ArticlePDF Available


At the turn of the 20th century, life expectancy at birth in most of today’s developed nations ranged between 45 and 50 years, with women routinely outliving men. About 22% of all individuals born in 1900 in the United States died before reaching the age of 10 years, mostly from infectious diseases.¹ Among those who survived into older ages in 1900, the common diseases of aging known today were present but less common.
From Lifespan to Healthspan
At the turn of the 20th century, life expectancy at birth
in most of today’s developed nations ranged between
45 and 50 years, with women routinely outliving men.
About 22% of all individuals born in 1900 in the United
States died before reaching the age of 10 years, mostly
from infectious diseases.
Among those who survived
into older ages in 1900, the common diseases of aging
known today were present but less common.
When public health emerged in the late 19th cen-
tury, including developments such as sanitation and
clean water,early mortality swiftly declined. A rapid shift
in the distribution of death from younger to older people
occurred during the first half of the 20th century, and
since then declining death rates at middle and older
ages have led to survival into increasingly older ages.
As a result, about 96% of infants born in developed na-
tions today will live to age 50 years or older, more than
84% will survive to age 65 years or older, and 75% to
77% of all deaths will predictably occur between age 65
and 95 years.
With declining early-age mortality and a shift in
the age distribution of death, the population of the
United States, and much of humanity in general,
achieved exactly what was desired: the first longevity
revolution. The 30-year increase in life expectancy at
birth in the past 100 years is one of humanity’s great-
est achievements.
Lifespan Limits and Decelerating Improvements
in Life Expectancy
Over the past century, the relatively easy gains in life ex-
pectancy have been achieved by reducing mortality of
younger people; more recently, scientists have focused
on how much higher life expectancy can increase and
what the maximum lifespan is for humans. The former
is a population-based metric that involves national vital
statistics for groups of people; the latter is the world rec-
ord for longevity held by 1 person.
Regarding maximum lifespan, only a small propor-
tion of all humans are capable of living to 115 years of age,
with a small number of statistical outliers capable of ap-
proaching the world record of 122 years.
Some ex-
perts suggest that if death rates plateau at older ages,
lifespans may continue to increase. This latter view has
been challenged because an unrealistically high num-
ber of people (estimated at 262 200) would have to
survive to age 105 years for just 1 person to exceed the
world record for longevity by 1 yearto 123 years.
As such,
the probability of any substantial increase in maximum
lifespan in this century is remote.
Regarding life expectancy, one view developed in
1990 suggested that the increase in life expectancy would
soon decelerate because the easy gains had already been
Any substantive future increases require im-
provements in mortality at older ages, although compo-
nents of the human body (eg, brain, heart, knees) are not
designed for long-term use. Others suggested that
historical trends in the increase in life expectancy will
continue indefinitely into the future due to yet-to-be-
developed medical advances and improved lifestyles.
Not one of the anticipated high-life-expectancy sce-
narios is remotely plausible today. In fact, a new trend
in the opposite direction has emerged in much of the de-
veloped world, indicating that death rates for many ma-
jor causes of death have either leveled off,experienced
declining improvement, or increased since 2008.
Biological Aging and Diminishing Returns
on Life Expectancy
Reductions in childhood diseases can occur only once
for a population; once such gains are achieved, the only
outlets for further gains in life expectancy must come
from extending the lives of older people. Given that
multiple fatal conditions accrue in older people because
of biological aging (eg, a fundamental and inevitable
risk that occurs independent of conventional behav-
ioral risk factors for diseases), once survival past age
65 years becomes common in a country, life expec-
tancy gains will decelerate, even with medical advances
and improved lifestyles. Because the
point of diminishing returns on life
expectancy (approximately 85 years for
men and women combined) and the
longevity limit (which has never been
exceeded) for the species has been
approached in many parts of the world,
there is good reason to conclude that the goal of life
extension has largely been achieved.
There is a dilemma. Modern medicine continues its
relentless pursuit of life extension without considering
either the consequences of success or the best way to
pursue it. The current focus of most of modern medi-
cine is on chronic fatal age-related diseases, in much the
same way infectious diseases were confronted more
than a century ago (ie, one at a time as if independent
of each other). Even though there havebeen some suc-
cesses, further life extension in an aging world will ex-
pose the saved population to an elevated risk for all other
aging-related diseases.
