Arkansas Biomedical Research Foundation
Our dauer lifespan project is part of our "MetaSENS" portfolio: projects that, rather than developing the seven SENS strands, validate the SENS strategy overall. We have projects exploring three broad areas: the comprehensiveness of the seven-strand partitioning of aging, the sociological and economic context of a post-aging world and the transition to it, and the possibility of simpler alternatives to SENS that could have a large impact on aging sooner than SENS can realistically be implemented. Our dauer project is in the last of these categories.
The consensus view of the evolution of aging is that there is no general program dictating how fast we age: that aging is the collection of gaps in our built-in automatic self-repair processes. This implies that any simple intervention, such as mutating a single gene or administering a chemical, can significantly postpone age-related ill-health only if it gets a lot of "help" from the organism, in the form of genetic machinery that senses the intervention and translates it into a wide variety of specific tweaks to metabolic priorities. But such machinery can only exist if it is also activated by some environmental circumstance that the species in question actually experiences, reasonably often, in the wild - otherwise, the genes in question would never have evolved, or would have mutated into oblivion over generations. Therefore, we can predict that no simple intervention, in any species, will elicit a substantially greater postponement of aging than any such environmental intervention.
So, what if we encounter an exception? That would tell us that the above theory, despite appearances, is somehow wrong, and that there might be simple ways to postpone human aging substantially after all, even though it's seeming increasingly likely that there are no environmental interventions (specifically, calorie restriction) can do that. Clearly, it would be unwise to neglect that possibility without very high confidence, because if such an intervention did exist we could potentially save a huge number of lives before SENS could be implemented.
Well, it turns out that there is an exception - just one, but a clear one. The nematode worm Caenorhabditis elegans can be induced to live ten times more than normal by mutating one gene, and no one has achieved more than a factor of 3 or 4 by starvation.
Unfortunately, there's a catch. It might be that the starvation approach has not been done as well as it could have been, and that in fact it can get a 10-fold life extension too. There are actually a few circumstantial reasons to suspect this. So we are funding a group in Arkansas - the very same group, in fact, that achieved the 10-fold result - to try several tricks for getting more longevity by starvation. If they fail, the possibility of a simple way to extend longevity becomes that much more likely. We still wouldn't know how to do it, to be sure, but we'd have much more reason to search than we do today.