View source for Life extension

{{Short description|Concept of extending human lifespan}}
{{Other uses}}
{{use dmy dates|date=May 2023}}
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'''Life extension''' is the concept of extending the human [[life expectancy|lifespan]], either modestly through improvements in medicine or dramatically by increasing the [[maximum lifespan]] beyond its generally-settled biological limit of [[Oldest people|around 125 years]].<ref>{{cite book | vauthors = Turner BS |title=Can We Live Forever? A Sociological and Moral Inquiry |publisher=Anthem Press |year=2009 |page=3}}</ref> Several researchers in the area, along with "life extensionists", "[[Immortality|immortalists]]", or "[[Longevity|longevists]]" (those who wish to achieve longer lives themselves), postulate that future breakthroughs in tissue [[rejuvenation (aging)|rejuvenation]], [[stem cell]]s, [[regenerative medicine]], [[molecular]] repair, [[gene therapy]], pharmaceuticals, and [[organ (anatomy)|organ]] replacement (such as with artificial organs or [[xenotransplantation]]s) will eventually enable humans to have indefinite lifespans through complete rejuvenation to a healthy youthful condition (agerasia<ref>{{OED|agerasia}}</ref>). The ethical ramifications, if life extension becomes a possibility, are debated by [[bioethicists]].

The sale of purported anti-aging products such as supplements and hormone replacement is a lucrative global industry. For example, the industry that promotes the use of hormones as a treatment for consumers to slow or reverse the [[aging]] process in the US market generated about $50&nbsp;billion of revenue a year in 2009.<ref name="AMA" /> The use of such hormone products has not been proven to be effective or safe.<ref name="AMA" /><ref name="Holliday">{{cite journal | vauthors = Holliday R | title = The extreme arrogance of anti-aging medicine | journal = Biogerontology | volume = 10 | issue = 2 | pages = 223–228 | date = April 2009 | pmid = 18726707 | doi = 10.1007/s10522-008-9170-6 | s2cid = 764136 }}</ref><ref name="PositionStatement" /><ref name="EMBOSENS">{{cite journal | vauthors = Warner H, Anderson J, Austad S, Bergamini E, Bredesen D, Butler R, Carnes BA, Clark BF, Cristofalo V, Faulkner J, Guarente L, Harrison DE, Kirkwood T, Lithgow G, Martin G, Masoro E, Melov S, Miller RA, Olshansky SJ, Partridge L, Pereira-Smith O, Perls T, Richardson A, Smith J, von Zglinicki T, Wang E, Wei JY, Williams TF | display-authors = 6 | title = Science fact and the SENS agenda. What can we reasonably expect from ageing research? | journal = EMBO Reports | volume = 6 | issue = 11 | pages = 1006–1008 | date = November 2005 | pmid = 16264422 | pmc = 1371037 | doi = 10.1038/sj.embor.7400555 }}</ref> Similarly, a variety of apps make claims to assist in extending the life of their users, or predicting their lifespans.<ref>{{Cite web |last=Ellefson |first=Lindsey |date=2025-02-12 |title=This 'Death Clock' App Made Me Rethink My Life |url=https://lifehacker.com/tech/this-death-clock-app-made-me-rethink-my-life |access-date=2025-06-27 |website=Lifehacker |language=en}}</ref><ref>{{Cite web |last=Downs |first=Maggie |date=2025-05-20 |title=The Death Clock App Uses AI to Predict When You'll Die |url=https://www.success.com/death-clock-ai-app/ |access-date=2025-06-27 |website=SUCCESS |language=en-US}}</ref><ref>{{Cite news |last=Petrow |first=Steven |date=9 June 2025 |title=How many years do I have left? An app gave me some helpful insights. |url=https://www.washingtonpost.com/health/2025/06/08/death-clock-ai-life-expectancy/ |access-date=27 June 2025}}</ref>

==Average life expectancy and lifespan==
{{Main|Senescence}}
During the process of [[aging]], an organism accumulates damage to its [[macromolecule]]s, [[cell (biology)|cells]], [[biological tissue|tissues]], and [[organ (anatomy)|organs]]. Specifically, aging is characterized as and thought to be caused by "genomic instability, telomere attrition, epigenetic alterations, loss of [[proteostasis]], deregulated nutrient sensing, mitochondrial dysfunction, [[cellular senescence]], stem cell exhaustion, and altered intercellular communication."<ref>{{cite journal | vauthors = López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G | title = The hallmarks of aging | journal = Cell | volume = 153 | issue = 6 | pages = 1194–1217 | date = June 2013 | pmid = 23746838 | pmc = 3836174 | doi = 10.1016/j.cell.2013.05.039 }}</ref> [[Oxidation]] damage to cellular contents caused by [[free radicals]] is believed to contribute to aging as well.<ref>Halliwell B, Gutteridge JMC (2007). Free Radicals in Biology and Medicine. Oxford University Press, USA, {{ISBN|019856869X}}, {{ISBN|978-0198568698}}</ref><ref>{{cite journal | vauthors = Holmes GE, Bernstein C, Bernstein H | title = Oxidative and other DNA damages as the basis of aging: a review | journal = Mutation Research | volume = 275 | issue = 3–6 | pages = 305–315 | date = September 1992 | pmid = 1383772 | doi = 10.1016/0921-8734(92)90034-M }}</ref>

The longest documented human lifespan is 122 years 164 days, the case of [[Jeanne Calment]], who according to records was born in 1875 and died in 1997, whereas the maximum lifespan of a [[wildtype]] mouse, commonly used as a model in research on aging, is about three years.<ref>{{cite web|url=http://www.informatics.jax.org/mgihome/other/mouse_facts1.shtml|title=Mouse Facts|publisher=informatics.jax.org}}</ref> Genetic differences between humans and mice that may account for these different aging rates include differences in efficiency of [[DNA repair]], [[antioxidant]] defenses, [[energy metabolism]], [[proteostasis]] maintenance, and recycling mechanisms such as [[autophagy]].<ref>{{cite web | vauthors =  Pedro de Magalhães J | date =  2014 | url =  http://www.senescence.info/causes_of_aging.html | title =  What Causes Aging? Damage-Based Theories of Aging | access-date =  24 January 2014 | archive-date =  5 July 2012 | archive-url =  https://web.archive.org/web/20120705183524/http://www.senescence.info/causes_of_aging.html | url-status =  dead }}</ref>

The average life expectancy in a population is lowered by [[infant mortality|infant]] and [[child mortality]], which are frequently linked to infectious diseases or nutrition problems. Later in life, vulnerability to [[accident]]s and age-related [[chronic disease]] such as [[cancer]] or [[cardiovascular disease]] play an increasing role in mortality. Extension of life expectancy and lifespan can often be achieved by access to improved medical care, [[vaccinations]], good [[diet (nutrition)|diet]], [[exercise]], and avoidance of hazards such as [[tobacco smoking|smoking]].

[[Maximum lifespan]] is determined by the rate of aging for a species inherent in its [[gene]]s and by environmental factors. Widely recognized methods of extending maximum lifespan in model organisms such as [[nematode]]s, fruit flies, and mice include [[caloric restriction]], [[gene manipulation]], and administration of pharmaceuticals.<ref>{{cite journal | vauthors = Verdaguer E, Junyent F, Folch J, Beas-Zarate C, Auladell C, Pallàs M, Camins A | title = Aging biology: a new frontier for drug discovery | journal = Expert Opinion on Drug Discovery | volume = 7 | issue = 3 | pages = 217–229 | date = March 2012 | pmid = 22468953 | doi = 10.1517/17460441.2012.660144 | s2cid = 24617426 }}</ref> Another technique uses evolutionary pressures such as breeding from only older members or altering levels of extrinsic mortality.<ref>{{cite journal | vauthors = Rauser CL, Mueller LD, Rose MR | title = The evolution of late life | journal = Ageing Research Reviews | volume = 5 | issue = 1 | pages = 14–32 | date = February 2006 | pmid = 16085467 | doi = 10.1016/j.arr.2005.06.003 | s2cid = 29623681 }}</ref><ref>{{cite journal | vauthors = Stearns SC, Ackermann M, Doebeli M, Kaiser M | title = Experimental evolution of aging, growth, and reproduction in fruitflies | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 97 | issue = 7 | pages = 3309–3313 | date = March 2000 | pmid = 10716732 | pmc = 16235 | doi = 10.1073/pnas.060289597 | doi-access = free | bibcode = 2000PNAS...97.3309S }}</ref>
Some animals such as [[hydra (genus)|hydra]], [[planarian| planarian flatworms]], and certain [[sponges]], [[corals]], and [[jellyfish]] do not die of old age and exhibit potential immortality.<ref>{{cite journal | vauthors = Newmark PA, Sánchez Alvarado A | title = Not your father's planarian: a classic model enters the era of functional genomics | journal = Nature Reviews. Genetics | volume = 3 | issue = 3 | pages = 210–219 | date = March 2002 | pmid = 11972158 | doi = 10.1038/nrg759 | s2cid = 28379017 }}</ref><ref>{{cite journal|year=1992 |title=Bi-directional conversion in ''Turritopsis nutricula'' (Hydrozoa) |journal=Scientia Marina |volume=56 |issue=2–3 |pages=137–140 |url=http://evolucionuader.yolasite.com/resources/Bavestrello%20et%20al%201992.pdf | vauthors = Bavestrello G, Sommer C, Sarà M |archive-url=https://web.archive.org/web/20150626120819/http://evolucionuader.yolasite.com/resources/Bavestrello%20et%20al%201992.pdf |archive-date=2015-06-26 }}</ref><ref>{{cite journal | vauthors = Martínez DE | title = Mortality patterns suggest lack of senescence in hydra | journal = Experimental Gerontology | volume = 33 | issue = 3 | pages = 217–225 | date = May 1998 | pmid = 9615920 | doi = 10.1016/S0531-5565(97)00113-7 | s2cid = 2009972 | citeseerx = 10.1.1.500.9508 }}</ref><ref>{{cite journal | vauthors = Petralia RS, Mattson MP, Yao PJ | title = Aging and longevity in the simplest animals and the quest for immortality | journal = Ageing Research Reviews | volume = 16 | pages = 66–82 | date = July 2014 | pmid = 24910306 | pmc = 4133289 | doi = 10.1016/j.arr.2014.05.003 }}</ref>

==History==
{{Further|Timeline of senescence research}}
The extension of life has been a desire of humanity and a mainstay motif in the history of scientific pursuits and ideas throughout history, from the Sumerian [[Epic of Gilgamesh]] and the Egyptian [[Edwin Smith Papyrus|Smith medical papyrus]], all the way through the [[Taoists]], [[Ayurveda]] practitioners, [[alchemists]], [[hygienist]]s such as [[Luigi Cornaro]], Johann Cohausen and [[Christoph Wilhelm Hufeland]], and philosophers such as [[Francis Bacon]], [[René Descartes]], [[Benjamin Franklin]] and Nicolas [[Condorcet]]. However, the beginning of the modern period in this endeavor can be traced to the end of the 19th – beginning of the 20th century, to the so-called "[[fin-de-siècle]]" (end of the century) period, denoted as an "end of an epoch" and characterized by the rise of scientific optimism and therapeutic activism, entailing the pursuit of life extension (or life-extensionism). Among the foremost researchers of life extension at this period were the Nobel Prize winning biologist [[Elie Metchnikoff]] (1845-1916) -- the author of the cell theory of immunity and vice director of Institut Pasteur in Paris, and [[Charles-Édouard Brown-Séquard]] (1817-1894) -- the president of the French Biological Society and one of the founders of modern endocrinology.<ref>{{cite book| vauthors = Stambler I |title=A History of Life-Extensionism in the Twentieth Century|date=2014|publisher=Longevity History|isbn=978-1-5008-1857-9|url=http://www.longevityhistory.com/}}</ref>

Sociologist [[James Hughes (sociologist)|James Hughes]] claims that science has been tied to a cultural narrative of conquering death since the [[Age of Enlightenment]]. He cites [[Francis Bacon]] (1561–1626) as an advocate of using science and reason to extend human life, noting Bacon's novel ''[[New Atlantis]]'', wherein scientists worked toward delaying aging and prolonging life. [[Robert Boyle]] (1627–1691), founding member of the [[Royal Society]], also hoped that science would make substantial progress with life extension, according to Hughes, and proposed such experiments as "to replace the blood of the old with the blood of the young". Biologist [[Alexis Carrel]] (1873–1944) was inspired by a belief in indefinite human lifespan that he developed after experimenting with [[Cell (biology)|cells]], says Hughes.<ref>{{cite book| vauthors = Hughes J |author-link=James Hughes (sociologist)|title=Leadership in Science and Technology: A Reference Handbook|date=October 20, 2011|publisher=[[SAGE Publications]]|isbn=978-1-4522-6652-7|page=587|chapter=Transhumanism| veditors = Bainbridge W |editor1-link=William Sims Bainbridge}}</ref>

===Contemporary===

Regulatory and legal struggles between the Food and Drug Administration (FDA) and the [[Biomedical Research & Longevity Society|Life Extension organization]] included seizure of merchandise and court action.<ref>{{cite web | vauthors = Zaleski A | url = https://www.popsci.com/forever-man-immortality-science/ | title = Is there any truth to anti-aging schemes? | work = Popular Science | date = 12 June 2018 }}</ref> In 1991, [[Saul Kent]] and [[Bill Faloon]], the principals of the organization, were jailed for four hours and were released on $850,000 bond each.<ref>{{Cite news |first=Matt |last=Schudel |url=https://www.sun-sentinel.com/news/fl-xpm-1992-12-06-9203040859-story.html/ |title=Is it a crime to live forever? |work=SunSentinel |date=December 6, 1992}}</ref> After 11 years of legal battles, Kent and Faloon convinced the US Attorney's Office to dismiss all criminal indictments brought against them by the FDA.<ref>{{cite web | url = https://lifeboat.com/ex/bios.william.faloon | title = William Faloon | work = lifeboatfoundation }}</ref>

In 2003, [[Doubleday (publisher)|Doubleday]] published "The Immortal Cell: One Scientist's Quest to Solve the Mystery of Human Aging," by [[Michael D. West]]. West emphasised the potential role of embryonic stem cells in life extension.<ref>{{cite book| vauthors = West MD |title=The Immortal Cell: One Scientist's Quest to Solve the Mystery of Human Aging|url=https://archive.org/details/imortalcell0000unse|url-access=registration |year=2003|publisher=Doubleday|isbn=978-0-385-50928-2}}</ref>

