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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 – discuss][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] |
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