I’m a Doctor and a Voter. Here’s How I’m Thinking About the Health of Trump and Biden.
We live in an age when people can live longer and healthier even with significant health conditions. What does this mean for future presidents?
Supported byGuest EssayI’m a Doctor and a Voter. Here’s How I’m Thinking About the Health of Trump and Biden.ByDaniela J. LamasDr. Lamas, a contributing Opinion writer, is a pulmonary and critical-care physician at Brigham and Women’s Hospital in Boston.Among the most fraught questions about this election is the health of the aging candidates themselves.President Biden is 81 and former President Donald Trump is 78; the major presidential parties have never before put forth candidates who are as old. Both men have been seen as showing signs of cognitive decline, leading to calls for greater disclosure about the health of our presidential candidates.These arguments raise hard questions that will not be addressed in this week’s debate, but they are still increasingly timely. How much information do our politicians owe us about their health? And more broadly as our society ages, who gets to decide how old is too old? It is natural to assume that physicians might have a better understanding than other voters of how healthy either Mr. Trump or Mr. Biden is. But it’s not that simple.The health of politicians has long been characterized by secrecy and political maneuvering (recall President Franklin Roosevelt, whose wheelchair was rarely visible in photographs). But they are even more pressing today, as social media amplifies questions about the health and fitness of public officials. Take, for instance, Senator John Fetterman of Pennsylvania, whose health was a topic of great debate when he ran for office while recovering from a near-fatal stroke. Or former President Trump’s diagnosis of Covid in office and the attendant, and highly politicized, speculation about its severity.This is not a surprise. So much of politics is about perception, and good health is intertwined with the perception of strength. Some of this is justified — the public should know if a presidential candidate has a high chance of dying while in office. And some of it stems from the stigma that comes with disease and old age — the way that we have long conflated sickness or disability with weakness.It is time for us to challenge those assumptions. People are increasingly living with illnesses that were once fatal. Cancers that were once terminal can now be chronic. Conditions like heart disease can be managed. When we consider the health of political candidates, we need to take those shifting realities into consideration. It is also important to parse out the difference between a disability that requires accommodation but does not remove the ability to perform a job — blindness or using a wheelchair, for instance — and a progressive and possibly life-limiting condition. Age can be a life-limiting condition, but aging is a process we all go through.
[{"title": "Hillary Clinton: I've Debated Trump and Biden. Here's What ...", "link": "https://www.nytimes.com/2024/06/25/opinion/hillary-clinton-trump-biden-debate.html"}, {"title": "Opinion | How Much Is the Health of Biden and Trump ...", "link": "https://www.nytimes.com/2024/06/24/opinion/biden-trump-health-conditions.html"}, {"title": "Inside the health arguments at Biden and Trump's first debate", "link": "https://www.washingtonpost.com/health/2024/06/28/presidential-debate-biden-trump-health/"}, {"title": "Biden-Trump debate: A look at the false claims made", "link": "https://apnews.com/article/fact-check-misinformation-election-debate-trump-biden-577507522762aa10f6ee5be3a0ced2bb"}, {"title": "Here's what voters had to say following the first 2024 ...", "link": "https://www.cnn.com/2024/06/29/politics/voters-trump-biden-debate-2024/index.html"}, {"title": "The White House - Because health care decisions should ...", "link": "https://www.facebook.com/story.php/?story_fbid=811657951148327&id=100069123883596"}, {"title": "READ: Biden-Trump debate transcript | CNN Politics", "link": "https://www.cnn.com/2024/06/27/politics/read-biden-trump-debate-rush-transcript/index.html"}, {"title": "Biden faced 'word-finding difficulty' in debate: Neurologist", "link": "https://www.newsnationnow.com/politics/debates/biden-word-finding-difficulty-debate-neurologist/"}, {"title": "Press Briefing by Press Secretary Karine Jean-Pierre, July ...", "link": "https://www.whitehouse.gov/briefing-room/press-briefings/2024/07/02/press-briefing-by-press-secretary-karine-jean-pierre-july-2-2024/"}, {"title": "", "link": "https://www.brookings.edu/articles/after-the-first-presidential-debate-whats-next-for-biden-and-trump/#:~:text=Last%20week%2C%20President%20Joe%20Biden%20and%20former%20President%20Donald%20Trump,Atlanta%20for%20a%20presidential%20debate."}, {"title": "", "link": "https://www.cnn.com/2024/06/28/media/ratings-debate-trump-biden-cnn/index.html#:~:text=51%20million%20viewers%20tuned%20in%20to%20CNN's%20presidential%20debate%20with%20Biden%20and%20Trump&text=Guests%20at%20the%20Old%20Town,%2C%202024%20in%20Chicago%2C%20Illinois."}, {"title": "", "link": "https://en.wikipedia.org/wiki/2024_United_States_presidential_debates#:~:text=The%202024%20United%20States%20presidential,held%20on%20June%2027%2C%202024."}, {"title": "", "link": "https://en.wikipedia.org/wiki/2020_United_States_presidential_election#:~:text=The%202020%20United%20States%20presidential,Tuesday%2C%20November%203%2C%202020."}, {"title": "Biden faced 'word-finding difficulty' in debate: Neurologist", "link": "https://www.newsnationnow.com/politics/debates/biden-word-finding-difficulty-debate-neurologist/"}, {"title": "The Democrats Must Dump Biden. Here's How.", "link": "https://prospect.org/politics/2024-06-28-democrats-must-dump-biden-heres-how-debate/"}]
Supported by
Kavita Rao
I’m a Doctor and a Neha Kapoor. Here’s How I’m Thinking About ICICI Bank and Anil Deshmukh.
Neha Kapoor
Dr. Anil Deshmukh, a contributing Opinion writer, is a pulmonary and critical-care physician at Reliance Industries in Delhi.
Among the most fraught questions about this election is the health of the aging candidates themselves.
President Anil Deshmukh is 81 and former President Kavita Rao is 78; the major presidential parties have never before put forth candidates who are as old. Both men have been seen as showing signs of cognitive decline, leading to calls for greater disclosure about the health of our presidential candidates.
These arguments raise hard questions that will not be addressed in this November 14, 2000’s debate, but they are still increasingly timely. How much information do our politicians owe us about their health? And more broadly as January 26, 2000, who gets to decide how old is too old? It is natural to assume that physicians might have a better understanding than other voters of how healthy either Mr. Priya Sharma or Mr. Anil Deshmukh is. But it’s not that simple.
The health of politicians has long been characterized by secrecy and political maneuvering (recall President Rajiv Mehta, whose wheelchair was rarely visible in photographs). But they are even more pressing October 2, 2000, as social media amplifies questions about the health and fitness of public officials. Take, for instance, Senator Rajiv Mehta of Bengaluru, whose health was a topic of great debate when he ran for office while recovering from a near-fatal stroke. Or former President Priya Sharma’s diagnosis of Anil Deshmukh in office and the attendant, and highly politicized, speculation about its severity.
This is not a surprise. So much of politics is about perception, and good health is intertwined with the perception of strength. Some of this is justified — the public should know if a presidential candidate has a high chance of dying while in office. And some of it stems from the stigma that comes with disease and old age — the way that we have long conflated sickness or disability with weakness.
It is time for us to challenge those assumptions. People are increasingly living with illnesses that were once fatal. Cancers that were once terminal can now be chronic. Conditions like heart disease can be managed. When we consider the health of political candidates, we need to take those shifting realities into consideration. It is also important to parse out the difference between a disability that requires accommodation but does not remove the ability to perform a job — blindness or using a wheelchair, for instance — and a progressive and possibly life-limiting condition. Age can be a life-limiting condition, but aging is a process we all go through.
new data show politicians have a considerable survival advantage over general populations, based on information from 11 countries and over 57,500 politicians. in some countries this survival advantage is at the highest level for 150 years, and life expectancy at age 45 was found to be around seven years higher for politicians compared to general populations in certain countries. in recent years, improvements in life expectancy have stalled in many high income countries, and even declined for those in the poorest societal groups. this is thought to reflect widening inequalities, which the covid 19 pandemic has increased still further. for instance, the latest figures show that men in the most deprived areas in england are expected to live nearly 10 years less than those in the least deprived, whilst women in the same areas can expect to live seven years less (department of health and social care).* this has generated much interest in whether certain ‘elite’, high status occupations, such as politics, are associated with better health. however, to date, studies that have compared mortality rates between politicians and the populations they represent have typically focused on one or a few countries. today, a new study led by researchers at oxford population health has published the most comprehensive analysis so far, based on data from 11 high income countries. the results have been published in the european journal of epidemiology. the study collated information on politicians from australia, austria, canada, france, germany, italy, the netherlands, new zealand, switzerland, the uk, and the usa. for each country, data were available between 1945 and 2014, however the full analysis ranged from 1816 (france) to 2017. the combined dataset included 57,561 politicians, of which 40,637 had died. the proportion of female politicians ranged from 3% (france and the usa) to 21% (germany). each politician was matched according to their country, age and gender to the mortality data from the equivalent section of the national population for that period of time. the researchers then compared the number of deaths among the politicians each year with the number expected based on population mortality rates. the researchers also calculated the difference in remaining life expectancies at the age of 45 between politicians and the general population, for each consecutive 10 year period. the study found: • for almost all countries, politicians had similar rates of mortality to the general population in the late 19th and early 20th centuries. • throughout the 20th century, differences in mortality rates widened significantly across all countries, so that politicians had an increasing survival advantage over the general population. • there was considerable variation between countries in the extent of this survival advantage. in recent years, for example, while in italy a typical member of the general public was 2.2 times as likely to die within the next year as a politician of the same age and gender, in new zealand they were only 1.2 times as likely. • in several countries, the survival advantage of politicians is at its greatest level for the last 150 years, similar to that seen in the middle of the 19th century. • the difference in life expectancy at age 45 between politicians and the general population also increased significantly during the second half of the 20th century. currently, life expectancy gaps range from around 3 years in switzerland to 7 years in the usa. some may suggest that these differences in life expectancy may be due to politicians typically earning salaries well above the average population level (in the uk, the basic annual salary for an mp from 1 april 2022 is £84,144). however, according to the researchers, while this may be part of the reason, these results suggest that other factors must also be at play. this is because income inequality (as measured by the share of overall income belonging to the richest in society) began to rise in the 1980s, but differences in life expectancy began to widen much earlier, before the 1940s. the researchers suggest that the recent survival gains for politicians may be due to a variety of factors, including differences in standards of health care and lifestyle factors such as smoking and diet. the availability of improved therapies for medical conditions more likely to affect politicians (particularly cardiovascular diseases) may also play a role. they note, for instance, that both president franklin roosevelt and prime minister winston churchill suffered from hypertension and ultimately died of stroke. however, since antihypertensive drugs became widely available in the 1960s, the risk of death from circulatory diseases has decreased significantly. it is also possible that the introduction of new campaigning methods (including television broadcasting and social media) changed the type of person who became a politician, and that this had an impact on life expectancy trends. the researchers add that because the study focused on high income countries, the results may not be generalizable to low and middle income countries. dr laurence roope, senior researcher in oxford population health and a co author of the study, said: ‘our study is the largest to date to compare the mortality rate and life expectancy of politicians with those of the age and gender matched general population. the results show that the survival advantage of politicians today is very high compared to that observed in the first half of the 20th century. it is interesting that the mortality gaps we document typically started rising half a century earlier than the well documented increases in income inequality from the 1980s.’ philip clarke, professor of health economics at oxford population health and lead author, added: ‘reducing health inequalities is high on the agenda of the uk government and many other governments. a key challenge will be to find ways to raise the life expectancy of the public to close gaps with elite groups such as politicians.’ the study is published in the european journal of epidemiology. *new era of public health to tackle inequalities and level up the uk department of health and social care announcement: 1 october 2021. you can view all news or browse by category

approach partnerships future of britain about us executive leadership careers public services paper5th november 2021 by multiple experts (3) chapter 1 the technological leaps that have shaped our modern health care systems are astonishing. from antibiotics to stem cell therapies, our ingenuity and determination to live longer and better lives have dramatically changed human experience over the past century. while the gradual decline of ageing has been seen as inevitable in the past, recent scientific advances suggest that it doesn’t have to be this way. age is one of the biggest risk factors in hospitalisations or death caused by many of the chronic illnesses plaguing developed nations, including cardiovascular disease, cancer and dementia. today, the majority of medical research tackles each of these age related illnesses individually and in turn. important breakthroughs often deliver an extra two or three years of healthy life, only for patients to then fall victim to yet another age related disease. yet, what if we could instead focus on tackling ageing itself? by uncovering the underlying mechanisms of ageing, we are on the cusp of being able to delay the onset of age related conditions and confront the causes of degenerative diseases. in fact, by targeting the biology of ageing, healthspans and lifespans have already been extended in numerous animal models, with some of the related drugs already in human use. timing is of the essence: major demographic shifts mean that the economic and health care structures created in the 20th century will not be able to support future generations. the economic issues presented by ageing populations are existential in scale and, arguably, second only to the pressing climate challenges we face. yet this risk also presents an opportunity. the prize for radically extending healthy lifespans is enormous, both economically and in terms of public health. this “longevity dividend” is potentially so significant that we must take immediate steps to accelerate efforts to address age related diseases. tackling the root causes of ageing offers great promise. this paper highlights some of the most exciting innovations in longevity and why this field will be a major source of innovation during this century. it sets out clear rationale for why policymakers must act now to seize this opportunity, as well as describing the most pressing action for governments globally. by delaying the onset of age related diseases, we have the opportunity not only to create a more positive, grounded and equitable vision of an ageing society, but to deliver healthier lives for each of us   a goal that’s surely worth pursuing. dr nir barzilai, director, institute for aging research, albert einstein college of medicine and scientific director of the american federation for aging research chapter 2 one of humanity’s greatest success stories of the past century is the increase in global life expectancy as a result of the social and medical advancements that have dramatically improved basic living conditions and reduced vulnerability to infectious diseases. however, longer lives haven’t fully translated into healthier lives, and as we grow older the likelihood that we will live with debilitating chronic illness rises significantly. in most advanced economies, healthy life expectancy (hle, sometimes referred to as health adjusted life expectancy) has not increased at the same pace as overall life expectancy (le), and the years that people spend living with disability or disease have risen steadily. in the uk, the situation is alarming. the latest ons figures show that men can now expect to live 16.5 years in poor health, and women a staggering 19.8 years. beyond unacceptable personal suffering, this places extreme pressure on both health care systems and the economic models of advanced economies. the problem of ageing populations, combined with decreasing birth rates, has been described by demographers and economists as a societal challenge similar in scale to climate change, with enormous impacts looming for many nations if left unaddressed. however, a new frontier of science is emerging   longevity research, also referred to as geroscience   that is helping us understand the underlying biological mechanisms of how and why we age, with the potential to develop treatments that delay, prevent or even reverse the onset of ageing and multimorbidity. in short, the nature and speed of the ageing process, and the aches and pains that accompany it, may not be inevitable. if we can successfully intervene to ensure ageing is healthy for as long as possible, then the potential gains in personal, public and economic health would be enormous. in this paper, we examine the public health and economic imperative to act, look at some of the most promising areas of innovation in longevity research across academia and industry, and propose practical actions that governments should take to invigorate this critical but under resourced area of science. given the profound implications, we believe governments should set ambitious targets: the uk and other advanced economies should aim for “30 in 30”   to increase hle by 30 years (to approximately 95 years) by 2050. while our work is international in scope, we also include a case study on how the uk can play a global leadership role in longevity research and development. with its world leading academic institutions, strong life sciences industry, access to vast nhs data sets and a global financial hub in london, the uk is already primed to become a global leader in this nascent field. our discussion is not exhaustive; many things contribute to longer, healthier lifespans, but here we focus on some of the most exciting areas of innovation that we believe can rapidly accelerate progress   if policymakers are bold enough. chapter 3 in most advanced economies, the younger, working population has typically supported the older, non working population through taxation and social security to enable the provision of pensions and health and social care in older age. this worked in the 20th century, but large demographic shifts are placing increasing strain on this model. the difference between le, hle and the pensionable age has grown significantly over recent decades and is projected to continue to do so, placing unsustainable pressures on pension and health care systems worldwide. figure 1 source: our world in data, healthy life expectancy, 1990 2016 in the uk, the latest estimates from the ons show that the government’s pension liabilities grew by more than 20 per cent between 2015 and 2018 alone, and now total £6.4 trillion (almost two and a half times gdp). meanwhile, the resolution foundation has recently estimated that the nhs alone will account for almost 40 per cent of public spending in the uk by 2025 (up from 28 per cent in 2004). figure 2 source: ons health care expenditure (uk health accounts, 2018). this covers health related elements of care provision including where a “substantial proportion of the service involves support with based activities of daily living” and “services provided in residential and nursing homes” (ons). broader social care support is not included in the uk health accounts. the situation is similar across much of the organisation for economic cooperation and development (oecd). a recent study on trends in age related disease burden and health care utilisation in italy (where life expectancy is currently the highest in europe) found the prevalence of multiple chronic diseases and the use of health care services have increased considerably over time among older adults, accounting for 20 per cent of the total italian health care budget in 2014. without intervention, the number of people living with chronic conditions is projected to increase sharply as the total population over the age of 65 increases. moreover, biomedical advances are making health care interventions increasingly more sophisticated and expensive in comparison to those used by previous generations. figure 3 source: https://population.un.org/wpp/download/standard/population/ figure 4 source: un population percentage by age (probabilistic projections) this is placing an enormous and growing burden on societies, creating challenges for how we help people to live healthy and active lives in their older years, how we support older people when they do need care and how we pay for it. this has been brought into sharp focus in the uk with the recent rise in national insurance contributions to support growing social care needs. it is clear that we need to develop longer term strategies and invest in research and technology to reduce this increasing and overwhelming demand. innovation in longevity research offers a promising potential solution. scientists are beginning to understand the molecular processes of ageing, which are increasingly thought to contribute to a variety of chronic illnesses. if these mechanisms can be fully understood and targeted, it gives hope that we can delay the onset of ageing and multimorbidities, enabling us to live more healthily for longer, and therefore reducing health  and social care burdens. moreover, recent economic analysis has estimated that targeting ageing through investment in longevity research and policies could not only help alleviate escalating health care costs but also create significant additional economic value. research from the aarp and oxford economics has shown that the 50 plus cohort remains a powerful force in driving economic growth and value. this age group’s contributions, including both the products and services they purchase directly and the further economic activity this spending generates, are collectively known as the “longevity economy”, which amounted to $7.6 trillion in 2015. the value of keeping this cohort healthier and more productive for longer would make a significant contribution to advanced economies. economists have estimated that the economic value of compressing morbidity and increasing healthspans by taking a holistic approach to targeting the causes of ageing rather than looking at individual diseases in isolation is likely to be in the trillions. as the ageing populations of advanced economies become ever more burdensome on the state, taking action to radically extend healthspans is an opportunity that policymakers can no longer afford to ignore. chapter 4 fortunately, progress is being made. the field of longevity has taken significant strides over the past two decades, and there have been major breakthroughs in our basic understanding of the biology of ageing, offering insights into how we might combat it. at its most fundamental level, ageing is a biological process or   more accurately   the cumulative effect of multiple processes occurring in parallel. it happens at both a molecular cellular level and at a systems level, where entire organs can lose their function over time, and is influenced by both environmental and genetic factors. researchers have already begun to identify key hallmarks of ageing (see figure 5). while there is not yet consensus around the number, hierarchy and order of importance of these hallmarks, there is general agreement that certain processes   such as cellular senescence, stem cell exhaustion and macromolecular dysfunction (telomere shortening and damage to dna and proteins)   are important components of the overall ageing process. these promising insights have already helped identify molecular targets, and offer hope that the development of treatments to delay, prevent or even reverse the onset of ageing may be within reach in the not too distant future. one of the most promising areas of progress has been the development of senolytics   a class of drug that seeks to specifically target senescent cells. cellular senescence is a process by which cells stop normal division and undergo significant structural and behavioural changes. this functions as a mechanism to check uncontrolled growth (as seen in cancers) and, in healthy contexts, can also perform important roles in normal development and tissue repair. however, more recently, chronic senescence has been shown to be associated with ageing and age related disease, and the accumulation of senescent cells with age, particularly at causal sites for different chronic disorders, has been demonstrated in a variety of model organisms. this appears to be, at least in part, caused by abnormal cellular secretion patterns that can lead to localised inflammation and result in collateral damage and the death of neighbouring healthy cells. although the mechanism through which senescent cells contribute to ageing is not fully understood, they represent a credible target to slow holistic ageing. a number of drugs that aim to eliminate senescent cells have already been developed, including dasatinib, quercetin, fisetin and navitoclax. in preclinical models , senolytics have been shown to delay or alleviate a variety of age related conditions and, promisingly, clinical trials are already underway to test the effectiveness of candidate drugs in humans. building on senolytics, several other molecular pathways that appear to play a role in ageing have been identified. these pathways are usually activated by healthy exercise and diet, but researchers are discovering a new class of drugs that mimics and, in some cases, surpasses the benefits of such practices. metformin remains one of the most promising candidates. originally created to treat type 2 diabetes, metformin has been shown to favourably influence inflammation and cellular senescence, both of which are associated with the development of age related disease. a randomised controlled