aged

• adj.

• 高齢の、老齢の、歳の

• n.

• 高齢者

関

age、elderly

　 　 　 　 　 　 　 　

WordNet

1. people who are old collectively; "special arrangements were available for the aged" (同)elderly
2. at an advanced stage of erosion (pronounced as one syllable); "aged rocks"
3. (used of tobacco) aging as a preservative process (`aged is pronounced as one syllable) (同)cured
4. advanced in years; (`aged is pronounced as two syllables); "aged members of the society"; "elderly residents could remember the construction of the first skyscraper"; "senior citizen" (同)elderly, older, senior
5. having attained a specific age; (`aged is pronounced as one syllable); "aged ten"; "ten years of age" (同)of age
6. of wines, fruit, cheeses; having reached a desired or final condition; (`aged pronounced as one syllable); "mature well-aged cheeses" (同)ripened
7. harmed or injured or spoiled; "I wont buy damaged goods"; "the storm left a wake of badly damaged buildings"
8. the property characteristic of old age (同)senescence
9. how long something has existed; "it was replaced because of its age"
10. a time of life (usually defined in years) at which some particular qualification or power arises; "she was now of school age"; "tall for his eld" (同)eld
11. begin to seem older; get older; "The death of his wife caused him to age fast"
12. make older; "The death of his child aged him tremendously"

PrepTutorEJDIC

1. 《補語にのみ用い,数詞を伴って》…『歳の』 / (酒・チーズなどが)熟成した
2. 年とった
3. 〈U〉(一般に)『年齢』,寿命;〈C〉(個々の)『年齢』,年 / 〈U〉成年(おとなとしての資格・権利を得る年齢;通例18または21歳) / 〈U〉『老齢』;《集合的に》老人たち / 〈U〉(人生の)『一時期』;〈C〉世代(generation) / 〈U〉〈C〉《しばしばA-》(歴史上の)『時代』 / 〈C〉《話》長い間 / 年をとる,ふける;〈物が〉古くなる / 〈年〉'を'とらせる;〈物〉'を'古びさせる
4. =aging

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2016/05/09 16:08:52」(JST)

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For other uses, see Ageing (disambiguation).

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Ageing
A human face showing signs of ageing
Classification and external resources
OMIM	502000
MeSH	D000375

Ageing (British English) or aging (American English) is the process of becoming older. In the narrow sense, the term refers to biological ageing of human beings, animals and other organisms. In the broader sense, ageing can refer to single cells within an organism (cellular ageing) or to the population of a species (population ageing).

In humans, ageing represents the accumulation of changes in a human being over time, encompassing physical, psychological, and social change. Reaction time, for example, may slow with age, while knowledge of world events and wisdom may expand. 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 die from age-related causes.

The causes of ageing are unknown; current theories are assigned to the damage concept, whereby the accumulation of externally induced damage (such as DNA point mutations) may cause biological systems to fail, or to the programmed ageing concept, whereby internal processes (such as DNA telomere shortening) may cause ageing.

The discovery, in 1934, that calorie restriction can extend lifespan twofold in rats, and the existence of species having negligible senescence and potentially immortal species such as Hydra, have motivated research into delaying and preventing ageing and thus age-related diseases.

Ageing versus immortality

Immortal Hydra, a relative of the jellyfish

Human beings and members of many other species necessarily experience ageing and mortality. In contrast, some species can be considered immortal: for example, bacteria fission to produce daughter cells, strawberry plants grow runners to produce clones of themselves, and animals in the genus Hydra have a regenerative ability with which they avoid dying of old age.

Even within humans and other mortal species, there are arguably cells with the potential for immortality: cancer cells which have lost the ability to die such as the HeLa cell line, stem cells, and specifically germ cells (producing ova and spermatozoa). In artificial cloning, adult cells can be rejuvenated back 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 Hayflick Limit, discovered by Leonard Hayflick in 1961).

