My own view has always been the "motor car" theory, namely that parts just wear out; just look at my knees. A nice example comes from elephants, some of whom die of old age when their teeth are so worn down that they can no longer eat. But the hot focus at present is on the telomeres. Telomeres? Hardly a term in everyday use, but it could become as familiar in relation to ageing as serotonin is to depression.
Telomeres are specialised DNA sequences at the ends of each chromosome. One of their functions is to protect the chromosome from damage by chemicals that could break it down. When the cell divides the chromosomes are duplicated, and there is a special enzyme that is involved in duplicating the telomeres. However, this enzyme is not present in all cells and its absence may be linked to ageing, for the telomeres may be used to count how many times a cell has divided.
The conventional wisdom until the Sixties was that when cells were placed in a suitable culture medium they would continue to proliferate for ever - they were essentially "immortal". But it was wrong. When human cells from connective tissue, for example, are cultured, they will go through about 50 divisions and then stop dividing. And the older the person from whom they are taken, the fewer times they will divide. It seems that telomeres are doing the counting, for each time one of those cells in culture divides, the end of the telomere is not properly duplicated, so that the telomere gets shorter and shorter with each division. The evidence for this, and it is a lovely experiment, is to add the enzyme that synthesises telomeres - telomerase - to the cells in culture; they then become "immortal" and will multiply indefinitely.
But cells stopping dividing in culture are a long way from the multiple aspects of ageing in the human body and seem hard to relate, for example, to impairment in thinking, memory and physical strength.
But very new work is suggestive. What they did was to make mice that had no telomerase, and so when the cells divided, their telomeres got shorter. After several generations of these mice being inbred, they showed premature greying and hair loss; they were ageing prematurely and had, for example, reduced capacity to repair wounds. There were also suggestive similarities with a human condition, known as Werner's syndrome, that results in premature ageing; growth at adolescence is reduced and sufferers have the disabilities of old age in their twenties. Most of them die before 50.
But telomeres are just part of the hunt for immortality. There is a mutant fruit fly - a favourite model for genetics - called Methuselah, which lives one-third longer than normal, but no one knows why. Even more striking is a worm - another model - which lives four times as long. This longevity is related to insulin and its effect on metabolism, and is thought to be similar to the effect of low-calorie intake being able significantly to increase the life span of rodents. But it is unlikely that there is just one cause of ageing. An attractive approach is the network model, which aims to take into account a whole range of processes, for example mutations in genes, and toxic substances produced by the cells themselves, that will in the end lead to the death of the cell.
Current evidence suggests that if you eat less you live longer - I like the idea that food is dangerous. And it is wise to be careful about your lifestyle, particularly how much exercise you take. For while telomeres and genes have a part to play, the evidence is that environmental influences can profoundly influence the outcomes of ageing. As a cyclist in London, should I rethink my attachment to my bike? Certainly not.
The writer is professor of biology as applied to medicine at University College London