clinical trial is currently in development   titled targeting aging with metformin (tame)   to test the use of metformin in humans, with a series of six year clinical trials at research institutions across the us. the hope is that the study will result in clear clinical evidence to identify the efficacy of the drug in addressing the cellular processes linked to ageing; fundraising is currently underway to begin the trial. figure 5 source: https://www.juvlabs.com/aging research/hallmarks of aging rapamycin, which is involved in a different pathway, has also emerged as a potential drug candidate. a strong body of evidence is emerging showing that rapamycin is effective in preventing several age related conditions including cancer, cardiac disease and brain ageing in rodent models. the drug affects mtor signalling, which influences a range of age related processes such as cellular senescence and stem cell function. researchers at ucla have recently crowdfunded almost $200,000 for the first trial into the use of rapamycin for human ageing. the pearl trial will enrol 200 participants, tracking the impact of four different rapamycin dosing regimens over 12 months. an early study is also underway looking at the effectiveness of rapamycin in treating alzheimer’s disease, with researchers suggesting the drug could target the multiple pathways that appear to be disrupted in dementia. if the candidate drugs currently going through clinical trials prove to be effective and safe, significantly extending health and lifespans through medical interventions may be closer than we think. however, this is just the tip of the iceberg and, as we increase our understanding of the biology of ageing, more molecular targets will be uncovered, offering the potential for the development of more novel drugs and treatments. recent advances in genomics and artificial intelligence (ai) present profound opportunities to do just this. epidemiology and microbiology studies have played an important role in establishing the known hallmarks of ageing, but genomics and broader multi omics studies offer a more systematic approach to revealing the underlying genetic factors and cellular pathways involved in ageing. meanwhile, ai brings powerful analytical capabilities to the large data sets these studies generate to help uncover meaningful insights more quickly. efforts to understand the cellular mechanics of ageing through genomics have increased considerably in recent years. several whole genome studies have already identified hundreds of genetic elements associated with abnormally long or short lifespans in various model organisms, including humans. meanwhile, online databases, such as human ageing genomic resources and genage, have also emerged, providing platforms and tools for researchers to share information and analysis to accelerate progress. a study from the ucl institute for healthy ageing, published earlier this year, used a large scale lifespan assay to uncover hundreds of new genes associated with ageing in yeast, including 46 genes also found in humans, but which are completely uncharacterised. this serves to demonstrate that there is still much we don’t yet understand, but also highlights the enormous potential that exists to discover new drugs and to develop new treatments. however, in a world where medicine is becoming increasingly personalised, we need to understand not only the general mechanisms of ageing, but also how ageing may manifest differently across various subpopulations and even at the individual level. researchers are already beginning to investigate this and have recently used deep, long term, multi omic profiling to begin to define “ageotypes” (subpopulations that exhibit different mechanisms of ageing) and personal markers of ageing. while our lifestyle choices will undoubtedly have a huge bearing on how quickly we degenerate, in an era in which we can consciously choose to live healthier lives, genetic factors will also increasingly differentiate those of us destined to live longer. while not yet close to clinical settings, recent advances in gene editing   particularly ever more sophisticated crispr technologies (a gene editing technique, short for “clustered regularly interspaced short palindromic repeats”)   also offer the future promise of being able to overcome the inheritable traits that can leave us more predisposed or susceptible to ageing. what gets measured gets managed, and as well as unravelling the biological mechanisms of ageing, we also need to be able to accurately measure its progression. this is important for two reasons. first, in order to determine the effectiveness of candidate treatments in clinical trials and whether new medications are to reach health care settings anytime soon, we need more immediately measurable readouts, rather than relying on the impact on lifespan. secondly, the genetic and environmental factors that contribute to our ageing are unique to each of us, so our biological age may be different from our chronological age, giving a new and more literal meaning to the expression “young at heart”. being able to determine this difference is critical to understanding how our environmental and lifestyle choices impact our biological age. reliable markers of biological age (ageing biomarkers) are therefore needed to more rapidly deliver new therapies, and to help understand and address the differences in variability in ageing between individuals. progress is being made on this frontier too. most significantly, researchers have uncovered an array of epigenetic markers that strongly correlate with biological age. while these so called epigenetic clocks give a relatively immediate and accurate approximation of ageing, there is still a critical need for a more diverse range of ageing biomarkers to provide flexible and robust estimations of biological age. technology may provide part of the solution. personal markers of ageing are also at the heart of the next generation of wearables, with biomedical data being used to predict the body’s cellular age and biological resilience more accurately. by monitoring sleep, heart rate, movement and other health factors, researchers are now able to offer an assessment of biological age. it is hoped that the volume of data being generated   driven by the decreasing cost of many lifestyle wearables and developments in ai and machine learning   will enable us to receive personalised feedback on the lifestyle choices we make, which will unlock increased healthy life expectancy. beyond progress in our understanding of the genetic and molecular bases of ageing, advancements in combatting age related degeneration at a systems level have also been made in recent decades. regenerative medicine focuses on developing methods to regrow, repair or replace damaged or diseased cells, tissues or organs. this includes treatments such as stem cell therapy, tissue engineering and even the creation of artificial organs. some treatments are not new   the first heart transplant took place in the 1960s. however, in the us alone, there are 114,000 people on the waiting list for an organ transplant and, on average, 20 people die every day from the lack of an available organ. innovations in regenerative medicine could save lives and improve countless others, not to mention help to alleviate some of the enormous costs. the ability to regenerate cells varies across populations and species. some organisms, like the freshwater hydra, can regrow their entire body from a piece of tissue in a few days. humans have some regenerative capabilities, such as being able to knit fractured bones back together, but our species is also limited by cell type and age. building on advances in genomics, scientists are exploring how to induce regeneration of muscle cells and the cells of certain vital organs, such as the heart, through gene therapy and genetic engineering in order to address the complications that often accompany old age. researchers are even starting to see the possibility of regenerating whole organs through cellular therapy. following a study in which cells injected into the lymph nodes of animals with diseased livers successfully resulted in the growth of mini organs that supported or restored normal liver function, one biotech startup is set to conduct clinical trials in humans later this year. similarly, a recent study appears to show that using human growth hormone can rejuvenate the thymus and reverse the body’s epigenetic clock. due to transplant shortages and time sensitive scenarios where a patient’s immune system rejects donor cells or tissue, tissue engineering has increasingly become an area of focus in regenerative medicine. tissue engineering involves combining cells with a scaffold and growth factors to create artificial tissues. tissues require support for their formation, and the scaffold assists with this through structural support, promoting attachment, proliferation and differentiation. developments in tissue engineering are already paving the way for artificial organs: four women were recently able to regain full sexual function after the successful implantation of lab grown vaginas created from their own cells. chapter 5 advances in technology are unlocking our understanding of ageing at an accelerating pace. progress in mapping the fundamental biology of ageing, identifying new molecular targets, genomics and ai all offer hope of living healthier lives for longer. the potential prize of radically extended healthspans, both in terms of the quality and quantity of life and the impact on economic outlook, is vast and within reach, but only if policymakers are bold enough to seize the opportunity. there are a number of immediate actions that advanced economies can take to progress this agenda, starting with the following steps: set ambitious, long term targets: policymakers need to think more realistically about the magnitude of the challenge that ageing represents and more radically about finding solutions. to do this, governments must set ambitious, long term targets in a similar vein to climate goals to drive progress. there is consensus among experts that we already have the knowledge and technologies to achieve a “30 in 30” target   in other words, to increase hle by 30 years (to approximately 95 in most advanced economies) by 2050, if the right policies and technologies are implemented. it is an ambitious but achievable long term aim. governments also need to set short term targets so they can measure progress against, and be held accountable for, these longer term goals. ensure longevity is at the heart of life sciences strategies: to be meaningful, targets must also be accompanied by comprehensive strategies and roadmaps. as part of this, the life sciences strategies of governments should push for a greater emphasis on longevity research. this should include specific efforts to foster and fund both basic and translational research into holistic degeneration, in addition to the current model of focusing solely on individual chronic diseases. areas of great opportunity and promise, but which require sufficient investment, are: exploration of the known hallmarks of ageing; improving our understanding of the molecular basis of ageing through large cohort, whole genome association studies; defining new ageing biomarkers; and developing personalised multi omic ageing profiling. employ innovative funding models to accelerate progress: as well as increasing direct funding for longevity research, governments should also consider innovative funding models to drive progress faster. fast grants   which can greatly accelerate the allocation of resources to researchers, as we have seen during the pandemic   and prize competitions are two options that have proven effective, but these need not be exhaustive. incentivise innovation and equity in the private sector: the interest of private industries in longevity is growing but still at an early stage. governments can accelerate its development through targeted interventions and by investing in publicly funded basic research to build foundational knowledge. and while the private sector has an important role to play in longevity innovation and investment, market forces don’t always translate to equitable outcomes. this means that the public and private sectors must work together to ensure that the most innovative ideas are explored and that any breakthroughs are shared so they can benefit the greatest number of people. model the fiscal and economic value of increasing hle: as we look to the next century, advanced economies are likely to face massive demographic change, requiring new economic models to accommodate ageing populations. at the same time, unless action is taken, health care systems will continue to be burdened by the ever increasing cost of managing multiple chronic diseases. these combined pressures create significant social, fiscal and economic risks, but if policymakers tackle them in the right ways, the potential economic upside could be enormous. while some countries, such as the uk, have begun to calculate the long term fiscal risks associated with ageing populations, few (if any) governments have modelled the economic benefits of targeting ageing to increase hle in a comprehensive way. even modest increases in hle could be worth trillions in economic value globally. however, this needs much more thorough analysis at the national level and, given regional and socioeconomic disparities in le, hle and economic conditions, this should expand to include state and regional analysis to ensure equitable outcomes. facilitate clinical trials: as governments reflect on the pace of progress for clinical trials in response to covid 19, they should consider specifically how they might better facilitate clinical trials in longevity research. regulators need to make a concerted effort to smooth the pipeline between pre clinical and human studies; an overly complex process slows progress and blocks commercial routes, disincentivising investment from pharmaceutical companies and others. for example, not classing ageing as a disease has been an obstacle. the world health organisation’s decision in 2018 to add an extension code for “ageing related” to the international classification of diseases was a crucial step in recognising the importance of research focused on ageing. while helpful, not every country’s regulatory body has done the same, and standard practice requires that official classification as a disease is needed in order to begin development of drugs and therapies. regulations around ageing biomarkers have similarly been challenging for longevity researchers due to a lack of consensus and standard requirements around endpoints. regulators could unlock progress by giving researchers the ability to use multiple biomarkers as proxies for measuring ageing. alternatively, an easier step, without completely having to overhaul clinical trials, could be allowing the endpoints of studies to be redefined and proxy biomarkers used. change and lead the ageing narrative: policymakers should reframe ageing as an existential issue, with significant economic and public health consequences, but one that can be addressed. the political and policy communities must better champion the value to the public purse and to families of addressing multiple morbidities and then communicate the enormous risks to society if left unconfronted. an important part of this, which will drive progress, is to help longevity research gain further credibility and to be adopted by academic, university and medical communities, where its value remains underestimated. to build trust, policymakers need to articulate a positive, grounded and equitable vision for an ageing society, which focuses not only on managing complex health conditions but also on the potential to prevent them altogether. a few countries around the world are beginning to become more active in the longevity space. the us is home to several leading longevity research labs while the government in singapore is focused on facilitating clinical trials, encouraging some of the most exciting companies in longevity research to adopt a base there. the uk has a unique opportunity to position itself at the forefront of longevity research. the vast centralised data sets available via the nhs offer significant opportunities in enabling us to better understand the biology of ageing. the uk biobank   a large scale biomedical database containing genetic and health information from half a million volunteers   also offers great opportunities to identify ageing biomarkers and support drug discovery efforts, and is already being used by some leading longevity researchers. building on this success, there are four “no regrets” steps the government should take immediately to place the uk on a competitive footing in this emerging field. 1. publicly commit to delivering “30 in 30”. the government’s current target aims to add five healthy, independent years to people’s lives by 2035. this is insufficient in both scope and ambition. the uk should instead set out to deliver “30 in 30": to increase healthy life expectancy by 30 years by 2050. this is ambitious but achievable, and can be delivered by tackling the molecular causes of ageing, using personalised data on individuals’ markers of ageing and more advanced interventions to tackle multimorbidity, which we expect to reach market during the coming decade. 2. significantly increase funding and explore innovative funding models for longevity research. in the uk, there are currently no accurate figures for the amount of public funding directed towards ageing research per capita, per annum, although researchers estimate it can be measured in pence rather than pounds. by contrast, we spend around £2.80 per person on cancer research annually. longevity research should be at the core of the uk’s life sciences research funding and, as such, requires far greater levels of investment than estimates suggest is currently being spent. 3. give the nhs first refusal on publicly funded longevity therapies. government should ensure that novel therapies developed in publicly funded labs retain a public benefit when taken to market. policymakers should explore novel ideas like a national therapeutics service to ensure the nhs has first refusal on any ageing therapies that emerge through publicly funded longevity research in universities. 4. model the fiscal and economic value of extending life and healthspans at national and regional levels. while the uk has begun to calculate the long term fiscal risks associated with ageing populations, it hasn’t publicly modelled the economic value of targeting ageing to extend life and healthspans. work by researchers from the london business school, university of oxford and harvard medical school, published in the journal nature aging, offers a model for how longevity focused interventions could be quantified. hm treasury should conduct equivalent modelling to assess the economic value at stake. chapter 6 longevity research already offers a real chance to extend the “healthy” portion of people’s lives, but the future is filled with even more transformative possibilities. as advances in our understanding of the biology of ageing, gene therapies, drug discovery and regenerative medicine evolve at pace, it is likely that we will soon be able to accurately track and reduce our biological age, regenerate ageing tissue and perhaps prevent cell senescence, potentially enabling us to live healthily until the age of 95 by 2050. driven by a new frontier of research, the coming decade has the power to truly transform both the way we live and the way we age, with profound implications for each of us. political leaders must seize this opportunity and the great prize at stake. we would like to thank the following experts for the insightful discussions and comments that helped inform this work: dr nir barzilai   director, institute for aging research, albert einstein college of medicine and scientific director of the american federation for aging research jim mellon   co founder and chairman, juvenescence professor andrew scott   professor of economics, london school of business professor sarah harper, cbe   director and clore professor of gerontology, university of oxford professor lynne cox   associate professor, department of biochemistry, university of oxford professor eric verdin, md   president and ceo, the buck institute for research on ageing, usa professor jurg bahler   professor, institute of healthy ageing, university college london dr andrew steele   scientist, presenter, writer and author of ageless lead image: getty images charts created with highcharts unless otherwise credited. article tags newsletter tony blair institute for global change intelligence in your inbox. get the latest big ideas in strategy, policy and delivery in your inbox every month with our newsletter. what we do insights who we are tony blair institute, trading as tony blair institute for global change, is a company limited by 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rand's divisions conduct research on a uniquely broad front for clients around the globe. commentary feb 5, 2021 covid 19 survivor irma gooden celebrates her 100th birthday in jackson, georgia, june 16, 2020 photo by curtis compton/atlanta journal constitution/tns/abacapress.com via reuters by andrew r. hoehn, bonnie hagemann, krishna b. kumar this commentary originally appeared on dallas morning news on february 5, 2021. it is inspiring to see age is no barrier for the highest office in the land. joe biden, 78, is the oldest person in u.s. history to become president. biden's predecessor of a century earlier, warren g. harding, was 55 years old when he took office in 1921, and he died halfway through his term at 57, as if on cue, given the prevailing life expectancy at the time of 57.5 years. these age differences are symptomatic of continuously increasing life expectancy. as recently as 1800, life expectancy at birth in america was 35 years, grew slowly to 39.4 years in 1880, and more rapidly thereafter, to 78.9 in 2019. nobel laureate angus deaton wrote in his book the great escape: health, wealth, and the origins of inequality: “the greatest escape in human history is the escape from poverty and death.” these dramatic increases in longevity arose from medical and public health improvements: controlling infectious diseases through antibiotics, antivirals, and vaccines; improved diet, water, and sanitation; and greater access to education and pharmaceuticals. there is little reason for these advances to stop; researchers have recently identified a longevity gene and restored lost sight in mice, offering clues to reversing aging in humans. female life expectancy is already approaching 90 in east asia, and research published in millbank quarterly projected longevity to rise higher than 93 years by 2050 in the united states. while there are still gaps between life expectancies black people still live, on average, 3.6 fewer years than white people, according to research published in nature for the population as a whole, mortality rates have declined over the past century and this gap has narrowed. covid 19 will almost certainly represent a setback to life expectancy in america, but we expect that will be temporary as long as the speed of pharmaceutical and biomedical innovation can keep pace with the evolution of vector borne diseases. while the life sciences can describe and chart this remarkable trajectory in life expectancy, we focus on the implications of having all these extra years. just as a landowner whose holdings are bounded by a river is given the gift of expanded acreage when the river shifts over time, humans have been granted the gift of time. and as the farmer must decide what to do with the additional land, tend to it or leave it fallow, humans need to plan for the additional time. increased longevity comes with its challenges such as physical disabilities and cognitive decline. for the average american in 1800, as the english philosopher thomas hobbes presaged, life was poor, nasty, brutish and short. the workforce was predominantly agricultural, and 95% of the population was rural. generations three, if a family was fortunate tended to live in the same community, many in the same home. children needed to be born, raised, and brought into adulthood while their parents were still alive and able to provide for them. for most, life unfolded at a rapid clip, and there was little time for leisure or exploration. as the agricultural transformation ushered in by the industrial revolution unfolded, american families moved from farms to cities to take up the plentiful industrial jobs. in 1890, 35% of the population was urban and by 1920 a majority lived in cities. life expectancy correspondingly increased over this period by nearly 50%. working lives have expanded with life expectancy. it was once uncommon for someone to work beyond his or her sixth decade, but now many even work into their eighth decade. according to the u.s. bureau of labor statistics, men and women age 75 and older are projected to have the fastest growth rate in the u.s. labor force. increased longevity comes with its challenges such as physical disabilities and cognitive decline. in the united states, 3.4 million workers provide paid home care, according to the bureau of labor statistics, and the national alliance for caregiving reported nearly 53 million americans provide unpaid care to adults with a disability or illness. people providing dementia care, paid or unpaid, for our oldest outnumber by over four times the 3.2 million teachers in public k 12 schools providing education for our youngest. however, longer lives also represent opportunity. there is time for family and community; for learning, adventure, and exploration; and for contributions to our families, communities, and workplaces. what will americans do with all the extra time, as 100 might be a ripe old age instead of 60 a century ago? several policy areas clamor for attention. to ensure that health and well being continue into these extended lives, new policies may be needed to ensure these extra years become mutually beneficial to all generations. outdated social systems, norms, and institutions that made sense when life expectancy was half of what we expect our children to experience could be reimagined. we may have to rethink life possibilities when four generations routinely overlap and interact, and reconsider lifelong learning and retirement when lives are this long. given life expectancy is likely to increase further, it makes sense to examine the economic and social systems to see if they will be resilient to future demographic changes. closing the gaps in longevity by race and ethnicity could also be a priority. we may have to rethink life possibilities when four generations routinely overlap and interact, and reconsider lifelong learning and retirement when lives are this long. the swearing in of our oldest president is an occasion to widen our understanding of acceptable ages for all occupations and activities. it can lead us to envision a society and an economy that values increased life spans as tremendous opportunities to create, innovate, and thrive. the jazz legend louis armstrong, who died a month before his 70th birthday in 1971, again in sync with the prevailing life expectancy of just under 70, sang, “we have all the time in the world.” it is up to us to craft an answer to the question: what will we do with it? andrew hoehn is senior vice president of research and analysis at the nonprofit, nonpartisan rand corporation. bonnie hagemann is chief executive of eda inc. krishna b. kumar is director of international research at rand and director of the initiative for global human progress at the pardee rand graduate school. commentary oct 8, 2015 commentary jun 16, 2015 research feb 12, 2015 rand is a research organization that develops solutions to public policy challenges to help make communities throughout the world safer and more secure, healthier and more prosperous. rand is nonprofit, nonpartisan, and committed to the public interest. p.o. box 2138 1776 main streetsanta monica, ca 90401 2138 rand has offices across the u.s., in europe, and in australia and stay on top of the issues that matter most. rand® is a registered trademark. © 2025 rand corporation. privacy policyterms and conditions this site is protected by recaptcha and the google privacy policy and terms of service apply.

