8 ms·

So to achieve longevity escape velocity [0] 1. Don't have unprotected sex if you're less than 44 years old. 2. Don't kill yourself, or do drugs, if you're les

by joshuak 13y ago

So to achieve longevity escape velocity [0] 1. Don't have unprotected sex if you're less than 44 years old. 2. Don't kill yourself, or do drugs, if you're less than 54 years old. 3. Invest heavily in heart disease, cancer, and alzheimer's research. [0] http://en.wikipedia.org/wiki/Longevity_escape_velocity http://en.wikipedia.org/wiki/Longevity_escape_velocity

leothekim 13y ago
Diabetes, heart disease, and arguably some forms of cancer are diseases of affluence [0] with known risk factors that are avoidable through lifestyle changes. If you're enumerating things to avoid in order to achieve longevity escape velocity, #3 should read something more like "Eat healthily and exercise daily to reduce your chances of getting diabetes and other vascular diseases." Incidentally, there is also some evidence of Alzheimer's disease being linked to risk factors typically associated with type 2 diabetes. [1] [0] http://en.wikipedia.org/wiki/Diseases_of_affluence http://en.wikipedia.org/wiki/Diseases_of_affluence [1] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2769828/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2769828/
- joshuak 13y ago
  Thanks, I agree. Of course my post is a bit tongue in cheek. Healthy nutrition and exercise are probably the biggest factors in living longer setting aside physical trauma. It even improves your mood, so I'm sure it lowers the suicide rate too. I considered listing it, but this is a list of things that will kill you, not a list of things that will make you live longer, healthier, and happier... I would love to have that list please.
exratione 13y ago
Not really. Actuarial escape velocity is a concept that emerges from the SENS proposals [0]. Next to nothing you do with your life has truly significant expected impact on your future longevity other than providing support and funding for SENS and SENS-like research aimed at repairing the root causes of all the big killer age-related conditions. (Less significant here means a ten year swing in life expectancy. Exercise, not smoking, calorie restriction - these are things that can make 5-10 year expected differences. Everything else is pretty marginal if you exclude the obvious exogenous line items like risk of accident. But an improving implementation of SENS provides indefinite extension of healthy life out to the expected limits due to accident rates, which is somewhere in the 1000-5000 year range for present data). The mainstream medical research community is largely focused on patching late stage manifestations of aging. Most work and funding goes towards either manipulating proximate causes rather than root causes, or trying to find ways to alter the operation of metabolism to make the disease process less terrible - but again without addressing causes. Until such time as the research community is overtaken by the "address root causes" disruption currently taking place, of which SENS is an exemplar, but by no means the only movement, then progress towards extended life and defeat of age-related disease will continue to be painfully expensive, slow, and marginal. The trends in life extension achieved through medicine to date are all largely incidental, unintentional. Where aging itself as a collection of processes [1] has been slowed it wasn't because that was the deliberate intent. Again, because until very recently no-one has been trying to address aging itself rather than focusing on the nature of its outcomes. It is the same difference as that between working to reverse or prevent rust in metal structures versus working on repairing structural failures that occur due to that rust. [0]: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC423155/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC423155/ [1]: http://sens.org/research/introduction-to-sens-research http://sens.org/research/introduction-to-sens-research
- epaladin 13y ago
  I'm a bioinformatics guy trying to move toward this research. Do you work in the field?
  - xaa 13y ago
    I do research at the interface between aging and bioinformatics. It's a great place to be because many aging researchers, while smart and capable at their own techniques, are basically in the informatics stone age. So there is a lot of collaboration potential. As for GP's comments, I'd agree that there needs to be more focus on "root causes" and fundamental mechanisms in aging research. But SENS itself is broadly considered hokum.
    - exratione 13y ago
      I expect the informatics stone age in aging research will start to dissipate more rapidly in the years ahead, given that Calico and Human Longevity look to be focused in that direction. I would love to see more of the people who dismiss SENS criticize it on the published details of ongoing or proposed research rather than just hand-waving. Sadly all too few seem to be willing to do so. Clearly it isn't nonsense, since there are SENS labs and allied research programs in a number of universities now, including Cambridge, Wake Forest, etc, and a range of important figures in aging research and other life science fields relevant to regenerative medicine support SENS.
      - xaa 13y ago
        My concern about Calico and the other commercial efforts at aging research is, will the tools and data they develop be made public so that others can build on them? Also, supposing they succeed, I find the idea of commercial ownership of a (real) anti-aging drug morally repugnant in the extreme, perhaps even dystopian. But I certainly can't deny that Google has informatics experience. SENS, as I understand it, can mean (at least) 3 different things: a) The idea that we should focus on root causes rather than late-stage manifestations. I agree with this. b) The idea that we should attempt to repair aging-related damage without needing to know what caused the damage. I find this debatable. We have stumbled on to some big treatments (aspirin, penicillin), without knowing how or why they worked. But in general, if you take a broken, complex system (e.g., a car, some source code) and attempt to repair it without understanding how it works, you will fail. With aging, many changes occur. How can you determine which changes are "damage" and which are compensatory regulatory changes without understanding the chain of causation? c) A specific list of 7 aging-associated markers of damage and proposals to clear that damage, with the implication that if we do so, we will drastically reduce or eliminate age-associated morbidity and mortality. This is the part that is seen as hokum. At best, it is a hypothesis. Let de Grey get a grant and prove it, like everyone else does, rather than publicity-hunting and implying that it is only the stodgy old aging research establishment keeping us from eternal youth. But if you want semi-technical criticisms: - On what basis are these 7 types of damage chosen and not others? - One of the proposed treatments for the natural shortening of telomeres over time is the periodic, whole-body addition of telomerase or the equivalent. Considering that telomerase is overexpressed in cancer and is an important ingredient to uncontrolled cell division, do you think this is a good idea? - On a related note, SENS presupposes that a cure for cancer must be found before the entire program can be made practical. A minor problem. - The technology for several other of his other proposed interventions does not currently exist; for example, expressing mitochondrial genes only in the nucleus. Anyway, I actually share SENS' goals but not its unwarranted confidence in its specific proposals to achieve them.
tootie 13y ago
Self-driving cars will be the biggest humanitarian boon since the Green Revolution or the invention of antibiotics.
ignostic 13y ago
Lumping all "drugs" together is pretty lazy. I'd like to know a lot more. Alcohol, Warfarin, and cocaine are all drugs. Alcohol, for example, tends to INCREASE life expectancy when consumed in moderation (1-2 drinks for women, 2-3 drinks for men).
- saddino 13y ago
  Apparently moderate alcohol consumption only increases life expectancy for people who are generally unhealthy (by reducing risk of heart attack) http://nutritionfacts.org/video/alcohol-risks-vs-benefits/ http://nutritionfacts.org/video/alcohol-risks-vs-benefits/

