Eternal youth

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For other uses, see Eternal youth (disambiguation).
Youth and Time, John William Godward, 1901

Eternal youth is the concept of human physical immortality free of aging. The youth referred to is usually meant to be in contrast to the depredations of aging, rather than a specific age of the human lifespan. Achieving eternal youth so far remains beyond the capabilities of scientific technology. However, much research is being conducted in the sciences of genetics which may allow manipulation of the aging process in the future.[citation needed] Eternal youth is common in mythology, and is a popular theme in fiction.

Mythology

Eternal youth is a characteristic of the inhabitants of Paradise in Abrahamic religions.

The Hindus believe that the Vedic and the post-Vedic rishis have attained immortality, which implies the ability to change one's body's age or even shape at will. These are some of the siddhas in Yoga. Markandeya is said to always stay at the age of 16.

The difference between eternal life and the more specific eternal youth is a recurrent theme in Greek and Roman mythology. The mytheme of requesting the boon of immortality from a god, but forgetting to ask for eternal youth appears in the story of Tithonus. A similar theme is found in Ovid regarding the Cumaean Sibyl.

In Norse mythology, Iðunn is described as providing the gods apples that grant them eternal youthfulness in the 13th century Prose Edda.

Telomeres

An individual's DNA plays a role in the aging process. Aging starts as soon as one is born. As soon as cells start to die and begin to need to be replaced. On the ends of each chromosome are repetitive sequences of DNA, telomeres, that protect the chromosome from joining with other chromosomes and have several key roles. One of these roles is to regulate cell division by allowing each cell division to take a small amount of genetic code off. The amount taken off varies by the type off cell being replicated. The slow wearing away of the telomeres restricts cell division to 40-60 times, also known as the Hayflick limit. Once this limit has been reached more cells die than can be replaced in the same amount of time. Thus soon after this limit is reached the organism dies. The importance of telomeres is now clearly evident: lengthen the telomeres, lengthen the life.[1]

However a study of the comparative biology of mammalian telomeres indicated that telomere length correlates inversely, rather than directly, with lifespan, and concluded that the contribution of telomere length to lifespan remains controversial.[2] Also, telomere shortening does not occur with age in a some postmitotic tissues, such in the rat brain.[3] In humans, skeletal muscle telomere lengths remain stable from ages 23 –74.[4] In baboon skeletal muscle, that consists of fully differentiated post-mitotic cells, less than 3% of myonuclei contain damaged telomeres and this percentage does not increase with age. [5] Thus telomere shortening does not appear to be a major factor in the aging of the differentiated cells of brain or skeletal muscle.

Studies have shown that 90 percent of cancer cells contain large amounts of an enzyme called telomerase.[6] Telomerase is an enzyme that replenishes the worn away telomeres by adding bases to the ends and thus renewing the telomere. A cancer cell has in essence, turned on the telomerase gene, and this allows them to have an unlimited amount of divisions without the telomeres wearing away. Other kinds of cells that can surpass the Hayflick limit are: stem cells, hair follicles, and germ cells.[7] This is because they contain raised amounts of telomerase.

See also

References

  1. ↑ Lee J. Siegel. "ARE TELOMERES THE KEY TO AGING AND CANCER?". 
  2. ↑ Gomes NM, Ryder OA, Houck ML, Charter SJ, Walker W, Forsyth NR, Austad SN, Venditti C, Pagel M, Shay JW, Wright WE (2011). Comparative biology of mammalian telomeres: hypotheses on ancestral states and the roles of telomeres in longevity determination. Aging Cell 10(5):761-768. doi: 10.1111/j.1474-9726.2011.00718.x. PMID: 21518243
  3. ↑ Cherif H, Tarry JL, Ozanne SE, Hales CN (2003). Ageing and telomeres: a study into organ- and gender-specific telomere shortening. Nucleic Acids Res 31(5):1576-1583. PMID: 12595567
  4. ↑ Renault V, Thornell LE, Eriksson PO, Butler-Browne G, Mouly V (2003). Regenerative potential of human skeletal muscle during aging. Aging Cell 1(2):132-139. PMID: 12882343
  5. ↑ Jeyapalan JC, Ferreira M, Sedivy JM, Herbig U (2007) Accumulation of senescent cells in mitotic tissue of aging primates. Mech Ageing Dev 128(1):36-44. PMID: 17116315
  6. ↑ Klaus Damm (2001). "A highly selective telomerase inhibitor limiting human cancer cell proliferation". The EMBO Journal 20 (24). doi:10.1093/emboj/20.24.6958. 
  7. ↑ Peter J. Hornsby (2007). "Telomerase and the aging process". PubMed 42 (7): 575–81. doi:10.1016/j.exger.2007.03.007. PMC 1933587. PMID 17482404. 
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