From Wikipedia, the free encyclopedia
Ageing or aging (see ) is the process of becoming older. The term refers especially to human beings, many animals, and fungi, whereas for example bacteria,
and some simple animals are potentially . In the broader sense, ageing can refer to single cells within an organism which have ceased dividing () or to the population of a species ().
In humans, ageing represents the accumulation of changes in a human being over time, encompassing , , and social changes. Reaction time, for example, may slow with age, while knowledge of world events and wisdom may expand. Ageing is among the greatest known
for most human diseases: of the roughly 150,000 people who die each day across the globe, about two thirds die from age-related causes.
The causes of
current theories are assigned to the damage concept, whereby the accumulation of damage (such as ) may cause biological systems to fail, or to the programmed ageing concept, whereby internal processes (such as ) may cause ageing. Programmed ageing should not be confused with programmed cell death ().
The discovery, in 1934, that
can extend lifespan by 50% in rats has motivated research into delaying and preventing ageing.
Immortal Hydra, a relative of the jellyfish
Human beings and members of other species, especially animals, necessarily experience ageing and mortality. Fungi, too, can age. In contrast, many species can be considered : for example,
fission to produce daughter cells,
plants grow runners to produce clones of themselves, and animals in the genus
have a regenerative ability by which they avoid dying of old age.
Early life forms on Earth, starting at least 3.7 billion years ago, were single-celled organisms. Such organisms (prokaryotes, protozoans, algae) multiply by fissioning thus do not age and are innately immortal.
Ageing and mortality of the individual organism became possible with the , which occurred with the emergence of the fungal/animal kingdoms approximately a billion years ago, and the evolution of
320 million years ago. The sexual organism could henceforth pass on some of its genetic material to produce new individuals and could itself
with respect to the survival of its species. This classic biological idea has however been perturbed recently by the discovery that the bacterium
may split into distinguishable daughter cells, which opens the theoretical possibility of "age classes" among bacteria.
Even within humans and other mortal species, there are cells with the potential for immortality: cancer cells which have lost the ability to die when maintained in a cell culture such as the
cell line, and specific
(producing
and ). In artificial , adult cells can be rejuvenated to embryonic status and then used to grow a new tissue or animal without ageing. Normal human cells however die after about 50 cell divisions in laboratory culture (the , discovered by
Enlarged ears and noses of old humans are sometimes blamed on continual cartilage growth, but the cause is more probably gravity.
Comparison of a normal aged brain (left) and a brain affected by
A number of characteristic ageing symptoms are experienced by a majority or by a significant proportion of humans during their lifetimes.
Teenagers lose the young child's ability to
high-frequency sounds above 20 kHz.
In the mid-20s, cognitive decline begins.
develop mainly due to , particularly affecting sun-exposed areas (face).
People over 35 years of age are at risk for developing . and most people benefit from reading glasses by age 45–50. The cause is lens hardening by decreasing levels of α-crystallin, a process which may be sped up by higher temperatures.
Around age 50, .
by the age of 50 affects about 30%-50% of males and a quarter of females.
typically occurs between 49 and 52 years of age.
In the 60–64 age cohort, the incidence of
rises to 53%. Only 20% however report disabling osteoarthritis at this age.
Almost half of people older than 75 have
inhibiting spoken communication.
By age 80, more than half of all Americans either have a
or have had .
, defined as loss of muscle mass and mobility, affects 25% of those over 85.
is classified as an ageing disease. It leads to cardiovascular disease (for example
and ) which globally is the most common cause of death.
The maximum human lifespan is suggested to be
"for the foreseeable future". The oldest reliably recorded human was
who attained 122 years and died in 1997.
becomes more common with age. About 3% of people between the ages of 65 and 74, 19% between 75 and 84, and nearly half of those over 85 years of age have dementia. The spectrum ranges from
to the neurodegenerative diseases of , ,
and . Furthermore, many types of , but not
or general knowledge such as vocabulary definitions, which typically increases or remains steady until late adulthood (see ).
declines with age, though the rate varies depending on the
and may in fact remain steady throughout most of the lifespan, dropping suddenly only as people near the end of their lives. Individual variations in rate of cognitive decline may therefore be explained in terms of people having different lengths of life. There are changes to the brain: after 20 years of age there is a 10% reduction each decade in the total length of the brain's
Age can result in , whereby
is reduced, which can lead to isolation and possible depression.
causes vision loss and increases with age, affecting nearly 12% of those above the age of 80. This degeneration is caused by systemic changes in the circulation of waste products and by growth of abnormal vessels around the retina.
A distinction can be made between "proximal ageing" (age-based effects that come about because of factors in the recent past) and "distal ageing" (age-based differences that can be traced to a cause in person's early life, such as childhood ).
Ageing is among the greatest known risk factors for most human diseases. Of the roughly 150,000 people who die each day across the globe, about two thirds—100,000 per day—die from age-related causes. In industrialised nations, the proportion is higher, reaching 90%.
95-year-old woman holding a five-month-old boy
At present, researchers are only just beginning to understand the biological basis of ageing even in relatively simple and short-lived organisms such as yeast. Less still is known of mammalian ageing, in part due to the much longer lives of even small mammals such as the mouse (around 3 years). A
for studying of ageing is the
, thanks to its short lifespan of 2–3 weeks, our ability to easily perform genetic manipulations or to suppress gene activity with , or other factors. Most known mutations and RNA interference targets that extend lifespan were first discovered in C. elegans.
The factors proposed to influence biological ageing fall into two main categories, programmed and damage-related. Programmed factors follow a biological timetable, perhaps one that might be a continuation of the one that regulates childhood growth and development. This regulation would depend on changes in gene expression that affect the systems responsible for maintenance, repair and defence responses. Damage-related factors include internal and environmental assaults to living organisms that induce cumulative damage at various levels.
In a detailed review, Lopez-Otin and colleagues (2013), who discuss ageing through the lens of the damage theory, propose nine metabolic "hallmarks" of ageing in various organisms but especially mammals:
genomic instability (mutations accumulated in nuclear DNA, in mtDNA, and in the nuclear lamina)
telomere attrition (the authors note that artificial telomerase confers non-cancerous immortality to otherwise mortal cells)
epigenetic alterations (including DNA methylation patterns, post-translational modification of histones, and chromatin remodelling)
(protein folding and proteolysis)
deregulated nutrient sensing (relating to the , which is the most conserved ageing-controlling pathway in evolution and among its targets are the / transcription factors and the mTOR complexes, probably responsive to )
mitochondrial dysfunction (the authors point out however that a causal link between ageing and increased mitochondrial production of reactive oxygen species is no longer supported by recent research)
cellular senescence (accumulation of no longer dividing cells in certain tissues, a process induced especially by p16INK4a/Rb and p19ARF/p53 to stop cancerous cells from proliferating)
stem cell exhaustion (in the authors' view caused by damage factors such as those listed above)
altered intercellular communication (encompassing especially inflammation but possibly also other intercellular interactions)
There are three main metabolic pathways which can influence the rate of ageing, discussed below:
the / pathway, probably responsive to
the activity levels of the
in mitochondria and (in plants) in chloroplasts.
It is likely that most of these pathways affect ageing separately, because targeting them simultaneously leads to additive increases in lifespan.
The rate of ageing varies substantially across different species, and this, to a large extent, is genetically based. For example, numerous
ranging from strawberries and potatoes to
typically produce clones of themselves by
and are thus potentially immortal, while
such as wheat and watermelons die each year and reproduce by sexual reproduction. In 2008 it was discovered that inactivation of only two genes in the annual plant Arabidopsis thaliana leads to its conversion into a potentially immortal perennial plant. The oldest animals known so far are 15,000-year-old Antarctic , which can reproduce both sexually and clonally.
