Humans possess the remarkable ability to recombine details of divergent memories into imaginings of future events. Such imaginings are useful, for example, because they foster planning and motivate farsighted decisions. Importantly, recurrently imagining feared situations can also undermine our well-being and may even contribute to the development of anxiety. Here, we demonstrate that fearful imaginings about the future can be inhibited by neural mechanisms that help to suppress the past. Importantly, suppression reduces later apprehensiveness about the feared events, a benefit that was diminished in individuals with greater trait anxiety. This pattern suggests that the observed inhibition mechanism serves to control people’s future fears and its disruption may foster psychological disorders characterized by intrusive prospective thoughts.

Abstract

Imagining future events conveys adaptive benefits, yet recurrent simulations of feared situations may help to maintain anxiety. In two studies, we tested the hypothesis that people can attenuate future fears by suppressing anticipatory simulations of dreaded events. Participants repeatedly imagined upsetting episodes that they feared might happen to them and suppressed imaginings of other such events. Suppressing imagination engaged the right dorsolateral prefrontal cortex, which modulated activation in the hippocampus and in the ventromedial prefrontal cortex (vmPFC). Consistent with the role of the vmPFC in providing access to details that are typical for an event, stronger inhibition of this region was associated with greater forgetting of such details. Suppression further hindered participants’ ability to later freely envision suppressed episodes. Critically, it also reduced feelings of apprehensiveness about the feared scenario, and individuals who were particularly successful at down-regulating fears were also less trait-anxious. Attenuating apprehensiveness by suppressing simulations of feared events may thus be an effective coping strategy, suggesting that a deficiency in this mechanism could contribute to the development of anxiety.