From Wikipedia, the free encyclopedia - View original article

Classification and external resources
A human face showing signs of ageing
  (Redirected from Octogenarian)
Jump to: navigation, search
Classification and external resources
A human face showing signs of ageing

Ageing (British English) or aging (American English) is the accumulation of changes in a person over time.[1] Ageing in humans refers to a multidimensional process of physical, psychological, and social change. Some dimensions of ageing grow and expand over time, while others decline. Reaction time, for example, may slow with age, while knowledge of world events and wisdom may expand. Research shows that even late in life, potential exists for physical, mental, and social growth and development.[2] Ageing is an important part of all human societies reflecting the biological changes that occur, but also reflecting cultural and societal conventions. Roughly 100,000 people worldwide die each day of age-related causes.[3]

Age is measured chronologically and a person's birthday is often an important event. However the term "ageing" is somewhat ambiguous. Distinctions may be made between "universal ageing" (age changes that all people share) and "probabilistic ageing" (age changes that may happen to some, but not all people as they grow older including diseases such as type two diabetes). Chronological ageing may also 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).[4] There is also a distinction 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).[5]

Differences are sometimes made between populations of elderly people. Divisions are sometimes made between the young old (65–74), the middle old (75–84) and the oldest old (85+). However problematic this may be, chronological age does not correlate perfectly with functional age, i.e. two people may be of the same age, but differ in their mental and physical capacities. Each nation, government and non-government organisation has different ways of classifying age.

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 commit most crimes, they are more likely to push for political and social change, to develop and adopt new technologies and to need education, the latter of which tend to lose political significance for people in the ageing process.[6] Older people have different requirements from society and government as opposed to young people and frequently differing values as well, such as for property and pension rights.[7] Older people are also far more likely to vote and in many countries the young are forbidden from voting. Thus, the aged have comparatively more, or at least different, political influence.[8]

Recent scientific successes in rejuvenation and extending a lifespan of model animals (mice 2.5 times, yeast and nematodes 10 times) and discovery of variety of species (including humans of advanced ages) having negligible senescence give hope to achieve negligible senescence (cancel ageing) for younger humans, reverse ageing or at least significantly delay it. In spite of the developments mentioned above and the fact that ageing is admitted to be the major cause of mortality in developed worlds,[9][10] scientists consider anti-ageing and life extension research to be greatly underfunded.[11] Although human life is declared to be a basic value in many societies, there is no strong awareness and thus demand for society to cancel human ageing.[12]

Early observations[edit]

The first formal studies of ageing appear to be those of Muhammad ibn Yusuf al-Harawi (1582) in his book entitled Ainul Hayat, published by Ibn Sina Academy of Medieval Medicine and Sciences.[13] This book is based only on ageing and its related issues. The original manuscript of Ainul Hayat was scribed in 1532 by the author Muhammad ibn Yusuf al-Harawi. Four copies of the manuscript survive and were reprinted in an edited and translated version by Hakim Syed Zillur Rahman (2007). The book discusses behavioural and lifestyle factors putatively influencing ageing including diet, environment and housing conditions. Also discussed are drugs that may increase and decrease ageing rates.


A map showing median age figures for 2001

In biology, senescence is the state or process of ageing. Cellular senescence is a phenomenon where isolated cells demonstrate a limited ability to divide in culture (the Hayflick Limit, discovered by Leonard Hayflick in 1961), while organismal senescence is the ageing of organisms. After a period of near perfect renewal (in humans, between 20 and 35 years of age), organismal senescence 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. Some researchers (specifically biogerontologists) are treating ageing as a disease. As genes that have an effect on ageing are discovered, ageing is increasingly being regarded in a similar fashion to other genetically influenced "conditions", potentially "treatable".[citation needed]

Some claim aging is an avoidable property of life, that it is the result of a genetic program. Numerous species show very low signs of aging ("negligible senescence"), the best known being trees like 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 quahog and sea anemone[14] and lobster.[15][16]

In humans and other animals, cellular senescence has been attributed to the shortening of telomeres with each cell cycle; when telomeres become too short, the cells die. The length of telomeres is therefore the "molecular clock", predicted by Hayflick. 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.[17] Stem cells regenerative capacity is affected by the age of the recipient.[18]

Among the signs of senescence subjective vertigo is reported.[19]

Other genes are known to affect the ageing process. The sirtuin family of genes have been shown to have a significant effect on the lifespan of yeast and nematodes. Over-expression of the RAS2 gene increases lifespan in yeast by 30%.[20]

In addition to genetic ties to lifespan, diet has been shown to substantially affect lifespan in many animals. Specifically, caloric restriction (that is, restricting calories to 30–50% less than an ad libitum animal would consume, while still maintaining proper nutrient intake), has been shown to increase lifespan in mice up to 50%.[citation needed] Caloric restriction works on many other species beyond mice (including species as diverse as yeast and Drosophila) and appears (though the data is not conclusive) to increase lifespan in primates according to a study done on Rhesus monkeys at the National Institute of Health (US), although the increase in lifespan is only notable if the caloric restriction is started early in life.[citation needed] Since, at the molecular level, age is counted not as time but as the number of cell doublings, this effect of calorie reduction could be mediated by the slowing of cellular growth and therefore, the lengthening of the time between cell divisions.[dubious ][citation needed]

Drug companies are currently searching for ways to mimic the lifespan-extending effects of caloric restriction without having to severely reduce food consumption.[weasel words][citation needed]

In his book, How and Why We Age, Hayflick notes a contradiction to the caloric restriction longevity increase theory for humans, noting that data from the Baltimore Longitudinal Study of Aging show that being thin does not favour longevity.[need quotation to verify][21]

