高骨折风险患者——比如曾经断过椎体或髋部、骨密度T值低于-3.0，或者用了好几年传统药骨量还是上不去的——他们最焦虑的就是：有没有一种药，能快点把骨头“长回来”？ 传统抗骨松药物多为单一机制：要么抑制骨吸收，让骨量不再快速流失；要么单纯促进骨形成。起效慢、骨量提升有限，患者往往用药一年半载，骨密度仍难见明显回升。而在此期间，每多等一天，骨折风险就高一分。 直到2025年12月，答案出现了。 全球首个且唯一双重作用的抗骨松生物制剂——罗莫索珠单抗（易稳泰®） 在国内获批。它跟以往所有药都不一样：既能强力促成骨（激活Wnt通路，加速新骨生成），又能快速抑骨吸收（减少骨流失）。一增一减，好比给骨头同时按下“加速生长”和“减慢流失”两个键。 临床数据显示，使用12个月，新发椎体骨折风险下降73%，腰椎骨密度平均提升13.3%，全髋骨密度提升6.8%。 这意味着，很多“久治不愈”的重度患者，终于有机会在短短一年内，让骨骼重新变得结实。每月仅需皮下注射一次，疗程12个月，后续序贯抗骨吸收药维持即可。 但新药上市了，患者什么时候能真正打上？ 他们多方打听、查阅专业资讯后得知：厦门弘爱医院骨科，是全市首个规范开展罗莫索珠单抗治疗的临床科室。更让他们意外的是，从特需申请审批、药品采购到患者用药，医院领导高度重视，在弘爱骨科牵头下，多部门共同协作，开通了绿色通道——24小时内完成全流程闭环，加速了罗莫索珠单抗在厦门的使用。让极高骨折风险患者不出厦门，很快用上国际前沿创新药。 何奶奶顺利完成了首剂注射。骨科何发胜主任团队为她制定了兼顾高龄、既往肾切除史的个体化方案。 目前虽然还在早期观察阶段，但家人很笃定：“我们了解过这个药的机制，它就是老人家最后的希望。” 无独有偶。55岁的余女士绝经后腰背反复酸痛两年，T值最低-3.6，常规治疗后症状依然反复。 一次偶然听说弘爱骨科有新药，她专门赶来，成为厦门第一位注射罗莫索珠单抗的患者。余女士说：“我相信，在规范治疗下，腰背痛会慢慢好起来，骨头也会越来越结实。” 在弘爱医院“有药用、有好药用”的机制支持下，骨科专业诊疗团队全程规范化管理与康复指导，从评估、注射到后续序贯抗骨吸收治疗，形成完整闭环，让患者不再奔波，不再焦虑等待。 如果您身边人： - 曾发生椎体/髋部/腕部脆性骨折 - 骨密度T值 ≤ -2.5，尤其 T值＜-3.0 - 多种危险因素叠加、既往抗骨松治疗效果不佳 欢迎至厦门弘爱医院【骨质疏松专病门诊】就诊评估，咨询专业建议。 医学的进步，有时就是一场与沉默的较量。骨质疏松被称为“沉默的杀手”，因为它从不预警，只在某次跌倒后突然宣判。如今，罗莫索珠单抗的出现，让这场较量有了新的转机。 声明：本文仅作健康科普，不用于任何商业广告目的，且不提供诊疗建议，也不能替代医院的检查和治疗。如有相关疾病，请及时就诊，谨遵医嘱。 通讯员：李盈宏 编辑：刘颖 一审：何发胜 二审：庄雅静 三审：夏天

Introduction  介绍 Longevity—the length of human life—is the subject of growing scientific and commercial interest. Often associated with “anti-aging,” the word carries connotations of cosmetic products, speculative therapies, and unproven claims. In our view, this association should not distract from the scientific progress now underway in aging biology research. Advances in aging biology suggest that aging is not a single process that occurs uniformly with chronological age. Instead, biological aging involves the progressive dysregulation of many measurable biological mechanisms that reduce resilience, increase disease risk, and erode function over time.长寿——即人类寿命的长度——正日益引起科学界和商业界的关注。长寿一词常常与“抗衰老”联系在一起，并带有化妆品、投机性疗法和未经证实的说法等含义。我们认为，这种联想不应分散人们对衰老生物学研究领域正在取得的科学进展的关注。衰老生物学的进展表明，衰老并非一个与实际年龄同步发生的单一过程。相反，生物衰老涉及许多可测量的生物机制的逐渐失调，这些机制会降低机体的抵抗力，增加患病风险，并随着时间的推移而逐渐丧失功能。 Our ability to quantify biological aging has improved markedly. Functional performance metrics, molecular biomarkers, multiomics data, and continuous digital signals now can measure what clinicians once inferred almost entirely from chronological age. These tools do not imply that aging has been “solved,” nor that extreme longevity is imminent, but they do make aging a more tractable target for serious scientific study, clinical evaluation, and medical intervention.我们对生物衰老的量化能力已显著提升。功能性指标、分子生物标志物、多组学数据和连续数字信号现在能够测量临床医生过去几乎完全根据年龄推断出的衰老信息。这些工具并不意味着衰老问题已被“解决”，也不意味着极长寿命即将到来，但它们确实使衰老成为更易于开展严肃科学研究、临床评估和医疗干预的目标。 What we call “longevity-relevant therapies” already are reaching patients, not through an "aging" indication, but through disease-specific approvals that reduce morbidity and mortality from conditions in which prevalence rises sharply with age. Regulatory and scientific shifts are opening new pathways, among them: the approval of GLP-1 receptor agonists, gene-editing therapies that target genes associated with cardiovascular risk, and a recent U.S. Food and Drug Administration (FDA) decision accepting bone mineral density as a surrogate endpoint for osteoporosis trials.我们称之为“长寿相关疗法”的药物已经开始惠及患者，其适应症并非“衰老”，而是针对特定疾病的审批，旨在降低那些患病率随年龄增长而急剧上升的疾病的发病率和死亡率。监管和科学领域的变革正在开辟新的途径，其中包括：GLP-1 受体激动剂的获批、靶向心血管风险相关基因的基因编辑疗法，以及美国食品药品监督管理局（FDA）近期批准将骨密度作为骨质疏松症试验的替代终点。 The economic stakes are substantial. Our modeling suggests that premature death in the US claims 46 million life-years each year—worth roughly $4.6 trillion at standard health-economics valuations. Modeling a scenario that eliminates non-accidental deaths and functional decline, we estimate the theoretical potential of the US longevity opportunity is ~$1.2 quadrillion, as further described later in this article.1 Even partial progress against aging biology would generate substantial value: slowing biological aging by 5–15% could generate ~$10–30 trillion in discounted incremental value across the lifetime of the current US population,2 the largest share accruing to younger cohorts thanks to the compounding benefit of slower aging. To put the longevity opportunity in more familiar terms: a 10% aging slowdown could be worth ~$930 billion per year on an annualized basis—roughly double the $467 billion the US spent on prescription drugs in 2024, as shown below.3经济利益巨大。我们的模型显示，美国每年因过早死亡而损失 4600 万个生命年——按标准卫生经济学估值，价值约 4.6 万亿美元。在排除非意外死亡和功能衰退的情况下，我们估计美国长寿机遇的理论潜在价值为 1.2 千万亿美元，本文稍后将对此进行更详细的描述。 即使仅部分延缓衰老，也能创造巨大的价值：将生物衰老速度减缓 5%至 15%，就能在当前美国人口的生命周期内创造 10 万亿至 30 万亿美元的折现增量价值， 其中 ，由于衰老速度减缓带来的复利效应，年轻群体将获得最大份额。用更通俗易懂的方式解释长寿带来的机遇：人口老龄化速度减缓 10% 每年可带来 9300 亿美元的收益——大约是美国 2024 年处方药支出 4670 亿美元的两倍， 如下所示。 Taken together, these developments suggest that “longevity” is best understood not as speculative "anti-aging" but as a tractable scientific problem at the intersection of biology, measurement, and intervention. We believe that the convergence among biology, AI, and broader innovation platforms is accelerating the progress that will unlock that value.综上所述，这些进展表明，“长寿”的最佳理解并非是推测性的“抗衰老”，而是一个生物学、测量和干预交叉领域的、可解决的科学问题。我们相信，生物学、人工智能和更广泛的创新平台之间的融合正在加速释放这一价值的进程。 Note: This chart compares US prescription drug spending in 2024 against the estimated annualized value of slowing biological aging by 10% across the US population. The annualized value is derived from a model that estimates the lifetime incremental quality-adjusted life years (QALYs) gained if each individual experienced a 10% reduction in the rate of biological aging, with non-accident mortality and health-related quality of life (EQ-5D-5L utility weights) evaluated at biological rather than chronological age, while accident mortality risk remains commensurate with chronological age. All future QALYs are discounted at 3% annually and valued at $100,000 per QALY. To produce an annual figure comparable to annual spending, each person's lifetime present value is converted to equal annual payments over their remaining life expectancy using the standard annuity formula at the same 3% discount rate, then multiplied by the US population at each age and summed across all ages (0–120). The annualized value (~$930 billion) represents willingness-to-pay for health gains, while prescription drug spending ($467 billion) represents actual expenditure—different units placed side by side to convey the scale of the longevity opportunity relative to current healthcare spending. Source: ARK Investment Management LLC, 2026, based on data from Centers for Medicare & Medicaid Services, National Health Expenditure Accounts 2024; Centers for Disease Control and Prevention, National Center for Health Statistics, United States Life Tables, 2023; United Nations Department of Economic and Social Affairs, Population Division, World Population Prospects 2024; Jiang et al. 2021; CDC WONDER 2025.4 For informational purposes only and should not be considered investment advice or a recommendation to buy, sell, or hold any particular security. Forecasts are inherently limited and cannot be relied upon.注：本图表对比了 2024 年美国处方药支出与美国人口生物衰老速度减缓 10%的估计年化价值。该年化价值源自一个模型，该模型估算了如果每个人的生物衰老速度降低 10%，其终生质量调整生命年（QALY）增量。模型中，非意外死亡率和健康相关生活质量（EQ-5D-5L 效用权重）的评估基于生物年龄而非实际年龄，而意外死亡风险则与实际年龄相符。所有未来的 QALY 均按每年 3%的贴现率进行折现，并按每 QALY 10 万美元的价值计算。为了得出与年度支出相当的年度数值，首先使用标准年金公式，以相同的 3%贴现率，将每个人的终生现值转换为在其剩余预期寿命内等额的年度支付额，然后乘以每个年龄段的美国人口数，最后将所有年龄段（0-120 岁）的支付额相加。年化价值（约 9300 亿美元）代表人们为获得健康收益愿意支付的金额，而处方药支出（4670 亿美元）则代表实际支出——将不同的单位并列，旨在展现长寿机会相对于当前医疗保健支出的规模。数据来源：ARK Investment Management LLC，2026 年，基于以下数据：美国医疗保险和医疗补助服务中心，《2024 年国家卫生支出账户》；美国疾病控制与预防中心，国家卫生统计中心，《2023 年美国生命表》；联合国经济和社会事务部人口司，《2024 年世界人口展望》；Jiang 等人，2021 年；CDC WONDER，2025 年。4 仅供参考，不应被视为投资建议或买卖或持有任何特定证券的建议。预测本身具有局限性，不能完全依赖。 The Longevity Shift: Mortality Has Shifted To Later In Life寿命延长趋势：死亡年龄已推迟至晚年 Over the past century, improvements in public health and medicine have reduced early deaths from infectious and chronic diseases, leading to major gains in life expectancy. As a result, the global distribution of deaths has shifted markedly toward older ages: globally, life expectancy has risen from 46.5 years in 1950 to 73 years as of 2023, as shown below.5过去一个世纪，公共卫生和医学的进步降低了传染病和慢性病导致的过早死亡，从而显著提高了预期寿命。