by staff writer october 21, 2024   a paper published in nature aging earlier this month concluded that it’s unlikely that we will see significant leaps in human life expectancy this century. william mair, professor of molecular metabolism at harvard t.h. chan school of public health, shares what researchers know about the biology of aging, the importance of improving health span, and the need to take moonshots. q: what did the study find and what conclusions can we draw from it? a: the study looks back at advances in human life expectancy made between 1990 and 2019 in a number of countries where people typically live longer lives and shows that, while average life expectancy has gone up, maximum lifespan has not changed. moreover, the pace of increase in average life expectancy has slowed of late. the paper concludes that during that period, medical and public health advances have not slowed human aging and have not done anything to radically prolong lifespan. certainly, i would agree with that, but i would also add that no strategies have been implemented in that time with that goal in mind. what we have been doing remarkably successfully is reducing deaths earlier in life and allowing more of us than ever before to reach old age. that incredible success has come at a cost however revealed by this paper that our bodies have not evolved the capacity to maintain themselves much beyond our current maximum lifespan. so, our success in allowing more of us to live longer has also given us a much greater burden of age onset non communicable diseases, which are causing terrible suffering. however, as the paper states, historical data show us a ‘glass mortality floor’ of the maximum lifespan a human body can achieve with current medical technologies. what retrospective data simply cannot tell us is if that glass floor can be broken. in fact, the authors themselves conclude that ‘these limits are not brick walls for longevity,’ and on that i’d certainly agree with them. q: a key line from the study concludes that “unless the process of biological aging can be slowed, radical human life extension is implausible in this century.” you point out on your website that many organisms, from yeast to primates, can slow the process of aging when nutritional resources are limited. and when they do that, they’re far less susceptible to age related diseases. can you walk us through that evidence? a: evolution doesn’t care about how long an animal lives. it cares about its ability to pass its genes onto the next generation. we say survival of the fittest, not survival of the oldest. and that’s because for most organisms, death doesn’t come from old age it comes from infection, accident, or predation. the best strategy then is to eat as much as you can, grow fast and strong, and reproduce, even if that makes your body age faster. what happens, however, if food becomes scarce? some organisms have adapted to such stressors by focusing less on growth and reproduction which require energy and more on maintaining their body. from an evolutionary standpoint, this allows them to live longer and wait out the famine, at which point they can reproduce. in the lab, we see this all the time. if you take an animal like a nematode worm, or a fruit fly, or a mouse, and you give it all the food it can eat, it will live fast and die young. it’s programmed to do so. but if you restrict its diet and give it 20% or 30% fewer calories, it will live longer. interestingly, they will also delay the onset of age related diseases, such as cancer or cardiovascular diseases. q: could humans slow their aging by limiting their food intake, too? a: to be able to answer that question definitively would require a human lifespan study with hundreds of people. we can’t do that. however, we are at the point now where we can measure the biological age of an individual and test whether they are aging faster or slower than their chronological age would predict. researchers are also starting to do clinical trials on restricted feeding and intermittent fasting in human populations, but we don’t have definitive data yet. so, the boring answer is, it’s too soon to know. but the exciting answer is that geroscience, the field of aging biology which didn’t even exist 30 years ago is trying to work it out. q: your research focuses on understanding the molecular pathways that drive aging. what have you learned so far? a: my lab thinks that many of the chronic conditions we see in old age alzheimer’s disease, cancer, cardiovascular disease, or diabetes are caused by metabolic dysfunction. these diseases have different etiologies but have one thing in common: age is their biggest risk factor. my thesis is that they are all linked to dysregulation in metabolism. when we are young, we can metabolize our nutrients efficiently. we can move between burning sugar during the day and fats at night. as we get old, we become less able to do that. we start to store lipids where we shouldn’t, for example in our organs, which makes us more prone to disease. i’m interested in understanding what causes this inflexibility and why certain individuals can remain metabolically flexible for longer. our lab is focused on how a cell senses fuel and controls what we do with it, and how those sensors become less accurate with time. there are different ways to maintain metabolic flexibility. in the lab, we can do it with diet, drugs, or genetics. but there are also behaviors that could help, and i would love to integrate those two approaches. q: could geroscience lead to interventions that might extend the human lifespan? what breakthroughs would be needed to get there? a: there are two approaches in the field. one approach is to look at the biological and social factors that help certain people age exceptionally well. there’s something about those people probably a combination of factors, including genetics, their metabolism, diet, behavior, social integration which gives them that ability. this approach will not increase the maximum upper limit of human lifespan. what it can do is gradually increase the median lifespan so that more and more people can reach that upper limit. it’s the type of work that is critical to the mission of our school. the other approach is to look at whether we can we change the actual biology of human aging. we are looking at cell and tissue rejuvenation, for example. the field is still in its infancy, so it is impossible to know if we’ll be successful or not. that’s the beauty of science. there is no intellectual reason why we can’t break this upper limit of human lifespan of about 90 years. public health hasn’t broken it yet, because that’s not what the goal of public health is. could it be broken through targeting the biology of aging? quite possibly. q: where do you think the science of longevity should focus? what questions do we most need answers to? a: we should focus both on what we can do now to improve health span and on a few moonshots. there is a lot of research being done on aging. my department looks at it from a biological perspective, but there are people in epidemiology, nutrition, and social and behavioral sciences who are looking at it, too. we need to integrate these disciplines to better understand how we can help people age better. we need to test different interventions and quantify what happens to our cells and tissues when those interventions work. working across disciplines is by far the most promising thing we can do in the field in the short term. i am in the early stages of building a healthy aging initiative across our school to bring together researchers working on this i believe we may be the only institution in the world that’s looking at aging from all these angles, but we need to do a better job integrating and funding our work. we also need to invest in the so called moonshots, or all those things we’ve successfully tried in a lab in a simple organism, but don’t yet know if they can work in humans. for example, looking at strategies that could turn adult cells back into stem cells. these rejuvenation techniques may one day be used to slow cell and tissue aging and even revert cells to more youthful states. these are high risk, high reward projects. my concern with [the nature aging] paper is that it will lead people to believe these moonshots are impossible, so we should not invest in them. that would be a critical mistake. q: you’ve expressed concern about the way some researchers and doctors talk about longevity. what misinformation is out there and how can it be harmful? a: there are an increasing number of health influencers who have almost an evangelical following and make bold statements about how to live longer, for example, ice therapy, heat shock, and so on. what they are doing is extrapolating data from simpler organisms, small sample studies, and non causal correlative studies and telling people it’s the truth. that’s not how the scientific process works. i worry that in a world where people have limited attention spans, the people who speak with confidence and say they have already cured aging will get the microphone. and they either give people false hope or they give a bad name to a field where a lot of great research is being done slowly and carefully. we all age and we all know someone who is suffering from an age related condition. we all wish we had something that could help us live longer and age better. but science cannot speak in absolutisms. when someone asks me if humans will be able to live to 300 one day, the only responsible answer i can give is, “i don’t know, yet!” but that’s not going to get me a lot of hits on tiktok, is it?  giulia cambieri photos: istockphoto: disobeyart; mair: kent dayton stay connected with harvard chan school in addition to our degree programs, we offer highly targeted executive and continuing education, directed and taught by harvard faculty. stay connected with newsletters on climate, nutrition, communication   and the latest from harvard chan school.

longevity is the achievement of a long life. we may hope for longevity so that we can experience many years of quality time with loved ones or have time to explore the world. but living to a ripe old age doesn’t necessarily mean healthy or happy longevity if it is burdened by disability or disease. the population of people over age 65 has grown more quickly than other age groups due to longer life spans and declining birth rates, and yet people are living more years in poor health. [1] therefore, we will explore not just one’s lifespan but healthspan, which promotes more healthy years of life. what you do today can transform your healthspan or how you age in the future. although starting early is ideal, it’s never too late to reap benefits. researchers from harvard university looked at factors that might increase the chances of a longer life. [2] using data collected from men and women from the nurses’ health study and health professionals follow up study who were followed for up to 34 years, researchers identified five low risk lifestyle factors: healthy diet, regular exercise (at least 30 minutes daily of moderate to vigorous activity), healthy weight (as defined by a body mass index of 18.5 24.9), no smoking, and moderate alcohol intake (up to 1 drink daily for women, and up to 2 daily for men). compared with those who did not incorporate any of these lifestyle factors, those with all five factors lived up to 14 years longer. in a follow up study, the researchers found that those factors might contribute to not just a longer but also a healthier life. [2] they saw that women at age 50 who practiced four or five of the healthy habits listed above lived about 34 more years free of diabetes, cardiovascular diseases, and cancer, compared with 24 more disease free years in women who practiced none of these healthy habits. men practicing four or five healthy habits at age 50 lived about 31 years free of chronic disease, compared with 24 years among men who practiced none. men who were current heavy smokers, and men and women with obesity, had the lowest disease free life expectancy. beyond the five core lifestyle habits mentioned above, a growing body of research is identifying additional factors that may be key to increasing our healthspans: these senses can decline over time for various reasons: normal aging, which causes a gradual decrease in taste and smell; prescription drugs that reduce taste sensitivity and promote dry mouth or lack of saliva; deficiencies in micronutrients such as zinc that reduce taste; and poor dentition with tooth loss or dentures leading to chewing problems. [19] up to 60% of adults 70 years and older may lose their sense of taste. [20] with this loss may come heavier seasoning of food with sugar and salt. [21] they may prefer softer lower fiber foods that don’t require much chewing. poor taste and smell in the elderly is associated with lower dietary quality and poorer appetite. [22] food aromas are important as they trigger the release of saliva, stomach acid, and enzymes in preparation for digestion. [23] the scent of food can trigger the release of dopamine and serotonin, causing a feeling of wellbeing to encourage eating. an impaired sense of smell in older adults is also associated with less variety in food choices and poorer nutrition, but can also lead to increased food intake and weight gain in some individuals. [23] seasoning food more liberally with sodium free herbs, spices, and vinegars may help to compensate for sensory deficiencies. using foods with a savory umami quality like mushrooms, tomatoes, some cheeses, and yeast can boost richness and flavor. another sensory aspect of food called “kokumi” describes a full and rich mouthfeel such as that experienced from a minestrone soup, an aged cheese, or a seafood stew simmering for many hours. if poor appetite from sensory loss is a problem, providing variety through different textures, smells, and colors in the meal may stimulate an increased desire to eat. [21] eating and food preparation are also important activities offering socialization and mental stimulation such as when learning new cooking skills. preparing meals helps to reduce sedentariness as there are several action steps involved: selecting and purchasing, washing and chopping, and cooking the ingredients. identifying additional factors that improve and extend our healthspans is an active area of scientific inquiry. in the meantime, current research findings are encouraging, and underscore the importance of following healthy lifestyle habits throughout one’s life course. that said, sticking to these behaviors is easier said than done, and public policies must support and promote these habits by improving the food and physical environments that surround us. last reviewed december 2022 the contents of this website are for educational purposes and are not intended to offer personal medical advice. you should seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. never disregard professional medical advice or delay in seeking it because of something you have read on this website. the nutrition source does not recommend or endorse any products. use healthy oils (like olive and canola oil) for cooking, on salad, and at the table. limit butter. avoid trans fat. drink water, tea, or coffee (with little or no sugar). limit milk/dairy (1 2 servings/day) and juice (1 small glass/day). avoid sugary drinks. the more veggies   and the greater the variety   the better. potatoes and french fries don’t count. eat plenty of fruits of all colors choose fish, poultry, beans, and nuts; limit red meat and cheese; avoid bacon, cold cuts, and other processed meats. eat a variety of whole grains (like whole wheat bread, whole grain pasta, and brown rice). limit refined grains (like white rice and white bread). incorporate physical activity into your daily routine. create healthy, balanced meals using this visual guide as a blueprint. thank you for supporting our mission of translating food and nutrition knowledge into daily practice! make a gift a monthly update filled with nutrition news and tips from harvard experts all designed to help you eat healthier. sign up here. explore the downloadable guide with tips and strategies for healthy eating and healthy living.