Clonal immortality apart, there are certain species whose individual lifespans stand out among Earth's life-forms, including the
at 5062 years or 5067 years (however Hayflick states that the bristlecone pine has no cells older than 30 years), invertebrates like the
(known as quahog in New England) at 508 years, the
at 400 years, various deep-sea
at over 300 years, fish like the
and the , and the
and . Such organisms are sometimes said to exhibit . The genetic aspect has also been demonstrated in studies of human .
In laboratory settings, researchers have demonstrated that selected alterations in specific genes can extend lifespan quite substantially in
and , less so in
and less again in . Some of the targeted genes have
across species and in some cases have been associated with human longevity.
: The strong effect of age on DNA methylation levels has been known since the late 1960s. Horvath hypothesised that DNA methylation age measures the cumulative effect of an epigenetic maintenance system but details are unknown. DNA methylation age of blood predicts all-cause mortality in later life. Furthermore, prematurely aged mice can be rejuvenated and their lives extended by 30% by partially "resetting" the methylation pattern in their cells (a full reset leads to undesirable immortal cancer cells). This resetting into a juvenile state was experimentally achieved by activating the four
DNA transcription factors – , ,
(which have previously been routinely used for producing young animals from cloned adult skin cells).
: In humans and other animals, cellular
has been attributed to the shortening o when telomeres become too short, the cells senesce and die or cease multiplying. The length of telomeres is therefore the "molecular clock", predicted by Hayflick. However, telomere length in wild mouse strains is unrelated to lifespan, and mice lacking the telomerase enzyme do not have a dramatically reduced lifespan. Laboratory mice's telomeres are many times longer than human ones. Another caveat is that a study following nearly 1000 humans for ten years showed that while some humans do shorten their telomeres over time, a third of the participants did not.
A variation in the gene A has a positive effect on the life expectancy of humans, and is found much more often in people living to 100 and beyond – moreover, this appears to be true worldwide. FOXO3A acts on the
family of genes which also have a significant effect on lifespan in
and in . Sirtuin in turn inhibits mTOR.
leads to longer lifespans in various species, an effect that is unclear, but probably mediated by the nutrient-sensing function of the
, a protein that inhibits , has been linked to ageing through the
signalling pathway. mTOR functions through nutrient and growth cues leading scientists to believe that dietary restriction and mTOR are related in terms of longevity. When organisms restrict their diet, mTOR activity is reduced, which allows an increased level of autophagy. This recycles old or damaged cell parts, which increases longevity and decreases the chances of being obese. This is thought to prevent spikes of
concentration in the blood, leading to reduced insulin signalling. This has been linked to less mTOR activation as well. Therefore, longevity has been connected to caloric restriction and insulin sensitivity inhibiting mTOR, which in turns allows autophagy to occur more frequently. It may be that mTOR inhibition and autophagy reduce the effects of
on the body, which damage DNA and other organic material, so longevity would be increased.
A decreased
has been associated with increased life span in various organisms including fruit flies, nematodes and mice. The precise mechanism by which decreased GH/IGF-1 signalling increases longevity is unknown, but various mouse strains with decreased GH and/or IGF-1 induced signalling share a similar phenotype which includes increased insulin sensitivity, enhanced stress resistance and protection from carcinogenesis. The studied mouse strains with decreased GH signalling showed between 20% and 68% increased longevity, and mouse strains with decreased IGF-1 induced signalling revealed a 19 to 33% increase in life span when compared to control mice.
Over-expression of the
gene increases lifespan in
by 30%. A yeast mutant lacking the genes sch9 and ras2 has recently been shown to have a tenfold increase in lifespan under conditions of calorie restriction and is the largest increase achieved in any organism.
: Many have argued that life span, like other , is . Traits that benefit early survival and reproduction will be
for even if they contribute to an earlier death. Such a genetic effect is called the
effect when referring to a gene (pleiotropy signifying the gene has a double function – enabling reproduction at a young age but costing the organism life expectancy in old age) and is called the
effect when referring to an entire genetic programme (the organism diverting limited resources from maintenance to reproduction). The biological mechanisms which regulate lifespan evolved several hundred million years ago.
Some evidence is provided by oxygen-deprived bacterial cultures.
The theory would explain why the
disease, , can persist even though it is inexorably lethal. Also, it has been suggested that some of the genetic variants that increase fertility in the young increase cancer risk in the old. Such variants occur in genes p53 and BRCA1.
argues that ageing is regulated specifically by reproductive hormones that act in an antagonistic
manner via cell cycle signalling, promoting growth and development early in life to achieve reproduction, but becoming dysregulated later in life, driving senescence (dyosis) in a futile attempt to maintain reproductive ability. The endocrine dyscrasia that follows the loss of follicles with menopause, and the loss of Leydig and Sertoli cells during andropause, drive aberrant cell cycle signalling that leads to cell death and dysfunction, tissue dysfunction (disease) and ultimately death. Moreover, the hormones that regulate reproduction also regulate cellular metabolism, explaining the increases in fat deposition during pregnancy through to the deposition of centralised adiposity with the dysregulation of the HPG axis following menopause and during andropause (Atwood and Bowen, 2006). This theory, which introduced a new definition of ageing, has facilitated the conceptualisation of why and how ageing occurs at the evolutionary, physiological and molecular levels.
Autoimmunity: The idea that ageing results from an increase in
that attack the body's tissues. A number of diseases associated with ageing, such as
and , are probably autoimmune in this way. However, while inflammation is very much evident in old mammals, even completely
mice raised in
laboratory conditions still experience senescence.[]
An elderly
The cellular balance between energy generation and consumption (energy homeostasis) requires tight regulation during ageing. In 2011, it was demonstrated that acetylation levels of
change with age in yeast and that preventing this change slows yeast ageing.
: DNA damage is thought to be the common basis of both cancer and ageing, and it has been argued that intrinsic causes of
are the most important drivers of ageing. Genetic damage (aberrant structural alterations of the DNA),
(changes in the DNA sequence), and epimutations ( or alterations of the
which ), can cause abnormal gene expression. DNA damage causes the cells to stop dividing or induces , often
and hence hindering regeneration. However, lifelong studies of mice suggest that most mutations happen during embryonic and childhood development, when cells divide often, as each cell division is a chance for errors in DNA replication.
: In heart muscle cells, dogs annually lose approximately 3.3% of the DNA in their heart muscle cells while humans lose approximately 0.6% of their heart muscle DNA each year. These numbers are close to the ratio of the maximum longevities of the two species (120 years vs. 20 years, a 6/1 ratio). The comparative percentage is also similar between the dog and human for yearly DNA loss in the brain and lymphocytes. As stated by lead author, , "... genetic damage (particularly gene loss) is almost certainly (or probably the) central cause of ageing."
Accumulation of waste:
A buildup of waste products in cells presumably interferes with metabolism. For example, a waste product called
is formed by a complex reaction in cells that binds fat to proteins. This waste accumulates in the cells as small granules, which increase in size as a person ages.
The hallmark of ageing yeast cells appears to be overproduction of certain proteins.
induction can enhance clearance of toxic intracellular waste associated with neurodegenerative diseases and has been comprehensively demonstrated to improve lifespan in yeast, worms, flies, rodents and primates. The situation, however, has been complicated by the identification that autophagy up-regulation can also occur during ageing. Autophagy is enhanced in obese mice by caloric restriction, exercise, and a low fat diet (but in these mice is evidently not related with the activation of , see above).
Wear-and-tear theory: The very general idea that changes associated with ageing are the result of chance damage that accumulates over time.
Accumulation of errors: The idea that ageing results from chance events that escape proof reading mechanisms, which gradually damages the genetic code.
Cross-linkage: The idea that ageing results from accumulation of
compounds that interfere with normal cell function.