Other modern life extensionists include writer [[Gennady Stolyarov II|Gennady Stolyarov]], who insists that death is "the enemy of us all, to be fought with medicine, science, and technology";<ref>{{cite book| vauthors = Stolyarov G |title = Death is Wrong|date = November 25, 2013|publisher = Rational Argumentator Press|isbn = 978-0-615-93204-0|url = http://rationalargumentator.com/Death_is_Wrong_Second_Edition_Full.pdf}}</ref> [[Transhumanism|transhumanist]] philosopher [[Zoltan Istvan]], who proposes that the "transhumanist must safeguard one's own existence above all else";<ref>{{cite news | vauthors = Istvan Z |url=http://www.huffingtonpost.com/zoltan-istvan/the-three-laws-of-transhu_b_5853596.html |title=The Morality of Artificial Intelligence and the Three Laws of Transhumanism |work=Huffington Post |date=October 2, 2014}}</ref> futurist [[George Dvorsky]], who considers aging to be a problem that desperately needs to be solved;<ref>{{cite web|title=Futurist: 'I will reap benefits of life extension'|url=http://america.aljazeera.com/watch/shows/fault-lines/articles/2015/5/7/futurist-itll-start-to-become-ridiculous-not-to-talk-about-curing-aging.html|website=Al Jazeera America|date=May 7, 2015|quote=To Dvorsky, aging is a problem that's desperately in need of solving.}}</ref> and recording artist [[Steve Aoki]], who has been called "one of the most prolific campaigners for life extension".<ref>{{cite web| vauthors = Tez RM |title=Steve Aoki, Dan Bilzerian, a giraffe and the search for eternal life|url=https://i-d.co/article/steve-aoki-dan-bilzerian-a-giraffe-and-the-search-for-eternal-life/|website=i-D|publisher=VICE|date=May 11, 2015|quote=Unknown to most, Steve is both an undeniable champion of life expansion as well as one of the most prolific campaigners for life extension. Understanding that the depth of his life's experience is limited by time alone, in his latest album Neon Future he pens lyrics such as 'Life has limitless variety... But today, because of ageing, it does not have limitless scope.' [...] Set up by the Steve Aoki Charitable Fund, the profits from the Dan Bilzerian party went to life extension research.}}</ref>

====Scientific research====
{{see also|Timeline of senescence research}}
In 1991, the [[American Academy of Anti-Aging Medicine]] (A4M) was formed. The [[American Board of Medical Specialties]] recognizes neither anti-aging medicine nor the A4M's professional standing.<ref>{{Cite news | vauthors = Kuczynski A |date=12 April 1998 |title=Anti-Aging Potion Or Poison? |url=https://www.nytimes.com/1998/04/12/style/anti-aging-potion-or-poison.html |work=[[The New York Times]] |access-date=17 July 2009}}</ref>

In 2003, [[Aubrey de Grey]] and [[David Gobel]] formed the [[Methuselah Foundation]], which gives financial grants to anti-aging research projects. In 2009, de Grey and several others founded the [[SENS Research Foundation]], a California-based scientific research organization which conducts research into aging and funds other anti-aging research projects at various universities.<ref>{{cite web | vauthors = Jones T, Rae M, de Grey A | url = http://sens.org/files/pdf/2011_Research_Report.pdf | title = Research Report 2011 | archive-url = https://web.archive.org/web/20120814133213/http://www.sens.org/files/pdf/2011_Research_Report.pdf | archive-date = 14 August 2012 | work = Sens Foundation }}</ref> In 2013, [[Google]] announced [[Calico (company)|Calico]], a new company based in San Francisco that will harness new technologies to increase scientific understanding of the biology of aging.<ref>{{cite web|url=http://www.cnn.com/2013/10/03/tech/innovation/google-calico-aging-death/|title=How Google's Calico aims to fight aging and 'solve death'| vauthors = McNicoll A |date=3 October 2013|work=CNN}}</ref> It is led by [[Arthur D. Levinson]],<ref>{{cite web|url=http://googlepress.blogspot.com/2013/09/calico-announcement.html|title=Google announces Calico, a new company focused on health and well-being|date=September 18, 2013}}</ref> and its research team includes scientists such as [[Hal V. Barron]], [[David Botstein]], and [[Cynthia Kenyon]]. In 2014, biologist [[Craig Venter]] founded Human Longevity Inc., a company dedicated to scientific research to end aging through genomics and cell therapy. They received funding with the goal of compiling a comprehensive human genotype, microbiome, and phenotype database.<ref>{{cite web|url=http://www.prnewswire.com/news-releases/human-longevity-inc-hli-launched-to-promote-healthy-aging-using-advances-in-genomics-and-stem-cell-therapies-248379091.html|title=Human Longevity Inc. (HLI) Launched to Promote Healthy Aging Using Advances in... – SAN DIEGO, March 4, 2014 /PRNewswire/ --|author=Human Longevity Inc.|date=4 March 2014|access-date=12 August 2014|archive-url=https://web.archive.org/web/20141021000819/http://www.prnewswire.com/news-releases/human-longevity-inc-hli-launched-to-promote-healthy-aging-using-advances-in-genomics-and-stem-cell-therapies-248379091.html|archive-date=21 October 2014}}</ref>

Aside from private initiatives, aging research is being conducted in university laboratories, and includes universities such as [[Harvard University|Harvard]] and [[University of California, Los Angeles|UCLA]]. University researchers have made a number of breakthroughs in extending the lives of mice and insects by reversing certain aspects of aging.<ref>{{cite web|url=http://www.cnn.com/2014/05/05/health/young-blood-mice-aging/|title=Young blood makes old mice more youthful |last=Landau |first= Elizabeth |date=5 May 2014|work=CNN}}</ref><ref>{{cite web |last=Wood |first=Anthony | date = 7 May 2014 | url = http://www.gizmag.com/gdf11-protein-aging-mice-harvard/31929/ | title = Harvard researchers find protein that could reverse the aging process | work = gizmag.com }}</ref><ref>{{cite web|url=http://newsroom.ucla.edu/releases/ucla-biologists-delay-the-aging-process-by-remote-control|title=UCLA biologists delay the aging process by 'remote control'|last=Wolpert |first=Stuart |work=UCLA Newsroom|date=September 8, 2014}}</ref><ref>{{cite web |url= http://www.abc.net.au/news/2013-12-20/scientists-develop-anti-ageing-process-in-mice/5168580 |title=Australian and US scientists reverse ageing in mice, humans could be next |work=ABC News|date=2013-12-19}}</ref>

==Research==
Theoretically, extension of maximum lifespan in humans could be achieved by reducing the rate of aging damage by [[tissue engineering|periodic replacement of damaged tissues]], [[nanobiotechnology|molecular repair]] or [[rejuvenation (aging)|rejuvenation]] of deteriorated cells and tissues, reversal of harmful epigenetic changes, or the enhancement of enzyme [[telomerase]] activity.<ref>{{cite journal | vauthors = Rando TA, Chang HY | title = Aging, rejuvenation, and epigenetic reprogramming: resetting the aging clock | journal = Cell | volume = 148 | issue = 1–2 | pages = 46–57 | date = January 2012 | pmid = 22265401 | pmc = 3336960 | doi = 10.1016/j.cell.2012.01.003 | author-link2 = Howard Y. Chang }}</ref><ref>{{cite journal | vauthors = Johnson AA, Akman K, Calimport SR, Wuttke D, Stolzing A, de Magalhães JP | title = The role of DNA methylation in aging, rejuvenation, and age-related disease | journal = Rejuvenation Research | volume = 15 | issue = 5 | pages = 483–494 | date = October 2012 | pmid = 23098078 | pmc = 3482848 | doi = 10.1089/rej.2012.1324 }}</ref>

Research geared towards life extension strategies in various organisms is currently under way at a number of academic and private institutions. Since 2009, investigators have found ways to increase the lifespan of nematode worms and yeast by 10-fold; the record in nematodes was achieved through [[genetic engineering]] and the extension in yeast by a combination of genetic engineering and [[caloric restriction]].<ref name=Shmookle>{{cite journal | vauthors = Shmookler Reis RJ, Bharill P, Tazearslan C, Ayyadevara S | title = Extreme-longevity mutations orchestrate silencing of multiple signaling pathways | journal = Biochimica et Biophysica Acta (BBA) - General Subjects | volume = 1790 | issue = 10 | pages = 1075–1083 | date = October 2009 | pmid = 19465083 | pmc = 2885961 | doi = 10.1016/j.bbagen.2009.05.011 }}</ref> A 2009 review of longevity research noted: "Extrapolation from worms to mammals is risky at best, and it cannot be assumed that interventions will result in comparable life extension factors. Longevity gains from dietary restriction, or from mutations studied previously, yield smaller benefits to Drosophila than to nematodes, and smaller still to mammals. This is not unexpected, since mammals have evolved to live many times the worm's lifespan, and humans live nearly twice as long as the next longest-lived primate. From an evolutionary perspective, mammals and their ancestors have already undergone several hundred million years of natural selection favoring traits that could directly or indirectly favor increased longevity, and may thus have already settled on gene sequences that promote lifespan. Moreover, the very notion of a "life-extension factor" that could apply across taxa presumes a linear response rarely seen in biology."<ref name=Shmookle/>

=== Anti-aging/life-extension drugs ===

There are numerous chemicals intended to slow the aging process under study in [[animal model]]s.<ref>{{cite journal | vauthors = Childs BG, Durik M, Baker DJ, van Deursen JM | title = Cellular senescence in aging and age-related disease: from mechanisms to therapy | journal = Nature Medicine | volume = 21 | issue = 12 | pages = 1424–1435 | date = December 2015 | pmid = 26646499 | pmc = 4748967 | doi = 10.1038/nm.4000 }}</ref> One type of research is related to the observed effects of a [[calorie restriction]] (CR) diet, which has been shown to extend lifespan in some animals.<ref>{{cite journal | vauthors = Anderson RM, Shanmuganayagam D, Weindruch R | title = Caloric restriction and aging: studies in mice and monkeys | journal = Toxicologic Pathology | volume = 37 | issue = 1 | pages = 47–51 | date = January 2009 | pmid = 19075044 | pmc = 3734859 | doi = 10.1177/0192623308329476 }}</ref> Based on that research, there have been attempts to develop drugs that will have the same effect on the aging process as a CR diet, which are known as [[caloric restriction mimetic]] drugs, such as [[rapamycin]]<ref>{{cite journal | vauthors = Harrison DE, Strong R, Sharp ZD, Nelson JF, Astle CM, Flurkey K, Nadon NL, Wilkinson JE, Frenkel K, Carter CS, Pahor M, Javors MA, Fernandez E, Miller RA | display-authors = 6 | title = Rapamycin fed late in life extends lifespan in genetically heterogeneous mice | journal = Nature | volume = 460 | issue = 7253 | pages = 392–395 | date = July 2009 | pmid = 19587680 | pmc = 2786175 | doi = 10.1038/nature08221 | bibcode = 2009Natur.460..392H }}</ref> and [[metformin]].<ref>{{cite journal | vauthors = Dhahbi JM, Mote PL, Fahy GM, Spindler SR | title = Identification of potential caloric restriction mimetics by microarray profiling | journal = Physiological Genomics | volume = 23 | issue = 3 | pages = 343–350 | date = November 2005 | pmid = 16189280 | doi = 10.1152/physiolgenomics.00069.2005 | citeseerx = 10.1.1.327.4892 }}</ref>

[[Sirtuin]] activating [[polyphenol]]s, such as [[resveratrol]] and [[pterostilbene]],<ref>{{cite journal | vauthors = Kaeberlein M | title = Resveratrol and rapamycin: are they anti-aging drugs? | journal = BioEssays | volume = 32 | issue = 2 | pages = 96–99 | date = February 2010 | pmid = 20091754 | doi = 10.1002/bies.200900171 | s2cid = 16882387 }}</ref><ref>{{cite journal | vauthors = Barger JL, Kayo T, Vann JM, Arias EB, Wang J, Hacker TA, Wang Y, Raederstorff D, Morrow JD, Leeuwenburgh C, Allison DB, Saupe KW, Cartee GD, Weindruch R, Prolla TA | display-authors = 6 | title = A low dose of dietary resveratrol partially mimics caloric restriction and retards aging parameters in mice | journal = PLOS ONE | volume = 3 | issue = 6 | article-number = e2264 | date = June 2008 | pmid = 18523577 | pmc = 2386967 | doi = 10.1371/journal.pone.0002264 | bibcode = 2008PLoSO...3.2264B | doi-access = free }}</ref><ref>{{cite journal | vauthors = McCormack D, McFadden D | title = A review of pterostilbene antioxidant activity and disease modification | journal = Oxidative Medicine and Cellular Longevity | volume = 2013 | article-number = 575482 | year = 2013 | pmid = 23691264 | pmc = 3649683 | doi = 10.1155/2013/575482 | doi-access = free }}</ref> and [[flavonoid]]s, such as [[quercetin]] and [[fisetin]],<ref name="Martel-2020">{{cite journal | vauthors = Martel J, Ojcius DM, Wu CY, Peng HH, Voisin L, Perfettini JL, Ko YF, Young JD | display-authors = 6 | title = Emerging use of senolytics and senomorphics against aging and chronic diseases | journal = Medicinal Research Reviews | volume = 40 | issue = 6 | pages = 2114–2131 | date = November 2020 | pmid = 32578904 | doi = 10.1002/med.21702 | s2cid = 220047655 }}</ref> as well as [[oleic acid]]<ref>{{cite journal | vauthors = Mutlu AS, Duffy J, Wang MC | title = Lipid metabolism and lipid signals in aging and longevity | journal = Developmental Cell | volume = 56 | issue = 10 | pages = 1394–1407 | date = May 2021 | pmid = 33891896 | pmc = 8173711 | doi = 10.1016/j.devcel.2021.03.034 }}</ref> are [[dietary supplement]]s that have also been studied in this context. Other common supplements with less clear biological pathways to target aging include [[lipoic acid]],<ref>{{cite journal | vauthors = Shay KP, Moreau RF, Smith EJ, Smith AR, Hagen TM | title = Alpha-lipoic acid as a dietary supplement: molecular mechanisms and therapeutic potential | journal = Biochimica et Biophysica Acta (BBA) - General Subjects | volume = 1790 | issue = 10 | pages = 1149–1160 | date = October 2009 | pmid = 19664690 | pmc = 2756298 | doi = 10.1016/j.bbagen.2009.07.026 }}</ref> [[senolytic]]s,<ref name="Martel-2020" /> and [[coenzyme Q10]].<ref>{{cite journal | vauthors = Arenas-Jal M, Suñé-Negre JM, García-Montoya E | title = Coenzyme Q10 supplementation: Efficacy, safety, and formulation challenges | journal = Comprehensive Reviews in Food Science and Food Safety | volume = 19 | issue = 2 | pages = 574–594 | date = March 2020 | pmid = 33325173 | doi = 10.1111/1541-4337.12539 | doi-access = free | hdl = 2445/181270 | hdl-access = free }}</ref> 

While agents such as these have some limited laboratory evidence of efficacy in animals, there are no studies to date in humans for drugs that may promote life extension, mainly because research investment remains at a low level, and regulatory standards are high.<ref name="aarp">{{cite web |first1=Rachel|last1=Nania |title=A pill to slow aging? |url=https://www.aarp.org/health/drugs-supplements/info-2023/pill-to-slow-aging.html |publisher=AARP |access-date=7 September 2024 |date=15 November 2023}}</ref> Aging is not recognized as a preventable condition by governments, indicating there is no clear pathway to approval of anti-aging medications.<ref name=aarp/> Further, anti-aging drug candidates are under constant review by regulatory authorities like the US [[Food and Drug Administration]], which stated in 2023 that "no medication has been proven to slow or reverse the aging process."<ref name="fda-fraud">{{cite web |title=Medication Health Fraud for Specific Diseases and Conditions |url=https://www.fda.gov/drugs/medication-health-fraud/medication-health-fraud-specific-diseases-and-conditions |archive-url=https://web.archive.org/web/20230825214009/https://www.fda.gov/drugs/medication-health-fraud/medication-health-fraud-specific-diseases-and-conditions |archive-date=25 August 2023 |publisher=US Food and Drug Administration |access-date=7 September 2024 |date=9 August 2023}}</ref>