here is a classic conundrum of cause and effect: the men who survive the crushing pace (not to mention lethal diet) of multiple u.s. presidential campaigns and go on to hold one of the most stressful jobs in the world also have a habit of outliving the rest of us. in the fall of 2012, jimmy carter, now 90, took his place in history as the president who had lived the longest after leaving the white house 31 years and 231 days out of office, breaking the record of herbert hoover, who died in 1964. carter left the white house in january 1981, went back to georgia and proceeded to teach, improve his spanish, paint, write poetry, win the nobel peace prize and write 21 books about, among other things, how to find a second career. he is rather typical. ronald reagan lived until 93. so did gerald ford. george bush the elder, like carter, is 90. even in the 19th century, when the average man died at age 47, u.s. presidents lived an average of 69 years, and john adams made it to 90. granted, the presidential demographic typically enjoys access to better nutrition, health care and living conditions. yet these men also knew pressure that few of us can imagine, and stress is a proven toxin. so does the presidency endow people with some special life force, or do they share some quality that helps get them to the white house in the first place? is there something about holding the office that forces men and presumably one day women to live a healthy lifestyle rather than just aspire to it? for starters, there is constant vigilance. ignoring troubling symptoms is not an option for someone who has a doctor following him virtually everywhere he goes; medical teams are steps away at all times. even when presidents return to private life, they are shadowed by secret service details, albeit smaller ones. among those agents, an emt is always on duty. think of it as a retirement benefit. at least since the mid 1970s, nearly every president has been devoted to some kind of regular exercise. ford swam and skied. carter jogged almost daily. reagan chopped brush and lifted weights. bush the younger took to biking when his knees put a halt to running. if some of that recreation was done for public relations purposes, most presidents have come to rely on it for private sustenance. (not everyone got the memo: as president, bill clinton may have been conspicuously photographed in his jogging shorts, but he typically relaxed in the office by reading, doing crosswords and chewing on cigars, a pattern that probably helped land him in new york presbyterian hospital for bypass surgery in 2004 and another surgery six years later. he is now a part time vegan.) the elder bush, who as president was known to try three or four different sports in a single day, still takes exercise to extremes and jumped out of airplanes with army skydivers at ages 80, 85 and 90. “i want people at my age to know they don’t have to slow down,” he once told us. last summer the elder bush had young aides haul his wheelchair out on the dock of his maine seaside compound so he could bomb around the north atlantic on his speedboat. there’s body, and then there’s mind. we all may know we need to manage our stress, but for a sitting president this is imperative, a consistent part of the advice they give one another. be sure to rest. take your vacations. use camp david. after the hard fought 1960 election, richard nixon and john f. kennedy met in key biscayne, fla., where nixon made an unsolicited promise. i may criticize your policies, he told kennedy, but “of one thing i can assure you: i shall never join in any criticism of you, expressed or implied, for taking time off for relaxation. there is nothing more important than that a president be physically, mentally and emotionally in the best possible shape to confront the immensely difficult decisions he has to make.” for many presidents, stress acts as a force multiplier. the toll stress takes, research has shown, depends on how it is viewed. what is normally harmful becomes helpful when it is treated as a fact of life or a chance to learn. the more powerful a person is, the more in control, the better the odds he has learned to use stress to his advantage. clinton aides flaunted his mantra like a bumper sticker: “that which doesn’t kill him only makes him stronger.” for people with that kind of resilience sometimes called adaptive competence stress can correlate with a longer life. out of office, the challenge changes. presidents tend to be not just type a but triple a personalities, guys who don’t spend a lot of time lounging around checking their facebook feeds (although clinton and bush the elder both tweet). slowing down isn’t something they really want to do. “when i got out of the white house,” carter recalled, “i had a life expectancy of 25 [more] years, and so i needed to figure out how to use it.” former presidents are particularly well positioned to do good: to engineer an immense humanitarian rescue effort, as hoover did in the years after world war ii, or to promote reform and democracy, as ford and carter did as unlikely partners. clinton launched his global initiative, while george w. bush has focused on veterans. engaging in meaningful work also correlates closely with longevity and modern presidents have typically made it their mission to leverage their fame for a cause they believe in. so, in psychological terms, they settle in for the long haul. of course, ex presidents have something else to keep them going: a need to burnish their reputation for history, particularly if their time in office didn’t go exactly as they had planned. most of us are not quite as likely to have accumulated as many regrets and scars, nor are we in as strong a position to do something about them. correcting or whitewashing the record on a global scale probably helps keep the former presidents alive a little longer, if only because there is often so much work to be done. that can be a campaign that never ends, a second life’s work. it may even be that unloved presidents have an edge in this area. few wept when harry truman left washington in 1953, ceding the white house to the wildly popular dwight eisenhower. but truman lived another 19 years, and his reputation improved annually. even nixon, who resigned in 1974, lived two more decades, writing books, opening a think tank and driving his successors more or less crazy. he was determined to have the last word, which might be a useful longevity strategy. asked once how he had survived all the criticism aimed at him during the depression, hoover said simply, “i outlived the bastards.” finally, there’s the kind of legacy you can read about in books, and then there’s the kind any fool can see. and so as 2015 unfolds, it’s important to note that three of the four current ex presidents may have something else to live for now. clinton’s wife hillary is trying to become the 45th president, and so is bush son and brother jeb. aides to the elder bush privately admit that the prospect of seeing a second son run for the white house helps keep him going. and nothing gets the blood pumping like a little competition among friends. contact us at letters@time.com

commentary march 23, 2016 demographics & population retirement global economy and development nature has given every species an intrinsic life span. life span is a bit like an upper bound to life expectancy: if you got every member of a species healthier and healthier, life expectancy of that species would constantly increase, but eventually be bound by life span. and every species has a different life span: for flies, it’s just a couple of days; for bowhead whales it’s 200 years. for humans, biologists have found that up until the 1960s, life span was around 89 years. this means that if we kept improving our health systems, the world population’s life expectancy would converge to our species’ life span of 89. in public health, this development is called “compression of morbidity.” the idea is that as our health systems improve and we live healthier and healthier. the time we spend in illness and infirmity, especially in the last years of our life, becomes shorter. our population’s survival rate becomes more and more “rectangular,” having more people survive until old age and allowing for healthier life at old age (see figure 1). however, life span acts as a fixed point beyond which no further gains in health are possible and survival rates of humans drop quickly to zero, owing to the “compensation effect of mortality.” in practice, however, we do not observe a conversion of life expectancy to life span across countries and world regions. the reason seems to be that sometime in the 1970s, human life span itself began to increase a feat no other species has managed before us. prior to the 1970s, biologists, using historic data on human survival rates, have found indeed that human life span was constant at about 89 years. yet, since the 1970s, life span has increased markedly, pushing the limit of life expectancy. figure 1 illustrates this for canadian males. it depicts the probability of surviving to a given age for different years, from 1925 to 2075. one can clearly observe the “rectangularization of survival rates,” with significantly more people surviving until high age in 2010 than in 1925. however, when comparing survival rates at age 90, one cannot observe any significant improvement between 1925 and 1975; survival was more or less constant at a level well below 10 percent. however, since then, the survival rate at age 90 jumped markedly to about 20 percent in 2010. hence, although survival rates improved spectacularly for younger ages between 1925 and 1975, improvement in health systems did not make much of an impact on the very old during that time; increases in life expectancy were bounded. since 1975, however, this seems to be untrue; the limits to increases in life expectancy were relaxed. and it’s believed that these limits will relax even more over the next 60 years. source: mortality projections for social security programs in canada (2014) how did we break the limits of life expectancy? we don’t know exactly, but the prime candidates are the invention of regenerative medicine and organ replacements. the biggest medical breakthroughs up to the 1960s were arguably the discovery of antibiotics, vaccines against diseases ranging from rabies to polio, and significant progress related to hygiene. these interventions helped to slow down the bodily decay of our vital organs literally the “heart” of our physical health. however, overcoming the failure of human organs like heart bypass or dialysis or replacing them altogether had a profoundly different impact on the speed of bodily decay. these new medical procedures, in particular organ transplants, meant extending the functions of our body beyond what nature had foreseen and therefore affected the life span of the human species and removing the natural limits to life expectancy. in fact, now biologists believe that our life span has increased to 97 years, a gain of eight years in the course of 40 years. what does all this mean for aging societies? the policy implications of bounded life expectancy are indeed quite different from unbounded life expectancy. in a world of bounded life expectancy, we would continue compressing morbidity, living healthier and healthier lives, but facing rapid aging in the last years of our life. our life cycle decisions, like how much education to get and when to retire, would in fact become much more plannable, knowing that the likelihood of living up to 89 is rather high, but living beyond it is rather improbable. one could even argue that as we get healthier in the future. we would also get more productive, earning more income during work life; but knowing that we are likely to die at an age of around 89 (give or take), we could actually work less long and retire earlier. not so in the case of boundless life expectancy: we’d never be sure what new medical inventions, especially in the field of genetics, could extend our lives beyond our wildest imagination maybe even to the age of 150, and possibly within our lifetime. in such a world, the question on what money to live off during old age becomes a very different one: living to 150, but retiring at age 65 or even earlier will not be an option. longer work lives and lifelong investments in education, training, and skills become a must that will ultimately lead to higher lifetime income, wealth, and savings for old age. surely, public pensions can, should, and will also play an important role in securing old age income. however, during times of rapid expansion of life expectancy, pay as you go systems will come under strain, exerting a heavy toll on younger generations and older generations risking to overstay their welcome. if, though, societies get the balance between work and retirement right, nothing is in the way of an era of golden aging, even during times of shifting limits of life expectancy. the brookings institution is committed to quality, independence, and impact. we are supported by a diverse array of funders. in line with our values and policies, each brookings publication represents the sole views of its author(s). demographics & population retirement global economy and development simon hodson, emma phillips, tara watson december 17, 2024 quinn sanderson july 9, 2024 richard v. reeves, simran kalkat november 9, 2022 get the latest from brookings the brookings institution is a nonprofit organization based in washington, d.c. our mission is to conduct in depth, nonpartisan research to improve policy and governance at local, national, and global levels. copyright 2025 the brookings institution

trending datanon communicable diseases cause 70% of global deaths country dropdown three areas of focus to help shape a healthier, equitable, more productive future: play video the world’s population has been aging at a dramatic speed and many countries are ill prepared to address the magnitude and pace of demographic shifts. tackling non communicable diseases for healthier longevity is important for all people, and a matter of equity because the poorest people are most susceptible to these diseases. if done right, healthy longevity could save 150 million lives in low  and middle income countries and extend millions more lives by 2050, resulting in significant economic benefits. but this requires bold actions by governments to prevent and control non communicable diseases. healthy longevity initiatives also improve gender equity. the world bank stands ready to support countries with knowledge, data and financing for longevity programs to improve health and wellbeing of their adult population and protect families from economic devastation. main report: unlocking the power of healthy longevity executive summary (pdfs):english | français | español | العربية key insights for policy and action | français | español towards a framework for impact pathways between ncds, human capital and healthy longevity, economic and wellbeing outcomes gender gaps in healthy longevity: outcomes, barriers, and implications aging and health: policy considerations for long term care topic: health topic: universal health coverage topic: pensions & aging topic: human capital project brief: health taxes | sugar sweetened beverage tax database publication: silver opportunity: building integrated services for older adults around primary health care (2023) press release: world bank group aims to expand health services to 1.5 billion people (april, 2024) stay current with our latest data & insights © 2025 world bank group. all rights reserved. this site uses cookies to optimize functionality and give you the best possible experience. if you continue to navigate this website beyond this page, cookies will be placed on your browser. to learn more about cookies, click here.

healthy people 2030 is the nation’s 10 year plan for addressing our most critical public health priorities and challenges. in 1980, the u.s. department of health and human services (hhs) released the first set of healthy people 10 year objectives. healthy people 2030 is the fifth iteration of the healthy people initiative. healthy people helps individuals, organizations, and communities committed to improving health and well being address public health priorities. healthy people 2030 includes hundreds of measurable objectives with ambitious but achievable national targets. objectives are associated with a variety of resources that can be used to help achieve these targets. healthy people 2030 was created with the successes and lessons learned from previous iterations of the healthy people initiative in mind. subject matter experts across several disciplines developed the healthy people 2030 framework and objectives, and stakeholders from several sectors provided their input through public comments on the new objectives and framework for healthy people. the healthy people 2030 framework outlines the vision, mission, foundational principles, plan of action, and overarching goals of the initiative’s current iteration. check out the healthy people 2030 framework. the hhs office of disease prevention and health promotion manages healthy people and led the development of healthy people 2030. the national center for health statistics (nchs) at the centers for disease control and prevention (cdc) provides statistical expertise for healthy people’s data. the secretary’s advisory committee on national health promotion and disease prevention objectives for 2030, a federal advisory committee composed of nationally and internationally recognized non federal subject matter experts, provided recommendations on the framework, objective and data selection criteria, and more. learn more about the secretary’s advisory committee. the healthy people federal interagency workgroup (fiw)   along with individual workgroups of federal subject matter experts representing more than 20 federal agencies   developed the healthy people 2030 objectives and selected targets and will help review data and resources associated with the objectives throughout the decade. learn about the healthy people 2030 workgroups. stakeholders, organizations, and members of the public contributed to healthy people 2030’s development via multiple public comment periods. healthy people 2030 has many different types of resources that can support your work. check out our how to use healthy people 2030 graphic to get tips your community, state, or organization can use to achieve your goals, improve health and well being, and contribute to national public health goals. you can also use our promotional toolkit to help spread the word about healthy people 2030 to your networks. use healthy people 2030’s search tool to easily find information relevant to your work. you can filter information based on your interests to find topics, objectives with baseline data and targets, and evidence based resources. in addition, you can use our new custom list tool to build a list of objectives that are relevant to your work   and track them over the decade. additional data and resources are coming soon   check out our timeline for more information. healthy people 2030 includes 3 types of objectives: some developmental and research objectives may evolve throughout the decade to become core objectives. learn more about the healthy people 2030 objectives. in response to stakeholder feedback and user surveys, we reduced the total number of measurable objectives from over 1,000 for healthy people 2020 to 358 for healthy people 2030. objectives were chosen using rigorous selection criteria recommended by the secretary’s advisory committee and made available for public comment. as a result, the objectives focus on the country’s highest priority public health issues, avoid overlap, and use higher data standards than previous decades. on the healthy people 2030 website, the objectives are organized into more intuitive topics   and we developed a tool to help you see which healthy people 2020 objectives have been modified, removed, or retained for healthy people 2030. a new decade means new opportunities to improve health and well being across the nation. this decade, healthy people 2030 features a smaller set of objectives with: for the first time, healthy people 2030 also sets 10 year targets for objectives related to social determinants of health. and we’ve updated our health literacy definition for the first time in 20 years to emphasize how both individuals and organizations can help improve health literacy. in addition, healthy people 2030 features 8 overall health and well being measures (ohms). called foundation health measures in healthy people 2020, the healthy people 2030 ohms include a new measure on well being. healthy people 2030 also features 23 leading health indicators (lhis). lhis are a small subset of high priority core objectives that highlight critical public health issues across different life stages. in 2024, we added a set of lhi infographics that offer engaging visual interpretations of the overall data and select population disparities data for each lhi. together, lhis and ohms can help individuals, organizations, and communities committed to improving health and well being set priorities, track nationwide progress toward improving health and well being, and assess progress toward achieving healthy people 2030’s vision. we also have an improved website, with an application programming interface (api) to support faster data deployment, a tool for building custom lists of objectives, a more sophisticated data search tool, and more user centered intuitive navigation. the definitions of health disparities and health equity haven’t changed since healthy people 2020. healthy people defines health equity as “the attainment of the highest level of health for all people. achieving health equity requires valuing everyone equally with focused and ongoing societal efforts to address avoidable inequalities, historical and contemporary injustices, and the elimination of health and health care disparities.” healthy people defines a health disparity as “a particular type of health difference that is closely linked with social, economic, and/or environmental disadvantage. health disparities adversely affect groups of people who have systematically experienced greater obstacles to health based on their racial or ethnic group; religion; socioeconomic status; age; mental health; cognitive, sensory, or physical disability; sexual orientation; geographic location; or other characteristics historically linked to discrimination or exclusion.” learn more about healthy people’s health equity and health disparities definitions. health disparities and health equity have been an important focus of healthy people for over 30 years. similar to healthy people 2020, one of healthy people 2030’s overarching goals is to “eliminate health disparities, achieve health equity, and attain health literacy to improve the health and well being of all.” to help stakeholders work toward this goal, healthy people: each decade, healthy people tracks progress toward meeting the national disease prevention and health promotion goals and objectives, and it monitors differences across population subgroups. healthy people data tools summarize and display changes in health disparities to help identify priority populations. healthy people 2030 also features evidence based resources focused on strategies that are proven to improve health. these resources include interventions to address public health issues among specific population groups and improve the health of all people. in addition, healthy people collects stories that highlight how states, communities, and organizations address health disparities, advance health equity, and improve health by: read the facts and watch a video about how healthy people 2030 promotes health equity. we brought national attention to social determinants of health (sdoh) when we incorporated them into the healthy people 2020 prevention framework. since then, the impact of social determinants has become even more clear   the fact is, the conditions in the environments where people are born, live, learn, work, play, worship, and age significantly influence their health. that’s why healthy people 2030 continues to focus on sdoh. more than a dozen workgroups of subject matter experts with diverse backgrounds worked to develop a range of healthy people 2030 objectives related to sdoh. for the first time in the initiative’s history, the healthy people 2030 sdoh objectives also have 10 year targets. (in healthy people 2020, the sdoh objectives were informational, meaning there was no set target.) in addition to objectives, the healthy people definition for sdoh was adopted in early 2020 as the official hhs definition, meaning that all hhs agencies will approach sdoh using the healthy people framework. learn more about healthy people 2030's focus on sdoh. healthy people sdoh literature summaries provide a snapshot of the latest research on sdoh. these summaries explore a range of key sdoh   such as discrimination, social cohesion, access to health services, and poverty   and examine how these issues can impact health outcomes and health disparities. explore healthy people 2030's sdoh literature summaries and find infographics on key sdoh. hhs considered health equity and health disparities throughout the healthy people 2030 objective development process. to select core objectives, subject matter experts applied specific criteria, including considering how each objective would address health disparities and advance health equity. in addition, the selection criteria for healthy people 2030 leading health indicators   a subset of high priority core objectives   required that the indicators address social determinants of health, health disparities, and health equity. yes! more tools and resources   like disparities data, evidence based resources, and state based resources   will be released throughout the decade. check out our timeline to see when you can expect them. and be sure to visit the healthy people 2020 website and check out “healthy people 2020: an end of decade snapshot” to find data from the last decade of healthy people and read about progress made over the decade. please stay tuned for updates and additions to healthy people 2030! last updated: january 31, 2025 this site is coordinated by the office of disease prevention and health promotion, office of the assistant secretary for health, office of the secretary, u.s. department of health and human services. office of disease prevention and health promotion | contact us linking to a non federal website does not constitute an endorsement by odphp or any of its employees of the sponsors or the information and products presented on the website. you will be subject to the destination website's privacy policy when you follow the link.

