This meta-analysis synthesized 102 effect sizes reflecting the relation between specific moods and creativity. Effect sizes overall revealed that positive moods produce more creativity than mood-neutral controls (r= .15), but no significant differences between negative moods and mood-neutral controls (r= -.03) or between positive and negative moods (r= .04) were observed. Creativity is enhanced most by positive mood states that are activating and associated with an approach motivation and promotion focus (e.g., happiness), rather than those that are deactivating and associated with an avoidance motivation and prevention focus (e.g., relaxed). Negative, deactivating moods with an approach motivation and a promotion focus (e.g., sadness) were not associated with creativity, but negative, activating moods with an avoidance motivation and a prevention focus (fear, anxiety) were associated with lower creativity, especially when assessed as cognitive flexibility. With a few exceptions, these results generalized across experimental and correlational designs, populations (students vs. general adult population), and facet of creativity (e.g., fluency, flexibility, originality, eureka/insight). The authors discuss theoretical implications and highlight avenues for future research on specific moods, creativity, and their relationships.

Oxytocin and Intergroup Conflict: Human society is organized into groups, such as those based on nationality or religion, which can lead to intergroup conflicts, with sometimes devastating consequences. Intergroup conflict engages a human behavior termed parochial altruism: For example, a soldier who fights against the enemy at risk to themselves to protect their country is a parochial altruist. De Dreu et al. (p. 1408 ; see the cover; see the News story by Miller ) have discovered a role for oxytocin, a neuropeptide produced in the hypothalamus, in regulating parochial altruism during human intergroup competition and conflict. Oxytocin is already known to play a role in trusting behavior, and naturally occurring genetic variants of the oxytocin receptor exist within the human population. Administration of oxytocin modulated defense-related aggression toward competing groups, but did not affect unprovoked, hateful behavior. Thus, there may be a neurobiological basis for intergroup conflict in humans.

To understand when and why mood states influence creativity, the authors developed and tested a dual pathway to creativity model; creative fluency (number of ideas or insights) and originality (novelty) are functions of cognitive flexibility, persistence, or some combination thereof. Invoking work on arousal, psychophysiological processes, and working memory capacity, the authors argue that activating moods (e.g., angry, fearful, happy, elated) lead to more creative fluency and originality than do deactivating moods (e.g., sad, depressed, relaxed, serene). Furthermore, activating moods influence creative fluency and originality because of enhanced cognitive flexibility when tone is positive and because of enhanced persistence when tone is negative. Four studies with different mood manipulations and operationalizations of creativity (e.g., brainstorming, category inclusion tasks, gestalt completion tests) support the model.

Anecdotes from creative eminences suggest that executive control plays an important role in creativity, but scientific evidence is sparse. Invoking the Dual Pathway to Creativity Model, the authors hypothesize that working memory capacity (WMC) relates to creative performance because it enables persistent, focused, and systematic combining of elements and possibilities (persistence). Study 1 indeed showed that under cognitive load, participants performed worse on a creative insight task. Study 2 revealed positive associations between time-on-task and creativity among individuals high but not low in WMC, even after controlling for general intelligence. Study 3 revealed that across trials, semiprofessional cellists performed increasingly more creative improvisations when they had high rather than low WMC. Study 4 showed that WMC predicts original ideation because it allows persistent (rather than flexible) processing. The authors conclude that WMC benefits creativity because it enables the individual to maintain attention focused on the task and prevents undesirable mind wandering.

Promotion-focused states generally boost creativity because they associate with enhanced activation and cognitive flexibility. With regard to prevention-focused states, research evidence is less consistent, with some findings suggesting prevention-focused states promote creativity and other findings pointing to no or even negative effects. We proposed and tested the hypothesis that whether prevention-focused states boost creativity depends on regulatory closure (whether a goal is fulfilled or not). We predicted that prevention-focused states that activate the individual (unfulfilled prevention goals, fear) would lead to similar levels of creativity as promotion-focused states but that prevention-focused states that deactivate (closed prevention goals, relief) would lead to lower levels of creativity. Moreover, we predicted that this effect would be mediated by feelings of activation. Predictions were tested in 3 studies on creative insights and 1 on original ideation. Results supported predictions. Implications for self-regulation, motivation, mood, and creativity are discussed.

Previous work suggests that trait behavioral activation may link to creativity, a possibility the authors empirically examine in this article. This research is grounded in the dual pathway to creativity model and experiments on approach orientation, and the authors propose that behavioral activation potentiates creativity when and because it facilitates global and flexible processing. Four experiments support this hypothesis and also reveal that when external cues sustain or facilitate local and bottom-up processing, trait behavioral activation negatively relates to creativity. Possible explanations and avenues for new research are discussed.