Shortening telomeres are a red herring. You need multiple generations of a mammal not having telomerase before you get premature ageing, and all the research you’ve heard about where they ‘reversed ageing’ with telomerase was putting it back into animals that had been engineered to lack it for generations. Plus lack of telomerase in most of your somatic cells is one of your big anti-cancer defenses.
Much more of a problem is things like nuclear pores never being replaced in post-mitotic cells (they’re only replaced during mitosis) and slowly oxidizing and becoming leaky, extracellular matrix proteins having a finite lifetime, and all kinds of metabolic dysregulation and protein metabolism issues.
This isn’t exactly my field, but there’s a few interesting actual lines of research I’ve seen. One is an apparent reduction in protein-folding chaperone activity with age in many animals from C. elegans to humans [people LOVE C. elegans for ageing studies because they can enter very long-lived quiescent phases in their life cycle, and there are mutations with very different lifespans]. People still aren’t quite sure what that means or where it comes from.
There’s lots of interest in caloric restriction still, with many organisms switching between high-fertility shorter-lifespan and loger-lifespan lower-fertility states, but with actual mechanisms quite up in the air and there being serious questions as to if it actually happens in primates at all.
That paper a year or two back where some people claimed to double mouse lifespans with buckyballs dissolved in olive oil has my attention. Nobody including me actually believes the results, not least because their experimental design and data storage/presentation was an absolute unmitigated mess, but their biological evidence of massive antioxidant effects from the buckyballs (numbers of oxidative molecules neutralized far in excess of the numbers of buckyballs) was interesting and possibly even true. You can bet there are a couple labs around Europe trying to replicate the results that we will hear back from in a few years. If it does actually have an effect I would expect far less of an effect in animals that are less metabolically frenetic than mice, which can metabolize a tenth of their body weight per day.
If I had to actually give advice though it would come from rather more prosaic sources than molecular biology. It would say get the hell up and moving fairly often, get sleep on a regular schedule and don’t expose yourself to blue light after sunset, don’t eat refined sugar, have friends you can rely on, and don’t take strong medicines when you don’t absolutely have to. And get cheap genetic tests when you can since they can tip you off about low-frequency high-impact things.
Sure, why not. I might be able (in a less busy time) to dig up that protein chaperone research too, somebody came to the university I’m at to give a talk on it a month or two ago.
Shortening telomeres are a red herring. You need multiple generations of a mammal not having telomerase before you get premature ageing, and all the research you’ve heard about where they ‘reversed ageing’ with telomerase was putting it back into animals that had been engineered to lack it for generations. Plus lack of telomerase in most of your somatic cells is one of your big anti-cancer defenses.
Much more of a problem is things like nuclear pores never being replaced in post-mitotic cells (they’re only replaced during mitosis) and slowly oxidizing and becoming leaky, extracellular matrix proteins having a finite lifetime, and all kinds of metabolic dysregulation and protein metabolism issues.
This isn’t exactly my field, but there’s a few interesting actual lines of research I’ve seen. One is an apparent reduction in protein-folding chaperone activity with age in many animals from C. elegans to humans [people LOVE C. elegans for ageing studies because they can enter very long-lived quiescent phases in their life cycle, and there are mutations with very different lifespans]. People still aren’t quite sure what that means or where it comes from.
There’s lots of interest in caloric restriction still, with many organisms switching between high-fertility shorter-lifespan and loger-lifespan lower-fertility states, but with actual mechanisms quite up in the air and there being serious questions as to if it actually happens in primates at all.
That paper a year or two back where some people claimed to double mouse lifespans with buckyballs dissolved in olive oil has my attention. Nobody including me actually believes the results, not least because their experimental design and data storage/presentation was an absolute unmitigated mess, but their biological evidence of massive antioxidant effects from the buckyballs (numbers of oxidative molecules neutralized far in excess of the numbers of buckyballs) was interesting and possibly even true. You can bet there are a couple labs around Europe trying to replicate the results that we will hear back from in a few years. If it does actually have an effect I would expect far less of an effect in animals that are less metabolically frenetic than mice, which can metabolize a tenth of their body weight per day.
If I had to actually give advice though it would come from rather more prosaic sources than molecular biology. It would say get the hell up and moving fairly often, get sleep on a regular schedule and don’t expose yourself to blue light after sunset, don’t eat refined sugar, have friends you can rely on, and don’t take strong medicines when you don’t absolutely have to. And get cheap genetic tests when you can since they can tip you off about low-frequency high-impact things.
Intriguing, and thank you for the detailed reply. May I respond in the future should I have further queries?
Sure, why not. I might be able (in a less busy time) to dig up that protein chaperone research too, somebody came to the university I’m at to give a talk on it a month or two ago.