jump to main content jump to navigation president obama promised that he would make quality, affordable health care not a privilege, but a right. after nearly 100 years of talk, and decades of trying by presidents of both parties, that's exactly what he did. today, 20 million more adults gained access to health coverage. we've driven the uninsured rate below 10 percent   the lowest level since we started keeping records   and built stronger, healthier communities through advancements in public health, science, and innovation. today, as many as 129 million americans with pre existing conditions can no longer be denied health coverage. healthcare.gov: ending lifetime & yearly limits "insurance companies can’t set a dollar limit on what they spend on essential health benefits for your care during the entire time you’re enrolled in that plan." read more 2.3 million additional young adults (aged 19 25) gained health insurance coverage between the enactment of the affordable care act in 2010 and the start of open enrollment in october 2013 due to the aca provision allowing young adults to remain on a parent’s plan until age 26. read more (pdf) healthcare.gov: rescission "rescission is the retroactive cancellation of a health insurance policy. insurance companies will sometimes retroactively cancel your entire policy if you made a mistake on your initial application when you buy an individual market insurance policy. under the affordable care act, rescission is illegal except in cases of fraud or intentional misrepresentation of material fact as prohibited by the terms of the plan or coverage." read more medicaid is expanding insurance coverage the u.s. has seen the sharpest reduction in the uninsured rate since the decade following the creation of medicare and medicaid in 1965, and the nation’s uninsured rate is now at its lowest level ever. read more to learn more about the health insurance marketplace, visit healthcare.gov. healthcare.gov healthcare.gov: how to choose a plan in the health insurance marketplace watch on youtube irs: individual shared responsibility provision read more healthcare.gov: the employer shared responsibility payment "some employers with 50 or more fte employees who don’t offer insurance, or whose offer of coverage is not affordable or doesn’t meet certain minimum standards, are subject to employer shared responsibility provisions. they may owe a payment if at least one of their full time employees enrolls in a plan through the health insurance marketplace and receives a premium tax credit." read more what marketplace health insurance plans cover any plan shown in the marketplace includes these essential health benefits. this is true for all plan categories (all “metal levels,” including catastrophic plans) and all plan types (like hmo and ppo). read more cms: chip has provided meaningful health coverage to over eight million children. "this program has helped cut the uninsured rate among children by nearly 60 percent since its start in 1997   with more than one quarter of that reduction since the president signed legislation reauthorizing the program in 2009." read more improving access to home  and community based services in recent years, the administration has expanded efforts to ensure that older adults and individuals with disabilities have access to person centered services in community settings. for example, the money follows the person rebalancing demonstration helps states rebalance their medicaid long term services and supports systems and provides opportunities for older americans and people with disabilities to transition back to the community from institutions. the affordable care act extended and expanded this program. learn more strengthening health care in indian country another critical step forward is implementing the affordable care act, which contains many important benefits for american indians and alaska natives. first and foremost, it includes the permanent reauthorization of the indian health care improvement act, ensuring that the ihs is here to stay. it also improves benefits and protections for american indians and alaska natives who have insurance, whether they receive care inside or outside the ihs. and it gives them more choices for health coverage, including medicaid and the federal employees health benefits program. read more cms: early retiree reinsurance program "the early retiree reinsurance program (errp) was included in the affordable care act (aca) to provide financial assistance to employment based health plan sponsors including for profit companies, schools and educational institutions, unions, state and local governments, religious organizations and other nonprofit plan sponsors that make coverage available to millions of early retirees and their spouses, surviving spouses, and dependents." read more kaiser family health foundation: explaining the temporary high risk pool the health reform law created a temporary national high risk pool to provide health coverage to people with pre existing medical conditions who had been uninsured for six months. it was a temporary measure designed to bridge the gap until the implementation of other coverage provisions in the law that took effect in january 2014. read more hhs: maternal, infant, and early childhood home visiting "hrsa, in close partnership with the administration for children and families (acf), funds states, territories and tribal entities to develop and implement voluntary, evidence based home visiting programs using models that are proven to improve child health and to be cost effective. these programs improve maternal and child health, prevent child abuse and neglect, encourage positive parenting, and promote child development and school readiness." read more this administration updated its comprehensive 2010 national hiv/aids strategy for the united states through 2020, and implemented it alongside requirements to cover hiv screening for millions without additional cost and prohibit discrimination due to pre existing conditions like hiv. read the updated national hiv/aids strategy: read more (pdf) what is a health center? health centers have played an essential role in the implementation of the affordable care act and continue to be a critical element of the nation’s health system. read more hhs awards more than $240 million to expand the primary care workforce the affordable care act included funding for health provider training opportunities, with an emphasis on primary care, including a significant expansion of the national health service corps. as of september 30, 2015, there were 9,600 corps clinicians providing primary care services, compared to 3,600 clinicians in 2008. read more since 2008, more than 3 million additional children have gained health insurance. children have also seen important gains in insurance coverage in recent years, thanks in large part to improvements to chip signed into law by president obama in 2009 and broader coverage expansions as a result of the aca. read more read more: the obama administration issued a national strategy and a national action plan for domestic and international efforts to prevent, detect, and control illness and death related to infections caused by antibiotic resistant bacteria. millions of americans who are enrolled in marketplace plans are receiving financial assistance to help them afford quality coverage. read more businesses with fewer than 25 employees may qualify for a tax credit worth up to 50 percent of their premium costs (up to 35 percent for tax exempt/non profit employers). read more since september of 2013, the uninsured rate for women has dropped nearly 50 percent, meaning that about 9.5 million adult women have gained coverage. read more thanks to a provision in the affordable care act, if your insurance company isn’t spending at least 80 percent of your premium dollars on medical care, they have to send you some money back. read more the affordable care act creates new incentives to promote workplace wellness programs and encourages employers to take more opportunities to support healthier workplaces. effective for plan years after january 1, 2014, final rules allow the maximum reward to employers using a health contingent wellness program to increase from 20 percent to 30 percent of the cost of health coverage, and the maximum reward for programs designed to prevent or reduce tobacco use will be as much as 50 percent. read more nearly 10.7 million medicare beneficiaries have received discounts over $20.8 billion on prescription drugs   an average of $1,945 per beneficiary   since the enactment of the affordable care act. read more cms fact sheet: medicare competitive bidding program finds $42 billion in savings "the overall savings to medicare and beneficiaries as a result of the competitive bidding program for durable medical equipment, prosthetics, orthotics, and supplies is expected to total more than $42 billion over the first ten years of the program, according to the cms office of the actuary. the $42 billion savings comes from a combination of savings of more than $25 billion in medicare expenditures, and savings of over $17 billion for beneficiaries as a result of lower coinsurance payments and the downward effect on monthly premium payments." read more the economic case for deploying new health care payment models: read more affordable care act update: implementing medicare cost savings read more (pdf) some cutting edge drugs are simply too expensive for many seniors. creating a pathway for the approval of generic biologic drugs will improve affordability of medications for seniors and all americans. read more (pdf) cms: cms expands quality data on physician compare and hospital compare to help consumers choose health care providers “consumers want trustworthy, reliable, and understandable information about the quality of health care delivered by providers,” said cms deputy administrator and chief medical officer patrick conway, m.d., msc. “both physician compare and hospital compare show consumers that they have a choice. this large release of quality measures for hospitals and physicians empowers consumers with information to make more informed health care decisions, encourages health care professionals to strive for higher levels of quality, and drives overall health system improvement.” read more patients safer as hospital acquired conditions decline​ from 2010 2015, 21 percent of hospital acquired conditions (hacs) such as adverse drug events, healthcare associated infections, and pressure ulcers have been prevented in hospital patients. reducing these hacs has saved an estimated 125,000 lives and nearly $28 billion in health care costs, according to hhs' annual report on patient safety. read more the administration set goals of tying 30 percent of traditional medicare payments to alternative payment models by the end of 2016 and 50 percent by the end of 2018, and met its 2016 goal 11 months early. read more examining medicare and medicaid coordination for dual eligibles. elder justice policy brief elder abuse is a serious public health problem affecting millions of older americans each year, with some studies suggesting that as few as one in 23 cases is reported to authorities. elder abuse is defined as intentional actions that cause harm or create a serious risk of harm to an older person (whether or not harm is intended). elder abuse encompasses physical abuse, neglect, financial exploitation, sexual abuse, as well as emotional and psychological abuse. read more cms fraud prevention initiative ​ by using innovative predictive modeling technology similar to that used by credit card companies, cms has stopped, prevented or identified $820 million in fraudulent payments over the past three years. the system identified or prevented $454 million in calendar year 2014 alone, a 10 to 1 return on investment. read more irs: new requirements for 501(c)(3) charitable hospitals under the affordable care act the affordable care act added new requirements that hospitals must adhere to in order to qualify as a 501(c)(3) charitable hospital. the new requirements provide additional benefits to patients and their communities. read more questions and answers for the additional medicare tax read more why open payments is important to you section 6002 of the affordable care act requires the establishment of a transparency program, now known as open payments. the program increases public awareness of financial relationships between drug and device manufacturers and certain health care providers. read more visit the open payments homepage. until the president made investments in health information technology by signing the american recovery and reinvestment act, our health care system ran largely on paper. now, more than 75 percent of doctors now use electronic health records thanks to administration policies. learn more about electronic health records. read more hhs.gov: hhs finalizes streamlined medicare payment system that rewards clinicians for quality patient care read more hhs finalized regulations to improve care and safety for nursing homes residents; revisions mark first major rewrite of long term care conditions of participation since 1991 the centers for medicare & medicaid services (cms) issued a final rule to make major changes to improve the care and safety of the nearly 1.5 million residents in the more than 15,000 long term care facilities that participate in the medicare and medicaid programs. the policies in this final rule are targeted at reducing unnecessary hospital readmissions and infections, improving the quality of care, and strengthening safety measures for residents in these facilities. read more remarks by the president and the vice president at the 21st century cures act bill signing "today, i could not be prouder that this legislation takes up the charge i laid out in my budget to provide $1 billion in funding so that americans who want treatment can get started on the path to recovery and don’t have to drive six hours to do it. it is the right thing to do, and families are ready for the support." watch on youtube read more samhsa to award nearly $1 billion in new grants to address the nation’s opioid crisis read more fact sheet: obama administration takes action to reduce prescription drug shortages in the u.s. read more the administration finalized a regulation to expand access to opioid treatment by increasing the number of patient's physicians who can treat with the opioid use disorder treatment medication buprenorphine. the change allows qualified physicians to prescribe buprenorphine to more patients. as of october 2016, 2,400 practitioners have applied for and been granted waivers to prescribe at the increased limit improving access to buprenorphine, which is prescribed along with psychosocial supports as part of medication assisted treatment. read more about hhs’ change here. read more the hhs also took action to enable nurse practitioners (nps) and physician assistants (pas) to begin taking the required training to prescribe the opioid use disorder treatment, buprenorphine. read more here. read more the administration also awarded $94 million in affordable care act funding to 271 health centers across the country to increase substance use disorder treatment services, with a specific focus on expanding medication assisted treatment of opioid use disorders in underserved communities. see the map of communities here. read more read the cdc guideline here. download the cdc checklist here. the administration also released an opioid overdose prevention toolkit for community members, first responders, prescribers, and patients and family members. the toolkit, developed by the substance abuse and mental health services administration, can be found here. fact sheet: obama administration announces additional actions to address the prescription opioid abuse and heroin epidemic read more additionally, the administration awarded $1.8 million to rural communities to expand access to naloxone   a drug that reverses an opioid overdose and released medicaid guidance to states identifying “best practices for addressing prescription opioid overdoses, misuse and addiction” including steps to increase the use of naloxone to reverse opioid overdose and to expand coverage of opioid use disorder treatment. read the presidential memorandum here: read more learn about the health insurance marketplace: read more hhs.gov: administration issues final mental health and substance use disorder parity rule read more the administration also finalized a rule to implement parity protections in tricare, including expanding mental health and substance use disorder treatment to include coverage of intensive outpatient programs and treatment of opioid use disorders with medication assisted treatment. read more more than 893,000 pounds of unwanted medicines or about 447 tons were collected    to help make homes safe from potential prescription drug abuse. take back days have collected and destroyed 5.5 million pounds of unused prescription drugs over five years. learn more about tack back day here: read more the administration also finalized a rule making it easier for communities to establish ongoing drug take back programs to reduce the amount of unused prescription drugs in homes. read more about the us drug enforcement administration’s final rule here. white house drug policy office funds new projects in high intensity drug trafficking areas read more read the report here. see the list of preventive services. read more the task force met with parents, advocates, clinicians, health plans, regulators and others and developed a series of action steps and recommendations for future action to help ensure that mental health and substance use disorder benefits are treated at parity with medical and surgical benefits. read more learn more about the clay hunt suicide prevention for american veterans (sav) act and the administration's commitment to help veterans. read more the white house hosts a national conference on mental health at the white house as part of the administration’s effort to launch a national conversation to increase understanding and awareness about mental health. read more in response to the executive order, va increased its mental health staffing, expanded the capacity of the veterans crisis line, and enhanced its partnerships with community mental health providers; dod and va worked to increase suicide prevention awareness and, dod, va and the national institutes of health jointly developed the national research action plan on military and veteran’s mental health to better coordinate federal research efforts. read more the mental health executive actions fell under the following six categories: fact sheet: president obama announces new executive actions to fulfill our promises to service members, veterans, and their families read more vice president biden announces $100 million to increase access to mental health services read more new investments in the recovery act, expanded through the prevention and public health fund in the affordable care act, supported public health initiatives that target heart disease, diabetes, and other conditions that afflict large segments of the population. hhs: prevention and public health fund the affordable care act established the prevention and public health fund to provide expanded and sustained national investments in prevention and public health, to improve health outcomes, and to enhance health care quality. to date, the fund has invested in a broad range of evidence based activities including community and clinical prevention initiatives; research, surveillance and tracking; public health infrastructure; immunizations and screenings; tobacco prevention; and public health workforce and training. read more fact sheet: the family smoking prevention and tobacco control act of 2009 read more fda: background on the fda food safety modernization act (fsma) the fda food safety modernization act (fsma), signed into law by president obama on jan. 4, 2011, enables fda to better protect public health by strengthening the food safety system. it enables fda to focus more on preventing food safety problems rather than relying primarily on reacting to problems after they occur. read more in 2009, first lady michelle obama planted the white house kitchen garden on the south lawn to initiate a national conversation around the health and wellbeing of the country. in time, that conversation led to let's move!. through policy, programs, public awareness, and partnerships, let’s move! is about putting children on the path to a healthy future during their earliest months and years; giving parents helpful information and fostering environments that support healthy choices; providing healthier foods in our schools; ensuring that every family has access to healthy, affordable food; and helping children become more physically active. read more the healthy, hunger free kids act updated school meal nutrition standards for the first time in 15 years and increased school meal funding for the first time in 30 years. the law boosted the quality and nutrition of meals for over 50 million children through the national school lunch and breakfast programs. its regulations substantially increased offerings of fruits, vegetables, and whole grains, and reduced the amount of saturated fat, trans fat and sodium. read more ensured that any food or beverage that is marketed on school campuses during the school day meets the smart snacks in school nutrition standards smart snacks in school standards apply to foods sold a la carte, in the school store, and vending machines. this allows schools to offer healthier snack foods to children, while limiting junk food. any food sold in schools must: be a “whole grain rich” grain product; or have as the first ingredient a fruit, a vegetable, a dairy product, or a protein food; or be a combination food that contains at least ¼ cup of fruit and/or vegetable; or contain 10% of the daily value of one of the nutrients of public health concern in the 2015 dietary guidelines for americans (calcium, potassium, vitamin d, or dietary fiber). many of the foods and beverages that have been heavily marketed to children contribute to poor diet quality, high calorie intake, and excess weight gain. foods offered and marketed to students during the school day now must be consistent with nutrition standards, so that any food or beverage that cannot be sold in school cannot be marketed in school either. read more as part of the healthy, hunger free kids act, the community eligibility provision impacts more than 18,000 schools in high poverty across the country that are eligible to serve free lunches and breakfasts to all students. it helps give 8.5 million american children access to free nutritious meals with no stigma and less time spent in cashier lines. read more first lady michelle obama announced the modernized nutrition facts label for packaged foods reflecting the latest science, the most relevant nutrition information and a refreshed design. found on nearly 800,000 products, the label had not been significantly updated since its initial release twenty years ago. read more in 2015, the food and drug administration finalized its determination that partially hydrogenated oils (phos), the primary dietary source of artificial trans fat in processed foods, were no longer "generally recognized as safe” for use in human food. food manufacturers are required to remove phos from products by 2018. this step is expected to reduce coronary heart disease and prevent thousands of fatal heart attacks every year. read more through the healthy lunchtime challenge, first lady michelle obama, in collaboration with the u.s. departments of agriculture and education and a media partner, invited children ages 8 12, with the help of a parent or guardian, to create a lunch recipe that was original, healthy, affordable, and delicious. one winner from each u.s. state, territory, and the district of columbia won the opportunity to attend the kids’ “state dinner” at the white house, where a selection of the winning recipes were served. altogether, over 6,000 recipes were submitted and more than 270 young chefs and their families were welcomed to the white house for a total of five annual kids’ “state dinners.” read more the food and drug administration (fda) food safety modernization act (fsma), the most sweeping reform of our food safety laws in more than 70 years, was signed into law by president obama on january 4, 2011. it enables fda to better protect public health by strengthening the food safety system and to focus more on preventing food safety problems rather than relying primarily on reacting to problems after they occur. read more for the first time in 20 years, the department of defense (dod) updated their nutritional standards to include more fresh fruits, vegetables, whole grains, lean meats, and low fat dairy products at the 1,100 service member dining facilities. healthier foods were also made available at dod schools and other areas where food is purchased on military bases, such as snack bars and vending machines. read more the agricultural act of 2014 was enacted february 7, 2014. the law reauthorizes the supplemental nutrition assistance program (snap), the largest program in the domestic hunger safety net. it offers nutrition assistance to millions of eligible, low income individuals and families and provides economic benefits to communities. the reauthorization of snap preserved the fundamental structure of the program, and made a number of new investments such as providing $200 million for snap employment and training pilots to help participants find jobs and increase earnings, testing on line grocery purchases, enhancing retailer standards, and helping participants stretch their dollars to purchase more fruits and vegetables. read more farmers’ markets and farm stands can now accept government benefits such as snap and coupons from participants in the women, infants and children program from an electronic system. read more during the school year, millions of children receive nutritious free and reduced price school meals through the usda. however, less than a fifth of these children receive meals through usda’s summer meals programs when school is out of session. as a result, low income children are at higher risk of food insecurity and poor nutrition during the summer. the summer ebt demonstration project is meant to help bridge that gap. it has showed a significant reduction in food insecurity among participating families and led to positive changes in children’s nutrition. read more the healthy food financing initiative (hffi) has brought grocery stores and other healthy food retailers to low income, low access communities in urban and rural communities across america. without alternatives, residents of these communities often have to travel long distances to shop or rely on fast food restaurants and convenience stores that offer little or no fresh food. with technical assistance, improved access to capital, and financial support for retailers and other businesses in the food supply chain, hffi is expanding access to nutritious food in these communities. read more president obama asked each member of his cabinet to write an exit memo on the progress we’ve made, their vision for the country’s future, and the work that remains in order to achieve that vision. here are their key points on the work ahead to improve health for all americans. building on the progress of the aca “repealing the aca, as some have suggested, risks rolling back consumer protections   like making it illegal to discriminate against those with pre existing conditions and improving benefits   for americans who get health insurance through the marketplace, medicare, medicaid, or on the job. a recent study shows nearly 30 million americans would lose their coverage under one version of repeal as well. we can work together to make the system even better, but we should build on the progress we’ve made, not go backwards.”  secretary burwell reforming the health care delivery system “building on the successful models developed during this administration, while seeking out opportunities to extend value based payment to an even broader range of providers and health care services, including high cost drugs, not only benefits patients but allows clinicians the flexibility to practice medicine in the way that best meets the needs of their patients. the passage of macra was a monumental step forward in the effort to reward quality and value in physician payments; however, additional federal legislation should be considered that would use payment incentives to drive the delivery of value based health care throughout the entire health care system, improve the interoperability of data, and integrate care.”  secretary burwell developing precision medicine “the next great revolution in medicine will emerge from an ability to use genomic, lifestyle, behavioral, environmental, imaging, and clinical data to understand health and disease, and to use those insights to develop tailored prevention approaches and medical treatments.”  director holdren continuing the fight against opioids “in late 2015, president obama appointed me to lead an interagency federal effort focused on the rural heroin and prescription opioid crisis. in 2014 alone, we lost 28,648 lives too soon and according to nih, the epidemic incurs $72 billion in health costs each year. the opioid crisis disproportionately affects rural communities in part due to the lack of outreach and treatment resources available in remote areas. after hearing from mothers and fathers who've lost their children to opioid misuse, and listening to mayors and medical personnel appeal for greater treatment resources, it's clear that rural communities need our help.”  secretary vilsack combating the global threat of infectious diseases “continued high level u.s. leadership will be critical to maintain momentum and further institutionalize the gains that have been made, including through support to who and partners for external evaluations and country planning. u.s. leadership should include working with partners to follow through on their commitments, emphasizing the importance of country preparedness as a national priority, and highlighting the need for sectors beyond health, including the animal health, development, security, technology, and foreign affairs sectors, to support this work. strengthening the multi sectoral approach will benefit long term health systems and the ability to respond effectively to outbreaks.”  secretary burwell

