Cyclic outbreaks of defoliating insects devastate forests, but their causes are poorly understood. Outbreak cycles are often assumed to be driven by density-dependent mortality due to natural enemies, because pathogens and predators cause high mortality and because natural-enemy models reproduce fluctuations in defoliation data. The role of induced defenses is in contrast often dismissed, because toxic effects of defenses are often weak and because induceddefense models explain defoliation data no better than naturalenemy models. Natural-enemy models, however, fail to explain gypsy moth outbreaks in North America, in which outbreaks in forests with a higher percentage of oaks have alternated between severe and mild, whereas outbreaks in forests with a lower percentage of oaks have been uniformly moderate. Here we show that this pattern can be explained by an interaction between induced defenses and a natural enemy. We experimentally induced hydrolyzable-tannin defenses in red oak, to show that induction reduces variability in a gypsy moth's risk of baculovirus infection. Because this effect can modulate outbreak severity and because oaks are the only genus of gypsy moth host tree that can be induced, we extended a natural-enemy model to allow for spatial variability in inducibility. Our model shows alternating outbreaks in forests with a high frequency of oaks, and uniform outbreaks in forests with a low frequency of oaks, matching the data. The complexity of this effect suggests that detecting effects of induced defenses on defoliator cycles requires a combination of experiments and models. host-pathogen model | Lymantria dispar | complex population dynamics | spatial model | hydrolyzable tannins P eriodic outbreaks of forest-defoliating insects severely damage valuable timber and increase atmospheric CO 2 levels by converting forests from carbon sinks to carbon sources (1). Decades of research have produced multiple hypotheses to explain defoliator outbreak cycles (2), but a decisive experiment to choose between competing hypotheses faces almost insurmountable logistical difficulties, because outbreaks occur at 5-30 y intervals and typically cover thousands of square kilometers (3). Efforts to support particular hypotheses have therefore instead relied on a mixture of observational field data, small-scale field and laboratory experiments, and mathematical models.For example, the most widely accepted hypothesis is that defoliator cycles are driven by natural enemies. Support for this hypothesis comes first of all from observational data showing that defoliators experience high rates of infection by specialist pathogens and parasitoids in peak populations (2, 4) and high rates of attack by generalist predators and parasitoids in trough populations (5). Second, experimental data have confirmed key assumptions of defoliator-natural-enemy models, and the models produce longperiod, large-amplitude cycles resembling time series of insect densities and defoliation levels (6).Neither data nor models have provided meani...