因此，全球死亡分布已明显向老年群体转移：如下图所示，全球预期寿命已从 1950 年的 46.5 岁提高到 2023 年的 73 岁。 5 Source: ARK Investment Management LLC, 2026, based on data from United Nations 2024; Our World in Data 2024.6 For informational purposes only and should not be considered investment advice or a recommendation to buy, sell, or hold any particular security.资料来源：ARK Investment Management LLC，2026 年，基于联合国 2024 年数据；Our World in Data 2024 年数据。 6 仅供参考，不应被视为投资建议或买卖或持有任何特定证券的推荐。 As more people live longer, the composition of mortality is shifting. In younger cohorts, accidents and perinatal or congenital conditions account for the majority of fatalities. Beginning in midlife, however, age-associated diseases—led by cardiovascular disease and cancer—begin to dominate. In 2024, Americans aged 55 and older accounted for roughly 90% of all US deaths, with cardiovascular disease and cancer responsible for more than half.7 Neurodegeneration, respiratory disease, and metabolic conditions contributed meaningfully as well, particularly in older age groups, as shown below. Note: For the 0–14 age group, “Other” primarily includes perinatal conditions (e.g., gestational disorders, birth complications), congenital malformations (e.g., circulatory, nervous system, chromosomal), and ill-defined or unknown causes of death. The vast majority of these deaths are concentrated in the under-1 age group. The composition of “Other” varies across older age groups. Source: ARK Investment Management LLC, 2026, based on data from based on data from Centers for Disease Control and Prevention, National Center for Health Statistics 2025.8 For informational purposes only and should not be considered investment advice or a recommendation to buy, sell, or hold any particular security.注：对于 0-14 岁年龄组，“其他”主要包括围产期疾病（例如妊娠紊乱、分娩并发症）、先天性畸形（例如循环系统、神经系统、染色体异常）以及死因不明或不明确的死亡。这些死亡病例绝大多数集中在 1 岁以下年龄组。“其他”的构成在不同年龄组中有所不同。数据来源：ARK Investment Management LLC，2026 年，基于美国疾病控制与预防中心国家卫生统计中心 2025 年的数据。 8 仅供参考，不应被视为投资建议或买卖或持有任何特定证券的推荐。 During the last century, the frontier of progress has shifted from preventing early-life deaths to addressing the biological processes that increase the risk of disease and drive age-related functional decline.9 That dynamic establishes a central question to longevity research: can we further extend healthy lifespans by targeting the biology of aging itself? Can Slowing The Process Of Biological Aging Extend Lifespans? Aging biology describes the cumulation of molecular and cellular changes that reduce function and increase vulnerability to disease gradually over time. A widely used framework—the “hallmarks of aging”—organizes those changes into categories, highlighting the diverse forms of damage and dysregulation interacting at the tissue and organism levels.10 Importantly, the hallmarks describe what changes with age. As a complement, geroscience reframes why what changes matters: because aging biology drives many chronic diseases, targeting fundamental aging processes could impact many diseases—not just one—simultaneously.11 More recently, information-based models have proposed a unifying mechanism that describes how all the changes accumulate. In this view, the progressive loss of epigenetic information—the chemical markers that help control which genes in a cell are turned on or off—primarily drives aging, as repeated stress and repair responses lead to imperfect restoration of gene regulation over time.12 Note: Aging mechanisms are likely not independent, the table is not intended to imply causal ordering nor is it exhaustive, and interventions targeting one process may influence others. Source: ARK Investment Management LLC, 2026, based on data from López-Otín et al. 2013; López-Otín et al. 2023; Lu et al. 2023.13 For informational purposes only and should not be considered investment advice or a recommendation to buy, sell, or hold any particular security. Evidence from animal models increasingly suggests that targeting these aging mechanisms directly can extend lifespan. Among the therapies demonstrating meaningful lifespan extension in mice later in life are: rapamycin, an inhibitor of the mTOR pathway, a central regulator of nutrient sensing14; senolytics, drugs that clear senescent or “zombie” cells—damaged cells that have stopped dividing but secrete inflammatory signals15; anti-inflammatory antibodies16; gene therapy17; and combination regimens.18 In some cases, depending on the intervention and timing, the therapies have extended lifespans by more than 100%, as shown in the chart below. These results span multiple hallmarks of aging, from deregulated nutrient-sensing and cellular senescence to chronic inflammation and epigenetic alterations, suggesting that the biological processes underlying aging are amenable to intervention. Indeed, the field is converging on a practical premise: aging reflects distinct biological processes that interventions can modify to extend healthy lifespans. Now, the practical question is how to quantify biological aging? Note: Chart reflects ARK’s approximations of median survival data based on published Kaplan-Meier survival curves where provided. Where studies reported sex-specific results, values shown represent averages across males and females. Remaining lifespan extension is calculated as the percentage increase in median survival time from treatment initiation relative to untreated controls, not total lifespan extension. Aging mechanism classifications reference López-Otín et al. 202319; mechanisms are likely not independent, and interventions targeting one process may influence others. Effect sizes are not directly comparable across studies due to differences in mouse strains, dosing regimens, treatment duration, and study design. Source: ARK Investment Management LLC, 2026, based on data from Harrison et al. 2009; Xu et al. 2018; Widjaja et al. 2024; Cano Macip et al. 2024; Gkioni et al. 2025.20 For informational purposes only and should not be considered investment advice or a recommendation to buy, sell, or hold any particular security. The Precision In Our Ability To Quantify Biological Aging Is Increasing For much of modern medicine, chronological age—simply the number of years a person has lived—has been the primary proxy for aging, guiding risk stratification and treatment decisions despite wide variations in health and function among individuals of the same age. Two 65-year-olds may differ dramatically in cardiovascular fitness, cognitive sharpness, and underlying disease risk. Clinical assessments can capture some of the differences through diagnostics and risk factors, while chronological age alone does not. The crucial gap between calendar age and actual biological condition has driven the search for better ways to measure the speed at which a person “ages.”在现代医学中，年龄（即一个人实际活了多少年）一直是衡量衰老的主要指标，用于指导风险分层和治疗决策，尽管同龄个体之间的健康和功能差异很大。两位65岁的老人可能在心血管健康、认知能力和潜在疾病风险方面存在显著差异。临床评估可以通过诊断和风险因素捕捉到部分差异，而仅凭年龄则无法做到这一点。日历年龄与实际生理状况之间的巨大差距促使人们寻求更好的方法来衡量人的“衰老”速度。 Early efforts focused on the physiological and functional markers correlated with mortality, disability, and loss of independence: blood pressure,21 aerobic capacity (a measure of cardiovascular fitness),22 bone mineral density,23 gait speed,24 and grip strength.25 While clinically useful, these measures largely capture the consequences of aging rather than its underlying biology, often identifying risks after a substantial decline in health. Weaker grip strength or lower bone mineral density suggests that aging processes have been underway for years.早期研究主要集中于与死亡率、残疾和丧失独立生活能力相关的生理和功能指标：血压、 21 有氧能力（衡量心血管健康的指标）、 22 骨密度、 23 步速、 24 和握力。 25 虽然这些指标在临床上很有用，但它们主要反映的是衰老的后果 ，而非其潜在的生物学机制，往往是在健康状况显著下降后才发现风险。握力减弱或骨密度降低表明衰老过程已持续多年。 Advances in molecular biology and computation have shifted the measurement of aging further upstream, closer to the biological processes themselves. Epigenetic clocks based on DNA methylation—small chemical tags that attach to DNA and change in predictable patterns over a person’s lifetime—can estimate biological age directly from molecular patterns in a person’s cells.