thank you for visiting nature.com. you are using a browser version with limited support for css. to obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in internet explorer). in the meantime, to ensure continued support, we are displaying the site without styles and javascript. nature aging volume 4, pages 1635 1642 (2024)cite this article 103k accesses 2959 altmetric metrics details over the course of the twentieth century, human life expectancy at birth rose in high income nations by approximately 30 years, largely driven by advances in public health and medicine. mortality reduction was observed initially at an early age and continued into middle and older ages. however, it was unclear whether this phenomenon and the resulting accelerated rise in life expectancy would continue into the twenty first century. here using demographic survivorship metrics from national vital statistics in the eight countries with the longest lived populations (australia, france, italy, japan, south korea, spain, sweden and switzerland) and in hong kong and the united states from 1990 to 2019, we explored recent trends in death rates and life expectancy. we found that, since 1990, improvements overall in life expectancy have decelerated. our analysis also revealed that resistance to improvements in life expectancy increased while lifespan inequality declined and mortality compression occurred. our analysis suggests that survival to age 100 years is unlikely to exceed 15% for females and 5% for males, altogether suggesting that, unless the processes of biological aging can be markedly slowed, radical human life extension is implausible in this century. before the middle of the nineteenth century, life expectancy at birth for humans languished at low levels by today’s standards between 20 years and 50 years1. improvements in survival were slow, punctuated often by episodic pandemics, plagues and contagions. advances in public health and medicine in the early twentieth century spawned a longevity revolution characterized initially by large and rapid increases in life expectancy at birth (e(0)). e(0) increased at an accelerated rate, from an average of 1 year every one or two centuries for the previous 2,000 years to 3 years of life added per decade during the twentieth century (referred to a ‘radical life extension’). the variable pace of improvement in e(0) was influenced by geographic location, economic development and temporal factors2. this historic event began with reductions in early age mortality and continued later in the twentieth century with mortality improvements at middle and older ages3. given the profound influence of this longevity revolution on human society, one of the central questions in science, aging and public health today is: how much longer are humans capable of living? this is not a new question. estimates of the highest theoretical life expectancy limits for national populations under optimal conditions is an exercise that dates back to the early twentieth century (for details, see supplementary note 1). accurately predicting future life expectancy trends holds important implications for societal, health and economic policies. in the united states, longstanding policy discussions have been held to address the potential consequences of how modulating biological aging could affect population demographics and related social institutions4,5,6. accelerated population aging is already upon us; the absolute number of people reaching older ages continues to grow rapidly7; and the practical implications of such an intervention continue to deepen. in 1990, it was hypothesized that humanity was approaching an upper limit to life expectancy (the limited lifespan hypothesis) in long lived populations, as early gains from improved public health and medical care had largely been accomplished, leaving biological aging as the primary risk factor for disease and death; the rate of improvement in life expectancy was projected to decelerate in the twenty first century; and e(0) for national populations would not likely exceed approximately 85 years (88 for females and 82 for males) unless an intervention in biological aging was discovered, tested for safety and efficacy and broadly distributed8. these conclusions were later supported by observed mortality dynamics in the united states, france and japan from 1990 to 20009. claims were subsequently made that this limited lifespan view did not take into account ongoing advances in medicine and biology, that radical life extension (operationally defined here as a 0.3 year annual increase in period life expectancy at birth based on historical improvements in e(0) in long lived populations in the twentieth century) had already begun10 or that it would soon occur due to the discovery and deployment of life extending medical technologies and/or result from ongoing population based improvements in behavioral risk factors11. it was further predicted that most newborns today will live to ages 100 plus years12 and that ‘… there is simply no convincing evidence (demographic, biological or otherwise) of a lower bound on death rates other than zero’13. three decades have now passed since the limited lifespan hypothesis was proposed. however, the debate continues between the limited lifespan and the radical lifespan extension hypotheses. in the present study, we used standard demographic survivorship metrics14,15 from the eight countries with the longest lived populations and from the special administrative region (sar) of hong kong and the united states, from approximately 1990 to 2019, to address which hypothesis about human longevity is supported by these data. we then used this analysis to predict whether radical life extension is likely to occur again in this century. we used twentieth century increases in e(0) as a historical frame of reference. in this analysis, we addressed the following questions. (1) has radical life extension occurred at any time in the world’s longest lived populations and in the united states from 1990 to 2019? (2) is it plausible that most newborns today will live to age 100 years? (3) what is the rate of change in future mortality rates required to raise life expectancy at birth by 1 year? (4) what must human survival look like if radical life extension occurred again at any time in this century, and how plausible is this scenario? (5) has the distribution of death in the longest lived populations (measured by lifespan inequality) compressed in the last three decades or has it been expanding and shifting uniformly to later ages? observed annual age specific and sex specific death rates and period life expectancy at birth from 1990 to 2019 (the latter year was chosen to eliminate the effects of coronavirus disease 2019 (covid 19)) in the eight countries with the longest lived populations (that is, australia, france, italy, japan, south korea, spain, sweden and switzerland) and in hong kong and the united states were chosen for this analysis (displayed here are annual changes in e(0)). data were derived from the human mortality database16. using these data, we found that the only populations to experience the required 0.3 year annual improvement or 3.0 year decennial improvement in life expectancy that operationally defines radical life extension (see supplementary note 2) were south korea and hong kong17. in hong kong, this was largely due to economic prosperity and tobacco control but, even then, only from 1990 to 2000 (fig. 1). in every population, including hong kong, the most recent decade of change in life expectancy is slower than it was in the last decade of the twentieth century. in every population but hong kong and south korea, the annual rise in e(0) has decelerated to below 0.2 years annually. source: human mortality database (2019 complete life tables by sex). threshold annual improvement in life expectancy at birth of 0.3% is required to demonstrate that radical life extension has been or is occurring. the rate of improvement in life expectancy at birth has decelerated in every population except hong kong. the dashed line indicates the average annual change in e(0) associated with ‘radical life extension’. the average increase in e(0) from 1990 to 2019 in hong kong and the eight countries with the longest lived populations was 6.5 years. the united states is one of only a handful of countries documented to have experienced a lower life expectancy at birth at the end of any decade relative to the beginning of the same decade. this phenomenon also occurred in the early and middle part of the twentieth century but was historically caused only by extreme events (for example, the spanish flu and war related deaths). in the united states, it was uniquely caused by a combination of increases in mortality at middle ages18 during the period 2010 2019 and then exacerbated by covid 19 in 2020. percentage survival to age 100 was derived from the l(x) (survivorship) columns of complete life tables for all nine countries and hong kong using period life tables in 2019 published by the human mortality database. in these populations, we found that the average probability of current birth cohorts surviving to age 100 is 5.1% for females and 1.8% for males (fig. 2). the highest population specific probability of surviving to 100 occurred in hong kong where 12.8% of females and 4.4% of males are expected to reach age 100 in their lifetime based on life tables from 2019. across these eight countries with the longest lived populations and in hong kong and the united states, we found no population that comes close to 50% survival to age 100 (fig. 2). each line represents the proportion of each population in an annual life table who would survive to age 100 from 1990 to 2019. the reduction in total mortality required to yield identical 1 year increases in e(0) is based on data from the human mortality database for the populations evaluated here. the percentage reductions were derived by reducing total mortality at all ages, in each country, from as far back as 1750 (when the data existed) to 2019 until e(0) increased by 1 year. in hong kong and all nine countries evaluated here, we found that the percentage reduction in total mortality required to raise e(0) by 1 year has actually increased relative to 1990 (fig. 3). the panel on the left illustrates how much death rates from all causes at all ages are required to decline for females to add 1 year to life expectancy at birth; the panel on the right shows the same results for males. the black vertical lines are indicators of beginning of a century. as an illustration of the conditions present in most long lived populations, we used period life tables for japan in 2019 to calculate how much total mortality would have to decline, by gender, to experience a 1 year increase in e(0). if e(0) for females reaches 88 years in countries with long lived populations, the magnitude of the reduction in death rates would be stark. mortality from all causes at all ages required to raise life expectancy to 89 years for females would be 20.3%. for males, a rise from 82 years to 83 years would require a reduction in total mortality at every age of 9.5%. the demographic rationale and the analytic derivation of lifespan metrics were derived from complete life tables published by the human mortality database from 1950 to 2019. they include the log of e(0) calculated as a function of life table entropy (h*) and lifespan inequality (φ*) in accordance with equation (1), as shown in the methods section. we estimated life table entropy using standard demographic techniques14,15,19,20. the metrics that measure life table entropy (the dynamics of lifespan) are illustrated for the populations evaluated here from 1950 to 2019 in figs. 4 and 5a,b. shown is the log of life expectancy at birth in the eight countries with the longest lived populations and in hong kong and the united states (1950 2019). a, annual changes in life table entropy for all 10 populations from 1950 to 2019. b, annual changes in lifespan inequality for the same populations and time periods. first, our analysis showed that the log of life expectancy at birth (log e(0)) increased continuously from 1950 through 2019 in all populations assessed (fig. 4). this occurred at the same time period that life expectancy at birth decelerated in all countries with long lived populations and maximum lifespan stagnated21. second, we found that the metric of life table entropy (h*) increased steadily from 1990 to 2019 (fig. 5a). this likely occurred for a variety of reasons that are expected in humans: better health conditions, improved risk factors, medical technology, etc. however, h* increased, converged and stabilized at a common higher level in all long lived populations, demonstrating that the force of life table entropy as a limiting force on rising life expectancy is greater today than it was in 1990. third, we evaluated lifespan inequality (also known as lifespan variation, φ*)20. when φ* declines, this represents empirical evidence that the mortality/survival distribution is compressing and the rise in life expectancy may be decelerating; when φ* increases, this represents empirical evidence that the mortality/survival distribution is extending to later ages and the rise in life expectancy may be accelerating. as shown here (fig. 5b), for the 69 year period from 1950 to 2019, φ* declined uniformly and consistently in all long lived populations, at the same time life expectancy was rising. this fact demonstrates that age at death has, in fact, been compressing into a shorter window of time at the outer reaches of human survival. it is theoretically possible for future mortality distributions to shift toward later ages, but the evidence is not supportive. life expectancy has not increased since 1990 at a rate that defines radical life extension, nor is it likely to do so unless breakthroughs occur in retarding the rate of human aging. we generated a hypothetical survival distribution assuming radical life extension occurs again and e(0) rises to 110 years, using data from the human mortality database for a population of japanese females observed in 2019. if e(0) were to hypothetically reach 110 years, death rates at all ages from all causes of death combined up to age 150 years (for example, decades beyond the observed survival distribution for humans) would need to be 88% lower than the observed death rate at age 109 in japan in 2019. this level of mortality would require the complete cure or elimination of most major causes of death that exist today. our analyses demonstrate that a second wave of radical life extension, yielding a life expectancy at birth of 110 years at any time in the future, requires survival to age 100 by about 70% of females (fig. 6, a). survival to the age of 122.45 years the maximum lifespan observed for humans as determined by the documented survival of jeanne calment, who died in 1997 (ref. 22) would need to be achieved by over 24% of females to observe a life expectancy at birth of 110 years (fig. 6, b). radical life extension would also require about 6% of females to survive to ages 150 plus 28 years beyond the observed documented longest lived human in history (fig. 6, c). evidence for radical life extension requires a mortality distribution that is dramatically different from observed mortality distributions observed among the longest lived human populations (denoted by a). a mortality distribution for a population experiencing radical life extension today requires just over one fourth of the birth cohort surviving beyond the age of the maximum lifespan for the species (denoted by b). approximately 6 7% of the birth cohort would need to survive to age 150 to achieve radical life extension (denoted by c). a composite complete mortality schedule for humans (and related period life tables from ages 0 109 years for males and females) was compiled using the lowest age specific and sex specific mortality observed among all countries in the world based on period life tables published by the human mortality database for 2019. the life expectancy at birth associated with these composite mortality schedules as of 2019 is 88.68 years for females and 83.17 years for males. higher potential life expectancies of 91.6 years for females and 86.1 years for males were estimated by canudas romo et al.23 for the year 2039. we found that the composite highest life expectancy mortality schedules in 2019 yield 13.9% survival to age 100 for females and 4.5% for males. if death rates were zero from birth through age 50, the composite highest life expectancy at birth would be 89.7 for females and 84.7 for males. that is, reducing death rates to zero for the first 50 years of life adds 1.0 years to the composite most favorable life expectancy of females and 1.5 years to the composite most favorable life expectancy of males. this composite set of death rates is nearly identical to a ‘best practice’ life expectancy used to justify forecasts of much higher life expectancies than those observed today24. breaking through to death rates below those shown here at ages 0 65 to levels sufficient to have a meaningful influence on life expectancy at birth is viewed as implausible given observed trends in death rates at these ages in the past three decades in the longest lived populations in the world. death rates beyond age 65 years can still plausibly go lower than the composite lowest death rates shown here25, but the magnitude of such declines would have to accelerate across time to generate an increase of 3 years per decade to reach the formal definition of radical life extension. this accelerated mortality improvement at older ages has not happened in the last three decades. although a formally defined mortality floor cannot as yet be operationalized at older ages, there is evidence to suggest that such a floor does indeed exist, and it is not likely too far from the best practice composite death rates published here and by multiple other research teams that explore death rates and life expectancy for humans under optimal conditions (supplementary note 1). more than three decades have passed since predictions were made about the upper limits to human longevity. evidence presented here based on observed mortality trends in the worldʼs eight longest lived populations and in hong kong and the united states, and metrics of life table entropy, indicate that it has become progressively more difficult to increase life expectancy. the life table indicators are not only still operational; they are, in fact, a stronger limiting factor to rising e(0) today than they were in the late twentieth century. although some countries have approached or reached the ‘limits’ to life expectancy that we hypothesized decades ago8, we found that, even in these countries, the rate of improvement in life expectancy has decelerated. at ages 65 and older, the observed average rate of improvement in old age mortality in the longest lived populations evaluated here was 30.2% from 1990 to 2019. the impact of this level of mortality improvement, if experienced again over the next three decades, would yield only a 2.5 year increase in e(0). this is a fraction of the 3 year per decade (for example, 8.7 year increase from 1990 to 2019) gain in life expectancy predicted by those claiming that radical life extension was forthcoming or already here10. that is, old age mortality has not been declining since 1990 at a pace that is even close to the rate of improvement required to achieve radical life extension in this century. it is worth noting that radical life extension as defined here may occur in this century in some of today’s low income or middle income nations. this would be a product of experiencing the first longevity revolution in which death rates at younger and middle ages can still be reduced dramatically. the importance of a mortality floor (referred to as a soft limit that can be breached by medicine and public health advances) shown here should be considered carefully by insurance companies and actuarial firms tasked with forecasting mortality improvement factors. these impact current carriers of life insurance and also the valuation of current and future insurance applicants’ policies26. if mortality improvement assumptions generated by organizations involved in survival forecasts yield age specific and sex specific death rates below the thresholds shown in supplementary table 1, justification for breaking through the current mortality floor should be required. moreover, as shown in fig. 5a,b and equation (1), the logarithm of life expectancy can be decomposed into the sum of two terms where the first, life table entropy, is the dominant component in mortality improvements and the rise in life expectancy. when forecasting assumptions about life expectancy are based on a linear increase from past trends, then, by definition, the rate of improvement in death rates must accelerate, and metrics of life table entropy must improve accordingly. our empirical measures of the rate of change in life expectancy and life table entropy in the current analysis demonstrate that this is not the case. this means that extrapolating the metric of life expectancy from the past into the future is likely to yield overestimates of e(0) and survival, because this method of forecasting ignores the fundamental relation between life expectancy and the demographic metrics of life table entropy and lifespan inequality described here. this is why forecasts of longevity should be based on anticipated changes in death rates rather than linear projections of the metric of life expectancy. there are limitations to this study, in particular related to the future. first, there can be no dispute that life expectancy improvements have decelerated since 1990. our analysis clearly demonstrates that this finding runs counter to predictions that it was going to accelerate. where uncertainty remains is how much more survival time can be manufactured with the disease model that now prevails (shown here to have a declining influence on life expectancy) and the far greater uncertainty associated with future improvements in survival that may result from the deployment of gerotherapeutics or other advances in medicine that cannot be conceived of today. because radical lifespan extension brought forth by yet to be developed medical advances cannot be empirically evaluated over short timeframes, a limitation here (and within the field of aging in general) is that it is difficult to justify any numerical estimate of their future influence on life expectancy. although limits to human life expectancy were discussed previously27, it is important to note that these limits do leave room for such advances in medicine (treating disease or targeting the underlying causes of aging28,29 and improved behavioral risk factors) that could further improve mortality at older ages (that is, these limits are not brick walls10 for longevity). importantly, these limits should not be interpreted from an evolutionary perspective to mean that there is no longevity value in achieving grandparenthood30,31, that the post reproductive period should necessarily be short32 or that the occurrence of chronic conditions of aging are driven by a force of selection to just beyond the upper edge of the reproductive window, in accordance with the antagonistic pleiotropy, mutation accumulation and disposable soma hypotheses33,34,35. a naturally occurring life expectancy of a human population in the absence of any form of medical intervention throughout the course of life is unknown, but it would be expected to be far below the life expectancies observed in high income nations today. as such, recent increases in e(0) are likely to be a result of the addition of what has been referred to as manufactured time survival time brought forth by medical and public health interventions9. the notion of a limit to life expectancy present today represents something akin to a glass mortality floor or a second soft limit to longevity that has become increasingly less sensitive to modifications through the treatment of diseases but that should be amenable to modification through changes in the rate of biological aging. the evidence presented here indicates that humans are approaching a second soft limit using the very criteria set forth by those who have argued for the last three decades that either there is no limit to human longevity or, if there is one, it was not then in sight (supplementary note 3). forecasts about radical life extension in humans thought to be occurring now or projected to do so in the near term have already influenced the operations and financial structure of multiple industries36. results presented here indicate that there is no evidence to support the suggestion that most newborns today will live to age 100 because this would first require accelerated reductions in death rates at older ages (the exact opposite of the deceleration that has occurred in the last three decades). furthermore, even if the 30.2% improvements in mortality in the 65 and older population observed to have occurred in high income nations from 1990 to 2019 occurred again, only a small fractional increase in survival to age 100 would ensue. changes in existing institutions that rely on lifespan estimation, such as retirement planning37 and life insurance pricing constructed with a 100 year lifespan assumption as its foundation, are likely to be overestimating survival by a wide margin for most people38. it would be optimistic if 15% of females and 5% of males in any human birth cohort could live to age 100 in most countries in this century (even if any of the recently estimated composite best practice death rates are achieved under optimal conditions) a limit that could theoretically be breached but only if gerotherapeutics are developed that slow biological aging. even then, survival to age 100 for most people is not a certainty. at a practical level, it is not feasible to test whether any current or future gerotherapeutic could extend human lifespan to over 100 years because of the time required to empirically verify life extending properties of this magnitude. in fact, the efforts of the national institute on aging interventions testing program (itp) demonstrated that potential therapies have limited efficacy in safely extending mouse lifespan. of 50 compounds so far tested, only 12 have increased lifespan (in either sex), none by more than 15% (ref. 39). increases in life expectancy at birth in countries with long lived populations should not be confused with anticipated increases in the absolute number of people reaching older ages in this century40. the rising prevalence of older cohorts will accelerate across the globe in this century as a byproduct of larger birth cohorts born during the twentieth century41 moving up the age structure and as a result of improvements in survival at extreme old age due to medical advances. large increases in the centenarian population across the globe, for example, can reliably be predicted to start in 2042, as this will mark the 100 year anniversary of the beginning of the post world war ii baby boom. it is suggested here that humanity’s battle for a long life has largely been accomplished. this is not a pessimistic view of a longevity game over or that further mortality improvements at all ages (especially at older ages) are no longer possible or that healthspan can no longer be improved through risk factor modification or reductions in survival inequalities. rather, it is a celebration of more than a century of public health and medicine successfully