Studies of mtDNA mutator mice have shown that increased levels of somatic mtDNA mutations directly can cause a variety of ageing phenotypes. The authors propose that mtDNA mutations lead to respiratory-chain-deficient cells and thence to apoptosis and cell loss. They cast doubt experimentally however on the common assumption that mitochondrial mutations and dysfunction lead to increased generation of reactive oxygen species (ROS).
: Damage by , or more generally
or , create damage that may gives rise to the symptoms we recognise as ageing. 's group has provided evidence that the effect of calorie restriction may be due to increased formation of
within the , causing a secondary induction of increased
defence capacity.
and caloric restriction: Caloric restriction reduces
DNA damage in organs of ageing rats and mice. Thus, reduction of oxidative DNA damage is associated with a slower rate of ageing and increased lifespan.
substantially affects lifespan in many animals, including the ability to delay or prevent many age-related diseases. Typically, this involves caloric intake of 60–70% of what an
animal would consume, while still maintaining proper nutrient intake. In rodents, this has been shown to increase lifespan by up to 50%; similar effects occur for yeast and Drosophila. No lifespan data exist for humans on a calorie-restricted diet, but several reports support protection from age-related diseases. Two major ongoing studies on
initially reveal while one study, by the University of Wisconsin, showed that caloric restriction does extend lifespan, the second study, by the National Institute on Ageing (NIA), found no effects of caloric restriction on longevity. Both studies nevertheless showed improvement in a number of health parameters. Notwithstanding the similarly low calorie intake, the diet composition differed between the two studies (notably a high
content in the Wisconsin study), and the monkeys have different origins (India, China), initially suggesting that genetics and dietary composition, not merely a decrease in calories, are factors in longevity. However, in a comparative analysis in 2014, the Wisconsin researchers found that the allegedly non-starved NIA control monkeys in fact are moderately underweight when compared with other monkey populations, and argued this was due to the NIA's apportioned feeding protocol in contrast to Wisconsin's truly unrestricted ad libitum feeding protocol. They conclude that moderate calorie restriction rather than extreme calorie restriction is sufficient to produce the observed health and longevity benefits in the studied rhesus monkeys.
In his book How and Why We Age, Hayflick says that caloric restriction may not be effective in humans, citing data from the Baltimore Longitudinal Study of Aging which shows that being thin does not favour longevity.[] Similarly, it is sometimes claimed that moderate obesity in later life may improve survival, but newer research has identified confounding factors such as weight loss due to terminal disease. Once these factors are accounted for, the optimal body weight above age 65 corresponds to a leaner
of 23 to 27.
Alternatively, the benefits of dietary restriction can also be found by changing the
profile to reduce protein intake without any changes to calorie level, resulting in similar increases in longevity. Dietary protein restriction not only inhibits mTOR activity but also IGF-1, two mechanisms implicated in ageing. Specifically, reducing
intake is sufficient to inhibit mTOR activity, achievable through reducing animal food consumption.
is credited with lowering the risk of heart disease and early death. The major contributors to mortality risk reduction appear to be a higher consumption of vegetables, fish, fruits, nuts and monounsaturated fatty acids, i.e., olive oil.
The amount of
has an impact on mortality. People who live the longest report sleeping for six to seven hours each night. Lack of sleep (&5 hours) more than doubles the risk of death from , but too much sleep (&9 hours) is associated with a doubling of the risk of death, though not primarily from cardiovascular disease. Sleeping more than 7 to 8 hours per day has been consistently associated with increased mortality, though the cause is probably other factors such as depression and socioeconomic status, which would correlate statistically. Sleep monitoring of hunter-gatherer tribes from Africa and from South America has shown similar sleep patterns across continents: their average sleeping duration is 6.4 hours (with a summer/winter difference of 1 hour), afternoon naps () are uncommon, and
is very rare (tenfold less than in industrial societies).
may increase life expectancy. People who participate in moderate to high levels of physical exercise have a lower mortality rate compared to individuals who are not physically active. Moderate levels of exercise have been correlated with preventing aging and improving quality of life by reducing inflammatory potential. The majority of the benefits from exercise are achieved with around 3500
(MET) minutes per week. For example, climbing stairs 10 minutes, vacuuming 15 minutes, gardening 20 minutes, running 20 minutes, and walking or bicycling for 25 minutes on a daily basis would together achieve about 3000 MET minutes a week.
Avoidance of
(as opposed to acute stress) is associated with a slower loss of
in most but not all studies, and with decreased
levels. A chronically high cortisol level compromises the immune system, causes cardiac damage/ and is associated with facial ageing, and the latter in turn is a marker for increased morbidity and mortality. A meta-analysis shows that loneliness carries a higher mortality risk than smoking. Stress can be countered by social connection, spirituality, and (for men more clearly than for women) married life, all of which are associated with longevity.
The following drugs and interventions have been shown to retard or reverse the biological effects of ageing in animal models, but none has yet been proven to do so in humans.
Evidence in both animals and humans suggests that
may be a caloric restriction mimetic.
As of 2015
was under study for its potential effect on slowing ageing in the worm
and the . Its effect on otherwise healthy humans is unknown.
was first shown to extend lifespan in eukaryotes in 2006 by Powers et al. who showed a dose-responsive effect of rapamycin on lifespan extension in yeast cells. In a 2009 study, the lifespans of
fed rapamycin were increased between 28 and 38% from the beginning of treatment, or 9 to 14% in total increased maximum lifespan. Of particular note, the treatment began in mice aged 20 months, the equivalent of 60 human years. Rapamycin has subsequently been shown to extend mouse lifespan in several separate experiments, and is now being tested for this purpose in nonhuman primates (the
Cancer geneticist
and his colleagues published research in mice where
activity was first genetically removed. Then, after the mice had prematurely aged, they restored telomerase activity by reactivating the telomerase gene. As a result, the mice were rejuvenated: Shrivelled testes grew back to normal and the animals regained their fertility. Other organs, such as the spleen, liver, intestines and brain, recuperated from their degenerated state. "[The finding] offers the possibility that normal human ageing could be slowed by reawakening the enzyme in cells where it has stopped working" says Ronald DePinho. However, activating telomerase in humans could potentially encourage the growth of tumours.
Most known genetic interventions in C. elegans increase lifespan by 1.5 to 2.5-fold. As of 2009, the record for lifespan extension in C. elegans is a single-gene mutation which increases adult survival by tenfold. The strong conservation of some of the mechanisms of ageing discovered in model organisms imply that they may be useful in the enhancement of human survival. However, the benefits may longevity gains are typically greater in C. elegans than fruit flies, and greater in fruit flies than in mammals. One explanation for this is that mammals, being much longer-lived, already have many traits which promote lifespan.
Some research effort is directed to slow ageing and extend healthy lifespan.
currently funds an intervention testing programme, whereby investigators nominate compounds (based on specific molecular ageing theories) to have evaluated with respect to their effects on lifespan and age-related biomarkers in outbred mice. Previous age-related testing in mammals has proved largely irreproducible, because of small numbers of animals and lax mouse husbandry conditions.[] The intervention testing programme aims to address this by conducting parallel experiments at three internationally recognised mouse ageing-centres, the
at Ann Arbor and the .
Several companies and organisations, such as , , , Gero, , and Science for Life Extension in Russia, declared stopping or delaying ageing as their goal.
Prizes for extending lifespan and slowing ageing in mammals exist. The
offers the Mprize. Recently, the $1 Million Palo Alto Longevity Prize was launched. It is a research incentive prize to encourage teams from all over the world to compete in an all-out effort to "hack the code" that regulates our health and lifespan. It was founded by .
Look up , , , , or
in Wiktionary, the free dictionary.