After a period of near perfect renewal (in humans, between 20 and 35 years of age), ageing is characterised by the declining ability to respond to stress, increasing homeostatic imbalance and the increased risk of disease. This currently irreversible series of changes inevitably ends in death.

Effects of ageing

Comparison of a normal aged brain (left) and the brain of a person with Alzheimer's disease (right). Characteristics that separate the two are pointed out.

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 hear high-frequency sounds above 20 kHz.
• A continuous decline in several cognitive processes occurs after a peak performance in the mid-20s age group.
• By age 30, wrinkles develop mainly due to photoageing, particularly affecting sun-exposed areas (face, hands) of fair-skinned individuals.
• Around age 35, female fertility declines sharply.
• In the mid-forties, presbyopia generally becomes apparent.
• Around age 50, hair turns grey in Caucasoids. Many men are affected by balding, and women enter menopause.
• In the 60–64 age cohort, osteoarthritis rises to 53%. Only 20% however report disabling osteoarthritis at this age.
• In the 70–79 age range, partial hearing loss affecting communication rises to 65%, predominantly among low-income males.
• Over the age of 85, thirst perception decreases, such that 41% of the elderly drink insufficiently. Frailty, defined as loss of muscle mass and mobility, affects 25% of those over 85.

Ageing furthermore is among the greatest known risk factors for most human diseases. Specifically, age is a major risk factor for most common neurodegenerative diseases. Dementia becomes more common with age. About 3% of people between the ages of 65–74 have dementia, 19% between 75 and 84 and nearly half of those over 85 years of age. The spectrum includes mild cognitive impairment, Alzheimer's disease, cerebrovascular disease, Parkinson's disease and Lou Gehrig's disease. Research has focused in particular on memory and ageing and has found decline in many types of memory with ageing, but not in semantic memory or general knowledge such as vocabulary definitions, which typically increases or remains steady until the late adulthood. Early studies on changes in cognition with age generally found declines in intelligence in the elderly, but studies were cross-sectional rather than longitudinal and thus results may be an artefact of cohort rather than a true example of decline. However, longitudinal studies could be confounded due to prior test experience. Intelligence may decline with age, though the rate may vary depending on the type 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: though neuron loss is minor after 20 years of age there is a 10% reduction each decade in the total length of the brain's myelinated axons.

Age can result in communication barriers, such as due to hearing loss and visual impairment. Sensory impairments include hearing and vision deficits. Changes in cognition, hearing, and vision are associated with healthy ageing and can cause problems when diagnosing dementia and aphasia due to the similarities. Common conditions that can increase the risk of hearing loss in elderly people are high blood pressure, diabetes or the use of certain medications harmful to the ear. Hearing aids are commonly referred to as personal amplifying systems, which can generally improve hearing by about 50%. In visual impairment, non-verbal communication is reduced, which can lead to isolation and possible depression. Macular degeneration is a common cause of vision loss in elderly people. This degeneration is caused by systemic changes in the circulation of waste products and growth of abnormal vessels around the retina causing the photoreceptors not to receive proper images.

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 back to a cause early in person's life, such as childhood poliomyelitis).

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 much higher, reaching 90%.

Biological basis of ageing

Main article: Senescence

95-year-old woman holding a five-month-old boy

At present, the biological basis of ageing is unknown, even in relatively simple and short-lived organisms. Less still is known about mammalian ageing, in part due to the much longer lives in even small mammals such as the mouse (around 3 years). A primary model organism for studying ageing is the nematode C. elegans, thanks to its short lifespan of 2–3 weeks, the ability to easily perform genetic manipulations or suppress gene activity with RNA interference, and other factors. Most known mutations and RNA interference targets that extend lifespan were first discovered in C. elegans.

Factors that are proposed to influence biological ageing fall into two main categories, programmed and damage-related. Programmed factors follow a biological timetable, perhaps 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 defense responses. Damage-related factors include environmental assaults to living organisms that induce cumulative damage at various levels.

