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Life expectancy
Life expectancy
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Life expectancy and healthy life expectancy in various countries of the world in 2019, according to WHO[1]
Map of the life expectancy at birth in the world in 2023 (UN estimate, smooth palette)[2]
  ⩾ 85
  82.5
  80
  77.5
  75
  72.5
  70
  67.5
  65
  62.5
  60
  57.5
  55
  ⩽ 53
Life expectancy at age 15 years[2]
  70
  67.5
  65
  62.5
  60
  57.5
  55
  52.5
  50
  47.5
Life expectancy at age 65 years[2]
  22.5
  20
  17.5
  15
  12.5
Life expectancy at age 80 years[2]
  10
  7.5
  5
Life expectancy development in several countries since 1960
Life expectancy at birth, measured by region, between 1950 and 2050
Life expectancy by world region, from 1770 to 2023

Human life expectancy is a statistical measure of the estimate of the average remaining years of life at a given age. The most commonly used measure is life expectancy at birth (LEB, or in demographic notation e0, where ex denotes the average life remaining at age x). This can be defined in two ways. Cohort LEB is the mean length of life of a birth cohort (in this case, all individuals born in a given year) and can be computed only for cohorts born so long ago that all their members have died. Period LEB is the mean length of life of a hypothetical cohort[3][4] assumed to be exposed, from birth through death, to the mortality rates observed at a given year.[5] National LEB figures reported by national agencies and international organizations for human populations are estimates of period LEB.

Human remains from the early Bronze Age indicate an LEB of 24.[6] In 2019, world LEB was 73.3.[7] A combination of high infant mortality and deaths in young adulthood from accidents, epidemics, plagues, wars, and childbirth, before modern medicine was widely available, significantly lowers LEB. For example, a society with a LEB of 40 would have relatively few people dying at exactly 40: most will die before 30 or after 55. In populations with high infant mortality rates, LEB is highly sensitive to the rate of death in the first few years of life. Because of this sensitivity, LEB can be grossly misinterpreted, leading to the belief that a population with a low LEB would have a small proportion of older people.[8] A different measure, such as life expectancy at age 5 (e5), can be used to exclude the effect of infant mortality to provide a simple measure of overall mortality rates other than in early childhood. For instance, in a society with a life expectancy of 30, it may nevertheless be common to have a 40-year remaining timespan at age 5 (but not a 60-year one[dubiousdiscuss]).

Aggregate population measures—such as the proportion of the population in various age groups—are also used alongside individual-based measures—such as formal life expectancy—when analyzing population structure and dynamics. Pre-modern societies had universally higher mortality rates and lower life expectancies at every age for both males and females.

Life expectancy, longevity, and maximum lifespan are not synonymous. Longevity refers to the relatively long lifespan of some members of a population. Maximum lifespan is the age at death for the longest-lived individual of a species. Mathematically, life expectancy is denoted [a] and is the mean number of years of life remaining at a given age , with a particular mortality.[9] Because life expectancy is an average, a particular person may die many years before or after the expected survival.

Life expectancy is also used in plant or animal ecology,[10] and in life tables (also known as actuarial tables). The concept of life expectancy may also be used in the context of manufactured objects,[11] though the related term[dubiousdiscuss] shelf life is commonly used for consumer products, and the terms "mean time to breakdown" and "mean time between failures" are used in engineering.

History

[edit]

The earliest documented work on life expectancy was done in the 1660s by John Graunt,[12] Christiaan Huygens, and Lodewijck Huygens.[13]

Human patterns

[edit]

Maximum

[edit]

The longest verified lifespan for any human is that of French woman Jeanne Calment, who is verified as having lived to age 122 years, 164 days, between 21 February 1875 and 4 August 1997. This is referred to as the "maximum life span", which is the upper boundary of life, the maximum number of years any human is known to have lived. Although maximum life expectancy is around 125 years, genetic enhancements could allow humans to live for a maximum of 245 years, according to InsideTracker.[14] According to a study by biologists Bryan G. Hughes and Siegfried Hekimi, there is no evidence for a limit on human lifespan.[15][16] However, this view has been questioned on the basis of error patterns.[17] A theoretical study shows that the maximum life expectancy at birth is limited by the human life characteristic value δ, which is around 104 years.[18]

Variation over time

[edit]

The following information is derived from the 1961 Encyclopædia Britannica and other sources, some with questionable accuracy. Unless otherwise stated, it represents estimates of the life expectancies of the world population as a whole. In many instances, life expectancy varied considerably according to class and gender.

Life expectancy at birth takes account of infant mortality and child mortality but not prenatal mortality.

Era Life expectancy at birth in years Notes
Paleolithic 22–33[19] With modern hunter-gatherer populations' estimated average life expectancy at birth of 33 years, life expectancy for the 60% reaching age 15 averages 39 remaining years.[20]
Neolithic 20[21]–33[22] Based on Early Neolithic data, life expectancy at age 15 would be 28–33 years.[23]
Bronze Age and Iron Age[24] 26 Based on Early and Middle Bronze Age data, life expectancy at age 15 would be 28–36 years.[23]
Classical Greece[25] 25[26]–28[27] Based on Athens Agora and Corinth data, life expectancy at age 15 would be 37–41 years.[23] Most Greeks and Romans died young. About half of all children died before adolescence. Those who survived to the age of 30 had a reasonable chance of reaching 50 or 60. The truly elderly, however, were rare. Because so many died in childhood, life expectancy at birth was probably between 20 and 30 years.[28]
Ancient Rome 20–33

[29][30][31][28][19][32]

Data is lacking, but computer models provide the estimate. If a person survived to age 20, they could expect to live around 30 years more. Life expectancy was probably slightly longer for women than men.[33]

Life expectancy at age 1 reached 34–41 remaining years for the 67[29]–75% surviving the first year. For the 55–65% surviving to age 5, remaining life expectancy reached around 40–45,[31] while the ~50% reaching age 10 could expect another 40 years of life.[29] Average remaining years fell to 33–39 at age 15; ~20 at age 40;[29] 14–18 at age 50; ~10–12 at age 60; and ~6–7 at age 70.[31][33]

Wang clan of China, 1st century AD – 1749 35 Life expectancy at age 1 reached 47 years for the 72% surviving the first year.[34][35]
Early Middle Ages (Europe, from the late 5th or early 6th century to the 10th century) 30–35 A Gaulish boy surviving to age 20 might expect to live 25 more years, while a woman at age 20 could normally expect about 17 more years. Anyone who survived until 40 had a good chance of another 15 to 20 years.[36]
Pre-Columbian Mesoamerica 20–40 Expectation of life at birth 13–36 years for various Pre-Columbian Mesoamerican cultures, most of the results lying in the range 24–32 years.[37] Aztec life expectancy 41.2 years for men and 42.1 for women.[38]
Late medieval English peerage[39][40] 30–33[32] Around a third of infants died in their first year.[19] Life expectancy at age 10 reached 32.2 remaining years, and for those who survived to 25, the remaining life expectancy was 23.3 years. Such estimates reflected the life expectancy of adult males from the higher ranks of English society in the Middle Ages, and were similar to that computed for monks of the Christ Church in Canterbury during the 15th century.[32] At age 21, life expectancy of an aristocrat was an additional 43 years.[41]
Early modern Britain (16th – 18th century)[24] 33–40 18th-century male life expectancy at birth was 34 years.[42] Female expectation of remaining years at age 15 rose from ~33 years around the 15th-16th centuries to ~42 in the 18th century.[43]
18th-century England[44][19] 25–40 For most of the century it ranged from 35 to 40; but in the 1720s it dipped as low as 25.[44] During the second half of the century it averaged 37,[45] while for the elite it passed 40 and approached 50.[34]
Pre-Champlain Canadian Maritimes[46] 60 Samuel de Champlain wrote that in his visits to Mi'kmaq and Huron communities, he met people over 100 years old. Daniel Paul attributes the incredible lifespan in the region to low stress and a healthy diet of lean meats, diverse vegetables, and legumes.[47]
18th-century Prussia[42] 24.7 For males.[42]
18th-century France[42] 27.5–30 For males:[42] 24.8 years in 1740–1749, 27.9 years in 1750–1759, 33.9 years in 1800–1809.[35]
18th-century American colonies[19] 28 Massachusetts colonists who reached the age of 50 could expect to live until 71, and those who were still alive at 60 could expect to reach 75.
Beginning of the 19th century[44] ~29 At the beginning of the 19th century, no country in the world had a life expectancy at birth longer than 40 years, England, Belgium and the Netherlands came closest, each reaching 40 years by the 1840s (by which time they had been surpassed by Norway, Sweden and Denmark). India's life expectancy is estimated at ~25 years,[44] while Europe averaged ~33 years.[45]
Early 19th-century England[24][44][34] 40 Remaining years of life averaged ~45[34]–47 for the 84% who survived the first year. Life expectancy fell to ~40 years at age 20, then ~20 years at age 50 and ~10 years at age 70.[44] For a 15-year-old girl it was ~40–45.[43] For the upper-class, LEB rose from ~45 to 50.[34]

Only half of the people born in the early 19th century made it past their 50th birthday. In contrast, 97% of the people born in 21st century England and Wales can expect to live longer than 50 years.[44]

19th-century British India[48] 25.4
19th-century world average[44] 28.5–32 Over the course of the century: Europe rose from ~33 to 43, the Americas from ~35 to 41, Oceania ~35 to 48, Asia ~28, Africa 26.[44] In 1820s France, LEB was ~38, and for the 80% that survived, it rose to ~47. For Moscow serfs, LEB was ~34, and for the 66% that survived, it rose to ~36.[34] Western Europe in 1830 was ~33 years, while for the people of Hau-Lou in China, it was ~40.[45] The LEB for a 10-year-old in Sweden rose from ~44 to ~54.[44]
1900 world average[49] 31–32[44] Around 48 years in Oceania, 43 in Europe, and 41 in the Americas.[44] Around 47 in the U.S.[19] and around 48 for 15-year-old girls in England.[43]
1950 world average[49] 45.7–48[44] Around 60 years in Europe, North America, Oceania, Japan, and parts of South America; but only 41 in Asia and 36 in Africa. Norway led with 72, while in Mali it was merely 26.[44]
2019–2020 world average 72.6–73.2
[44][50][51]
  • Females: 75.6 years
  • Males: 70.8 years
  • Range: ~54 (Central African Republic) – 85.3 (Hong Kong)[51]

English life expectancy at birth averaged about 36 years in the 17th and 18th centuries, one of the highest levels in the world although infant and child mortality remained higher than in later periods. Life expectancy was under 25 years in the early Colony of Virginia,[52] and in seventeenth-century New England, about 40% died before reaching adulthood.[53] During the Industrial Revolution, the life expectancy of children increased dramatically.[54] Recorded deaths among children under the age of 5 years fell in London from 74.5% of the recorded births in 1730–49 to 31.8% in 1810–29,[55][56] though this overstates mortality and its fall because of net immigration (hence more dying in the metropolis than were born there) and incomplete registration (particularly of births, and especially in the earlier period). English life expectancy at birth reached 41 years in the 1840s, 43 in the 1870s and 46 in the 1890s, though infant mortality remained at around 150 per thousand throughout this period.

