Very good points. The obvious solutions are either really low birth rates and/or aggressive expansion into space. Both of which are hard.
In a certain sense it’s correct to say that resetting the whole body to a 25 year olds level would fix most health problems. The problem with this is that it’s also the solution to fixing a broken vase. Biology has a very nasty habit of turning out to be even more complicated than you expected when you start digging deeper. Cleaning up doesn’t have to suffice—there are various intra- and extracellular (i.e. hormones) interactions, cascades and what not which would also have to be set appropriately.
The biologist in me would also like to point out the existence of zombie genes, which start expressing themselves after death—more as a curiosity than a specific point—animal physiology is fascinating.
Suppose a future technological trick allows our civilisation to magically size and control anything material within a spheric bubble growing at light speed: that means what we own would grow as a polynomial (2 or 3, depending on your TOE). But polynomial growth is not enough to cope with any fixed grow rate of the population (that’s exponential), so that’s why I think amortals should play on time to make space. In permutation city, Greg Egan imagine the uploaded could play with their refreshing speed. In the context of biological immortality, taking long naps could serve the same purpose.
Always glad to see Greg Egan referenced. The important thing to me is that although population growth could be exponential (for the reasons cousin_it gave), it’s going to be very slow relative to the rate of technological progress. Unless fertility rises significantly, it’s likely to be hundreds of years before population would grow by 10x, by which point we’re well into Greg Egan territory and all bets are off anyway. So population could be a concern, but we’ll have plenty of time to address it via methods that don’t involve literally everyone dying.
On second thought, strong upvote for this answer because I think it’s key to pinpoint our divergence.
You think that we will likely be well into Greg Egan territory in a few hundred years, whereas new tools in biology are so fantastic we are a few decades to, yes immortality, but I guess you see that as a direct consequence of reaching biological universality (when we can basically at will make cells do whatever one cell can do).
To me (and, in a sense, echoing Vladimir_Nesov´s comment above) that’s the contrary: not only I expect new biological limitations to show up nearly as fast as we solve old problems (like decoding the human genome was fantastic, and fruitful, but not as fruitful as I was naively thinking at the time), but I also fully expect we will taste Greg Egan territory several decades before we will fully master our own biology.
Late late late disclaimer: I’m toying with the idea of starting a series of post called Road to amortality, so you should expect me to be biased and stubbornly attached to my ideas. 😉
To fight the latter, here’s one result that would move me toward your position: if we can print or grow any complex organ within the next decade. Do you accept this criteria as fair and to the point? Would you mind thinking of some results that would make you strongly update toward my position?
Naps would handle the amount of people walking around, but would probably require some novel approaches to ownership to work properly. Or synchronization of when people wake up? With the current norms, you’d end up with empty cities, because a large fraction of the inhabitants would be asleep at each given moment. Though magically sizing stuff would also handle that issue.
After reflexion I still don’t get your point, e.g. what problems intermittent naps would make us need new approach to ownership. Say we the people agree for sustainability purpose to set a fix number A as the number of people allowed & required to be awake, and P is the total number of people, sleeping or awake. Then everyone would have a right to be awake A/P of the years, or A/P decades within each millennia, and from that we might want to trade synchronisation with Star War MCXIV release for synchronisation with Harry upcoming new biography, the way Smith intended capitalism. What am I missing?
Assume you have a population of 1000 billion people on earth (what with the hibernation tech), with most of them sleeping at any given time, so that you only have 10 billion awake. If everyone has their own apartment/house then at any given time, only 1% of the houses will be in use. This in itself is fine, as people can simply synchronize when they wake up to have empty/full neighborhoods. But it would also require either having 100x more infrastructure to handle the larger cities (or paving over the world, or more exotic solutions), giving everyone a lot less living room (e.g. pod skyscrapers) or having shared accommodations (like hotels or shared bedrooms).
My main point is that the current approach, where a house with a large garden is the default to strive for, would be totally untenable. Which in turn would require a lot of cultural changes (people tend to like having lots of room for themselves). This by no means invalidates the idea of napping, it’s just something that would have to be handled.
I’m guessing compounded interest could also be troublesome in the long run, e.g. you start a savings account now, and someone else starts in a million years—that would introduce some scary inequality. For the same reason that the older the vampire, the more powerful.