Of the roughly 150,000 people who die each day across the globe, about two thirds—100,000 per day—die of age-related causes.[3] In industrialized nations, the proportion is much higher, reaching 90%.[3]

The evolution of ageing[edit]

Because evolution is the unifying theory of biology, understanding how evolution works is essential for explaining why we age. Ageing evolves because of the interaction of two effects. First, natural selection is stronger on the young than on the old; this explains why the autosomal dominant disease, Huntington's Disease, can persist even though it is inexorably lethal. Second, any genetic, developmental, or physiological effect that increases the reproductive performance of the young will evolve so long as the costs that it imposes on the old are not too great.[22] Or put another way, traits that benefit early survival and reproduction will be selected for even if they contribute to an earlier death. Such genetic effects are called antagonistic pleiotropy. "Antagonistic" refers to the impact on fitness in the young, which is positive and the negative effect on the old. Genetic pleiotropy refers to genes that have multiple effects. Antagonistic pleiotropy has been identified both in model organisms and in humans.[23] In humans, 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[24] and BRCA1.[25]

Dividing the lifespan[edit]

An elderly Caucasian woman

An animal's life is often divided into various age ranges. However, because biological changes are slow-moving and can vary within one's own species, arbitrary dates are usually set to mark periods of life. The human divisions given below are not valid in all cultures:

People from 13 to 19 years of age are also known as teens or teenagers. Tween or Twelvie is an American neologism referring to someone aged 10 through 12.[26] The casual terms "twentysomething", "thirtysomething", etc. are also in use to describe people by decades of age, along with the systematic terms such as "vicenarian", "tricenarian", "quadragenarian", etc.

Cultural variations[edit]

In some cultures there are other ways to express age: by counting years with or without including current year. For example, it could be said for the same person that he is twenty years old or that he is in the twenty-first year of his life. In Russian the former expression is generally used, the latter one has restricted usage: it is used for age of a deceased person in obituaries and for the age of an adult when it is desired to show him/her older than he/she is. (Psychologically, a woman in her 20th year seems older than one who is 19 years old.)

Depending on cultural and personal philosophy, ageing can be seen as an undesirable phenomenon, reducing beauty and bringing one closer to death; or as an accumulation of wisdom, mark of survival and a status worthy of respect. In some cases numerical age is important (whether good or bad), whereas others find the stage in life that one has reached (adulthood, independence, marriage, retirement, career success) to be more important.

East Asian age reckoning is different from that found in Western culture. Traditional Chinese culture uses a different ageing method, called Xusui (虛歲) with respect to common ageing which is called Zhousui (周歲). In the Xusui method, people are born at age 1, not age 0, possibly because conception is already considered to be the start of the life span and possibly because the number '0' was not historically present in Ancient China,[citation needed] and another difference is the ageing day: Xusui grows up at the Spring Festival (aka. Chinese New Year's Day), while Zhousui grows up at one's birthday.



An elderly Caucasian man.

There are variations in many countries as to what age a person legally becomes an adult.

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.

Similarly in many countries in jurisprudence, the defence of infancy is a form of defence by which a defendant argues that, at the time a law was broken, they were not liable for their actions and thus should not be held liable for a crime. Many courts recognise that defendants who are considered to be juveniles may avoid criminal prosecution on account of their age and in borderline cases the age of the offender is often held to be a mitigating circumstance.


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.[27] 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.[28] 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.[28]

Health care demand[edit]

Many societies in Western Europe and Japan have ageing population issues. 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.[29]

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.[30] 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. (Main article: Dementia).

Even so, 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 Medicare decreased elderly spending on home health care by 12.5 percent per year between 1996 and 2000.[31] This would suggest that the impact of ageing populations on health care costs is not inevitable.

Impact on prisons[edit]

As of July 2007, medical costs for a typical inmate in the United States might run an agency around $33 per day, while costs for an ageing inmate could run upwards of $100. Most State DOCs report spending more than 10 percent of the annual budget on elderly care. That is expected to rise over the next 10–20 years. Some states have talked about releasing ageing inmates early.[32]

Cognitive effects[edit]

Steady decline in many cognitive processes is seen across the lifespan, accelerating from the twenties or even thirties.[33] 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.[34] 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.[35] 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.[5] 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.[36]

Coping and well-being[edit]

Elderly Gambian woman.

Psychologists have examined coping skills in the elderly. Various factors, such as social support, religion and spirituality, active engagement with life and having an internal locus of control have been proposed as being beneficial in helping people to cope with stressful life events in later life.[37][38][39] Social support and personal control are possibly the two most important factors that predict well-being, morbidity and mortality in adults.[40] Other factors that may link to well-being and quality of life in the elderly include social relationships (possibly relationships with pets as well as humans), and health.[41]

Individuals in different wings in the same retirement home have demonstrated a lower risk of mortality and higher alertness and self-rated health in the wing where residents had greater control over their environment,[42][43] though personal control may have less impact on specific measures of health.[39] Social control, perceptions of how much influence one has over one's social relationships, shows support as a moderator variable for the relationship between social support and perceived health in the elderly and may positively influence coping in the elderly.[44]


Religion is an important factor used by the elderly in coping with the demands of later life and appears more often than other forms of coping later in life.[45] Religiosity is a multidimensional variable; while participation in religious activities in the sense of participation in formal and organised rituals may decline, it may become a more informal, but still important aspect of life such as through personal or private prayer.[46]

Self-rated health[edit]

Self-ratings of health, the beliefs in one's own health as excellent, fair or poor, has been correlated with well-being and mortality in the elderly; positive ratings are linked to high well-being and reduced mortality.[47][48] 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.[49] This finding is generally stronger for men than women,[48] though the pattern between genders is not universal across all studies and some results suggest sex-based differences only appear in certain age groups, for certain causes of mortality and within a specific sub-set of self-ratings of health.[49]


Retirement, a common transition faced by the elderly, may have both positive and negative consequences.[50]

Successful ageing[edit]

Two men practicing Tahtib. One of them is balding, suggesting vigorous activity at an advanced age.