The principal outcome and most
important metric of success should be
the extension of healthspan.
S. Jay Olshansky,
Division of
Epidemiology and
University of Illinois
at Chicago School of
Public Health,
Author: S. Jay
Olshansky, PhD,
Division of
Epidemiology and
University of Illinois
at Chicago School of
Public Health, 1603
W Taylor St, Room
885, Chicago, IL
60612 (sjayo@uic
Opinion (Reprinted) JAMA Published online September 17,2018 E1
© 2018 American Medical Association. All rights reserved.
Downloaded From: by MAURIZIO BASSI on 09/24/2018
The longer people live, the more important aging biology be-
comes as a primary risk factor in determining both length and qual-
ity of life. In long-lived populations, a substantialpar t of life,and cer-
tainly most deaths, now occur in a period in the lifespan when the
risk for frailty and disability increases exponentially.
In this period,
which could be called the red zone, it becomes increasingly more dif-
ficult to intervene using conventional disease-oriented ap-
proaches; the further into this period that humans venture, the more
resistant diseases become (Figure).
Because the biological processes of aging force human bodies
to become ever more susceptible to fatal and disabling conditions,
unwanted health conditions emerge in the red zone not so much be-
cause of how life has been lived (although harmful lifestyles can ac-
celerate their emergence and progression) but because of how long
life has already been lived. Time becomes the greatest challenge.
With death inevitable, the modern attempt to counteract
aging-related diseases reveals a phenomenon known as competing
risks. When the risk of death from a disease decreases, the risk
of death from other diseases increases or becomes more ap-
parent. With advancing age, the period between the emergence
of competing diseases shortens. The hazard in old age is not
so much that one disease displaces another but that the new dis-
eases are often much more debilitating. For example, finding a cure
for cancer may cause an unintended increase in the prevalence of
Alzheimer disease.
The inescapable conclusion from these observations is that life
extension should no longer be the primary goal of medicine when
applied to people older than 65 years of age. The principal out-
come and most important metric of success should be the exten-
sion of healthspan.
The First Health Revolution
The conventional approaches used to counteract the diseases of
older age have been to improve behavioral risk factors, find ways
to detect them earlier, and use medical technology to extend sur-
vival for those who already have diseases. The more important goal
of public health, medicine, biotechnology, and the health sciences
should now shift toward delaying and compressing the period of the
lifespan when frailty and disability increase substantially. Referred
to as the first health revolution,
this new approach for public health
(which is to target aging) is seen as a highly effective method of pri-
mary prevention.
A consortium of scientists as well as public health experts
and organizations has formed with the purpose of developing this
new approach to extend healthspan, address the diseases of ag-
ing, and help to ameliorate the economic challenges of an antici-
pated rising prevalence of late-onset diseases. This effort is called
the Longevity Dividend Initiative
or geroscience.
Clinical trials de-
signed to target aging have been approved by the US Foodand Drug
Administration, with the first trial set to begin in 2019.Large invest-
ments in aging biology have already begun through Google Calico
and Human Longevity Inc. The National Institute on Aging has es-
tablished the Interventions TestingProgram to rigorously and quickly
test prospective aging interventions for free. The National Insti-
tutes of Health has reduced the barriers between its disease-
oriented research silos, and the American Federation for Aging Re-
search is spearheading a global effort to secure funds to launch the
Longevity Dividend Initiative in 2019.
The time has come to recognize the achievement of life extension.
Efforts should be focused on achieving the goals of extending and
improving the healthspan.
Published Online: September 17,2018.
Conflict of Interest Disclosures: The author has
completed and submitted the ICMJE Form for
Disclosure of Potential Conflicts of Interest. Dr
Olshansky reported being cofounder and chief
scientist at Lapetus Solutions Inc. Elements of the
Longevity Dividend Initiative were funded by the
MacArthur Foundation Research Network on an
Aging Society and The Glenn Award from the Glenn
Foundation for Medical Research. No other
disclosures were reported.
