Chris Driver <drierac at deakin.edu.au> writes:
>The two pillars of the theory do not hold up: measures of radical damage only
>occasionally correlate with longevity, and free radical trappers do not give
>reproducable lifespan extension. So where is the case?
Actually, the evidence that free radicals are involved in inflammatory
and degenerative processes is pretty overwhelming, if admittedly
indirect. Superoxide dismutase is even a pretty good antiinfalmmatory
agent. In as far as degenerative diseases are associated with
decreased longevity, the case is pretty well established. You
might call this the " weak " theory of free radical aging.
As for the "strong" theory: that free radicals are involved
directly in aging, the evidence is less strong, but still pretty
interesting. One problem is that many radical scavengers can
also act as pro-oxidants and so may give entirely different
results depending on the circumsatnces.
A "natural" example. Uric acid levels are associated with
increased longevity in primates. OTOH, this same reducing
substance may mediate gout by free radical mechanisms.
Peter H. Proctor, PhD, MD
