The popular press pieces are, as usual, breathlessly overhyped. Some commentary on this: http://www.fightaging.org/archives/2011/02/another-proposed-link-betwe

The popular press pieces are, as usual, breathlessly overhyped. Some commentary on this: http://www.fightaging.org/archives/2011/02/another-proposed-link-between-short-telomeres-and-dysfunctional-mitochondria.php http://www.fightaging.org/archives/2011/02/another-proposed-... "it is certainly the case that damaged mitochondria and shortening telomeres are only two of the possible reasons we suffer age-related degeneration. Many of the other causes of aging involve a build up of varying forms of damaging waste product that the body cannot remove - mechanisms which are quite capable of causing disability and death on their own, telomere shortening or no telomere shortening. "That said, telomeres, mitochondria, and p53 are all large and healthy areas of research when it comes to the biology of aging. I imagine that anyone would be pleased to produce good evidence that might mechanically tie them all together, such that one or more are secondary effects rather than primary causes. From an economic perspective, we should all be hoping that some of our present candidates for the primary causes of aging turn out to be secondary effects - because then we don't have to devote any time towards developing repair biotechnologies to fix them. "On a closer reading of the new research, I have to say that it looks to me very much like an independent confirmation of discoveries from 2007 and 2008 relating to mitochondrial damage, telomere length, and the enzyme telomerase. In a nutshell, it may be that telomere shortening is entirely driven by mitochondrial dysfunction" Etc. Links to more in the post.