Ok, thanks for clarifying (I misunderstood « approaches » as implying new economical system). Yes, that scenario would need us to change some of our habits, for example we could share home with P/A family member, or rent it while sleeping.
compounded interest could also be troublesome in the long run
Interesting thought. On the other hand, the more sleepers, the more capital, the lower the interest rate. And what kind of bank could we trust for one million years?
You may well turn out to be correct—biology is indeed fiendishly complex and still very poorly understood, and it may turn out that clearing the damage types identified by the SENS platform is insufficient for comprehensive rejuvenation. However, I’ve tried to separate that particular claim from a different, more defensible, more immediately relevant one: that damage repair should become our main approach to medical research in a world where infectious disease is largely conquered, and most suffering is due to (mostly age related) chronic illnesses. Most bodily disorders these days are caused not by infection by an external pathogen, but by damage to the body itself, most of which is self-inflected by ordinary metabolic processes. Yet for some reason, we continue to treat the (often arbitrarily defined) diseases themselves, as though they were infectious diseases, instead of even trying to repair the damage that causes them. This must change, and it is changing. To me, damage repair is a first and foremost a new, fundamentally different approach to medicine, one that emphasizes fixing things that are obviously broken, which I expect to work much better than the old paradigm of treating diseases separately. The whole “ageing” thing is almost secondary to me. We’ve literally not been fixing people’s bodies this entire time, and now people are finally trying to fix a bunch of obviously broken things, that’s why I’m excited.
To me, damage repair is a first and foremost a new, fundamentally different approach to medicine, one that emphasizes fixing things that are obviously broken, which I expect to work much better than the old paradigm of treating diseases separately. The whole “ageing” thing is almost secondary to me. We’ve literally not been fixing people’s bodies this entire time, and now people are finally trying to fix a bunch of obviously broken things, that’s why I’m excited.
I like the parts of the post I’ve read so far, and I’m just making a local argument to this specific bit.
People have been fixing people’s bodies insofar as they can, since the dawn of medicine. They’ve been setting bones, stitching wounds, treating or preventing inflammation and autoimmune reactions, and more recently, destroying or removing cancer and transplanting organs.
What unites SENS interventions is that they require sophisticated cellular and subcellular therapies that depend on the stack of biomedical technologies we’ve produced at an accelerating pace over the last century. Cellular senescence was discovered in vitro a little over 60 years ago, and as recently as 1996, a Berkeley cancer biologist was still writing in Cell that “a limited number of in vivo experiments… strongly suggest that cellular senescence is not an artifact of culture,” i.e. that it takes place in the body, not just in a dish, though the potential mechanistic links between senescence as a tumor suppression mechanism and driver of aging were already well-known. We only sequenced the human genome in 2003, and Crispr-CAS9 has only been around since 2012.
Point being that we’ve been trying to fix people’s bodies for millennia, but we’ve only had the scientific knowledge and bioengineering technology that might potentially allow us to treat the cellular and subcellular precursors of homeostatic breakdown (“aging”) for a matter of years.
Yes we’ve always been trying to fix damage—anything that restores function must fix damage somehow—but it’s a matter of what we consider to be damage, i.e. “bad stuff that we should try to fix because it would restore function”. Historically we’ve focused on trauma, infection and cancer, and although we’ve known about age-related changes like lipofuscin accumulation for a long time, it’s only recently that we started thinking of them as potential targets. Gerontology has historically been a field of basic science, with few gerontologists willing to venture that we could even in principle do something about age-related changes until very recently. They were too afraid to challenge the deeply held notion that ageing is normal, natural and fundamentally immutable. I’m not without sympathy though—anyone who had made that claim would have been attacked and likely would have lost their livelihood—Aubrey de Grey was only able to do it because he was financially independent.
If you look at things like atherosclerosis and AMD, both of which have long been known to be driven by the accumulation of toxic metabolites, I think we could and should have started working on the root causes of these diseases much earlier than we did. Sure, we’re only now figuring out how to remove 7KC and A2E, but that’s because we only just started working on it! Likewise, we’ve known about thymic involution for a long time and it’s always been clear that it damages your immune system in the long run, so why is it that only Greg Fahy is working on fixing it, and why does he get so little funding that his trials have to be funded by their own participants? We declared war on cancer long ago, when our models and tools were still hopelessly crude, and because of that we are further advanced now than we would have been otherwise.