1. Bell F, Miller ML. Life tables for the United States
Social Security Area 1900-2100. Actuarial Study
No. 120.
/LifeTables_Tbl_6_1900.html. Accessed
August 30, 2018.
2. Human Mortality Database. https://www Accessed July 22, 2018.
3. Dong X, Milholland B, Vijg J. Evidence for a limit
to human lifespan. Nature. 2016;538(7624):257-259.
4. Olshansky SJ, Carnes BA. Mortality plateaus
and unlimited lifespans: let’s get real. Science.
/1459/tab-e-letters. Accessed August 30, 2018.
5. Olshansky SJ, Carnes BA, Cassel C. In search of
Methuselah: estimating the upper limits to human
longevity.Science. 1990;250(4981):634-640.
6. Fried LP, Tangen CM, Walston J, et al;
Cardiovascular Health Study Collaborative Research
Group. Frailty in older adults: evidence for a
phenotype. J Gerontol A Biol Sci Med Sci. 2001;56
(3):M146-M156. doi:10.1093/gerona/56.3.M146
7. Olshansky SJ, Carnes BA. Primary prevention
with a capital P. Perspect Biol Med. 2017;60(4):478-
496. doi:10.1353/pbm.2017.0037
8. Olshansky SJ, Martin G, Kirkland J, eds. Aging:
The Longevity Dividend. Cold Spring Harbor,NY:
Cold Spring Harbor Laboratory Press; 2015.
9. Sierra F, Kohanski R, eds. Advances in Geroscience.
New York, NY: Springer; 2016.
10. American Federation for Aging Research.
/mission-statement/. Accessed August 30, 2018.
Figure. Age Distribution of Life TableDeaths for Women
in the United States, per 100 000 People, 1900 and 2016
No. of Deaths per 100
Age, y
1111 611 16 10610121 26 31 36 41 46 51 56 61 66 71 76 81 86 91 96
The red zone represents a period in life when the risk of frailty and disability
begins to increase rapidly.The goal of aging science is to delay and compress
the red zone, which may extend healthy life. Sources: 1900 data from Bell and
; 2016 data from Human Mortality Database.
Opinion Viewpoint
E2 JAMA Published online September 17, 2018 (Reprinted)
© 2018 American Medical Association. All rights reserved.
Downloaded From: by MAURIZIO BASSI on 09/24/2018
... Current estimates indicate that delaying the onset of these chronic diseases by one year would save $38 trillion in the US alone (Scott et al., 2021). Therefore, major research efforts are dedicated to understanding how to increase the time spent in good health (i.e., healthspan) and to postpone and compress the time spent suffering from age-related pathologies and chronic diseases (i.e., sickspan) (Kaeberlein, 2017;Kennedy et al., 2014;Olshansky, 2018;Partridge et al., 2018). ...
... On the other hand, there are several interventions that increase healthspan without increasing lifespan per SE identified in mice (Fischer et al., 2016;Garcia-Valles et al., 2013) and Rhesus monkeys (Mattison et al., 2012). Thus, studying longevity is an important first step of identifying molecular mechanisms promoting healthy aging, but our study and others (Fischer et iScience Article crucially important for geroscience to start investigating interventions that improve healthspan directly in future studies (Olshansky, 2018). Initial steps in defining healthspan (Kaeberlein, 2017;Kennedy et al., 2014) and also tools and experimental setups, including this study, are being developed to reliably quantify healthspan (Bellantuono et al., 2020;Collins et al., 2008;Haefke and Ewald, 2020;Teuscher et al., 2019;Teuscher and Ewald, 2018). ...
Full-text available
Human centenarians and longevity mutants of model organisms show lower incidence rates of late-life morbidities than the average population. However, whether longevity is caused by a compression of the portion of life spent in a state of morbidity, i.e., “sickspan,” is highly debated even in isogenic C. elegans. Here, we developed a microfluidic device that employs acoustophoretic force fields to quantify the maximum muscle strength and dynamic power in aging C. elegans. Together with different biomarkers for healthspan, we found a stochastic onset of morbidity, starting with a decline in dynamic muscle power and structural integrity, culminating in frailty. Surprisingly, we did not observe a compression of sickspan in longevity mutants but instead observed a temporal scaling of healthspan. Given the conservation of these longevity interventions, this raises the question of whether the healthspan of mammalian longevity interventions is also temporally scaled.
