Professor Alan Hipkiss, of King's College, University of London, writing in Human Ageing and Later Life (edited by Anthony Warnes and published by Edward Arnold, London, 1989) tells us that free radicals are also responsible for the damage which occurs in cataracts due to cross-linkage of proteins, and he says: 'Oxygen free radicals can also damage DNA which, if it is not repaired, could give rise to altered, mutant proteins.'

Some free radical activity is actually essential for good healthy functioning. For example, when certain of our immune functions are operating, say when white blood cells are attacking and deactivating invading micro-organisms (bacteria, viruses, fungi etc.) they generate free radicals in order to do their job. It should not be surprising to discover, therefore, that in the face of the flood of free radicals produced both by normal metabolism and other functions of the body, as well as those received from outside the body (radiation, low level radiation, cigarette smoke, environmental pollution, alcohol and many other 'contributors') our bodies have, of necessity, had to find ways of coping.

Can ageing due to free radicals be slowed down?
Professor Hipkiss is not sure. He says:

Ageing may be inevitable in complex organisms; indeed it is surprising that we live so long given the multiplicity of insults to which our cells are continuously subjected. Only homoeostatic mechanisms (self-repairing, self-balancing, including antioxidant functions) enable our survival. Maybe, if we wish either to live longer or to resist the ravages of time, we should design further homoeostatic systems to repair our repair systems.

Doctors Cranton and Frackelton dramatically underline the importance of dealing with free radicals:

When free radicals in living tissues exceed safe levels, the result is cell destruction, malignant mutation, tumor growth, damage to enzymes and inflammations, which manifest clinically as age-related, chronic degenerative diseases. Each uncontrolled free radical has the potential to multiply a million-fold. But, when functioning properly, our antioxidant systems suppress excessive free radical reactions.

They point out that the life expectancy of mammals (such as ourselves) is in direct proportion to the free radical control enzymes, like superoxide dismutase. The use of antioxidant and dietary restriction approaches would seem to be able to boost and enhance antioxidant activity, given the evidence accumulated to date. We are literally repairing the repair system (or allowing it to repair itself) when we fast or modify what is eaten in the manner suggested by Drs Weindruch and Walford's experiments. The question seems not only to be whether such repairs influence life expectancy rather than health, but also what are the best ways of achieving this end?

Since Dr Denham Harman of the University of Nebraska first proposed that free radicals were the keys to ageing, as far back as the mid-1950s, the study of ageing has spent much time examining the possibilities of slowing down both free radical damage and ageing. Recently, however, although the theory still looks accurate in many respects, some doubts have begun to be cast on just how antioxidant activity at cellular level can be achieved. Our self-produced defense against free radicals comes in the form of substances which literally sacrifice themselves so that the rogue free radical molecules are mopped up, thus preventing their ability to latch onto electrons in healthy tissues, and damaging or altering them in the process.