An elderly man
Different cultures express age in different ways. The age of an adult human is commonly measured in whole years since the day of birth. Arbitrary divisions set to mark periods of life may include:
(via , , , ), , , and . More casual terms may include "teenagers," "," "twentysomething", "thirtysomething", etc. as well as "denarian", "vicenarian", "tricenarian", "quadragenarian", etc.
Most legal systems define a specific age for when an individual is allowed or obliged to do particular activities. These age specifications include , , , , , , , and . Admission to a movie for instance, may depend on age according to a . A bus fare might be discounted for the young or old. Each nation, government and non-governmental organisation has different ways of classifying age. In other words,
ageing may be distinguished from "social ageing" (cultural age-expectations of how people should act as they grow older) and "biological ageing" (an organism's physical state as it ages).
In a UNFPA report about ageing in the 21st century, it highlighted the need to "Develop a new rights-based culture of ageing and a change of mindset and societal attitudes towards ageing and older persons, from welfare recipients to active, contributing members of society." UNFPA said that this "requires, among others, working towards the development of international human rights instruments and their translation into national laws and regulations and affirmative measures that challenge age discrimination and recognise older people as autonomous subjects." Older persons make contributions to society including caregiving and volunteering. For example, "A study of Bolivian migrants who [had] moved to Spain found that 69% left their children at home, usually with grandparents. In rural China, grandparents care for 38% of children aged under five whose parents have gone to work in cities."
A map showing median age figures for 2015
Population ageing is the increase in the number and proportion of older people in society. Population ageing has three possible causes: migration, longer
(decreased death rate) and decreased birth rate. Ageing has a significant impact on society. Young people tend to have fewer legal privileges (if they are below the ), they are more likely to push for political and social change, to develop and adopt new technologies, and to need education. Older people have different requirements from society and government, and frequently have differing values as well, such as for property and pension rights.
In the 21st century, one of the most significant population trends is ageing. Currently, over 11% of the world's current population are people aged 60 and older and the
(UNFPA) estimates that by 2050 that number will rise to approximately 22%. Ageing has occurred due to development which has enabled better nutrition, sanitation, health care, education and economic well-being. Consequently, fertility rates have continued to decline and life expectancy have risen. Life expectancy at birth is over 80 now in 33 countries. Ageing is a "global phenomenon," that is occurring fastest in developing countries, including those with large youth populations, and poses social and economic challenges to the work which can be overcome with "the right set of policies to equip individuals, families and societies to address these challenges and to reap its benefits."
As life expectancy rises and
decline in developed countries, the
age rises accordingly. According to the , this process is taking place in nearly every country in the world. A rising median age can have significant social and economic implications, as the workforce gets progressively older and the number of old workers and retirees grows relative to the number of young workers. Older people generally incur more health-related costs than do younger people in the workplace and can also cost more in worker's compensation and pension liabilities. In most developed countries an older workforce is somewhat inevitable. In the United States for instance, the
estimates that one in four American workers will be 55 or older by 2020.
Among the most urgent concerns of older persons worldwide is income security. This poses challenges for governments with ageing populations to ensure investments in pension systems continues in order to provide economic independence and reduce poverty in old age. These challenges vary for developing and developed countries. UNFPA stated that, "Sustainability of these systems is of particular concern, particularly in developed countries, while social protection and old-age pension coverage remain a challenge for developing countries, where a large proportion of the labour force is found in the informal sector."
The global economic crisis has increased financial pressure to ensure economic security and access to health care in old age. In order to elevate this pressure "social protection floors must be implemented in order to guarantee income security and access to essential health and social services for all older persons and provide a safety net that contributes to the postponement of disability and prevention of impoverishment in old age."
It has been argued that population ageing has undermined economic development. Evidence suggests that pensions, while making a difference to the well-being of older persons, also benefit entire families especially in times of crisis when there may be a shortage or loss of employment within households. A study by the Australian Government in 2003 estimated that "women between the ages of 65 and 74 years contribute A$16 billion per year in unpaid caregiving and voluntary work. Similarly, men in the same age group contributed A$10 billion per year."
Due to increasing share of the elderly in the population, health care expenditures will continue to grow relative to the economy in coming decades. This has been considered as a negative phenomenon and effective strategies like labour productivity enhancement should be considered to deal with negative consequences of ageing.
In the field of sociology and mental health, ageing is seen in five different views: ageing as , ageing as decline, ageing as a life-cycle event, ageing as generation, and ageing as survival. Positive correlates with ageing often include economics, employment, marriage, children, education, and sense of control, as well as many others. The
includes disengagement theory, activity theory, selectivity theory, and continuity theory. , a common transition faced by the elderly, may have both positive and negative consequences. As cyborgs currently are on the rise some theorists argue there is a need to develop new definitions of ageing and for instance a bio-techno-social definition of ageing has been suggested.
With age inevitable biological changes occur that increase the risk of illness and disability. UNFPA states that,
"A life-cycle approach to health care – one that starts early, continues through the reproductive years and lasts into old age – is essential for the physical and emotional well-being of older persons, and, indeed, all people. Public policies and programmes should additionally address the needs of older impoverished people who cannot afford health care."
Many societies in Western Europe and Japan have ageing populations. While the effects on society are complex, there is a concern about the impact on health care demand. The large number of suggestions in the literature for specific interventions to cope with the expected increase in demand for long-term care in ageing societies can be organised under four headings: improv redes support and shift demographic parameters.
However, the annual growth in national health spending is not mainly due to increasing demand from ageing populations, but rather has been driven by rising incomes, costly new medical technology, a shortage of health care workers and informational asymmetries between providers and patients. A number of health problems become more prevalent as people get older. These include mental health problems as well as physical health problems, especially .
It has been estimated that population ageing only explains 0.2 percentage points of the annual growth rate in medical spending of 4.3% since 1970. In addition, certain reforms to the Medicare system in the United States decreased elderly spending on home health care by 12.5% per year between 1996 and 2000.
has been correlated with higher well-being and reduced mortality in the elderly. Various reasons have been proposed
people who are objectively healthy may naturally rate their health better than that of their ill counterparts, though this link has been observed even in studies which have controlled for , psychological functioning and health status. This finding is generally stronger for men than women, though this relationship is not universal across all studies and may only be true in some circumstances.
As people age, subjective health remains relatively stable, even though objective health worsens. In fact, perceived health improves with age when objective health is controlled in the equation. This phenomenon is known as the "paradox of ageing." This for instance, the older people get, the more they may consider themselves in better health than their same-aged peers. Elderly people often associate their functional and physical decline with the normal ageing process.
The concept of successful ageing can be traced back to the 1950s and was popularised in the 1980s. Traditional definitions of successful ageing have emphasised absence of physical and cognitive disabilities. In their 1987 article, Rowe and Kahn characterised successful ageing as involving three components: a) freedom from disease and disability, b) high cognitive and physical functioning, and c) social and productive engagement.
The ancient Greek dramatist
(5th century BC) describes the multiply-headed mythological monster
as having a regenerative capacity which makes it immortal, which is the historical background to the name of the biological genus . The
(c. 6th century BC) describes human lifespan as inherently limited and makes a comparison with the innate immortality that a felled tree may have when undergoing vegetative regeneration.
Bowen, Richard L.; Atwood, Craig S. (2004). "Living and Dying for Sex". Gerontology. 50 (5): 265–90. :.  .
Dillin A, Gottschling DE, Nystr?m T (2014). . Curr Opin Cell Biol. 26: 107–12. :.   .  .
Nutman AP, Bennett VC, Friend CR, Van Kranendonk MJ, Chivas AR (2016). "Rapid emergence of life shown by discovery of 3,700-million-year-old microbial structures". Nature. 537 (7621): 535–538. :. :.  .
Rose MR (1991). Evolutionary Biology of Aging. New York: Oxford University Press.
Partridge L, Barton NH (1993). "Optimality, mutation and the evolution of ageing". Nature. 362 (6418): 305–311. :. :.  .