LDL-C lowering drugs such as statins and PCSK9 inhibitors present with some of the most promising candidates for increasing lifespan since there is substantial randomized genetic and clinical evidence that reduced risk of atherosclerotic cardiovascular disease via reducing LDL-C would yield a net gain in lifespan.<ref>{{Cite journal |last=Daghlas |first=Iyas |last2=Gill |first2=Dipender |date=2021 |title=Low‐density lipoprotein cholesterol and lifespan: A Mendelian randomization study |url=https://bpspubs.onlinelibrary.wiley.com/doi/10.1111/bcp.14811 |journal=British Journal of Clinical Pharmacology |language=en |volume=87 |issue=10 |pages=3916–3924 |doi=10.1111/bcp.14811 |issn=0306-5251|doi-access=free }}</ref><ref>{{Cite journal |last=Ference |first=Brian A. |last2=Ginsberg |first2=Henry N. |last3=Graham |first3=Ian |last4=Ray |first4=Kausik K. |last5=Packard |first5=Chris J. |last6=Bruckert |first6=Eric |last7=Hegele |first7=Robert A. |last8=Krauss |first8=Ronald M. |last9=Raal |first9=Frederick J. |last10=Schunkert |first10=Heribert |last11=Watts |first11=Gerald F. |last12=Borén |first12=Jan |last13=Fazio |first13=Sergio |last14=Horton |first14=Jay D. |last15=Masana |first15=Luis |date=2017-08-21 |title=Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel |url=https://academic.oup.com/eurheartj/article/38/32/2459/3745109 |journal=European Heart Journal |language=en |volume=38 |issue=32 |pages=2459–2472 |doi=10.1093/eurheartj/ehx144 |issn=0195-668X |pmc=5837225 |pmid=28444290}}</ref>

=== Nanotechnology ===
Future advances in [[nanomedicine]] could give rise to life extension through the repair of many processes thought to be responsible for aging. [[K. Eric Drexler]], one of the founders of [[nanotechnology]], postulated [[Cell (biology)|cell]] repair machines, including ones operating within cells and utilizing as yet hypothetical molecular [[computers]], in his 1986 book ''[[Engines of Creation]]''. [[Raymond Kurzweil]], a [[futurist]] and [[transhumanist]], stated in his book ''[[The Singularity Is Near]]'' that he believes that advanced medical [[nanorobotics]] could completely remedy the effects of aging by 2030.<ref>{{Cite book | vauthors = Kurzweil R |author-link=Raymond Kurzweil |year=2005 |title=The Singularity Is Near |publisher=[[Viking Press]] |location=[[New York City]] |isbn=978-0-670-03384-3 |oclc=57201348|title-link=The Singularity Is Near }}{{Page needed|date=September 2010}}</ref> According to [[Richard Feynman]], it was his former graduate student and collaborator [[Albert Hibbs]] who originally suggested to him (circa 1959) the idea of a ''medical'' use for Feynman's theoretical [[nanomachines]] (see [[biological machine]]). Hibbs suggested that certain repair machines might one day be reduced in size to the point that it would, in theory, be possible to (as Feynman put it) "[[Molecular machine#Biological|swallow the doctor]]". The idea was incorporated into Feynman's 1959 essay ''[[There's Plenty of Room at the Bottom]].''<ref>{{cite web |url = http://www.its.caltech.edu/~feynman/plenty.html|title = There's Plenty of Room at the Bottom| vauthors = Feynman RP |date = December 1959 |access-date   = 22 March 2016 |archive-url  = https://web.archive.org/web/20100211190050/http://www.its.caltech.edu/~feynman/plenty.html |archive-date = 2010-02-11 }}</ref>

=== Cyborgs ===
{{Main|Cyborg}}
Replacement of biological (susceptible to diseases) organs with mechanical ones could extend life. This is the goal of the [[2045 Initiative]].<ref>{{cite web | vauthors = Segal D | work = The New York Times | date = 1 June 2013 | url = https://www.nytimes.com/2013/06/02/business/dmitry-itskov-and-the-avatar-quest.html?pagewanted=all&_r=0 | title = This Man Is Not a Cyborg. Yet. }}</ref>
=== Cryonics ===
{{Main|Cryonics}}
Cryonics is the [[Cryopreservation|low-temperature freezing]] (usually at {{cvt|−196|C|F K|disp=or}}) of a human corpse, with the hope that [[wikt:resuscitate|resuscitation]] may be possible in the [[future]].<ref>{{cite news| vauthors = McKie R |title=Cold facts about cryonics|url=https://www.theguardian.com/education/2002/jul/14/medicalscience.science|access-date=1 December 2013|newspaper=[[The Observer]]|date=13 July 2002|quote=Cryonics, which began in the Sixties, is the freezing – usually in liquid nitrogen – of human beings who have been legally declared dead. The aim of this process is to keep such individuals in a state of refrigerated limbo so that it may become possible in the [[future]] to resuscitate them, cure them of the condition that killed them, and then restore them to functioning life in an era when medical science has triumphed over the activities of the Grim Reaper.
}}</ref><ref>{{cite news | vauthors = Day E |title=Dying is the last thing anyone wants to do – so keep cool and carry on|url=https://www.theguardian.com/science/2015/oct/11/cryonics-booms-in-us|access-date=21 February 2016|work=[[The Guardian]]|date=10 October 2015}}</ref> It is regarded with [[skepticism]] within the mainstream scientific community and has been characterized as [[quackery]].<ref>{{cite book | vauthors = Butler K |title=A Consumer's Guide to "Alternative" Medicine |publisher=Prometheus Books |year=1992 |page=173}}</ref>

=== Strategies for engineered negligible senescence ===
{{Main|Strategies for engineered negligible senescence|Genetics of aging}}
Another proposed life extension technology aims to combine existing and predicted future biochemical and genetic techniques. SENS proposes that rejuvenation may be obtained by removing aging damage via the use of [[stem cell]]s and [[tissue engineering]], [[telomere]]-lengthening machinery, [[allotopic expression]] of [[mitochondrial]] proteins, targeted ablation of cells, [[immunotherapy|immunotherapeutic]] clearance, and novel [[lysosome|lysosomal]] [[hydrolases]].<ref>{{Cite book | vauthors = de Grey A, Rae M  |author-link=Aubrey de Grey | title=Ending Aging: The Rejuvenation Breakthroughs that Could Reverse Human Aging in Our Lifetime |publisher=[[St. Martin's Press]] |year=2007 |location=[[New York City]] |isbn= 978-0-312-36706-0 |oclc=132583222|title-link=Ending Aging }}{{Page needed|date=September 2010}}</ref>

While some [[Biogerontology|biogerontologists]] find these ideas "worthy of discussion",<ref>{{cite web | vauthors = Pontin J | date = 11 July 2006 | url = http://www.technologyreview.com/sens/ | title = Is Defeating Aging Only A Dream? | work = Technology Review | access-date = 15 February 2013 | archive-date = 11 September 2012 | archive-url = https://archive.today/20120911155923/http://www.technologyreview.com/sens/ }}</ref><ref>{{cite news | vauthors = Garreau J | date = 31 October 2007 | url = https://www.washingtonpost.com/wp-dyn/content/article/2007/10/30/AR2007103002222.html?hpid=features1&hpv=national | title = The Invincible Man | newspaper = Washington Post }}</ref> others contend that the alleged benefits are too speculative given the current state of technology, referring to it as "fantasy rather than science".<ref name=Holliday /><ref name="EMBOSENS" />

==Genetic editing==
{{Main|Genetics of aging|Genome editing}}
[[Genome editing]], in which [[nucleic acid]] polymers are delivered as a [[Biologic medical product|drug]] and are either [[gene expression|expressed]] as proteins, interfere with the expression of proteins, or correct genetic mutations, has been proposed as a future strategy to prevent aging.<ref>{{cite journal | vauthors = Goya RG, Bolognani F, Hereñú CB, Rimoldi OJ | title = Neuroendocrinology of aging: the potential of gene therapy as an interventive strategy | journal = Gerontology | volume = 47 | issue = 3 | pages = 168–173 | date = 2001-01-08 | pmid = 11340324 | doi = 10.1159/000052792 | s2cid = 10069927 }}</ref><ref>{{cite journal | vauthors = Rattan SI, Singh R | title = Progress & prospects: gene therapy in aging | journal = Gene Therapy | volume = 16 | issue = 1 | pages = 3–9 | date = January 2009 | pmid = 19005494 | doi = 10.1038/gt.2008.166 | doi-access =  }}</ref>

===CRISPR/Cas9===
{{Main|CRISPR}}
CRISPR/Cas9 edits genes by precisely cutting DNA and then harnessing natural DNA repair processes to modify the gene in the desired manner. The system has two components: the Cas9 enzyme and a guide RNA.<ref>{{cite web | url=https://crisprtx.com/gene-editing | title=Gene Editing }}</ref>  A large array of genetic modifications have been found to increase lifespan in model organisms such as yeast, nematode worms, fruit flies, and mice. As of 2013, the longest extension of life caused by a single gene manipulation was roughly 50% in mice and 10-fold in [[nematode]] worms.<ref>{{cite journal | vauthors = Tacutu R, Craig T, Budovsky A, Wuttke D, Lehmann G, Taranukha D, Costa J, Fraifeld VE, de Magalhães JP | display-authors = 6 | title = Human Ageing Genomic Resources: integrated databases and tools for the biology and genetics of ageing | journal = Nucleic Acids Research | volume = 41 | issue = Database issue | pages = D1027–D1033 | date = January 2013 | pmid = 23193293 | pmc = 3531213 | doi = 10.1093/nar/gks1155 }}</ref>

[[File:Healthspan, parental lifespan, and longevity are highly genetically correlated.webp|thumb|right|200px|"Healthspan, parental lifespan, and longevity are highly genetically correlated."<ref name="Multivariate"/>]]
In July [[2020 in science|2020]] scientists, using public [[List of biological databases|biological data]] on 1.75 m people with known lifespans overall, identify 10 [[Locus (genetics)|genomic loci]] which appear to intrinsically influence [[healthspan]], lifespan, and longevity – of which half have not been reported previously at [[Genome-wide association study|genome-wide significance]] and most being associated with [[cardiovascular disease]] – and identify [[Human iron metabolism|haem metabolism]] as a promising candidate for further research within the field. Their study suggests that high levels of iron in the blood likely reduce, and genes involved in metabolising iron likely increase healthy years of life in humans.<ref>{{cite news |title=Blood iron levels could be key to slowing ageing, gene study shows |url=https://phys.org/news/2020-07-blood-iron-key-ageing-gene.html |access-date=18 August 2020 |language=en |work=Phys.org |date=July 16, 2020 |author=University of Edinburgh}}</ref><ref name="Multivariate">{{cite journal |vauthors=Timmers PR, Wilson JF, Joshi PK, Deelen J |date=July 2020 |title=Multivariate genomic scan implicates novel loci and haem metabolism in human ageing |journal=Nature Communications |volume=11 |issue=1 |article-number=3570 |bibcode=2020NatCo..11.3570T |doi=10.1038/s41467-020-17312-3 |pmc=7366647 |pmid=32678081}} [[File:CC-BY_icon.svg|50x50px|class=noviewer]] Text and images are available under a [[creativecommons:by/4.0/|Creative Commons Attribution 4.0 International License]].</ref> The same month other scientists report that yeast cells of the same genetic material and within the same environment age in two distinct ways, describe a biomolecular mechanism that can determine which process dominates during aging and [[genetically engineer]] a novel aging route with substantially extended lifespan.<ref>{{cite news |title=Researchers discover 2 paths of aging and new insights on promoting healthspan |url=https://phys.org/news/2020-07-paths-aging-insights-healthspan.html |access-date=17 August 2020 |work=Phys.org |language=en |date=July 16, 2020 |author=University of California}}</ref><ref>{{cite journal | vauthors = Li Y, Jiang Y, Paxman J, O'Laughlin R, Klepin S, Zhu Y, Pillus L, Tsimring LS, Hasty J, Hao N | display-authors = 6 | title = A programmable fate decision landscape underlies single-cell aging in yeast | journal = Science | volume = 369 | issue = 6501 | pages = 325–329 | date = July 2020 | pmid = 32675375 | pmc = 7437498 | doi = 10.1126/science.aax9552 | bibcode = 2020Sci...369..325L }}</ref>

===Fooling genes===
In ''[[The Selfish Gene]]'', [[Richard Dawkins]] describes an approach to life-extension that involves "fooling genes" into thinking the body is young.<ref>{{Cite book | vauthors = Dawkins R |author-link=Richard Dawkins |title=The Selfish Gene |publisher=[[Oxford University Press]] |orig-date=1976|year=2006 |location=[[New York City|New York]] |isbn= 978-0-19-929115-1 | pages = 41–42|title-link=The Selfish Gene }}</ref> Dawkins attributes inspiration for this idea to [[Peter Medawar]]. The basic idea is that our bodies are composed of genes that activate throughout our lifetimes, some when we are young and others when we are older. Presumably, these genes are activated by environmental factors, and the changes caused by these genes activating can be lethal. It is a statistical certainty that we possess more lethal genes that activate in later life than in early life. Therefore, to extend life, we should be able to prevent these genes from switching on, and we should be able to do so by "identifying changes in the internal chemical environment of a body that take place during aging... and by simulating the superficial chemical properties of a young body".<ref>{{Cite book | vauthors = Dawkins R |author-link=Richard Dawkins |title=The Selfish Gene |publisher=[[Oxford University Press]] |orig-date=1976|year=2006 |location=[[New York City|New York]] |isbn= 978-0-19-929115-1 | page = 42|title-link=The Selfish Gene }}</ref>

=== Cloning and body part replacement ===
Some life extensionists suggest that [[therapeutic cloning]] and [[stem cell]] research could one day provide a way to generate cells, body parts, or even entire bodies (generally referred to as [[reproductive cloning]]) that would be genetically identical to a prospective patient. In 2008, the US Department of Defense announced a program to research the possibility of growing human body parts on mice.<ref>{{cite magazine |last1=Saletan |first1=William |title=Rearming America |url=https://slate.com/technology/2008/04/the-military-s-plan-to-regrow-body-parts.html |website=Slate |date=18 April 2008 |publisher=Slate |access-date=8 June 2024 |ref=WS2008}}</ref> Complex biological structures, such as mammalian joints and limbs, have not yet been replicated. Dog and primate brain transplantation experiments were conducted in the mid-20th century but failed due to [[transplant rejection|rejection]] and the inability to restore nerve connections. As of 2006, the implantation of bio-engineered bladders grown from patients' own cells has proven to be a viable treatment for bladder disease.<ref>{{cite magazine | vauthors = Khamsi R |date= April 4, 2006 |title=Bio-engineered bladders successful in patients |url=https://www.newscientist.com/article/dn8939-bioengineered-bladders-successful-in-patients.html |magazine=[[New Scientist]] |access-date=January 26, 2011}}</ref> Proponents of body part replacement and cloning contend that the required biotechnologies are likely to appear earlier than other life-extension technologies.