... Advancing age is a predominant risk factor for developing frailty as well as a variety of diseases and degeneration, such as Alzheimer's disease, cardiovascular disease, stroke, and cancer (López-Otín et al., 2013). Although life expectancy has nearly doubled over the past 150 years, increasing from 40 years in 1850 to an average life expectancy of ~80 years in 2019 for many countries, the age of onset of most health problems has not been significantly delayed in a commensurate manner (Kingston et al., 2018;Olshansky, 2018). This means that most people live to old age but spend greater time at older ages suffering from various age-associated diseases, frailty, disability, and functional loss (Crimmins, 2015). ...
Full-text available
Life expectancy has increased substantially over the last 150 years. Yet this means that now most people also spend a greater length of time suffering from various age-associated diseases. As such, delaying age-related functional decline and extending healthspan, the period of active older years free from disease and disability, is an overarching objective of current aging research. Geroprotectors, compounds that target pathways that causally influence aging, are increasingly recognized as a means to extend healthspan in the aging population. Meanwhile, FOXO3 has emerged as a geroprotective gene intricately involved in aging and healthspan. FOXO3 genetic variants are linked to human longevity, reduced disease risks, and even self-reported health. Therefore, identification of FOXO3-activating compounds represents one of the most direct candidate approaches to extending healthspan in aging humans. In this work, we review compounds that activate FOXO3, or influence healthspan or lifespan in a FOXO3-dependent manner. These compounds can be classified as pharmaceuticals, including PI3K/AKT inhibitors and AMPK activators, antidepressants and antipsychotics, muscle relaxants, and HDAC inhibitors, or as nutraceuticals, including primary metabolites involved in cell growth and sustenance, and secondary metabolites including extracts, polyphenols, terpenoids, and other purified natural compounds. The compounds documented here provide a basis and resource for further research and development, with the ultimate goal of promoting healthy longevity in humans.
... At the same time, it has become painfully evident that not all of the gained extra years are healthy: estimates have shown that the proportion of life characterised by good health has remained rather constant between 1990 and 2019 (GBD 2019Demographic Collaborators, 2020, implying that most of the life years gained is lived largely in poor health (Scott et al., 2021). As pointed by Olshansky (2018), this leads to a situation where a significant portion of lifespan is lived during a window of exponentially increasing risk of frailty and chronic disability, with the simultaneous manifestation of many chronic conditions as late life comorbidities (Cutler & Mattson, 2006;de Grey, 2007;Zhavoronkov et al., 2021). Therefore, there is an increasing understanding of the importance of so called "healthy ageing" 3 (Seals & Melov, 2014;Campisi et al., 2019) and an unprecedented advance in the research that focuses on the biology of ageing (Skulachev, 2012;Moskalev et al., 2013;Sinclair, 2019;Barzilai, 2020). 1 Posthumanism seeks to improve human nature by using technology to transcend the limitations of body and mind (Bostrom, 2003(Bostrom, , 2005(Bostrom, , 2009Hughes, 2007). 2 Such an approach presupposes that death could be interactively delayed by anticipating and fixing the damaging effects of ageing across the lifespan (de Grey, 2012). ...
Full-text available
There is a growing consensus that chronological age (CA) is not an accurate indicator of the ageing progress and that biological age (BA) instead is a better measure of an individual's risk of age-related outcomes and a more accurate predictor of mortality than actual CA. In this context BA measures the "true" age that is an integrated result of an individual's level of damage accumulation across all levels of biological organization, along with preserved resources. The BA is plastic and depends upon epigenetics. Brain state is an important factor contributing to health-and lifespan. Quantitative electroencephalography (qEEG) derived brain BA (BBA) is a suitable and promising measure of brain ageing. In the present study we aimed to show that BBA can be decelerated or even reversed in humans (N = 89) by using customised programs of nutraceutical compounds or lifestyle changes (Mean duration = 13 months). We observed that the BBA was younger than CA in both groups at the end of the intervention. Further, the BBA of participants in the nutraceuticals group was 2.83 years younger at the endpoint of the intervention compared with BBA score at the beginning of the intervention, while the participants' BBA of the lifestyle group scored only 0.02 years younger at the end of the intervention. These results were accompanied by improvement in mental health and other comorbidities in both groups. Pre-intervention BBA score, as well as sex of participants were considered as confounding factors and analyzed separately. Overall, the obtained results support the feasibility of the goal of this study and also provide the first robust evidence that halting and reversal of brain ageing is possible in humans within a reasonable (practical) timeframe of around one year.
