How does insulin signalling regulate longevity (in worms)?

Imagine a happily fed animal, say a worm on a rotting apple in an orchard. This worm has plenty of food, thanks to the ready supply of bacteria that flourishes as the apple decays. With plenty of nutrients at its disposal, the right “decision” for the worm is to develop as quickly as possible and to have as many children as it can while times are good. Under these circumstances, in response to the food cues that the worm senses, an insulin that binds to and activates the insulin/IGF-1 receptor is released from neurons and circulates, turning all of the worm’s DAF-2 receptors to the “on” position [… allowing] the young worm develop into adulthood
(p. 104, Kindle Edition)

Now imagine this same worm, or more likely one of its unlucky progeny, that is still around when the apple has been devoured and the bacterial supply is starting to run out. If the worm manages to avoid starving in the first larval stage (L1), it won’t go into dauer [hibernation-like], but it may get pretty hungry while it’s growing. There’s still hope: maybe the worm can crawl to a new apple and find another source of bacteria. If this is likely, then it’s a better strategy for the worm to buy itself some time before reproducing. When the worm’s neurons sense that there is a low amount of food but it is not yet starving, the insulin signaling pathway essentially turns “off,” causing DAF-16 to enter the nucleus (and, concomitantly, PQM-1 to leave) and to start turning on all kinds of protective genes that help the worm’s body survive longer while it looks for food. (p. 105)

So all of this business about slowing down aging isn’t really to help the hungry individual live to the ripe old age of three to four weeks, but rather to make sure that the next generation has the best chance of survival.