Jacob Kimmel

And you ended up with these quite similar, quite homologous genes that now have specialized functions.

So it's like when evolution has a new problem to solve, it doesn't have to start from scratch.

It starts from, like, what was the last copy of the parameters for encoding a gene that is getting close to solving this?

Okay, let's do a copy-paste on that and then iterate and fine-tune on those parameters as opposed to having to start with, like, ab initio, some random stretch of sequence somewhere in the genome has to become a gene.

Interesting.

Right.

The number of calories they can gather for the population.

Yeah, I think that's correct.

I don't think that there is a single monocausal explanation for aging.

I think there are layers of molecular regulation that explain a lot.

For instance, I have dedicated my career now to working on epigenetics and trying to change which gene cells use because I think that explains a lot of it.

But it's not that there is like some upstream bad gene X and all we have to do is turn that off and suddenly aging is solved.

And so I think the most likely outcome is that when we eventually develop medicines that prolong health in each of us, it's not going to fix everything all at once.

There's not going to be a singular magic pill, but rather you're going to have medicines that add multiple healthy years to your life, years you can't otherwise get back.

But it's not going to fix everything at the same time.

You are still going to experience for the first medicine some amount of decline over time.

And this gives you an example of if you think about evolution as a medicine maker in this sort of anthropomorphic context, why it might not have been selected for immediately.

Yeah.

So we're working on something called epigenetic reprogramming, which very broadly is using genes called transcription factors.

I like to think about these as sort of the orchestra conductors of the genome.