Life extension possible today - Revision history

Dmitry Dzhagarov: /* References */

2023-08-16T16:08:23Z

References

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	== References ==		== References ==
	<references />		<references />
			[[Category:Drafts]]
			[[Category:Lifespan interventions]]
			[[Category:Longevity concepts]]
			[[Category:Longevity genes]]
			[[Category:Main list]]

Dmitry Dzhagarov: /* Ways to extend life */

2023-08-16T16:04:15Z

Ways to extend life

← Older revision		Revision as of 16:04, 16 August 2023
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	== Ways to extend life ==		== Ways to extend life ==
	According to the hypothesis put forward by professor of molecular biogerontology João Pedro de Magalhães "we have a very complicated set of computerlike programs in our DNA that turn us into an adult human being, and maybe some of these same programs, as they continue into later life, become detrimental.” He believes that the medical intervention necessary for extremely long lives will require finding a way to eliminate aging at the cellular level by reprograming cells and genes critical to the aging process. “In terms of caner resistance and probably overall aging as well, it’s their (cells) ability to respond to and repair DNA damage,” he said, adding he believes aging is more a software problem than a hardware problem.<ref>[https://www.popularmechanics.com/science/health/a44713943/humans-can-live-20000-years-aging-expert/ An Aging Expert Thinks Humans Can Live for 20,000 Years. He's Not Crazy.]</ref>		According to the hypothesis put forward by professor of molecular biogerontology João Pedro de Magalhães "we have a very complicated set of computerlike programs in our DNA that turn us into an adult human being, and maybe some of these same programs, as they continue into later life, become detrimental.” He believes that the medical intervention necessary for extremely long lives will require finding a way to eliminate aging at the cellular level by reprograming cells and genes critical to the aging process. “In terms of caner resistance and probably overall aging as well, it’s their (cells) ability to respond to and repair DNA damage,” he said, adding he believes aging is more a software problem than a hardware problem.<ref>[https://www.popularmechanics.com/science/health/a44713943/humans-can-live-20000-years-aging-expert/ An Aging Expert Thinks Humans Can Live for 20,000 Years. He's Not Crazy.]</ref> Many other theories also, suppose development and aging are part of the same molecular mechanisms—or at least very intersected.<ref>Silva-García, C.G. (2023). [https://doi.org/10.1007/s11357-023-00809-2 Devo-Aging: Intersections Between Development and Aging.] GeroScience, 1-15. PMID: 37160658 DOI: 10.1007/s11357-023-00809-2</ref>

	Back in 2013 '''the synergistic extension by a "double mutant" technique''', when applied to nematode worms, '''makes them live five times longer than usual'''. On their own, one of the mutations - in the insulin signalling pathway - doubles their lifespan (169%), while the other - known as the TOR pathway - adds 20% percent. But together, something magical happens. This synergistic longevity phenotype (454%) cannot be explained by the hypothesis that daf-2 (IGF-1 receptor) and rsks-1 (ribosomal S6 kinase) function in parallel to modulate lifespan independently since an additive effect will be expected under such an assumption. Synergistic lifespan extension is achieved through positive feedback regulation of DAF-16 by AMPK. Tissue-specific analysis suggests that this enhanced activation of DAF-16 is initiated by signals from the germ line and that '''the germ line tissue may play a key role in integrating the interactions between daf-2 and rsks-1 to cause synergistic lifespan extension'''. "These pathways are 'conserved', meaning that they have been passed down to humans through evolution," the research team said in a statement. <ref name="fivetimes">Chen, D., Li, P. W. L., Goldstein, B. A., Cai, W., Thomas, E. L., Chen, F., ... & Kapahi, P. (2013). Germline signaling mediates the synergistically prolonged longevity produced by double mutations in daf-2 and rsks-1 in C. elegans. Cell reports, 5(6), 1600-1610. PMID: 24332851 PMCID: PMC3904953 DOI: 10.1016/j.celrep.2013.11.018</ref>		Back in 2013 '''the synergistic extension by a "double mutant" technique''', when applied to nematode worms, '''makes them live five times longer than usual'''. On their own, one of the mutations - in the insulin signalling pathway - doubles their lifespan (169%), while the other - known as the TOR pathway - adds 20% percent. But together, something magical happens. This synergistic longevity phenotype (454%) cannot be explained by the hypothesis that daf-2 (IGF-1 receptor) and rsks-1 (ribosomal S6 kinase) function in parallel to modulate lifespan independently since an additive effect will be expected under such an assumption. Synergistic lifespan extension is achieved through positive feedback regulation of DAF-16 by AMPK. Tissue-specific analysis suggests that this enhanced activation of DAF-16 is initiated by signals from the germ line and that '''the germ line tissue may play a key role in integrating the interactions between daf-2 and rsks-1 to cause synergistic lifespan extension'''. "These pathways are 'conserved', meaning that they have been passed down to humans through evolution," the research team said in a statement. <ref name="fivetimes">Chen, D., Li, P. W. L., Goldstein, B. A., Cai, W., Thomas, E. L., Chen, F., ... & Kapahi, P. (2013). Germline signaling mediates the synergistically prolonged longevity produced by double mutations in daf-2 and rsks-1 in C. elegans. Cell reports, 5(6), 1600-1610. PMID: 24332851 PMCID: PMC3904953 DOI: 10.1016/j.celrep.2013.11.018</ref>

