In fact, the two aims (health and long life) are inseparable since the only methods of life extension so far researched and proved to work (namely methods of calorie restriction within a framework of a diet providing all other essential nutrients, as described in detail in later chapters) have shown that with an extension of life come major health benefits in terms of lower incidence of the diseases we normally associate with age, as well as the disappearance of many of those ailments that already exist when the programmes are begun.
While the ageing process quite obviously takes place with the progression of time, it is not necessarily directly linked to it. People can and do age at different rates and, in some instances (Down's Syndrome is an example) ageing can be seen to speed up and sometimes become extremely rapid. The study of ageing has led to the development of a variety of theories to explain the 'why' of the process, since the 'what' is all too clear. All or some of the mechanisms described in the different theories may be involved in ageing in any given instance.
Some experts prefer to use the expression 'failure to survive' rather than 'ageing', since this word has overtones of an inevitable decline and degeneration, which some believe to be inaccurate. The two main lines of investigation into the ageing process focus on either those cellular changes which might be involved, or on the whole organism and the changes which occur in it. As Alan Hipkiss and Alan Bittles state in their contribution to Human Ageing and Later Life (edited by Anthony Warnes and published by Edward Arnold, London, 1989): 'It is accepted by most biologists that ageing ultimately has a molecular basis and that, whatever the changes in molecular structures or functions which accompany or cause ageing, these changes are manifested by deleterious alterations in cellular, organ and organismic behavior.'
What we've got to look at, then, is not just what is happening in the basic cells which make up the whole, but also at the whole organism and how changes which have occurred in it (for whatever reason) influence its totality, including its cellular function.
There have been many ideas put forward on cellular ageing. One is that a variety of errors and changes in our genetic information control mechanism (deoxyribonucleic acid or DNA) contained in every cell of our bodies take place with ageing, resulting in either mutation or damage to cells. This then leads to inadequate (both in quality and quantity) protein manufacture with an inevitable decline in function, since continuous synthesis of protein is essential for repair and maintenance of our multitude of organs and parts.
Free radicals (toxic by-products of oxygen metabolism) are also pinpointed as havoc producers at a cellular level, and these are thought to lead to the sort of damage to our cellular information storage (DNA) described above, or alternatively to an impairment of the energy status of cells and a consequent malfunction in detoxification activity and other functions. Free radical activity induces proteins and fats to combine to produce age-pigments called lipofuscin ('liver spots') which overload cells reducing their efficient working.
The development of cross-links between cells as a result of faulty enzyme activity, free radical activity or sugar-related alterations (known as glycosylization) are also thought to lead to age-related changes (wrinkles are a superficial example). Cross linking of this sort is often associated with poor protein synthesis. Connective tissue (collagen) which supports and gives shape and cohesion to other soft tissues is commonly affected by cross linkage associated with ageing. It is thought by some researchers that ageing is a preprogrammed process, and that just as we grow and develop at a certain rate so do we age at a certain rate, with the whole process determined by genetic factors (DNA again).