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HandWiki. Indefinite Lifespan. Encyclopedia. Available online: https://encyclopedia.pub/entry/31267 (accessed on 23 December 2024).
HandWiki. Indefinite Lifespan. Encyclopedia. Available at: https://encyclopedia.pub/entry/31267. Accessed December 23, 2024.
HandWiki. "Indefinite Lifespan" Encyclopedia, https://encyclopedia.pub/entry/31267 (accessed December 23, 2024).
HandWiki. (2022, October 26). Indefinite Lifespan. In Encyclopedia. https://encyclopedia.pub/entry/31267
HandWiki. "Indefinite Lifespan." Encyclopedia. Web. 26 October, 2022.
Indefinite Lifespan
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Indefinite lifespan (also known as indefinite life extension or bio-indefinite) is a term used in the life extension movement and transhumanism to refer to the hypothetical longevity of humans (and other life-forms) under conditions in which ageing is effectively and completely prevented and treated. Their lifespans would be "indefinite" (that is, they would not be "immortal"), because protection from the effects of aging on health does not guarantee survival. Such individuals would still be susceptible to death by disease, starvation, accidents, or deliberate killing, but not death from aging. Semantically, "indefinite lifespan" is more accurate than "immortality" which, especially in religious contexts, implies an inability to die.

life extension transhumanism longevity

1. Longevity Escape Velocity

“The first 1000-year-old is probably only ~10 years younger than the first 150-year-old”

Longevity escape velocity is a term used in the life extension movement. It is a hypothetical situation in which life expectancy is being increased faster than time is being expended. For example, in a given year in which longevity escape velocity would be maintained, technological advances would increase life expectancy more than that year took away by passing by.

2. Not Immortality

The terms "immortality" and "eternal youth" are often used as synonyms for "indefinite lifespan", but they carry connotations from their other contexts which science has deemed to be impossible. That is, immortal means "incapable of dying". Eternal implies guaranteed existence for eternity, and in this context is also implausible because of entropy. Even if cures were found for all the degenerative diseases, and effective treatments were developed for all the processes of aging, so that bodies could be maintained as easily as cars can be repaired, people would still be killed in accidents, slain in wars, choose to die, etc.

The term indefinite lifespan represents a more achievable state of affairs, because it merely implies freedom from death by aging or infirmity.

The use of the term is also sometimes favored for reasons of linguistic aesthetics, in the same way that the term birth control is preferred to "birth prevention" or "birth elimination" which both imply, as does 'immortality', that the choice is one-time only and has permanent consequences. Whereas the point of 'indefinite lifespan', like the point of 'birth control', is to gain the opportunity to lead one's life in a more conscious and deliberate manner.

3. Probability

This question is twofold. On the one hand it can be interpreted to mean, "Will a cure (or program of effective treatments) for aging ever be developed?" while on the other hand it could mean "Will the effective treatment of aging become available soon enough for those alive today to take advantage of it?" The answer to the first question is conditional on medical advancement: if medical science continues to advance in the fields of biogerontology and bioengineering, then some people hope the answer is "yes, that it will happen eventually, except if some event or series of events were to prevent the further advance of biological science" (see Risks to civilization, humans and planet Earth and the Doomsday Clock). Many scientists researching this area at the moment do not agree. They see a problem in not just individual diseases but in failure of repair mechanisms alluded to above in the discussion of thermodynamic considerations.

While science is constantly advancing and technology is becoming ever more sophisticated, the human body and mind are only evolving very slowly, and the aging process has not, in that time, become any more damaging (which, in short, is why we live three times as long on average in the twenty-first century as we did ten thousand years before).[1]

The answer to the second question depends on two factors: the first being how fast medical science advances, and the second being how well each person takes care of themself (such as utilizing the best available life extension technology or not, and generally eating and behaving in a healthful and non-degrading way), both of which may affect whether or not a given person is still alive when the cure (or set of treatments) becomes available. This strategy is captured in the subtitle "Live Long Enough to Live Forever" of the life extension book Fantastic Voyage, by Ray Kurzweil and Terry Grossman.

The second factor to the second question hinges on the first factor - no amount of healthy living will enable somebody alive today to reach the point of indefinite lifespan if medical science is curtailed significantly, or if aging turns out to be massively more complex than currently believed. However, if biomedical gerontology continues to improve, if somatic genetic engineering becomes safe and effective (and is not banned by opponents) within the relatively near future, it may be conceivable for some of those now alive to attain indefinite lifespans.

4. Proposed Techniques

Strategies for Engineered Negligible Senescence is a proposed research program for repairing all types of age-related damage.

