From Ouroboros: "Aging is what geneticists like to call a 'complex trait' - simply put, a trait that is controlled by a large number of genes and the interactions between them. Complex traits differ from simple traits in the following way: When one is studying a simple trait, one simply identifies a mutant in the relevant trait and, after an ingenious combination of clever crosses and muscular cloning steps, finds the defective gene - thus gaining a great deal of explanatory power about the trait in question. When one is studying a complex trait, however, approaches like a mutant screen fall short. They don't fall totally flat - one of the great innovations of the last decade or so is the realization that we can learn quite a bit by studying aging at the single-gene level - but they can't get us all the way home. Suppose you do a screen and find fifty mutants that all lengthen lifespan by forty percent (not far from the situation in worms) - or, speaking more generally about complex traits, you find fifty loci in the human genome that are associated with a higher risk of schizophrenia. What then? What have you really learned about how the system works?" This complexity is why slowing aging by metabolic manipulation is a much harder path forward than aiming to preserve the metabolism we have by repairing the known damage of aging.

Link: http://ouroboros.wordpress.com/2009/02/04/systems-biology-of-aging-understanding-yeast-cr-by-network-inference/