As Elmer Cranton MD states Journal of Holistic Medicine (1984 6(1):6-31)): 'Research in senility, dementia, brain ischaemia, stroke, and spinal cord injury provides a wealth of evidence incriminating free radicals as a cause of nervous system disease, and also provides a rationale for treatment.' He points out that the central nervous system not only contains the highest concentrations of fat of any organ, but that in good health it also contains vitamin C in concentrations 100 times greater than that found in most other tissues and organs of the body.

The concentrations of antioxidants in our tissues is, along with the level of free radicals active in those tissues, a key determining factor of length of life (as well, of course, as the level of health). An important function of vitamin C is protection of the central nervous system from peroxidative damage caused by free radical activity on fatty tissues.

Can antioxidants in the diet increase protection from free radicals?

1. Dr E. Calebrese and colleagues examined the protective effect of vitamin E supplementation against exposure to ozone (commonly present in polluted air) which degrades to form hydrogen peroxide (bleach) one of the most potent of all free radical producers. In this study, 12 adult human volunteers were supplemented daily with 600iu of vitamin E for a month. Samples of their blood - taken before the study started, and after two weeks and then after four weeks of supplementation - were exposed to varying levels of ozone in order to test the amount of damage taking place to cells, with and without different degrees of supplemented vitamin E in the donors of the blood. When blood is exposed to ozone it forms a damage by-product called methaemoglobin. This byproduct was found in far lower levels during the second and fourth weeks of vitamin E supplementation, especially at the highest exposure to ozone.

2. Much research confirms that as red blood cells reach the end of their useful life (as they age in fact) 'markers' appear on their surface (called 'senescent cell antigens') which alert defense mechanism cells (immunoglobulin-G auto-antibodies) to target them for removal from the circulatory system. A study was conducted in which red blood cells taken from vitamin E deficient rats were examined in relation to this whole phenomenon. The results showed that vitamin E deficiency caused premature ageing of the red blood cells and that this led to binding with the cells of the antibodies. The cells of vitamin E deficient animals - of all ages - were seen to behave in the same way as the red blood cells of old animals on normal diets. The researchers said: 'Results of the experiments indicate that erythrocytes (red blood cells) from vitamin E deficient rats age prematurely, indicating that oxidation accelerates cellular ageing.'

3. Dr A. Blackett, of the General Infirmary, University of Leeds, has studied the relationship between vitamin E levels and the accumulation of lipofuscin (the fat/protein substance-'age pigment - associated with ageing) in mice Journal of Gerontology (1981 36:529-33)). Half the mice were supplemented with vitamin E and half were not, and it was found that the levels of vitamin E in the tissues of the supplemented animals rose by 400 per cent over the length of the study (two years) and that the supplemented mice had lower levels of lipofuscin throughout their lives. By the time they were 28 months old they had levels which were similar to non supplemented mice aged 23 months. If accumulation of age pigments is an indication of the rate of ageing, then this is clear evidence that the process is slowed by antioxidant supplementation. Unfortunately the study did not show any consistent increase in life span for the supplemented mice despite their ability to stay young longer. One argument against expecting any life extension for supplemented mice is that other factors, such as the content of their overall diet and levels of other antioxidants, were unchanged. Clearly, altering just one factor, as in this example of supplementing one antioxidant, while having health enhancing benefits, does not necessarily prolong life.