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..
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..