As you age, your mitochondria become ever more damaged and dysfunctional, a process that causes further biochemical damage throughout your body, and is in fact an important component of aging.

cells entirely populated with damaged mitochondria start churning out large quantities of free radicals - through another, more forceful mechanism - into the body at large. That's a path to age-related degeneration and fatal conditions like atherosclerosis. The free radical theory of aging is based upon the harm done to tissues, structures and processes by these damaging biochemicals.

Can ongoing mitochondrial degeneration be slowed? Well, yes - calorie restriction appears to slow down every catalogued aspect of aging, and evidence suggests that regular exercise is just about as good for everything except extending maximum species longevity. But can we do better than this for failing mitochondria via new medical technologies?

I stumbled over recent research that suggests there are comparatively simple genetic changes that will slow the rate at which your mitochondria cause the damage that leads to aging:

Doing something about the decay of mitochondrial function has a number of evident benefits, as demonstrated above. But slowing things down is a second rate strategy at best - especially if it involves genetic engineering, a technology unlikely to be in widespread use for humans for another ten to twenty years. A slowing of damage does little for those who are already damaged and aged. What we really want to be capable of achieving is reversal of existing damage - to be able to restore old and damaged mitochondria to a pristine state.

This goal is unlikely to be any more expensive or time-consuming than engineering a slowing of mitochondrial decay, so it should be the first priority. If you look back in the Fight Aging! and Longevity Meme archives, you'll find mention of a range of potential technologies at varying stages of research: