The alterations which are seen in cells, as this array of changes occur, were outlined in the previous chapter, and are listed here once more, since they represent the very center of our search for the processes which have to be slowed or reversed if we are to achieve life extension.
These changes are dominated by the slow build-up in cells of 'altered proteins' which result in all or some of the following states:
- Build up of age pigments (lipofuscin). The presence of these fat/protein granules (found in nerve and muscle cells) is largely the result of the loss of the ability to normalize cross-linkage of proteins and fats following free radical activity.
- Enzymes which have changed in their sensitivity to heat and their functional ability to act as catalysts in various cellular activities.
- Enzymes which behave poorly in their defensive roles as part of our immune function.
- Plaque and tangles of tissue found in aged brain tissue (e.g. in Alzheimer's disease).
As well as these accumulating deposits and changes there seems, with ageing, to be a tendency for both the quality and rate of protein synthesis to become increasingly disturbed. Whether these alterations are the result of a gradual loss of efficiency in dealing with the hazards of life, or whether they are the result of a built-in (genetically programmed) decline feature, remains a major question for research. What is known for certain is that where the efficiency of cell detoxification and DNA repair is operating at its best there is a coincidental increase in life expectancy.
These factors, therefore, lie at the heart of our search for an understanding of how to increase our normal life span, and they involve some of the problems and processes, on a cellular level, which are thought to play a large part in the ageing process.
If we accept a 'wear-and-tear' theory of ageing it seems to be
the likely outcome of a gradual overwhelming of the efficient
conduct of cells, as they start to work less productively,
accumulating more toxic debris, slowing down in their energy
production and generally failing to protect and repair themselves
in the face of a combination of undernutrition and toxicity (in its
widest sense) including free radical activity . . . unless there is
another factor, which most of us would recognize in relation to modern manufacturing techniques: built-in obsolescence.
Cars and refrigerators have a time-span of normal use which the manufacturers estimate to be so many years, after which time they become uneconomical to repair. You then have to buy a new one. It is considered possible by many experts that just such a feature has been built into our DNA. That a genetic code exists which says, at a given point in time, 'Enough, it's time to go.' It may also be the case that this 'switching off' decision, if it is genetically programmed, is only activated once a certain level of toxicity and inefficiency is reached, at which time the organism somehow recognizes a point of no return a moment to give up the struggle.
As indicated in Chapter 1, the best results to date in extending life experimentally have been achieved by dietary manipulation, using either individually or in combination:
- A degree of calorie restriction, or
- Antioxidant nutrition (this quenches free radical activity).
- Use of amino-acid substances to trigger growth-hormone