Williams, George C. (1957). "Pleiotropy, Natural Selection, and the Evolution of Senescence". Evolution. 11 (4): 398–411. :.  . .
Stewart EJ, Madden R, Paul G, Taddei F (2005). . PLoS Biology. 3 (2): e45. :.   .  .
Pereira-Smith OM, Ning Y (1992). "Molecular genetic studies of cellular senescence". Exp Gerontol. 27 (5–6): 519–22.  .
Forster P, Hohoff C, Dunkelmann B, Schürenkamp M, Pfeiffer H, Neuhuber F, Brinkmann B (2015). . Proc R Soc B. 282 (1803): 1–6. :.   .  .
Wakayama S, Kohda T, Obokata H, Tokoro M, Li C, Terashita Y, Mizutani E, Nguyen VT, Kishigami S, Ishino F, Wakayama T (2013). "Successful serial recloning in the mouse over multiple generations". Cell Stem Cell. 12 (3): 293–297. :.  .
Stephen Moss (July 2013). . MeshID:D000375; OMIM:6.
Rodriguez Valiente A, Trinidad A, Garcia Berrocal JR, Gorriz C, Ramirez Camacho R (April 2014). "Review: Extended high-frequency (9–20 kHz) audiometry reference thresholds in healthy subjects". Int J Audiol. 53 (8): 531–545. :.  .
Desjardins, R Warnke, Arne Jonas (2012). "Ageing and Skills". OECD Education Working Papers. :.
Finkel, D Reynolds, Chandra A. (9 July 2013). . Springer Science & Business Media – via Google Books.
Thurstan SA, Gibbs NK, Langton AK, Griffiths CE, Watson RE, Sherratt MJ (2012). . Chem Cent J. 6 (1): 34. :.   .  .
pmhdev (25 March 2015).
– via www.ncbi.nlm.nih.gov.
. Last Reviewed October 2010: National Eye Institute 2016.
Weale RA (2003). "Epidemiology of refractive errors and presbyopia". Surv Ophthalmol. 48 (5): 515–43. :.  .
Truscott RJ (2009). "Presbyopia. Emerging from a blur towards an understanding of the molecular basis for this most common eye condition". Exp Eye Res. 88 (2): 241–7. :.  .
Pathai, S; Shiels, PG; Lawn, SD; Cook, C; Gilbert, C (March 2013). "The eye as a model of ageing in translational research--molecular, epigenetic and clinical aspects". Ageing research reviews. 12 (2): 490–508. :.  .
Pandhi, D; Khanna, D (2013). "Premature graying of hair". Indian journal of dermatology, venereology and leprology. 79 (5): 641–53. :.  .
Vary JC, Jr (November 2015). "Selected Disorders of Skin Appendages--Acne, Alopecia, Hyperhidrosis". The Medical clinics of North America. 99 (6): . :.  .
Takahashi, TA; Johnson, KM (May 2015). "Menopause". The Medical clinics of North America. 99 (3): 521–34. :.  .
Thomas, E Peat, G Croft, Peter (2014). . Rheumatology (Oxford). 53 (2): 338–345. :.   .  .
(Last Updated June 3, 2016). National Institute on Deafness and Other Communication Disorders 2016.
. September .
Fried, LP; Tangen, CM; Walston, J; Newman, AB; Hirsch, C; Gottdiener, J; Seeman, T; Tracy, R; Kop, WJ; Burke, G; McBurnie, MA (Mar 2001). "Frailty in older adults: evidence for a phenotype". The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences. 56 (3): M146–56. :.  .
Percentage derived from Table 2 in Fried et al. 2001
Wang JC, Bennett M (2012). "Aging and atherosclerosis: mechanisms, functional consequences, and potential therapeutics for cellular senescence". Circ Res. 111 (2): 245–59. :.  .
Herrington W, Lacey B, Sherliker P, Armitage J, Lewington S (2016). "Epidemiology of Atherosclerosis and the Potential to Reduce the Global Burden of Atherothrombotic Disease". Circ Res. 118 (4): 535–46. :.  .
(October 5, 2016). .
Dong, X Milholland, B Vijg, Jan (October 5, 2016). . Nature. 538 (7624): 257–259. :.   2016.
Larson, EB; Yaffe, K; Langa, KM (12 December 2013). . The New England Journal of Medicine. 369 (24): 2275–7. :.   .  .
Umphred, Darcy (2012).
(6th ed.). St. Louis, Mo.: Elsevier Mosby. p. 838.  .
Schaie, K. Warner (2005). Developmental Influences on Adult Intelligence. :.  .[]
Stuart-Hamilton, Ian (2006). The Psychology of Ageing: An Introduction. London: Jessica Kingsley Publishers.  .
Marner, L Nyengaard, Jens R.; Tang, Y Pakkenberg, Bente (2003). "Marked loss of myelinated nerve fibers in the human brain with age". The Journal of Comparative Neurology. 462 (2): 144–52. :.  .
Peters, Alan (1 January 2007). Riddle, David R., ed. . CRC Press/Taylor & Francis.  .
Worrall, L.,& Hickson, L. M. (2003). "Theoretical foundations of communication disability in aging", pp. 32–33 in Linda E. Worrall & Louise M. Hickson(Eds.). Communication disability in aging: from prevention to intervention. Clifton Park, NY: Delmar Learning
Mehta, S (September 2015). "Age-Related Macular Degeneration". Primary care. 42 (3): 377–91. :.  .
Nussbaum, J. F., Thompson, T. L., & Robinson, J. D. (1989). "Barriers to conversation", pp. 234–253 in Jon F. Nussbaum, Teresa Thompson, James D. Robinson (Eds.). Communication and aging. New York: Harper & Row
De Grey, Aubrey D.N.J (2007). "Life Span Extension Research and Public Debate: Societal Considerations". Studies in Ethics, Law, and Technology. 1. :.
Lopez, Alan D; Mathers, Colin D; Ezzati, M Jamison, Dean T; Murray, Christopher JL (2006). "Global and regional burden of disease and risk factors, 2001: Systematic analysis of population health data". The Lancet. 367 (9524): 1747–57. :.  .
. Stanford.edu. Retrieved on 11 April 2012.
Janssens GE, Meinema AC, González J, Wolters JC, Schmidt A, Guryev V, Bischoff R, Wit EC, Veenhoff LM, Heinemann M (2015). . ELife. 4: e08527. :.   .  .
Deepti S. W Rebecca C. T Andrew Dillin (2012). "Analysis of Aging in Caenorhabditis elegans". In Joel H. R Andrew Singson. . Academic Press. pp. 353–381.  .
Shmookler Reis RJ, Bharill P, Tazearslan C, Ayyadevara S (2009). . Biochim Biophys Acta. 1790 (10): 1075–83. :.   .  .
. 1Vigor 2013.
Jin, Kunlin (2010). . Aging Dis. 1 (2): 72–74.   .  .
Lopez-Otin, C; Blasco, MA; Partridge, L; Serrano, M; Kroemer, G (2013). . Cell. 153 (6): . :.   .  .
Guarente, Leonard P.; Partridge, L Wallace, Douglas C. (2008). Molecular Biology of Aging. New York: Cold Spring Harbor. pp. 347–362.  .
Taylor RC, Dillin A (2011). . Cold Spring Harb Perspect Biol. 3 (5): a004440. :.   .  .
Melzer, S; Lens, F; Gennen, J; Vanneste, S; Rohde, A; Beeckman, T (2008). "Flowering-time genes modulate meristem determinacy and growth form in Arabidopsis thaliana". Nature Genetics. 40 (12): 1489–92. :.  .
. BBC. 12 June .
. Rocky Mountain Tree Ring Research.
