The Scientist has published two interesting pieces on biochemistry, genetics and longevity as of today. The first provides more information, perspectives (and a brace of links to further resources) on the nematode longevity research noted at the Longevity Meme.

Long lifespan inhibits tumors:

Longevity mutations in C. elegans are unfriendly to tumor cells, contradicting research that's suggested the opposite effect

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"With reduced growth factors, you'd expect reduced tumor growth," according to Wayne Van Voorhies from New Mexico State University in Las Cruces, who was not involved in the study. "The thing that was really surprising, though, was that it seems those daf-2 mutants have increased rates of apoptosis in the tumor cells," Van Voorhies said. "That's not an anticipated result."

The researchers found that apoptosis was upregulated in both normal and cancerous daf-2 cells, but decreased cell division was specific to tumor cells. "I was really surprised by that," Kenyon told The Scientist. "I expected to see [reduced cell division] in normal cells and we didn't."

You'll find all sorts of interesting things if you keep working away at a very complex environment with ever-better tools. Here we see more grist for the debate over what exactly determines relationships between cancer mechanisms and longevity in the biochemistry of various species. Continuing on, this same question is explored in commentary on another set of papers. These relate to research into the mechanisms of calorie restriction in mammals, centering around a small group of interacting genes and pathways:

Long Life and Forkhead Deacetylation:

The seemingly opposite results on gene expression suggested an intriguing mechanism: SIRT1 might urge FOXO-regulated processes away from death and towards survival. "It seemed that SIRT1 was providing a dream scenario for longevity," says Guarente, "whereby it was able to repress apoptosis while boosting DNA repair." But, complexity is never far behind a new pathway, and recent results suggest SIRT1 is quite pleiotropic and may even be an oncogene.

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It all points to a balance, in that modulating SIRT1 could be good for longevity, but dangerous in terms of cancer risk. Experiments in mice, underway in a number of labs, should get at a big question of whether longevity and cancer can be uncoupled, says Brunet. But answers will take time, since mice live longer than yeast and worms. "It's another race," says Brunet, "just on a longer time scale."

It's always more complex than you think - and there is a compelling argument that this is the wrong direction for hopes of greatly increased longevity. There are many benefits to be had from a greater understanding of metabolic processes and the means by which calorie restriction increases healthy longevity and maximum life span - but this does not seem to the road to radical life extension. Could we reengineer human biochemistry to produce something more like whale longevity? Or would it be easier to work on fixing the known damage that causes aging?

My hat is in the latter court; I'm buying in on the argument that continually repairing the root causes of aging - thus reversing its progression - is easier than learning how to merely slow aging via metabolic, genetic and biochemical manipulations. Moreover, we seem to know more about how to get started.

Technorati tags: aging, biotechnology, calorie restriction, medical research, science,

Posted by Reason at August 17, 2006 9:08 PM | TrackBack (0)