Mitochondria and Wormish Longevity

It's all worms and mice over at the Longevity Meme today - so worms it will be here too. We should be thankful that evolution has chanced to produce an biosphere in which we are so closely related in structure and biochemistry to creatures that are efficient to study. I can't think of work that shows this is anything but likely, given the way in which evolution works, but for all we know we are very lucky to be in this circumstance. Imagine the slow crawl of longevity research if we could only usefully learn from close relatives like primates.

But back to the worms:

Microscopic worms used for scientific research are living longer despite cellular defects, a discovery that is shedding light on how the human body ages and how doctors could one day limit or reverse genetic mutations that cause inherited diseases ... researchers manipulated the metabolic state of genetically engineered lab worms called C. elegans and discovered a window of high-efficiency cellular processing that enabled the worms to slow their rate of aging.


Rea and his team used RNAi to produce worms with varying levels of mitochondrial dysfunction with the hope of solving a mystery that has baffled scientists for years. They wanted to know why the genetically engineered worms, known as "Mit mutants," lived longer despite cellular defects that would have caused similarly damaged human cells to become diseased or die off in the lab.


The research suggests that the worms' cells receive signals from their nuclei as DNA problems are sensed and not, as previously thought, from their disrupted mitochondrial power sources. The signal-sending nuclei order cells to shut down DNA replication, allowing them time to fix problems and create an environment that copes better with DNA damage and stress, researchers believe.

"It is only in this window that survival is enhanced. Once you move too far outside, then, like human cells, worm cells also die," Rea said. "We think there's a whole shift in the metabolism and the way it protects DNA. We show very clearly in our work that long life is intimately linked with the control of cell division."

The process appears to mimic the "hunker down" survival mode that stressed animals adopt during times of famine and danger. When conditions improve, the animals procreate again to ensure the survival of their species.

In the future, Rea and his collaborators hope to build on these findings with biochemistry and genetics to discover what controls this pro-longevity mode and how humans can reduce oxidative stress that causes cellular damage. "Life extension in humans is around the corner. There is no doubt about it," Rea said.

Very pleasing to see more researchers openly expressing their views on healthy life extension through modern biotechnology in humans. This work is an intriguing way of implementing something that looks like calorie restriction - in worms, in any case. We shall see in time whether it is one of the many commonalities or many differences between humans and nematodes.

This research does present a novel window into methodologies by which metabolism could be improved, to thereby cause less cellular and biomolecular damage over time and increase longevity - but it still doesn't make that path more attractive than the path of sticking with the metabolism we have and learning to repair it really well. You can tweak the efficiency of a system as much as you like, but it's still going to degrade, age and die. The only efficient way to greatly extend longevity is through repair - so why not just direct the lion's share of resources in that direction?

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