Background/Question/Methods Bet hedging – stochastic switching between phenotypic states – is a canonical example of an evolutionary adaptation that facilitates persistence in the face of fluctuating environmental conditions. While bet hedging is found in organisms ranging from bacteria to humans, direct evidence for an adaptive origin of this behaviour is lacking. Informed by new theory, which shows the selective significance of exclusion rules combined with population bottlenecks, I will describe an experiment in which we observed the de novo evolution of bet hedging in experimental bacterial populations. Results/Conclusions Bacteria were subjected to an environment that continually favoured new phenotypic states. Initially, this regime drove the successive evolution of novel phenotypes via mutation and selection; however, in two (of twelve) replicates this trend was broken by the evolution of bet-hedging genotypes that persisted on account of rapid stochastic phenotype switching. Genome re-sequencing of one of these switching types revealed that it differed from the ancestor by nine mutations. The final mutation was both necessary and sufficient for rapid phenotype switching; nonetheless, the evolution of bet hedging was contingent upon earlier mutations that altered the relative fitness effect of the final mutation. I will account for the adaptive significance of each of the nine mutations and describe in some detail the effect of the final mutation that establishes a bi-stable (epigenetic) switch. Together these findings capture the adaptive evolution of bet hedging in the simplest of organisms, and suggest that risk-spreading strategies may have been among the earliest evolutionary solutions to life in fluctuating environments