It is well established that emotion plays a key role in human social and economic decision making. The recent literature on emotion regulation (ER), however, highlights that humans typically make efforts to control emotion experiences. This leaves open the possibility that decision effects previously attributed to acute emotion may be a consequence of acute ER strategies such as cognitive reappraisal and expressive suppression. In Study 1, we manipulated ER of laboratory-induced fear and disgust, and found that the cognitive reappraisal of these negative emotions promotes risky decisions (reduces risk aversion) in the Balloon Analogue Risk Task and is associated with increased performance in the prehunch/hunch period of the Iowa Gambling Task. In Study 2, we found that naturally occurring negative emotions also increase risk aversion in Balloon Analogue Risk Task, but the incidental use of cognitive reappraisal of emotions impedes this effect. We offer evidence that the increased effectiveness of cognitive reappraisal in reducing the experience of emotions underlies its beneficial effects on decision making.
Early-life adversity has been associated with a life-long increased risk for psychopathology and chronic health problems. These long-term negative effects have been explained through stress sensitization, which may involve dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis through either increased or decreased reactivity. The present meta-analysis assessed for the first time the effect of early-life adversity on cortisol response to social stress. Thirty data sets were included in the meta-analysis, in which early-life adversity and salivary cortisol response to social stress were assessed in 4292 individuals of different ages. Results indicated a moderate effect size (g = −0.39) in overall cortisol levels across studies. Separate analyses of cortisol at different stages of response showed large effect sizes at peak and recovery, and a moderate effect at baseline. Heterogeneity was large in this sample of studies and several moderators were identified. The effect size was larger in studies that focused on maltreatment compared to those that included other adversities, and in adults compared to children and adolescents. Percent of women in each sample and methodological quality were positive predictors of the effect size. Publication bias may be present, but the analysis was hampered by the high heterogeneity. Therefore, these results support the association between early-life adversity and blunted cortisol response to social stress, and they suggest that the long-term negative effects of early-life adversity may reach maximum levels in adults.
Serotonin (5-HT) modulates emotional and cognitive functions such as fear conditioning (FC) and decision making. This study investigated the effects of a functional polymorphism in the regulatory region (5-HTTLPR) of the human 5-HT transporter (5-HTT) gene on observational FC, risk taking and susceptibility to framing in decision making under uncertainty, as well as multidimensional anxiety and autonomic control of the heart in healthy volunteers. The present results indicate that in comparison to the homozygotes for the long (l) version of 5-HTTLPR, the carriers of the short (s) version display enhanced observational FC, reduced financial risk taking and increased susceptibility to framing in economic decision making. We also found that s-carriers have increased trait anxiety due to threat in social evaluation, and ambiguous threat perception. In addition, s-carriers also show reduced autonomic control over the heart, and a pattern of reduced vagal tone and increased sympathetic activity in comparison to l-homozygotes. This is the first genetic study that identifies the association of a functional polymorphism in a key neurotransmitter-related gene with complex social-emotional and cognitive processes. The present set of results suggests an endophenotype of anxiety disorders, characterized by enhanced social learning of fear, impaired decision making and dysfunctional autonomic activity.
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