Danuta Sosnowska, Chris Richardson, William E. Sonntag, Anna Csiszar, Zoltan Ungvari, Iain Ridgway (2014). . J Gerontol a Biol Sci Med Sci. 69 (12): 1448–61. :.   .  .
Julius Nielsen, Rasmus B. Hedeholm, Jan Heinemeier, Peter G. Bushnell, J?rgen S. Christiansen, Jesper Olsen, Christopher Bronk Ramsey, Richard W. Brill, Malene Simon, Kirstine F. Steffensen, John F. Steffensen (2016). "Eye lens radiocarbon reveals centuries of longevity in the Greenland shark (Somniosus microcephalus)". Science. 353 (6300): 702–704. :. :.  .
Durkin, A., Fisher, C.R. & Cordes, E.E. (2017). "Extreme longevity in a deep-sea vestimentiferan tubeworm and its implications for the evolution of life history strategies". The Science of Nature. 104: 63. :.  .
Timiras, Paola S. (2003) Physiological Basis of Ageing and Geriatrics. Informa Health Care.  . p. 26.
Silverman, Jacob. . .
Wallace, David Foster (2005). . .  .[]
Guerin, J (2004). "Emerging area of aging research: long-lived animals with "negligible senescence"". Ann N Y Acad Sci. 1019: 518–20. :. :.  .
Bartke A (2011). . Philos Trans R Soc Lond B Biol Sci. 366 (1561): 28–34. :.   .  .
Berdyshev, G; Korotaev, G; Boiarskikh, G; Vaniushin, B (1967). "Nucleotide composition of DNA and RNA from somatic tissues of humpback and its changes during spawning". Biokhimiia. 31: 88–993.
Marioni, R; Shah, S; McRae, A; Chen, B; Colicino, E; Harris, S; Gibson, J; Henders, A; Redmond, P; Cox, S; Pattie, A; Corley, J; Murphy, L; Martin, N; Montgomery, G; Feinberg, A; Fallin, M; Multhaup, M; Jaffe, A; Joehanes, R; Schwartz, J; Just, A; Lunetta, K; Murabito, JM; Starr, J; Horvath, S; Baccarelli, A; Levy, D; Visscher, P; Wray, N; Deary, I (2015). . Genome Biology. 16 (1): 25. :.   .  .
Christiansen, L (2015). . Aging Cell. 15 (1): 149–154. :.   .  .
Horvath, S (2015). . Aging (Dec).
Ocampo, A.; et al. (2016). "In Vivo Amelioration of Age-Associated Hallmarks by Partial Reprogramming". Cell. 167 (7): . :.  .
Tina Hesman Saey (15 December 2013).
Stibich, Mark (19 April 2009) .
m. Mikhelson, V Gamaley, Irina (2013). "Telomere Shortening is a Sole Mechanism of Aging in Mammals". Current Aging Science. 5 (3): 203–8. :.  .
Hayflick, L. (1987) Origins of longevity. In Warner, H.R., Butler, R.N., Sprott, R.L. and Schneider, E.L. (eds), Modern Biological Theories of Aging. Raven Press, New York, pp. 21–34.  
Bernstein C, Bernstein H. (1991) Aging, Sex, and DNA Repair. Academic Press, San Diego.  . pp. 314, 320 and 326
Hemann, M. T.; Greider, CW (2000). . Nucleic Acids Research. 28 (22): 4474–8. :.   .  .
Blasco, María A; Lee, Han-W Hande, M.P Samper, E Lansdorp, Peter M; Depinho, Ronald A; Greider, Carol W (1997). "Telomere Shortening and Tumor Formation by Mouse Cells Lacking Telomerase RNA". Cell. 91 (1): 25–34. :.  .
Kipling, D Cooke, Howard J. (1990). "Hypervariable ultra-long telomeres in mice". Nature. 347 (6291): 400–2. :. :.  .
Nordfj?ll, K; Svenson, U; Norrback, K. F.; Adolfsson, R; Lenner, P; Roos, G (2009). . PLoS Genetics. 5 (2): e1000375. :.   .  .
Willcox B. J. (2008). . PNAS. 105 (37): 1. :. :.   .  .
Flachsbart F, Caliebe A, Kleindorp R, Blanché H, von Eller-Eberstein H, Nikolaus S, Schreiber S, Nebel A (2009). . PNAS. 106 (8): 2700–5. :. :.   .  .
Ghosh, H. S.; McBurney, M; Robbins, P. D. (2010). . PLoS ONE. 5 (2): e9199. :. :.   .  .
Fontana L, Partridge L, Longo VD (2010). . Science. 328 (5976): 321–6. :. :.   .  .
Johnson, Simon C.; Rabinovitch, Peter S.; Kaeberlein, Matt (2013). . Nature. 493 (7432): 338–45. :. :.   .  .
Junnila, RK; List, EO; Berryman, DE; Murrey, JW; Kopchick, JJ (2013). . Nat Rev Endocrinol. 9 (6): 366–76. :.   .  .
J S Kale, SP; Childress, AM; Pinswasdi, C; Jazwinski, SM (15 July 1994). "Divergent roles of RAS1 and RAS2 in yeast longevity". Journal of Biological Chemistry. 269 (28): 18638–45.  .
Wei M, Fabrizio P, Hu J, Ge H, Cheng C, Li L, Longo VD (2008). . PLoS Genet. 4 (1): 139–149. :.   .  .
. University of Southern California.
Nystr?m, T. (2003). "The free-radical hypothesis of aging goes prokaryotic". Cellular and Molecular Life Sciences (CMLS). 60 (7): 1333–41. :.  .
Kang, H.-J.; Feng, Z.; Sun, Y.; Atwal, G.; Murphy, M. E.; Rebbeck, T. R.; Rosenwaks, Z.; Levine, A. J.; Hu, W. (2009). . Proceedings of the National Academy of Sciences. 106 (24): 9761–6. :. :.   .  .
Smith, K. R.; Hanson, H. A.; Mineau, G. P.; Buys, S. S. (2011). . Proceedings of the Royal Society B: Biological Sciences. 279 (1732): 1389–95. :.   .  .
Atwood, Craig S.; Bowen, Richard L. (2011). "The reproductive-cell cycle theory of aging: An update". Experimental Gerontology. 46 (2–3): 100–7. :.  .
Mair W, Steffen KK, Dillin A (2011). "SIP-ing the elixir of youth". Cell. 146 (6): 859–60. :.  .
Gensler, Helen L.; Bernstein, Harris (1981). "DNA Damage as the Primary Cause of Aging". The Quarterly Review of Biology. 56 (3): 279–303. :.  .  .
Sinha, Jitendra K Ghosh, S Swain, U Giridharan, Nappan V Raghunath, Manchala (2014). "Increased macromolecular damage due to oxidative stress in the neocortex and hippocampus of WNIN/Ob, a novel rat model of premature aging". Neuroscience. 269: 256–64. :.  .
Freitas, Alex A.; De Magalh?es, Jo?o Pedro (2011). "A review and appraisal of the DNA damage theory of ageing". Mutation Research/Reviews in Mutation Research. 728 (1–2): 12–22. :.  .
L. R J. Labat-R A. M. Robert (2010). "Genetic, epigenetic and posttranslational mechanisms of aging". Biogerontology. 11 (4): 387–399. :.  .
Strehler, Bernard L. (1986). "Genetic instability as the primary cause of human aging". Experimental Gerontology. 21 (4–5): 283–319. :.  .
Gavrilov, L. A.; Gavrilova, N. S. (2006), "Reliability Theory of Aging and Longevity", pp. 3–42 in Handbook of the Biology of Aging, ed. Masoro E. J. and Austad S. N, Academic Press, San Diego, CA.
Carroll B, Hewitt G, Korolchuk VI (2013). "Autophagy and ageing: implications for age-related neurodegenerative diseases". Essays Biochem. 55: 119–31. :.  .