There are three main metabolic pathways which can influence the rate of ageing:

• the FOXO3/Sirtuin pathway, probably susceptible to caloric restriction
• the Growth hormone/IGF-1-like signalling pathway
• the activity levels of the electron transport chain 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.

Programmed factors

The rate of ageing varies substantially across different species, and this, to a large extent, is genetically based. For example, perennial plants can produce clones of themselves by vegetative reproduction and are thus potentially immortal, while annual plants die each year and reproduce by sexual reproduction. Clonal immortality apart, there are certain species whose individual lifespans stand out among Earth's life-forms, including the bristlecone pine (however Hayflick states that the bristlecone pine has no cells older than 30 years), fish like the sturgeon and the rockfish, invertebrates like the hard clam (known as quahog in New England) and the sea anemone and lobster. The genetic aspect has also been demonstrated in studies of human centenarians.

In laboratory settings, researchers have demonstrated that selected alterations in specific genes can extend lifespan quite substantially in yeast and roundworms, less so in fruit flies and less again in mice. Some of the targeted genes have homologues across species and in some cases have been associated with human longevity.

• Telomeres: In humans and other animals, cellular senescence has been attributed to the shortening of telomeres at each cell division; when telomeres become too short, the cells senesce or die. The length of telomeres is therefore the "molecular clock", predicted by Hayflick. This agrees with the 'ageing-clock theory', which suggests that an ageing sequence is built into the operation of the nervous or endocrine system of the body. In rapidly dividing cells, shortening of the telomeres would provide such a clock. This idea is in contradiction with the evolutionary theory of ageing. Telomeres have experimentally been shown to shorten with each successive cell division. Shortened telomeres activate a mechanism that prevents further cell multiplication. This may be particularly limiting to tissues such as bone marrow and the arterial lining where cell division occurs repeatedly throughout life. The quantity of the hematopoietic stem cells that produce the blood components residing in the bone marrow of human beings have been found to decline with ageing. Mice lacking the telomerase enzyme do not have a dramatically reduced lifespan, although laboratory mice may be an exception due to their long hypervariable telomeres. Telomere length in wild mouse strains is unrelated to lifespan.
• A variation in the gene FOXO3A is known to have 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 sirtuin family of genes which have also been shown to have a significant effect on lifespan, in yeast and in nematodes.
• DNA methylation: 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. The fact that DNA methylation age of blood predicts all-cause mortality in later life suggests that it relates to a process that causes aging.
• Over-expression of the Ras2 gene increases lifespan in yeast 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.
• Diet (specifically, caloric restriction) substantially increases lifespan in many animals, including the delay or prevention of many age-related diseases. Typically, this involves caloric intake of 60–70% of what an ad libitum animal would consume, while still maintaining proper nutrient intake. In rodents, this has been shown to increase lifespan by up to 50%; this effect occurs for many other species besides mice, including species as diverse as yeast and Drosophila, and likely includes primates as well. There are two major studies of caloric restriction being performed in rhesus monkeys, one at the US National Institutes of Health, and the other at the University of Wisconsin-Madison. The basis for caloric restriction remains unclear, though it is likely mediated by nutrient-sensing pathways such as the mTOR pathway. Evidence in both animals and humans suggests that resveratrol may be a caloric restriction mimetic. However, 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. Alternatively, the benefits of dietary restriction can also be found by changing the macro nutrient profile to reduce protein intake with similar increases in longevity. Dietary protein restriction not only inhibits mTOR activity but also IGF-1, two other mechanisms implicated in ageing. Specifically, reducing leucine intake is sufficient to inhibit mTOR activity, achievable through reducing animal food consumption.
• mTOR, a protein that inhibits autophagy, has been linked to ageing through the insulin signalling pathway. It has been found, in various species, that caloric restriction leads to longer lifespans, an effect that is likely mediated by the nutrient-sensing function of the mTOR 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 glucose 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 reactive oxygen species on the body, which damage DNA and other organic material, so longevity would be increased.
• A decreased Growth hormone (GH)/Insulin Growth Factor-1 (IGF-1) signaling pathway has been associated with increased life span in various organisms including fruit flies, nematodes and mice. Even though the mechanism by which decreased GH/IGF-1 signaling increases longevity is unknown; various long-lived mice models with decreased GH and/or IGF-1 induced signaling have similar phenotype. This phenotype includes increased insulin sensitivity, enhanced stress resistance and protection from carcinogenesis. Long lived mice with decreased GH signaling (Ames, Snell, Ghrh and GHR -/- mice) showed between 20% and 68% increased longevity when compared with control mice. On the other hand, mice with decreased IGF-1 induced signaling, such as the IGF1R +/- and the Klotho transgenic mice revealed a 19 to 33% increase in life span when compared to control mice.
• Evolutionary theories of aging: Many have argued that life span, like other phenotypes, is selected. Traits that benefit early survival and reproduction will be selected for even if they contribute to an earlier death. Such a genetic effect is called the antagonistic pleiotropy 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 disposable soma effect when referring to an entire genetic programme (the organism diverting limited resources from maintenance to reproduction). Some evidence is provided by oxygen-deprived bacterial cultures. This would explain why the autosomal dominant disease, Huntington's disease, can persist even though it is inexorably lethal. Also, some of the genetic variants that increase fertility in the young are now known to increase cancer risk in the old. Such genes include p53 and BRCA1. The biological mechanisms which regulate lifespan evolved several hundred million years ago.
• Reproductive-cell cycle theory: The idea that ageing is regulated by reproductive hormones that act in an antagonistic pleiotropic 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 signaling 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 centralized 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 aging, has facilitated the conceptualization of why and how aging occurs at the evolutionary, physiological and molecular levels.
• Autoimmunity: The idea that ageing results from an increase in autoantibodies that attack the body's tissues. A number of diseases associated with ageing, such as atrophic gastritis and Hashimoto's thyroiditis, are probably autoimmune in this way. While inflammation is very much evident in old mammals, even SCID mice in SPF colonies still experience senescence.