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.[51][52]

Successful ageing consists of three components:[53]

  1. Low probability of disease or disability;
  2. High cognitive and physical function capacity;
  3. Active engagement with life.

A greater number of people self-report successful ageing than those that strictly meet these criteria.[51]

Successful ageing may be viewed an interdisciplinary concept, spanning both psychology and sociology, where it is seen as the transaction between society and individuals across the life span with specific focus on the later years of life.[54] The terms "healthy ageing"[51] and "optimal ageing" have been proposed as alternatives to successful ageing, partly because the term "successful ageing" has been criticised for making healthy ageing sound too competitive.

Six suggested dimensions of successful ageing include:[39]

  1. No physical disability over the age of 75 as rated by a physician;
  2. Good subjective health assessment (i.e. good self-ratings of one's health);
  3. Length of undisabled life;
  4. Good mental health;
  5. Objective social support;
  6. Self-rated life satisfaction in eight domains, namely marriage, income-related work, children, friendship and social contacts, hobbies, community service activities, religion and recreation/sports.

Political struggle against ageing[edit]

Though many scientists state that radical life extension, delaying and stopping ageing are achievable,[55] there are still no international or national programmes focused on stopping ageing or on radical life extension. There are political forces staying for and against life extension. In 2012 the Longevity political parties started in Russia, then in the USA, Israel and the Netherlands. These parties aim to provide political support to anti-ageing and radical life extension research and technologies and want to ensure the fastest possible and at the same time the softest societal transition to the next step: radical life extension and life without ageing, that will make it possible to provide the access to such technologies to the most of the currently living people.[56]


Biological theories[edit]

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

At present, the biological basis of ageing is unknown. Most scientists agree that substantial variability exists in the rates of ageing across different species and that this, to a large extent, is genetically based. In model organisms and laboratory settings, researchers have been able to demonstrate that selected alterations in specific genes can extend lifespan quite substantially in nematodes, less so in fruit flies and less again in mice. Life span extension can occur as the result of genetic alterations that increase DNA repair, reduce oxidative damage or reduce cell suicide (apoptosis) due to DNA damage.[57] Even in the relatively simple and short-lived organisms, the mechanism of ageing remain to be elucidated. Less is known about mammalian ageing, in part due to the much longer lives in even small mammals such as the mouse (around 3 years).

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.[58] 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.

Many have argued that life-span, like other phenotypes, is selected.

Some theories suggest that ageing is a disease. The examples are

Genetic theories[edit]

An elderly Somali woman.

Many theories suggest that ageing results from the accumulation of damage to DNA in the cell, or organ. Since DNA is the formative basis of cell structure and function, damage to the DNA molecule, or genes, can lead to its loss of integrity and early cell death.

Examples include:

Some have argued that ageing is programmed: that an internal clock detects a time to end investing in the organism, leading to death. This ageing-Clock Theory suggests, as in a clock, 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 based theory of ageing.[71][72]

  1. There is no original damage left unrepaired in a living being. If damage was left unrepaired a life threatening condition (such as bleeding, infection, or organ failure) would develop.
  2. Misrepair, the repair with less accuracy, does not happen accidentally. It is a necessary measure of the reparation system to achieve sufficiently quick reparation in situations of serious or repeated damage, to maintain the integrity and basic function of a structure, which is important for the survival of the living being.
  3. Hence the appearance of Misrepair increases the chance for the survival of individual, by which the individual can live at least up to the reproduction age, which is critically important for the survival of species. Therefore the Misrepair mechanism was selected by nature due to its evolutionary advantage.
  4. However, since Misrepair as a defective structure is invisible for the reparation system, it accumulates with time and causes gradually the disorganisation of a structure (tissue, cell, or molecule); this is the actual source of ageing.
  5. Ageing hence is the side-effect for survival, but important for species survival. Thus Misrepair might represent the mechanism by which organisms are not programmed to die but to survive (as long as possible) and ageing is just the price to be paid.

Non-biological theories[edit]

An elderly Iraqi man.
Disengagement Theory
This is the idea that separation of older people from active roles in society is normal and appropriate, and benefits both society and older individuals. Disengagement theory, first proposed by Cumming and Henry, has received considerable attention in gerontology, but has been much criticised.[5][77] The original data on which Cumming and Henry based the theory were from a rather small sample of older adults in Kansas City and from this select sample Cumming and Henry then took disengagement to be a universal theory.[78] There are research data suggesting that the elderly who do become detached from society are those who were initially reclusive individuals and such disengagement is not purely a response to ageing.[5]
Activity theory
In contrast to disengagement theory, this theory implies that the more active elderly people are, the more likely they are to be satisfied with life. The view that elderly adults should maintain well-being by keeping active has had a considerable history and since 1972, this has come to be known as activity theory.[78] However, this theory may be just as inappropriate as disengagement for some people as the current paradigm on the psychology of ageing is that both disengagement theory and activity theory may be optimal for certain people in old age, depending on both circumstances and personality traits of the individual concerned.[5] There are also data which query whether, as activity theory implies, greater social activity is linked with well-being in adulthood.[78]
Selectivity Theory
This theory mediates between Activity and Disengagement Theory, which suggests that it may benefit older people to become more active in some aspects of their lives, more disengaged in others.[78]
Continuity Theory
The view that in ageing people are inclined to maintain, as much as they can, the same habits, personalities and styles of life that they have developed in earlier years. Continuity theory is Atchley's theory that individuals, in later life, make adaptations to enable them to gain a sense of continuity between the past and the present and the theory implies that this sense of continuity helps to contribute to well-being in later life.[41] Disengagement theory, activity theory and continuity theory are social theories about ageing, though all may be products of their era rather than a valid, universal theory.