			There was provided a proof-of-concept evidence that '''even close to the end of an individual’s lifespan, it is possible to slow aging and promote longevity'''. For example, Venz et al. genetically engineered the nematode worm C. elegans so that they could trigger the rapid degradation of the insulin/IGF-1 receptor and observed that reducing insulin/IGF-1 receptor very late during lifespan at a time at which already approximately 50–75% of the population had died doubled the lifespan of these animals at this late stage.<ref>Venz, R., Pekec, T., Katic, I., Ciosk, R., & Ewald, C. Y. (2021). End-of-life targeted degradation of DAF-2 insulin/IGF-1 receptor promotes longevity free from growth-related pathologies. Elife, 10, e71335. PMID: 34505574 PMCID: PMC8492056 DOI: 10.7554/eLife.71335</ref><ref>Zhang, Y. P., Zhang, W. H., Zhang, P., Li, Q., Sun, Y., Wang, J. W., ... & Dong, M. Q. (2022). Intestine-specific removal of DAF-2 nearly doubles lifespan in Caenorhabditis elegans with little fitness cost. Nature communications, 13(1), 6339. PMID: 36284093 PMCID: PMC9596710 DOI: 10.1038/s41467-022-33850-4</ref>

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Dmitry Dzhagarov at 14:05, 16 August 2023

2023-08-16T14:05:30Z

← Older revision		Revision as of 14:05, 16 August 2023
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	According to the hypothesis put forward by professor of molecular biogerontology João Pedro de Magalhães "we have a very complicated set of computerlike programs in our DNA that turn us into an adult human being, and maybe some of these same programs, as they continue into later life, become detrimental.” He believes that the medical intervention necessary for extremely long lives will require finding a way to eliminate aging at the cellular level by reprograming cells and genes critical to the aging process. “In terms of caner resistance and probably overall aging as well, it’s their (cells) ability to respond to and repair DNA damage,” he said, adding he believes aging is more a software problem than a hardware problem.<ref>[https://www.popularmechanics.com/science/health/a44713943/humans-can-live-20000-years-aging-expert/ An Aging Expert Thinks Humans Can Live for 20,000 Years. He's Not Crazy.]</ref>		According to the hypothesis put forward by professor of molecular biogerontology João Pedro de Magalhães "we have a very complicated set of computerlike programs in our DNA that turn us into an adult human being, and maybe some of these same programs, as they continue into later life, become detrimental.” He believes that the medical intervention necessary for extremely long lives will require finding a way to eliminate aging at the cellular level by reprograming cells and genes critical to the aging process. “In terms of caner resistance and probably overall aging as well, it’s their (cells) ability to respond to and repair DNA damage,” he said, adding he believes aging is more a software problem than a hardware problem.<ref>[https://www.popularmechanics.com/science/health/a44713943/humans-can-live-20000-years-aging-expert/ An Aging Expert Thinks Humans Can Live for 20,000 Years. He's Not Crazy.]</ref>