Life expectancy in 1800, 1950, and 2015 – visualization by Our World in Data

Public health measures are credited with much of the recent increase in life expectancy. During the 20th century, despite a brief drop due to the 1918 flu pandemic,[57] the average lifespan in the United States increased by more than 30 years, of which 25 years can be attributed to advances in public health.[58]

Regional variations

[edit]

There are great variations in life expectancy between different parts of the world, mostly caused by differences in public health, medical care, and diet.[59]

Human beings are expected to live on average 60 years in Eswatini[60] and 82.6 years in Japan.[b] An analysis published in 2011 in The Lancet attributes Japanese life expectancy to equal opportunities, excellent public health, and a healthy diet.[62][63]

The World Health Organization announced that the COVID-19 pandemic reversed the trend of steady gain in life expectancy at birth. The pandemic wiped out nearly a decade of progress in improving life expectancy.[64]

Africa

[edit]
Graphs of life expectancy at birth for some sub-Saharan countries showing the fall in the 1990s primarily due to the HIV pandemic[65]

During the last 200 years, African countries have generally not had the same improvements in mortality rates that have been enjoyed by countries in Asia, Latin America, and Europe.[66][67] This is most apparent by the impact of AIDS on many African countries. According to projections made by the United Nations in 2002, the life expectancy at birth for 2010–2015 (if HIV/AIDS did not exist) would have been:[68]

  • 70.7 years instead of 31.6 years, Botswana
  • 69.9 years instead of 41.5 years, South Africa
  • 70.5 years instead of 31.8 years, Zimbabwe

Eastern Europe

[edit]

On average, eastern Europeans tend to live shorter lives than their western counterparts. For example, Spaniards from Madrid can expect to live to 85, but Bulgarians from the region of Severozapaden are predicted to live just past their 73rd birthday. This is in large part due to poor health habits, such as heavy smoking and high alcoholism in the region, and environmental factors, such as high air pollution.[69]

United States

[edit]
Life expectancy from 1990 to 2021 in the US, UK, Netherlands, and Austria

In 2023, the life expectancy at birth was 78.4 in the United States, a 0.9 year increase from 2022. Although American life expectancy has been on a general increase, from 73.7 in 1980 to 78.4 in 2023. Compared to other industrialized countries, the United States has fallen significantly behind, with the gap between the U.S and "peer countries" increasing from 0.9 years in 1980 to 4.1 years in 2023.[70]

In what has been described as a "life expectancy crisis", there were a total of 14.7 million "missing Americans" from 1980 to 2023, deaths that would have been averted if it had the standard mortality rate of "wealthy nations".[71] The annual number of "missing Americans" has been increasing, with 622,534 in 2019 alone.[72]

Black Americans have generally shorter life expectancies than their White American counterparts. For example, white Americans in 2010 are expected to live until age 78.9, but black Americans only until age 75.1. This 3.8-year gap, however, is the lowest it has been since 1975 at the latest, the greatest difference being 7.1 years in 1993.[73] In contrast, Asian American women live the longest of all ethnic and gender groups in the United States, with a life expectancy of 85.8 years.[74] The life expectancy of Hispanic Americans is 81.2 years.[73]

Japan

[edit]

In 2023, the life expectancy was 84.5 in Japan, 4.2 years above the OECD average, and one of the highest in the world. This represents a significant change from the 1960s, when Japan's life expectancy used to be among the lower G7 countries, due to high rates of cerebrovascular disease and stomach cancer. Since then, these rates have significantly decreased, as have the rates of coronary artery disease and other types of cancer, which were already low. High intake of fish and plant food with a modest intake of meat, milk, and dairy products is thought to contribute to these changes.[75]

In cities

[edit]

Cities also experience a wide range of life expectancy based on neighborhood breakdowns. This is largely due to economic clustering and poverty conditions that tend to associate based on geographic location. Multi-generational poverty found in struggling neighborhoods also contributes. In American cities such as Cincinnati, the life expectancy gap between low income and high-income neighborhoods touches 20 years.[76]

Economic circumstances

[edit]
Life expectancy vs healthcare spending of rich OECD countries. US average of $10,447 in 2018.[77]

Economic circumstances also affect life expectancy. For example, in the United Kingdom, life expectancy in the wealthiest and richest areas is several years higher than in the poorest areas. This may reflect factors such as diet and lifestyle, as well as access to medical care. It may also reflect a selective effect: people with chronic life-threatening illnesses are less likely to become wealthy or to reside in affluent areas.[78] In Glasgow, the disparity is amongst the highest in the world: life expectancy for males in the heavily deprived Calton area stands at 54, which is 28 years less than in the affluent area of Lenzie, which is only 8 km (5.0 mi) away.[79][80]

A study published in the American Geriatrics Society found that the average life expectancy of the Chinese emperors (which have much wealth) from the first Qin Dynasty (221–207 BC) to the last Qing Dynasty, was 41.3 years. This is much lower than that of the Buddhist monks (66.9 years) traditional Chinese doctors (75.1 years) and the emperors' servant, who survived to 71.3 years (range 55–94), during the same time.[81]

A 2013 study found a pronounced relationship between economic inequality and life expectancy.[82] However, in contrast, a study by José A. Tapia Granados and Ana Diez Roux at the University of Michigan found that life expectancy actually increased during the Great Depression, and during recessions and depressions in general.[83] The authors suggest that when people are working harder during prosperous economic times, they undergo more stress, exposure to pollution, and the likelihood of injury among other longevity-limiting factors.

Life expectancy is also likely to be affected by exposure to high levels of highway air pollution or industrial air pollution. This is one way that occupation can have a major effect on life expectancy. Coal miners (and in prior generations, asbestos cutters) have lower life expectancies than average. Other factors affecting an individual's life expectancy are genetic disorders, drug use, tobacco smoking, excessive alcohol consumption, obesity, access to health care, diet, and exercise.

Sex differences

[edit]
Life expectancy and healthy life expectancy by sex in 2019[1]
Pink: Countries where female life expectancy at birth is higher than males. Blue: A few countries in southern Africa where females have shorter lives due to AIDS. (2015)[84]
"Gender Die Gap": global female life expectancy gap at birth for countries and territories as defined by WHO for 2019. Open the original svg-file and hover over a bubble to show its data. The area of the bubbles is proportional to country population based on estimation of the UN.

Modern female human life expectancy is greater than that of males, despite females having higher morbidity rates (see health survival paradox). There are several potential reasons for this. Traditional arguments tend to favor sociology-environmental factors: historically, men have consumed more tobacco, alcohol, and drugs than women in most societies, and are more likely to die from many associated diseases such as lung cancer, tuberculosis, and cirrhosis of the liver.[85] Men are also more likely to die from injuries, whether unintentional (such as occupational, war, or car wrecks) or intentional (suicide).[85] Men are also more likely to die from the leading causes of death (some already stated) than women. Some of these in the United States include cancer of the respiratory system, motor vehicle accidents, suicide, cirrhosis of the liver, emphysema, prostate cancer, and coronary heart disease.[14] These far outweigh the female mortality rate from breast cancer and cervical cancer. In the past, mortality rates for females in child-bearing age groups were higher than for males at the same age.

A paper from 2015 found that female foetuses have a higher mortality rate than male foetuses.[86] This finding contradicts papers dating from 2002 and earlier that attribute the male sex to higher in-utero mortality rates.[87][88][89] Among the smallest premature babies (those under 2 pounds (910 grams)), females have a higher survival rate. At the other extreme, about 90% of individuals aged 110 are female. The difference in life expectancy between men and women in the United States dropped from 7.8 years in 1979 to 5.3 years in 2005, with women expected to live to age 80.1 in 2005.[90] Data from the United Kingdom shows the gap in life expectancy between men and women decreasing in later life. This may be attributable to the effects of infant mortality and young adult death rates.[91]

Some argue that shorter male life expectancy is another manifestation of the general rule, seen in all mammal species, that larger-sized individuals within a species tend, on average, to have shorter lives.[92][93] This biological difference[clarification needed] occurs because women have more resistance to infections and degenerative diseases.[14]

In her extensive review of the existing literature, Kalben concluded that the fact that women live longer than men was observed at least as far back as 1750 and that, with relatively equal treatment, modern males in all parts of the world experience greater mortality than females. However, Kalben's study was restricted to data in Western Europe alone, where the demographic transition occurred relatively early. United Nations statistics from mid-twentieth century onward, show that in all parts of the world, females have a higher life expectancy at age 60 than males.[94] Of 72 selected causes of death, only 6 yielded greater female than male age-adjusted death rates in 1998 in the United States. Except for birds, males of almost all animal species studied have higher mortality than females. Evidence suggests that the sex mortality differential in humans is due to both biological/genetic and environmental/behavioral risk and protective factors.[87]

One recent suggestion is that mitochondrial mutations which shorten lifespan continue to be expressed in males (but less so in females) because mitochondria are inherited only through the mother. By contrast, natural selection weeds out mitochondria that reduce female survival; therefore, such mitochondria are less likely to be passed on to the next generation. This thus suggests that females tend to live longer than males. The authors claim that this is a partial explanation.[95][96]

Another explanation is the unguarded X hypothesis. According to this hypothesis, one reason for why the average lifespan of males is shorter than females––by 18% on average, according to the study––is that they have a Y chromosome which cannot protect an individual from harmful genes expressed on the X chromosome, while a duplicate X chromosome, as present in female organisms, can ensure harmful genes are not expressed.[97][98]

