Amazing substances
Our bodies have evolved defensive substances such as the enzyme catalyst which can deactivate hydrogen peroxide (bleach), one of the substances our immune system uses in its own attacks on unwelcome, invading, micro-organisms. Catalase and other antioxidant enzymes, such as superoxide dismutase (SOD) and glutathione peroxidase, are also present as defenders of body tissues against oxidative processes. These enzymes are dependent upon a number of trace elements and vitamins (mainly of the B-complex group) for their function, including copper, zinc and manganese (for SOD), selenium (for glutathione peroxidase) and iron (for catalase).
There are also non-enzyme free radical deactivators, some of which are literally consumed in their battle against radicals, including beta carotene (the precursor of vitamin A),vitamins E and C, amino acids glutathione, methionine and cysteine, and the mineral selenium which is symbiotically active with vitamin E.
A surprise defender
One of the more surprising antioxidants, which we produce in our own cells, is cholesterol. This substance helps protect the cell membrane against free radical damage, as well as itself being a precursor of vitamin D. Vitamin D is formed by the body, from cholesterol in the skin, in response to radiation from sunlight (ultraviolet light). When too much vitamin D is formed in some tissues this attracts the deposition of calcium into cells in the region, in turn interfering with normal cell transportation functions and energy production.
The health benefits which have been seen as a result of reducing cholesterol in the diet seem to be a result of a coincidental reduction in fat intake, which reduces free radical potential (fats peroxidize easily under free radical attack.) However, use of drugs which reduce cholesterol levels in the blood (nine-tenths of which is self-produced rather than result of the food we eat) have had a history of side-effects, mainly because of the failure to recognize the protection cholesterol gives us as an antioxidant.
Another extremely powerful antioxidant, universally present in the system, is uric acid, which, although toxic in excess, is easily metabolized by the body if adequate nutritional levels of vitamin C are present.
What about ageing?
Now, since we know that antioxidants can slow down or switch off free radical activity, should it not be the case that ageing automatically slowed down when these are supplied in increased quantities? Weindruch and Walford are not sure, saying that feeding antioxidants to animals has so far failed to demonstrate increase in life span (this statement has been challenged, see below They suggest that the 'excuses' which believers in oxidant nutrition offer for this failure are that the antioxidants given to the experimental animals may not be able to penetrate he sites of free radical activity in the cells, or that the body adjusts its own production of natural antioxidants downwards when these are supplemented in the diet, so that no net gain is seenin antioxidant activity (and therefore no improvement in terms of lessened damage or life expectancy). The second 'excuse' come at least partially accurate. As mentioned previously, we come equipped with a wide array of self-repair and protection mechanisms including an assortment of antioxidant enzymes which quench free radicals.
Evidence
Richard Cutler of the National Institute of Aging in the US , studied more than 20 species, including rats and humans. In cases those that live longest have the highest and most active levels of antioxidant enzymes which literally soak up free radical activity (remember a squeeze of lemon juice on a browning apple, rust-proofing metal?). However, some studies show that when antioxidants such as vitamin A are provided, cells respond by reducing their own production of antioxidants, allowing the same amount of free radical activity to continue. This does not stand as absolute proof that antioxidant methods are not going to work, but certainly puts a question mark on just how this can best be achieved, and I tackle this later in the book.
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