by joshuak 13y ago

leothekim 13y ago

Diabetes, heart disease, and arguably some forms of cancer are diseases of affluence [0] with known risk factors that are avoidable through lifestyle changes. If you're enumerating things to avoid in order to achieve longevity escape velocity, #3 should read something more like "Eat healthily and exercise daily to reduce your chances of getting diabetes and other vascular diseases." Incidentally, there is also some evidence of Alzheimer's disease being linked to risk factors typically associated with type 2 diabetes. [1] [0] http://en.wikipedia.org/wiki/Diseases_of_affluence http://en.wikipedia.org/wiki/Diseases_of_affluence [1] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2769828/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2769828/

joshuak 13y ago
Thanks, I agree. Of course my post is a bit tongue in cheek. Healthy nutrition and exercise are probably the biggest factors in living longer setting aside physical trauma. It even improves your mood, so I'm sure it lowers the suicide rate too. I considered listing it, but this is a list of things that will kill you, not a list of things that will make you live longer, healthier, and happier... I would love to have that list please.

exratione 13y ago

Not really. Actuarial escape velocity is a concept that emerges from the SENS proposals [0]. Next to nothing you do with your life has truly significant expected impact on your future longevity other than providing support and funding for SENS and SENS-like research aimed at repairing the root causes of all the big killer age-related conditions. (Less significant here means a ten year swing in life expectancy. Exercise, not smoking, calorie restriction - these are things that can make 5-10 year expected differences. Everything else is pretty marginal if you exclude the obvious exogenous line items like risk of accident. But an improving implementation of SENS provides indefinite extension of healthy life out to the expected limits due to accident rates, which is somewhere in the 1000-5000 year range for present data). The mainstream medical research community is largely focused on patching late stage manifestations of aging. Most work and funding goes towards either manipulating proximate causes rather than root causes, or trying to find ways to alter the operation of metabolism to make the disease process less terrible - but again without addressing causes. Until such time as the research community is overtaken by the "address root causes" disruption currently taking place, of which SENS is an exemplar, but by no means the only movement, then progress towards extended life and defeat of age-related disease will continue to be painfully expensive, slow, and marginal. The trends in life extension achieved through medicine to date are all largely incidental, unintentional. Where aging itself as a collection of processes [1] has been slowed it wasn't because that was the deliberate intent. Again, because until very recently no-one has been trying to address aging itself rather than focusing on the nature of its outcomes. It is the same difference as that between working to reverse or prevent rust in metal structures versus working on repairing structural failures that occur due to that rust. [0]: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC423155/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC423155/ [1]: http://sens.org/research/introduction-to-sens-research http://sens.org/research/introduction-to-sens-research