An elderly Somali woman

Damage-related factors (non-programmed factors)

• DNA damage theory of ageing: Genetic damage, including mutations (damages to the DNA sequence) and epimutations (damage to the DNA scaffolding which regulates gene expression), causes abnormal gene expression and can lead to diseases such as cancer. 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. Known causes of cancer (radiation, chemical and viral) account for about 30% of the total cancer burden and for about 30% of the total DNA damage. DNA damage causes the cells to stop dividing or induces apoptosis, often affecting stem cell pools and hence hindering regeneration. DNA damage is thought to be the common pathway causing both cancer and ageing. Viral infection would appear to be the most likely cause of the other 70% of DNA damage, especially in cells that are not exposed to smoking and sunlight. It has also been argued that intrinsic causes of DNA damage are more important drivers of ageing.
• Genetic instability: 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, Bernard L. Strehler, "... genetic damage (particularly gene loss) is almost certainly (or probably the) central cause of aging."
• Accumulation of waste: A buildup of waste products in cells presumably interferes with metabolism. For example, a waste product called lipofuscin 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.
• 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 cross-linked compounds that interfere with normal cell function.
• Free-radical theory: Damage by free radicals, or more generally reactive oxygen species or oxidative stress, create damage that may gives rise to the symptoms we recognise as ageing. Michael Ristow's group has provided evidence that the effect of calorie restriction may be due to increased formation of free radicals within the mitochondria, causing a secondary induction of increased antioxidant defence capacity.