分子生物学和计算技术的进步已将衰老测量向前推进，更接近生物过程本身。基于 DNA 甲基化的表观遗传时钟——DNA 甲基化是一种附着在 DNA 上的小型化学标记，会在人的一生中以可预测的模式发生变化——可以直接根据人体细胞中的分子模式来估算生物年龄。 Horvath’s original multi-tissue clock estimated biological age with a median error of 3.6 years across 51 different tissue and cell types, and subsequent models frequently outperformed chronological age in predicting mortality, morbidity, and functional decline.26 Instead of inferring biological condition from physical performance or clinical markers that reflect the consequences of aging, researchers were able to estimate a person’s biological age directly from molecular data, effectively transforming “aging” from an inevitable passage of time into a measurable, and potentially modifiable, biological state.Horvath 最初开发的多组织生物钟模型，在 51 种不同的组织和细胞类型中，对生物年龄的估计误差中位数为 3.6 年。后续模型在预测死亡率、发病率和功能衰退方面，通常优于实际年龄。 26 研究人员不再需要从反映衰老后果的体能表现或临床指标来推断生物状况，而是能够直接从分子数据中估计个体的生物年龄，从而有效地将“衰老”从不可避免的时间流逝转变为一种可测量且可能可改变的生物状态。 More recently, proteomic, immune-based, and wearable-derived measures have added new layers of biological depth and temporal resolution, linking circulating protein signatures,27 inflammatory pathways,28 and real-world activity patterns captured by wearable devices29 to aging trajectories and health risks. Together, these advances reflect a broader transition: aging is transforming from an implicit assumption based on years lived to a measurable, multidimensional variable spanning molecular, physiological, and behavioral domains. As measurement of those variables improves, the central question is shifting from whether biological aging can be quantified to whether it can be intervened upon within existing medical and regulatory frameworks.近年来，蛋白质组学、免疫学和可穿戴设备衍生的测量方法为生物学研究增添了新的深度和时间分辨率，将循环蛋白特征 、 炎症通路以及可穿戴设备捕捉到的真实世界活动模式与衰老轨迹和健康风险联系起来。这些进展共同反映了一种更广泛的转变：衰老正从基于寿命的隐性假设转变为一个可测量的、涵盖分子、生理和行为领域的多维变量。随着这些变量测量技术的进步，核心问题也从能否量化生物衰老转变为能否在现有的医疗和监管框架内对其进行干预。 Source: ARK Investment Management LLC, 2026, based on data from Kannel et al. 1961; Blair et al. 1989; Cummings et al. 1993; Guralnik et al. 1994; Studenski et al. 2011; Leong et al. 2015; Horvath 2013; Levine et al. 2018; Lu et al. 2019; Lehallier et al. 2020; Sathyan et al. 2020; Pyrkov et al. 2021; McIntyre et al. 2021.30 For informational purposes only and should not be considered investment advice or a recommendation to buy, sell, or hold any particular security.资料来源：ARK Investment Management LLC，2026 年，数据基于 Kannel 等人（1961 年）、Blair 等人（1989 年）、Cummings 等人（1993 年）、Guralnik 等人（1994 年）、Studenski 等人（2011 年）、Leong 等人（2015 年）、Horvath（2013 年）、Levine 等人（2018 年）、Lu 等人（2019 年）、Lehallier 等人（2020 年）、Sathyan 等人（2020 年）、Pyrkov 等人（2021 年）和 McIntyre 等人（2021 年）的研究。 30 仅供参考，不应被视为投资建议或买卖或持有任何特定证券的推荐。 What Is A “Longevity Treatment” In Today’s Regulatory Framework?在当今的监管框架下，什么是“长寿疗法”？ As aging biology becomes more measurable, pharma and biotech companies will face key translation challenges. Regulators in the US evaluate and approve drugs based on specific disease indications and clinically meaningful endpoints, such as event reduction, symptom improvement, or functional preservation.31 Even therapies that target aging mechanisms, like the accumulation of senescent cells, the breakdown of cellular quality-control systems, or the gradual loss of the molecular signals that maintain cell identity, must satisfy those disease-specific regulatory criteria.32 Consequently, longevity solutions typically enter the market indirectly.随着衰老生物学变得越来越可测量，制药和生物技术公司将面临关键的转化挑战。美国监管机构根据特定的疾病适应症和具有临床意义的终点（例如事件减少、症状改善或功能保留）来评估和批准药物。 31 即使是针对衰老机制的疗法，例如衰老细胞的积累、细胞质量控制系统的破坏或维持细胞身份的分子信号的逐渐丧失，也必须满足这些疾病特定的监管标准。 32 因此，延寿解决方案通常以间接的方式进入市场。 The most immediate and broadly accessible longevity interventions are behavioral. Collectively, improved diet, regular physical activity, adequate sleep, and avoidance of harmful exposures like tobacco influence a wide range of aging-related outcomes, from cardiometabolic disease and cognitive decline to all-cause mortality.33 Regular physical activity alone is associated with a 20–35% reduction in the relative risk of death.34 In other words, behavioral interventions are among the most evidence-based methods available for extending healthy lifespans and require no regulatory approval to access. That said, adherence to these interventions is a challenge: only ~10% of US adults adhere to recommendations for fruit and vegetable intake,35 ~24% meet recommended levels of both aerobic and muscle-strengthening physical activity—a figure that drops to ~15% among adults aged 65 and older,36 while adherence to long-term medical therapies averages ~50% in developed countries.37 Certain categories of medical intervention—particularly those reducing dosing frequency or requiring only one administration—can lower the adherence barrier structurally, complementing behavior change rather than replacing it.最直接、最易获得的长寿干预措施是行为干预。总体而言，改善饮食、规律运动、充足睡眠以及避免接触烟草等有害物质，能够影响一系列与衰老相关的健康结果，包括心血管代谢疾病、认知能力下降以及全因死亡率。 33 仅规律运动一项就能使死亡相对风险降低 20%至 35%。 34 换句话说，行为干预是目前延长健康寿命最有循证依据的方法之一，而且无需监管部门批准即可获得。尽管如此，坚持这些干预措施仍然是一个挑战：只有~10%的美国成年人能够达到水果和蔬菜摄入量的推荐标准， 35 ~24%的人能够达到有氧运动和肌肉强化运动的推荐水平——在 65 岁及以上的老年人中，这一比例下降到~15%， 36 而在发达国家，长期药物治疗的依从性平均为~50%。 37 某些类别的医疗干预——特别是那些减少给药频率或只需要一次给药的干预——可以从结构上降低依从性障碍，补充行为改变，而不是取代行为改变。 Medical therapies increasingly address longevity—not by targeting “aging” directly, but by reducing morbidity and mortality from diseases that increase sharply with age. By entering the market through disease-specific regulatory pathways, these therapies then generate broader value as their mechanisms impact shared biological pathways like inflammation, metabolism, and vascular risk.医疗疗法正日益关注延长寿命——并非直接针对“衰老”，而是通过降低随年龄增长而显著增加的疾病的发病率和死亡率。这些疗法通过针对特定疾病的监管途径进入市场，其作用机制会影响炎症、代谢和血管风险等共同的生物学通路，从而产生更广泛的价值。 GLP-1 receptor agonists illustrate this dynamic clearly. Originally developed for Type 2 diabetes, GLP-1s—a class of drugs that mimic a gut hormone involved in regulating blood sugar and appetite—have expanded to address obesity and cardiovascular risk. The FDA approved semaglutide, a GLP-1 receptor agonist marketed as Wegovy for chronic weight management. Thereafter, the SELECT cardiovascular outcomes trial—enrolling ~17,600 overweight/obese adults with established cardiovascular disease but without diabetes—demonstrated that semaglutide reduced the combined risk of cardiovascular death, heart attack, and stroke by 20%38 compared to placebo. Based on those results, in March 2024 the FDA approved Wegovy as the first weight-management medication with an additional indication for cardiovascular risk reduction—a survival-linked endpoint directly linked to longevity.39 As each successive indication has expanded the treatable population, GLP-1 receptor agonist revenue has grown rapidly, as shown below, illustrating how longevity value compounds as therapies approved for one condition can benefit others. Note: The chart reflects full-year revenue encompassing GLP-1 based therapeutics from Eli Lilly, Novo Nordisk, and Sanofi. Source: ARK Investment Management LLC, 2026, based on data from SEC filings and press releases from Eli Lilly, Novo Nordisk, and Sanofi through 2020 to 2025. For informational purposes only and should not be considered investment advice or a recommendation to buy, sell, or hold any particular security.注：图表反映的是礼来、诺和诺德和赛诺菲基于 GLP-1 疗法的全年收入。数据来源：ARK Investment Management LLC，2026 年，基于礼来、诺和诺德和赛诺菲 2020 年至 2025 年期间向美国证券交易委员会提交的文件和新闻稿数据。仅供参考，不应被视为投资建议或买卖或持有任何特定证券的推荐。 Our research suggests that one-time gene-editing therapies targeting genes involved in lipid metabolism—such as ANGPTL3 and LPA—could extend that logic further, potentially compressing decades of chronic cardiovascular dosing into a single treatment. ARK has explored the scientific basis and market opportunity for this approach in a companion piece, Harnessing Nature’s Wisdom: Gene-Editing Therapy For Cardiovascular Disease.40 A recent regulatory shift could open the door wider to longevity-relevant therapies. In December 2025, the FDA qualified treatment-related change in hip bone mineral density (BMD) as a surrogate endpoint—a measurable biomarker that regulators accept as a substitute for longer-term clinical outcomes like fractures—for clinical trials of osteoporosis drugs in postmenopausal women.41 The FDA based its decision on SABRE, the Study to Advance BMD as a Regulatory Endpoint initiative, a public-private partnership managed by the Foundation for the National Institutes of Health (FNIH) Biomarkers Consortium. SABRE assembled data from more than 160,000 participants across 52 clinical trials of anti-osteoporosis drugs that showed a strong statistical relationship between treatment-related BMD gains and fracture risk reduction.42近期监管政策的转变可能为延长寿命的疗法打开更广阔的大门。