In developed countries, starting around 1880, death rates decreased faster among women, leading to differences in mortality rates between males and females. Before 1880, death rates were the same. In people born after 1900, the death rate of 50- to 70-year-old men was double that of women of the same age. Men may be more vulnerable to cardiovascular disease, but this susceptibility was evident only after deaths from other causes, such as infections, started to decline.[99] Most of the difference in life expectancy between the sexes is accounted for by differences in the rate of death by cardiovascular diseases among persons aged 50–70.[100]

Genetics

[edit]

The heritability of lifespan is estimated to be less than 10%, meaning the majority of variation in lifespan is attributable due to differences in environment rather than genetic variation.[101] However, researchers have identified regions of the genome which can influence the length of life and the number of years lived in good health. For example, a genome-wide association study of 1 million lifespans found 12 genetic loci which influenced lifespan by modifying susceptibility to cardiovascular and smoking-related disease.[102] The locus with the largest effect is APOE. Carriers of the APOE ε4 allele live approximately one year less than average (per copy of the ε4 allele), mainly due to increased risk of Alzheimer's disease.[102]

"Healthspan, parental lifespan, and longevity are highly genetically correlated."[103]

In July 2020, scientists identified 10 genomic loci with consistent effects across multiple lifespan-related traits, including healthspan, lifespan, and longevity.[103] The genes affected by variation in these loci highlighted haem metabolism as a promising candidate for further research within the field. This study suggests that high levels of iron in the blood likely reduce, and genes involved in metabolising iron likely increase healthy years of life in humans.[104]

A follow-up study which investigated the genetics of frailty and self-rated health in addition to healthspan, lifespan, and longevity also highlighted haem metabolism as an important pathway, and found genetic variants which lower blood protein levels of LPA and VCAM1 were associated with increased healthy lifespan.[105]

Centenarians

[edit]

In developed countries, the number of centenarians is increasing at approximately 5.5% per year, which doubles the centenarian population every 13 years, pushing it from some 455,000 in 2009 to 4.1 million in 2050.[106] Japan has the highest ratio of centenarians (347 for every 1 million inhabitants in September 2010). Shimane Prefecture had an estimated 743 centenarians per million inhabitants.[107]

In the United States, the number of centenarians grew from 32,194 in 1980 to 71,944 in November 2010 (232 centenarians per million inhabitants).[108]

Mental illness

[edit]

Mental illness is reported to occur in approximately 18% of the American population.[109][110]

Life expectancy in the seriously mentally ill is much shorter than the general population.[111]

The mentally ill have been shown to have a 10- to 25-year reduction in life expectancy.[112] The reduction of lifespan in the mentally ill population compared to the mentally stable population has been studied and documented.[113][114][115][116][117]

The greater mortality of people with mental disorders may be due to death from injury, from co-morbid conditions, or medication side effects.[118] For instance, psychiatric medications can increase the risk of developing diabetes.[119][120][121][122] The psychiatric medication olanzapine can increase risk of developing agranulocytosis, among other comorbidities.[123][124] Psychiatric medicines also affect the gastrointestinal tract; the mentally ill have a four times risk of gastrointestinal disease.[125][126][127]

As of 2020 and the COVID-19 pandemic, researchers have found an increased risk of death in the mentally ill.[128][129][130]

Other illnesses

[edit]

The life expectancy of people with diabetes, which is 9.3% of the U.S. population, is reduced by roughly 10–20 years.[131][132] People over 60 years old with Alzheimer's disease have about a 50% life expectancy of 3–10 years.[133] Other people that tend to have a lower life expectancy than average include transplant recipients[134] and the obese.[135]

Education

[edit]

Education on all levels has been strongly associated with increased life expectancy.[136] This association may be due partly to higher income,[137] which can lead to increased life expectancy. Despite the association, among identical twin pairs with different education levels, there is only weak evidence of a relationship between educational attainment and adult mortality.[136]

According to a paper from 2015, the mortality rate for the Caucasian population in the United States from 1993 to 2001 is four times higher[dubiousdiscuss] for those who did not complete high school compared to those who have at least 16 years of education.[136] In fact, within the U.S. adult population, people with less than a high school education have the shortest life expectancies.

Preschool education also plays a large role in life expectancy. It was found that high-quality early-stage childhood education had positive effects on health. Researchers discovered this by analyzing the results of the Carolina Abecedarian Project, finding that the disadvantaged children who were randomly assigned to treatment had lower instances of risk factors for cardiovascular and metabolic diseases in their mid-30s.[138]

Evolution and aging rate

[edit]

Various species of plants and animals, including humans, have different lifespans. Evolutionary theory states that organisms which—by virtue of their defenses or lifestyle—live for long periods and avoid accidents, disease, predation, etc. are likely to have genes that code for slow aging, which often translates to good cellular repair. One theory is that if predation or accidental deaths prevent most individuals from living to an old age, there will be less natural selection to increase the intrinsic life span.[139] That finding was supported in a classic study of opossums by Austad;[140] however, the opposite relationship was found in an equally prominent study of guppies by Reznick.[141][142]

One prominent and very popular theory states that lifespan can be lengthened by a tight budget for food energy called caloric restriction.[143] Caloric restriction observed in many animals (most notably mice and rats) shows a near doubling of life span from a very limited calorific intake. Support for the theory has been bolstered by several new studies linking lower basal metabolic rate to increased life expectancy.[144][145][146] That is the key to why animals like giant tortoises can live so long.[147] Studies of humans with life spans of at least 100 have shown a link to decreased thyroid activity, resulting in their lowered metabolic rate.[citation needed]

The ability of skin fibroblasts to perform DNA repair after UV irradiation was measured in shrew, mouse, rat, hamster, cow, elephant and human.[148] It was found that DNA repair capability increased systematically with species life span. Since this original study in 1974, at least 14 additional studies were performed on mammals to test this correlation.[149] In all, but two of these studies, lifespan correlated with DNA repair levels, suggesting that DNA repair capability contributes to life expectancy.[149] See DNA damage theory of aging.

In a broad survey of zoo animals, no relationship was found between investment of the animal in reproduction and its life span.[150]

Calculation

[edit]
A survival tree to explain the calculations of life-expectancy. Red numbers indicate a chance of survival at a specific age, and blue ones indicate age-specific death rates.

In actuarial notation, the probability of surviving from age to age is denoted and the probability of dying during age (i.e. between ages and ) is denoted . For example, if 10% of a group of people alive at their 90th birthday die before their 91st birthday, the age-specific death probability at 90 would be 10%. This probability describes the likelihood of dying at that age, and is not the rate at which people of that age die.[c] It can be shown that

The curtate future lifetime, denoted , is a discrete random variable representing the remaining lifetime at age , rounded down to whole years. Life expectancy, more technically called the curtate expected lifetime and denoted ,[a] is the mean of —that is to say, the expected number of whole years of life remaining, assuming survival to age .[151] So,

Substituting (1) into the sum and simplifying gives the final result[152]

If the assumption is made that, on average, people live a half year on the year of their death, the complete life expectancy at age would be , which is denoted by e̊x, and is the intuitive definition of life expectancy.

By definition, life expectancy is an arithmetic mean. It can also be calculated by integrating the survival curve from 0 to positive infinity (or equivalently to the maximum lifespan, sometimes called 'omega'). For an extinct or completed cohort (all people born in the year 1850, for example), it can of course simply be calculated by averaging the ages at death. For cohorts with some survivors, it is estimated by using mortality experience in recent years. The estimates are called period cohort life expectancies.

The starting point for calculating life expectancy is the age-specific death rates of the population members. If a large amount of data is available, a statistical population can be created that allow the age-specific death rates to be simply taken as the mortality rates actually experienced at each age (the number of deaths divided by the number of years "exposed to risk" in each data cell). However, it is customary to apply smoothing to remove (as much as possible) the random statistical fluctuations from one year of age to the next. In the past, a very simple model used for this purpose was the Gompertz function, but more sophisticated methods are now used.[153] The most common modern methods include:

  • fitting a mathematical formula (such as the Gompertz function, or an extension of it) to the data.
  • looking at an established mortality table derived from a larger population and making a simple adjustment to it (such as multiplying by a constant factor) to fit the data. (In cases of relatively small amounts of data.)
  • looking at the mortality rates actually experienced at each age and applying a piecewise model (such as by cubic splines) to fit the data. (In cases of relatively large amounts of data.)
A 2024 study estimated that each cigarette reduces life expectancy by 20 minutes.[154][155]

The age-specific death rates are calculated separately for separate groups of data that are believed to have different mortality rates (such as males and females, or smokers and non-smokers) and are then used to calculate a life table from which one can calculate the probability of surviving to each age. While the data required are easily identified in the case of humans, the computation of life expectancy of industrial products and wild animals involves more indirect techniques. The life expectancy and demography of wild animals are often estimated by capturing, marking, and recapturing them.[156] The life of a product, more often termed shelf life, is also computed using similar methods. In the case of long-lived components, such as those used in critical applications (e.g. aircraft), methods like accelerated aging are used to model the life expectancy of a component.[11]

The life expectancy statistic is usually based on past mortality experience and assumes that the same age-specific mortality rates will continue. Thus, such life expectancy figures need to be adjusted for temporal trends before calculating how long a currently living individual of a particular age is expected to live. Period life expectancy remains a commonly used statistic to summarize the current health status of a population. However, for some purposes, such as pensions calculations, it is usual to adjust the life table used by assuming that age-specific death rates will continue to decrease over the years, as they have usually done in the past. That is often done by simply extrapolating past trends, but some models exist to account for the evolution of mortality, like the Lee–Carter model.[157]

As discussed above, on an individual basis, some factors correlate with longer life. Factors that are associated with variations in life expectancy include family history, marital status, economic status, physique, exercise, diet, drug use (including smoking and alcohol consumption), disposition, education, environment, sleep, climate, and health care.[14] As of 2025, some AI apps claim to be able to predict individual life expectancy and death dates through a combination of population statistics and individual factors.[158][159]

Healthy life expectancy

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To assess the quality of these additional years of life, 'healthy life expectancy' has been calculated for the last 30 years.[when?] Since 2001, the World Health Organization has published statistics called healthy life expectancy (HALE), defined as the average number of years that a person can expect to live in "full health" excluding the years lived in less than full health due to disease and/or injury.[160][161] Since 2004, Eurostat publishes annual statistics called Healthy Life Years (HLY) based on reported activity limitations. The United States uses similar indicators in the framework of the national health promotion and disease prevention plan "Healthy People 2010". More and more countries are using health expectancy indicators to monitor the health of their population.