	Back in 2013 '''the synergistic extension by a "double mutant" technique''', when applied to nematode worms, '''makes them live five times longer than usual'''. On their own, one of the mutations - in the insulin signalling pathway - doubles their lifespan (169%), while the other - known as the TOR pathway - adds 20% percent. But together, something magical happens. This synergistic longevity phenotype (454%) cannot be explained by the hypothesis that daf-2 (IGF-1 receptor) and rsks-1 (ribosomal S6 kinase) function in parallel to modulate lifespan independently since an additive effect will be expected under such an assumption. Synergistic lifespan extension is achieved through positive feedback regulation of DAF-16 by AMPK. Tissue-specific analysis suggests that this enhanced activation of DAF-16 is initiated by signals from the germ line and that '''the germ line tissue may play a key role in integrating the interactions between daf-2 and rsks-1 to cause synergistic lifespan extension'''. "These pathways are 'conserved', meaning that they have been passed down to humans through evolution," the research team said in a statement.<ref>Chen, D., Li, P. W. L., Goldstein, B. A., Cai, W., Thomas, E. L., Chen, F., ... & Kapahi, P. (2013). Germline signaling mediates the synergistically prolonged longevity produced by double mutations in daf-2 and rsks-1 in C. elegans. Cell reports, 5(6), 1600-1610. PMID: 24332851 PMCID: PMC3904953 DOI: 10.1016/j.celrep.2013.11.018</ref>		Back in 2013 '''the synergistic extension by a "double mutant" technique''', when applied to nematode worms, '''makes them live five times longer than usual'''. On their own, one of the mutations - in the insulin signalling pathway - doubles their lifespan (169%), while the other - known as the TOR pathway - adds 20% percent. But together, something magical happens. This synergistic longevity phenotype (454%) cannot be explained by the hypothesis that daf-2 (IGF-1 receptor) and rsks-1 (ribosomal S6 kinase) function in parallel to modulate lifespan independently since an additive effect will be expected under such an assumption. Synergistic lifespan extension is achieved through positive feedback regulation of DAF-16 by AMPK. Tissue-specific analysis suggests that this enhanced activation of DAF-16 is initiated by signals from the germ line and that '''the germ line tissue may play a key role in integrating the interactions between daf-2 and rsks-1 to cause synergistic lifespan extension'''. "These pathways are 'conserved', meaning that they have been passed down to humans through evolution," the research team said in a statement. <ref name="fivetimes">Chen, D., Li, P. W. L., Goldstein, B. A., Cai, W., Thomas, E. L., Chen, F., ... & Kapahi, P. (2013). Germline signaling mediates the synergistically prolonged longevity produced by double mutations in daf-2 and rsks-1 in C. elegans. Cell reports, 5(6), 1600-1610. PMID: 24332851 PMCID: PMC3904953 DOI: 10.1016/j.celrep.2013.11.018</ref>
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Dmitry Dzhagarov: /* Ways to extend life */

2023-08-16T11:17:20Z

Ways to extend life

← Older revision		Revision as of 11:17, 16 August 2023
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	== Ways to extend life ==		== Ways to extend life ==
	According to the hypothesis put forward by professor of molecular biogerontology João Pedro de Magalhães "we have a very complicated set of computerlike programs in our DNA that turn us into an adult human being, and maybe some of these same programs, as they continue into later life, become detrimental.” He believes that the medical intervention necessary for extremely long lives will require finding a way to eliminate aging at the cellular level by reprograming cells and genes critical to the aging process. “In terms of caner resistance and probably overall aging as well, it’s their (cells) ability to respond to and repair DNA damage,” he said, adding he believes aging is more a software problem than a hardware problem.<ref>[https://www.popularmechanics.com/science/health/a44713943/humans-can-live-20000-years-aging-expert/ An Aging Expert Thinks Humans Can Live for 20,000 Years. He's Not Crazy.]</ref>		According to the hypothesis put forward by professor of molecular biogerontology João Pedro de Magalhães "we have a very complicated set of computerlike programs in our DNA that turn us into an adult human being, and maybe some of these same programs, as they continue into later life, become detrimental.” He believes that the medical intervention necessary for extremely long lives will require finding a way to eliminate aging at the cellular level by reprograming cells and genes critical to the aging process. “In terms of caner resistance and probably overall aging as well, it’s their (cells) ability to respond to and repair DNA damage,” he said, adding he believes aging is more a software problem than a hardware problem.<ref>[https://www.popularmechanics.com/science/health/a44713943/humans-can-live-20000-years-aging-expert/ An Aging Expert Thinks Humans Can Live for 20,000 Years. He's Not Crazy.]</ref>