2025 年 12 月，美国食品药品监督管理局（FDA）将治疗相关的髋部骨密度（BMD）变化认定为绝经后女性骨质疏松症药物临床试验的替代终点——一种可测量的生物标志物，监管机构认可其可替代骨折等长期临床结局。 41 FDA 的这一决定基于 SABRE（推进 BMD 作为监管终点的研究）计划，该计划是由美国国立卫生研究院基金会（FNIH）生物标志物联盟管理的公私合作项目。SABRE 收集了来自 52 项抗骨质疏松症药物临床试验的超过 16 万名参与者的数据，结果显示治疗相关的 BMD 增加与骨折风险降低之间存在显著的统计学关联。 42 What is the impact of this FDA decision on longevity? Osteoporosis is one of the clearest manifestations of biological aging: bone mass declines progressively with age, resulting in fractures that are a leading cause of disability and death in older adults. More than 10 million older adults in the US have osteoporosis, and the International Osteoporosis Foundation projects that the condition will cause 3.2 million fractures annually by 2040 and ~$95 billion per year in related healthcare costs.43 Historically, clinical trials for new osteoporosis drugs required thousands of patients to demonstrate a decline in the number of fractures over several years, a costly and time-consuming barrier that led to a development drought. Indeed, the FDA has not approved a novel-mechanism osteoporosis therapy since romosozumab (Evenity) in 2019.44 By accepting non-invasive imaging of BMD as a primary endpoint, the FDA has lowered the barrier to innovation substantially. Future pivotal trials might require ~500-1000 patients followed over two years—not 10,000+ patients over three to five years.45 Two effects compound under the new paradigm: smaller patient enrollment lowers Phase 3 trial cost, and shorter trial duration extends years of patent-protected revenue post-approval. Our modeling illustrates how these effects could improve return on Phase 3 capital investment by ~7x over the status quo, as shown in the case study below.FDA 的这项决定对寿命有何影响？骨质疏松症是生物衰老最明显的表现之一：骨量随着年龄增长而逐渐下降，导致骨折，而骨折是老年人致残和死亡的主要原因。美国有超过 1000 万老年人患有骨质疏松症，国际骨质疏松症基金会预测，到 2040 年，该疾病每年将导致 320 万例骨折，并带来每年 950 亿美元的相关医疗保健费用。 以往 ，新骨质疏松症药物的临床试验需要数千名患者在数年内证明骨折次数减少，这既耗时又费钱，导致了药物研发的停滞。事实上，自 2019 年批准 romosozumab（Evenity）以来，FDA 尚未批准任何一种具有全新作用机制的骨质疏松症疗法 。FDA 将非侵入性骨密度成像作为主要终点，大大降低了创新的门槛。未来的关键性试验可能需要对 500 至 1000 名患者进行为期两年的随访，而不是像现在这样对 10000 多名患者进行为期三到五年的随访。在新模式下， 两项优势叠加：较小的患者入组规模降低了 III 期试验的成本，而较短的试验周期则延长了获批后专利保护期的收入。我们的模型显示，如下案例研究所示，这些优势可使 III 期资本投资回报率比现状提高 7 倍。 Note: Illustrative analysis comparing fracture-endpoint and BMD surrogate-endpoint trial economics and Phase 3 capital return on investment (ROI). Return on Phase 3 capital investment defined as (estimated cumulative patent-protected revenue minus Phase 3 trial cost) divided by Phase 3 trial cost. The metric isolates the regulatory change's effect on Phase 3 economics, capturing both the lower trial cost (from smaller, shorter surrogate-based trials) and the additional years of patent-protected revenue (from earlier market entry). It does not reflect total R&D investment, risk-adjusted returns, or profit margins. Cumulative revenue benchmarked from approximation of Amgen’s approved osteoporosis drug Prolia (denosumab) estimated from five annual revenue data points with intervening years interpolated using compound annual growth rates between anchors.46 Drug approved following fracture endpoint assumes 12 years of patent-protected sales while drug approved following BMD endpoint assumes 14 years, reflecting two additional years of patent-protected revenue from shorter pivotal trial duration. Phase 3 trial cost and enrollment estimates based on published osteoporosis trial benchmarks referenced in Institute for Progress 2026; Eastell et al. 2026.47 Source: ARK Investment Management LLC, 2026. For informational purposes only and should not be considered investment advice or a recommendation to buy, sell, or hold any particular security. More broadly, in ARK’s view, the BMD decision illustrates a pattern that could accelerate development of longevity-relevant therapies across many age-associated conditions. When regulators accept biomarkers closely tied to aging biology as endpoints for clinical trials, they are creating new regulatory on-ramps for therapies that preserve function and extend healthy lifespan—even without explicit approval for "aging." For drug developers, validated surrogate endpoints like BMD can mean smaller and shorter pivotal trials to test those targets clinically.48 Relation Therapeutics is one company that we believe is positioned to benefit, as its machine-learning platform maps causal biology across bone, immunologic, and metabolic disorders to identify novel drug targets that could be tested through these more efficient trial designs. Combined with advances in AI-driven drug discovery and the ability to measure and target the biological mechanisms associated with age-related disease, the regulatory evolution suggests that the pipeline of longevity-relevant medical interventions is likely to expand in the years ahead. Reflecting the expanding scope of medical interventions and, more recently, the aging of the population, US healthcare spending already has increased inexorably over the last 50 years, as shown below. Source: ARK Investment Management LLC, 2026, based on data from Centers for Medicare & Medicaid Services (CMS), National Health Expenditure Accounts 2024.49 For informational purposes only and should not be considered investment advice or a recommendation to buy, sell, or hold any particular security. Against the backdrop of rising expenditures, and as interventions accumulate, a natural question follows: what is the value of extending healthy lifespans? Standard health-economics frameworks offer a way to estimate the theoretical added value associated with longevity and the resulting figures underscore the magnitude of the opportunity. What Might The US Longevity Market Be Worth? Each year, premature death claims an estimated ~46 million years of life in the US.50 When someone dies at age 55, for example, actuarial tables estimate that he or she had ~27 more years of life remaining—“years of life lost.” Summed across all deaths in the US, those lost years total ~46 million annually. Cardiovascular disease and cancer account for the largest share of years lost across most age brackets, but neurological disorders, respiratory diseases, and metabolic conditions contribute increasingly at older ages as multiple aging-related pathologies converge later in life, as shown below. Valued at $100,000 per life-year, a commonly cited willingness-to-pay threshold in US health-economics analyses,51 those lost years represent ~$4.6 trillion worth of healthy life lost each year. Note: Years of life lost are calculated by multiplying deaths in each age group by remaining life expectancy at the midpoint age of the bracket. Source: ARK Investment Management LLC, 2026, based on data from Centers for Disease Control and Prevention, National Center for Health Statistics 2025; Arias et al. 2025.52 For informational purposes only and should not be considered investment advice or a recommendation to buy, sell, or hold any particular security. Health economists often evaluate medical interventions using quality-adjusted life years, or QALYs, a standard metric that captures both the length and quality of life.53 A QALY weights each year lived on a scale from 0 (death) to 1 (perfect health): a year lived in excellent health counts as 1.0, while a year lived with a significant disability might count as 0.6. Health economists use QALYs in cost-effectiveness analyses to compare treatments that extend life, and/or improve quality of life.54 Using this theoretical framework, we estimated the healthy life potential of the US population in an ideal world that eliminates non-accidental deaths and functional decline. Under those conditions, the current US population could gain ~11.9 billion QALYs, effectively doubling its healthy life potential, as shown below.55 *Note: To calculate the longevity gain, this model assumes a theoretical max lifespan of 120 years old, elimination of functional decline, while accidental deaths persist. Analysis from Winton and Wihlborg, ARK Big Ideas 2026 research report. Source: ARK Investment Management LLC, 2026, based on data from Centers for Disease Control and Prevention, National Center for Health Statistics 2025; Arias et al. 2022; United Nations Department of Economic and Social Affairs, Population Division 2024.56 In addition to those sources, certain information presented may be the result of ARK’s internal analyses, which draw on various additional sources of information. For informational purposes only and should not be considered investment advice or a recommendation to buy, sell, or hold any particular security. Forecasts are inherently limited and cannot be relied upon.