The use of human [[stem cells]], particularly [[embryonic stem cells]], is controversial. Opponents' objections generally are based on interpretations of religious teachings or ethical considerations.<ref>{{cite journal |last1=Lo |first1=Bernard |last2=Parham |first2=Lindsay |date=1 May 2009 |title=Ethical Issues in Stem Cell Research |journal=Endocrine Reviews |volume=30 |issue=3 |pages=204–213 |doi=10.1210/er.2008-0031 |pmid=19366754 |pmc=2726839 }}</ref> Proponents of stem cell research point out that cells are routinely formed and destroyed in a variety of contexts. Use of stem cells taken from the umbilical cord or parts of the adult body may not provoke controversy.<ref>{{Cite news| vauthors = White C |date=19 August 2005 |title=Umbilical stem cell breakthrough |url=http://www.stemcellnews.com/articles/stem-cells-umbilical-breakthrough.htm |work=[[The Australian]] |access-date=17 July 2009 |archive-url=https://web.archive.org/web/20090720054316/http://www.stemcellnews.com/articles/stem-cells-umbilical-breakthrough.htm |archive-date=20 July 2009 }}</ref>

The controversies over cloning are similar, except general public opinion in most countries stands in opposition to [[reproductive cloning]]. Some proponents of therapeutic cloning predict the production of whole bodies, lacking consciousness, for eventual brain transplantation.

==Ethics and politics ==

===Scientific controversy===
Some critics dispute the portrayal of aging as a disease. For example, [[Leonard Hayflick]], who determined that [[fibroblast]]s are limited to around 50&nbsp;cell divisions, reasons that aging is an unavoidable consequence of [[entropy]]. Hayflick and fellow [[biogerontologist]]s [[S. Jay Olshansky|Jay Olshansky]] and Bruce Carnes have strongly criticized the anti-aging industry in response to what they see as unscrupulous profiteering from the sale of unproven [[anti-aging supplements]].<ref name="PositionStatement">{{cite journal | vauthors = Olshansky SJ, Hayflick L, Carnes BA | title = Position statement on human aging | journal = The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences | volume = 57 | issue = 8 | pages = B292–B297 | date = August 2002 | pmid = 12145354 | doi = 10.1093/gerona/57.8.B292 | doi-access = free | citeseerx = 10.1.1.541.3004 }}</ref><!--This may be a good place to link into the broader social debate on life extension ethics. Hayflick is not the only one to object to the portrayal/treatment of aging as a disease. Many doctors, social scientists, feminists, etc. do-->

===Consumer motivations ===
Research by Sobh and Martin (2011) suggests that people buy anti-aging products to obtain a hoped-for self (e.g., keeping a youthful skin) or to avoid a feared-self (e.g., looking old). The research shows that when consumers pursue a hoped-for self, it is expectations of success that most strongly drive their motivation to use the product. The research also shows why doing badly when trying to avoid a feared self is more motivating than doing well. When product use is seen to fail it is more motivating than success when consumers seek to avoid a feared-self.<ref>{{cite journal | year = 2011 | title = Feedback Information and Consumer Motivation. The Moderating Role of Positive and Negative Reference Values in Self-Regulation | url = http://www.basmartin.com/wp-content/uploads/2011/12/S-and-M.pdf | journal = European Journal of Marketing | volume = 45 | issue = 6 | pages = 963–986 | doi = 10.1108/03090561111119976 | archive-url = https://web.archive.org/web/20140818073959/http://www.basmartin.com/wp-content/uploads/2011/12/S-and-M.pdf | archive-date = 2014-08-18 | vauthors = Sobh R, Martin BA | hdl = 10576/52103 }}</ref>

===Political parties===
Though many scientists state<ref>{{cite web|url=http://www.imminst.org/cureaging/ |title=Scientists' Open Letter on Aging |publisher=Imminst.org |access-date=2012-10-07}}</ref> that life extension and radical life extension are possible, there are still no international or national programs focused on radical life extension. There are political forces working both for and against life extension. By 2012, in Russia, the United States, Israel, and the Netherlands, the Longevity political parties started. They aimed to provide political support to radical life extension research and technologies, and ensure the fastest possible and at the same time soft transition of society to the next step – life without aging and with radical life extension, and to provide access to such technologies to most currently living people.<ref>{{cite web |url=http://www.fightaging.org/archives/2012/07/a-single-issue-political-party-for-longevity-science.php |title=A Single-Issue Political Party for Longevity Science |publisher=Fightaging.org |access-date=2012-10-07|date=2012-07-27 }}</ref>

===Political leaders===
[[General Secretary of the Chinese Communist Party]] [[Xi Jinping]] and [[President of Russia]] [[Vladimir Putin]] discussed [[Organ transplantation|organ transplants]] and "immortality" during the [[2025 China Victory Day Parade]]. This conversation is caught recorded by [[China Central Television]]'s public broadcast. During the conversation, Putin spoke about [[biotechnology]] and "human organs will continue to be transplanted, and people will became younger and younger". Xi responded Putin, talking about how people predicted that [[life expectancy]] can reach up to 150 years and how 70 years old still is quite young compared to the past.<ref>{{Cite news |date=2025-09-03 |title=Hot mic picks up Putin and Xi discussing organ transplants and immortality |url=https://www.reuters.com/business/media-telecom/hot-mic-picks-up-putin-xi-discussing-organ-transplants-immortality-2025-09-03/ |access-date=2025-09-05 |work=Reuters |language=en}}</ref><ref>{{Cite web |date=2025-09-03 |title=Hot mic catches Xi and Putin discussing organ transplants and immortality |url=https://www.bbc.com/news/articles/cr70rvrd41ko |access-date=2025-09-05 |website=www.bbc.com |language=en-GB}}</ref><ref>{{Cite web |last=中央通訊社 |date=2025-09-03 |title=習近平蒲亭討論器官移植、長生不老 央視直播出去[影] {{!}} 兩岸 |url=https://www.cna.com.tw/news/acn/202509030345.aspx |access-date=2025-09-05 |website=中央社 CNA |language=zh-Hant-TW}}</ref> At the press conference during the evening, Putin clarified to Russian media that he and Xi did discuss about the topic of human lifespan.<ref>{{Cite web |last=Troianovski |first=Anton |last2=储百亮 |date=2025-09-04 |title=习近平和普京谈及器官移植与"长生不老" |url=https://cn.nytimes.com/world/20250904/putin-xi-immortality-organ-transplants/ |access-date=2025-09-05 |website=纽约时报中文网 |language=zh-cmn-hans}}</ref>

===Silicon Valley===
Some tech innovators and Silicon Valley entrepreneurs have invested heavily into anti-aging research. This includes [[Jeff Bezos]] (founder of [[Amazon (company)|Amazon]]), [[Larry Ellison]] (founder of [[Oracle Corporation|Oracle]]), [[Peter Thiel]] (former [[PayPal]] CEO),<ref>{{cite web | url = https://www.youtube.com/watch?v=yQHrJvwnOzo&list=PLCNNepS_4NcyOSlUdWOcTUCeUbK8nuywQ | title = Veritas Forum Q&A with Peter Thiel | work = YouTube | date = 25 June 2015 }}</ref> [[Larry Page]] (co-founder of [[Google]]), [[Peter Diamandis]],<ref>{{cite magazine|url=https://www.newyorker.com/magazine/2017/04/03/silicon-valleys-quest-to-live-forever|title=Silicon Valley's Quest to Live Forever|date=April 3, 2017| vauthors = Friend T |magazine=The New Yorker}}</ref> [[Sam Altman]] (CEO of [[OpenAI]], invested in [[Joe Betts-LaCroix#Biotechnology_&_biomedicine|Retro Biosciences]]), [[Brian Armstrong (businessman)|Brian Armstrong]] (founder of [[Coinbase]] and NewLimit),<ref>{{cite web |title=Sam Altman invested $180 million into a company trying to delay death |url=https://www.technologyreview.com/2023/03/08/1069523/sam-altman-investment-180-million-retro-biosciences-longevity-death/ |website=MIT Technology Review |language=en |date=8 March 2023}}</ref> and [[Bryan Johnson]] (Founder of [[Kernel (neurotechnology company)|Kernel]]).<ref>{{cite magazine |last1=ALTER |first1=CHARLOTTE |title=The Man Who Thinks He Can Live Forever |url=https://time.com/6315607/bryan-johnsons-quest-for-immortality/ |magazine=TIME |date=20 September 2023 |publisher=Time |access-date=31 March 2024}}</ref>

===Commentators===
[[Leon Kass]] (chairman of the US [[President's Council on Bioethics]] from 2001 to 2005) has questioned whether potential exacerbation of [[Human overpopulation|overpopulation]] problems would make life extension unethical.<ref>{{cite web | vauthors = Smith S |date=3 December 2002 |title=Killing Immortality |url=http://www.betterhumans.com/Features/Columns/Forward_Thinking/column.aspx?articleID=2002-12-03-4 |archive-url= https://web.archive.org/web/20040607195722/http://www.betterhumans.com/Features/Columns/Forward_Thinking/column.aspx?articleID=2002-12-03-4 |archive-date=7 June 2004 |publisher=Betterhumans |access-date=17 July 2009}}</ref> He states his opposition to life extension with the words:
{{Blockquote|"simply to covet a prolonged life span for ourselves is both a sign and a cause of our failure to open ourselves to procreation and to any higher purpose ... [The] desire to prolong youthfulness is not only a childish desire to eat one's life and keep it; it is also an expression of a childish and [[narcissistic]] wish incompatible with devotion to posterity."<ref>{{Cite book | vauthors = Kass L |author-link= Leon Kass |year=1985 |title=Toward a more natural science: biology and human affairs |publisher=[[Free Press (publisher)|Free Press]] |location=[[New York City]] |isbn=978-0-02-918340-3 |oclc=11677465 |page= 316}}</ref>}}

John Harris, former editor-in-chief of the Journal of Medical Ethics, argues that as long as life is worth living, according to the person himself, we have a powerful moral imperative to save the life and thus to develop and offer life extension therapies to those who want them.<ref>Harris J. (2007) ''Enhancing Evolution: The ethical case for making better people''. Princeton University Press, New Jersey.</ref>

[[Transhumanist]] [[philosopher]] [[Nick Bostrom]] has argued that any technological advances in life extension must be equitably distributed and not restricted to a privileged few.<ref>{{Cite news | vauthors = Sutherland J |date=9 May 2006 |title=The ideas interview: Nick Bostrom |url=https://www.theguardian.com/science/2006/may/09/academicexperts.genetics |work=[[The Guardian]] |access-date= 17 July 2009 |location=London}}</ref> In an extended metaphor entitled "[[The Fable of the Dragon-Tyrant]]", Bostrom envisions death as a monstrous dragon who demands human sacrifices. In the fable, after a lengthy debate between those who believe the dragon is a fact of life and those who believe the dragon can and should be destroyed, the dragon is finally killed. Bostrom argues that political inaction allowed many preventable human deaths to occur.<ref>{{cite journal | vauthors = Bostrom N | title = The fable of the dragon tyrant | journal = Journal of Medical Ethics | volume = 31 | issue = 5 | pages = 273–277 | date = May 2005 | pmid = 15863685 | pmc = 1734155 | doi = 10.1136/jme.2004.009035 }}</ref>

===Overpopulation concerns===

Controversy about life extension is due to fear of [[Human overpopulation|overpopulation]] and possible effects on society.<ref name="Superlongevity Without Overpopulation">{{cite web|url=https://www.fightaging.org/archives/2005/02/superlongevity-without-overpopulation-1.php|title=Superlongevity Without Overpopulation|work=Fight Aging!|date=2005-02-06}}</ref> Biogerontologist [[Aubrey De Grey]] counters the overpopulation critique by pointing out that the therapy could postpone or eliminate [[menopause]], allowing women to space out their pregnancies over more years and thus ''decreasing'' the yearly population growth rate.<ref>{{cite web|url=http://www.project-syndicate.org/commentary/the-ethics-of-anti-aging-by-peter-singer|title=Peter Singer on Should We Live to 1,000? – Project Syndicate|work=Project Syndicate|date=2012-12-10}}</ref> Moreover, the philosopher and futurist [[Max More]] argues that, given that the worldwide population growth rate is slowing down and is projected to eventually stabilize and begin falling, superlongevity would be unlikely to contribute to overpopulation.<ref name="Superlongevity Without Overpopulation"/>

===Opinion polls===

A Spring 2013 [[Pew Research]] poll in the United States found that 38% of Americans would want life extension treatments, and 56% would reject it. However, it also found that 68% believed most people would want it and that only 4% consider an "ideal lifespan" to be more than 120 years. The median "ideal lifespan" was 91 years of age and the majority of the public (63%) viewed medical advances aimed at prolonging life as generally good. 41% of Americans believed that radical life extension (RLE) would be good for society, while 51% said they believed it would be bad for society.<ref name="pewforum.org"/> One possibility for why 56% of Americans claim they would reject life extension treatments may be due to the cultural perception that living longer would result in a longer period of decrepitude, and that the elderly in our current society are unhealthy.<ref>{{cite journal | vauthors = de Magalhães JP | title = The scientific quest for lasting youth: prospects for curing aging | journal = Rejuvenation Research | volume = 17 | issue = 5 | pages = 458–467 | date = October 2014 | pmid = 25132068 | pmc = 4203147 | doi = 10.1089/rej.2014.1580 }}</ref>

Religious people are no more likely to oppose life extension than the unaffiliated,<ref name="pewforum.org">{{cite web|url=http://www.pewforum.org/2013/08/06/living-to-120-and-beyond-americans-views-on-aging-medical-advances-and-radical-life-extension/|title=Living to 120 and Beyond: Americans' Views on Aging, Medical Advances and Radical Life Extension|date=6 August 2013|work=Pew Research Center's Religion & Public Life Project}}</ref> though some variation exists between religious denominations.

