One argument against free radical damage being a major cause ageing is based on the fact that the ageing process seems to a well-organized progression, whereas the damage cause by e radicals appears more chaotic and random. So, although it might well be that most if not all the major diseases of old age have roots which link them to free radical damage, this does not necessarily connect ageing itself to the activity of free radicals, only to poor health.

Genetics again
There is also the argument that when a certain degree of damage has taken place on a cellular level, a preprogrammed, genetically based process might be called into play, a sort of 'self-destruct button' having been pressed. Just when this happens will depend upon the degree of damage caused by free radicals (or other factors), which are themselves to a large extent the product of the rate at which metabolic activity is going on, which takes us back to the 'thrifty' and 'burner' types described by Weindruch and Walford.

As I explain in Chapter 9, there is much evidence to support the importance, in the delaying of ageing, of lowering internal temperature levels, which naturally enough means slowing down metabolic processes. When metabolic processes are slower, free radical activity slows down, and ageing is delayed. Once again we see the interconnection between one aspect of the picture with another - slow metabolism, leading to less free radical damage, leading to less cellular damage and disease, leading to lesser likelihood of programmed obsolescence via the genes being triggered.

The idea that a genetic programme exists which decides that enough is enough, and that ageing should be accelerated is not completely fanciful, as it fits into some of the evolutionary concepts which I have previously talked about. It is quite certain that antioxidant techniques can lead to a reduction in oxidation damage caused by free radicals, resulting in improved health (both in animals and humans). It is also reasonably certain that youthful qualities can be generated by such an approach, but what remains very unclear is whether this would have any noticeable impact on life expectancy.

Can anti-free radical approaches lengthen life?
Over the years, three approaches to 'using' the understanding of free radical activity for promotion of life extension have been suggested:

1. Employment (in the diet) of free radical deactivators (antioxidants) such as vitamins A, C, E, and B6; minerals zinc and selenium; amino acids cysteine, methionine and glutathione, as well as enzymes such as SOD and catalase (which are now known to survive the bodys digestion process and to be able to increase tissue levels when supplemented in certain forms, such as freeze-dried wheat grass juice). Some (e.g. Pearson and Shaw) also recommend the use of artificial substances such as BHT in this quest (see below).

2. Reduction in the diet, as far as is possible, of foods and substances which add to the free radical burden, including polyunsaturated fats and metals such as copper. A logical extension of this sort of tactic would be to avoid wherever possible exposure to environmental pollution, whether in the workplace or at home, as well as curbing lifestyle habits which might add to the burden (smoking and alcohol consumption, for example).

3. Dietary restriction, which reduces metabolic rate, and therefore free radical activity, as well as actually increasing the presence of some of the most important antioxidants. Some experts suggest that one of the main reasons why dietary restriction actually increases life span is its effect on free radicals.