Prevention and reversal[edit]

Old man at a nursing home in Norway.

Several drugs and food supplements have been shown to retard or reverse the biological effects of ageing in animal models; none has yet been proven to do so in humans.

Transcendental Meditation (TM technique) may have beneficial age-related effects.[79][80][81][82][83]

In 2002, a team led by Professor Bruce Ames at UC Berkeley discovered that feeding aged rats a combination of acetyl-L-carnitine and alpha-lipoic acid (both substances are already approved for human use and sold in health food stores) produced a rejuvenating effect.[84] Ames said, "With these two supplements together, these old rats got up and did the macarena. The brain looks better, they are full of energy – everything we looked at looks like a young animal." UC Berkeley has patented the use of these supplements in combination and a company, Juvenon, has been established to market the treatment.

In 2007, researchers at the Salk Institute for Biological Studies identified a critical gene in nematode worms that specifically links eating fewer calories with living longer. Professor Andrew Dillin and colleagues showed that the gene pha-4 regulates the longevity response to calorie restriction.[85] In the same year Dr Howard Chang of the Stanford University School of Medicine was able to rejuvenate the skin of two-year-old mice to resemble that of newborns by blocking the activity of the gene NF-kappa-B.[86]

In 2008, a team at the Spanish National Cancer Research Center genetically engineered mice to produce ten times the normal level of the telomerase enzyme.[87] The mice lived 26% longer than normal.[88]

Also in 2008, a team led by Professor Michael O Thorner at the University of Virginia discovered that the drug MK-677 restored 20% of muscle mass lost due to ageing in humans aged 60 to 81. The subjects' growth hormone and insulin-like growth factor 1 (IGF-1) levels increased to that typical of healthy young adults.[89]

In 2009, a drug called rapamycin, discovered in the 1970s in the soil of Easter Island in the South Pacific, was found to extend the life expectancy of 20-month-old mice by up to 38%.[90] Rapamycin is approved for human use and is generally used to suppress the immune system and prevent the rejection of transplanted organs. It is thought to mimic the effect of calorie restriction.[91] Dr Arlan Richardson of the Barshop Institute said, "I never thought we would find an anti-ageing pill in my lifetime; however, rapamycin shows a great deal of promise to do just that."[this quote needs a citation] Professor Randy Strong of the University of Texas Health Science Center at San Antonio said, "We believe this is the first convincing evidence that the ageing process can be slowed and lifespan can be extended by a drug therapy starting at an advanced age."[this quote needs a citation]

Sign outside a modern anti-ageing clinic in Germany.

Also in 2009, the British Journal of Nutrition reported a study at Tufts University in Boston which showed that brain function and motor skills in aged rats could be improved by adding walnuts to their diet. The human equivalent would be to eat seven to nine walnuts per day.[92]

Another drug already approved for human use (for the treatment of diabetes), metformin has been shown to increase mouse lifespan by about five percent when treatment is started in middle age.[93]

In September 2009, researchers at UC Berkeley discovered they could restore youthful repair capability to muscle tissue taken from men aged 68 to 74 by in vitro treatment with mitogen-activated protein kinase.[94] This protein was found to be essential for the production of the stem cells necessary to repair muscle[95] after exercise and is present at reduced levels in aged individuals.

Ronald A. DePinho, a cancer geneticist at the Dana-Farber Cancer Institute and Harvard Medical School, published a paper[96] in Nature magazine in November 2010 which indicated that the organs of genetically altered mice, designed to activate telomerase after feeding them with a chemical, 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. Dr Lynne Cox of Oxford University said, "This paper is extremely important as it provides proof of the principle that short-term treatment to restore telomerase in adults already showing age-related tissue degeneration can rejuvenate aged tissues and restore physiological function."[this quote needs a citation]

In this experiment mice were engineered to not produce telomerase naturally but after a chemical "switch" the system would then restore telomerase. Importantly, this chemical does not have the ability to produce telomerase in animals that are not genetically altered. Moreover, telomerase activation is also associated with the growth of cancerous tumours which could prevent anti-ageing treatments using this discovery.

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 damage, which is another major proposed cause to aging. It has become clear that autophagy activation in the body by mTOR inhibition increases longevity. mTOR inhibition reduces Reactive Oxygen Species 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 aging 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.[70]

In December 2013 a study, published in the journal Cell, detailed work carried out by researchers in: Australia - (University of NSW), in Portugal - (Center for Neurosciences and Cell Biology; University of Coimbra; and University of Aveiro) and in the USA - (Harvard University; Massachusetts Institute of Technology; and National Institutes of Health). Researchers reversed the ageing process in the muscles of mice, making two-year-old mice appear to be six months old. Research has shown that declining NAD+ during aging causes pseudohypoxia and that raising nuclear NAD+ in old mice reverses pseudohypoxia and metabolic dysfunction, thus reversing the aging process.[97] [98] The study involved injecting NAD into the mice. This reversed pseudohypoxia and metabolic dysfunction and thus the ageing process. It has been reported that human trials will begin in 2014. [99]

Measure of age[edit]

The age of an adult human is commonly measured in whole years since the day of birth. Fractional years, months or even weeks may be used to describe the age of children and infants for finer resolution. The time of day the birth occurred is not commonly considered.

The measure of age has historically varied from this approach in some cultures. In parts of Tibet, age is counted from conception i.e. one is usually 9 months old when one is born.[100]

Age in prenatal development is normally measured in gestational age, taking the last menstruation of the mother as a point of beginning. Alternatively, fertilisation age, beginning from fertilisation can be taken.