Healthy Life Expectancy (HALE) vs GDP per Capita in different countries
Healthy Life Expectancy (HALE) vs GDP per Capita in different countries

The long-standing quest for longer life led in the 2010s to a focus on increasing HALE, also known as a person's "healthspan". Besides the benefits of keeping people healthier longer, a goal is to reduce health-care expenses on the many diseases associated with cellular senescence. Approaches being explored include fasting, exercise, and senolytic drugs.[162]

Forecasting

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Forecasting life expectancy and mortality form an important subdivision of demography. Future trends in life expectancy have huge implications for old-age support programs (like U.S. Social Security and pension) since the cash flow in these systems depends on the number of recipients who are still living (along with the rate of return on the investments or the tax rate in pay-as-you-go systems). With longer life expectancies, the systems see increased cash outflow; if the systems underestimate increases in life-expectancies, they will be unprepared for the large payments that will occur, as humans live longer and longer.

Life expectancy forecasting is usually based on one of two different approaches:

  1. Forecasting the life expectancy directly, generally using ARIMA or other time-series extrapolation procedures. This has the advantage of simplicity, but it cannot account for changes in mortality at specific ages, and the forecast number cannot be used to derive other life table results. Analyses and forecasts using this approach can be done with any common statistical/mathematical software package, like EViews, R, SAS, Stata, Matlab, or SPSS.
  2. Forecasting age-specific death rates and computing the life expectancy from the results with life table methods. This is usually more complex than simply forecasting life expectancy because the analyst must deal with correlated age-specific mortality rates, but it seems to be more robust than simple one-dimensional time series approaches. It also yields a set of age-specific rates that may be used to derive other measures, such as survival curves or life expectancies at different ages. The most important approach in this group is the Lee-Carter model,[163] which uses the singular value decomposition on a set of transformed age-specific mortality rates to reduce their dimensionality to a single time series, forecasts that time series, and then recovers a full set of age-specific mortality rates from that forecasted value. The software includes Professor Rob J. Hyndman's R package called 'demography' and UC Berkeley's LCFIT system Archived 18 April 2022 at the Wayback Machine.

Policy uses

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Life expectancy is one of the factors in measuring the Human Development Index (HDI) of each nation along with adult literacy, education, and standard of living.[164]

Life expectancy is used in describing the physical quality of life of an area. It is also used for an individual when the value of a life settlement is determined a life insurance policy is sold for a cash asset.[clarification needed]

Disparities in life expectancy are often cited as demonstrating the need for better medical care or increased social support. A strongly associated indirect measure is income inequality. For the top 21 industrialized countries, if each person is counted equally, life expectancy is lower in more unequal countries (r = −0.907).[165] There is a similar relationship among states in the U.S. (r = −0.620).[166]

Life expectancy vs. other measures of longevity

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"Remaining" life expectancy—expected number of remaining years of life as a function of current age—is used in retirement income planning.[167]

Life expectancy may be confused with the average age an adult could expect to live, creating the misunderstanding that an adult's lifespan would be unlikely to exceed their life expectancy at birth. This is not the case, as life expectancy is an average of the lifespans of all individuals, including those who die before adulthood. One may compare the life expectancy of the period after childhood to estimate also the life expectancy of an adult.[168]

As a measure of the years of life remaining, life expectancy decreases with age after initially rising in early childhood, but the average age to which a person is likely to live increases as they survive to successive higher ages.[169] In the table above, the estimated modern hunter-gatherer average expectation of life at birth of 33 years (often considered an upper-bound for Paleolithic populations) equates to a life expectancy at 15 of 39 years, so that those surviving to age 15 will on average die at 54.

In England in the 13th–19th centuries with life expectancy at birth rising from perhaps 25 years to over 40, expectation of life at age 30 has been estimated at 20–30 years,[170] giving an average age at death of about 50–60 for those (a minority at the start of the period but two-thirds at its end) surviving beyond their twenties.

Life expectancy[167] increases with age already achieved.

The table above gives the life expectancy at birth among 13th-century English nobles as 30–33, but having surviving to the age of 21, a male member of the English aristocracy could expect to live:

  • 1200–1300: to age 64
  • 1300–1400: to age 45 (because of the bubonic plague)
  • 1400–1500: to age 69
  • 1500–1550: to age 71[41]

A further concept is that of modal age at death, the single age when deaths among a population are more numerous than at any other age. In all pre-modern societies the most common age at death is the first year of life: it is only as infant mortality falls below around 33–34 per thousand (roughly a tenth of estimated ancient and medieval levels) that deaths in a later year of life (usually around age 80) become more numerous. While the most common age of death in adulthood among modern hunter-gatherers (often taken as a guide to the likely most favourable Paleolithic demographic experience) is estimated to average 72 years,[171] the number dying at that age is dwarfed by those (over a fifth of all infants) dying in the first year of life, and only around a quarter usually survive to the higher age.

Maximum life span is an individual-specific concept, and therefore is an upper bound rather than an average.[168] Science author Christopher Wanjek writes, "[H]as the human race increased its life span? Not at all. This is one of the biggest misconceptions about old age: we are not living any longer." The maximum life span, or oldest age a human can live, may be constant.[168] Further, there are many examples of people living significantly longer than the average life expectancy of their time period, such as Socrates (71), Saint Anthony the Great (105), Michelangelo (88), and John Adams (90).[168]

However, anthropologist John D. Hawks criticizes the popular conflation of life span (life expectancy) and maximum life span when popular science writers falsely imply that the average adult human does not live longer than their ancestors. He writes, "[a]ge-specific mortality rates have declined across the adult lifespan. A smaller fraction of adults die at 20, at 30, at 40, at 50, and so on across the lifespan. As a result, we live longer on average... In every way we can measure, human lifespans are longer today than in the immediate past, and longer today than they were 2000 years ago... age-specific mortality rates in adults really have reduced substantially."[172]

See also

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Increasing life expectancy

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Notes

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References

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Further reading

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Revisions and contributorsEdit on WikipediaRead on Wikipedia
from Grokipedia
Life expectancy at birth is a statistical measure of the average number of years a newborn can expect to survive if subjected to the age-specific mortality rates prevailing in a given during a specified period, typically derived from period life tables that sum survivorship probabilities across ages. It serves as a synthetic indicator of overall mortality levels and , reflecting cumulative risks from infancy through old age rather than actual cohort experiences, which can differ due to changing conditions. Unlike modal age at , which highlights typical endpoints for long-lived individuals, life expectancy emphasizes outcomes and is sensitive to high early-life mortality, historically pulling estimates downward in pre-modern societies. Over human history, life expectancy at birth has risen dramatically from around 30-40 years in pre-industrial eras—dominated by high and infectious diseases—to a global average of 73.3 years in 2024, driven empirically by reductions in child deaths through , , clean water, and antibiotics, alongside nutritional gains and control of epidemics. This near-doubling since 1900 underscores causal impacts of engineering over isolated medical advances, with regional disparities persisting: high-income nations like exceed 84 years, while some low-income African countries lag below 60 due to persistent poverty-related vulnerabilities, , and . Females consistently exhibit 4-6 years higher expectancy than males across s, attributable to biological differences in disease susceptibility and behavioral risks like or occupational hazards, though gaps narrow with socioeconomic parity. Recent trends reveal plateaus or reversals in certain developed nations, including the , linked to rising non-communicable diseases from , opioids, and factors, challenging assumptions of inexorable despite healthcare expansions; empirical correlations show weak links between per-capita spending and gains beyond basic thresholds, prioritizing preventive and environmental determinants. Projections anticipate modest future increases to 77 years globally by 2050 under medium variants, contingent on addressing aging-related burdens and inequalities, but underscore that expectancy conflates lifespan with healthspan, where healthy years lag behind total years amid chronic conditions.

Definition and Measurement

Calculation Methods

Life expectancy, denoted as exe_x, represents the average number of additional years a aged xx is expected to live under prevailing mortality conditions, calculated via life tables that summarize age-specific mortality probabilities. This conditional measure means that individuals reaching older ages, such as 64, have a total expected lifespan (x+exx + e_x) exceeding life expectancy at birth (e0e_0), as they have survived higher mortality risks in earlier life stages. These tables begin with a , typically a hypothetical cohort of 100,000 individuals at birth (l0l_0), and derive subsequent values using observed rates qxq_x, the probability of dying between ages xx and x+1x+1. For each age interval, deaths dxd_x are computed as lx×qxl_x \times q_x, survivors to the next age lx+1l_{x+1} as lxdxl_x - d_x, and person-years lived in the interval LxL_x approximately as lx+1+0.5dxl_{x+1} + 0.5 d_x to account for timing of deaths within the year. Total person-years from age xx onward (TxT_x) sum the LyL_y values from y=xy = x to the maximum age, yielding ex=Tx/lxe_x = T_x / l_x. Most reported figures employ period life tables, which apply contemporaneous age-specific mortality rates from a single year or short interval as if fixed throughout the cohort's lifetime, providing a snapshot of current conditions rather than realized outcomes. This method assumes future mortality rates remain constant at recent levels, though actual lifespans may vary due to health improvements, lifestyle changes, medical progress, or other factors. This method, used by agencies like the CDC and SSA for national estimates, relies on vital registration data for deaths and censuses or surveys for denominators to compute rates mx=m_x = deaths between xx and x+1x+1 divided by mid-interval . Conversion to qxq_x often uses qx=mx1+0.5mxq_x = \frac{m_x}{1 + 0.5 m_x} for approximation in complete tables covering single-year ages. Period measures can underestimate true if mortality improves over time, as seen in historical U.S. data where cohort values exceed period ones by 2–5 years for recent generations. In contrast, cohort life expectancy tracks a specific birth group's actual or projected mortality experiences across their lifespan, incorporating changing rates from diagonal slices of period tables or direct cohort data. This approach, less common due to data requirements—needing rates up to extinction age—is applied by the ONS for projections, revealing higher values (e.g., 1–3 years more than period for UK cohorts born post-1950) as improvements accrue. For incomplete cohorts, projections assume future trends, introducing uncertainty absent in period tables. Abridged life tables aggregate ages into broader intervals (e.g., 5-year bands) for data-scarce settings, using formulas like qx=2mx/(2+mx+mx+n)q_x = 2 m_x / (2 + m_x + m_{x+n}) for survival probabilities npx=1qx_n p_x = 1 - q_x over nn years, then deriving exe_x similarly but with adjusted LxL_x. Organizations like the UN and WHO compile global estimates from national period or abridged tables, harmonizing via models like the GBD for underreported regions, prioritizing empirical registration over modeled extrapolations where possible. Complete cohort tables, feasible only post-extinction (e.g., for 19th-century groups), confirm period underestimation but are rare for modern analyses.

