Abstract

As the popular saying goes, the only certain things in life are death and taxes. Given its inevitability, it is no surprise that death—and the ageing process that precedes it—has fascinated humans for centuries. However, it is only with the development of modern science that we are now beginning to understand why our bodies grow older and more frail until we eventually die. As theories have been put forward and refuted, the field of ageing research has oscillated between optimism and pessimism, flitting between the hope that ageing can be slowed or stopped, and the fear that it is inevitable and irreversible. The present mood is one of cautious optimism, based on studies showing that the average and maximum lifespans of rodents can be increased by 25–80% through restricting calorie intake or inhibiting the insulin growth factor 1 (IGF1) receptor (Holzenberger et al , 2003). In the worm Caenorhabditis elegans , in which increased longevity is easier to attain, the restriction of various reproductive and energy‐production pathways has increased maximum lifespan more than sixfold from 20 to 126 days (Kenyon et al , 1993; Murphy et al , 2003). According to Cynthia Kenyon from the University of California, San Francisco, USA, recent research—on C. elegans in her own laboratory, and on mammals, birds, insects, yeast and other organisms by other groups—has ushered in a new era in which significantly increasing human lifespan might be possible. “The real value of the work so far is that we now know lifespan is not a passive phenomenon. It's controlled by genes,” said Kenyon. Although some researchers are wary of drawing too many conclusions about mammalian ageing from work in lower organisms, it is now widely accepted that free radicals are the principal mediators of ageing in most species. During the synthesis of ATP, mitochondria produce …

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