Peter Attia· MD
What about something far less impressive but but but still um worth worthwhile so consider you know if we could get to the point where we could locally deliver vectors that would epigenetically change condra sites so that you could take osteoarthritis in the knee and just regenerate cartilage regenerate cartilage regenerate useful by changing the EPO but is that biological aging right I wouldn't be convinced that's modulating the biological aging process I would be convinced that's a clinically useful strategy for people who benefit from that therapy I guess it kind of dep depends on why we think an individual would be experiencing osteoarthritis right how much of that is sence how much of that is infl trigger here before we go down that path is it the s word or what yeah yeah let's talk about sesses but before we think if you think uh ostearthritis of the knee requires a knee joint replacement and that's going to help your patient you are not rejuvenating it's perfectly possible to do great things with technology including con condra site regeneration without having to decide that that's related to aging people don't age because they fail to have titanium knee joints or something and one way I think about this and again this this may be completely wrong but it but it's a useful way for me to think about it is I think about age related disease as the sort of Downstream effect of biological aging and then in for most diseases there becomes a point where the pathology of that disease mechanistically is no longer the same as biological Aging in which case very good you should listen to him in and one of the implications of that is the interventions that slow biological aging may not work once you get past that point but things that do work for that disease may have nothing to do with biological aging does that make sense yeah go go deeper on that idea though let's use let's use the example yeah well I think um so let's just I mean what's your favorite disease my favorite disease let's talk about is an easy one right we know with cancer in many cancers the process is you have one or more mutations which then often lead to additional mutations you get genome instability eventually you get an enco gen that gets activated and that leads to uncontrolled cell division there messor that gets deactivated yeah right so at and if we accept that immune surveillance is one important anti-cancer mechanism we know that immune surveillance declines with age so early on we're clearing a lot of our cancers as our immune system declines these cancers are going to escape immune surveillance they're going to accumulate all these mutations they're eventually going to go into uncontrolled cell division that uncontrolled cell division at that point you can treat the cancer right but uncontrolled cell division is not biological aging right it's not a normal part it's not a part of the normative aging process right so the treatment there so the mechanism now is fundamentally different from normative aging and the treatment let's just say the treatment in this case is chemotherapy might benefit the cancering right