Metabolism is very complex, and our present grasp of that complexity - for all the rapidity of present progress in biotechnology - is inadequate in the grand scheme of things. A few examples from recent papers illustrate the distance yet to go; so much remains unknown, and the closer you look the more there is to discover:

Long-lived dwarf mice: are bile acids a longevity signal?

Pathways that control aging act via regulated biochemical processes, among which metabolism of xenobiotics (potentially harmful chemical agents encountered as environmental toxicants, for example, drugs, or produced internally) is one possible candidate. A new study of long-lived Ghrhr mutant mice reports that increased bile acid levels activate xenobiotic metabolism via the nuclear receptor, farnesoid X receptor. This increases resistance to xenobiotic stress, possibly contributing to longevity.

Role of VEGF gene variability in longevity: A lesson from the Italian population

Vascular endothelial growth factor (VEGF) gene polymorphisms have been associated with an increased risk of developing a wide variety of disorders from diabetes to neurodegenerative diseases suggesting functions not confined to its vascular effects originally described. Based on the VEGF protective roles undisclosed in pathological conditions, we evaluate whether VEGF variability might be a determinant also for longevity. ... These results suggest that VEGF gene variability can be inserted among the genetic factors influencing the lifespan.

The right path forward is research - a great deal of research - but not to direct that research in service to efforts to rebuild our biochemistry for greater longevity. That is the hard path, and the longer path. Consider the different between the level of knowledge required to maintain an engine and the level of knowledge required to build a better engine. At the present time, the mainstream of medical science appears to be heading along the path of building a better engine: of attempting to slow the accumulation of age-related damage by manipulating metabolism.

This is a hard, expensive road, but there is a better way. Instead of reengineering the system - our biochemistry - to work in a new and different way, we could be identifying and working to reverse those changes that occur with aging. Instead of building a better engine that wears out more slowly, instead learn to repair the engine you have. This is most likely easier, and certainly more cost effective: a better engine still wears out in the end, but repairs can be made over and over again.

We are faced with a massive, complex problem - our bodies beset by aging in many different ways at the cellular and molecular level. We can try to change our biochemistry in ways that will require more work to understand the new system, or we can leave our biochemistry as it stands and learn how to repair it. Every effort counts, when we have all too few years to come to a solution. It matters whether or not the path taken is the most efficient.

Where would you rather the research community directed their efforts?

Technorati tags: aging, longevity, medical research

Posted by Reason at June 29, 2007 9:33 PM | TrackBack (0)