*注：为计算寿命增益，本模型假设理论最大寿命为 120 岁，功能衰退消除，但意外死亡仍然存在。分析来自 Winton 和 Wihlborg 的《ARK Big Ideas 2026》研究报告。数据来源：ARK Investment Management LLC，2026 年，基于美国疾病控制与预防中心国家卫生统计中心 2025 年的数据；Arias 等人 2022 年的研究；联合国经济和社会事务部人口司 2024 年的数据。 56 除上述数据来源外，部分信息可能来自 ARK 的内部分析，这些分析参考了其他各种信息来源。仅供参考，不应被视为投资建议或买卖或持有任何特定证券的推荐。预测本身具有局限性，不可依赖。 Valuing each healthy life year at $100,000 per QALY, this longevity gain could create a theoretical addressable market (TAM) valued at ~$1.2 quadrillion. To put that figure into perspective, global gross domestic product (GDP) totals ~$110 trillion per year57 and the global biotech market size is ~$1.5-$2 trillion—only ~0.1% of the $1.2 quadrillion US longevity TAM.58如果将每个健康生命年的价值定为每质量调整生命年 (QALY) 10 万美元，那么这种寿命延长带来的预期市场规模 (TAM) 可能高达 1.2 千万亿美元。为了更好地理解这个数字，全球国内生产总值 (GDP) 总额为每年 110 万亿美元 ， 而全球生物技术市场规模为 1.5 万亿至 2 万亿美元，仅占美国 1.2 千万亿美元寿命延长预期市场的 0.1% 。 The $1.2 quadrillion figure measures the gross theoretical scale of the longevity opportunity. It values every healthy life-year equally, regardless of when in the future it is experienced, because the figure is sizing a gap—not evaluating a specific intervention. In contrast, when health economists assess particular treatments, the standard convention is to apply a 3% time-value discount to both costs and outcomes, reflecting society's preference for sooner-realized health benefits over later ones. That convention, established by the Institute for Clinical and Economic Review (ICER) and the Second Panel on Cost-Effectiveness in Health and Medicine, is designed for intervention-level analysis—where the timing of costs and benefits affects whether a specific therapy is favorable enough to adopt.59 Applied to the same underlying longevity gap, it yields a discounted longevity opportunity of ~$350 trillion. The two figures answer different questions: the undiscounted ~$1.2 quadrillion measures the full theoretical scale of what is at stake; the discounted ~$350 trillion expresses that scale under the intervention-evaluation convention. Importantly, neither figure forecasts market penetration nor suggests that a single therapy or even a class of therapies will be able to deliver provocative outcomes in the near term. Rather, these figures represent both an upper-bound valuation based on today’s economic conventions and a framework for understanding value, analogous to the computed economic value of electricity or computing in the early years of conceptualizing those models. To estimate the value of modest progress against aging, we modeled the impact of biological aging proceeding at 95%, 90%, or 85% of its current rate, in other words, slowing aging by 5%, 10%, or 15%, respectively. The premise is straightforward: slower aging should delay the diseases and functional decline that cumulate with biological age. For instance, slowing biological aging by 10% would suggest nine years of biological wear and tear per decade. The earlier the intervention, the larger the gap between chronological and biological age and the greater compounding benefit in physical function, quality of life, and lowering mortality risk. Even a modest slowdown in aging could generate substantial value. In the 15% slowdown scenario, the incremental value added per person peaks at roughly $107,000 for individuals in their mid-twenties and declines steadily with age as remaining life expectancy shortens, as shown below. Even a 5% slowdown would generate ~$35,000 in per-person value for younger adults. Why? Compounding. Slowing biological aging does not deliver a one-time benefit but extends healthier functions across every year remaining in a young person’s life: the greater the number of years, the more the benefit accumulates. Note: Incremental value per person represents the additional quality-adjusted life years (QALYs) gained under each aging slowdown scenario relative to baseline, valued at $100,000 per QALY. The model simulates remaining lifetime QALYs for individuals at each age by projecting year-by-year survival under two mortality components: non-accident mortality, which shifts according to biological age (slowed by 5%, 10%, or 15%), and accident mortality, which remains fixed at chronological age. Health-related quality of life at each age is estimated using EQ-5D-5L utility weights and is also evaluated at biological age, meaning that individuals that age more slowly spend more time at the higher utility levels associated with younger biology—the value reflects both longer life and better quality of life during those years. All future QALYs are discounted at 3% annually, consistent with ICER's reference case for cost-effectiveness analysis. Because the survival gains from slowing aging accrue primarily at older ages—decades in the future for younger individuals—quality-of-life adjustment and discounting together substantially compress their present value. For example, a 10% slowdown beginning at age 20 is estimated to add several additional life years, but because those years arrive mostly after age 75, the discounted present value is approximately $71,000. Maximum lifespan is capped at 120 years. Source: ARK Investment Management LLC, 2026, based on data from Arias et al. 2025; Centers for Disease Control and Prevention, National Center for Health Statistics 2025; United Nations Department of Economic and Social Affairs, Population Division 2024; Jiang et al. 2021.60 For informational purposes only and should not be considered investment advice or a recommendation to buy, sell, or hold any particular security. Forecasts are inherently limited and cannot be relied upon. When aggregated across the US population and weighted by cohort size, the distribution of the value added is striking. Younger age groups account for the largest share of total incremental value under every scenario—not because of their disease burden today, but because larger cohorts and decades of expected remaining life allow the benefits of slower aging to compound. In contrast, adults aged 85 and older—the group most associated with aging—contribute negligibly to the value added, because this group’s remaining life expectancy limits the compounding of benefits. Across the US population, slowing biological aging by 5–15% could generate ~$10–30 trillion in total value added at $100,000 per QALY, as shown below.61 Note: Total incremental value per age group represents the population-weighted sum of additional quality-adjusted life years (QALYs) gained under each aging slowdown scenario (5%, 10%, and 15%) for all individuals within the age bracket, valued at $100,000 per QALY. The concentration of value in younger age groups reflects both larger cohort sizes and greater remaining life expectancy over which the benefits of slowed biological aging compound. The 0–14 age bracket accounts for the largest share of total incremental value under every scenario, driven by the combination of a wide cohort window (15 birth-year cohorts versus 10 for subsequent brackets through age 84) and decades of remaining life. The model simulates remaining lifetime QALYs for individuals at each age by projecting year-by-year survival under two mortality components: non-accident mortality, which shifts according to biological age under each slowdown scenario, and accident mortality, which remains fixed at chronological age. Health-related quality of life is estimated using EQ-5D-5L utility weights, all future QALYs are discounted at 3% annually, and maximum lifespan is capped at 120 years. Source: ARK Investment Management LLC, 2026 based on data from Arias et al. 2025; Centers for Disease Control and Prevention, National Center for Health Statistics 2025; United Nations Department of Economic and Social Affairs, Population Division 2024; Jiang et al. 2021.62 For informational purposes only and should not be considered investment advice or a recommendation to buy, sell, or hold any particular security. Forecasts are inherently limited and cannot be relied upon. Realizing increasing shares of that potential likely depends upon the convergence of multiple innovation platforms, including multiomics sequencing, artificial intelligence, and robotics. In a world of rising productivity and abundance, individuals are likely to place increasing value on extending healthy lifespans, or living longer with a higher quality of life.  