Obtaining survey data on ageing[edit]

Numerous worldwide health, ageing and retirement surveys contain questions pertaining to pensions. The Meta Data Repository – created by the non-profit RAND Corporation and sponsored by the National Institute on Aging at the National Institutes of Health – provides access to meta data for these questions as well as links to obtain respondent data from the originating surveys.

See also[edit]


  1. ^ a b Bowen, Richard L.; Atwood, Craig S. (2004). "Living and Dying for Sex". Gerontology 50 (5): 265–90. doi:10.1159/000079125. PMID 15331856. 
  2. ^ Papalia, Diane. "Physical and Cognitive Development in Late Adulthood". Human Development. Mc-Graw Hill. 
  3. ^ a b c De Grey, Aubrey D.N.J (2007). "Life Span Extension Research and Public Debate: Societal Considerations". Studies in Ethics, Law, and Technology 1. doi:10.2202/1941-6008.1011. 
  4. ^ Phillips, Judith, Kristine Ajrouch, and Sarah Hillcoat-Nallétamby, Key Concepts in Social Gerontology (SAGE Publications, 2010) 12-13.
  5. ^ a b c d e Stuart-Hamilton, Ian (2006). The Psychology of Ageing: An Introduction. London: Jessica Kingsley Publishers. ISBN 1-84310-426-1. 
  6. ^ Cattaneo, M. Alejandra; Wolter, Stefan C. (2009). "Are the elderly a threat to educational expenditures?". European Journal of Political Economy 25 (2): 225–36. doi:10.1016/j.ejpoleco.2008.10.002. 
  7. ^ Vincent, John A. (2005). "Understanding generations: Political economy and culture in an ageing society". The British Journal of Sociology 56 (4): 579–99. doi:10.1111/j.1468-4446.2005.00084.x. PMID 16309437. 
  8. ^ Powell, Jason L. (2010). "The Power of Global Aging". Ageing International 35 (1): 1–14. doi:10.1007/s12126-010-9051-6. 
  9. ^ Lopez, Alan D; Mathers, Colin D; Ezzati, Majid; 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. doi:10.1016/S0140-6736(06)68770-9. PMID 16731270. 
  10. ^ Brunet Lab: Molecular Mechanisms of Longevity and Age Related Diseases. Retrieved on 11 April 2012.
  11. ^ Scientists' Open Letter on Aging. Retrieved on 12 December 2012.
  12. ^ "3d International Conference of "Genetics of Aging and Longevity"". Science for Life Extension Foundation. Retrieved 4 October 2013. 
  13. ^ Ainul Hayat. Edited by Hakim Syed Zillur Rahman, Ibn Sina Academy of Medieval Medicine and Sciences. 2007. ISBN 978-81-901362-9-7[page needed]
  14. ^ Physiological Basis of Ageing and Geriatrics, by Paola S. Timiras, p. 26, Informa Health Care, 2003, ISBN 0-8493-0948-4
  15. ^ Jacob Silverman. "Is there a 400 pound lobster out there?". howstuffworks. 
  16. ^ David Foster Wallace (2005). Consider the Lobster and Other Essays. Little, Brown & Company. ISBN 0-316-15611-6. [page needed]
  17. ^ Dedeepiya, Vidyasagar Devaprasad; Rao, Yegneswara Yellury; Jayakrishnan, Gosalakkal A.; Parthiban, Jutty K. B. C.; Baskar, Subramani; Manjunath, Sadananda Rao; Senthilkumar, Rajappa; Abraham, Samuel J. K. (2012). "Index of CD34+ Cells and Mononuclear Cells in the Bone Marrow of Spinal Cord Injury Patients of Different Age Groups: A Comparative Analysis". Bone Marrow Research 2012: 1. doi:10.1155/2012/787414. PMC 3398573. PMID 22830032. 
  18. ^ Birbrair, A.; Zhang, T.; Wang, Z.-M.; Messi, M. L.; Mintz, A.; Delbono, O. (2013). "Type-1 pericytes participate in fibrous tissue deposition in aged skeletal muscle". AJP: Cell Physiology 305 (11): C1098. doi:10.1152/ajpcell.00171.2013. 
  19. ^ Trinus, K.F. (2010). Types of dizziness, evidence-based approach. ASN. 
  20. ^ J Sun; Kale, SP; Childress, AM; Pinswasdi, C; Jazwinski, SM (1994-07-15). "Divergent roles of RAS1 and RAS2 in yeast longevity". Journal of Biological Chemistry 269 (28): 18638–45. PMID 8034612. 
  21. ^ Hayflick, Leonard. (1994). How and why we age. New York: Ballantine Books. p. 261. ISBN 978-0-345-33918-8. OCLC 29908633. 
  22. ^ Williams, George C. (1957). "Pleiotropy, Natural Selection, and the Evolution of Senescence". Evolution 11 (4): 398–411. doi:10.2307/2406060. JSTOR 2406060. 
  23. ^ Kirkwood, T. B. L.; Rose, M. R. (1991). "Evolution of Senescence: Late Survival Sacrificed for Reproduction". Philosophical Transactions of the Royal Society B: Biological Sciences 332 (1262): 15–24. doi:10.1098/rstb.1991.0028. PMID 1677205. 
  24. ^ Kang, H.-J.; Feng, Z.; Sun, Y.; Atwal, G.; Murphy, M. E.; Rebbeck, T. R.; Rosenwaks, Z.; Levine, A. J.; Hu, W. (2009). "Single-nucleotide polymorphisms in the p53 pathway regulate fertility in humans". Proceedings of the National Academy of Sciences 106 (24): 9761–6. doi:10.1073/pnas.0904280106. PMC 2700980. PMID 19470478. 
