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As demonstrated in various animal models, organismal longevity can be achieved via interventions that at the mechanistic level could be considered to entail 'defensive' responses: most long-lived mutants focus on somatic maintenance, while reducing growth pathway signalling and protein translation and turnover. We here provide evidence that the opposite mechanism can also lead to longevity and improved health.We report on the mode of action of royalactin, a glycoprotein activator of epidermal growth factor signalling, capable of extending lifespan in several animals. We show that in Caenorhabditis elegans, royalactin-induced longevity depends on increased protein translation and entails increased proteasome activity. We propose the term 'copious longevity' to describe this newly-elucidated mechanism. In contrast to what is true for many other lifespan-extending interventions, we observed no obvious trade-offs between royalactininduced longevity and several life history traits. Our data point towards increased protein turnover to support healthy ageing, and provide a means for future comparative studies of defensive vs. copious mechanisms.