===Aging as a disease===
Most mainstream medical organizations and practitioners do not consider aging to be a disease. Biologist [[David Sinclair (biologist)|David Sinclair]] says: "I&nbsp;don't see aging as a disease, but as a collection of quite predictable diseases caused by the deterioration of the body."<ref>{{cite journal | vauthors = Hayden EC | title = Age research: a new angle on 'old' | journal = Nature | volume = 450 | issue = 7170 | pages = 603–605 | date = November 2007 | pmid = 18046373 | doi = 10.1038/450603a | doi-access = free | bibcode = 2007Natur.450..603H }}</ref> The two main arguments used are that aging is both inevitable and universal while diseases are not.<ref>Hamerman D. (2007) ''Geriatric Bioscience: The link between aging & disease''. The Johns Hopkins University Press, Maryland.</ref> However, not everyone agrees. Harry R. Moody, director of academic affairs for [[AARP]], notes that what is normal and what is disease strongly depend on a historical context.<ref>{{cite journal| vauthors = Moody HR |title=Who's afraid of life extension?|journal= Generations|volume=25|issue= 4 |year=2002|pages= 33–7}}</ref> [[David Gems]], assistant director of the Institute of Healthy Ageing, argues that aging should be viewed as a disease.<ref>{{cite journal | vauthors = Gems D | year = 2011 | title = Aging: To Treat, or Not to Treat? The possibility of treating aging is not just an idle fantasy | journal = American Scientist | volume = 99 | issue = 4| pages = 278–80 | doi = 10.1511/2011.91.278 | s2cid = 123698910 }}</ref> In response to the universality of aging, David Gems notes that it is as misleading as arguing that [[Basenji]] are not dogs because they do not bark.<ref name=Gems2>{{cite journal | vauthors = Gems D | title = Tragedy and delight: the ethics of decelerated ageing | journal = Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences | volume = 366 | issue = 1561 | pages = 108–112 | date = January 2011 | pmid = 21115537 | pmc = 3001315 | doi = 10.1098/rstb.2010.0288 }}</ref> Because of the universality of aging he calls it a "special sort of disease". Robert M. Perlman, coined the terms "aging syndrome" and "disease complex" in 1954 to describe aging.<ref>{{cite journal | vauthors = Perlman RM | title = The aging syndrome | journal = Journal of the American Geriatrics Society | volume = 2 | issue = 2 | pages = 123–129 | date = February 1954 | pmid = 13129024 | doi = 10.1111/j.1532-5415.1954.tb00884.x | s2cid = 45894370 }}</ref>

The discussion whether aging should be viewed as a disease or not has important implications. One view is, this would stimulate pharmaceutical companies to develop life extension therapies and in the United States of America, it would also increase the regulation of the anti-aging market by the [[Food and Drug Administration]] (FDA). Anti-aging now falls under the regulations for cosmetic medicine which are less tight than those for drugs.<ref name=Gems2/><ref>{{cite journal | vauthors = Mehlman MJ, Binstock RH, Juengst ET, Ponsaran RS, Whitehouse PJ | title = Anti-aging medicine: can consumers be better protected? | journal = The Gerontologist | volume = 44 | issue = 3 | pages = 304–310 | date = June 2004 | pmid = 15197284 | doi = 10.1093/geront/44.3.304 | doi-access =  }}</ref>

==Beliefs and methods==
{{See also|Ageing#Prevention and delay|Brain aging}}

===Senolytics and prolongevity drugs===
{{See also|Geroprotector|MTOR inhibitors#Rapamycin and rapalogs}}
{{Excerpt|Senolytic|paragraphs=|file=}}

Senolytics eliminate senescent cells whereas [[senomorphic]]s – with candidates such as [[Apigenin]], [[Everolimus]]<!--(RAD001 in ref)--> and [[Rapamycin]] – modulate properties of senescent cells without eliminating them, suppressing phenotypes of senescence, including the [[Senescence-associated secretory phenotype|SASP]].<ref name="Di Micco-2021">{{cite journal | vauthors = Di Micco R, Krizhanovsky V, Baker D, d'Adda di Fagagna F | title = Cellular senescence in ageing: from mechanisms to therapeutic opportunities | journal = Nature Reviews. Molecular Cell Biology | volume = 22 | issue = 2 | pages = 75–95 | date = February 2021 | pmid = 33328614 | pmc = 8344376 | doi = 10.1038/s41580-020-00314-w }}</ref><ref name="Robbins-2021">{{cite journal | vauthors = Robbins PD, Jurk D, Khosla S, Kirkland JL, LeBrasseur NK, Miller JD, Passos JF, Pignolo RJ, Tchkonia T, Niedernhofer LJ | display-authors = 6 | title = Senolytic Drugs: Reducing Senescent Cell Viability to Extend Health Span | journal = Annual Review of Pharmacology and Toxicology | volume = 61 | issue = 1 | pages = 779–803 | date = January 2021 | pmid = 32997601 | pmc = 7790861 | doi = 10.1146/annurev-pharmtox-050120-105018 }}</ref> Senomorphic effects may be one major effect mechanism of a range of prolongevity drug candidates. Such candidates are however typically not studied for just one mechanism, but multiple. There are [[biological database]]s of prolongevity drug candidates under research as well as of potential gene/protein targets. These are enhanced by longitudinal [[cohort study|cohort studies]], [[electronic health records]], [[In silico medicine|computational]] (drug) screening methods, computational biomarker-discovery methods and computational biodata-interpretation/[[personalized medicine]] methods.<ref name="Donertas-2019">{{cite journal | vauthors = Dönertaş HM, Fuentealba M, Partridge L, Thornton JM | title = Identifying Potential Ageing-Modulating Drugs In Silico | journal = Trends in Endocrinology and Metabolism | volume = 30 | issue = 2 | pages = 118–131 | date = February 2019 | pmid = 30581056 | pmc = 6362144 | doi = 10.1016/j.tem.2018.11.005 }}</ref><ref name="Zhavoronkov-2019"/><ref name="Partridge-2018">{{cite journal | vauthors = Partridge L, Deelen J, Slagboom PE | title = Facing up to the global challenges of ageing | journal = Nature | volume = 561 | issue = 7721 | pages = 45–56 | date = September 2018 | pmid = 30185958 | doi = 10.1038/s41586-018-0457-8 | bibcode = 2018Natur.561...45P | s2cid = 52161707 | hdl = 1887/75460 | hdl-access = free }}</ref>

Besides rapamycin and senolytics, the [[Drug repositioning|drug-repurposing]] candidates studied most extensively include [[metformin]], [[acarbose]], [[spermidine]] and [[Nicotinamide adenine dinucleotide|NAD+]] enhancers.<ref>{{cite journal | vauthors = Partridge L, Fuentealba M, Kennedy BK | title = The quest to slow ageing through drug discovery | journal = Nature Reviews. Drug Discovery | volume = 19 | issue = 8 | pages = 513–532 | date = August 2020 | pmid = 32467649 | doi = 10.1038/s41573-020-0067-7 | s2cid = 218912510 | url = https://discovery.ucl.ac.uk/id/eprint/10101648/ | hdl = 21.11116/0000-0007-868D-3 | hdl-access = free }}</ref>

Many prolongevity drugs are synthetic alternatives or potential complements to existing nutraceuticals, such as various [[sirtuin-activating compound]]s under investigation like [[SRT2104]].<ref>{{cite journal | vauthors = Bonkowski MS, Sinclair DA | title = Slowing ageing by design: the rise of NAD<sup>+</sup> and sirtuin-activating compounds | journal = Nature Reviews. Molecular Cell Biology | volume = 17 | issue = 11 | pages = 679–690 | date = November 2016 | pmid = 27552971 | pmc = 5107309 | doi = 10.1038/nrm.2016.93 }}</ref> {{anchor|GlyNAC}}In some cases pharmaceutical administration is combined with that of neutraceuticals – such as in the case of [[glycine]] combined with [[N-acetylcysteine|NAC]].<ref name="Sekhar-2021">{{cite journal | vauthors = Sekhar RV | title = GlyNAC Supplementation Improves Glutathione Deficiency, Oxidative Stress, Mitochondrial Dysfunction, Inflammation, Aging Hallmarks, Metabolic Defects, Muscle Strength, Cognitive Decline, and Body Composition: Implications for Healthy Aging | journal = The Journal of Nutrition | volume = 151 | issue = 12 | pages = 3606–3616 | date = December 2021 | pmid = 34587244 | doi = 10.1093/jn/nxab309 | doi-access = free }}</ref> Often studies are structured based on or thematize specific prolongevity targets, listing both nutraceuticals and pharmaceuticals (together or separately) such as [[FOXO3]]-activators.<ref>{{cite journal | vauthors = McIntyre RL, Liu YJ, Hu M, Morris BJ, Willcox BJ, Donlon TA, Houtkooper RH, Janssens GE | display-authors = 6 | title = Pharmaceutical and nutraceutical activation of FOXO3 for healthy longevity | journal = Ageing Research Reviews | volume = 78 | article-number = 101621 | date = June 2022 | pmid = 35421606 | doi = 10.1016/j.arr.2022.101621 | s2cid = 248089515 | doi-access = free }}</ref>

Researchers are also exploring ways to mitigate side-effects from such substances (possibly most notably [[MTOR inhibitors#Rapamycin and rapalogs|rapamycin and its derivatives]]) such as via protocols of intermittent administration<ref>{{cite journal | vauthors = Kirkland JL, Tchkonia T | title = Senolytic drugs: from discovery to translation | journal = Journal of Internal Medicine | volume = 288 | issue = 5 | pages = 518–536 | date = November 2020 | pmid = 32686219 | pmc = 7405395 | doi = 10.1111/joim.13141 }}</ref><ref name="Robbins-2021"/><ref name="Di Micco-2021"/><ref>{{cite journal | vauthors = Palmer AK, Gustafson B, Kirkland JL, Smith U | title = Cellular senescence: at the nexus between ageing and diabetes | journal = Diabetologia | volume = 62 | issue = 10 | pages = 1835–1841 | date = October 2019 | pmid = 31451866 | pmc = 6731336 | doi = 10.1007/s00125-019-4934-x }}</ref><ref>{{cite journal | vauthors = Blagosklonny MV | title = Fasting and rapamycin: diabetes versus benevolent glucose intolerance | journal = Cell Death & Disease | volume = 10 | issue = 8 | article-number = 607 | date = August 2019 | pmid = 31406105 | pmc = 6690951 | doi = 10.1038/s41419-019-1822-8 }}</ref> and have called for research that helps determine optimal [[treatment schedules]] (including timing) in general.<ref>{{cite journal | vauthors = Martel J, Chang SH, Wu CY, Peng HH, Hwang TL, Ko YF, Young JD, Ojcius DM | display-authors = 6 | title = Recent advances in the field of caloric restriction mimetics and anti-aging molecules | journal = Ageing Research Reviews | volume = 66 | article-number = 101240 | date = March 2021 | pmid = 33347992 | doi = 10.1016/j.arr.2020.101240 | s2cid = 229351578 }}</ref>

===Diets and supplements===
====Vitamins and antioxidants====
{{See also|Inflammaging|DNA damage theory of aging}}
The [[free-radical theory of aging]] suggests that [[antioxidant]] supplements might extend human life. Reviews, however, have found that use of vitamin A (as β-carotene) and vitamin E supplements possibly can increase mortality.<ref>{{cite journal | vauthors = Bjelakovic G, Nikolova D, Gluud LL, Simonetti RG, Gluud C | title = Mortality in randomized trials of antioxidant supplements for primary and secondary prevention: systematic review and meta-analysis | journal = JAMA | volume = 297 | issue = 8 | pages = 842–857 | date = February 2007 | pmid = 17327526 | doi = 10.1001/jama.297.8.842 }}</ref><ref>{{cite journal | vauthors = Bjelakovic G, Nikolova D, Gluud LL, Simonetti RG, Gluud C | title = Antioxidant supplements for prevention of mortality in healthy participants and patients with various diseases | journal = The Cochrane Database of Systematic Reviews | volume = 2012 | issue = 3 | article-number = CD007176 | date = March 2012 | pmid = 22419320 | pmc = 8407395 | doi = 10.1002/14651858.CD007176.pub2 | hdl-access = free | hdl = 10138/136201 }}</ref> Other reviews have found no relationship between vitamin E and other vitamins with mortality.<ref>{{cite journal | vauthors = Jiang S, Pan Z, Li H, Li F, Song Y, Qiu Y | title = Meta-analysis: low-dose intake of vitamin E combined with other vitamins or minerals may decrease all-cause mortality | journal = Journal of Nutritional Science and Vitaminology | volume = 60 | issue = 3 | pages = 194–205 | year = 2014 | pmid = 25078376 | doi = 10.3177/jnsv.60.194 | quote = Neither vitamin E intake alone nor combined with other agents is associated with a reduction in all-cause mortality. | doi-access = free }}</ref> [[Vitamin D]] supplementation of various dosages is investigated in trials<ref>{{cite journal | vauthors = Garay RP | title = Investigational drugs and nutrients for human longevity. Recent clinical trials registered in ClinicalTrials.gov and clinicaltrialsregister.eu | journal = Expert Opinion on Investigational Drugs | volume = 30 | issue = 7 | pages = 749–758 | date = July 2021 | pmid = 34081543 | doi = 10.1080/13543784.2021.1939306 | s2cid = 235334397 }}</ref> and there also is research into GlyNAC {{see above|[[#GlyNAC|above]]}}.<ref name="Sekhar-2021"/>

====Complications====
Complications of antioxidant supplementation (especially continuous high dosages far above the [[Recommended Daily Allowance|RDA]]) include that [[reactive oxygen species]] (ROS), which are mitigated by antioxidants, "have been found to be physiologically vital for signal transduction, gene regulation, and redox regulation, among others, implying that their complete elimination would be harmful". In particular, one way of multiple they can be detrimental is by inhibiting adaptation to exercise such as [[muscle hypertrophy]] (e.g. during [[bodybuilding|dedicated periods]] of caloric surplus).<ref>{{cite journal | vauthors = Damiano S, Muscariello E, La Rosa G, Di Maro M, Mondola P, Santillo M | title = Dual Role of Reactive Oxygen Species in Muscle Function: Can Antioxidant Dietary Supplements Counteract Age-Related Sarcopenia? | journal = International Journal of Molecular Sciences | volume = 20 | issue = 15 | article-number = E3815 | date = August 2019 | pmid = 31387214 | pmc = 6696113 | doi = 10.3390/ijms20153815 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Badran A, Nasser SA, Mesmar J, El-Yazbi AF, Bitto A, Fardoun MM, Baydoun E, Eid AH | display-authors = 6 | title = Reactive Oxygen Species: Modulators of Phenotypic Switch of Vascular Smooth Muscle Cells | journal = International Journal of Molecular Sciences | volume = 21 | issue = 22 | page = 8764 | date = November 2020 | pmid = 33233489 | doi = 10.3390/ijms21228764 | pmc = 7699590 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Sohal RS, Orr WC | title = The redox stress hypothesis of aging | journal = Free Radical Biology & Medicine | volume = 52 | issue = 3 | pages = 539–555 | date = February 2012 | pmid = 22080087 | pmc = 3267846 | doi = 10.1016/j.freeradbiomed.2011.10.445 }}</ref> There is also research into stimulating/activating/fueling endogenous antioxidant generation, in particular e.g. of neutraceutical glycine and pharmaceutical NAC.<ref>{{cite journal | vauthors = McCarty MF, O'Keefe JH, DiNicolantonio JJ | title = Dietary Glycine Is Rate-Limiting for Glutathione Synthesis and May Have Broad Potential for Health Protection | journal = The Ochsner Journal | volume = 18 | issue = 1 | pages = 81–87 | date = 2018 | pmid = 29559876 | pmc = 5855430 }}</ref> Antioxidants can change the oxidation status of different e.g. tissues, targets or sites each with potentially different implications, especially for different concentrations.<ref>{{cite journal | vauthors = Griffiths HR | title = Antioxidants and protein oxidation | journal = Free Radical Research | volume = 33 | issue = Supplement | pages = S47–S58 | date = November 2000 | pmid = 11191275 | url = https://publications.aston.ac.uk/id/eprint/39762/ }}</ref><ref>{{cite journal | vauthors = Cobley JN | title = Mechanisms of Mitochondrial ROS Production in Assisted Reproduction: The Known, the Unknown, and the Intriguing | journal = Antioxidants | volume = 9 | issue = 10 | page = 933 | date = September 2020 | pmid = 33003362 | pmc = 7599503 | doi = 10.3390/antiox9100933 | doi-access = free }}</ref><ref>{{cite journal | title = Nutritional Antioxidants: It Is Time to Categorise | journal = Antioxidants in Sport Nutrition | date = 2015 | pmid = 26065087 | publisher = CRC Press/Taylor & Francis | isbn = 978-1-4665-6757-3 | last1 = Bast | first1 = A. | author2 = Haenen GRMM | last3 = Lamprecht | first3 = M. }}</ref><ref>{{cite journal |last1=Lobo |first1=V |last2=Patil |first2=A |last3=Phatak |first3=A |last4=Chandra |first4=N |date=2010 |title=Free radicals, antioxidants and functional foods: Impact on human health |journal=Pharmacognosy Reviews |volume=4 |issue=8 |pages=118–126 |doi=10.4103/0973-7847.70902 |pmid=22228951 |pmc=3249911 |doi-access=free }}</ref> A review suggests [[mitochondria]] have a [[hormesis|hormetic]] response to ROS, whereby low oxidative damage can be beneficial.<ref>{{cite journal | vauthors = Hood WR, Zhang Y, Mowry AV, Hyatt HW, Kavazis AN | title = Life History Trade-offs within the Context of Mitochondrial Hormesis | journal = Integrative and Comparative Biology | volume = 58 | issue = 3 | pages = 567–577 | date = September 2018 | pmid = 30011013 | pmc = 6145418 | doi = 10.1093/icb/icy073 }}</ref>