Society and culture

Main article: Aging and society

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: juvenile (via infancy, childhood, preadolescence, adolescence), early adulthood, middle adulthood, and late adulthood. More casual terms may include "teenagers," "tweens," "twentysomething", "thirtysomething", etc. as well as "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 voting age, drinking age, age of consent, age of majority, age of criminal responsibility, marriageable age, age of candidacy, and mandatory retirement age. Admission to a movie for instance, may depend on age according to a motion picture rating system. 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, chronological 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 aging in the 21st century, it highlighted the need to "Develop a new rights-based culture of aging 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 vast contributions to society including caregiving and volunteering. For example, "A study of Bolivian migrants who moved to Spain found that 69 percent left their children at home, usually with grandparents. In rural China, grandparents care for 38 percent of children aged under five whose parents have gone to work in cities."

Economics

See also: Population ageing

A map showing median age figures for 2001

Population ageing is the increase in the number and proportion of older people in society. Population ageing has three possible causes: migration, longer life expectancy (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 age of majority), 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 aging. Currently, over 11% of the world's current population are people aged 60 and older and the United Nations Population Fund (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 birth rates decline in developed countries, the median age itself rises accordingly. According to the United Nations, 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 Bureau of Labor Statistics 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 labor productivity enhancement should be considered to deal with negative consequences of ageing.

Sociology

In the field of sociology and mental health, aging is seen in five different views: aging as maturity, aging as decline, aging as a life-cycle event, aging as generation, and aging as survival. Positive correlates with aging often include economics, employment, marriage, children, education, and sense of control, as well as many others. The social science of aging includes disengagement theory, activity theory, selectivity theory, and continuity theory. Retirement, 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 aging and for instance a bio-techno-social definition of aging has been suggested.

Health care demand

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: improve system performance; redesign service delivery; support informal caregivers; 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 dementia.

It has been estimated that population ageing only explains 0.2 percentage points of the annual growth rate in medical spending of 4.3 percent since 1970. In addition, certain reforms to the Medicare system in the United States decreased elderly spending on home health care by 12.5 percent per year between 1996 and 2000.

Self-perception of ageing

Positive self-perception of health has been correlated with higher well-being and reduced mortality in the elderly. Various reasons have been proposed for this association; 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 socioeconomic status, 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 may be a result of social comparison; 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.

Successful ageing

See also: Successful ageing

The concept of successful ageing can be traced back to the 1950s and was popularised in the 1980s. Previous research into ageing exaggerated the extent to which health disabilities, such as diabetes or osteoporosis, could be attributed exclusively to age, and research in gerontology exaggerated the homogeneity of samples of elderly people. Other research shows that even late in life, potential exists for physical, mental, and social growth and development.

Traditional definitions of successful aging have emphasised absence of physical and cognitive disabilities. In their 1987 article, Rowe and Kahn characterised successful aging as involving three components: a) freedom from disease and disability, b) high cognitive and physical functioning, and c) social and productive engagement.

Management and reversal

See also: Life extension

Some researchers (specifically biogerontologists) who study the biology of ageing believe that the development of interventions which slow ageing is inevitable. Several drugs and food supplements 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.

Cancer geneticist Ronald A. DePinho and his colleagues published research in mice where telomerase 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.

mTOR inhibition and the frequent activation of autophagy has been shown to increase longevity in model organisms such as yeast, flies and mice. mTor inhibition and autophagy have also been linked to insulin sensitivity and the reduction of reactive oxygen species (ROS) damage, which is another major proposed cause to ageing. It has become clear that autophagy activation in the body by mTOR inhibition increases longevity. mTOR inhibition reduces ROS damage by activating autophagy, which will recycle the damaged parts of cells and re use them for functioning parts. This process reduces ROS damage to a reasonable amount, therefore increasing longevity. mTOR inhibition has also been linked to other major ageing diseases. mTOR inhibition has helped treat neurodegenerative diseases like Alzheimer's in mice. It has also been used to reduce tumor growth in several cancers including renal, breast and several other rare cancers. Finally mTOR inhibition is also linked to reducing obesity and increasing immune function. The mTOR inhibition reduces the likelihood of diet induced and age induced obesity in mice, but in some cases led to glucose intolerance. Caloric restriction and exercise are two ways to activate autophagy and inhibit mTOR which can help resolve all of these common age related health issues. Reducing dietary protein intake without any changes to calorie level as an alternative to caloric restriction has also been shown to have similar effects on inhibiting mTOR activity. Specifically, reducing leucine intake from protein sources was considered most beneficial in inhibiting mTOR activity, primarily achieved through consuming more plant based foods.

