Estimate of the timing of results:
I [Aubrey] think there’s a 50% chance of getting the first-generation SENS therapies working within 25-30 years. But that’s only an estimate, and it’s a highly speculative one: I think there’s at least a 10% chance that we will hit so many unforeseen problems that we won’t get there for 100 years. This is not something special about SENS, though: any technology that’s two or more years away could easily be 100 years away.
Which anti-aging treatments soonest ?
..probably the closest is in fact not the enzyme therapy you mention, but the use of vaccines to eliminate extracellular aggregates (especially amyloid). But when we consider the others, actually I wouldn’t like to make the call, because the hardest ones are the ones that the Methuselah Foundation and I are prioritising in terms of the early research. In other words, we’re hoping that they will start to catch up with the easier ones. I suspect that the challenge of genetically modifying a high proportion of cells by somatic gene therapy will have been largely solved before we complete the development of all the genes that we want to introduce.
What will early anti-aging stem cell treatments be like ?
Stem cell treatments are mostly done with injections, but some of them (including ones for WILT) will be done from the outside, using technologies borrowed from cosmetic surgery for example. At first, these therapies will be quite experimental, so people will need to be monitored carefully for a while, but that will be a temporary phase. I don’t think the patient will feel unusual or experience any change of appearance. There should be no perceptible “macro-changes” as a result of WILT—the idea is to stop cancers from getting large enough to be noticed at all.
SENS will upgrade over time
Because SENS has so many components, it’ll be undergoing enhancements continuously after its first version arrives. Most of these enhancements will be conceptually quite minor – one more enzyme to get rid of a slowly accumulating target junk molecule, one more cell type that we need to replenish because too many cells have died, etc. But you’re right; occasionally there will need to be more major enhancements. I don’t know in detail how we’d cope with non-specific mutation accumulation – if I did, I’d suggest that we deal with it now, just in case my analysis of the non-importance of those mutations in a currently normal lifetime is wrong – but I expect it’ll involve an increased use of tissue engineering for most tissues, and in those where that’s impractical (especially the brain) a very mild stimulation of cell death combined with cell replacement from stem cells.