			Back in 2013 '''the synergistic extension by a "double mutant" technique''', when applied to nematode worms, '''makes them live five times longer than usual'''. On their own, one of the mutations - in the insulin signalling pathway - doubles their lifespan (169%), while the other - known as the TOR pathway - adds 20% percent. But together, something magical happens. This synergistic longevity phenotype (454%) cannot be explained by the hypothesis that daf-2 (IGF-1 receptor) and rsks-1 (ribosomal S6 kinase) function in parallel to modulate lifespan independently since an additive effect will be expected under such an assumption. Synergistic lifespan extension is achieved through positive feedback regulation of DAF-16 by AMPK. Tissue-specific analysis suggests that this enhanced activation of DAF-16 is initiated by signals from the germ line and that '''the germ line tissue may play a key role in integrating the interactions between daf-2 and rsks-1 to cause synergistic lifespan extension'''. "These pathways are 'conserved', meaning that they have been passed down to humans through evolution," the research team said in a statement.<ref>Chen, D., Li, P. W. L., Goldstein, B. A., Cai, W., Thomas, E. L., Chen, F., ... & Kapahi, P. (2013). Germline signaling mediates the synergistically prolonged longevity produced by double mutations in daf-2 and rsks-1 in C. elegans. Cell reports, 5(6), 1600-1610. PMID: 24332851 PMCID: PMC3904953 DOI: 10.1016/j.celrep.2013.11.018</ref>
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Dmitry Dzhagarov: /* Human life extension benefits and risks */

2023-08-16T09:37:15Z

Human life extension benefits and risks

← Older revision		Revision as of 09:37, 16 August 2023
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	One argument against extending human life beyond the norm is that it would lead to overpopulation, requiring more resources, while creating more waste, carbon emissions and pollution on a planet we've already stressed to breaking point.<ref>Hayley Bennett (2021).([https://www.sciencefocus.com/the-human-body/extend-human-lifespan We could radically extend the human lifespan. Here’s why we shouldn’t]. BBC Science Focus</ref>		One argument against extending human life beyond the norm is that it would lead to overpopulation, requiring more resources, while creating more waste, carbon emissions and pollution on a planet we've already stressed to breaking point.<ref>Hayley Bennett (2021).([https://www.sciencefocus.com/the-human-body/extend-human-lifespan We could radically extend the human lifespan. Here’s why we shouldn’t]. BBC Science Focus</ref>

			== Ways to extend life ==
			According to the hypothesis put forward by professor of molecular biogerontology João Pedro de Magalhães "we have a very complicated set of computerlike programs in our DNA that turn us into an adult human being, and maybe some of these same programs, as they continue into later life, become detrimental.” He believes that the medical intervention necessary for extremely long lives will require finding a way to eliminate aging at the cellular level by reprograming cells and genes critical to the aging process. “In terms of caner resistance and probably overall aging as well, it’s their (cells) ability to respond to and repair DNA damage,” he said, adding he believes aging is more a software problem than a hardware problem.<ref>[https://www.popularmechanics.com/science/health/a44713943/humans-can-live-20000-years-aging-expert/ An Aging Expert Thinks Humans Can Live for 20,000 Years. He's Not Crazy.]</ref>
	{{Draft-article }}		{{Draft-article }}

Dmitry Dzhagarov at 07:52, 16 August 2023

2023-08-16T07:52:19Z

← Older revision		Revision as of 07:52, 16 August 2023
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			== Human life extension benefits and risks ==
			Advantages of the life extension according to the ChatGPT:
			"The concept of life extension has the potential to promote intelligent evolution by allowing individuals to live longer and therefore have more time to accumulate knowledge, experience, and make well-informed decisions. With increased lifespans, people can dedicate more years to education, research, and self-improvement, which can contribute to personal growth and the advancement of societies as a whole. Additionally, longer lives offer the opportunity to witness and participate in future advancements and discoveries, which can further fuel intelligent evolution. However, it is important to consider ethical implications and ensure equitable access to life extension technologies to avoid creating disparities that hinder overall progress."

			One argument against extending human life beyond the norm is that it would lead to overpopulation, requiring more resources, while creating more waste, carbon emissions and pollution on a planet we've already stressed to breaking point.<ref>Hayley Bennett (2021).([https://www.sciencefocus.com/the-human-body/extend-human-lifespan We could radically extend the human lifespan. Here’s why we shouldn’t]. BBC Science Focus</ref>

	{{Draft-article }}		{{Draft-article }}

MarcS: MarcS moved page Life extension percentage per intervention to Life extension possible today: Shorter and easier title

2021-12-07T09:05:08Z

MarcS moved page Life extension percentage per intervention to Life extension possible today: Shorter and easier title

← Older revision	Revision as of 09:05, 7 December 2021
(No difference)

Bogdan at 11:15, 5 December 2021

2021-12-05T11:15:39Z

← Older revision		Revision as of 11:15, 5 December 2021
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			{{Draft-article }}

	This is draft, conceptual page presenting how life extension data representation may look like.		This is draft, conceptual page presenting how life extension data representation may look like.

Bogdan at 11:15, 5 December 2021

2021-12-05T11:15:12Z

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Bogdan at 11:14, 5 December 2021

2021-12-05T11:14:29Z

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			== References ==
			<references />