Limitations and Common Misconceptions

Life expectancy at birth, as a period measure, applies contemporaneous age-specific mortality rates to a hypothetical cohort, assuming static conditions that do not reflect actual future improvements in survival rates experienced by real birth cohorts. This underestimates cohort life expectancy, which tracks observed and projected mortality for specific generations; for instance, in high-income countries, cohort estimates often exceed period figures by several years due to ongoing declines in mortality at older ages. The metric is particularly sensitive to infant and child mortality rates, which historically lowered averages significantly without implying short adult lifespans; for example, in pre-modern societies, those reaching age 15 could expect to live another 50-60 years, comparable to modern conditional expectancies. As a value, it obscures variability and inequality in survival distributions, where skewed outcomes—such as rare extreme —can distort the average without representing typical experiences. Life expectancy does not differentiate between total lifespan and healthspan, potentially overstating quality-adjusted years; metrics like healthy life expectancy, which subtract disability-adjusted periods, reveal that gains in have not always paralleled improvements in functional . limitations further compromise reliability, including incomplete vital registration in low-income regions and inconsistencies in cause-of-death attribution, leading to underreporting of certain risks. A prevalent misconception equates low historical life expectancies—often around 30-40 years—with widespread early adult deaths, ignoring that high perinatal and childhood mortality inflated those figures while conditional adult expectancies remained substantial. Another error confuses life expectancy increases solely with reduced , whereas empirical data show gains across all age groups, driven by , , and later medical interventions. Claims that modern longevity merely reflects extended morbidity overlook evidence of compressed morbidity in some populations, where healthier years predominate before terminal decline.

Pre-Modern and Industrial Era Developments

In pre-modern societies, life expectancy at birth averaged 25 to 35 years across various regions, largely attributable to elevated infant and from infectious diseases, inadequate , and limited . Estimates derived from skeletal analyses and historical records indicate that for populations and early agricultural communities, these figures reflected annual mortality risks exceeding 1-2% for adults but approaching 20-30% for infants. Conditional on surviving to age 15, remaining life expectancy extended to approximately 50-60 years in many cases, with modal adult lifespans reaching 60-70 years among elites and healthier cohorts, as evidenced by European nobility records from 800-1400 showing average adult death ages around 48 years. Plagues, such as the in 14th-century , episodically reduced population life expectancies to as low as 20 years in affected areas by decimating 30-60% of inhabitants. Medieval Europe exemplified these patterns, with life expectancy at birth for land-owning males estimated at 31.3 years, driven by perinatal risks and childhood infections; however, those reaching adulthood often lived into their 50s or beyond, countering misconceptions of universal short lifespans. Data from parish registers and demographic reconstructions confirm that while average figures were depressed by early deaths, adult survival curves resembled modern patterns up to age 70 for a significant minority, limited primarily by , , and periodic famines rather than inherent biological . The Industrial Era, spanning the late 18th to early 20th centuries, initially stalled or reversed gains in regions like , where life expectancy at birth hovered around 35-40 years from 1780-1850 amid rapid , labor, and overcrowded slums fostering epidemics of and . Mortality rates surged in the 1830s, particularly among children in industrial towns, due to contaminated water and poor ventilation, with urban death rates exceeding rural by 20-50%. By mid-century, public health interventions— including the 1848 Public Health Act in Britain establishing sanitary commissions, chlorination of water supplies from the 1850s, and smallpox campaigns initiated in 1796—yielded incremental improvements, elevating life expectancy to 40-45 years by 1900 through reduced waterborne diseases and infant mortality declines from 150-200 per 1,000 births to under 100. These advances, rooted in engineering feats like sewage systems rather than medical cures, underscore causal roles of environmental over therapeutic interventions in pre-antibiotic era gains.

20th Century Gains and Drivers

Global life expectancy at birth rose from 32 years in 1900 to approximately 67 years by 2000, more than doubling over the century despite interruptions from world wars and the 1918 influenza pandemic. This increase reflected declines in mortality across all ages, not solely infancy, though child survival improvements accounted for a substantial portion of early gains; for instance, nearly half of Canadian life expectancy advances from 1921 to 1951 stemmed from reduced infant mortality. In developed nations like the United States, life expectancy climbed from 47 years in 1900 to 77 years by 2000, driven by similar patterns. Public health measures targeting infectious diseases formed the primary drivers in the century's first half. Access to clean water via chlorination and filtration, alongside sanitation infrastructure, drastically cut waterborne illnesses such as , typhoid, and diarrheal diseases, which had previously caused high infant and child death rates. practices, informed by germ theory, including handwashing and food , further reduced transmission of pathogens. These interventions, often low-cost and scalable, yielded outsized impacts; for example, U.S. typhoid mortality fell over 90% in cities adopting by . Mid-century advances in accelerated gains. Widespread eliminated globally by 1980 and curbed , pertussis, and , averting millions of deaths among children. The introduction of antibiotics like penicillin in the 1940s transformed outcomes for bacterial infections, slashing mortality from , , and wound across age groups. Improved , bolstered by agricultural productivity and , mitigated malnutrition-related vulnerabilities, enhancing resistance to infections. Later in the century, gains shifted toward chronic conditions, though these built on foundations laid earlier. Declines in mortality, aided by antihypertensive drugs, statins, and reduced prevalence, contributed to extended adult lifespans. enabled broader healthcare access and living standard improvements, facilitating the spread of these benefits to developing regions post-1950. Overall, attributes over 70% of 20th-century U.S. gains to infectious disease control rather than curative medicine alone.

Recent Stagnations and Declines

In the United States, life expectancy at birth stagnated following a period of steady gains, increasing by just 0.1 years from to 2019 compared to an average 1.2-year rise among peer high-income nations. This halt stemmed largely from decelerating reductions in cardiovascular mortality rates after , particularly among adults aged 65 and older, where progress in heart disease prevention and treatment plateaued. Beginning in 2014, when it reached a peak of 78.8 years, U.S. life expectancy entered outright decline, driven by surges in midlife mortality from overdoses—especially synthetic opioids like —suicides, and alcohol-induced causes, often termed "deaths of despair." Opioid-related deaths alone accounted for an estimated 3.1 million years of life lost in 2022, equivalent to reducing average life expectancy by about 0.11 years annually in recent years. The accelerated these declines, causing U.S. life expectancy to fall 1.8 years to 77.0 in 2020 and another 0.9 years to 76.1 in 2021—the lowest level since 1996—due to excess deaths from the alongside persistent rises in overdoses and other preventable causes. During the pandemic's early phases, opioids contributed an additional eight months to the life expectancy shortfall. By 2023, provisional data showed a partial recovery to 78.4 years, reflecting reduced mortality, though this remained 2.4 years below the peak and highlighted ongoing vulnerabilities from behavioral risk factors like and . Globally, life expectancy continued rising through 2019 to 73.1 years but experienced sharp reversals during the , declining 0.92 years from 2019 to 2020 and 0.72 years from 2020 to 2021 for a total drop of 1.8 years—the largest in over five decades—primarily from infections disproportionately affecting older populations in lower-income regions. In and other developed areas, gains slowed post-2010 relative to earlier decades, with some nations like the and parts of seeing minor plateaus linked to cardiovascular stalls and rising , though declines were less severe than in the U.S. absent comparable opioid epidemics. These trends underscore causal roles of modifiable factors such as drug policy failures, delayed chronic disease management, and pandemic response variations over systemic inequities alone.

Biological Foundations

Genetic and Heritable Factors

Twin studies estimate the of lifespan at 20-30%, indicating that genetic factors explain a moderate portion of variation in after accounting for shared environmental influences. A Danish twin of individuals born 1870-1900 found of 0.26 for males and 0.23 for females, with genetic effects becoming more pronounced after age 60. Recent analyses suggest potentially higher estimates, up to 50%, when controlling for confounding factors like , though these remain preliminary. Parental lifespan serves as a strong predictor of offspring , reflecting shared genetic endowment. Age-adjusted models show that both paternal and maternal ages at death positively associate with offspring reaching 90 years, with maternal often exerting a slightly stronger influence. This intergenerational correlation underscores the heritable component, as genetic variants transmitted from parents contribute to resilience against age-related decline. Genome-wide association studies (GWAS) reveal as a polygenic trait influenced by numerous variants of small effect, rather than single genes of large impact. Analyses of large cohorts, such as participants, have identified over 25 loci associated with lifespan, implicating pathways like insulin/IGF-1 signaling, APOE variants linked to and Alzheimer's risk, and in stress resistance. Genetic correlations exist between , healthspan, and parental lifespan, with variants also tying to reduced risks of and certain cancers, though environmental interactions modulate expression. These findings highlight causal genetic mechanisms in delaying intrinsic aging processes, independent of modifiable risks.

Sex-Based Differences

![Comparison of male and female life expectancy - world][float-right] Females consistently outlive males across human populations, with the global life expectancy gap averaging about 5 years in 2021: 73.8 years for females versus 68.8 years for males. This difference has been observed historically wherever reliable records exist, predating modern behavioral disparities like smoking rates, and persists even in controlled environments such as monasteries. The gap originates at birth, where male infant mortality exceeds female rates due to greater vulnerability to congenital anomalies and infections, and widens during adolescence and young adulthood primarily from external causes. Biological mechanisms contribute substantially to this disparity. Females possess two s, providing a genetic buffer against X-linked deleterious mutations, whereas males' single lacks this redundancy, increasing susceptibility to conditions like hemophilia and certain immune deficiencies. exerts cardioprotective effects, reducing and cardiovascular mortality—males face 50% higher heart disease death rates partly due to lower and higher testosterone levels, which correlate with elevated risks of and metabolic stress. Females also demonstrate stronger immune responses, linked to X-chromosome , conferring advantages against infections and cancers, though potentially heightening incidence. Evolutionary pressures may favor female longevity for prolonged offspring care, evident in comparative biology where sex-dimorphic lifespan advantages align with reproductive roles. Behavioral and environmental factors amplify the innate gap. Males exhibit higher mortality from injuries, suicides, homicides, and , with death rates from these causes often triple those of females; for instance, men are three times more likely to die from unintentional injuries or . These patterns stem partly from testosterone-driven risk-taking, as evidenced by consistent differences in across cultures and eras. Cardiovascular diseases account for a larger share of excess mortality at midlife, influenced by both and modifiable risks like , which historically widened the gap before converging with female declines. Despite females enduring more years with morbidity from inflammatory conditions, their overall lower premature death rates sustain the expectancy advantage. Recent data indicate the gap may be widening in some high-income nations due to stalled male gains post-COVID and persistent behavioral excesses.