Point taken that this is all extremely difficult and ambitious, and it’s not entirely unreasonable that researchers have been intimidated by that. Rejuvenation is indeed highly dependent on very recent technological breakthroughs, and those new capabilities are a huge part of why this shift is occurring. In my defense, there is a bit where I say
I don’t mean to imply that prior researchers had been stupid here; humans don’t come equipped with enzymes capable of degrading A2E so it wasn’t exactly obvious how to get rid of it.
Perhaps I could have stressed that more. To whatever extent there is blame, I place it more on grant committees than on medical researchers. The stuff SENS works on is all high-risk high-reward, which public purse-holders and investors are both cagey about—that’s why it all has to be philanthropically funded. For example, the idea to copy mitochondrial DNA into the nucleus where it is safer (which I ignored completely in the post) has been around for a long time, but SENS had to work on it because no one else would.
Anyway, I don’t want to fixate on whose fault things were. The point is that for whatever reason, we were pursuing a broken paradigm of “one disease one target one drug”, which was never going to work because the diseases were not naturally separable things and their root causes mostly lay in fundamental age-related changes, which we are now beginning to target, and it seems likely to work.
Agreed, I like this elaboration. As I see it, the argument really is that we’ve been neglecting preventative medicine in favor of treating disease after it has become symptomatic. This is a familiar critique that normal doctors and laypeople already subscribe to, and showing that anti-aging medicine is really just another familiar form of preventative medicine (which we have historically neglected) will make more immediate sense than claiming that “we haven’t been fixing people’s bodies” which is only true in the specific sense you just articulated.
Along with that is emphasizing that it’s normal and natural to use preventative medicine. You brush your teeth, you try to eat a good diet and get enough sleep and exercise, you might stake preventative statins or blood thinners or get LASEK. If you’ll do all these things to maintain your health, then why not take low-dose rapamycin? It’s really going to be about normalizing the use of pill-form preventatives at an earlier age, and breaking the association between pills and “being sick.” Instead, it’s about creating an association between pills and “maintaining health.”
It’s both prevention and cure—prevent disease by reversing damage before it gets bad enough to cause problems, but if you already have a chronic disease, then reversing the damage that causes it will be the only way to cure it (though prevention is better of course).
I agree the preventative medicine angle is a good one that people will buy easily, but you can make the same argument against it—that we’ve always been trying to prevent disease just as we’ve always been trying to fix damage.
It’s important to note that statins, blood thinners and rapamycin are not damage repair—they’re not useless, but I think damage repair will make them obsolete. These approaches focus on slowing the buildup of damage rather than reversing damage that’s already there. The problem is that a) this tries to modify human metabolism to “run more cleanly”, which is super difficult and prone to unforeseen consequences and b) you have to take these medicines every day, which makes it all the more dangerous. Statins are well known to have side effects, and rapamycin is an immunosuppressant, which unsurprisingly has a lot of side effects too. You don’t want to take this stuff every day.
The reason people associate things like statins with “being sick” is that they don’t actually make you less sick, they just slow the progression of a disease while causing side effects. Damage repair is far less prone to side effects because it targets stuff that’s definitely not supposed to be there instead of trying to change the way the body works. You won’t get side effects from removing atheromatous plaques (so long as that’s all the treatment does do), but you do get side effects from mucking around with liver chemistry. And because ageing damage accumulates so slowly, you’ll only have to take these therapies every 10 years or so (eventually, once they’re mature). And of course, because it reverses damage instead of merely slowing it, you’ll actually feel, look and be healthier and fitter after the treatment. That’s why I say it’s a new kind of medicine—the public are absolutely not used to medicine that makes them feel younger after they take it.
That’s a reasonable point of view. I don’t think we should be certain that the effects of rapamycin at high doses will be reflective of its effects at low doses, which is why we need to test it. This era is all about precision medicine, figuring out how to control dosing, release, and specific delivery in the context of much better knowledge of how these drugs affect the body to cut side effects and enhance benefit.
The heuristic of leaning toward occasional damage repair by engineered interventions rather than continuous damage slowdowns by manipulating evolved biochemistry makes sense, but so does the heuristic of focusing on an available tool that we have extensive data works pre-clinically right now. I think the “don’t mess with evolution” heuristic is oversubscribed for antagonistic pleiotropy and declining selection pressure with age reasons when it comes to anti-aging medicine.
