Rhonda Patrick· PhD
So we think by measuring these people's ageotypes, if you will, it's in a timeframe that's actionable, you can see how people are aging, you try an intervention and see if you can reverse it or at least slow it down.
The headline is broadly defensible, but the qualifications matter. Effect sizes vary by population, the strongest claims rest on shorter trials, and credible voices push back on how it's typically framed.
So we think by measuring these people's ageotypes, if you will, it's in a timeframe that's actionable, you can see how people are aging, you try an intervention and see if you can reverse it or at least slow it down.
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So we think by measuring these people's ageotypes, if you will, it's in a timeframe that's actionable, you can see how people are aging, you try an intervention and see if you can reverse it or at least slow it down.
So, these aren't out yet but the idea is that, if you can build a clock that's going to, essentially, try and proxy what your brain aging is or your liver aging or your kidney aging, then you can have multiple kind of epigenetic-age estimates and really understand more of the profile of the person. And so, yeah, it's kind of getting back to this idea of ageotypes. We both age at a different rate from each other but also in a different way. Right? So, I might diverge more down kind of this way and be more of a metabolic ager, or whatever it is, and someone else might be more of an immune ager. And understanding that is going to give people both, potentially, insight into what interventions might be the most helpful for them and also what they might be most at risk for.