Intrinsic Aging Processes

Intrinsic aging encompasses the time-dependent accumulation of molecular and cellular damage through endogenous mechanisms that progressively impair physiological function, distinct from extrinsic factors such as or . These processes underlie the universal decline in organismal resilience, culminating in increased vulnerability to and establishing an upper bound on human lifespan, empirically observed to rarely exceed 122 years as in the case of (1875–1997). Central to intrinsic aging are the primary hallmarks identified in comprehensive frameworks: genomic arises from unrepaired DNA damage, replication errors, and endogenous oxidants, leading to mutations that disrupt cellular and elevate cancer risk with advancing age.01377-0) attrition involves the progressive shortening of protective chromosomal end-caps with each , eventually triggering replicative ; shorter telomeres correlate with reduced across , with human studies showing baseline length and attrition rate predicting survival better than chronological age alone. Epigenetic alterations, including aberrant patterns and modifications, alter without sequence changes, fostering a pro-aging transcriptional ; global hypomethylation and site-specific hypermethylation intensify post-maturity, associating with frailty.01377-0) Loss of manifests as declining efficiency in protein synthesis, folding, and clearance, resulting in toxic aggregates like that impair organ function. Antagonistic hallmarks emerge as responses to primary damage but exacerbate aging when dysregulated: mitochondrial dysfunction entails bioenergetic failure from mtDNA mutations, cristae remodeling, and overproduction, contributing to energy deficits and that heighten mortality risk in age-related pathologies. Deregulated nutrient-sensing pathways, such as insulin/IGF-1 and hyperactivity, promote anabolic excess over repair, shortening lifespan in model organisms where caloric restriction mitigates this effect.01377-0) Cellular senescence imposes permanent cell-cycle arrest to suppress tumorigenesis but secretes pro-inflammatory factors (, SASP) that propagate tissue dysfunction systemically. Integrative hallmarks reflect downstream systemic failures: stem cell exhaustion diminishes regenerative capacity due to niche alterations and self-renewal defects, while altered intercellular communication—via chronic and disrupted endocrine signaling—amplifies multi-organ decline. These interconnected processes enforce a species-specific lifespan limit, with data indicating that even in optimal conditions, survival beyond 115 years becomes improbable due to cumulative frailty rather than single failures. Interventions targeting hallmarks, like activation or senolytics, extend healthspan in but await robust validation for lifespan extension.01377-0)

Modifiable Risk Factors

Behavioral and Lifestyle Influences

Regular physical activity is associated with increased life expectancy, with meta-analyses of cohort studies estimating gains ranging from 0.4 to 6.9 years depending on intensity and duration. Higher volumes and intensities of exercise, such as moderate-to-vigorous aerobic activities combined with , further reduce all-cause mortality risk by 20-40%, independent of baseline fitness levels. For instance, accumulating 8,000-12,000 daily steps correlates with progressively lower mortality rates, plateauing around 10,000 steps for younger adults and lower thresholds for those over 60. Optimal sleep duration of 7-9 hours per night minimizes mortality risk, while deviations—particularly chronic short sleep under 6 hours—elevate all-cause rates by up to 15% or more, even after adjusting for confounders like age and comorbidities. Individuals meeting multiple sleep quality metrics (e.g., regularity, satisfaction, and efficiency) exhibit life expectancies extended by 2.4 to 4.7 years compared to those with poor profiles. Long sleep exceeding 9 hours similarly predicts higher mortality, though short sleep shows stronger causal links in longitudinal data tracking midlife patterns over decades. Strong social connections, including frequent interactions with , friends, and , predict longer survival, with even modest socializing linked to reduced mortality comparable to quitting or exercising regularly. Meta-analyses and prospective studies confirm that higher in midlife correlates with exceptional , lowering all-cause mortality by mechanisms including stress reduction and behavioral reinforcement for maintenance. or , conversely, elevates death risk akin to smoking 15 cigarettes daily, based on pooled evidence from large cohorts. A strong sense of purpose in life, reflecting meaning and direction, independently predicts reduced all-cause mortality, with higher purpose associated with approximately 17% lower risk in large U.S. cohorts of adults over 50, after adjusting for health behaviors and demographics. This benefit contributes to outliving national averages when combined with healthy routines and higher education. Adherence to multiple behavioral factors—such as consistent exercise, adequate , robust social ties, and sense of purpose—yields synergistic effects, potentially adding 10-14 years to life expectancy when combined with other modifiable habits like those influenced by education, as evidenced by population modeling from the and Health Professionals Follow-up Study. These gains persist into late life, with individuals over 80 adopting such behaviors showing marked reductions in premature mortality. Empirical data underscore through dose-response relationships and intervention trials, though self-reported metrics in observational studies warrant caution due to potential .

Socioeconomic and Environmental Contributors

Socioeconomic status exerts a profound influence on life expectancy, with higher , , and consistently associated with longer lifespans across populations. In the United States, the life expectancy gap between the richest 1% and poorest 1% of individuals stands at 14.6 years for men and 10.1 years for women, based on analysis of tax records spanning 1988 to 2011. This disparity has widened over time; for men born in 1960, those in the top income quintile could expect to live 12.7 years longer at age 50 than those in the bottom quintile. similarly predicts , with each additional year of schooling linked to a roughly 2% reduction in adult mortality risk globally, an effect comparable to the benefits of quitting . Individuals with a degree in the U.S. live approximately 9 years longer than those without one, reflecting not only direct gains but also improved access to resources and behaviors. Lower socioeconomic groups face compounded risks from manual occupations, rental housing instability, and , which correlate with substantially reduced life expectancy—working-class Americans, for instance, die at least 7 years earlier on average than the wealthiest. These socioeconomic effects operate through causal pathways including limited healthcare access, , poorer , and exposure to hazardous work environments, rather than mere correlation with or alone. Higher socioeconomic status enables better mitigation of modifiable risks, such as early disease detection and adherence to preventive measures, while lower status amplifies vulnerabilities like interpersonal violence and inadequate . In regions with greater income inequality, the life expectancy gradient steepens, as evidenced by stalled gains for low-income groups amid overall population improvements. Cross-nationally, children in poorer countries face 13 times higher under-5 mortality, underscoring how economic deprivation curtails early-life survival and compounds lifelong deficits. Environmental exposures, particularly , independently shorten life expectancy by imposing physiological burdens like and cardiovascular strain. Globally, ambient fine particulate matter (PM2.5) from sources such as vehicle emissions and industrial activity reduced average life expectancy by about 1 year in 2019, with household air pollution adding another 0.7 years of loss. In heavily polluted regions of and , PM2.5 exposure alone subtracts 1.2 to 1.9 years from life expectancy. from U.S. policy interventions shows that a 10 µg/m³ decrease in PM2.5 concentrations correlates with a 0.35-year increase in mean life expectancy. Beyond particulates, broader —including elevated carbon emissions and chemical pollutants—negatively impacts by exacerbating respiratory and oncogenic risks, with human studies confirming shortened lifespans from chronic exposure. Urban built environments lacking spaces or safe infrastructure further diminish healthspan through reduced and heightened accident rates, though improvements in and have historically yielded the largest gains in modifiable environmental factors.

Nutrition, Obesity, and Substance Use

Poor dietary patterns, characterized by high intake of processed foods, sugars, and unhealthy fats, contribute to chronic diseases such as and , which shorten life expectancy. Modeling studies indicate that shifting from typical Western diets to optimized patterns emphasizing whole foods, such as increased consumption of legumes, whole grains, nuts, and fruits while reducing red/processed meats and sugars, could extend life expectancy by up to 10 years at age 20 and 8.4 years at age 60 for men, and 10.7 years at age 20 and 8.0 years at age 60 for women. In human trials, without has demonstrated slowed biological aging markers, with participants reducing calorie intake by 12-25% showing a 2-3% annual decrease in the pace of aging over two years. Obesity, defined by (BMI) ≥30 kg/m², causally links to reduced through increased risks of , , and inflammation-driven pathologies. Moderate obesity (BMI 30-35) shortens life expectancy by approximately 3 years compared to normal weight, while severe obesity (BMI ≥40) can reduce it by up to 14 years, based on cohort analyses adjusting for and other factors. For a 40-year-old never-smoker, obesity at BMI 30-35 correlates with a 4.2-year loss in remaining lifespan for men and 3.5 years for women. Tobacco smoking substantially diminishes life expectancy, primarily via , , and cardiovascular events, with smokers losing at least 10 years on average relative to non-smokers. Each smoked equates to roughly 11-20 minutes of life lost, accumulating to 6-10 years for pack-a-day smokers over decades. Excessive alcohol consumption (>40-50g/day) reduces lifespan by 4-5 years through liver , accidents, and cancers, while even moderate intake shows no net benefit in studies accounting for confounders like abstainer bias. Illicit drug use, particularly opioids and stimulants, further erodes expectancy; opioid-dependent individuals exhibit mortality rates 10-20 times higher than the general population, often halving remaining lifespan from diagnosis.

