I thought I'd draw your attention to a couple of worthy updates at Ouroboros from the past few days. We'll start by revisiting the biochemistry of clam longevity once more:

So: long-lived molluscs have much higher antioxidant capacities than short-lived molluscs, suggesting a mechanism by which their much slower (possibly "negligible" senescence) might have evolved.

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No defense based on prevention of damage (in this case, oxidation of protein and DNA) is 100% efficient. Assuming that protein and DNA oxidation contributes to the aging process in bivalves, even a very efficient SOD system will eventually allow oxidative adducts to accumulate to dangerous (i.e., gerontogenic) levels. If A. islandica is truly biologically ageless, then it must also have efficient repair systems in order to reverse, as opposed to merely prevent, oxidative damage. Then again, if this clam is simply aging very, very slowly, then maybe high levels of SOD are enough. Which is it? Only time will tell.

The long-lived actic quahog species of clam, the one with all the antioxidants, manages about nine times the lifespan of a more common or garden species of bivalve. That is interesting, because it calls to mind the difference between naked mole-rat lifespan and that of similarly sized rodents - also about a factor of nine, give or take. In both cases, the research focus appears to be on oxidative damage, mitochondria, and antioxidants in the right place to slow down resulting damage:

Mitochondria churn out damaging free radicals as a side-effect of their job as the cell's power plants. The chain of biochemical events that follows on from this fact is a major component of age-related damage, disease and degeneration. You can look back into the Fight Aging! archives for an introduction to that topic.

It has been demonstrated that soaking up the free radicals produced by mitochondria right at the source extends life span. This has been achieved by means of antioxidants like catalase, targeted to the mitochondria by gene therapy or other bioengineering means. This is quite different from taking antioxidants as a supplement, I should add; those don't go anywhere near your mitochondria, and thus don't do much good.

So it's reasonable to theorize that if you happen to be a member of a species that naturally generates a lot of antioxidants around the mitochondria, you're going to live longer than members of another, similar species with worse luck in the antioxidant stakes.

As Chris Patil at Ouroboros points out, it's a little too early to say that this isn't just a case of looking where the lamp shines, but it all hangs together well.

Moving on, the "human dignity" backlash: you can only claim for so long that our worth as human beings requires us to live in dirt and suffering, renouncing progress, before getting called on it.

the theoconservative movement cites considerations of "dignity" in cautioning against broad classes of biological research, including stem cell therapeutics and - more recently, as the idea becomes more thinkable - biogerontology ... Thus, in the process of enumerating the shortcomings of dignity as a desideratum, Pinker incidentally engages in a brief but cogent defense of life extension technologies.

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I believe that dignity does have a place in the discussion, in the following sense: There is nothing dignified about pain, senility, incontinence, or frailty; therefore, one of the primary justifications for studying the processes of aging in human beings is that we might hope to someday prevent the scourges of late-life disease and thereby increase dignity for all.

I feel it is necessary - as many times as it takes - to examine and hold up to just ridicule those who call for an enforced relinquishment of medical progress towards increased healthy longevity. They would have us, we billions, all suffer and die before our time because the whim pleases them; ridicule is effective and humane, but too kind.

Posted by Reason at June 3, 2008 5:05 PM | TrackBack (0)