All the same, I expect that over time we’ll come up with a wide range of both preventative and damage reversal interventions, perhaps along SENS lines. But in that context, a damage-slowing drug (perhaps rapamycin) that might reduce the frequency of the need for damage reversal therapies will be highly valuable, and particularly because it may well be the cheapest and most accessible option to get started, especially in countries that don’t yet have fully developed medical systems..
Very good points. The obvious solutions are either really low birth rates and/or aggressive expansion into space. Both of which are hard.
In a certain sense it’s correct to say that resetting the whole body to a 25 year olds level would fix most health problems. The problem with this is that it’s also the solution to fixing a broken vase. Biology has a very nasty habit of turning out to be even more complicated than you expected when you start digging deeper. Cleaning up doesn’t have to suffice—there are various intra- and extracellular (i.e. hormones) interactions, cascades and what not which would also have to be set appropriately.
The biologist in me would also like to point out the existence of zombie genes, which start expressing themselves after death—more as a curiosity than a specific point—animal physiology is fascinating.
Suppose a future technological trick allows our civilisation to magically size and control anything material within a spheric bubble growing at light speed: that means what we own would grow as a polynomial (2 or 3, depending on your TOE). But polynomial growth is not enough to cope with any fixed grow rate of the population (that’s exponential), so that’s why I think amortals should play on time to make space. In permutation city, Greg Egan imagine the uploaded could play with their refreshing speed. In the context of biological immortality, taking long naps could serve the same purpose.
Always glad to see Greg Egan referenced. The important thing to me is that although population growth could be exponential (for the reasons cousin_it gave), it’s going to be very slow relative to the rate of technological progress. Unless fertility rises significantly, it’s likely to be hundreds of years before population would grow by 10x, by which point we’re well into Greg Egan territory and all bets are off anyway. So population could be a concern, but we’ll have plenty of time to address it via methods that don’t involve literally everyone dying.
On second thought, strong upvote for this answer because I think it’s key to pinpoint our divergence.
You think that we will likely be well into Greg Egan territory in a few hundred years, whereas new tools in biology are so fantastic we are a few decades to, yes immortality, but I guess you see that as a direct consequence of reaching biological universality (when we can basically at will make cells do whatever one cell can do).
To me (and, in a sense, echoing Vladimir_Nesov´s comment above) that’s the contrary: not only I expect new biological limitations to show up nearly as fast as we solve old problems (like decoding the human genome was fantastic, and fruitful, but not as fruitful as I was naively thinking at the time), but I also fully expect we will taste Greg Egan territory several decades before we will fully master our own biology.
Late late late disclaimer: I’m toying with the idea of starting a series of post called Road to amortality, so you should expect me to be biased and stubbornly attached to my ideas. 😉
To fight the latter, here’s one result that would move me toward your position: if we can print or grow any complex organ within the next decade. Do you accept this criteria as fair and to the point? Would you mind thinking of some results that would make you strongly update toward my position?
Naps would handle the amount of people walking around, but would probably require some novel approaches to ownership to work properly. Or synchronization of when people wake up? With the current norms, you’d end up with empty cities, because a large fraction of the inhabitants would be asleep at each given moment. Though magically sizing stuff would also handle that issue.
After reflexion I still don’t get your point, e.g. what problems intermittent naps would make us need new approach to ownership. Say we the people agree for sustainability purpose to set a fix number A as the number of people allowed & required to be awake, and P is the total number of people, sleeping or awake. Then everyone would have a right to be awake A/P of the years, or A/P decades within each millennia, and from that we might want to trade synchronisation with Star War MCXIV release for synchronisation with Harry upcoming new biography, the way Smith intended capitalism. What am I missing?
Assume you have a population of 1000 billion people on earth (what with the hibernation tech), with most of them sleeping at any given time, so that you only have 10 billion awake. If everyone has their own apartment/house then at any given time, only 1% of the houses will be in use. This in itself is fine, as people can simply synchronize when they wake up to have empty/full neighborhoods. But it would also require either having 100x more infrastructure to handle the larger cities (or paving over the world, or more exotic solutions), giving everyone a lot less living room (e.g. pod skyscrapers) or having shared accommodations (like hotels or shared bedrooms).
My main point is that the current approach, where a house with a large garden is the default to strive for, would be totally untenable. Which in turn would require a lot of cultural changes (people tend to like having lots of room for themselves). This by no means invalidates the idea of napping, it’s just something that would have to be handled.