Population Variations

Geographic and National Disparities

Life expectancy at birth displays marked geographic and national variations, with high-income countries in and consistently outperforming those in and parts of . According to 2023 United Nations estimates incorporated in global datasets, records 84.6 years, 83.5 years, and 83.4 years among the highest, while reports 52.5 years, 53.9 years, and 54.7 years among the lowest. These extremes underscore a global range spanning over 30 years, reflecting divergent epidemiological profiles and infrastructural capacities. Regional aggregates amplify these national differences: the Western Pacific Region, per WHO data, averages around 78 years, driven by effective interventions and low infectious disease burdens, whereas the African Region lags at approximately 63 years, hampered by persistent challenges including prevalence, endemicity, and inadequate coverage. Empirical analyses link such gaps to foundational factors like access and childhood rates, which explain up to 70% of variance in low-versus-high expectancy nations through reduced early-life mortality. In contrast, affluent outliers like the achieve 78.4 years despite substantial healthcare investments, trailing peers due to elevated rates of drug overdoses, violence, and obesity-related conditions, highlighting behavioral and social determinants over mere expenditure. This underperformance persists beyond early-life mortality; remaining life expectancy at age 57 is approximately 23 years for males and 27 years for females in the US, lower than in countries with higher overall life expectancy such as Japan, Switzerland, and Australia, while global averages remain lower, especially in lower-income regions.
RegionAverage Life Expectancy (years, circa 2021-2023)Key Contributing Factors
77-80Advanced healthcare, low
82-85Dietary patterns, universal health coverage
60-65Infectious diseases, , conflict
74-76 benefits offset by violence in some areas
Socioeconomic metrics correlate strongly with these disparities, as nations with GDP above $20,000 typically exceed 80 years, while those below $2,000 rarely surpass 65, though causal pathways involve not just wealth but efficacy and . Studies emphasize that improvements in and yield disproportionate gains in low-expectancy settings, outpacing gains from GDP growth alone in econometric models. Persistent conflicts and institutional weaknesses in regions like further entrench low figures by disrupting supply chains for essentials like vaccines and antiretrovirals.

Ethnic, Racial, and Genetic Group Differences

In the , life expectancy at birth exhibits notable variation across racial and ethnic groups, reflecting a combination of genetic, behavioral, and environmental influences. As of 2021 data from the Institute for Health Metrics and Evaluation, recorded the highest average at 84.0 years, surpassing at 76.4 years, Hispanics at 77.6 years, at 70.8 years, and American Indians/ at 65.2 years. These figures represent post-COVID-19 adjustments, with American Indians/ experiencing the steepest declines due to elevated mortality from infectious diseases, chronic conditions, and external causes. Provisional 2022 estimates from the indicate partial recovery, with non-Hispanic Black life expectancy rising from 71.2 to 72.8 years and Asian non-Hispanic holding steady near 83 years, though full 2023 breakdowns by group remain pending. The Black-White gap has narrowed from approximately 7 years in 1990 to 3.6 years by 2018, driven by reductions in and among Blacks, yet disparities in midlife mortality from , , and persist. Globally, analogous patterns emerge when comparing populations by ancestral origins, though national data confound with socioeconomic and infectious disease burdens. East Asian-descended groups, such as those in and , achieve life expectancies exceeding 84 years, correlating with lower rates of , , and certain cancers. In contrast, sub-Saharan African populations average below 65 years in many nations, attributable partly to high from and , but adult gaps remain after age 15. Ashkenazi Jewish populations demonstrate elevated , with British census data indicating 5-6 years greater lifespan than non-Jewish counterparts, linked to genetic homogeneity from founder effects and potential selection for disease resistance. Exceptional longevity cohorts among Ashkenazi centenarians show enrichment for variants in genes like FOXO3A, which regulate insulin signaling and stress resistance. Genetic factors underpin these group differences, with twin studies estimating lifespan heritability at 20-30%, independent of shared environment. Genome-wide association studies (GWAS) identify polygenic scores for traits, such as cardiovascular and , that vary by ancestry due to differences; for instance, East Asian populations carry higher frequencies of protective variants in genes. While some analyses claim fully explains racial gaps in premature death, such assertions overlook residual differences after adjusting for , , and access to care, as well as ancestry-specific genetic predictors that fail to transfer across groups (e.g., European-derived lifespan variants underperform in African ancestries). Paradoxes, like longer telomeres in despite shorter expectancy, suggest compensatory mechanisms but underscore distinct genetic architectures influencing and disease susceptibility. Causal realism demands recognizing these heritable components, as environmental interventions alone cannot erase ancestry-correlated polygenic effects observed in diverse cohorts.

Urban-Rural and Economic Class Variations

In the , life expectancy in rural areas trails that of urban areas, with the disparity expanding over recent decades due to divergent mortality trends. From 2010 to 2019, rural counties recorded absolute declines in life expectancy—0.20 years for women and 0.30 years for men—while urban counties achieved modest gains, reversing earlier patterns where the rural-urban gap was narrower. By 2019, age-adjusted death rates in rural areas stood 20% higher than in urban areas, up from 7% in 1999, driven primarily by excess deaths from heart disease, cancer, and chronic lower respiratory diseases. These rural-urban gaps manifest at older ages as well; a 60-year-old rural man expects to live about two fewer years than an urban counterpart, while the female differential is roughly six months, reflecting higher rural burdens of , , and chronic conditions like . Rural working-age adults (ages 25-54) face 43% higher natural-cause mortality rates than urban peers, including from and cancer, contributing to stalled life expectancy improvements in non-metropolitan regions. Globally, urban areas consistently show higher life expectancies than rural ones, though data is sparser outside high-income countries and often reflects similar patterns of better healthcare access and lower chronic prevalence in cities. Life expectancy also exhibits stark gradients by economic class and socioeconomic status, with higher and levels strongly predictive of longer lifespans. In the , the life expectancy gap between the richest 1% and poorest 1% reached 14.6 years for men and 10.1 years for women during 2001-2014, widening due to differential vulnerabilities to preventable deaths among lower- groups. Between the top and bottom income deciles, men's life expectancy differential grew from 5 years in the late to 12 years by the , attributable to poorer behaviors, limited preventive care, and higher exposure to occupational hazards in lower strata. Lower socioeconomic indicators compound these risks: adults with less education, higher , manual occupations, or rental experience substantially reduced life expectancies compared to college-educated professionals or homeowners, often by several years, as evidenced by county-level analyses linking affluence to reduced mortality from amenable causes. Working-class individuals, particularly in lower-income rural or suburban counties, face life expectancies up to 7 years below those in affluent urban areas with median household incomes exceeding $100,000, where averages surpass 81 years. These class-based variations intersect with urban-rural divides, as rural economies often feature lower wages and fewer high-skill jobs, amplifying overall disparities through correlated factors like healthcare access and .

Evolutionary Perspectives

Natural Selection and Senescence

Natural selection operates primarily to maximize reproductive fitness, exerting stronger pressure on traits expressed early in life when reproduction is likely, while weakening its influence on post-reproductive periods, thereby permitting the evolution of as an accumulation of age-related declines in function. This results in organisms prioritizing energy allocation toward growth and over long-term somatic maintenance, leading to inevitable deterioration after peak reproductive years. Empirical support comes from observations across where extrinsic mortality rates inversely correlate with : high early-life hazards reduce selection for , accelerating aging processes. The accumulation theory, proposed by in 1952, posits that late-acting deleterious persist because their fitness costs manifest after most individuals have reproduced, evading strong purifying selection. Under this framework, intensifies with age as these express unchecked, supported by genomic analyses revealing an age-related increase in burden in humans and model organisms. Complementary evidence from in fruit flies demonstrates that relaxed late-life selection allows buildup, hastening decline. Antagonistic pleiotropy, articulated by George C. Williams in 1957, explains through genes that confer fitness advantages early in life—such as enhanced fertility or growth—but impose detrimental effects later, with net positive selection favoring their retention. Molecular examples include the dao-4 gene in nematodes, which boosts early reproduction but shortens lifespan, and human variants like those in APOE linked to early benefits yet late-onset pathology. This theory predicts trade-offs observable in longitudinal studies, where higher early reproductive output correlates with accelerated aging trajectories. The disposable soma theory, developed by Thomas Kirkwood, frames senescence as a resource allocation conflict: finite cellular energy is diverted preferentially to germline propagation over indefinite somatic repair, rendering the body "disposable" post-reproduction. Physiological data from mammals substantiate this, showing caloric restriction extends lifespan by mimicking scarcity and reallocating resources from reproduction to maintenance, though at the cost of fertility. In humans, this manifests as menopause signaling a shift away from reproductive investment, aligning with evolved limits where maximum lifespan hovers around 115–125 years despite average expectancy gains from medicine and hygiene. These theories collectively imply that while human life expectancy has doubled since 1800 through reduced early mortality, senescence imposes a biological ceiling resistant to further extension without overriding evolutionary trade-offs.

Cross-Species Comparisons

Human lifespan, with a maximum recorded age of 122 years, substantially exceeds that of other great apes; wild chimpanzees typically survive 40–50 years, while captives may reach 50–60 years. Phylogenetic comparative analyses across confirm that Homo sapiens deviates markedly from expected lifespan patterns based on body size and metabolic rate, exhibiting exceptional relative to closely related . This disparity arises from reduced extrinsic mortality—predation, injury, and infection—enabled by advanced , tool use, and cooperative social structures, which permit survival well beyond reproductive primes observed in other . Among mammals, lifespan variation spans over 100-fold, from ~2–3 years in mice to over 200 years in bowhead whales, with generally ranking among the longest-lived orders due to slower developmental paces and lower juvenile mortality. Humans occupy an intermediate position by body mass (scaling laws predict longer lifespans in larger via reduced metabolic rates), yet outperform expectations for their size class, as evidenced by epigenetic predictors estimating an innate female advantage conserved across 17 mammalian , including humans. Group-living , including humans, evolve extended lifespans compared to solitary counterparts, correlating with enhanced protection against environmental hazards. Exceptions highlight mechanistic diversity: naked mole rats achieve 30+ years with despite small size, via hypoxia tolerance and cancer resistance, while cetaceans like bowhead whales sustain 211-year maximums through efficiencies. Cross-species genomic studies reveal no single pathway dominates ; instead, duplications in human-associated genes (e.g., those regulating insulin signaling) appear enriched in long-lived mammals, underscoring evolutionary convergence on somatic maintenance over rapid . These comparisons inform human exceptionalism not as absolute maximum duration but as prolonged healthy lifespan amid variable extrinsic risks.

