Keynote: mechanisms of senescence--complificationists versus simplificationists.

It strikes me that among our relatively small community of gerontologists concerned with genetic approaches to our science, there is somewhat of a dichotomization. On the one hand, there are those of us, like myself, who tend to be dour 'complificationists'. Journalists talk to us, but are usually disappointed by the encounter. We are perhaps too impressed with the enormous diversity of genetic modulations of human senescence and with our interpretations of the implications of the evolutionary biological theory of senescence, namely that senescent phenotypes per se are non-adaptive, non-determinative, subject to stochastic events as well as highly polygenic modulations, with resulting wide variability in mechanisms of senescence among and within species. Quite happily, however, there are wonderful optimists among us. They seem to be convinced that there are likely to be a rather small number of major gene effects for a few major mechanisms. They include most Saccharomyces cerevisiae and Caenorhabditis elegans geneticists, some Drosophila melanogaster geneticists, and some mouse geneticists. They also include caloric restriction enthusiasts. Let's call these colleagues 'simplificationists'. Journalists and friends generally find them to be delightful companions. Where does the truth lie? Perhaps the truth lies somewhere between these two extremes and is largely dependent upon the organisms and the range of environments being investigated.