I’m guessing compounded interest could also be troublesome in the long run, e.g. you start a savings account now, and someone else starts in a million years—that would introduce some scary inequality. For the same reason that the older the vampire, the more powerful.
Ok, thanks for clarifying (I misunderstood « approaches » as implying new economical system). Yes, that scenario would need us to change some of our habits, for example we could share home with P/A family member, or rent it while sleeping.
Interesting thought. On the other hand, the more sleepers, the more capital, the lower the interest rate. And what kind of bank could we trust for one million years?
You may well turn out to be correct—biology is indeed fiendishly complex and still very poorly understood, and it may turn out that clearing the damage types identified by the SENS platform is insufficient for comprehensive rejuvenation. However, I’ve tried to separate that particular claim from a different, more defensible, more immediately relevant one: that damage repair should become our main approach to medical research in a world where infectious disease is largely conquered, and most suffering is due to (mostly age related) chronic illnesses. Most bodily disorders these days are caused not by infection by an external pathogen, but by damage to the body itself, most of which is self-inflected by ordinary metabolic processes. Yet for some reason, we continue to treat the (often arbitrarily defined) diseases themselves, as though they were infectious diseases, instead of even trying to repair the damage that causes them. This must change, and it is changing. To me, damage repair is a first and foremost a new, fundamentally different approach to medicine, one that emphasizes fixing things that are obviously broken, which I expect to work much better than the old paradigm of treating diseases separately. The whole “ageing” thing is almost secondary to me. We’ve literally not been fixing people’s bodies this entire time, and now people are finally trying to fix a bunch of obviously broken things, that’s why I’m excited.
I like the parts of the post I’ve read so far, and I’m just making a local argument to this specific bit.
People have been fixing people’s bodies insofar as they can, since the dawn of medicine. They’ve been setting bones, stitching wounds, treating or preventing inflammation and autoimmune reactions, and more recently, destroying or removing cancer and transplanting organs.
What unites SENS interventions is that they require sophisticated cellular and subcellular therapies that depend on the stack of biomedical technologies we’ve produced at an accelerating pace over the last century. Cellular senescence was discovered in vitro a little over 60 years ago, and as recently as 1996, a Berkeley cancer biologist was still writing in Cell that “a limited number of in vivo experiments… strongly suggest that cellular senescence is not an artifact of culture,” i.e. that it takes place in the body, not just in a dish, though the potential mechanistic links between senescence as a tumor suppression mechanism and driver of aging were already well-known. We only sequenced the human genome in 2003, and Crispr-CAS9 has only been around since 2012.
Point being that we’ve been trying to fix people’s bodies for millennia, but we’ve only had the scientific knowledge and bioengineering technology that might potentially allow us to treat the cellular and subcellular precursors of homeostatic breakdown (“aging”) for a matter of years.
Yes we’ve always been trying to fix damage—anything that restores function must fix damage somehow—but it’s a matter of what we consider to be damage, i.e. “bad stuff that we should try to fix because it would restore function”. Historically we’ve focused on trauma, infection and cancer, and although we’ve known about age-related changes like lipofuscin accumulation for a long time, it’s only recently that we started thinking of them as potential targets. Gerontology has historically been a field of basic science, with few gerontologists willing to venture that we could even in principle do something about age-related changes until very recently. They were too afraid to challenge the deeply held notion that ageing is normal, natural and fundamentally immutable. I’m not without sympathy though—anyone who had made that claim would have been attacked and likely would have lost their livelihood—Aubrey de Grey was only able to do it because he was financially independent.
If you look at things like atherosclerosis and AMD, both of which have long been known to be driven by the accumulation of toxic metabolites, I think we could and should have started working on the root causes of these diseases much earlier than we did. Sure, we’re only now figuring out how to remove 7KC and A2E, but that’s because we only just started working on it! Likewise, we’ve known about thymic involution for a long time and it’s always been clear that it damages your immune system in the long run, so why is it that only Greg Fahy is working on fixing it, and why does he get so little funding that his trials have to be funded by their own participants? We declared war on cancer long ago, when our models and tools were still hopelessly crude, and because of that we are further advanced now than we would have been otherwise.
