He doesn’t fully disagree with you here. I’m sure he thinks fixing mitochondria is an important part of reversing aging, he just thinks that it’s just one of many things that need to be fixed. His approach is that there are several important damages that need to be fixed and mitochondria is just one of those. Fixing one of them is not going to automatically fix the rest, and that’s what he thinks, or else there would not be several types of important damages listed under the SENS repair approach. I agree with him in the sensse that I think there are several types of damages that need to be fixed, and that while fixing some of them may improve some other ones a little, it’s not enough. In the end you need to fix all the types.
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I think it is an important disagreement. I think there are two key biochemical issues
a) Mitochondrial inefficiency (which is the development/aging clock)
b) The presence of senescent cells
On top of that is DNA damage, but I think that is a lesser (and harder) issue to deal with.
Aubrey thinks there are more issues. However, he is not clear what they are or how to deal with them so he feeds mice various mixtures of substances to see what happens.
The RMR is not a bad experiment, but it could be a lot better. However, I am not stressed.
That’s a strange statement to make. The SENS approach lists 7 types of damages that need to be fixed, only one of which is mitochondrial damage. See here: Strategies for engineered negligible senescence - Wikipedia
The question is what causes things to fail to function. I think there are two primary causes (as above). This causes a lot of what can be perceived as “damage”.
Ok, but even if you were right you would still need to fix the several types of damages. It wouldn’t be enough to just rejuvenate/fix the mitochondria. That would at best top further damage. You would also need to fix all the other types of damages to get full rejuvenation.
The question here is what the effect of fixing the mitochondria is. This is where cytosolic levels of acetyl-CoA come in. Those affect acetylation of both the histone and splicing factors. That reinstates more general homeostasis.
That’s why I look for issues around splicing and long genes.
