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Although many believe that creativity associates with a vulnerability to psychopathology, research findings are inconsistent. Here we address this possible linkage between risk of psychopathology and creativity in nonclinical samples. We propose that propensity for specific psychopathologies can be linked to basic motivational approach and avoidance systems, and that approach and avoidance motivation differentially influences creativity. Based on this reasoning, we predict that propensity for approach-based psychopathologies (e.g., positive schizotypy and risk of bipolar disorder) associates with increased creativity, whereas propensity for avoidance-based psychopathologies (e.g., anxiety, negative schizotypy, and depressive mood) associates with reduced creativity. Previous meta-analyses resonate with this proposition and showed small positive relations between positive schizotypy and creativity and small negative relations between negative schizotypy and creativity and between anxiety and creativity. To this we add new meta-analytic findings showing that risk of bipolar disorder (e.g., hypomania, mania) positively associates with creativity (k = 28, r = .224), whereas depressive mood negatively associates (albeit weakly) with creativity (k = 39, r = -.064). Our theoretical framework, along with the meta-analytic results, indicates when and why specific psychopathologies, and their inclinations, associate with increased or, instead, reduced creativity. (PsycINFO Database Record

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Our findings suggest that goal-directed motivation may drive the enhanced real-world creative achievements of people with ADHD. Moreover, people with ADHD may selectively engage and excel in creative domains that fit their skills and preferences.

RationaleElectrophysiological studies have identified a scalp potential, the late positive potential (LPP), which is modulated by the emotional intensity of observed stimuli. Previous work has shown that the LPP reflects the modulation of activity in extrastriate visual cortical structures, but little is known about the source of that modulation.ObjectivesThe present study investigated whether beta-adrenergic receptors are involved in the generation of the LPP.MethodsWe used a genetic individual differences approach (experiment 1) and a pharmacological manipulation (experiment 2) to test the hypothesis that the LPP is modulated by the activation of β-adrenergic receptors.ResultsIn experiment 1, we found that LPP amplitude depends on allelic variation in the β1-receptor gene polymorphism. In experiment 2, we found that LPP amplitude was modulated by the β-blocker propranolol in a direction dependent on subjects' level of trait anxiety: In participants with lower trait anxiety, propranolol led to a (nonsignificant) decrease in the LPP modulation; in participants with higher trait anxiety, propranolol increased the emotion-related LPP modulation.ConclusionsThese results provide initial support for the hypothesis that the LPP reflects the downstream effects, in visual cortical areas, of β-receptor-mediated activation of the amygdala.