The word senescence is derived from the Latin word “senex” (meaning old). In biology, senescence is a process by which a cell ages and permanently stops dividing. Senescence is a natural universal phenomenon affecting all living organisms (e.g., humans, animals, and plants). It is the process of growing old (aging). The underlying mechanisms of senescence and aging at the cellular level are not fully understood. Senescence is a multifactorial process that can be induced by several stimuli including cellular stress, DNA damage, telomere shortening, and oncogene activation. The most popular theory to explain aging is the free radical theory. Senescence plays a role in the development of several age-related chronic diseases in humans (e.g., ischemic heart disease, osteoporosis, and cancer). Lifespan is a biological characteristic of every species. The lifespan of living organisms ranges from few hours (with mayfly) to potential eternity (with jellyfish and hydra). The maximum theoretical lifespan in humans is around 120 years. The lifespan in humans is influenced by multiple factors including genetic, epigenetic, lifestyle, environmental, metabolic, and endocrine factors. There are several ways to potentially extend the lifespan of humans and eventually surpass the maximum theoretical lifespan of 120 years. The tools that can be proposed include lifestyle, reduction of several life-threatening diseases and disabilities, hormonal replacement, antioxidants, autophagy inducers, senolytic drugs, stem cell therapy, and gene therapy.
Zum einen prädisponiert die Organalterung einschließlich der aus ihr resultierenden Funktionseinbußen im höheren Lebenslater für das Auftreten von akuten und chronischen Erkrankungen. Zum anderen ist der Einfluss individueller Komorbiditäten auf die Funktionalität im Alter stärker als in jüngeren Jahren ausgeprägt. Dabei gilt es zu berücksichtigen, dass dieser je nach dem vorliegenden Erkrankungsspektrum und dem Schweregrad der einzelnen Erkankungen sehr unterschiedlich ausgesprägt ist. Komorbidität und Funktionalität durchdringen sich somit wechselseitig. Sie haben damit beide wenstlichen Einfluss auf die Entwicklung des individuellen biologischen Alters. Es gilt nun für die biologisch-medizinische Forschung herauszufinden, welche Ansätze es jenseits der Behandlung der individuellen Komorbiditäten zukünftig vermögen werden, den Verlauf der Funktionalität im Alter günstig zu beeinflussen. Bislang sind hier körperliches Training und eine optimierte Ernährung als Standards anzusehen. Ob neue medikamentöse Ansätze die an sie gestellten Erwartungen erfüllen können, müssen zukünftige Studien zeigen.
Full-text available
In understanding how health has changed over the past 100 years, sociology health presentation seeks to: Ascertain what is health? Examine a systems thinking approach framework for analysis. Determine 7 ways in which health has changed globally over the past century. Explore the outcomes.
Imagination and idealism are particularly important creative epistemic virtues for the medical sciences if we hope to improve the health of the world's ageing population. To date, imagination and idealism within the medical sciences have been dominated by a paradigm of disease control, a paradigm which has realised significant, but also limited, success. Disease control proved particularly successful in mitigating the early-life mortality risks from infectious diseases, but it has proved less successful when applied to the chronic diseases of late life (like cancer). The time is ripe for the emergence and prominence of a supplementary medical research paradigm, the paradigm of 'healthy ageing' which prioritises the goal of rate (of ageing) control rather than disease control. This is the difference between extending the human healthspan versus extending survival by managing (or trying to eliminate) the multi-morbidities, frailty and disability currently prevalent in late life. The idealism of the disease control paradigm is myopic because it ignores the health constraints imposed by the inborn ageing process itself, a biological reality which is already inflicting significant economic and disease burdens on the world's ageing populations. Unless the medical sciences retard the rate of biological ageing, these problems will continue to be amplified as larger numbers of persons survive into late life.