====Dietary restriction====
{{main|Diet and longevity}}
{{See also|Caloric restriction mimetic}}
As of 2021, there is no [[evidence-based medicine|clinical evidence]] that any dietary restriction practice contributes to human longevity.<ref>{{cite journal |vauthors=Lee MB, Hill CM, Bitto A, Kaeberlein M |date=November 2021 |title=Antiaging diets: Separating fact from fiction |journal=Science |volume=374 |issue=6570 |article-number=eabe7365 |doi=10.1126/science.abe7365 |pmc=8841109 |pmid=34793210}}</ref>

====Healthy diet====
Research suggests that increasing adherence to [[Mediterranean diet]] patterns is associated with a reduction in total and cause-specific mortality, extending health- and lifespan.<ref>{{cite journal | vauthors = Dominguez LJ, Di Bella G, Veronese N, Barbagallo M | title = Impact of Mediterranean Diet on Chronic Non-Communicable Diseases and Longevity | journal = Nutrients | volume = 13 | issue = 6 | page = 2028 | date = June 2021 | pmid = 34204683 | doi = 10.3390/nu13062028 | pmc = 8231595 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Eleftheriou D, Benetou V, Trichopoulou A, La Vecchia C, Bamia C | title = Mediterranean diet and its components in relation to all-cause mortality: meta-analysis | journal = The British Journal of Nutrition | volume = 120 | issue = 10 | pages = 1081–1097 | date = November 2018 | pmid = 30401007 | doi = 10.1017/S0007114518002593 | s2cid = 53226475 | doi-access = free | hdl = 2434/612956 | hdl-access = free }}</ref><ref>{{cite journal | vauthors = Ekmekcioglu C | title = Nutrition and longevity - From mechanisms to uncertainties | journal = Critical Reviews in Food Science and Nutrition | volume = 60 | issue = 18 | pages = 3063–3082 | date = 2020 | pmid = 31631676 | doi = 10.1080/10408398.2019.1676698 | s2cid = 204815279 }}</ref><ref name="niha"/> Research is identifying the key beneficial components of the Mediterranean diet.<ref>{{cite journal | vauthors = Hidalgo-Mora JJ, García-Vigara A, Sánchez-Sánchez ML, García-Pérez MÁ, Tarín J, Cano A | title = The Mediterranean diet: A historical perspective on food for health | language = English | journal = Maturitas | volume = 132 | pages = 65–69 | date = February 2020 | pmid = 31883665 | doi = 10.1016/j.maturitas.2019.12.002 | s2cid = 209510802 }}</ref><ref>{{cite journal | vauthors = Vasto S, Barera A, Rizzo C, Di Carlo M, Caruso C, Panotopoulos G | title = Mediterranean diet and longevity: an example of nutraceuticals? | journal = Current Vascular Pharmacology | volume = 12 | issue = 5 | pages = 735–738 | date = 2014 | pmid = 24350926 | doi = 10.2174/1570161111666131219111818 }}</ref> Studies suggest dietary changes are a factor of [[List of countries by life expectancy|national]] relative rises in life-span.<ref>{{cite journal | vauthors = Tsugane S | title = Why has Japan become the world's most long-lived country: insights from a food and nutrition perspective | journal = European Journal of Clinical Nutrition | volume = 75 | issue = 6 | pages = 921–928 | date = June 2021 | pmid = 32661353 | pmc = 8189904 | doi = 10.1038/s41430-020-0677-5 }}</ref>

====Optimal diet====
{{See also|Sustainable consumption#Sustainable food consumption}}
Approaches to develop optimal diets for health- and lifespan (or "longevity diets")<ref name="Longo-2022"/> include:
* modifying the Mediterranean diet as the baseline via [[nutrition science]]. For instance, via:
**(additional) increase in [[plant-based diet|plant-based]]<ref>{{cite journal | vauthors = Mariotti F, Gardner CD | title = Dietary Protein and Amino Acids in Vegetarian Diets-A Review | journal = Nutrients | volume = 11 | issue = 11 | page = 2661 | date = November 2019 | pmid = 31690027 | pmc = 6893534 | doi = 10.3390/nu11112661 | doi-access = free }}</ref><ref name="Longo-2022"/> foods alongside additional restriction of [[Meat#Health|meat intake]]<ref>{{cite journal | vauthors = Fong BY, Chiu WK, Chan WF, Lam TY | title = A Review Study of a Green Diet and Healthy Ageing | journal = International Journal of Environmental Research and Public Health | volume = 18 | issue = 15 | page = 8024 | date = July 2021 | pmid = 34360317 | doi = 10.3390/ijerph18158024 | pmc = 8345706 | doi-access = free }}</ref> – [[Environmental impact of meat production#Meat reduction and health|meat reduction is (or can be) typically healthy]],<ref>{{cite journal | vauthors = Parlasca MC, Qaim M |title=Meat Consumption and Sustainability |journal=Annual Review of Resource Economics |date=5 October 2022 |volume=14 |issue=1 |pages=17–41 |doi=10.1146/annurev-resource-111820-032340 |issn=1941-1340|doi-access=free }}</ref>
**keeping alcohol consumption of any type at a minimum – conventional Mediterranean diets include alcohol consumption (i.e. [[Health effects of wine#Moderate consumption|of wine]]), which is under research due to [[long-term impact of alcohol on the brain|data suggesting negative long-term brain impacts]] even at low/moderate consumption levels.<ref>{{cite journal | title = Alcohol use and burden for 195 countries and territories, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016 | journal = Lancet | volume = 392 | issue = 10152 | pages = 1015–1035 | date = September 2018 | pmid = 30146330 | pmc = 6148333 | doi = 10.1016/S0140-6736(18)31310-2 | last1 = Griswold | first1 = Max G. | last2 = Fullman | first2 = Nancy | last3 = Hawley | first3 = Caitlin | last4 = Arian | first4 = Nicholas | last5 = Zimsen | first5 = Stephanie R M. | last6 = Tymeson | first6 = Hayley D. | last7 = Venkateswaran | first7 = Vidhya | last8 = Tapp | first8 = Austin Douglas | last9 = Forouzanfar | first9 = Mohammad H. | last10 = Salama | first10 = Joseph S. | last11 = Abate | first11 = Kalkidan Hassen | last12 = Abate | first12 = Degu | last13 = Abay | first13 = Solomon M. | last14 = Abbafati | first14 = Cristiana | last15 = Abdulkader | first15 = Rizwan Suliankatchi | last16 = Abebe | first16 = Zegeye | last17 = Aboyans | first17 = Victor | last18 = Abrar | first18 = Mohammed Mehdi | last19 = Acharya | first19 = Pawan | last20 = Adetokunboh | first20 = Olatunji O. | last21 = Adhikari | first21 = Tara Ballav | last22 = Adsuar | first22 = Jose C. | last23 = Afarideh | first23 = Mohsen | last24 = Agardh | first24 = Emilie Elisabet | last25 = Agarwal | first25 = Gina | last26 = Aghayan | first26 = Sargis Aghasi | last27 = Agrawal | first27 = Sutapa | last28 = Ahmed | first28 = Muktar Beshir | last29 = Akibu | first29 = Mohammed | last30 = Akinyemiju | first30 = Tomi | display-authors = 1 }}</ref><ref>{{cite web |title=Facts about moderate drinking {{!}} CDC |url=https://www.cdc.gov/alcohol/fact-sheets/moderate-drinking.htm |website=www.cdc.gov |language=en-us |date=19 April 2022}}</ref> 
**fully replacing refined grains – some guidelines of Mediterranean diets do not clarify or include the principle of [[whole-grain]] consumption instead of refined grains. Whole grains are included in Mediterranean diets.<ref>{{cite journal | vauthors = Widmer RJ, Flammer AJ, Lerman LO, Lerman A | title = The Mediterranean diet, its components, and cardiovascular disease | journal = The American Journal of Medicine | volume = 128 | issue = 3 | pages = 229–238 | date = March 2015 | pmid = 25447615 | pmc = 4339461 | doi = 10.1016/j.amjmed.2014.10.014 }}</ref><ref>{{cite journal | vauthors = Ventriglio A, Sancassiani F, Contu MP, Latorre M, Di Slavatore M, Fornaro M, Bhugra D | title = Mediterranean Diet and its Benefits on Health and Mental Health: A Literature Review | journal = Clinical Practice and Epidemiology in Mental Health | volume = 16 | issue = Suppl-1 | pages = 156–164 | date = 2020 | pmid = 33029192 | pmc = 7536728 | doi = 10.2174/1745017902016010156 }}</ref>

===Other approaches===
Further advanced biosciences-based approaches include:
* '''Genetic and epigenetic alterations''': [[Human genetic enhancement]] for pro-longevity and protective genes – see [[genetics of aging]]<ref>{{cite journal | vauthors = Delhove J, Osenk I, Prichard I, Donnelley M | title = Public Acceptability of Gene Therapy and Gene Editing for Human Use: A Systematic Review | journal = Human Gene Therapy | volume = 31 | issue = 1–2 | pages = 20–46 | date = January 2020 | pmid = 31802714 | doi = 10.1089/hum.2019.197 | s2cid = 208645665 }}</ref><ref name="Zhavoronkov-2019"/>
* '''Cellular reprogramming''': in vivo [[Induced pluripotent stem cell|reprogramming]] to complement or augment [[Regeneration in humans|human regenerative capacity]] and rejuvenate or replace cells<ref>{{cite journal | vauthors = Beyret E, Martinez Redondo P, Platero Luengo A, Izpisua Belmonte JC | title = Elixir of Life: Thwarting Aging With Regenerative Reprogramming | journal = Circulation Research | volume = 122 | issue = 1 | pages = 128–141 | date = January 2018 | pmid = 29301845 | pmc = 5823281 | doi = 10.1161/CIRCRESAHA.117.311866 }}</ref><ref>{{cite journal | vauthors = Yener Ilce B, Cagin U, Yilmazer A | title = Cellular reprogramming: A new way to understand aging mechanisms | journal = Wiley Interdisciplinary Reviews. Developmental Biology | volume = 7 | issue = 2 | date = March 2018 | pmid = 29350802 | doi = 10.1002/wdev.308 | s2cid = 46743444 }}</ref><ref name="Zhavoronkov-2019"/>
* '''Epigenetic reprogramming''': early-stage research about rejuvenating/repairing [[epigenetic]] machinery<ref>{{cite journal | vauthors = Topart C, Werner E, Arimondo PB | title = Wandering along the epigenetic timeline | journal = Clinical Epigenetics | volume = 12 | issue = 1 | article-number = 97 | date = July 2020 | pmid = 32616071 | pmc = 7330981 | doi = 10.1186/s13148-020-00893-7 | doi-access = free }}</ref>
* '''Stem-cell interventions''': "Increasing the number and quality of stem cells and activate regenerative signals"<ref name="Ullah-2018"/><ref>{{cite journal |last1=Baraniak |first1=Priya R |last2=McDevitt |first2=Todd C |title=Stem cell paracrine actions and tissue regeneration |journal=Regenerative Medicine |date=January 2010 |volume=5 |issue=1 |pages=121–143 |doi=10.2217/rme.09.74 |pmid=20017699 |pmc=2833273 }}</ref>
* '''[[Nanobiotechnology#Nanomedicine|Nanomedicine]]''': early-stage research of in vivo pro-longevity nanotechnology<ref>{{cite journal | vauthors = Rzigalinski BA, Meehan K, Davis RM, Xu Y, Miles WC, Cohen CA | title = Radical nanomedicine | journal = Nanomedicine | volume = 1 | issue = 4 | pages = 399–412 | date = December 2006 | pmid = 17716143 | doi = 10.2217/17435889.1.4.399 }}</ref><ref>{{cite journal |last1=Ventola |first1=CL |title=The nanomedicine revolution: part 2: current and future clinical applications. |journal=P & T: A Peer-Reviewed Journal for Formulary Management |date=October 2012 |volume=37 |issue=10 |pages=582–91 |pmid=23115468 |pmc=3474440 }}</ref>
* '''[[Tissue engineering]]''': of tissues and organs<ref>{{cite journal | vauthors = Khorraminejad-Shirazi M, Dorvash M, Estedlal A, Hoveidaei AH, Mazloomrezaei M, Mosaddeghi P | title = Aging: A cell source limiting factor in tissue engineering | journal = World Journal of Stem Cells | volume = 11 | issue = 10 | pages = 787–802 | date = October 2019 | pmid = 31692986 | doi = 10.4252/wjsc.v11.i10.787 | pmc = 6828594 | s2cid = 207894219 | doi-access = free }}</ref> (see also: [[xenotransplantation]] and [[artificial organ]])
*{{anchor|EndogenousCirculatingBiomolecules}}'''Endogenous circulating biomolecules''': [[Blood protein]]s of blood from young animals have shown some pro-longevity potential in animal studies (e.g. via transfer of blood or plasma, and of plasma proteins).<ref name="Partridge-2018"/> Moreover, [[exerkine]]s – signalling biomolecules released during/after exercise – have also shown promising results.<ref name="Chow-2022">{{cite journal | vauthors = Chow LS, Gerszten RE, Taylor JM, Pedersen BK, van Praag H, Trappe S, Febbraio MA, Galis ZS, Gao Y, Haus JM, Lanza IR, Lavie CJ, Lee CH, Lucia A, Moro C, Pandey A, Robbins JM, Stanford KI, Thackray AE, Villeda S, Watt MJ, Xia A, Zierath JR, Goodpaster BH, Snyder MP | display-authors = 6 | title = Exerkines in health, resilience and disease | journal = Nature Reviews. Endocrinology | volume = 18 | issue = 5 | pages = 273–289 | date = May 2022 | pmid = 35304603 | doi = 10.1038/s41574-022-00641-2 | pmc = 9554896 | s2cid = 247524287 }}</ref> Exerkines include [[myokine]]s. [[Extracellular vesicles]] were shown to be secreted concomitantly with exerkines and are also investigated.<ref>{{cite journal | vauthors = Nederveen JP, Warnier G, Di Carlo A, Nilsson MI, Tarnopolsky MA | title = Extracellular Vesicles and Exosomes: Insights From Exercise Science | journal = Frontiers in Physiology | volume = 11 | article-number = 604274 | date = 2020 | pmid = 33597890 | pmc = 7882633 | doi = 10.3389/fphys.2020.604274 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Lananna BV, Imai SI | title = Friends and foes: Extracellular vesicles in aging and rejuvenation | journal = FASEB BioAdvances | volume = 3 | issue = 10 | pages = 787–801 | date = October 2021 | pmid = 34632314 | pmc = 8493967 | doi = 10.1096/fba.2021-00077 | doi-access = free }}</ref> (See also: [[body fluid]] and [[cerebrospinal fluid]])
*{{anchor|PersonalizedInterventions}}'''Personalized interventions''': future studies may tailor and investigate [[personalized medicine]]-type interventions.<ref name="Campisi-2019">{{cite journal | vauthors = Campisi J, Kapahi P, Lithgow GJ, Melov S, Newman JC, Verdin E | title = From discoveries in ageing research to therapeutics for healthy ageing | journal = Nature | volume = 571 | issue = 7764 | pages = 183–192 | date = July 2019 | pmid = 31292558 | pmc = 7205183 | doi = 10.1038/s41586-019-1365-2 | bibcode = 2019Natur.571..183C }}</ref> For instance, effects of interventions or e.g. dosages may vary per age<ref name="Longo-2022"/> and/or genome. A review suggests that the field of [[precision medicine]] and geroscience will have to interact closely<ref name="Campisi-2019"/> (see also: [[combination therapy]])
* '''Peptides''': such as [[MT-RNR1|MOTS-c]] released by mitochondria<ref name="Lopez-Otin-2016">{{cite journal | vauthors = López-Otín C, Galluzzi L, Freije JM, Madeo F, Kroemer G | title = Metabolic Control of Longevity | journal = Cell | volume = 166 | issue = 4 | pages = 802–821 | date = August 2016 | pmid = 27518560 | doi = 10.1016/j.cell.2016.07.031 | s2cid = 2316555 | doi-access = free | hdl = 10651/39940 | hdl-access = free }}</ref>
* '''Mitochondria modulation''': early-stage research indicates mitochondrial interventions such as mitochondrial transplantation may have potential to be efficacious<ref>{{cite journal | vauthors = Tomita K, Kuwahara Y, Igarashi K, Roudkenar MH, Roushandeh AM, Kurimasa A, Sato T | title = Mitochondrial Dysfunction in Diseases, Longevity, and Treatment Resistance: Tuning Mitochondria Function as a Therapeutic Strategy | journal = Genes | volume = 12 | issue = 9 | page = 1348 | date = August 2021 | pmid = 34573330 | doi = 10.3390/genes12091348 | pmc = 8467098 | doi-access = free }}</ref><ref name="Zhavoronkov-2019"/><ref>{{cite journal | vauthors = Akbari M, Kirkwood TB, Bohr VA | title = Mitochondria in the signaling pathways that control longevity and health span | journal = Ageing Research Reviews | volume = 54 | article-number = 100940 | date = September 2019 | pmid = 31415807 | pmc = 7479635 | doi = 10.1016/j.arr.2019.100940 }}</ref><ref>{{cite journal | vauthors = Akbari M, Kirkwood TB, Bohr VA | title = Mitochondria in the signaling pathways that control longevity and health span | journal = Ageing Research Reviews | volume = 54 | article-number = 100940 | date = September 2019 | pmid = 31415807 | doi = 10.1016/j.arr.2019.100940 | pmc = 7479635 | s2cid = 199544098 }}</ref><ref>{{cite journal | vauthors = Santoro A, Martucci M, Conte M, Capri M, Franceschi C, Salvioli S | title = Inflammaging, hormesis and the rationale for anti-aging strategies | journal = Ageing Research Reviews | volume = 64 | article-number = 101142 | date = December 2020 | pmid = 32814129 | doi = 10.1016/j.arr.2020.101142 | s2cid = 221136388 }}</ref> (See also: [[mitochondrial theory of ageing]])