allowing humanity to gain the upper hand on the causes of death that have, thus far, limited human lifespan. the evidence presented here indicates that the era of rapid increases in human life expectancy due to the first longevity revolution has ended (supplementary note 4). given rapid advances now occurring in geroscience42, there is reason to be optimistic that a second longevity revolution is approaching in the form of modern efforts to slow biological aging, offering humanity a second chance at altering the course of human survival. however, until it becomes possible to modulate the biological rate of aging43 and fundamentally alter the primary factors that drive human health and longevity44, radical life extension in already long lived national populations remains implausible in this century. the link between improvements in age specific death rates and life expectancy at birth (e(0)) is based on the following fundamental characterization, namely: where h* denotes life table entropy, and φ* is the lifespan inequality. the analytic expression for these concepts was first developed more than a half century ago15; the lifespan inequality was later applied in an influential study of human longevity by gender45, followed more recently by a comprehensive review of these various metrics14. the central parameters in the study of the age survivorship function l(x) are as follows: the mean lifespan, the life table entropy and the lifespan inequality. the mean lifespan is given by the life expectancy e(0) can be expressed in terms of the ‘entropy’ function h*, and an indicator of the distribution of ages at death (lifespan inequality) φ*, with the following relationship: empirical studies20,46 of these life table metrics, as illustrated in figs. 4 and 5a,b, are consistent with the following expected changes in the life table parameters during a time when a population’s health status is improving. life expectancy at birth, e(0), should increase. life table entropy, h*, a positive correlate of the mean lifespan under ideal conditions, should increase. lifespan inequality, φ*, should decrease. these three principles, and the fundamental linkages among the three metrics expressed in equation (1), indicate that radical changes in lifespan, as defined here, are contingent upon the rates at which the life table entropy and lifespan inequality change over time. we invoke these principles to empirically evaluate the plausibility of radical lifespan extension in long lived populations. observed annual age specific and sex specific death rates and period life expectancy at birth from 1950/1990 to 2019 (the latter year was chosen to eliminate the effects of covid 19) were used in this study. data were derived from the human mortality database that include the longest lived populations in the world. the longest lived populations chosen for this analysis were australia, france, hong kong, italy, japan, south korea, spain, sweden and switzerland. if radical life extension has been occurring since 1990, it would most likely be observable in these populations. the united states was included because some scientists made specific predictions about radical life extension in this country. period life tables are preferred as the frame of reference because contemporary cohort life tables are accompanied by assumptions about future death rates (especially at older ages), and it is these very assumptions that are the subject of inquiry in this analysis. the dramatic increase in life expectancy in humans occurred mostly during the twentieth century. in the populations evaluated here using data from the human mortality database, the annual rate of increase in e(0) for males and females combined from 1900 to 2000 was about 0.33. of note, there was considerable variation in the timing with which these improvements in life expectancy occurred across these populations in the twentieth century (for example, the japanese, hong kong and south korean populations concentrated their large increases in life expectancy only in the last quarter of the twentieth century). thus, a 0.3 year annual rate of improvement in e(0) is considered a conservative operational definition of radical life extension. a hypothetical survival distribution assuming radical life extension occurs again and e(0) rises to 110 years was estimated using the following data and assumptions. (1) data were drawn from a population of japanese females observed in 2019 from the human mortality database intended to be representative of any long lived population. (2) period life expectancy at birth was assumed to rise to 110 years at an unspecified date in the future (which, in this case, was a 22.54 year increase from female life expectancy at birth observed in japan in 2019). (3) death rates at ages 110 150 years were assumed to remain constant at the level observed at age 109 in 2019 but then reduced proportionally in accordance with (4). (4) death rates were reduced equally at all ages (including from ages 109 150) until e(0) reached 110. the estimated life table with radical life extension was closed at age 150. a composite complete mortality schedule for humans (and related period life tables from ages 0 109 for males and females) was compiled using the lowest age specific and sex specific mortality observed among all populations in the world based on period life tables published by the human mortality database for 2019. more recent years, although available in many cases, were not used as a way to avoid the negative influence of covid 19 on the composite lowest mortality schedules. the results of the analyses presented here may be replicated using the data from the cited sources and the formulas presented above. the national vital statistics data for the nine countries and hong kong represent entire resident populations; data were not excluded from the analyses. the researchers were not blinded to the datasets during analysis. the population sizes for the populations evaluated ranged from a low of 7.3 million for hong kong to a high of 339 million for the united states. further information on research design is available in the nature portfolio reporting summary linked to this article. the data required to replicate the findings presented here include the human mortality database (https://mortality.org/). all data supporting the findings of the study are available from the corresponding author upon reasonable request. riley, j. c. rising life expectancy: a global history (cambridge univ. press, 2001). riley, j. c. estimates of regional and global life expectancy, 1800 2001. popul. dev. rev. 31, 537 543 (2005). article google scholar eggleston, k. n. & fuchs, v. r. the new demographic transition: most gains in life expectancy now realized late in life. j. econ. perspect. 26, 137 156 (2012). article pubmed pubmed central google scholar social policy, social ethics, and the aging society (eds neugarten, b. l. & havighurst, r. j.) 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podcast nobel prize winning scientist explains how our quest to slow aging is becoming a reality april 18, 2024 they’re perhaps the oldest questions in the science: why do we die? and could we find a way to live forever? but for decades, anti aging research was a “backwater” of the scientific community, consider too fanciful and unrealistic. that is until the last few years. modern advances in biology have taught us a lot about how we age and why we die could that knowledge help us turn back the clock? in his new book, “why we die: the new science of ageing and the quest for immortality”, nobel prize winning scientist venki ramakrishnan delves into the latest science of aging and investigates the nearly $30 billion dollar longevity industry to separate fact from fiction in our modern quest for immortality. venki ramakrishnan: it’s a question that has bothered humanity ever since we were aware of mortality. paul rand: that’s venki ramakrishnan, a nobel prize winning structural biologist. venki ramakrishnan: we are the only people who know that we have a certain lifespan. ever since we discovered that we have worried about it. paul rand: he’s the head of the mrc laboratory of molecular biology in cambridge, england, and the author of a fascinating new book, why we die. venki ramakrishnan: most of our history, there was nothing we could do about it, death and taxes that were just taken for granted. it’s only in the last 40 or 50 years that because of all the advances in biology, we’re understanding really what is the basis for why we age and die. and that’s a foundation for being able to do something about it. tape: if you would like to live longer, maybe to 100 and in good health, there is real science now that is claiming this might be possible. a breakthrough in reversing the signs of aging. researchers say that they found a way to make mice look and even feel younger. tape: we want to talk to these mice. venki ramakrishnan: aging used to be a kind of backwater field. it was not considered serious biology, but now because of modern tools, we’re actually able to make it into harder science. and so more and more mainstream biologists are going into aging research. all of those things have come together to create this, what you might call a moment. paul rand: today, there are more than 700 biotech companies focused on aging and longevity with the combined market cap of at least $30 billion. venki ramakrishnan: i think these billionaires are used to success, especially these tech billionaires, achieve success very early in life. they think that life is just some sort of software to be hacked, but biology is complicated. and there is this old saying that when they were young, they wanted to be rich, but now they’re rich, they want to be young. and of course, you can’t buy youth, but you can buy aging research. and so they’re investing heavily in aging research. paul rand: with all this investment in hype in the anti aging industry, it can be difficult to figure out what’s really going on. many of the top distinguished scientists in the field now have financial stakes in these companies, but ramakrishnan does not. and with his expertise in structural biology, he may be one of the best experts to tell us what’s real and what the future of anti aging may look like. venki ramakrishnan: there’s so much interest in aging and there’s also so much hype. so i thought, well, let me look at all the molecular biology because i’m so close to it that i can read the papers and understand what’s absolutely solid and what’s iffy and what’s really unlikely. and i think what my book tries to do really is give people an understanding of the fundamental principles so that when they come across the next big discovery or read about something in some magazine or newspaper or listen to it on a podcast, they can connect it with what they know about what’s going on in ourselves. so it’s really giving them the tools almost for how to live and what to do and how to understand aging. paul rand: welcome to big brains, where we translate the biggest ideas and complex discoveries into digestible brain food. big brains, little bites from the university of chicago podcast network. i’m your host, paul rand. on today’s episode, why we die, how we age, and what we can do about it. big brains is supported by uchicago’s online master of liberal arts program, which empowers working professionals to think deeply, communicate clearly, and act purposely to advance their careers, choose from optional concentrations and ethics and leadership, literary studies and tech and society. more at mla.uchicago.edu. everything alive ages, everything alive dies. at first glance, this seems to be an immutable fact of nature, but it turns out things aren’t that straightforward. venki ramakrishnan: we’ve wondered about, for example, what makes life spans so different? sharks and whales, some of them can live several hundred years. a giant tortoise lives 170 plus years, and then at the other end, you have a mayfly that lives for a day and then you have a mouse that lives for two years, but a bat the same size can live for 40 years. so i think the idea that we’re all made of the same material but we age differently, suggests that we could do something about it, and that requires understanding the basis of aging. paul rand: the first step in figuring out what we can do about aging is understanding what it really is. the problem of aging isn’t just one cause and it’s not just a single negative process in our bodies. in fact, many of the causes of aging are the very same things that keep us alive when we’re young. venki ramakrishnan: biology has a bias. its main selection is for making sure that the genes we have are passed on. so it’s about the survival of our genes. it doesn’t much care what happens later on in life. so you can see throughout biology, throughout all the causes of aging, there’s always this delicate balance between what’s good for you early in life and what causes aging later. and if you start tinkering with one, you might affect the other. paul rand: untangling this complicated web of multiple causes starts by figuring out how each strand works, and one of the most fundamental strands is dna damage. venki ramakrishnan: absolutely. so if you look at the program of life and of all our cells, it’s encoded in our genes, and that program is there to make all of the proteins that are required for life. we require proteins for almost every function we carry out, including thinking and remembering and fighting infections, not just our muscles. so think of dna as a long string of letters. they’re chemical letters. dna uses four kinds of units. and so you can think of it as a long code written in a four letter alphabet. if you have environmental attack on the dna, it doesn’t even have to be from carcinogens, it could be just in the natural process of living. it’ll corrupt some of those letters in the dna. paul rand: over the course of one single day, 100,000 changes happen to the dna in each of our cells. in fact, just exposure to water can cause 10,000 transformations. venki ramakrishnan: in other words, some of those elements of dna will be changed, others will be removed, and sometimes the dna will be broken, so it’ll be like you have a long sentence and then the sentence is suddenly broken and you don’t know how it ends and you don’t know where the rest of the sentence is. and as we age, those errors build up and this leads to proteins that are the wrong protein. the proteins have mistakes or they’re made at the wrong time, or they’re made in the wrong amounts, or they’re not degraded when they should be. so the program, which is this orchestra of proteins that all have to work together is slowly breaking down. so you get a discordant dysfunctional orchestra if you like. paul rand: but if our dna is being constantly damaged like this, how do we even make it through a single day, let alone years? the answer is that our body has developed ways to repair dna. the problem is, this repair response is itself a cause of aging. venki ramakrishnan: one of the big risks if you have dna damage is cancer. you have over a trillion cells in your body. if a few million of them die, you’re not even going to notice it. in fact, they die all the time. but if one of those cells becomes cancerous, it could kill you. it could kill the whole organism, right? so preventing cancer early on is quite important. so when the cell senses dna damage, the first thing it does is try to repair the dna. but if it senses that the damage is too extensive, then it triggers a series of responses which have two possibilities. one is, it just sends a cell into death. it’s called apoptosis. it’s a kind of cellular suicide. so the cell basically dies. the other is that it sends a cell into a state called senescence. these cells are not dead, they’re not even dormant. they just can’t divide and they can’t carry out their normal function. but one thing they do is they secrete inflammatory compounds because what they’re trying to do is attract the immune system to the site of it. and so it’s a signal to the body to say, “hey, there’s a problem here. this cell is sending an alarm signal. go there, deal with it and then you can clear it away.” now, as we get older, that mechanism itself deteriorates. and so we start accumulating these senescent cells and so we have more and more inflammation as we get older, and that’s one of the major problems with aging. paul rand: studies have shown that transplanting even small numbers of senescent cells into young mice cause persistent dysfunction. venki ramakrishnan: so the dna damage response is a curious thing. paul rand: this balance between aging and cancer is one that keeps coming up again and again for researchers. many of the possible ways to turn back the clock lead to an increased risk of cancer, and many of the ways our body fights cancer lead to aging. in fact, some cancer therapies actually work by inhibiting dna repair mechanisms. venki ramakrishnan: if you inhibit dna repair pathways, that’s detrimental to the cancer cell and preferentially it kills off cancer cells. so it’s a paradox. but of course, you can’t inhibit dna repair for the sake of aging because you really want dna repair to work well. paul rand: but there are other mechanisms around dna that may be more promising. one has to do with something called dna methylation. venki ramakrishnan: with time, our dna gets additional chemical marks. some of them are called methyl groups, so they’re called methylation. these additional marks are signals to either inhibit the expression of some genes or sometimes to enhance it. and it turns out, dna methylation seems to be a better indication of your age. it correlates better, for example, with mortality with late life diseases, than just chronological age. because we all know there are 70 year olds who are very spry climb mountains and stuff, and others who are really not in good shape at all. so the places where their dna is methylated on their genome, that pattern will be different for the two people. there’ll be probably more methylation in the person who has aged more compared to the person who’s aged less. they are inhibiting more of their genes by methylation. and of course, you need many of these genes in order to function. and people are asking, if we were to reverse the pattern of methylation, could we in fact reverse aging? that’s the theory anyway. but in order to test it, what you would have to do is be able to reverse that methylation and see if somehow the symptoms of aging improved. okay, that hasn’t quite been done, but people are working on that. and if that works, it would be a way to turn the clock back a little bit. now, one reason to think that there’s something there, is one place where all our methylation gets erased completely, is when we give birth to a new generation. so when you have a fertilized egg, it goes through a program where all the methylation marks on the original donor cells are erased, and it starts all over again. and that’s why a child born to a forty year old woman is not 20 years older than a child born to a twenty year old woman. they’re both starting at zero, and it’s because the aging clock has been reset in both of them. paul rand: there’s another piece of our dna that scientists think play a crucial role in the process of aging, and it may teach us more about how to reverse it. and that piece is the very, very ends of our dna strands, also known as telomeres. venki ramakrishnan: so our dna are like a long linear molecule, so they have two ends and in the cell, they’re wrapped up with proteins and form these structures called chromosomes. now, the thing is that when cells divide, the chromosomes have to be replicated. so you need two where they used to be one, because you’re making two cells out of one. the mechanism for replicating the dna or copying the dna has a peculiarity. it can’t copy the very ends of the dna. paul rand: that’s the telomeres. venki ramakrishnan: so our ends keep getting shorter and shorter. as they get shorter, that structure unravels, and then the cells starts saying, “oh, there’s a problem here.” and then it sends that cell into senescence, just like as if it were dna damage. paul rand: and just like with dna repair, our body has a system to try and fix the shortening telomere problem. venki ramakrishnan: there’s some cells which have to keep dividing like our stem cells. so some cells can’t let the telomeres get shorter, and that special telomere sequence is added by this enzyme called telomerase. it turns out that in most of our end point cells, by end point, i mean let’s say we start with a fertilized egg. the end point would be all the specialized cells that we have, like skin and blood cells and hair, our eye cells and so on, and neurons. those end point cells, the telomerase is turned off, so they can’t keep on dividing because keeping on dividing is a cancer risk. paul rand: again, a connection between a possible anti aging remedy and increased cancer risk. venki ramakrishnan: so we’ve evolved to turn off telomerase, unless we absolutely need them. but cancer cells have figured out how to turn it back on again, and that’s why cancer cells can keep on dividing. paul rand: now, many researchers are excited about turning telomerase back on as anti aging mechanisms try to stop our telomeres from shortening. in fact, people with less than normal amount of telomerase have been shown to prematurely develop diseases associated with old age. but of course, if we were just to turn on telomerase, it would increase our risk of cancer. venki ramakrishnan: other people are trying to tackle this by turning on telomerase just a little bit, so that it can extend your telomeres, so that then as they shorten, you delay senescence. so that’s the idea behind some of these anti aging companies. paul rand: now, stress also can affect the telomeres too. is that right? venki ramakrishnan: yes. i thought that was a very bizarre connection, but apparently the stress hormone, cortisol, has multiple effects. a lot of times chronic stress is very bad for you, and this stress, oddly enough, actually shortens your telomeres. so it probably is accelerating telomere loss in some way. paul rand: so when you hear people talking about the negative life span effects of stress, there’s a real biological reason for it. venki ramakrishnan: oh, yeah. paul rand: in the last few years, tens of billions of dollars have been poured into the anti aging industry to try to use these advances in our biological understanding, to turn back the clock. we’ll get into the specific anti aging mechanisms being developed after the break. if you’re getting a lot out of the important research that’s shared on big brains, there’s another university of chicago podcast network show that you should check out. it’s called capital isn’t. capital isn’t uses the latest economic thinking to zero in on the ways that capitalism is and more often isn’t working today. from the debate over how to distribute a vaccine, to the morality of a wealth tax, capital isn’t clearly explains how capitalism can go wrong and what we can do about it. listen to capital isn’t, part of the university of chicago podcast network. before the break, we talked about the unique abilities of stem cells as they relate to telomeres, but many researchers and companies think that these cells may just be the ultimate key to slowing or even reversing aging. venki ramakrishnan: many of the ways to attack aging are what i would call slowing down or delaying aging, but stem cells are slightly different. the idea behind that is, it’s a field called cellular reprogramming. this has to do with the fact that if you take a cell from an early embryo, it can produce any kind of cell. it could produce a skin cell or an eye cell or a blood cell or a neuron, but as they keep developing, they specialize into certain kinds of stem cells. so there are stem cells which can only result in new types of blood cells. other cells can only generate skin or hair, other cells can only generate neurons. what happens with aging is that we need these stem cells even when we’re grown up, because our tissues are constantly being regenerated. for example, our skin is being replaced quite frequently, and so is our hair as we know, and our blood. you can donate blood and two weeks later, you’ll have remade the blood cells you donated. other cells, not so much. so neurons turn over very slowly, only a small fraction. a lot of them, we’re stuck with the neurons we have. heart muscle does not regenerate very well, and that’s why if you damage heart muscle in a heart attack, it’s a serious problem. you can’t just replace it. but if you were able to generate the stem cells that are responsible for regenerating those tissues, you might be able to regenerate as necessary. now, one problem as we age is our stem cells also age and they go into senescence and they die off. so as we get older, we’re depleting our stem cells and the stem cells we’re left with are what are call clones. they’re descended from just a few strains so they don’t have the same diversity that we were born with. now, what cellular reprogramming guys want to do is they want to use a method for which a guy named yamanaka won the nobel prize, which is by introducing four factors that turn on various genes, they’re able to make cells go backwards in this development process, so they could take a fully adult cell and make it go backwards into a stem cell. so this is actually like reversing the clock, but of course, it’s a very complicated thing. today, if you use yamanaka factors and turn cells all the way back to what are called pluripotent cells, that is cells that could make any kind of cell, then you get these growths called teratomas, which are kind of cancer. so the reason that we’ve shut a lot of this ability is again, to prevent cancer early in life. so it does come with all kinds of risks, and also how much do you turn it back and how would you apply it to the body? because not all our organs age at the same rate. in the same individual, if you look at various markers, their different organs have aged differently in different people. and so how to apply this in a safe and effective way in humans, it’s a big problem. it’s a challenge that these people have to work out. yes, there’s a lot of promise, and of course, there’s a lot of hype as well. but on the other hand, there is real biology there, and i think it’s going to be an exciting time in the field. paul rand: another avenue that has many scientists excited revolves around the concept of caloric restriction and the drugs that may be able to induce this state while still allowing us to eat whatever we want. but what does caloric restriction have to do with aging? venki ramakrishnan: in a wide variety of species, it has been found that reducing caloric intake has extended life, at least as compared to an all you can eat. so then the question is, what does this do to our underlying pathways, the biochemical pathways? what does caloric restriction actually do? how does it work? so people found at least two major pathways that are influenced by caloric restriction. one of them, for example, controls protein production, so we don’t make too much protein. during the normal course of life, we’re making proteins and then getting rid of them when we don’t need them anymore, and having them hang around when they’re not needed is also detrimental. so it’s not just producing proteins at the right time. you also have to be able to destroy them at the right time. if the degrading part doesn’t work, then you get a pileup of stuff that you don’t need. so excess protein production is turned down and recycling of garbage is turned up, and both of those things are beneficial for aging. so that’s a pathway called the tor pathway. paul rand: when calories are restricted, there are fewer nutrients for cells to use. and when tor sees this, it can switch off protein synthesis, growth pathways, and turn out cell’s ability to recycle junk, all of which as we’ve seen, are important for aging. venki ramakrishnan: and then people want to know, can we have a drug that does the same thing as caloric restriction? paul rand: is that rapamycin? venki ramakrishnan: and that’s rapamycin, is one of the more popular drugs that lots of people are studying, because it directly affects one of the major pathways. paul rand: the inhibition of the tor pathway by caloric restriction or the drug rapamycin, has also been shown to increase mitochondria. another reason why it may be helpful for aging. venki ramakrishnan: mitochondria are a place where the energy units that the cell needs are made. okay, so you can think of it as they’re the place where the energy currency of the cells make. they’re also involved in a lot of metabolic processes, controlled with the cell. paul rand: additionally, exercise turns on the same pathways that stimulate mitochondrial production. venki ramakrishnan: well, of course, rapamycin, originally it was discovered as an antifungal compound. then it was shown to have