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The concept is interesting and well-formed, but in order to earn better than a 'C,' the idea must be feasible. A Yale University management professor in response to Fred Smith's paper proposing reliable overnight delivery service. (Smith went on to found Federal Express Corp.)

9. DEATH Previous | Next

Evolution’s problem with self-destruction

WHY do living things die? Obviously, things kill each other – that’s part of the natural order. But what causes “natural” death? It is a question that splits biologists. It has become like a game of ping pong – over the years, theories have been batted back and forth as new evidence comes to light.

One answer is that death is simply necessary – to avoid overcrowding, for instance. But evolution doesn’t – can’t – select for a “death switch” because evolution is supposed to be all about the individual. And yet there does seem to be a death switch – researchers have managed to locate genetic switches that massively extend the lifespan of some nematode worms.

That might seem a long way removed from where we’re at, but there are vertebrates that live a very, very long time. Blandings Turtles, just don’t seem to get old and decrepit, for example. Teasing out why that might be is a tricky job – but potentially worth it.

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Location:Lewes, UK
Joined:7/23/2008
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#1 - Posted: 7/25/2008 7:53 AM

So, Stanford researchers are reporting that “specific genetic instructions drive aging in worms.” We kind of knew that, thanks to Cynthia Kenyon’s research. The thing is, they have to keep saying it, because other aging (ageing?) researchers keep saying there’s no genetic switches. You can’t win.

The Stanford news release suggests the research “implies science might eventually halt or even reverse the ravages of age.” Gosh, the ageing-is-just-like-rusting camp are going to hate that, and call it snake oil, moonshine, hogwash and other nasty things.

Here’s some edited highlights from the Stanford release:

Comparing young worms to old worms, Kim’s team discovered age-related shifts in levels of three transcription factors, the molecular switches that turn genes on and off. They found hundreds of age-regulated genes switched on and off by a single transcription factor called elt-3, which becomes more abundant with age. Two other transcription factors that regulate elt-3 also changed with age.

Basically, they argue, key regulatory pathways optimized for youth have drifted off track in older animals. Since natural selection can’t fix problems that arise late in the animals’ life spans, the genetic pathways for aging become entrenched by mistake.

Now they can begin searching for this new aging mechanism in other creatures. It’s likely they won’t find it in some – which is what’s really exciting. Some tortoises lay eggs at the age of 100. There are whales that live to be 200, and clams that make it past 400. Those species use the same building blocks for their DNA, proteins and fats as humans, mice and nematode worms. The chemistry of the wear-and-tear process, including damage from oxygen free-radicals, should be the same in all cells, which makes it hard to explain why species have dramatically different life spans. “A free radical doesn’t care if it’s in a human cell or a worm cell,” Kim said.

If aging is not a cost of unavoidable chemistry but is instead driven by changes in regulatory genes, the aging process may not be inevitable.  How cool is that? Certainly worth looking into – which makes it so odd that a group of leading scientists have to write a letter pointing it out. Sometimes, science is so strange – and so human…

 

 

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