  25. ^ Smith, K. R.; Hanson, H. A.; Mineau, G. P.; Buys, S. S. (2011). "Effects of BRCA1 and BRCA2 mutations on female fertility". Proceedings of the Royal Society B: Biological Sciences 279 (1732): 1389–95. doi:10.1098/rspb.2011.1697. PMC 3282366. PMID 21993507. 
  26. ^ "Special Issues for Tweens and Teens". MediaSmarts. 2010. Retrieved 4 December 2012. 
  27. ^ "UN Human Development Report 2005" (PDF). United Nations Development Programme. Archived from the original on 2008-05-27. Retrieved 2010-10-07. 
  28. ^ a b Chosewood, L. Casey. "Safer and Healthier at Any Age: Strategies for an Aging Workforce". NIOSH Science Blog. National Institute for Occupational Safety and Health. Retrieved 6 August 2012. 
  29. ^ Chawla, Mukesh; 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. doi:10.2190/AUL1-4LAM-4VNB-3YH0. PMID 17175843. 
  30. ^ Reinhardt, U. E. (2003). "Does the Aging of the Population Really Drive the Demand for Health Care?". Health Affairs 22 (6): 27–39. doi:10.1377/hlthaff.22.6.27. PMID 14649430. 
  31. ^ Meara, E.; White, C.; Cutler, D. M. (2004). "Trends in Medical Spending by Age, 1963-2000". Health Affairs 23 (4): 176–83. doi:10.1377/hlthaff.23.4.176. PMID 15318578. 
  32. ^ Aday, Ronald H. (2003). Aging Prisoners: Crisis in American Corrections. Praeger. ISBN 0-275-97123-6. [page needed]
  33. ^ Salthouse, Timothy A. (2009). "When does age-related cognitive decline begin?". Neurobiology of Aging 30 (4): 507–14. doi:10.1016/j.neurobiolaging.2008.09.023. PMC 2683339. PMID 19231028. 
  34. ^ Schaie, K. Warner (2005). Developmental Influences on Adult Intelligence. doi:10.1093/acprof:oso/9780195156737.001.0001. ISBN 978-0-19-515673-7. [page needed]
  35. ^ Desjardins, Richard; Warnke, Arne Jonas (2012). Ageing and Skills. OECD Education Working Papers. doi:10.1787/5k9csvw87ckh-en. 
  36. ^ Marner, Lisbeth; Nyengaard, Jens R.; Tang, Yong; Pakkenberg, Bente (2003). "Marked loss of myelinated nerve fibers in the human brain with age". The Journal of Comparative Neurology 462 (2): 144–52. doi:10.1002/cne.10714. PMID 12794739. 
  37. ^ Schulz, Richard; Heckhausen, Jutta (1996). "A life span model of successful aging". American Psychologist 51 (7): 702–14. doi:10.1037/0003-066X.51.7.702. PMID 8694390. 
  38. ^ Windsor, T. D.; Anstey, K. J.; Butterworth, P.; Luszcz, M. A.; Andrews, G. R. (2007). "The Role of Perceived Control in Explaining Depressive Symptoms Associated with Driving Cessation in a Longitudinal Study". The Gerontologist 47 (2): 215–23. doi:10.1093/geront/47.2.215. PMID 17440126. 
  39. ^ a b c Diane F. Gilmer; Aldwin, Carolyn M. (2003). Health, illness, and optimal aging: biological and psychosocial perspectives. Thousand Oaks: Sage Publications. ISBN 0-7619-2259-8. [page needed]
  40. ^ Smith, G. C.; Kohn, S. J.; Savage-Stevens, S. E.; Finch, J. J.; Ingate, R.; Lim, Y.-O. (2000). "The Effects of Interpersonal and Personal Agency on Perceived Control and Psychological Well-Being in Adulthood". The Gerontologist 40 (4): 458–68. doi:10.1093/geront/40.4.458. PMID 10961035. 
  41. ^ a b Bowling, Ann (2005). Aging well: quality of life in old age. [Milton Keynes]: Open University Press. ISBN 0-335-21509-2. [page needed]
  42. ^ Langer, Ellen J.; Rodin, Judith (1976). "The effects of choice and enhanced personal responsibility for the aged: A field experiment in an institutional setting". Journal of Personality and Social Psychology 34 (2): 191–8. doi:10.1037/0022-3514.34.2.191. PMID 1011073. 
  43. ^ Rodin, Judith; Langer, Ellen J. (1977). "Long-term effects of a control-relevant intervention with the institutionalized aged". Journal of Personality and Social Psychology 35 (12): 897–902. doi:10.1037/0022-3514.35.12.897. PMID 592095. 
  44. ^ Bisconti, T. L.; Bergeman, C. S. (1999). "Perceived Social Control as a Mediator of the Relationships Among Social Support, Psychological Weil-Being, and Perceived Health". The Gerontologist 39 (1): 94–103. doi:10.1093/geront/39.1.94. PMID 10028775. 
  45. ^ McFadden, Susan H. "Points of Connection: Gerontology and the Psychology of Religion". In Paloutzian, Raymond F.; Park, Crystal L. Handbook of the Psychology of Religion and Spirituality. Guiliford. pp. 162–76. ISBN 978-1-57230-922-7. 
  46. ^ Mindel, CH; Vaughan, CE (1978). "A multidimensional approach to religiosity and disengagement". Journal of gerontology 33 (1): 103–8. doi:10.1093/geronj/33.1.103. PMID 618958. 
  47. ^ 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. doi:10.1093/geront/43.3.372. 