Conclusion  结论 As the understanding of aging biology and its measurement improves, so should designing interventions that slow, halt, or reverse mechanisms of aging. In this context, no single therapy will define the longevity opportunity. Instead, the cumulative value of healthcare innovation will manifest in delaying disease and preserving function. Advances in longevity are likely to unfold gradually, in response to scientific evolution and regulatory breakthroughs. Near-term, improved measurement and prevention are likely to define progress, giving way in the mid-term to therapies targeting aging through disease-specific endpoints and, in the long-term to experimental approaches aimed at partial restoration or regeneration, as illustrated below. This horizon-based view underscores that longevity is not a single breakthrough but a compounding process in which value is likely to accrue as converging innovations help extend healthy lifespans over time. Note: Time horizons reflect ARK’s estimates based on scientific progress and regulatory feasibility, not guaranteed outcomes. Effects on lifespan or function are likely to be incremental, context-dependent, and mediated through disease-specific endpoints rather than “aging” as a clinical indication. Source: ARK Investment Management LLC, 2026. For informational purposes only and should not be considered investment advice or a recommendation to buy, sell, or hold any particular security. Forecasts are inherently limited and cannot be relied upon.1 See the figure entitled “US Longevity Potential.” QALYs are quality-adjusted life years, a standard health-economics metric that weights each year lived from 0 (death) to 1 (perfect health). ARK’s analysis reflects an undiscounted, theoretical value of what extended lives lived in better health would be worth if the US population could live to a theoretical maximum lifespan of 120 years in perfect health, with the risk of accidental deaths remaining. It is a measure of magnitude at a standard health-economics willingness-to-pay benchmark of $100,000 per QALY. The Institute for Clinical and Economic Review (ICER) is an independent non-profit that conducts cost-effectiveness analyses for healthcare interventions; its reference case applies a 3% time-value discount to both costs and outcomes, per the Second Panel on Cost-Effectiveness in Health and Medicine. Applying that convention here would yield a longevity opportunity of ~$350 trillion. The undiscounted figure measures the magnitude of the longevity opportunity as it exists. The discounted figure reflects standard health-economics convention that counts a healthy life-year experienced further in the future as worth less than one experienced soon. See the presentation in the section above entitled, “What Might the US Longevity Market Be Worth?” for further discussion.2 Cumulative value across the lifetime of the current US population, applying a 3% time-value discount to QALYs, as described above.3 See the figure entitled “Slowing Biological Aging by 10% Could Be Worth Nearly Double US Prescription Drug Spending Annually.” The $930 billion annualizes the lifetime QALY gains from a 10% aging slowdown—converting each person's discounted lifetime value to equal annual payments over their remaining life expectancy, then summed across the US population. The 10% case is the same scenario underlying the $10–30 trillion lifetime range cited above, expressed as an annual flow rather than a lifetime aggregate. Prescription drug spending represents actual annual expenditure, while the longevity figure represents annualized willingness-to-pay for health gains; the two are placed side-by-side to convey scale, not direct substitutability.参见题为“减缓生物衰老 10%的价值可能相当于美国处方药年支出的近两倍”的图表。图中 9300 亿美元的价值是将衰老减缓 10%所带来的终身质量调整生命年（QALY）收益按年计算得出的——即将每个人的折现终身价值转化为在其剩余预期寿命内每年支付的等额款项，然后将该金额汇总到美国人口总数。10%的情况与上文提到的 10 万亿至 30 万亿美元的终身价值范围所依据的情景相同，只是以年度金额而非终身总额来表示。处方药支出代表实际的年度支出，而寿命延长带来的收益则代表人们为获得健康收益而愿意支付的年度金额；两者并列展示是为了体现规模，而非直接的替代性。4 Centers for Medicare & Medicaid Services (CMS). 2024. “National Health Expenditure Data: Historical.” See also Arias, E. et al. 2025. "United States Life Tables, 2023.” National Vital Statistics Reports. See also Centers for Disease Control and Prevention, National Center for Health Statistics. 2025. “National Vital Statistics System (NVSS): Mortality Data, 2018–2024.” CDC WONDER Online Database. See also Jiang, R. et al. 2021. "US Population Norms for the EQ-5D-5L and Comparison of Norms from Face-to-Face and Online Samples." Quality of Life Research.美国医疗保险和医疗补助服务中心 (CMS)。2024 年。“国家卫生支出数据：历史数据”。另见 Arias, E. 等人。2025 年。“2023 年美国生命表”。《国家生命统计报告》。另见美国疾病控制与预防中心，国家卫生统计中心。2025 年。“国家生命统计系统 (NVSS)：2018-2024 年死亡率数据”。CDC WONDER 在线数据库。另见 Jiang, R. 等人。2021 年。“EQ-5D-5L 的美国人口常模以及面对面样本和在线样本常模的比较”。《生活质量研究》。5 United Nationals Department of Economic and Social Affairs, Population Division. 2024. “World Population Prospects 2024.” See also Our World in Data. 2024. “Life Expectancy.”联合国经济和社会事务部人口司，2024年，《2024年世界人口展望》。另见“数据世界”，2024年，《预期寿命》。6 Ibid.   同上。7 Note: Data are from the Multiple Cause of Death Files, 2018–2024, as compiled from data provided by the 57 vital statistics jurisdictions through the Vital Statistics Cooperative Program. Centers for Disease Control and Prevention, National Center for Health Statistics. 2025. “National Vital Statistics System (NVSS): Mortality Data, 2018–2024.” CDC WONDER Online Database.注：数据来自 2018-2024 年多重死因档案，该档案由 57 个生命统计管辖区通过生命统计合作计划提供的数据汇编而成。美国疾病控制与预防中心，国家卫生统计中心。2025 年。“国家生命统计系统（NVSS）：2018-2024 年死亡率数据。” CDC WONDER 在线数据库。8 Ibid.9 Partridge, L. et al. 2018. “Facing up to the global challenges of ageing.” Nature.10 López-Otín, C. et al. 2013. “The Hallmarks of Aging.” Cell. See also López-Otín, C. et al. 2023. “Hallmarks of Aging: An Expanding Universe.” Cell.11 Kennedy, B.K. et al. 2014. “Geroscience: Linking Aging to Chronic Disease.” Cell.12 Lu, Y.R., et al. 2023. “The Information Theory of Aging.” Nature Aging.13 López-Otín, C. et al. 2013. “The Hallmarks of Aging.” Cell. See also López-Otín, C. et al. 2023. “Hallmarks of Aging: An Expanding Universe.” Cell. See also Lu, Y.R., et al. 2023. “The Information Theory of Aging.” Nature Aging.López-Otín, C. 等人，2013 年。“衰老的标志”。《细胞》。另见 López-Otín, C. 等人，2023 年。“衰老的标志：一个不断扩展的宇宙”。《细胞》。另见 Lu, YR 等人，2023 年。“衰老的信息论”。《自然衰老》。14 Harrison, D.E. et al. 2009. “Rapamycin fed late in life extends lifespan in genetically heterogeneous mice.” Nature.Harrison, DE 等人 2009 年。“在生命后期喂食雷帕霉素可延长遗传异质小鼠的寿命。” Nature。15 Xu, M. et al. 2018. “Senolytics improve physical function and increase lifespan in old age.” Nature Medicine.Xu, M. 等. 2018.“衰老细胞清除剂改善老年人的身体机能并延长寿命。”自然医学。16 Widjaja, A.A. et al. 2024. “Inhibition of IL-11 signalling extends mammalian healthspan and lifespan.” Nature.Widjaja, AA 等人 2024。“抑制 IL-11 信号传导可延长哺乳动物的健康寿命和寿命。” Nature。17 Cano Macip, C. et al. 2024. “Gene Therapy-Mediated Partial Reprogramming Extends Lifespan and Reverses Age-Related Changes in Aged Mice.” Cellular Reprogramming.Cano Macip, C. 