The cellular balance between energy generation and consumption (energy homeostasis) requires tight regulation during ageing. In 2011, it was demonstrated that acetylation levels of AMP-activated protein kinase change with age in yeast and that preventing this change slows yeast ageing.

Caloric restriction substantially affects lifespan in many animals, including the ability to delay or prevent many age-related diseases. Evidence in both animals and humans suggests that resveratrol may be a caloric restriction mimetic.

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 not be proportional; 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.

Research projects and prizes

Some research effort is directed to slow ageing and extend healthy lifespan.

The US National Institute on Aging currently funds an intervention testing program, 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 program aims to address this by conducting parallel experiments at three internationally recognised mouse ageing-centres, the Barshop Institute at UTHSCSA, the University of Michigan at Ann Arbor and the Jackson Laboratory.

Several companies and organisations, such as Google Calico, Human Longevity, Craig Venter, Gero, SENS Research Foundation, 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 Methuselah Foundation 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 Joon Yun.

See also

• Aging brain
• Aging movement control
• Aging of Europe
• Anti-aging movement
• Biodemography of human longevity
• Biological immortality
• Biomarkers of aging
• Clinical Geropsychology
• Death
• Epigenetic clock
• Genetics of aging
• List of life extension-related topics
• Longevity
• Old age
• Population aging
• Progeria
• Stem cell theory of aging
• Supercentenarian
• Transgenerational design

References

External links

• Global AgeWatch Statistics on population ageing and life expectancy
• HelpAge International and UNFPA (2012). Ageing in the 21st Century – A Celebration and A Challenge.
• The dictionary definition of ageing at Wiktionary
• Media related to Ageing at Wikimedia Commons

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• 1. 正常な加齢 normal aging
• 2. 高齢者の衰え frailty
• 3. 小児における弱視：マネージメントおよび転帰 amblyopia in children management and outcome
• 4. 変形性関節症の臨床症状と診断 clinical manifestations and diagnosis of osteoarthritis
• 5. 無症候性心筋梗塞 previously undiagnosed myocardial infarction

English Journal

• Estimating prevalence of osteoporosis: examples from industrialized countries.

• Wade SW1, Strader C, Fitzpatrick LA, Anthony MS, O'Malley CD.
• Archives of osteoporosis.Arch Osteoporos.2014 Dec;9(1):182. doi: 10.1007/s11657-014-0182-3. Epub 2014 May 16.
• In nine industrialized countries in North America, Europe, Japan, and Australia, country-specific osteoporosis prevalence (estimated from published data) at the total hip or hip/spine ranged from 9 to 38 % for women and 1 to 8 % for men. In these countries, osteoporosis affects up to 49 million in
• PMID 24847682

• Comparison of peripheral forearm DXA and clinical risk factor screening using FRAX® to assess the risk of HIV-associated low bone mass: a cross-sectional study.

• Short CE1, Shaw SG, Fisher MJ, Gilleece YC, Walker-Bone K.
• Archives of osteoporosis.Arch Osteoporos.2014 Dec;9(1):181. doi: 10.1007/s11657-014-0181-4. Epub 2014 May 14.
• There is growing awareness that HIV infection is associated with low bone mass and fracture. DXA is a relatively scarce resource. Therefore, we evaluated two tools: peripheral DXA (pDXA) at the forearm and Fracture Risk Assessment Tool (FRAX®) to see which performed best at identifying men who shou
• PMID 24847675

• Relationship between 25-hydroxyvitamin D concentrations, serum calcium, and parathyroid hormone in apparently healthy Syrian people.