Objectives This study aims to investigate sex-based differences in the diabetes status and cognition relationship using a representative sample of older Americans. Methods Using a sample of 19,190 females and 15,580 males from the Health and Retirement Study, we conduct mixed-effects linear regression analyses to examine sex differences in the association between diabetes and cognition over a 20-year follow-up period among older adults in the United States. Main Findings Females experience slightly steeper declines in cognition that are further exacerbated by diabetes. At age 65, females without diabetes have significantly higher cognition than males; this gap is eliminated by age 85. Among diabetics, there is no initial sex disparity, but females’ cognition becomes significantly lower than males’ over the following 20 years. Principal Conclusions Relative to males, females are particularly susceptible to diabetes-related declines in cognition with increasing age.
This chapter describes the current state of urban population and the impact of ageing, and examines the potential role of social innovation could improve the physical, mental, and social wellbeing of urban residents and promote healthspan. The idea of co‐mentoring allows both the younger and older persons to be each other's mentors and learn from one another. This is in line with the life course approach to healthy longevity. The chapter illustrates the solutions of social practices that facilitate ageing in place and intergenerational coexistence and collaboration, and also examines how integrative co‐located programmes can contribute to inclusive, sustainable urban communities. Responsive and adaptive solutions at the systems‐level create a liveable city; they could improve the wellbeing of the individual for his or her entire life course. Brainstorming between the young and the seniors encourage participants to share entrepreneurial knowledge and ideas, understand different perspectives, and explore new business opportunities.
Full-text available
Healthspan is the period of our life without major debilitating diseases. In the modern world where unhealthy lifestyle choices and chronic diseases taper the healthspan, which lead to an enormous economic burden, finding ways to promote healthspan becomes a pressing goal of the scientific community. Exercise, one of humanity’s most ancient and effective lifestyle interventions, appears to be at the center of the solution since it can both treat and prevent the occurrence of many chronic diseases. Here, we will review the current evidence and opinions about regular exercise promoting healthspan through enhancing the functionality of our organ systems and preventing diseases.
Full-text available
The survival of large segments of human populations to advanced ages is a crowning achievement of improvements in public health and medicine, but in the 21st century, our continued desire to extend life brings forth a unique dilemma. The risk of death from chronic fatal diseases has declined, but even if it continues to do so in the future, the resulting longevity benefits are likely to diminish. It is even possible that unhealthy life expectancy could rise in the future as major fatal diseases wane. The reason for this is that the longer we live, the greater the influence of biological aging on the expression of fatal and disabling diseases. Research in gerontology has already demonstrated that aging is inherently modifiable, and that a therapeutic intervention that slows aging in people is a plausible target for science and public health. Given the speed with which population aging is progressing and chronic fatal and disabling conditions are challenging health-care costs across the globe, the case is now being made that delayed aging could be one of the most efficient and promising ways to combat disease, extend healthy life, compress morbidity, and reduce health-care costs.
Full-text available
Estimates of the upper limits to human longevity have important policy implications that directly affect forecasts of life expectancy, active life expectancy, population aging, and social and medical programs tied to the size and health status of the elderly population. In the past, investigators have based speculations about the upper limits of human longevity on observations of past trends in mortality. Here the estimate of the upper bound is based on hypothesized reductions in current mortality rates necessary to achieve a life expectancy at birth from 80 to 120 years and an expectation of life at age 50 from 30 to 70 years. With the use of conditional probabilities of death from complete life tables for the United States, reductions in mortality required to achieve extreme longevity (that is, 80 to 120 years) were compared with those resulting from hypothetical cures for all cardiovascular diseases, ischemic heart disease, diabetes, and cancer. Results indicate that in order for life expectancy at birth to increase from present levels to what has been referred to as the average biological limit to life (age 85), mortality rates from all causes of death would need to decline at all ages by 55%, and at ages 50 and over by 60%. Given that hypothetical cures for major degenerative diseases would reduce overall mortality by 75%, it seems highly unlikely that life expectancy at birth will exceed the age of 85.