等人 2024。“基因治疗介导的部分重编程延长了老年小鼠的寿命并逆转了与年龄相关的变化。”细胞重编程。18 Gkioni, L. et al. 2025. “The geroprotectors trametinib and rapamycin combine additively to extend mouse healthspan and lifespan.” Nature Aging.Gkioni, L. 等人 2025。“抗衰老药物曲美替尼和雷帕霉素协同作用，延长小鼠的健康寿命和寿命。”《自然衰老》。19 López-Otín, C. et al. 2023. “Hallmarks of Aging: An Expanding Universe.” Cell.López-Otín, C. 等人 2023. “衰老的标志：一个不断扩展的宇宙。” Cell.20 Harrison, D.E. et al. 2009. “Rapamycin fed late in life extends lifespan in genetically heterogeneous mice.” Nature. See also Xu, M. et al. 2018. “Senolytics improve physical function and increase lifespan in old age.” Nature Medicine. See also Widjaja, A.A. et al. 2024. “Inhibition of IL-11 signalling extends mammalian healthspan and lifespan.” Nature. See also Cano Macip, C. et al. 2024. “Gene Therapy-Mediated Partial Reprogramming Extends Lifespan and Reverses Age-Related Changes in Aged Mice.” Cellular Reprogramming. See also Gkioni, L. et al. 2025. "The Geroprotectors Trametinib and Rapamycin Combine Additively to Extend Mouse Healthspan and Lifespan." Nature Aging.Harrison, DE 等，2009 年。“晚年服用雷帕霉素可延长遗传异质性小鼠的寿命。”《自然》。另见 Xu, M. 等，2018 年。“衰老细胞清除剂可改善老年人的身体机能并延长寿命。”《自然医学》。另见 Widjaja, AA 等，2024 年。“抑制 IL-11 信号通路可延长哺乳动物的健康寿命和寿命。”《自然》。另见 Cano Macip, C. 等，2024 年。“基因治疗介导的部分重编程可延长老年小鼠的寿命并逆转其与年龄相关的变化。”《细胞重编程》。另见 Gkioni, L. 等，2025 年。“抗衰老药物曲美替尼和雷帕霉素联合使用可叠加延长小鼠的健康寿命和寿命。”《自然衰老》。21 Kannel, W.B. et al. 1961. “Factors of risk in the development of coronary heart disease.” Annals of Internal Medicine.Kannel, WB 等. 1961. “冠心病发展中的危险因素。”《内科年鉴》。22 Blair, S.N. et al. 1989. “Physical fitness and all-cause mortality.” JAMA.Blair, SN 等人，1989 年。“身体素质与全因死亡率。” JAMA。23 Cummings, S.R. et al. 1993. “Bone density and hip fracture prediction.” The Lancet.Cummings, SR 等人，1993 年。“骨密度和髋部骨折预测。”《柳叶刀》。24 Studenski, S. et al. 2011. “Gait speed and survival in older adults.” JAMA.Studenski, S. 等人 2011. “老年人的步速与生存率。” JAMA。25 Leong, D.P. et al. 2015. “Prognostic value of grip strength: findings from the PURE study.” The Lancet.Leong, DP 等人，2015 年。“握力的预后价值：PURE 研究的发现。”《柳叶刀》。26 Horvath, S. 2013. “DNA methylation age of human tissues.” Genome Biology. See also Levine, M.E. et al. 2018. “An epigenetic biomarker of aging.” Aging. See also Lu, A.T. et al. 2019. “GrimAge predicts lifespan and healthspan.” Aging.Horvath, S. 2013. “人类组织的 DNA 甲基化年龄。”《基因组生物学》。另见 Levine, ME 等. 2018. “衰老的表观遗传生物标志物。”《衰老》。另见 Lu, AT 等. 2019. “GrimAge 预测寿命和健康寿命。”《衰老》。27 Lehallier, B. et al. 2020. “Data mining of human plasma proteins generates a multitude of highly predictive aging clocks that reflect different aspects of aging.” Aging Cell. See also Sathyan, S. et al. 2020. “Plasma proteomic profile of age, health span, and all-cause mortality in older adults.” Aging Cell.Lehallier, B. 等人，2020 年。“人类血浆蛋白数据挖掘生成了多种高度预测性的衰老时钟，反映了衰老的不同方面。”《衰老细胞》。另见 Sathyan, S. 等人，2020 年。“老年人血浆蛋白质组学特征与年龄、健康寿命和全因死亡率的关系。”《衰老细胞》。28 Sayed, N. et al. 2021. “An inflammatory aging clock (iAge).” Nature Aging.Sayed, N. 等人 2021.“炎症衰老时钟 (iAge)。”《自然衰老》。29 Pyrkov, T.V. et al. 2021. “Deep longitudinal phenotyping of wearable sensor data reveals independent markers of longevity, stress, and resilience.” Aging. See also McIntyre, R.L. et al. 2021. “Biological Age Prediction From Wearable Device Movement Data Identifies Nutritional and Pharmacological Interventions for Healthy Aging.” Frontiers in Aging.Pyrkov, TV 等人，2021 年。“对可穿戴传感器数据进行深度纵向表型分析，揭示长寿、压力和韧性的独立标志物。”《衰老》。另见 McIntyre, RL 等人，2021 年。“基于可穿戴设备运动数据的生物年龄预测，识别促进健康老龄化的营养和药物干预措施。”《衰老前沿》。30 Kannel, W.B. et al. 1961. “Factors of risk in the development of coronary heart disease.” Annals of Internal Medicine. See also Blair, S.N. et al. 1989. “Physical fitness and all-cause mortality.” JAMA. See also Cummings, S.R. et al. 1993. “Bone density and hip fracture prediction.” The Lancet. See also Guralnik, J.M. et al. 1994. "A Short Physical Performance Battery Assessing Lower Extremity Function: Association with Self-Reported Disability and Prediction of Mortality and Nursing Home Admission." Journal of Gerontology. See also Studenski, S. et al. 2011. “Gait speed and survival in older adults.” JAMA. See also Leong, D.P. et al. 2015. “Prognostic value of grip strength: findings from the PURE study.” The Lancet. See also Horvath, S. 2013. “DNA methylation age of human tissues.” Genome Biology. See also Levine, M.E. et al. 2018. “An epigenetic biomarker of aging.” Aging. See also Lu, A.T. et al. 2019. “GrimAge predicts lifespan and healthspan.” Aging. See also Lehallier, B. et al. 2020. “Data mining of human plasma proteins generates a multitude of highly predictive aging clocks that reflect different aspects of aging.” Aging Cell. See also Sathyan, S. et al. 2020. “Plasma proteomic profile of age, health span, and all-cause mortality in older adults.” Aging Cell. See also Pyrkov, T.V. et al. 2021. “Deep longitudinal phenotyping of wearable sensor data reveals independent markers of longevity, stress, and resilience.” Aging. See also McIntyre, R.L. et al. 2021. “Biological Age Prediction From Wearable Device Movement Data Identifies Nutritional and Pharmacological Interventions for Healthy Aging.” Frontiers in Aging.Kannel, WB 等，1961 年。“冠心病发展中的危险因素”。《内科年鉴》。另见 Blair, SN 等，1989 年。“体能与全因死亡率”。《美国医学会杂志》。另见 Cummings, SR 等，1993 年。“骨密度与髋部骨折预测”。《柳叶刀》。另见 Guralnik, JM 等，1994 年。“评估下肢功能的简短体能测试：与自我报告的残疾程度以及死亡率和养老院入住率的关联”。《老年医学杂志》。另见 Studenski, S. 等，2011 年。“老年人的步速与生存率”。《美国医学会杂志》。另见 Leong, DP 等，2015 年。“握力的预后价值：来自 PURE 研究的发现”。《柳叶刀》。另见 Horvath, S. 2013. “人类组织的 DNA 甲基化年龄。”《基因组生物学》。另见 Levine, ME 等. 2018. “衰老的表观遗传生物标志物。”《衰老》。另见 Lu, AT 等. 2019. “GrimAge 预测寿命和健康寿命。”《衰老》。另见 Lehallier, B. 等. 2020. “人类血浆蛋白数据挖掘生成大量高度预测性的衰老时钟，反映衰老的不同方面。”《衰老细胞》。另见 Sathyan, S. 等. 2020. “老年人血浆蛋白质组学特征与年龄、健康寿命和全因死亡率的关系。”《衰老细胞》。另见 Pyrkov, TV 等. 2021. “可穿戴传感器数据的深度纵向表型分析揭示了长寿、压力和韧性的独立标志物。”《衰老》。另见 McIntyre, RL 等人 2021 年发表的《基于可穿戴设备运动数据的生物年龄预测识别健康老龄化的营养和药物干预措施》。《老龄化前沿》。31 U.S. Food and Drug Administration. 2022. “Development & Approval Process | Drugs.” See also U.S. Food and Drug Administration. 2018 “How FDA Approves Drugs and Regulates Their Safety and Effectiveness.”美国食品药品监督管理局。2022 年。“药物研发与审批流程”。另见美国食品药品监督管理局。2018 年。“FDA 如何审批药物并监管其安全性和有效性”。32 National Institute on Aging. 2024. "Information on FDA review of geroscience-related IND applications."美国国家老龄研究所。2024 年。“关于 FDA 对老年科学相关 IND 申请的审查信息。”33 Centers for Disease Control and Prevention (CDC). 2024. “Benefits of Quitting Smoking.” See also World Health Organization (WHO). 2020. “WHO guidelines on physical activity and sedentary behaviour.”美国疾病控制与预防中心（CDC）。2024 年。“戒烟的好处”。另见世界卫生组织（WHO）。2020 年。“世卫组织关于身体活动和久坐行为的指南”。34 Reimers, C.D. et al. 2012. "Does Physical Activity Increase Life Expectancy? A Review of the Literature." Journal of Aging Research. See also Löllgen, H. et al. 2009. "Physical activity and all-cause mortality: an updated meta-analysis with different intensity categories." International Journal of Sports Medicine. See also Nocon, M. et al. 2008. "Association of physical activity with all-cause and cardiovascular mortality: a systematic review and meta-analysis." European Journal of Cardiovascular Prevention & Rehabilitation.Reimers, CD 等，2012 年。“体育锻炼能延长预期寿命吗？文献综述。”《老年研究杂志》。另见 Löllgen, H. 等，2009 年。“体育锻炼与全因死亡率：一项包含不同强度类别的最新荟萃分析。”《国际运动医学杂志》。另见 Nocon, M. 等，2008 年。“体育锻炼与全因死亡率和心血管死亡率的关联：一项系统评价和荟萃分析。”《欧洲心血管预防与康复杂志》。35 Centers for Disease Control and Prevention. 2024. "State Indicator Report on Fruits and Vegetables."美国疾病控制与预防中心。2024年。《各州水果和蔬菜指标报告》。36 Centers for Disease Control and Prevention, National Center for Health Statistics. 2022. "Physical Activity Among Adults Aged 18 and Over: United States, 2020."美国疾病控制与预防中心，国家卫生统计中心。2022 年。“18 岁及以上成年人的身体活动：美国，2020 年。”37 World Health Organization. 2003. "Adherence to Long-term Therapies: Evidence for Action."世界卫生组织。2003 年。“长期治疗的依从性：行动的证据。”38 The SELECT trial reported a hazard ratio of 0.80 (95% CI, 0.72–0.90; P<0.001) for the primary composite endpoint of cardiovascular death, nonfatal myocardial infarction, or nonfatal stroke. Lincoff, A.M. et al. 2023. "Semaglutide and Cardiovascular Outcomes in Obesity without Diabetes." New England Journal of Medicine.SELECT 试验报告称，对于心血管死亡、非致死性心肌梗死或非致死性卒中的主要复合终点，风险比为 0.80（95% CI，0.72–0.90；P<0.001）。