This artificial antioxidant acts, according to Pearson and Shaw, 'in all metabolic functions' exactly like vitamin E, one of the most powerful of all antioxidants. It is tempting to ask why vitamin E is not therefore used in chicken feed? One answer might be that there is no patent on vitamin E and therefore there would be little commercial advantage to the company producing and marketing this feed additive, since anyone else could simply copy the product. A less cynical answer might be that when the body receives a quantity of an antioxidant which it should be producing for itself, there may occur an automatic reduction in its own production, leaving a no-gain situation in terms of potential for deactivating free radicals (as seen in the supplementation of vitamin A).

Could it be that the body does not recognize the artificial antioxidants as readily as it might recognize materials which are part of its normal everyday economy, such as vitamins A and E? And that it then continues to manufacture its own antioxidants which work alongside the artificial ones to keep free radical activity low?

Weindruch and Walford's views
When animals are placed on dietary restriction programmes there seems to be a 'selective' improvement in levels of certain antioxidants and not of others. For example, no change is seen in levels of production of superoxide dismutase or glutathione peroxidase, two of our most potent free radical fighters, when restricted diets are followed. However, there is a significant increase in levels of catalase with dietary restriction, especially in the liver and kidneys, and interestingly one of the signs of ageing is a marked lessening of catalase activity in these organs. Weindruch and Walford have now clearly demonstrated that an average of 50 per cent improvement in catalase activity occurs during dietary restriction. They caution that, in their opinion, other systems and effects divorced from free radical activity theories are the main factors in ageing. However, it remains clear that dietary restriction influences important aspects of the body's ability to cope with free radicals, and it is hard to see how this cannot but be significant, bearing in mind the importance of the damage free radicals can cause.

In the section on strategies I give guidelines for modifying or preventing free radical activity. This will involve diet, supplementation of specific nutrients, moderation of lifestyle habits and exercise, as well as other methods such as chelation therapy which have been found to have marked and beneficial effects on free radical activity.

What about natural vitamins?
I said early in this chapter that supplementation of artificial antioxidants seems to offer cell protection and some life extension potential. I also mentioned that when some nutrients are supplemented, such as pro-vitamin A (beta carotene) the tissues may be induced to synthesize or produce lower levels of other antioxidants, thus leaving the overall level of free radical fighters much the same as before supplementation. There is, however, much evidence that disappointing results such as this are not universal, even when the supplemented vitamins and other nutrients are not synthetic.

Background
Professor B. Ames of the Department of Chemistry, University of California, Berkeley, has stated that there exists a growing amount of evidence which shows that ageing, cancer, heart disease and other degenerative diseases are mainly due damage caused to cells by lipid peroxidation, including their DNA (Science (1983 221:1256-64)). Such peroxidation is, as we know, caused by free radicals which in turn are generated by a variety of factors including dietary fats, heavy metals (lead, cadmium) radiation, heavy exercise, increased metabolic rate, infectious or inflammatory processes and others, including deficiencies of antioxidants.