Full-text available
Frailty is considered highly prevalent in old age and to confer high risk for falls, disability, hospitalization, and mortality. Frailty has been considered synonymous with disability, comorbidity, and other characteristics, but it is recognized that it may have a biologic basis and be a distinct clinical syndrome. A standardized definition has not yet been established. To develop and operationalize a phenotype of frailty in older adults and assess concurrent and predictive validity, the study used data from the Cardiovascular Health Study. Participants were 5,317 men and women 65 years and older (4,735 from an original cohort recruited in 1989-90 and 582 from an African American cohort recruited in 1992-93). Both cohorts received almost identical baseline evaluations and 7 and 4 years of follow-up, respectively, with annual examinations and surveillance for outcomes including incident disease, hospitalization, falls, disability, and mortality. Frailty was defined as a clinical syndrome in which three or more of the following criteria were present: unintentional weight loss (10 lbs in past year), self-reported exhaustion, weakness (grip strength), slow walking speed, and low physical activity. The overall prevalence of frailty in this community-dwelling population was 6.9%; it increased with age and was greater in women than men. Four-year incidence was 7.2%. Frailty was associated with being African American, having lower education and income, poorer health, and having higher rates of comorbid chronic diseases and disability. There was overlap, but not concordance, in the cooccurrence of frailty, comorbidity, and disability. This frailty phenotype was independently predictive (over 3 years) of incident falls, worsening mobility or ADL disability, hospitalization, and death, with hazard ratios ranging from 1.82 to 4.46, unadjusted, and 1.29-2.24, adjusted for a number of health, disease, and social characteristics predictive of 5-year mortality. Intermediate frailty status, as indicated by the presence of one or two criteria, showed intermediate risk of these outcomes as well as increased risk of becoming frail over 3-4 years of follow-up (odds ratios for incident frailty = 4.51 unadjusted and 2.63 adjusted for covariates, compared to those with no frailty criteria at baseline). This study provides a potential standardized definition for frailty in community-dwelling older adults and offers concurrent and predictive validity for the definition. It also finds that there is an intermediate stage identifying those at high risk of frailty. Finally, it provides evidence that frailty is not synonymous with either comorbidity or disability, but comorbidity is an etiologic risk factor for, and disability is an outcome of, frailty. This provides a potential basis for clinical assessment for those who are frail or at risk, and for future research to develop interventions for frailty based on a standardized ascertainment of frailty.
Driven by technological progress, human life expectancy has increased greatly since the nineteenth century. Demographic evidence has revealed an ongoing reduction in old-age mortality and a rise of the maximum age at death, which may gradually extend human longevity. Together with observations that lifespan in various animal species is flexible and can be increased by genetic or pharmaceutical intervention, these results have led to suggestions that longevity may not be subject to strict, species-specific genetic constraints. Here, by analysing global demographic data, we show that improvements in survival with age tend to decline after age 100, and that the age at death of the world's oldest person has not increased since the 1990s. Our results strongly suggest that the maximum lifespan of humans is fixed and subject to natural constraints.
Mortality plateaus and unlimited lifespans: let's get real
  • S J Olshansky
  • B A Carnes
Olshansky SJ, Carnes BA. Mortality plateaus and unlimited lifespans: let's get real. Science. /1459/tab-e-letters. Accessed August 30, 2018.
Life tables for the United States Social Security Area 1900-2100. Actuarial Study No
  • F Bell
  • M L Miller
Bell F, Miller ML. Life tables for the United States Social Security Area 1900-2100. Actuarial Study No. 120. /LifeTables_Tbl_6_1900.html. Accessed August 30, 2018. 2. Human Mortality Database. https://www Accessed July 22, 2018.
Aging: The Longevity Dividend
  • S J Olshansky
  • G Martin
  • J Kirkland
Olshansky SJ, Martin G, Kirkland J, eds. Aging: The Longevity Dividend. Cold Spring Harbor, NY: Cold Spring Harbor Laboratory Press; 2015.