• Sayed-Hassan R1, Abazid N, Alourfi Z.
• Archives of osteoporosis.Arch Osteoporos.2014 Dec;9(1):176. doi: 10.1007/s11657-014-0176-1. Epub 2014 Apr 9.
• Vitamin D deficiency (25-hydroxyvitamin D (25OHD) <25 nmol/L) was common in a convenience sample of apparently healthy Syrian adults. Female gender, season, and concealing clothing were independent predictors of vitamin D deficiency. Community-based research is needed to identify vulnerable subgr
• PMID 24715441

• The incidence rate of hip fracture in Shiraz, Iran during 2008-2010.

• Maharlouei N1, Khodayari M, Forouzan F, Rezaianzadeh A, Lankarani KB.
• Archives of osteoporosis.Arch Osteoporos.2014 Dec;9(1):165. doi: 10.1007/s11657-013-0165-9. Epub 2014 Jan 15.
• This study aimed to estimate the incidence rate of hip fracture during 2008-2010 in Shiraz, Iran. Overall, the standardized age-related incidence were 329.6/100,000 in men and 1,589.7/100,000 in women. The incidence rate in females was remarkably higher than the previous studies in Iran.PURPOSE: Thi
• PMID 24424876

Japanese Journal

• 終末期ケアにおける専門職間協働の現状と課題 —特別養護老人ホームにおける調査から—

• 岡山県立大学保健福祉学部紀要 = BULLETIN OF FACULTY OF HEALTH AND WELFARE SCIENCE, OKAYAMA PREFECTURAL UNIVERSITY 22, 167-176, 2016-03-12
• NAID 120005719335

• 学校予防教育プログラム TOP SELF「向社会性の育成」 : 小学校5年生での実施と効果の検討

• 鳴門教育大学研究紀要 31, 121-135, 2016-03-11
• NAID 120005728033

• 超高齢社会の地域医療と療養指導を考える (第43回内科学の展望 体質から生活までを考える代謝内科学) -- (予防と治療を考える)

• 日本内科学会雑誌 105(3), 417-421, 2016-03-10
• NAID 40020765447

• 若年成人における運動習慣の有無が筋内脂肪蓄積に及ぼす影響

• 愛知教育大学研究報告. 芸術・保健体育・家政・技術科学・創作編 65, 39-44, 2016-03-01
• NAID 120005727052

Related Links

• agedの意味 - goo辞書 英和和英

agedとは。意味や和訳。[形容詞]1 ((限定的)) 年老いた，老齢の；年を経た，古びた，古色を帯びた.⇒OLD【類語】an aged man老人an aged tree老木.2 老齢に特有の，老いのan aged complexion老人特有の顔色.3 …歳の[で]a man ...

• AGED FREE(エイジドフリー)は中高年やシニア層に向けた ...

AGED FREE(エイジドフリー)は中高年やシニア層に向けたアルバイト・お仕事紹介サイトです。 社会貢献と生きがいを求める高齢者を応援しています。 ヘルプ・よくある質問 お問合わせ サイトマップ 12月17日更新 全国掲載件数： 1020 件 ...

• Aged - definition of aged by The Free Dictionary

ag·ed (ā′jĭd) adj. 1. Being of advanced age; old. 2. Characteristic of old age. 3. (ājd) Having reached the age of: aged three. 4. (ājd) Brought to a desired ripeness or maturity: aged cheese. 5. Geology Approaching the base level of ...