epaladin 13y ago
I'm a bioinformatics guy trying to move toward this research. Do you work in the field?
- xaa 13y ago
  I do research at the interface between aging and bioinformatics. It's a great place to be because many aging researchers, while smart and capable at their own techniques, are basically in the informatics stone age. So there is a lot of collaboration potential. As for GP's comments, I'd agree that there needs to be more focus on "root causes" and fundamental mechanisms in aging research. But SENS itself is broadly considered hokum.
  - exratione 13y ago
    I expect the informatics stone age in aging research will start to dissipate more rapidly in the years ahead, given that Calico and Human Longevity look to be focused in that direction. I would love to see more of the people who dismiss SENS criticize it on the published details of ongoing or proposed research rather than just hand-waving. Sadly all too few seem to be willing to do so. Clearly it isn't nonsense, since there are SENS labs and allied research programs in a number of universities now, including Cambridge, Wake Forest, etc, and a range of important figures in aging research and other life science fields relevant to regenerative medicine support SENS.
    - xaa 13y ago
      My concern about Calico and the other commercial efforts at aging research is, will the tools and data they develop be made public so that others can build on them? Also, supposing they succeed, I find the idea of commercial ownership of a (real) anti-aging drug morally repugnant in the extreme, perhaps even dystopian. But I certainly can't deny that Google has informatics experience. SENS, as I understand it, can mean (at least) 3 different things: a) The idea that we should focus on root causes rather than late-stage manifestations. I agree with this. b) The idea that we should attempt to repair aging-related damage without needing to know what caused the damage. I find this debatable. We have stumbled on to some big treatments (aspirin, penicillin), without knowing how or why they worked. But in general, if you take a broken, complex system (e.g., a car, some source code) and attempt to repair it without understanding how it works, you will fail. With aging, many changes occur. How can you determine which changes are "damage" and which are compensatory regulatory changes without understanding the chain of causation? c) A specific list of 7 aging-associated markers of damage and proposals to clear that damage, with the implication that if we do so, we will drastically reduce or eliminate age-associated morbidity and mortality. This is the part that is seen as hokum. At best, it is a hypothesis. Let de Grey get a grant and prove it, like everyone else does, rather than publicity-hunting and implying that it is only the stodgy old aging research establishment keeping us from eternal youth. But if you want semi-technical criticisms: - On what basis are these 7 types of damage chosen and not others? - One of the proposed treatments for the natural shortening of telomeres over time is the periodic, whole-body addition of telomerase or the equivalent. Considering that telomerase is overexpressed in cancer and is an important ingredient to uncontrolled cell division, do you think this is a good idea? - On a related note, SENS presupposes that a cure for cancer must be found before the entire program can be made practical. A minor problem. - The technology for several other of his other proposed interventions does not currently exist; for example, expressing mitochondrial genes only in the nucleus. Anyway, I actually share SENS' goals but not its unwarranted confidence in its specific proposals to achieve them.

tootie 13y ago

Self-driving cars will be the biggest humanitarian boon since the Green Revolution or the invention of antibiotics.

ignostic 13y ago

Lumping all "drugs" together is pretty lazy. I'd like to know a lot more. Alcohol, Warfarin, and cocaine are all drugs. Alcohol, for example, tends to INCREASE life expectancy when consumed in moderation (1-2 drinks for women, 2-3 drinks for men).

saddino 13y ago
Apparently moderate alcohol consumption only increases life expectancy for people who are generally unhealthy (by reducing risk of heart attack) http://nutritionfacts.org/video/alcohol-risks-vs-benefits/ http://nutritionfacts.org/video/alcohol-risks-vs-benefits/