5 replies to this topic

[smithx]

I posted this elsewhere, but perhaps it needs its own topic:

This very interesting study induced telomerase in mice with modified viruses. They report a 24% increase in lifespan and no increase in cancers.

http://scitechdaily....lifespan-by-24/

[Turnbuckle]

I posted this elsewhere, but perhaps it needs its own topic:

This very interesting study induced telomerase in mice with modified viruses. They report a 24% increase in lifespan and no increase in cancers.

http://scitechdaily....lifespan-by-24/

This is a bit surprising since rodents have much longer telomeres than we do, enough for several lifetimes. The paper turns to another paper for a possible explanation--

Given that mice have much longer telomeres compared to humans, it may seem surprising that telomere erosion could contribute to aging and aging associated disorders in this short-lived animal. However, telomeres do erode with advancing age in mice, including in stem cell compartments (Flores et al, 2008), suggesting that telomere shortening and dysfunction also limits growth of mouse cells and consequently contributes to aging.

And Flores says that it's not the average cell, but certain stem cells that are aging faster than normal.

Finally, we make the novel finding that telomeres shorten with age in different mouse stem cell compartments, which parallels a decline in stem cell functionality, suggesting that telomere loss may contribute to stem cell dysfunction with age.

Edited by Turnbuckle, 10 December 2012 - 12:58 PM.

[smithx]

The really interesting things about that article for me were:

- Longer lifespan

- No additional cancers

That last one is a biggie.

[niner]

No additional cancers is indeed a biggie, given all the concern regarding telomerase and cancer. I'd be even happier if they'd said "No" cancers, instead of "No additional", but you can't have everything. Or can you? Telomerase genotherapy plus c60-oo? If you're a rodent, anyway. I've been wondering if there's any connection between this telomerase result and Baati's results. This is stepping a ways out on the speculatory limb, but it's known that oxidative damage to telomeres is not well repaired, and is implicated in telomere shortening. Along with that, if one of the problems of rodent aging is stem cells crapping out, resulting in fewer differentiated cells, it's conceivable that c60 is assisting in stem cell differentiation, which has an important mitochondrial component. (thx Turnbuckle for finding that) That might explain some of the life extension effect of c60, along with some of the other effects like hair growth.

[Mind]

Call me "Mr. stick in the mud"

That might explain some of the life extension effect of c60

Life extension effect based on a single study of 6 rats. Just a reminder that most health studies are unable to be replicated. I am really hoping that C60 will turn out to be a life/health extension substance, but I am also a realist.

Thanks for posting the study SmithX. I am very surprised at the Telomerase Up-regulating=Cancer meme - how it has remained so strong for so long with scant evidence. I know in theory it makes sense - it is one of those ideas that "clicks" for those familiar with cellular replication and cancer, but it seems like the available science has negated this theory (in non-human models) pretty well, right? Or am I missing a couple of key explosive studies?

[niner]

Call me "Mr. stick in the mud"

That might explain some of the life extension effect of c60

Life extension effect based on a single study of 6 rats. Just a reminder that most health studies are unable to be replicated. I am really hoping that C60 will turn out to be a life/health extension substance, but I am also a realist.

Thanks for posting the study SmithX. I am very surprised at the Telomerase Up-regulating=Cancer meme - how it has remained so strong for so long with scant evidence. I know in theory it makes sense - it is one of those ideas that "clicks" for those familiar with cellular replication and cancer, but it seems like the available science has negated this theory (in non-human models) pretty well, right? Or am I missing a couple of key explosive studies?

Well, the evidence that telomerase activation doesn't cause cancer is about as good as Baati. Because you can never really prove a negative, only accumulate evidence that it doesn't happen, it will take a lot to convince people that telomeres can safely be lengthened, given that decrementing telomeres seem to be such a powerful anti-cancer device. (The vast majority of cancers have mutated telomerase that's "stuck in the on position".)

Regarding the health studies that are unable to be repeated, doesn't that take into account a lot of nonsense like in vitro experiments that are rarely applicable to humans? Or work in flies or worms or zebrafish that is only slightly better? Or compounds with horrible bioavailability that were given to mice as i.p. injections, or other issues? In this case, the data is in mammals, and the compound is bioavailable in humans. Small N is a problem when the effects are small, causing the entire experiment to have a different outcome if one animal lived instead of dying, for example. In this case, the effect was huge, so the statistics are actually very solid. In addition, the rats met MR's criteria of being genetically normal, rather than some sickly mutant strain. Finally, just repeating the experiment in rats or mice isn't a very high bar, compared to getting a spectacular result in humans, which is far less likely. (depends how you define "spectacular"- I'm not expecting anything like a 90% life extension in humans.)

Edited by niner, 12 December 2012 - 09:19 PM.