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.
Point taken. I guess the main difference for me is that with age reversal, we’ve got a framework that makes sense and de-mystifies it, and it implies that if we just do this and this and this and this then the problem should be solved. We can actually see a path between where we are right now and where we want to be. Do we have something like that with AGI, or is it more a matter of “these language models are starting to look pretty smart”? I’m not saying I would bet against AGI, the way things are going… but I wouldn’t want to rely on it without a rational model of it, either.