Point taken that this is all extremely difficult and ambitious, and it’s not entirely unreasonable that researchers have been intimidated by that. Rejuvenation is indeed highly dependent on very recent technological breakthroughs, and those new capabilities are a huge part of why this shift is occurring. In my defense, there is a bit where I say
Perhaps I could have stressed that more. To whatever extent there is blame, I place it more on grant committees than on medical researchers. The stuff SENS works on is all high-risk high-reward, which public purse-holders and investors are both cagey about—that’s why it all has to be philanthropically funded. For example, the idea to copy mitochondrial DNA into the nucleus where it is safer (which I ignored completely in the post) has been around for a long time, but SENS had to work on it because no one else would.
Anyway, I don’t want to fixate on whose fault things were. The point is that for whatever reason, we were pursuing a broken paradigm of “one disease one target one drug”, which was never going to work because the diseases were not naturally separable things and their root causes mostly lay in fundamental age-related changes, which we are now beginning to target, and it seems likely to work.
Agreed, I like this elaboration. As I see it, the argument really is that we’ve been neglecting preventative medicine in favor of treating disease after it has become symptomatic. This is a familiar critique that normal doctors and laypeople already subscribe to, and showing that anti-aging medicine is really just another familiar form of preventative medicine (which we have historically neglected) will make more immediate sense than claiming that “we haven’t been fixing people’s bodies” which is only true in the specific sense you just articulated.
Along with that is emphasizing that it’s normal and natural to use preventative medicine. You brush your teeth, you try to eat a good diet and get enough sleep and exercise, you might stake preventative statins or blood thinners or get LASEK. If you’ll do all these things to maintain your health, then why not take low-dose rapamycin? It’s really going to be about normalizing the use of pill-form preventatives at an earlier age, and breaking the association between pills and “being sick.” Instead, it’s about creating an association between pills and “maintaining health.”
It’s both prevention and cure—prevent disease by reversing damage before it gets bad enough to cause problems, but if you already have a chronic disease, then reversing the damage that causes it will be the only way to cure it (though prevention is better of course).
I agree the preventative medicine angle is a good one that people will buy easily, but you can make the same argument against it—that we’ve always been trying to prevent disease just as we’ve always been trying to fix damage.
It’s important to note that statins, blood thinners and rapamycin are not damage repair—they’re not useless, but I think damage repair will make them obsolete. These approaches focus on slowing the buildup of damage rather than reversing damage that’s already there. The problem is that a) this tries to modify human metabolism to “run more cleanly”, which is super difficult and prone to unforeseen consequences and b) you have to take these medicines every day, which makes it all the more dangerous. Statins are well known to have side effects, and rapamycin is an immunosuppressant, which unsurprisingly has a lot of side effects too. You don’t want to take this stuff every day.
The reason people associate things like statins with “being sick” is that they don’t actually make you less sick, they just slow the progression of a disease while causing side effects. Damage repair is far less prone to side effects because it targets stuff that’s definitely not supposed to be there instead of trying to change the way the body works. You won’t get side effects from removing atheromatous plaques (so long as that’s all the treatment does do), but you do get side effects from mucking around with liver chemistry. And because ageing damage accumulates so slowly, you’ll only have to take these therapies every 10 years or so (eventually, once they’re mature). And of course, because it reverses damage instead of merely slowing it, you’ll actually feel, look and be healthier and fitter after the treatment. That’s why I say it’s a new kind of medicine—the public are absolutely not used to medicine that makes them feel younger after they take it.
That’s a reasonable point of view. I don’t think we should be certain that the effects of rapamycin at high doses will be reflective of its effects at low doses, which is why we need to test it. This era is all about precision medicine, figuring out how to control dosing, release, and specific delivery in the context of much better knowledge of how these drugs affect the body to cut side effects and enhance benefit.
The heuristic of leaning toward occasional damage repair by engineered interventions rather than continuous damage slowdowns by manipulating evolved biochemistry makes sense, but so does the heuristic of focusing on an available tool that we have extensive data works pre-clinically right now. I think the “don’t mess with evolution” heuristic is oversubscribed for antagonistic pleiotropy and declining selection pressure with age reasons when it comes to anti-aging medicine.
All the same, I expect that over time we’ll come up with a wide range of both preventative and damage reversal interventions, perhaps along SENS lines. But in that context, a damage-slowing drug (perhaps rapamycin) that might reduce the frequency of the need for damage reversal therapies will be highly valuable, and particularly because it may well be the cheapest and most accessible option to get started, especially in countries that don’t yet have fully developed medical systems..
Totally agree and am glad you wrote this post