====Within the field====
{{See also|Biogerontology}}
There is a need and research into the development of aging [[biomarker]]s such as the [[epigenetic clock]] "to assess the ageing process and the efficacy of interventions to bypass the need for large-scale longitudinal studies".<ref name="Campisi-2019"/><ref name="Zhavoronkov-2019">{{cite journal | vauthors = Zhavoronkov A, Mamoshina P, Vanhaelen Q, Scheibye-Knudsen M, Moskalev A, Aliper A | title = Artificial intelligence for aging and longevity research: Recent advances and perspectives | journal = Ageing Research Reviews | volume = 49 | pages = 49–66 | date = January 2019 | pmid = 30472217 | doi = 10.1016/j.arr.2018.11.003 | s2cid = 53755842 | doi-access = free }}</ref> Such biomarkers may also include in vivo [[brain imaging]].<ref>{{cite journal | vauthors = Ingram DK, Chefer S, Matochik J, Moscrip TD, Weed J, Roth GS, London ED, Lane MA | display-authors = 6 | title = Aging and caloric restriction in nonhuman primates: behavioral and in vivo brain imaging studies | journal = Annals of the New York Academy of Sciences | volume = 928 | pages = 316–326 | date = April 2001 | issue = 1 | pmid = 11795523 | doi = 10.1111/j.1749-6632.2001.tb05661.x | s2cid = 35478202 }}</ref>

Reviews sometimes include structured tables that provide systematic overviews of intervention/drug candidates with a review calling for integrating "current knowledge with multi-omics, health records, and drug safety data to predict drugs that can improve health in late life" and listing [[research question|major outstanding questions]].<ref name="Donertas-2019"/> [[Biological database]]s of prolongevity drug candidates under research as well as of potential gene/protein targets include GenAge, DrugAge and Geroprotectors.<ref name="Donertas-2019"/><ref>{{cite journal | vauthors = Cardoso AL, Fernandes A, Aguilar-Pimentel JA, de Angelis MH, Guedes JR, Brito MA, Ortolano S, Pani G, Athanasopoulou S, Gonos ES, Schosserer M, Grillari J, Peterson P, Tuna BG, Dogan S, Meyer A, van Os R, Trendelenburg AU | display-authors = 6 | title = Towards frailty biomarkers: Candidates from genes and pathways regulated in aging and age-related diseases | journal = Ageing Research Reviews | volume = 47 | pages = 214–277 | date = November 2018 | pmid = 30071357 | doi = 10.1016/j.arr.2018.07.004 | s2cid = 51865989 | doi-access = free | hdl = 10807/130553 | hdl-access = free }}</ref>

A review has pointed out that the approach of "'epidemiological' comparison of how a low versus a high consumption of an isolated macronutrient and its association with health and mortality may not only fail to identify protective or detrimental nutrition patterns but may lead to misleading interpretations". It proposes a multi-pillar approach, and summarizes findings towards constructing – multi-system-considering and at least age-personalized dynamic – refined longevity diets. Epidemiological-type observational studies included in meta-analyses should according to the study at least be complemented by "(1) basic research focused on lifespan and healthspan, (2) carefully controlled clinical trials, and (3) studies of individuals and populations with record longevity".<ref name="Longo-2022">{{cite journal | vauthors = Longo VD, Anderson RM | title = Nutrition, longevity and disease: From molecular mechanisms to interventions | language = English | journal = Cell | volume = 185 | issue = 9 | pages = 1455–1470 | date = April 2022 | pmid = 35487190 | pmc = 9089818 | doi = 10.1016/j.cell.2022.04.002 }}</ref>

===Hormone treatment===
The [[anti-aging]] industry offers several [[hormone therapies]]. Some of these have been criticized for possible dangers and a lack of proven effect. For example, the [[American Medical Association]] has been critical of some anti-aging hormone therapies.<ref name=AMA>{{Cite news | vauthors = Japsen B |date=15 June 2009 |title=AMA report questions science behind using hormones as anti-aging treatment |url=https://www.chicagotribune.com/2009/06/15/anti-aging-treatment-on-amas-radar/ |work=[[The Chicago Tribune]] |access-date=17 July 2009}}</ref>

While [[growth hormone]] (GH) decreases with age, the evidence for use of growth hormone as an anti-aging therapy is mixed and based mostly on animal studies. There are mixed reports that GH or [[IGF-1]] modulates the aging process in humans and about whether the direction of its effect is positive or negative.<ref>{{cite journal | vauthors = Sattler FR | title = Growth hormone in the aging male | journal = Best Practice & Research. Clinical Endocrinology & Metabolism | volume = 27 | issue = 4 | pages = 541–555 | date = August 2013 | pmid = 24054930 | pmc = 3940699 | doi = 10.1016/j.beem.2013.05.003 | quote = In animal models, alterations in GH/IGF-1 signaling with reductions in these somatotrophs appear to increase life span. &nbsp;... Administration of IGF-1Eb (mechanogrowth factor) stimulates proliferation of myoblasts and induces muscle hypertrophy. Increases in GH and IGF-1 during adolescence are beneficial for brain and cardiovascular function during the aging process and GH administration during adolescence is vasoprotective and increases life-span.<sup>15</sup>&nbsp;... Studies relating GH and IGF-1 status to longevity provide inconsistent evidence as to whether decreased (somatopause) or high levels (e.g. acromegaly) of these hormones are beneficial or detrimental to longevity.&nbsp;... It is difficult to reconcile the largely protective effects of GH/IGF-1 deficiency on longevity in animals with the inconsistent or deleterious effects of low levels or declining GH/IGF-1 during human aging. }}</ref>

[[Klotho (biology)#Effects on aging|Klotho]]<ref name="Ullah-2018">{{cite journal | vauthors = Ullah M, Sun Z | title = Stem cells and anti-aging genes: double-edged sword-do the same job of life extension | journal = Stem Cell Research & Therapy | volume = 9 | issue = 1 | article-number = 3 | date = January 2018 | pmid = 29321045 | pmc = 5763529 | doi = 10.1186/s13287-017-0746-4 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Baranowska B, Kochanowski J | title = The metabolic, neuroprotective cardioprotective and antitumor effects of the Klotho protein | journal = Neuro Endocrinology Letters | volume = 41 | issue = 2 | pages = 69–75 | date = September 2020 | pmid = 33185993 }}</ref> and exerkines<ref name="Chow-2022"/> {{See above|[[#EndogenousCirculatingBiomolecules|above]]}} like [[irisin]]<ref>{{cite journal | vauthors = Fossati C, Papalia R, Torre G, Vadalà G, Borrione P, Grazioli E, Mazzola C, Parisi A, Pigozzi F, Denaro V | display-authors = 6 | title = Frailty of the elderly in orthopaedic surgery and body composition changes: the musculoskeletal crosstalk through irisin | journal = Journal of Biological Regulators and Homeostatic Agents | volume = 34 | issue = 4 Suppl. 3 | pages = 327–335. Congress of the Italian Orthopaedic Research Society | date = July 2020 | pmid = 33261297 }}</ref> are being investigated for potential pro-longevity therapies.

===Lifestyle factors===
{{See also|Lifestyle disease}}
[[Loneliness]]/isolation, social life and support,<ref name="niha"/><ref>{{cite journal | vauthors = Vila J | title = Social Support and Longevity: Meta-Analysis-Based Evidence and Psychobiological Mechanisms | journal = Frontiers in Psychology | volume = 12 | article-number = 717164 | date = 2021 | pmid = 34589025 | pmc = 8473615 | doi = 10.3389/fpsyg.2021.717164 | doi-access = free }}</ref> exercise/physical activity (partly via [[neurobiological effects of physical exercise|neurobiological effects]] and increased NAD+ levels),<ref name="niha">{{cite web |title=What Do We Know About Healthy Aging? |date=23 February 2022 |url=https://www.nia.nih.gov/health/what-do-we-know-about-healthy-aging |publisher=[[National Institute on Aging]] |access-date=1 June 2022 |language=en |archive-date=26 May 2022 |archive-url=https://web.archive.org/web/20220526235840/https://www.nia.nih.gov/health/what-do-we-know-about-healthy-aging |url-status=dead }}</ref><ref>{{cite journal | vauthors = O'Keefe EL, Torres-Acosta N, O'Keefe JH, Lavie CJ | title = Training for Longevity: The Reverse J-Curve for Exercise | journal = Missouri Medicine | volume = 117 | issue = 4 | pages = 355–361 | date = July 2020 | pmid = 32848273 | pmc = 7431070 | quote = Current studies suggest that 2.5 to 5 hours/week of moderate or vigorous physical activity will confer maximal benefits; >10 hours/week may reduce these health benefits. }}</ref><ref name="Campisi-2019"/><ref name="Lopez-Otin-2016"/><ref>{{cite journal | vauthors = Min S, Masanovic B, Bu T, Matic RM, Vasiljevic I, Vukotic M, Li J, Vukovic J, Fu T, Jabucanin B, Bujkovic R, Popovic S | display-authors = 6 | title = The Association Between Regular Physical Exercise, Sleep Patterns, Fasting, and Autophagy for Healthy Longevity and Well-Being: A Narrative Review | journal = Frontiers in Psychology | volume = 12 | article-number = 803421 | date = 2 December 2021 | pmid = 34925198 | pmc = 8674197 | doi = 10.3389/fpsyg.2021.803421 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Hofer SJ, Davinelli S, Bergmann M, Scapagnini G, Madeo F | title = Caloric Restriction Mimetics in Nutrition and Clinical Trials | journal = Frontiers in Nutrition | volume = 8 | article-number = 717343 | date = 2021 | pmid = 34552954 | doi = 10.3389/fnut.2021.717343 | pmc = 8450594 | doi-access = free }}</ref> psychological characteristics/personality (possibly highly indirectly),<ref>{{cite journal | vauthors = Chapman BP, Roberts B, Duberstein P | title = Personality and longevity: knowns, unknowns, and implications for public health and personalized medicine | journal = Journal of Aging Research | volume = 2011 | article-number = 759170 | date = 10 July 2011 | pmid = 21766032 | doi = 10.4061/2011/759170 | pmc = 3134197 | s2cid = 16615606 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Kern ML, Friedman HS | title = Do conscientious individuals live longer? A quantitative review | journal = Health Psychology | volume = 27 | issue = 5 | pages = 505–512 | date = September 2008 | pmid = 18823176 | doi = 10.1037/0278-6133.27.5.505 }}</ref> sleep duration,<ref name="niha"/> [[circadian rhythm]]s (patterns of sleep, drug-administration and feeding),<ref>{{cite journal | vauthors = Froy O, Miskin R | title = Effect of feeding regimens on circadian rhythms: implications for aging and longevity | journal = Aging | volume = 2 | issue = 1 | pages = 7–27 | date = December 2010 | pmid = 20228939 | pmc = 2837202 | doi = 10.18632/aging.100116 }}</ref><ref>{{cite journal | vauthors = Froy O | title = Circadian rhythms, aging, and life span in mammals | journal = Physiology | volume = 26 | issue = 4 | pages = 225–235 | date = August 2011 | pmid = 21841071 | doi = 10.1152/physiol.00012.2011 }}</ref><ref>{{cite journal | vauthors = Acosta-Rodríguez VA, Rijo-Ferreira F, Green CB, Takahashi JS | title = Importance of circadian timing for aging and longevity | journal = Nature Communications | volume = 12 | issue = 1 | article-number = 2862 | date = May 2021 | pmid = 34001884 | doi = 10.1038/s41467-021-22922-6 | pmc = 8129076 | bibcode = 2021NatCo..12.2862A | s2cid = 234770669 }}</ref> type of leisure activities,<ref name="niha"/> not smoking,<ref name="niha"/> altruistic emotions and behaviors,<ref>{{cite journal | vauthors = Post SG | title = Altuism, happiness, and health: it's good to be good | journal = International Journal of Behavioral Medicine | volume = 12 | issue = 2 | pages = 66–77 | date = 2005 | pmid = 15901215 | doi = 10.1207/s15327558ijbm1202_4 | s2cid = 12544814 }}</ref><ref>{{cite journal | vauthors = Gottlieb BH, Gillespie AA | title = Volunteerism, health, and civic engagement among older adults | journal = Canadian Journal on Aging | volume = 27 | issue = 4 | pages = 399–406 | date = 2008 | pmid = 19416800 | doi = 10.3138/cja.27.4.399 | s2cid = 24698644 }}</ref> subjective [[well-being]],<ref>{{cite journal | vauthors = Diener E, Oishi S, Tay L | title = Advances in subjective well-being research | journal = Nature Human Behaviour | volume = 2 | issue = 4 | pages = 253–260 | date = April 2018 | pmid = 30936533 | doi = 10.1038/s41562-018-0307-6 | s2cid = 4726262 }}</ref> mood<ref name="niha"/> and stress (including via [[heat shock protein]])<ref name="niha"/><ref>{{cite journal | vauthors = Gomez CR | title = Role of heat shock proteins in aging and chronic inflammatory diseases | journal = GeroScience | volume = 43 | issue = 5 | pages = 2515–2532 | date = October 2021 | pmid = 34241808 | pmc = 8599533 | doi = 10.1007/s11357-021-00394-2 }}</ref> are investigated as potential (modulatable) factors of life extension.