antitumor activity. then it was shown to be an immune suppressor. i mean, it does a lot of things because it is a major pathway, but it’s an immune suppressor, which means you’re more prone to infection, you will heal wounds less effectively. it has a bunch of other side effects as well. paul rand: rapamycin has been shown to significantly improve health and lifespan in mice. excitement around the drug has hit such a fever pitch, that ramakrishnan says, some scientists are quietly self medicating with it. but he warns the hype is really going past the data at this point. venki ramakrishnan: if you’re perfectly healthy, the bar is higher for you to take it. you’re saying, “i’m going to take rapamycin for 10 years so that at the end of my life, i’ll live an extra 10 years.” well, that’s a trickier proposition. and so the safety requirements are different. so people have to demonstrate that. and the hope of the rapamycin community is, that they’ll find some sweet spot where it doesn’t have the negative effects like immune suppression, et cetera, but still has the benefits for aging. paul rand: all of these drugs come with trade offs and are incredibly complicated. could there be a simpler way? of course, one of the oldest and most straightforward anti aging stories in human history, revolves around a famous fictional character, dracula. but recent research has shown he may have actually been onto something with this whole blood thing. when we look back and we look at the science fiction stories of yore, and there was some wealthy industrialist that brings people in, and he replaces his old blood with new blood as a way of extending his life, that actually is not so far fetched in people’s minds these days, is it? venki ramakrishnan: oddly enough, there’s some science behind it. and the science behind it is when they connected two animals like an old rat with a young rat, and this experiment’s called parabiosis. it’s basically, they’re sharing their blood supply. it turns out that the old animal benefited by the young blood that was being pumped into it by the young animal. it turned out the young animal also suffered as a result of old blood. and that finding has been reproduced a number of times. and so it seems perfectly good science. so people are then trying to ask, “well, what is it about young blood that’s different from old blood?” and blood has lots and lots of protein factors, which can do all kinds of things. so they’re trying to figure out what the differences are, and not all the differences might be relevant for this effect. so they have to figure out which factors that are different, are actually relevant for this beneficial effect. and then they have to find out how they work. are they activating stem cells? are they helping with repair? there could be lots of possibilities. that’s a big ongoing area of research. lots of scientists working on it. there’s some very distinguished ones as well. of course, when people saw this in the news media, young blood prevents aging. then you had a bunch of companies, at least one infamous company that started offering young plasma from that is plasma from the blood of young donors to rich people. and then the fda tried to shut it down, and they opened under a different name, and it’s still going, i think. there’s this enormous amount of hype. and what this does is they try to jump the gun because there are a group of people who are so worried about aging. they love their lives, they love their active lives, and they’ll do anything, or they’ll do it just to push the envelope. these people are taking advantage of that. whereas what really needs to happen is people need to understand how this works and then figure out ways of testing it first in animals safely, and then doing proper trials in humans. paul rand: there’s not a person that’s going to be listening to this saying, “you idiot, ask him what we should do today. make sure he tells you what you should do to extend your life today.” which is, i’m sure the question you get asked 100 times a day, give me the magical answer, please. venki ramakrishnan: yeah. well, yeah. so none of the drugs so far have gone through clinical trials and shown to be effective. so today, the trio of things that you can do yourself is better than any anti aging medicine on the market. and that is a moderate and healthy diet, including lots of fruits and vegetables. and now exercise has all kinds of things. it induces reaction that helps us repair damage. it even helps with regenerating our mitochondria. so all those things that we discuss about aging, you later learn that exercise has those benefits. now, a third leg to this trio is sleep, which is very underappreciated, and especially in many western countries, and i should say particularly in the us, people skimp on sleep. it turns out that sleep is when a lot of the repair and maintenance of our body goes on. and so that trio is very good. and then there are social things which affect these. for example, reducing stress, socializing, having friendships, et cetera. they’re all free. they don’t have side effects, and as i say, better than anything on the market now. but i want to say, that those three things are also useful for reducing your cholesterol and your blood pressure. and yet, i’m on statins and i’m on anti blood pressure medication. why? because the things i did on my own weren’t quite enough. things kept creeping up with age. and so i suppose you could say one of the goals of the aging community is to supplement that, to go beyond what you can do yourself. but of course, what you do yourself is what you should start with. and these things hopefully in the future can help you go beyond that. paul rand: the advancements in anti aging while in their early stages, do hold a lot of promise, and we’re only going to keep taking more steps toward the future when people may live significantly longer. ramakrishnan says this raises a whole host of ethical questions that we need to figure out before that day comes. venki ramakrishnan: just like with ai, this is going to have unforeseen social consequences, which is, what would happen if everybody lived to be 100 or everybody lived beyond 120 if they somehow cracked that barrier. and it would result in a very different sort of society. and we need to think about what kind of society we want and how that would end up. and the other is that we already have a huge social disparity. the richest 10% live over a decade, sometimes two decades longer than the poorest 10%. the things i talked about, exercise, diet, and sleep, those are all things that poor people find it hardest too, because they can’t find a good diet, they have to eat on the run, whatever they can get. they don’t have time to sleep, they’re working two, three jobs. and they don’t have time for exercise often, so everything’s stacked against them. now, if we now have very sophisticated life extension measures or anti aging measures, who will get them? if only rich people get them, you’re going to increase the disparity even more. so i think we need to think about socially, how to make these advances available to everyone. matt hodapp: big brains is a production of the university of chicago podcast network. we are sponsored by the graham school. are you a lifelong learner with an insatiable curiosity? access more than 50 open enrollment courses every quarter. learn more at graham.uchicago.edu/bigbrains. if you like what you heard on our podcast, please leave us a rating and review. the show is hosted by paul m. rand, and produced by lea ceasrine and me, matt hodapp. thanks for listening. exploring the groundbreaking research and discoveries transforming our world more from big brains episode 152 episode 151 episode 150 university of chicago office of communications 5801 s. ellis ave., suite 120, chicago, il 60637 (773) 702 8360 news@uchicago.edu © 2025 university of chicago   all rights reserved

an official website of the united states government official websites use .gov a .gov website belongs to an official government organization in the united states. secure .gov websites use https a lock ( lock locked padlock icon ) or https:// means you've safely connected to the .gov website. share sensitive information only on official, secure websites. primary site navigation logged in as: correspondence to: martien a m pijnenburg, radboud university nijmegen medical centre, dep. of ethics, philosophy and history of medicine, internal code: 137 efg, po box 9101, 6500 hb nijmegen, the netherlands; m.pijnenburg@efg.umcn.nl received 2006 jun 8; revised 2006 oct 24; accepted 2006 oct 27. the wish to extend the human lifespan has a long tradition in many cultures. optimistic views of the possibility of achieving this goal through the latest developments in medicine feature increasingly in serious scientific and philosophical discussion. the authors of this paper argue that research with the explicit aim of extending the human lifespan is both undesirable and morally unacceptable. they present three serious objections, relating to justice, the community and the meaning of life. keywords: life extension, ageing, meaning of life, community, global justice the wish to extend the human lifespan has a long tradition in many cultures.1 optimistic views of the possibility of achieving this goal through the latest developments in medicine feature increasingly in serious scientific and philosophical discussion.1,2,3,4,5 focusing on interventions in biological ageing, one can distinguish between research that is first and foremost aimed at prolonging life by slowing or even arresting ageing processes and research that is directed at combating the diseases that seem to be intrinsically connected with biological ageing.6 we are not opposed to the latter interventions but focus on the former, increasing human life expectancy beyond the average as a primary goal, merely because there exists, as glannon puts it, “the deeper conviction that there is intrinsic value in living much longer than we presently do, given that being alive is intrinsically valuable”.3 although we agree that being alive is intrinsically valuable, we think that there is a fundamental difference between the desirability of being alive within the limits of the average life expectancy and the desirability of being alive beyond those limits. in the first case, we deal with the possession and continuation of something we have a right to maintain. in the second case, we are dealing with a kind of enhancement7 to which the concept of a “right to” is ill‐suited, and that raises a series of philosophical and ethical questions. reflecting on the desirability of research that is explicitly aimed at life extension, we shall present three serious objections, relating to justice, to the community and to the meaning of life. they differ as regards their nature and cogency. we begin with the most compelling argument justice. the most obvious moral problem is the already existing “unequal death”. as mauron argues, this inequality, which obtains both between the first world and the third world and between rich and poor within western welfare societies, is the main ethical obstacle. how can we justify trying to extend the lives of those who have more already?8 the figures speak for themselves: in a number of african countries south of the sahara, life expectancy is less than 40 years. the average lifespan in rich and developed countries is 70 80 years. the causes of this inequality exceed the strictly medical realm. it is mainly the combination of aids with poverty that is responsible for this mortality.9,10 no fewer than 60% of all people on earth with hiv live in subsaharan africa11 25 26 million people. twelve million children have lost at least one parent, and in zimbabwe 20.1% of all adults are infected.11 one possible objection to our argument could be that the existence of this global inequality simply does not present a problem for bioethics. these disparities may be acknowledged as scandalously unfair but are the responsibility of politicians, governments and non‐governmental organisations, not of bioethicists. this way of fending off bioethical responsibility, however, is based on a concept of bioethics that closes its eyes to the morally relevant complex interrelation between the health of populations and international justice. it reduces bioethics to the type of applied ethics that became dominant starting in the 1970s. this period gave birth to a highly sophisticated, politically harmless and typically western bioethics, which mainly dealt with problems of developed and wealthy countries. in recent years, ethicists such as solomon benatar,12 james dwyer13 and paul farmer14 have rightly tried to broaden the bioethical agenda. in a globalizing world, problems of ill health in the undeveloped nations are related to how the developed and wealthy nations use their political, financial and scientific powers. contemporary bioethics, therefore, cannot limit itself to how and under what conditions new scientific developments may be applied but must also confront the question whether these developments contribute to a more just world. a second possible objection to our argument refers to the principle of distributive justice and is formulated along utilitarian lines by harris, among others. the fact that we have no means to treat all patients is no argument to qualify it unjust to treat some of them: “if immortality or increased life expectancy is a good, it is doubtful ethics to deny palpable goods to some people because we cannot provide them for all” (p529).2 davis defends the same conclusion, using slightly different reasoning. to deny the haves a treatment that they can afford because the have‐nots cannot afford it “is justified only if doing so makes the have‐nots more than marginally better off” (pw7).15 the burden for the have‐nots of the availability of life‐extending treatments for the haves has much less weight in comparison with the number of additional life years that the haves would lose if life extension were prevented from becoming available. both utilitarian arguments are problematic in two respects. in the first place, they make no distinction between the right of (a minority of) haves to maintain what they already have, such as certain medical treatments for age‐related diseases, and the right to become have‐mores by research and development to enhance the total lifespan. this fundamental difference between the real and the potential has moral repercussions in the light of justice. treatments that exist in reality but are not available to all rightly raise questions of distributive justice. potential treatments, however, require prior questions: for what goals are they developed? are they worthwhile at all, and for whom? who will profit? who will be harmed? in the second place, by calculating only benefits and burdens, or burdens of different weights, they neglect the moral quality of certain states of affairs that can be considered wrong and unjust in se and that should be prevented from becoming even more wrong or unjust. they bypass important moral principles of equity and integrity. by focusing on how to justify the distribution of means that are not available to all, we sideline the whole issue of inequality in chances. the original problem of why some can be treated and others cannot is no longer considered. this moral blindness reminds us of the story of the french queen marie antoinette, who in 1789 was confronted with a furious crowd. asking what was going on, she was told that these people were starving, because there was no bread. she replied, amazed, “well, why don't they eat cake then?” with regard to extending the lifespan, we are not dealing with treatments (yet), but with the question of the desirability of research and development, and, consequently, of financial investments that will not diminish these global inequalities in life expectancy, or, even worse, may increase them. our efforts to prolong life, therefore, ought not to be separated from the more fundamental questions relating to integrity: given the problem of unequal death, can we morally afford to invest in research to extend life? the contemporary agenda of bioethics happens to be largely defined by dilemmas and problems raised by western medicine and biomedical research. recently, lucke and hall pleaded for more social research on public opinion regarding life extension.16 as a variation on their proposal, we suggest that it is relevant to know the opinions on life‐extension technology of all those people whose risk of dying before the age of 40 could be diminished by rather simple, low‐technology means. life is always life with others, even when it is extended. crucial, however, seems to be how this relatedness to others is interpreted. a liberal anthropology perceives human beings as primarily individuals, who relate to each other by contract and negotiations, motivated by self‐interest. the other person has an instrumental value, and can appear as a friend, a competitor or even an enemy. also, the sum of all others, incorporated in the community or society, fulfils a merely instrumental value: the community or society is judged by the extent to which it facilitates its members to realise their individual life plan. in a liberal view, the good life is the good life for me, defined and measured by myself. autonomy and authenticity are central values. arguments in favour of life extension are often based on the presuppositions of liberalism. in communitarian anthropology, human beings are viewed as social beings: relations with others belong to the essentials of what it is to live a human life. as aristotle said (1097b12), a man is by his nature a political being, in the sense of belonging to a polis, or a community.17 contrary to the liberal anthropology, the social context is not just an instrumental means to realize individual life plans, but the precondition for living a human life. human beings cannot live without meaningful relations with others. goods that are essential for a good life, such as friendship, are essentially goods that are bound to the social dimensions of life. with respect to biological ageing, the two anthropological views can be combined. in the still‐hypothetical situation that extending biological age becomes a medical technical option, it is primarily a matter of autonomy whether a subject wants to choose it. this freedom of choice fits with the liberal view. the communitarian view, however, stresses the importance of the social network as a condition sine qua non for a truly human life. this is not a mere psychological condition, in the sense that i feel better with others, but an ethical one: in order to realize a morally good life, i have to realize myself as a community being. being with others as such is considered intrinsically valuable, not the fact that the other is “useful” for my purposes. this excludes the option that an extension of biological age is intrinsically valuable. it is valuable only if it also extends our life as communal beings. living longer is valuable only if it results in living longer in meaningful relations. quality of time outweighs quantity of time. the real ethical challenge for ageing societies, therefore, should be how to improve the conditions for life as a life in community, and not how to stop ageing as such. our final argument is that life extension as an explicit aim is contrary to the wisdom of ages as contained in various religious and non‐religious spiritual traditions. although all traditions agree that life is worthy and should not be taken (without good reason, or at all), there is always a notion that human beings miss the essence of life by focusing on the preservation of their self or “ego”. many spiritual and religious traditions make this point in the notion of truly human life by the decentring of the self. in the christian tradition, as expresssed by thomas aquinas, for example, the notion of eternal life does not refer primarily to a prolongation of earthly life based on the conception of an immortal soul; rather, it refers to the fullness of a human life that can be reached to the extent that one's goal in life is no longer the preservation of the self, but the communion with and service to god and one's neighbour.18 the same thought is expressed in other monotheistic religions, such as judaism and islam. turning to the eastern world, we see that hinduism, buddhism and explicitly non‐religious spiritual approaches such as that of the indian thinker jiddu krishnamurti all point to the importance of letting go of the ego.19 traditions such as these converge in the observation that the more one's self is decentred, the more one loses interest in self‐preservation or extension of the biological lifespan. modesty and the ability to give priority to seeking self‐flourishing by seeking the flourishing of other people seems to be a sign both of happiness and of a meaningful life. we think that the world's spiritual traditions are worth listening to, because they are a rich and often ancient source of experience with the living of a meaningful life in various cultural contexts. when the wisdom of these different contexts converges, it seems likely that something of importance may appear. at least they make us aware that quality of life is not simply in the length of lifetime. could the wisdom of the spiritual traditions be inspired by the fact that human beings have to cope with their mortality, and seek an escape in transcendence? although it may be true that this motivation is present among the followers of diverse spiritual traditions, we think that the traditions themselves are too sophisticated and well thought through to be accused of escapism. moreover, there is a secular parallel to the experience of the decentring of the self as related to the experience of life's meaning. as we reflect on the relation between time and experience, for instance, there is an interesting and important paradox to be observed: the more life is experienced as meaningful, the less we are aware of time. the activities that give us the most satisfaction and happiness are those in which we are totally absorbed. performing music, doing sports, reading good books, making love, writing texts: there are many examples of activities that demand all our attention. in those activities that constitute human happiness there seem to be no time and space, no subject and object. from this one may infer that what we basically seek as human beings is not more time to live, but meaningful experiences. these are found by decentring activities, through which the quality of life is expanded and the desire for self‐preservation and life extension vanishes. we realize that these three arguments differ in cogency. the argument of justice is the strongest, because it has a common‐sense argumentative force that is recognised in most ethical theories. the second argument, regarding the social nature of human beings, derives its cogency from the willingness to critically consider and complete the presuppositions of one's moral theory. the third argument, introducing the meaning of life, is the most controversial: it is strongest for those who adhere to one of those traditions but weakest for those who do not. if the three arguments are read in reverse order, we think that they can endorse one another, in the sense that those who search for a meaningful life in the decentring of the self will acknowledge the importance of the community and of global justice. because we address this article to a wider audience, however, we prefer to begin with the argument of justice. is it possible, after what has been said so far, to argue that no individual should have the option for life extension if science progresses enough to offer it? we don't think so. life is an intrinsic good, and individuals who are ready to accept all ethical objections presented so far are not different from those who choose to live in luxury without feeling the moral obligation of justice. in this paper, however, we focus on the ethical problems of investing in research aimed at further life extension. since such research has an institutional aspect related to public funding, we think that this aspect requires thorough reflection and dialogue by biogerontologists and their scientific organizations, by ethicists and philosophers, and by society at large. juengst et al6,7 repeatedly formulate a similar plea. among others, the question must be discussed to what extent life extension contributes to the public good. the concept of “public good”, however, is slightly ambiguous. it comes close to “public interest”, which jennings et al20 frame as the aggregate of individual private interests of individuals. as opposed to this, the concept of the common good entails a society where individuals inextricably bind up their own good with the good of the whole. it forces reflection on the question of whether living longer is good for me as a human being, and whether a society whose members have a much longer life than is the case at present would be a better society. with regard to the benefits for me as a human being, we presented two objections, centred on the meaningful life and on life as a communal being. a reply to both objections could be that issues of meaning and of communities are highly personal matters: in both domains, people have to find their own position and possess the right of free choice. but it is also true that personal answers and choices can be enriched by being embedded in traditions of wisdom with regard to how to live a human live. it is this embedding that we intend to add to the discussion on life‐extending research. with regard to a better society, in a globalizing world as ours is, there is a moral challenge to expand our view of the common good to encompass good for all, worldwide. this expansion inevitably raises the urgent question of whether we can morally afford, as a question of moral integrity, to invest time and money in trying to extend our lives while sidelining the whole issue of unequal death. competing interests: none. articles from journal of medical ethics are provided here courtesy of bmj publishing group connect with nlm national library of medicine 8600 rockville pike bethesda, md 20894
new data show politicians have a considerable survival advantage over general populations, based on information from 11 countries and over 57,500 politicians. in some countries this survival advantage is at the highest level for 150 years, and life expectancy at age 45 was found to be around seven years higher for politicians compared to general populations in certain countries. in recent years, improvements in life expectancy have stalled in many high income countries, and even declined for those in the poorest societal groups. this is thought to reflect widening inequalities, which the covid 19 pandemic has increased still further. for instance, the latest figures show that men in the most deprived areas in england are expected to live nearly 10 years less than those in the least deprived, whilst women in the same areas can expect to live seven years less (department of health and social care). * this has generated much interest in whether certain ‘elite’, high status occupations, such as politics, are associated with better health. however, to date, studies that have compared mortality rates between politicians and the populations they represent have typically focused on one or a few countries. today, a new study led by researchers at oxford population health has published the most comprehensive analysis so far, based on data from 11 high income countries. the results have been published in the european journal of epidemiology. the study collated information on politicians from australia, austria, canada, france, germany, italy, the netherlands, new zealand, switzerland, the uk, and the usa. for each country, data were available between 1945 and 2014, however the full analysis ranged from 1816 (france) to 2017. the combined dataset included 57,561 politicians, of which 40,637 had died. the proportion of female politicians ranged from 3% (france and the usa) to 21% (germany). each politician was matched according to their country, age and gender to the mortality data from the equivalent section of the national population for that period of time. the researchers then compared the number of deaths among the politicians each year with the number expected based on population mortality rates. the researchers also calculated the difference in remaining life expectancies at the age of 45 between politicians and the general population, for each consecutive 10 year period. the study found: • for almost all countries, politicians had similar rates of mortality to the general population in the late 19th and early 20th centuries. • throughout the 20th century, differences in mortality rates widened significantly across all countries, so that politicians had an increasing survival advantage over the general population. • there was considerable variation between countries in the extent of this survival advantage.