Projections and Uncertainties

Forecasting Methodologies

Forecasting life expectancy relies on projecting future mortality rates by age, sex, and cohort, typically through statistical , demographic modeling, or probabilistic frameworks that account for historical trends and uncertainties. Extrapolative methods dominate due to their data-driven nature, assuming persistence or deceleration in past mortality declines, while incorporating adjustments for emerging risks like pandemics or . These approaches distinguish between period life expectancy, which reflects cross-sectional mortality at a given time, and cohort life expectancy, which tracks birth cohorts forward using age-specific rates. The Lee-Carter model, introduced in , represents a foundational extrapolative technique, modeling the logarithm of age-specific mortality rates as the product of a stable age pattern and a time-varying index forecasted via (ARIMA) processes. It has been applied globally for its simplicity and accuracy in medium-term projections, though variants address limitations like cohort effects or sex-specific patterns by incorporating additional factors. Extensions, such as coherent forecasting across populations, reduce errors by linking related groups like countries or sexes, yielding optimistic yet bounded estimates; for instance, projections for high-mortality nations show convergence toward lower-mortality frontiers. Demographic agencies like the employ cohort-component methods within probabilistic frameworks, starting with historical vital registration or census data to baseline age-specific rates, then assuming medium-variant improvements in life expectancy—such as 2.5 years per decade for females and 2.3 for males in low-mortality countries through 2050—adjusted via Bayesian hierarchical models for uncertainty. These projected improvements are driven by factors including better chronic disease management for cardiovascular diseases, cancer, and diabetes; advancements in personalized medicine; vaccine progress; and enhancements in lifestyle and public health measures. These integrate and migration assumptions, using model life tables to fill data gaps in developing regions, and generate fan charts for 80-95% prediction intervals. The U.S. similarly projects cohort life expectancies by extrapolating recent mortality trends with ultimate annual reductions (e.g., 0.73% for males post-2050), calibrated to intermediate assumptions that have overestimated gains in recent decades due to unforeseen events like COVID-19. Alternative approaches include gap models, which forecast a global record life expectancy (e.g., Japan's) then estimate convergence gaps for specific populations, and cause-decomposition methods that project disease-specific mortality using spatiotemporal regressions. Emerging hybrids combine Lee-Carter with for nonlinear patterns, improving out-of-sample accuracy, though all methods face challenges from decelerating gains—evident in cohorts born after 1940, where improvements slow to under 0.2 years per decade—and require sensitivity to biomedical limits around 115 years maximum lifespan. Probabilistic variants, emphasizing trajectories over deterministic points, better capture variance from behavioral or environmental shifts.

Demographic and Global Challenges

Demographic shifts, including rapid population aging and persistently low fertility rates, pose significant challenges to life expectancy projections. Globally, the proportion of individuals aged 60 and older is projected to nearly double from 12% in 2015 to 22% by 2050, driven by sustained increases in life expectancy that reached 73.3 years at birth in 2024. This aging trend exacerbates dependency ratios, with the global population aged 65 and older expected to surpass the number of children under 18 by the late 2070s, reaching 2.2 billion elderly individuals by 2080. Such shifts strain healthcare systems and labor forces, potentially slowing further gains in longevity through reduced innovation and economic productivity, as evidenced by forecasts of shrinking working-age populations in high-income regions. Low fertility rates compound these issues, with the global (TFR) anticipated to decline to the replacement level of 2.1 births per woman by 2050 before falling further to 1.8. In many developed nations, TFRs already below 1.5 signal inverted population pyramids, where fewer young cohorts support larger elderly s, introducing uncertainties into mortality projections as intergenerational support erodes and morbidity rises. These dynamics challenge first-principles assumptions in forecasting models, which often rely on historical mortality declines without fully accounting for causal feedbacks like reduced public investment in health amid fiscal pressures from depopulation. Global inequalities further complicate projections, with life expectancy in lagging 7 years below the world average of 73.3 years in 2024. Regional disparities persist, as seen in Sub-Saharan Africa's slower convergence toward global norms despite overall rebounds post-COVID-19, where life expectancy returned to pre-pandemic levels of approximately 73 years by 2023 but with uneven recovery. Social determinants, including inequities in access to healthcare and nutrition, continue to shorten healthy life expectancy by up to decades in vulnerable populations, undermining optimistic UN projections that assume uniform progress. Uncertainties in these projections arise from external shocks and methodological assumptions, such as the pandemic's temporary dip in global life expectancy, which erased gains and highlighted vulnerabilities in over-reliant models. Forecasts like those from the UN Prospects 2024 incorporate probabilistic elements for and mortality but may underestimate risks from geopolitical conflicts, climate-induced stressors, or stalled fertility rebounds, particularly in regions with entrenched low TFRs. While global life expectancy is expected to rise to 77 years by 2050 under baseline scenarios, demographic realities demand cautious interpretation, prioritizing empirical tracking over assumptive convergence.

Policy and Societal Implications

Applications in Health and Economic Policy

Life expectancy metrics guide by informing toward interventions with proven impacts on mortality reduction, such as measures including , , and , which have historically driven the majority of gains in developed nations since the mid-20th century. For instance, policies targeting priority conditions like and cancer, which account for over 80% of life expectancy disparities in many populations, prioritize preventive strategies over to maximize years of life saved. However, evidence indicates diminishing returns from increased healthcare spending beyond basic access, as demonstrated by the ' high expenditures—over $4,000 more than the next highest nation in —yet lowest life expectancy among wealthy peers at 76.1 years, attributable more to behavioral risks like and drug overdoses than medical system deficiencies. In , life expectancy projections underpin actuarial assumptions for and social systems, where rising —such as the increase in remaining life expectancy at age 65 from 13.7 years in 1940 to 18.1 years for men and 20.6 years for women by 2019—necessitates reforms like gradual increases to maintain solvency without eroding lifetime benefits. Socioeconomic disparities in life expectancy exacerbate challenges, as lower-income groups experience shorter lifespans, potentially reducing net benefits from age-linked reforms unless progressive adjustments protect vulnerable cohorts. Policies incorporating these metrics also evaluate productivity, linking longer healthy lifespans to sustained , though interventions must address inequality to equitably distribute gains. Cross-domain applications integrate life expectancy into cost-benefit analyses for interventions, favoring those compressing morbidity—such as promotions yielding up to one year of added expectancy—over expensive with marginal extensions. Despite associations between universal coverage and higher expectancy in some studies, causal evidence remains limited, with non-medical factors like and infrastructure showing stronger correlations. Policymakers thus prioritize evidence-based targets, such as elevating U.S. life expectancy from its 49th global ranking, through multifaceted strategies beyond expenditure alone.

Effectiveness of Interventions and Critiques

Public health interventions such as and access to clean water have historically driven substantial gains in life expectancy. In the United States, clean water initiatives from the early reduced by three-quarters and by nearly two-thirds over the first four decades of implementation. Similarly, advancements in and antibiotics have been pivotal, with vaccines identified as the medical intervention yielding the greatest impact on and by preventing infectious diseases that previously curtailed lifespans. Global efforts have averted at least 154 million deaths over the past 50 years, equating to 10.2 billion years of full gained. Lifestyle modifications, particularly , demonstrate high effectiveness in extending life expectancy. Quitting smoking at age 35 can add 6.1 to 8.5 years to life expectancy for both men and women compared to continued . Broader adoption of healthy —including regular , balanced , and avoidance of —could prolong U.S. life expectancy by up to 14 years for women and 12 years for men if fully implemented from age 50. alone correlates with 0.4 to 4.2 years of additional life expectancy after adjusting for confounders. Critiques of medical interventions highlight diminishing marginal returns, especially in high-income settings with elevated healthcare spending. Cross-country data reveal that while initial increases in health expenditure yield significant life expectancy gains, further spending beyond certain thresholds produces progressively smaller benefits, as seen in where health costs far exceed peers but life expectancy lags. factors often outperform advanced medical care in preventive impact, with evidence suggesting that behavioral risks explain much of the variance in outcomes where spending inefficiencies persist. Anti-aging and longevity interventions face skepticism due to limited human evidence and potential overhyping. While compounds like rapamycin show promise in animal models for extending lifespan, clinical translation remains uncertain, with critiques noting inconsistent results across studies and challenges in biomarkers for aging reversal. Public deployment of such therapies risks , including extended morbidity without quality-of-life improvements, underscoring the need for rigorous, long-term trials over speculative claims.

Controversies in Data Reporting and Interpretation

Life expectancy is susceptible to biases from incomplete or erroneous reporting, particularly in regions with weak vital registration systems, where omissions of deaths and age misreporting can distort mortality rates and lead to underestimated late-life mortality. For instance, in low-income countries, undercounting of and deaths inflates apparent lifespans, while age exaggeration among the elderly compresses mortality curves at advanced ages, challenging claims of a human mortality plateau. A persistent interpretive controversy surrounds the heavy influence of infant mortality on life expectancy at birth, which can mislead comparisons across eras or populations by averaging in high early-life death rates that do not reflect adult outcomes. Historical data from 19th-century , for example, showed life expectancy at birth around 40 years due to exceeding 150 per 1,000, yet expectancy at age 5 reached 73-75 years, indicating that survivors often lived comparably long lives to modern standards. Critics argue this skew fosters misconceptions, such as underestimating pre-modern adult , while proponents of at-birth metrics emphasize their utility for capturing overall burdens from perinatal risks. Methodological choices, such as period versus cohort approaches, introduce further distortions; period life expectancy, based on current age-specific rates, can bias estimates downward during improving mortality trends by hypothetically applying to future cohorts. Tempo effects exacerbate this, temporarily depressing period figures amid delayed mortality (e.g., from medical advances), which some demographers interpret as stagnation rather than transient artifacts. During shocks like the , standard period methods overstated declines by conflating temporary spikes with permanent losses, whereas hybrid cohort-adjusted approaches reveal smaller net reductions, such as halving estimated U.S. drops when accounting for survivors' regained years. In the United States, recent life expectancy declines—falling to 76.4 years by 2021—spark debate over causal attribution, with official analyses emphasizing "deaths of despair" (overdoses, suicides) and , yet underplaying chronic factors like and sedentary lifestyles amid critiques of healthcare-centric narratives. data during 2020-2021 suggests underreporting of non-COVID causes, widening racial gaps (e.g., 2-3 times larger drops for and groups), while methodological assumptions in ethnic breakdowns amplify errors from missing records. Precision to decimal places in reported figures compounds misinterpretation, as inherent sampling variability renders sub-year distinctions unreliable for policy, often masking true uncertainty in small populations or volatile periods. Global estimates from bodies like the WHO face scrutiny for aggregating heterogeneous data, where model-based imputations for under-registered deaths introduce in developing regions, potentially overstating progress by smoothing over local inaccuracies. These issues underscore the need for transparency in assumptions, as interpretive overreliance on flawed aggregates can propagate narratives prioritizing inequality over verifiable causal drivers like infectious disease control or behavioral risks.

References

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