Cui M, Yu H, Wang J, Gao J, Li J (2013). . J Diabetes Res. 2013: 852754. :.   .  .
Jin K (2010). . Aging Dis. 1 (2): 72–74.   .  .
Bjorksten, J Tenhu, Heikki (1990). "The crosslinking theory of aging — Added evidence". Experimental Gerontology. 25 (2): 91–5. :.  .
Trifunovic, A.; Larsson, N.-G. (). . Journal of Internal Medicine. 263 (2): 167–178. :.  .
Harman, D. (1981). . Proceedings of the National Academy of Sciences. 78 (11): 7124–8. :. :.   .  .
Schulz, Tim J.; Zarse, K Voigt, A Urban, N Birringer, M Ristow, Michael (2007). "Glucose Restriction Extends Caenorhabditis elegans Life Span by Inducing Mitochondrial Respiration and Increasing Oxidative Stress". Cell Metabolism. 6 (4): 280–93. :.  .
Hamilton ML, Van Remmen H, Drake JA, Yang H, Guo ZM, Kewitt K, Walter CA, Richardson A (2001). . Proc. Natl. Acad. Sci. U.S.A. 98 (18): 10469–74. :. :.   .  .
Wolf FI, Fasanella S, Tedesco B, Cavallini G, Donati A, Bergamini E, Cittadini A (2005). "Peripheral lymphocyte 8-OHdG levels correlate with age-associated increase of tissue oxidative DNA damage in Sprague-Dawley rats. Protective effects of caloric restriction". Exp. Gerontol. 40 (3): 181–8. :.  .
Anson, R. M.; Bohr, V. A. (October 2000). . Journal of the American Aging Association. 23 (4): 199–218. :.  .   .  .
Guarente L, Picard F (2005). "Calorie restriction—the SIR2 connection". Cell. 120 (4): 473–82. :.  .
Agarwal B, Baur JA (2011). "Resveratrol and life extension". Ann N Y Acad Sci. 1215 (1): 138–43. :. :.  .
Larson-Meyer DE; et al. (2008). "Effect of 6-month calorie restriction and exercise on serum and liver lipids and markers of liver function". Obesity (Silver Spring). 16 (6): . :.
Heilbronn LK; et al. (2006). "Effect of 6-month calorie restriction on biomarkers of longevity, metabolic adaptation, and oxidative stress in overweight individuals: a randomized controlled trial". JAMA. 295: . :.
Colman RJ, Anderson RM, Johnson SC, Kastman EK, et al. (2009). . Science. 325 (5937): 201–4. :. :.   .  .
Mattison, Julie A.; et al. (2012). . Nature. 489 (7415): 318–321. :. :.   .  .
Colman RJ; Beasley TM; Kemnitz JW; Johnson SC; Weindruch R; Anderson RM (Apr 1, 2014). . Nature Communications. 5: 3557. :. :.   .   2014.
"There may be little advantage of moderate CR over modest CR—this would be an extremely important discovery and one that merits further investigation."
Hayflick, Leonard. (1994). How and why we age. New York: Ballantine Books. p. 261.  .  .
Bowman K; Delgado J; Henley WE; Masoli JA; Kos K; Brayne C; Thokala P; Lafortune L; Kuchel GA; Ble A; Melzer D; Ageing Well Programme of the NIHR School for Public Health Research, England (Aug 4, 2016). . J Gerontol a Biol Sci Med Sci. 72 (2): 203–209. :.   .  .
Nakagawa, S Lagisz, M Hector, Katie L.; Spencer, Hamish G. (). "Comparative and meta-analytic insights into life extension via dietary restriction". Aging Cell. 11 (3): 401–409. :.  .  .
Simpson, Stephen J.; Raubenheimer, David (). . Aging. 1 (10): 875–880. :.  .   .  .
Melnik, Bodo C. (). . World Journal of Diabetes. 3 (3): 38–53. :.  .   .  .
Yan, L Lamb, Richard F. (). "Amino acid sensing and regulation of mTORC1". Seminars in Cell & Developmental Biology. 23 (6): 621–625. :.  .  .
Rees, K; Hartley, L; Flowers, N; Clarke, A; Hooper, L; Thorogood, M; Stranges, S (12 August 2013). "'Mediterranean' dietary pattern for the primary prevention of cardiovascular disease". The Cochrane database of systematic reviews. 8 (8): CD009825. :.  .
Sofi F, Cesari F, Abbate R, Gensini GF, Casini A (2008). . BMJ (Clinical research ed.). 337 (sep11 2): a1344. :.   .  .
de Gaetano, Giovanni (). . ScienceDaily.
Rhonda Rowland (15 February 2002). . CNN 2013.
Patel SR, Ayas NT, Malhotra MR, White DP, Schernhammer ES, Speizer FE, Stampfer MJ, Hu FB (May 2004). "A prospective study of sleep duration and mortality risk in women". Sleep. 27 (3): 440–4.  .
Ferrie JE, Shipley MJ, Cappuccio FP, Brunner E, Miller MA, Kumari M, Marmot MG (December 2007). . Sleep. 30 (12): 1659–66.   .  .
– University of Warwick.
Patel SR, Malhotra A, Gottlieb DJ, White DP, Hu FB (July 2006). . Sleep. 29 (7): 881–9.   .  .; cf. Irwin MR, Ziegler M (February 2005). "Sleep deprivation potentiates activation of cardiovascular and catecholamine responses in abstinent alcoholics". Hypertension. 45 (2): 252–7. :.  .
Yetish G, Kaplan H, Gurven M, Wood B, Pontzer H, Manger PR, Wilson C, McGregor R, Siegel JM (November 2015). . Curr. Biol. 25 (21): 2862–8. :.   .  .
Gremeaux, V; Gayda, M; Lepers, R; Sosner, P; Juneau, M; Nigam, A (December 2012). "Exercise and longevity". Maturitas. 73 (4): 312–7. :.  .
Department Of Health And Human Services, United States (1996). . United States Department of Health.  .
Woods, Jeffrey A.; Wilund, Kenneth R.; Martin, Stephen A.; Kistler, Brandon M. (). . Aging and Disease. 3 (1): 130–140.  .   .  .
Kyu, Hmwe H; Bachman, Victoria F; Alexander, Lily T; Mumford, John E Afshin, A Estep, K Veerman, J L Delwiche, K Iannarone, Marissa L; Moyer, Madeline L; Cercy, K Vos, T Murray, Christopher J L; Forouzanfar, Mohammad H (9 August 2016). . BMJ. 354: i3857. :.   .  .
Notterman DA, Mitchell C (2015). . Pediatric Clinics of North America (Review). 62 (5): 1227–40. :.   .  .
Quinlan J, Tu MT, Langlois EV, Kapoor M, Ziegler D, Fahmi H, Zunzunegui MV (2014). . Syst Rev (Review). 3 (40): 40. :.   .  .
Noordam R, Gunn DA, Tomlin CC, Rozing MP, Maier AB, Slagboom PE, Westendorp RG, van Heemst D, de Craen AJ, Leiden Longevity Study group (2012). "Cortisol serum levels in familial longevity and perceived age: the Leiden longevity study". Psychoneuroendocrinology. 37 (10): 1669–75. :.  .
Lazzarino AI, Hamer M, Gaze D, Collinson P, Steptoe A (2013). . J Am Coll Cardiol. 62 (18): . :.   .  .
Holt-Lunstad J, Smith TB, Layton JB (2010). . PLOS Medicine. 7 (7): e1000316. :.   .  .
. stanford.edu. Archived from
on 11 September 2016.
Koenig H. G., King D. E., Carson V. B (2012). Handbook of religion and health (2nd ed.). New York: Oxford University Press. p476
. <. 2 April 2015.
