The comments I have seen so far in response to this relate to or may relate to
free radicals and pathology. There is fairly good evidence that free radicals
are involved in reperfusion damage. I would also accept the suggestion that
free radicals may have a role in atherosclerosis and inflammation processes.
None of these are ageing.
The free radical theory has been around for nearly five decades now. Time
enough for workers to tie it down and develop commercial anti-oxidants which
will substantially extend human lifespan. This has not happened.
To qualify as an ageing process, you need to meet Strehler's criteria: the
processes should be universal (effect every member of the species),
progressive, irreversible and deleterious.
We can now add that free radical scavengers should reduce the rate of
physiological declines and onset of age assocaited pathologies. There may be
some data relating to atherosclerosis by now. To my knowledge there is no
other data set that answers this criteria. In fact in the case of Alzheimers,
it is clear that free radical trappers are worthless.
Back to your court.
Chris Driver
Chris Driver, Ph D
School of Biology and Chemistry, Rusden Campus
Deakin University
662 Blackburn Rd
Clayton, VIC, 3168
AUSTRALIA