Lincoff, AM等. 2023.“Semaglutide and Cardiovascular Outcomes in Obesity without Diabetes.” New England Journal of Medicine.39 U.S. Food and Drug Administration (FDA). 2024. "FDA Approves First Treatment to Reduce Risk of Serious Heart Problems Specifically in Adults with Obesity or Overweight." See also: Novo Nordisk. 2024. "Wegovy® receives FDA approval for cardiovascular risk reduction in adults with known heart disease and overweight or obesity."美国食品药品监督管理局 (FDA)。2024 年。“FDA 批准首个专门针对肥胖或超重成年人降低严重心脏疾病风险的治疗方案。”另见：诺和诺德。2024 年。“Wegovy® 获得 FDA 批准，用于降低已知患有心脏病且超重或肥胖的成年人的心血管风险。”40 Wihlborg, S. 2025. "Harnessing Nature’s Wisdom: Gene-Editing Therapy For Cardiovascular Disease.” ARK Investment Management LLC.Wihlborg, S. 2025. “利用自然的智慧：心血管疾病的基因编辑疗法。” ARK 投资管理有限责任公司。41 Foundation for the National Institutes of Health. 2025. "FNIH Announces FDA Qualification of First Surrogate Endpoint for Use in Osteoporosis Clinical Trials." See also Beth Israel Deaconess Medical Center. 2025. "BIDMC Investigator Contributes To FDA Approval of New and Better Way To Test Osteoporosis Treatments."美国国立卫生研究院基金会 (FNIH)。2025 年。“FNIH 宣布 FDA 批准首个用于骨质疏松症临床试验的替代终点指标。”另见贝斯以色列女执事医疗中心 (BIDMC)。2025 年。“BIDMC 研究人员助力 FDA 批准一种新的、更有效的骨质疏松症治疗测试方法。”42 Ibid.   同上。43 Ibid.   同上。44 Romosozumab (Evenity), a monoclonal antibody sclerostin inhibitor, was approved by the FDA in April 2019 for the treatment of osteoporosis in postmenopausal women at high risk of fracture. Since then, no novel-mechanism osteoporosis therapy has been approved. See also Entera Bio. 2025. "Entera Bio Congratulates the FNIH-ASBMR-SABRE Team on FDA's Qualification of Total Hip BMD as Regulatory Endpoint."罗莫索单抗（Evenity）是一种单克隆抗体硬骨素抑制剂，于 2019 年 4 月获得 FDA 批准，用于治疗绝经后高骨折风险女性的骨质疏松症。自此之后，尚无其他新型机制的骨质疏松症疗法获得批准。另见 Entera Bio 公司 2025 年发布的报告：“Entera Bio 祝贺 FNIH-ASBMR-SABRE 团队获得 FDA 对全髋骨密度作为监管终点的认可。”45 Eastell, R. et al. 2026. "Recognising a new surrogate endpoint for osteoporosis trials: the SABRE project." Hospital Healthcare Europe. See also Institute for Progress. 2026. "Proxy Praxis: Why Validating an Endpoint Took 12 Years."Eastell, R. 等人，2026 年。“识别骨质疏松症试验的新替代终点：SABRE 项目”。《欧洲医院医疗保健》。另见进步研究所，2026 年。“代理实践：验证一个终点为何耗时 12 年”。46 Amgen. 2026. “Amgen reports fourth quarter and full year 2025 financial results.”安进公司。2026年。“安进公司公布2025年第四季度及全年财务业绩。”47 Eastell, R. et al. 2026. "Recognising a new surrogate endpoint for osteoporosis trials: the SABRE project." Hospital Healthcare Europe. See also Institute for Progress. 2026. "Proxy Praxis: Why Validating an Endpoint Took 12 Years."Eastell, R. 等人，2026 年。“识别骨质疏松症试验的新替代终点：SABRE 项目”。《欧洲医院医疗保健》。另见进步研究所，2026 年。“代理实践：验证一个终点为何耗时 12 年”。48 Relation Therapeutics. 2024. "Relation Therapeutics secures $35 million of new seed financing led by DCVC and co-lead NVentures, NVIDIA's venture arm."Relation Therapeutics. 2024.“Relation Therapeutics 获得由 DCVC 领投、NVIDIA 旗下风险投资机构 NVentures 联合领投的 3500 万美元新种子轮融资。”49 Centers for Medicare & Medicaid Services. 2024. “National Health Expenditure Data: Historical.”美国医疗保险和医疗补助服务中心。2024 年。“国家医疗支出数据：历史数据”。50 Arias, E. et al. 2025. "United States Life Tables, 2023.” National Vital Statistics Reports. See also Centers for Disease Control and Prevention, National Center for Health Statistics. 2025. “National Vital Statistics System (NVSS): Mortality Data, 2018–2024.” CDC WONDER Online Database.Arias, E. 等. 2025. “2023 年美国生命表”。国家生命统计报告。另见美国疾病控制与预防中心，国家卫生统计中心。2025. “国家生命统计系统 (NVSS)：2018-2024 年死亡率数据”。CDC WONDER 在线数据库。51 Institute for Clinical and Economic Review (ICER). 2023 (updated). “ICER Value Assessment Framework.”临床与经济评价研究所（ICER）。2023（更新版）。“ICER 价值评估框架。”52 Centers for Disease Control and Prevention, National Center for Health Statistics. 2025. “National Vital Statistics System (NVSS): Underlying Cause of Death, 2018–2024.” CDC WONDER Online Database. See also Arias, Elizabeth et al. 2025. "United States Life Tables, 2023." National Vital Statistics Reports.美国疾病控制与预防中心，国家卫生统计中心。2025。“国家生命统计系统（NVSS）：2018-2024 年根本死因”。CDC WONDER 在线数据库。另见 Arias, Elizabeth 等人。2025。“2023 年美国生命表”。国家生命统计报告。53 Gold, M.R. et al. 1996. “Cost-Effectiveness in Health and Medicine.” Oxford University Press. See also Neumann, P.J. et al. 2016. “Cost-Effectiveness in Health and Medicine: Second Panel on Cost-Effectiveness in Health and Medicine." JAMA.Gold, MR 等. 1996. “卫生和医学中的成本效益。”牛津大学出版社。另见 Neumann, PJ 等. 2016. “卫生和医学中的成本效益：卫生和医学成本效益第二届专家组会议。”JAMA。54 Ibid.   同上。55 Centers for Disease Control and Prevention, National Center for Health Statistics. 2025. “National Vital Statistics System (NVSS): Underlying Cause of Death, 2018–2024.” CDC WONDER Online Database. See also Arias, Elizabeth et al. 2025. "United States Life Tables, 2023." National Vital Statistics Reports.美国疾病控制与预防中心，国家卫生统计中心。2025。“国家生命统计系统（NVSS）：2018-2024 年根本死因”。CDC WONDER 在线数据库。另见 Arias, Elizabeth 等人。2025。“2023 年美国生命表”。国家生命统计报告。56 Ibid. See also United Nations Department of Economic and Social Affairs, Population Division. 2024. "World Population Prospects 2024."同上。另见联合国经济和社会事务部人口司，2024年，《2024年世界人口展望》。57 World Bank. 2024. “World Development Indicators: GDP (current US$).”世界银行。2024年。“世界发展指标：国内生产总值（现价美元）”。58 Biotech market size broadly encompasses bio-related applications including pharmaceutical, agricultural and industrial applications. BioSpace. 2025. “Biotechnology Market Size Expected to Surpass USD 5.71 Trillion by 2034: Biologics, Regenerative Therapies, Chromatography and Tissue Engineering in Focus.” See also Grand View Research. 2024. “Biotechnology Market Size, Share & Trends Analysis Report.”生物技术市场规模涵盖生物相关应用，包括制药、农业和工业应用。BioSpace，2025 年。“预计到 2034 年，生物技术市场规模将超过 5.71 万亿美元：生物制剂、再生疗法、色谱技术和组织工程是重点关注领域。”另见 Grand View Research，2024 年。“生物技术市场规模、份额和趋势分析报告。”59 Note: ICER is an independent non-profit that conducts cost-effectiveness analyses for healthcare interventions. Institute for Clinical and Economic Review (ICER). 2023. “ICER Value Assessment Framework.” See also Neumann, P.J. et al. 2016. “Cost-Effectiveness in Health and Medicine: Second Panel on Cost-Effectiveness in Health and Medicine.” JAMA.注：ICER 是一个独立的非营利组织，致力于开展医疗干预措施的成本效益分析。临床与经济评价研究所 (ICER)。2023 年。“ICER 价值评估框架”。另见 Neumann, PJ 等人。2016 年。“卫生和医学中的成本效益：卫生和医学成本效益第二期专家组会议”。JAMA。60 Arias, Elizabeth et al. 2025. "United States Life Tables, 2023." National Vital Statistics Reports. See also Centers for Disease Control and Prevention, National Center for Health Statistics. 2025. "National Vital Statistics System (NVSS), Underlying Cause of Death, 2018–2024." CDC WONDER Online Database. See also United Nations Department of Economic and Social Affairs, Population Division. 2024. "World Population Prospects 2024." See also Jiang, R. et al. 2021. "US Population Norms for the EQ-5D-5L and Comparison of Norms from Face-to-Face and Online Samples." Quality of Life Research.Arias, Elizabeth 等. 2025. “2023 年美国生命表”。《国家生命统计报告》。另见美国疾病控制与预防中心，国家卫生统计中心。2025. “国家生命统计系统 (NVSS)，根本死因，2018-2024”。CDC WONDER 在线数据库。另见联合国经济和社会事务部，人口司。2024. “2024 年世界人口展望”。另见 Jiang, R. 等. 2021. “EQ-5D-5L 的美国人口常模及面对面样本和在线样本常模的比较”。《生活质量研究》。61 At $100,000 per QALY, a 5% aging slowdown generates ~$10 trillion, a 10% slowdown ~$20 trillion, and a 15% slowdown ~$30 trillion in total incremental value across the US population.按每质量调整生命年 (QALY) 10 万美元计算，人口老龄化速度减缓 5% 将产生 10 万亿美元，减缓 10% 将产生 20 万亿美元，减缓 15% 将产生 30 万亿美元。62 Arias, Elizabeth et al. 2025. "United States Life Tables, 2023." National Vital Statistics Reports. See also Centers for Disease Control and Prevention, National Center for Health Statistics. 2025. "National Vital Statistics System (NVSS), Underlying Cause of Death, 2018–2024." CDC WONDER Online Database. See also United Nations Department of Economic and Social Affairs, Population Division. 2024. "World Population Prospects 2024." See also Jiang, R. et al. 2021. "US Population Norms for the EQ-5D-5L and Comparison of Norms from Face-to-Face and Online Samples." Quality of Life Research.Arias, Elizabeth 等. 2025. “2023 年美国生命表”。《国家生命统计报告》。另见美国疾病控制与预防中心，国家卫生统计中心。2025. “国家生命统计系统 (NVSS)，根本死因，2018-2024”。CDC WONDER 在线数据库。另见联合国经济和社会事务部，人口司。2024. “2024 年世界人口展望”。另见 Jiang, R. 等. 2021. “EQ-5D-5L 的美国人口常模及面对面样本和在线样本常模的比较”。《生活质量研究》。