  48. ^ a b 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. doi:10.1093/geront/43.3.369. PMID 12810900. 
  49. ^ a b 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. doi:10.1093/geront/43.3.396. PMID 12810904. 
  50. ^ Panek, Paul E.; Hayslip, Bert (1989). Adult development and aging. San Francisco: Harper & Row. ISBN 0-06-045012-6. [page needed]
  51. ^ a b c Strawbridge, W. J.; Wallhagen, M. I.; Cohen, R. D. (2002). "Successful Aging and Well-Being: Self-Rated Compared with Rowe and Kahn". The Gerontologist 42 (6): 727–33. doi:10.1093/geront/42.6.727. PMID 12451153. 
  52. ^ Rowe, J.; Kahn, R. (1987). "Human aging: Usual and successful". Science 237 (4811): 143–9. doi:10.1126/science.3299702. PMID 3299702. 
  53. ^ Rowe, J. W.; Kahn, R. L. (1997). "Successful Aging". The Gerontologist 37 (4): 433–40. doi:10.1093/geront/37.4.433. PMID 9279031. 
  54. ^ Featherman, David L.; Smith, Jacqui; Peterson, James G. (1993). "Successful aging in a post-retired society". In Baltes, Paul B.; Baltes, Margret M. Successful Aging: Perspectives from the Behavioral Sciences. Cambridge University Press. pp. 50–93. ISBN 978-0-521-43582-6. 
  55. ^[full citation needed]
  56. ^[full citation needed]
  57. ^ Bernstein C, Bernstein H. (2004) Aging and Sex, DNA Repair in. See page 58. Encyclopedia of Molecular Cell Biology and Molecular Medicine, 2nd edition. Robert A. Meyers (Editor) pages 55–98. Wiley-VCH. ISBN 3-527-30543-2 ISBN 978-3-527-30543-8
  58. ^ Miller, Richard A.; Harrison, David E.; Astle, Clinton M.; Floyd, Robert A.; Flurkey, Kevin; Hensley, Kenneth L.; Javors, Martin A.; Leeuwenburgh, Christiaan; Nelson, James F.; Ongini, Ennio; 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. doi:10.1111/j.1474-9726.2007.00311.x. PMID 17578509. 
  59. ^ Stibich, Mark [1]., 19 April 2009
  60. ^ m. Mikhelson, Victor; Gamaley, Irina (2013). "Telomere Shortening is a Sole Mechanism of Aging in Mammals". Current Aging Science 5 (3): 203–8. doi:10.2174/1874609811205030006. PMID 23387887. 
  61. ^ "Mitochondrial Theory of Aging and Other Aging Theories". 1Vigor. Retrieved 4 October 2013. 
  62. ^ Minamino, Tohru; Komuro, I (2008). "Role of telomeres in vascular senescence". Frontiers in Bioscience 13 (13): 2971–9. doi:10.2741/2902. PMID 17981770. 
  63. ^ Blasco, María A; Lee, Han-Woong; Hande, M.Prakash; Samper, Enrique; 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. doi:10.1016/S0092-8674(01)80006-4. PMID 9335332. 
  64. ^ Kipling, David; Cooke, Howard J. (1990). "Hypervariable ultra-long telomeres in mice". Nature 347 (6291): 400–2. doi:10.1038/347400a0. PMID 2170845. 
  65. ^ Hemann, M. T.; Greider, CW (2000). "Wild-derived inbred mouse strains have short telomeres". Nucleic Acids Research 28 (22): 4474–8. doi:10.1093/nar/28.22.4474. PMC 113886. PMID 11071935. 
  66. ^ Atwood, Craig S.; Bowen, Richard L. (2011). "The reproductive-cell cycle theory of aging: An update". Experimental Gerontology 46 (2–3): 100–7. doi:10.1016/j.exger.2010.09.007. PMID 20851172. 
  67. ^ Birbrair, A.; Zhang, T.; Wang, Z.-M.; Messi, M. L.; Mintz, A.; Delbono, O. (2013). "Type-1 pericytes participate in fibrous tissue deposition in aged skeletal muscle". AJP: Cell Physiology 305 (11): C1098. doi:10.1152/ajpcell.00171.2013. 
  68. ^ Gensler, Helen L.; Bernstein, Harris (1981). "DNA Damage as the Primary Cause of Aging". The Quarterly Review of Biology 56 (3): 279–303. doi:10.1086/412317. JSTOR 2826464. PMID 7031747. 
  69. ^ Freitas, Alex A.; De Magalhães, João Pedro (2011). "A review and appraisal of the DNA damage theory of ageing". Mutation Research/Reviews in Mutation Research 728 (1–2): 12–22. doi:10.1016/j.mrrev.2011.05.001. 
  70. ^ a b Johnson, Simon C.; Rabinovitch, Peter S.; Kaeberlein, Matt (2013). "MTOR is a key modulator of ageing and age-related disease". Nature 493 (7432): 338–45. doi:10.1038/nature11861. PMC 3687363. PMID 23325216. 
  71. ^ 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. ISBN 0-88167-310-2
  72. ^ a b c Bernstein C, Bernstein H. (1991) Aging, Sex, and DNA Repair (see pages 314, 320 and 326) Academic Press, San Diego. ISBN 0-12-092860-4 ISBN 978-0-12-092860-6
  73. ^ Bjorksten, Johan; Tenhu, Heikki (1990). "The crosslinking theory of aging — Added evidence". Experimental Gerontology 25 (2): 91–5. doi:10.1016/0531-5565(90)90039-5. PMID 2115005. 
  74. ^ Harman, D. (1981). "The aging process". Proceedings of the National Academy of Sciences 78 (11): 7124–8. doi:10.1073/pnas.78.11.7124. PMC 349208. PMID 6947277. 