Related Pictures

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★リンクテーブル★

リンク元	「高齢者」「老齢」「高齢」「歳」
拡張検索	「middle-aged」「caged」
関連記事	「age」

「高齢者」

　　[★]

英

elderly、aged

関

老化、加齢、歳、初老、老齢、年輩、高齢、老人、老齢者、老年者、高年齢

定義

• 国連の世界保健機関による定義：高齢者とは65歳以上。前期高齢者とは65歳以上74歳未満。後期高齢者とは75歳以上。末期高齢者とは85歳以上。

特徴

• 精神：人格変化(柔軟性の低下、自発性の低下、感情の制御困難(涙もろい、怒りっぽい)、社会的引きこもり)。若い頃の性格が先鋭化。
• 神経：反射低下

• 樹状突起棘の減少 >> ニューロンの脱落(ADでは優位)、軸索の変性
• 老人斑(大脳皮質、扁桃体)、神経原線維変化(海馬、嗅内皮質)

• 呼吸：残気量増加、肺活量低下、分時換気量低下、最大酸素摂取量低下　　←　呼吸数は不変

[show details]

増加	RV	DLCO	コンプライアンス	ガス不均等分布
低下	PaO2	VC	FEV1.0	FEV1.0%	弾性収縮力

• 心臓：一回心拍出量減少
• 血管

• 収縮期血圧上昇

• 消化器：吸収機能低下、食欲低下、便秘
• 肝臓：肝機能低下

• 薬物代謝のI相(加水分解、酸化、還元)の機能低下

• 腎臓：糸球体濾過量減少
• 骨：骨塩量減少
• 筋肉：筋力低下
• 関節：可動域低下(拘縮)、変形
• 水分量：細胞外液・細胞内液減少　→　脱水になりやすい
• 血液

• 脂質増加
• BUN増加　←　腎機能低下を反映
• 血清Cr増加　←　腎機能低下を反映

• 内分泌

• インスリン抵抗性増大
• ゴナドトロピン上昇

高齢者と医療

SUB12.

• 年齢階級別国民医療費(H20)「国民医療費」：65歳以上が54.6%と半数以上を占める。
• 年齢階級別一人あたり国民医療費(H20)「国民医療費」：65歳以上67万円、75歳以上83万円　⇔　それ以外の年齢階級はは10-25万円
• 傷病別・年齢階級別一般診療医療費の割合(H20)「国民医療費」：65歳以上では循環器疾患(27.1%)が最も多く、新生物(13.1%)がこれに次ぐ。
• 疾病別外来・入院受診率「患者調査」：(外来)循環器系疾患(高血圧性疾患)。(入院)循環器疾患(脳血管疾患)
• 年齢階級別死因順位(H21)「人口動態統計」：(65～89歳)①悪性新生物、②心疾患。(89～99歳)①心疾患、②肺炎

• 医療保険制度：後期高齢者医療制度：65-74歳で一定の障害がある者と75歳以上を対象とする。各都道府県の全市町村が加入する広域連合が保険者。財源は公費(5割)、支援(4割)、保険料(1割)
• 介護保険制度：65歳以上(第1号被保険者)と40-64歳(第2号被保険者)が対象となる。市町村が保険者。財源は公費(5割。国20%、調節交付金5%、都道府県12.5%、市町村12.5%)、保険料(第1号被保険者20%、第2号被保険者30%)

「老齢」

　　[★]

英

aged、elderly

関

歳、初老、高齢者、年輩、高齢、老人、老齢者、老年者、高年齢

「高齢」

　　[★]

英

aged、elderly

関

歳、初老、老齢、高齢者、年輩、老人、老齢者、老年者、高年齢

「歳」

　　[★]

英

age、aged

関

加齢、年齢、老齢、高齢者、熟成、高齢

「middle-aged」

　　[★]

• 中年の

関

middle age、midlife

　 　

「caged」

　　[★]

• ケージ化、ケージド

「age」

　　[★]

• n.

• 年齢、歳

• v.

• 加齢する、熟成する

関

aged、ageing、aging、year old