Calorie restriction has been presented as a piece of the puzzle of reaching actuarial escape velocity.[2][3][4] Other proposed techniques include genetic engineering, telomere extension, organ regeneration, nanotechnology, and even mind uploading.[5]

On the theory that the primary cause of aging is DNA damage [see DNA damage theory of aging and DNA damage (naturally occurring)], there are, in principle, two ways of reducing DNA damage in cells, and thus allowing indefinite extension of lifespan. These are:

  1. Preventing the occurrence of DNA damage, and
  2. Repairing the DNA damage after it has occurred.

There is a large body of literature on antioxidant phytochemicals that reduce the occurrence of oxidative DNA damage. However, when intervention trials were carried out using these antioxidants as dietary supplements and cancer as the endpoint, the results generally proved disappointing.[6][7]

On the other hand, there seems to be evidence that certain dietary components stimulate repair of DNA damage, and protect against cancer as an endpoint. One of these is chlorogenic acid, a major component of, and absorbable from, coffee.[8] Coffee is protective against colorectal cancer,[9] and chlorogenic acid and its metabolites increase the protein expression levels of two DNA repair enzymes: Pms2 and PARP.[10] Another compound that protects against the early stages of cancer is naringenin, a citrus flavonoid.[11] Naringenin was shown to increase the mRNA expression levels of two DNA repair enzymes, DNA pol beta and OGG1.[12]

References

  1. Cairns J (1997). “Matters of Life and Death” Princeton University Press, Princeton, N.J. (see pages 8-13) ISBN:9780691002507
  2. Traister, Rebecca (November 22, 2006), "Diet your way to a long, miserable life!", Salon.com, archived from the original on January 29, 2009, https://web.archive.org/web/20090129015832/http://www.salon.com/mwt/feature/2006/11/22/cr_diets/index.html, retrieved 2008-10-31 
  3. Dibbell, Julian (October 23, 2006), "The Fast Supper", New York Magazine, http://nymag.com/nymag/features/23169/ 
  4. Birnbaum, Ben (2006), "Extension program", Boston College Magazine, http://bcm.bc.edu/issues/fall_2006/prologue/extension-program.html 
  5. Grossman, Lev (February 10, 2011). "2045: The Year Man Becomes Immortal". TIME. http://www.time.com/time/health/article/0,8599,2048138,00.html. Retrieved 2011-10-04. 
  6. Collins, Andrew R. (2005). "Antioxidant intervention as a route to cancer prevention". European Journal of Cancer 41 (13): 1923–30. doi:10.1016/j.ejca.2005.06.004. PMID 16111883.  https://dx.doi.org/10.1016%2Fj.ejca.2005.06.004
  7. Williams, Christina D. (2013). "Antioxidants and prevention of gastrointestinal cancers". Current Opinion in Gastroenterology 29 (2): 195–200. doi:10.1097/MOG.0b013e32835c9d1b. PMID 23274317.  https://dx.doi.org/10.1097%2FMOG.0b013e32835c9d1b
  8. Del Rio, Daniele; Stalmach, Angelique; Calani, Luca; Crozier, Alan (2010). "Bioavailability of Coffee Chlorogenic Acids and Green Tea Flavan-3-ols". Nutrients 2 (8): 820–33. doi:10.3390/nu2080820. PMID 22254058.  http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3257704
  9. Li, Guowei; Ma, Defu; Zhang, Yumei; Zheng, Wei; Wang, Peiyu (2013). "Coffee consumption and risk of colorectal cancer: a meta-analysis of observational studies". Public Health Nutrition 16 (2): 346–57. doi:10.1017/S1368980012002601. PMID 22694939.  https://dx.doi.org/10.1017%2FS1368980012002601
  10. Bernstein, Harris; Crowley-Skillicorn, Cheray; Bernstein, Carol; Dvorak, Katerina; Garewal, Harinder (2007). "Dietary Compounds that Enhance DNA Repair and their Relevance to Cancer and Aging". in Landseer, Breehn R.. New Research on DNA Repair. pp. 99–113. ISBN 978-1-60021-385-4. https://books.google.com/books?id=KxzvDlS90tUC&pg=PA99. 
  11. Leonardi, T.; Vanamala, J.; Taddeo, S. S.; Davidson, L. A.; Murphy, M. E.; Patil, B. S.; Wang, N.; Carroll, R. J. et al. (2010). "Apigenin and naringenin suppress colon carcinogenesis through the aberrant crypt stage in azoxymethane-treated rats". Experimental Biology and Medicine 235 (6): 710–7. doi:10.1258/ebm.2010.009359. PMID 20511675.  http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2885760
  12. Gao, K; Henning, S; Niu, Y; Youssefian, A; Seeram, N; Xu, A; Heber, D (2006). "The citrus flavonoid naringenin stimulates DNA repair in prostate cancer cells". The Journal of Nutritional Biochemistry 17 (2): 89–95. doi:10.1016/j.jnutbio.2005.05.009. PMID 16111881.  https://dx.doi.org/10.1016%2Fj.jnutbio.2005.05.009
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