  75. ^ Schulz, Tim J.; Zarse, Kim; Voigt, Anja; Urban, Nadine; Birringer, Marc; Ristow, Michael (2007). "Glucose Restriction Extends Caenorhabditis elegans Life Span by Inducing Mitochondrial Respiration and Increasing Oxidative Stress". Cell Metabolism 6 (4): 280–93. doi:10.1016/j.cmet.2007.08.011. PMID 17908557. 
  76. ^ Wang, Jicun; Michelitsch, Thomas; Wunderlin, Arne; Mahadeva, Ravi (2009). Aging as a consequence of misrepair -- a novel theory of aging 0904. p. 575. arXiv:0904.0575. Bibcode:2009arXiv0904.0575W. 
  77. ^ Benjamin Cornwell, Edward O. Laumann, and L. Philip Schumm. (2008). "The Social Connectedness of Older Adults: A National Profile." American Sociological Review 73(2):185-203.
  78. ^ a b c d Willis, Sherry L. (1996). Adult development and aging. New York, NY: HarperCollins College Publishers. ISBN 0-673-99402-3. [page needed]
  79. ^ Schneider, Robert H.; Alexander, Charles N.; Staggers, Frank; Rainforth, Maxwell; Salerno, John W.; Hartz, Arthur; Arndt, Stephen; Barnes, Vernon A.; Nidich, Sanford I. (2005). "Long-Term Effects of Stress Reduction on Mortality in Persons ≥55 Years of Age with Systemic Hypertension". The American Journal of Cardiology 95 (9): 1060–4. doi:10.1016/j.amjcard.2004.12.058. PMC 1482831. PMID 15842971. 
  80. ^ Wallace, RK; Dillbeck, M; Jacobe, E; Harrington, B (1982). "The effects of the transcendental meditation and TM-Sidhi program on the aging process". The International journal of neuroscience 16 (1): 53–8. doi:10.3109/00207458209147602. PMID 6763007. 
  81. ^ Alexander, CN; Langer, EJ; Newman, RI; Chandler, HM; Davies, JL (1989). "Transcendental meditation, mindfulness, and longevity: An experimental study with the elderly". Journal of personality and social psychology 57 (6): 950–64. doi:10.1037/0022-3514.57.6.950. PMID 2693686. 
  82. ^ Glaser, JL; Brind, JL; Vogelman, JH; Eisner, MJ; Dillbeck, MC; Wallace, RK; Chopra, D; Orentreich, N (1992). "Elevated serum dehydroepiandrosterone sulfate levels in practitioners of the Transcendental Meditation (TM) and TM-Sidhi programs". Journal of behavioral medicine 15 (4): 327–41. doi:10.1007/BF00844726. PMID 1404349. 
  83. ^ References of related research
  84. ^ Dietary Supplements Make Old Rats Youthful, May Rejuvenate Aging Humans. (2002-02-19). Retrieved on 11 April 2012.
  85. ^ Retrieved on 11 April 2012.
  86. ^ Adler, A. S.; Sinha, S.; Kawahara, T. L.A.; Zhang, J. Y.; Segal, E.; Chang, H. Y. (2007). "Motif module map reveals enforcement of aging by continual NF- B activity". Genes & Development 21 (24): 3244–57. doi:10.1101/gad.1588507. PMC 2113026. PMID 18055696. 
  87. ^ Spanish National Cancer Research Center. Retrieved on 11 April 2012.
  88. ^ Telomere enzyme a likely key to longevity. Retrieved on 11 April 2012.
  89. ^ Nass, Ralf; Pezzoli, SS; Oliveri, MC; Patrie, JT; Harrell Jr, FE; Clasey, JL; Heymsfield, SB; Bach, MA; Vance, ML; Thorner, MO (2008). "Effects of an Oral Ghrelin Mimetic on Body Composition and Clinical Outcomes in Healthy Older Adults". Annals of Internal Medicine 149 (9): 601–11. doi:10.7326/0003-4819-149-9-200811040-00003. PMC 2757071. PMID 18981485. 
  90. ^ Tests raise life extension hopes. BBC News (2009-07-08). Retrieved on 11 April 2012.
  91. ^ Bjedov, I; Toivonen, JM; Kerr, F; Slack, C; Jacobson, J; Foley, A; Partridge, L (2010). "Mechanisms of life span extension by rapamycin in the fruit fly Drosophila melanogaster". Cell metabolism 11 (1): 35–46. doi:10.1016/j.cmet.2009.11.010. PMC 2824086. PMID 20074526. 
  92. ^ Adding Walnuts To Good Diet May Help Older People Improve Motor And Behavioral Skills. (2009-04-19). Retrieved on 11 April 2012.
  93. ^[full citation needed]
  94. ^ Yang, Sarah. (2009-09-30) Scientists discover clues to what makes human muscle age. Retrieved on 11 April 2012.
  95. ^ Birbrair, Alexander; Zhang, Tan; Wang, Zhong-Min; Messi, Maria Laura; Enikolopov, Grigori N.; Mintz, Akiva; Delbono, Osvaldo (2013). "Role of Pericytes in Skeletal Muscle Regeneration and Fat Accumulation". Stem Cells and Development 22 (16): 2298–314. doi:10.1089/scd.2012.0647. PMC 3730538. PMID 23517218. 
  96. ^ Callaway, Ewen (2010). "Telomerase reverses ageing process". Nature. doi:10.1038/news.2010.635. 
  97. ^ [2] Declining NAD+ Induces a Pseudohypoxic State Disrupting Nuclear-Mitochondrial Communication during Aging, Cell, Dec 2013
  98. ^ [3]Guardian Newspaper - Online, Dec 2013
  99. ^ [4]Guardian Newspaper - Online, Dec 2013
  100. ^ Maddison, Angus (2006). The World Economy. Paris: OECD. p. 31. ISBN 92-64-02261-9. Retrieved 28 June 2008. 


External links[edit]