The process of ageing makes death increasingly likely, involving a random aspect that produces a wide distribution of lifespan even in homogeneous populations1,2. The study of this stochastic behaviour may link molecular mechanisms to the ageing process that determines lifespan. Here, by collecting high-precision mortality statistics from large populations, we observe that interventions as diverse as changes in diet, temperature, exposure to oxidative stress, and disruption of genes including the heat shock factorhsf-1, the hypoxia-inducible factorhif-1, and the insulin/IGF-1 pathway componentsdaf-2,age-1, anddaf-16all alter lifespan distributions by an apparent stretching or shrinking of time. To produce such temporal scaling, each intervention must alter to the same extent throughout adult life all physiological determinants of the risk of death. Organismic ageing inCaenorhabditis eleganstherefore appears to involve aspects of physiology that respond in concert to a diverse set of interventions. In this way, temporal scaling identifies a novel state variable,r(t), that governs the risk of death and whose average decay dynamics involves a single effective rate constant of ageing,kr. Interventions that produce temporal scaling influence lifespan exclusively by alteringkr. Such interventions, when applied transiently even in early adulthood, temporarily alterkrwith an attendant transient increase or decrease in the rate of change inrand a permanent effect on remaining lifespan. The existence of an organismal ageing dynamics that is invariant across genetic and environmental contexts provides the basis for a new, quantitative framework for evaluating the manner and extent to which specific molecular processes contribute to the aspect of ageing that determines lifespan.