Sir

The growing number of elderly people in society is attracting much interest. Because the matter is of much concern to many people, care must be taken when journals report on ageing matters.

Take, for example, the report of N. Ishii et al. on the oxygen-sensitive mev-1 mutant of the nematode worm (Nature 394, 694–697; 1998). This well-known mutant appears to be defective in mitochondrial electron transport, which could explain its high sensitivity to oxygen poisoning, as shown by its decreased longevity. However, the title of the paper links this result not only to oxidative stress, but also to ageing. Further, the front cover of Nature inaccurately states “Ageing: role of oxidative stress”, and the entry on the contents summary page was entitled “Ageing gene”. This choice of title is unfortunate.

First, Ishii et al. report longevity, not ageing, data, even though the authors equate a shortening of longevity with premature ageing. Longevity does not provide the same information as ageing data for individuals; many laboratories rightly use biological markers of ageing, such as those provided by the study of behaviour, rather than relying solely on longevity data. Longevity is a measure of duration, not of content. We all know people of the same longevity, say 90 years old, who were bedridden or who were able to go jogging — knowing the longevity of individuals is not the same as knowing their physiological status or quality of life.

Second, Nature's title “Ageing gene” gives the impression that there could be genes governing the way we age. It is well-known that many genes may have effects on various features of the ageing process, but it is not correct to suggest that mendelian genes determine the ageing process. It is well-recognized by gerontologists that genes decreasing longevity are not strong arguments for a genetic determinism of longevity. Many mutants, due to their negative defects, have a low longevity, and attempts to find mutants where lifespan is increased have failed except in nematodes. Human genetic diseases often decrease lifespan, but it is generally accepted that their study is of little help in understanding normal ageing.

Our purpose is not to criticize the interesting work of Ishii et al. But we do wish to draw attention to the need to use the word ‘ageing’ with care when reporting on longevity, and we do wish to ask authors and journals to avoid titles that may misrepresent gerontological research.