Healthy lifestyle practices and healthy diet have been suggested as "first-line function-preserving strategies, with pharmacological agents, including existing and new pharmaceuticals and novel 'nutraceutical' compounds, serving as potential complementary approaches".<ref>{{cite journal | vauthors = Seals DR, Justice JN, LaRocca TJ | title = Physiological geroscience: targeting function to increase healthspan and achieve optimal longevity | journal = The Journal of Physiology | volume = 594 | issue = 8 | pages = 2001–2024 | date = April 2016 | pmid = 25639909 | doi = 10.1113/jphysiol.2014.282665 | pmc = 4933122 | s2cid = 9776021 }}</ref>

===Societal strategies===
{{See also|#Ethics and politics|#Scientific research|Clinical trial|Metascience|Telehealth|Health economics|Health education|Medical research}}
[[File:Life expectancy vs healthcare spending.jpg|thumb|Life expectancy vs healthcare spending of rich OECD countries. [[List of countries by total health expenditure per capita|US average of $10,447 in 2018]].<ref>{{cite journal |author-link1=Max Roser |vauthors=Roser M |date=26 May 2017 |title=Link between health spending and life expectancy: US is an outlier |url=https://ourworldindata.org/the-link-between-life-expectancy-and-health-spending-us-focus |journal=[[Our World in Data]]}} Click the sources tab under the chart for info on the countries, healthcare expenditures, and data sources. See the later version of the chart [https://ourworldindata.org/us-life-expectancy-low here].</ref>]]
Collectively, addressing [[List of causes of death by rate|common causes of death]] could extend lifespans of populations and humanity overall. For instance, a 2020 study indicates that the global mean [[loss of life expectancy]] (LLE) from [[air pollution]] in 2015 was 2.9 years, substantially more than, for example, 0.3 years from all forms of direct violence, albeit a significant fraction of the LLE (a measure similar to [[years of potential life lost]]) is considered to be unavoidable.<ref>{{cite journal | vauthors = Lelieveld J, Pozzer A, Pöschl U, Fnais M, Haines A, Münzel T | title = Loss of life expectancy from air pollution compared to other risk factors: a worldwide perspective | journal = Cardiovascular Research | volume = 116 | issue = 11 | pages = 1910–1917 | date = September 2020 | pmid = 32123898 | pmc = 7449554 | doi = 10.1093/cvr/cvaa025 }}</ref>

Regular [[Screening (medicine)|screening]] and doctor visits has been suggested as a lifestyle-societal intervention.<ref name="niha"/> (See also: [[medical test]] and [[biomarker (medicine)|biomarker]])

[[Health policy]] and changes to standard healthcare could support the adoption of the field's conclusions – a review suggests that the longevity diet would be a "valuable complement to standard healthcare and that, taken as a preventative measure, it could aid in avoiding morbidity, sustaining health into advanced age" as a form of [[preventive healthcare]].<ref name="Longo-2022"/>

It has been suggested that in terms of healthy diets, Mediterranean-style diets could be promoted by countries for ensuring healthy-by-default choices ("to ensure the healthiest choice is the easiest choice") and with highly effective measures including [[Nutrition education|dietary education]], food [[checklist]]s and [[recipe]]s that are "simple, palatable, and affordable".<ref>{{cite journal | vauthors = Murphy KJ, Parletta N | title = Implementing a Mediterranean-Style Diet Outside the Mediterranean Region | journal = Current Atherosclerosis Reports | volume = 20 | issue = 6 | article-number = 28 | date = May 2018 | pmid = 29728772 | doi = 10.1007/s11883-018-0732-z | s2cid = 21658334 }}</ref>

A review suggests that "targeting the aging process per se may be a far more effective approach to prevent or delay aging-associated pathologies than treatments specifically targeted to particular clinical conditions".<ref>{{cite journal | vauthors = Vaiserman A, Lushchak O | title = Implementation of longevity-promoting supplements and medications in public health practice: achievements, challenges and future perspectives | journal = Journal of Translational Medicine | volume = 15 | issue = 1 | article-number = 160 | date = July 2017 | pmid = 28728596 | pmc = 5520340 | doi = 10.1186/s12967-017-1259-8 | doi-access = free }}</ref>

===Low ambient temperature===
Low ambient temperature as a physical factor affecting free radical levels was identified as a treatment producing exceptional lifespan increase in Drosophila melanogaster and other living beings.<ref>{{cite journal | vauthors = Shaposhnikov MV, Guvatova ZG, Zemskaya NV, Koval LA, Schegoleva EV, Gorbunova AA, Golubev DA, Pakshina NR, Ulyasheva NS, Solovev IA, Bobrovskikh MA, Gruntenko NE, Menshanov PN, Krasnov GS, Kudryavseva AV, Moskalev AA | display-authors = 6 | title = Molecular mechanisms of exceptional lifespan increase of Drosophila melanogaster with different genotypes after combinations of pro-longevity interventions | journal = Communications Biology | volume = 5 | issue = 1 | article-number = 566 | date = June 2022 | pmid = 35681084 | pmc = 9184560 | doi = 10.1038/s42003-022-03524-4 }}</ref>
===Young blood transfusion===
{{Further|Young blood transfusion}}
As of 2017, some clinics offered injection of [[blood plasma]] from young donors. The alleged benefits of the treatment, none of which had been proven, included a longer life.<ref name="guard">{{Cite news| url=https://www.theguardian.com/society/shortcuts/2017/aug/21/ambrosia-the-startup-harvesting-the-blood-of-the-young|title=Ambrosia: the startup harvesting the blood of the young| vauthors = Haynes G |date=August 21, 2017|newspaper=The Guardian|access-date=November 5, 2017}}</ref><ref name="cnbc">{{Cite news|url=https://www.cnbc.com/2017/05/31/blood-transfusions-from-teenagers-start-up-charging-8000-apiece.html|title=This start-up is offering $8,000 blood transfusions from teens to people who want to fight aging| vauthors = Farr C |date=May 31, 2017|work=CNBC|access-date=November 5, 2017}}</ref> The approach was based on [[parabiosis]] studies in mice.<ref name=cnbc/> 

In 2019, after receiving an [[FDA warning letter]] to cease giving people plasma infusions, one American company that promoted the treatment, ''Ambrosia'', withdrew from clinical trials it had conducted without FDA approval.<ref name="cnn">{{cite news |vauthors=Scutti S |title=Young blood company stops unproven anti-aging treatments after FDA warning |url=https://www.cnn.com/2019/02/19/health/plasma-infusion-young-blood-fda-bn/index.html |access-date=1 July 2025 |work=CNN |date=20 February 2019|quote=There is no proven clinical benefit of infusion of plasma from young donors to cure, mitigate, treat, or prevent these conditions, and there are risks associated with the use of any plasma product}}</ref> The FDA had stated "that some patients are being preyed upon by unscrupulous actors touting treatments of plasma from young donors as cures and remedies."<ref name=cnn/>

The treatment appeared in HBO's ''[[Silicon Valley (TV series)|Silicon Valley]]'' fiction series.<ref name=cnbc/>

===Microbiome alterations===
[[Fecal microbiota transplant]]ation<ref>{{cite news | vauthors = Haridy R |title=Gut bacteria from young mice reverse signs of brain aging in old mice |url=https://newatlas.com/science/microbiome-brain-aging-gut-bacteria-neuroscience/ |access-date=21 September 2021 |work=New Atlas |date=10 August 2021}}</ref><ref>{{cite journal | vauthors = Boehme M, Guzzetta KE, Bastiaanssen TF, Van De Wouw M, Moloney GM, Gual-Grau A, Spichak S, Olavarría-Ramírez L, Fitzgerald P, Morillas E, Ritz NL, Jaggar M, Cowan CS, Crispie F, Donoso F, Halitzki E, Neto MC, Sichetti M, Golubeva AV, Fitzgerald RS, Claesson MJ, Cotter PD, O'Leary OF, Dinan TG, Cryan JF | display-authors = 6 |title=Microbiota from young mice counteracts selective age-associated behavioral deficits |journal=Nature Aging |date=August 2021 |volume=1 |issue=8 |pages=666–676 |doi=10.1038/s43587-021-00093-9 | pmid = 37117767 |language=en |issn=2662-8465|doi-access=free }}</ref> and [[probiotics]] are being investigated as means for life and healthspan extension.<ref>{{cite journal | vauthors = Sharma D, Kober MM, Bowe WP | title = Anti-Aging Effects of Probiotics | journal = Journal of Drugs in Dermatology | volume = 15 | issue = 1 | pages = 9–12 | date = January 2016 | pmid = 26741377 }}</ref><ref>{{cite journal | vauthors = Ayala FR, Bauman C, Cogliati S, Leñini C, Bartolini M, Grau R | title = Microbial flora, probiotics, ''Bacillus subtilis'' and the search for a long and healthy human longevity | journal = Microbial Cell | volume = 4 | issue = 4 | pages = 133–136 | date = March 2017 | pmid = 28435840 | pmc = 5376353 | doi = 10.15698/mic2017.04.569 }}</ref><ref>{{cite journal | vauthors = Tsai YC, Cheng LH, Liu YW, Jeng OJ, Lee YK | title = Gerobiotics: probiotics targeting fundamental aging processes | journal = Bioscience of Microbiota, Food and Health | volume = 40 | issue = 1 | pages = 1–11 | date = 2021 | pmid = 33520563 | pmc = 7817508 | doi = 10.12938/bmfh.2020-026 }}</ref>

==Mind uploading==
{{Main|Mind uploading}}
One hypothetical future strategy that, as some suggest,{{who|date=July 2017}} "eliminates" the complications related to a physical body, involves the copying or transferring (e.g. by progressively replacing neurons with transistors) of a conscious mind from a biological brain to a non-biological computer system or computational device. The basic idea is to scan the structure of a particular brain in detail, and then construct a software model of it that is so faithful to the original that, when run on appropriate hardware, it will behave in essentially the same way as the original brain.<ref>{{Cite book| vauthors = Sandberg A, Boström N | author2-link=Nick Bostrom|title=Whole Brain Emulation: A Roadmap|quote=The basic idea is to take a particular brain, scan its structure in detail, and construct a software model of it that is so faithful to the original that, when run on appropriate hardware, it will behave in essentially the same way as the original brain.|url=http://www.fhi.ox.ac.uk/Reports/2008-3.pdf|access-date=7 March 2013|series= Technical Report #2008-3|year=2008| publisher = Future of Humanity Institute, Oxford University}}</ref> Whether or not an exact copy of one's mind constitutes actual life extension is matter of debate.

However, critics argue that the uploaded mind would simply be a clone and not a true continuation of a person's consciousness.<ref>{{cite news|url=https://www.wsj.com/articles/will-your-uploaded-mind-still-be-you-11568386410|title=Will Your Uploaded Mind Still Be You?| vauthors = Graziano M |date=September 13, 2019|access-date=May 19, 2020|newspaper=[[Wall Street Journal]]}}</ref>

Some scientists believe that the dead may one day be "resurrected" through simulation technology.<ref>{{cite web | vauthors = Bostrom N |title=Are You Living in a Computer Simulation? |date=19 January 2010 |url=http://www.simulation-argument.com/simulation.html}}</ref>

== See also ==
{{Main|List of life extension topics|Index of life extension-related articles}}
<!-- keep alphabetical -->
{{div col|colwidth=20em}}
* [[Advanced glycation end product]]
* [[Aging brain]]
* [[Biological immortality]]
* [[Centenarian]]
* [[DNA damage theory of aging]]
* [[Human enhancement]]
* [[Immortality]]
* [[Maximum lifespan]]
* [[Senescence]]
* [[Slow aging]]
* [[Supercentenarian]]

{{div col end}}
<!-- keep alphabetical -->

== References ==
{{Reflist|30em}}

== Further reading ==
{{refbegin}}
* {{cite web | url = http://www.nickbostrom.com/fable/dragon.html | title = The Fable of the Dragon Tyrant | vauthors = Bostrum N | author-link1 = Nick Bostrom }}
* {{cite news | url = http://news.bbc.co.uk/1/hi/uk/4003063.stm | vauthors = de Grey A | title = We will be able to live to 1,000 | work = BBC News | date = 3 December 2004 }}
* {{cite web | vauthors = Easterbrook G | url = https://www.theatlantic.com/features/archive/2014/09/what-happens-when-we-all-live-to-100/379338/ | title = What Happens When We All Live to 100? | work = The Atlantic | date = October 2014 | pages = 60–72 }}
* {{cite web | vauthors = Emanuel EJ | url = https://www.theatlantic.com/features/archive/2014/09/why-i-hope-to-die-at-75/379329/ | title = Why I Hope to Die at 75 | work = The Atlantic | date = October 2014 | pages = 74–81 }}
{{refend}}

== External links ==
* {{Wikiversity inline}}

{{Life extension}}
{{Longevity}}
{{emerging technologies|topics=yes|biomed=yes}}
{{Effective altruism}}
{{Authority control}}

[[Category:Life extension| ]]
[[Category:Ageing]]
[[Category:Population]]
[[Category:Anti-aging substances| ]]
[[Category:Transhumanism]]