Light at the end of the tunnel

Even distinguished biologists such as the authors of this excellent book cannot give many answers to the questions posed by biological ageing, but they do clarify them. Robert Ricklefs and Caleb Finch nicely distinguish between "how" and "why" questions. Accumulation of mechanical damage literally abrades the wings of houseflies and the teeth of lions beyond the point of viability and wears our joints into arthritis. Free radicals cumulatively impair cell metabolism; cells can replace themselves, but for each species there is a limit to the number of viable replacements (our own 40-60 fibroblast doublings compare with up to 35 for chickens and 100 for tortoises).

Some changes, can be successfully delayed or minimised by lifestyle. Muscle atrophy and osteoporosis can be deferred by exercise. Stress, which is known to result in cortoicosteroid elevations accompanied by hippocampal damage in rats, and inferred also to do so in humans, can perhaps be reduced by lifestyle adjustment. The aetiology and the therapy of other changes are much more obscure. The immune system becomes less efficient so that both B and T cells find it hard to respond to new antigens, and infections become more serious.

However our defence system against infection also provides a provocative caution against the idea that all changes are for the worse because with age macrophages appear to maintain or increase their abundance and aggression. The task of deducing general principles of ageing from studies of physiological subsystems that exhibit very different trajectories of change provokes feelings of inadequacy in gerontologists, even those as doughty as Ricklefs and Finch: "I it is the nature of ageing that it begets changes across all levels of biological organisation. An equivalent task might be to deduce from the laws of physics of subnuclear particles how the brain works, a challenge that few physicists could take on."

There are intriguingly powerful statistical consistencies in ageing, most notably the ubiquitous Gompertz functions, but these remain cryptic. Mammals, birds and reptiles all show an inverse relationship between rate of ageing and body size, and body size is quite closely related to metabolic rate, so that animals as different as hamsters and elephants metabolise the same amount of glucose and synthesise the same amount of protein per unit of their mass, and experience roughly the same number of heartbeats during the course of their lives. However the gain in longevity with size - and slowing of metabolic rate - is greater in mammals, for unknown reasons, than in reptiles, and less than in birds.

There are, understandably, even fewer answers on the "why" of ageing: the reasons why it is a good survival strategy for immortal, and selfish, genes to accept temporal limitation of the disposable individual bodies that transmit them. Ricklefs and Finch give a lucid account of essential evolutionary theories of ageing. Depending on environmental pressures species of animals and birds can show population growth rates of 9 per cent to 102 per cent. Obviously these would be curtailed by unlimited life spans resulting in overpopulation but, for selfish genes, maximum growth rate is an advantageous investment.

However, given that population attrition is limited by ageing, however slow, population growth will be boosted more by increases in reproductive rate early rather than late in the average life span. Thus genes that promote early fecundity will tend to be selected, even if they carry penalties, in terms of later loss of fecundity, increase in mortality or more rapid ageing. This sets out only very rough rules for an evolutionary "ageing game", and the many further questions it provokes will, no doubt, provide intriguing answers. For those of us who have already chosen our parents the authors can offer little help in the way of advice except to moderate in all things, especially food, to take exercise, reduce stress, avoid tobacco smoke and, having taken these precautions, to manage to have as good a life as possible in the years that our selfish genes have programmed for us.

Patrick Rabbitt is at the Age and Cognitive Performance Research Centre, University of Manchester.