Lam YY, Peterson CM, Ravussin E (2013). "Resveratrol vs. calorie restriction: data from rodents to humans". Exp Gerontol. 48 (10): 1018–24. :. &#160;.
Pryor, R; Cabreiro, F (1 November 2015). . The Biochemical Journal. 471 (3): 307–22. :. &#160; . &#160;.
Powers RW, Kaeberlein M, Caldwell SD, Kennedy BK, Fields S (2006). . Genes Dev. 20 (2): 174–84. :. &#160; . &#160;.
Harrison DE, Strong R, Sharp ZD, Nelson JF, Astle CM, Flurkey K, Nadon NL, Wilkinson JE, Frenkel K, Carter CS, Pahor M, Javors MA, Fernandez E, Miller RA (2009). . Nature. 460 (7253): 392–5. :. :. &#160; . &#160;.
– The Times (8 July 2009).
Miller RA, Harrison DE, Astle CM, Baur JA, Boyd AR, de Cabo R, Fernandez E, Flurkey K, Javors MA, Nelson JF, Orihuela CJ, Pletcher S, Sharp ZD, Sinclair D, Starnes JW, Wilkinson JE, Nadon NL, Strong R (February 2011). . J. Gerontol. A Biol. Sci. Med. Sci. 66 (2): 191–201. :. &#160; . &#160;.
Ingram DK, Roth GS (March 2011). "Glycolytic inhibition as a strategy for developing calorie restriction mimetics". Experimental Gerontology (review). 46 (2–3): 148–154. :. &#160;.
Tardif, S; Ross, C; Bergman, P; Fernandez, E; Javors, M; Salmon, A; Spross, J; Strong, R; Richardson, A (19 July 2014). . J Gerontol a Biol Sci Med Sci. 70 (5): 577–588. :. &#160; . &#160;.
Callaway, Ewen (2010). "Telomerase reverses ageing process". Nature. :.
Blagosklonny, M. V. (2009). . Aging. 1 (3): 281–8. &#160; . &#160;.
Kogan, V Molodtcov, I Menshikov, Leonid I.; Shmookler Reis, Robert J.; Fedichev, Peter (2015). . Scientific Reports. 5. :.
29 April 2015 at the .. imminst.org.
Miller, Richard A.; Harrison, David E.; Astle, Clinton M.; Floyd, Robert A.; Flurkey, K Hensley, Kenneth L.; Javors, Martin A.; Leeuwenburgh, C Nelson, James F.; Ongini, E Nadon, Nancy L.; Warner, Huber R.; Strong, Randy (2007). "An aging Interventions Testing Program: Study design and interim report". Aging Cell. 6 (4): 565–75. :. &#160;.
. Science against aging foundation. Archived from
on 18 February 2015.
. Palo Alto Longevity Prize 2014.
Ashlee Vance (9 September 2014). .
(Press release). . 9 September 2014. Archived from the original on 6 October .
Aaron Kinney (14 September 2014). .
Victoria Thorp (23 November 2014). . Palo Alto Pulse 2014.
Phillips, Judith, Kristine Ajrouch, and Sarah Hillcoat-Nallétamby (2010) Key Concepts in Social Gerontology. SAGE Publications. &#160;. pp. 12–13.
. UNFPA. 2012.
Vincent, John A. (2005). "Understanding generations: Political economy and culture in an ageing society". The British Journal of Sociology. 56 (4): 579–99. :. &#160;.
. UNFPA. 2002.
. unfpa.org.
(PDF). United Nations Development Programme. Archived from
(PDF) on 27 May .
Chosewood, L. Casey. . NIOSH Science Blog. National Institute for Occupational Safety and Health 2012.
Basakha M; Yavari K; Sadeghi H; Naseri A. (2015). . Payavard Salamat. 9 (2): 131–146.
Basakha M, Yavari K, Sadeghi H, Naseri A (2014). . Journal of Research in Health Sciences. 14 (2): 152–6. &#160;.
Scheid, Teresa L.; Brown, Tony N. (2010). A Handbook for the Study of Mental Health (Second ed.). New York: Cambridge University Press.
Panek, Paul E.; Hayslip, Bert (1989). Adult development and aging. San Francisco: Harper & Row. &#160;.[]
Anita Wejbrandt (2014) Defining aging in cyborgs: A bio-techno-social definition of aging, Journal of Aging Studies, Volume 31, Pages 104–109
Chawla, M Dubois, Hans F. W.; Chawla, Richard B. (2006). "The Impact of Aging on Long-Term Care in Europe and Some Potential Policy Responses". International Journal of Health Services. 36 (4): 719–46. :. &#160;.
Reinhardt, U. E. (2003). "Does the Aging of the Population Really Drive the Demand for Health Care?". Health Affairs. 22 (6): 27–39. :. &#160;.
Meara, E.; White, C.; Cutler, D. M. (2004). "Trends in Medical Spending by Age, ". Health Affairs. 23 (4): 176–83. :. &#160;.
Idler, E. L. (2003). "Discussion: Gender Differences in Self-Rated Health, in Mortality, and in the Relationship Between the Two". The Gerontologist. 43 (3): 372–375. :.
Deeg, D. J. H.; Bath, P. A. (2003). "Self-Rated Health, Gender, and Mortality in Older Persons: Introduction to a Special Section". The Gerontologist. 43 (3): 369–71. :. &#160;.
Benyamini, Y.; Blumstein, T.; Lusky, A.; Modan, B. (2003). "Gender Differences in the Self-Rated Health-Mortality Association: Is It Poor Self-Rated Health That Predicts Mortality or Excellent Self-Rated Health That Predicts Survival?". The Gerontologist. 43 (3): 396–405; discussion 372–5. :. &#160;.
Kunzmann, U Little, Todd D; Smith, Jacqui (2000). "Is age-related stability of subjective well-being a paradox? Cross-sectional and longitudional evidence from the Berlin Aging Study". Psychology and Aging. 15 (3): 511–526. :.
Jylh?, M Guralnik, Jack M; Balfour, J Fried, Linda P (2001). "Walking Difficulty, Walking Speed, and Age as Predictors of Self-Rated Health: The Women's Health and Aging Study". Journal of Gerontology. 56A (10): M609–17. &#160;.
Heckhausen, Jutta (1999). Developmental Regulation in Adulthood: Age-Normative and Sociostructural Constraints as Adaptive Challenges. Cambridge University Press. &#160;.
Sargent-Cox, K Anstey, K Luszcz, Mary (2008). "Determinants of Self-Rated Health Items With Different Points of Reference". Journal of Aging and Health. 20 (6): 739–761. :.
Idler, Ellen L (1993). "Age differences in self-assessments of health: Age changes, cohort difference, or survivorship?". Journal of Gerontology. 48 (6): S289. :.
Williamson, JD; Fried, LP (1996). "Characterization of older adults who attribute functional decrements to "old age"". Journal of the American Geriatrics Society. 44 (12): . :.
Baltes, Paul B.; Baltes, Margret M. (1990). "Psychological perspectives on successful aging: The model of selective optimization with compensation". In Baltes, Paul B.; Baltes, Margret M. Successful Aging. pp.&#160;1–34. :. &#160;.
Rowe, J.; Kahn, R. (1987). "Human aging: Usual and successful". Science. 237 (4811): 143–9. :. :. &#160;.
Job 14:5-7 A man’s days are numbered. You know the number of his months. He cannot live longer than the time You have set. So now look away from him that he may rest, until he has lived the time set for him like a man paid to work. For there is hope for a tree, when it is cut down, that it will grow again, and that its branches will not stop growing
Find more aboutAgeingat Wikipedia's
from Wiktionary
from Commons
from Wikiquote
from Wikibooks
from Wikidata
Statistics on population ageing and life expectancy
HelpAge International and UNFPA (2012).
development
: Hidden categories: