Emotion regulation strategies provide a means by which to modulate our social behavior. In this study, we investigated the effect of using reappraisal to both up- and downregulate social decision making. After being instructed on how to use reappraisal, participants played the Ultimatum Game while undergoing functional magnetic resonance imaging and applied the strategies of upregulation (reappraising the proposer's intentions as more negative), down-regulation (reappraising the proposer's intentions as less negative), as well as a baseline "look" condition. As hypothesized, when reappraising, decision acceptance rates were altered, with a greater number of unfair offers accepted while down-regulating and a greater number of unfair offers rejected while upregulating, both relative to the baseline condition. At the neural level, during reappraisal, significant activations were observed in the inferior and middle frontal gyrus (MFG), in addition to the medial prefrontal cortex and cingulate gyrus for unfair offers only. Regulated decisions involved left inferior frontal gyrus for upregulation and MFG for down-regulation strategies, respectively. Importantly, the effects of emotion modulation were evident in posterior insula, with less activation for down-regulation and more activation for upregulation in these areas. Notably, we show for the first time that top-down strategies such as reappraisal strongly affect our socioeconomic decisions.

Previous studies have reported the effect of emotion regulation (ER) strategies on both individual and social decision-making, however, the effect of regulation on socially driven emotions independent of decisions is still unclear. In the present study, we investigated the neural effects of using reappraisal to both up- and down-regulate socially driven emotions. Participants played the Dictator Game (DG) in the role of recipient while undergoing fMRI, and concurrently applied the strategies of either up-regulation (reappraising the proposer's intentions as more negative), down-regulation (reappraising the proposer's intentions as less negative), as well as a baseline “look” condition. Results showed that regions responding to the implementation of reappraisal (effect of strategy, that is, “regulating regions”) were the inferior and middle frontal gyrus, temporo parietal junction and insula bilaterally. Importantly, the middle frontal gyrus activation correlated with the frequency of regulatory strategies in daily life, with the insula activation correlating with the perceived ability to reappraise the emotions elicited by the social situation. Regions regulated by reappraisal (effect of regulation, that is, “regulated regions”) were the striatum, the posterior cingulate and the insula, showing increased activation for the up-regulation and reduced activation for down-regulation, both compared to the baseline condition. When analyzing the separate effects of partners' behavior, selfish behavior produced an activation of the insula, not observed when subjects were treated altruistically. Here we show for the first time that interpersonal ER strategies can strongly affect neural responses when experiencing socially driven emotions. Clinical implications of these findings are also discussed to understand how the way we interpret others' intentions may affect the way we emotionally react.

Anxiety is a mental state characterized by an intense sense of tension, worry or apprehension, relative to something adverse that might happen in the future. Researchers differentiate aspects of anxiety into state and trait, respectively defined as a more transient reaction to an adverse situation, and as a more stable personality attribute in experiencing events. It is yet unclear whether brain structural and functional features may distinguish these aspects of anxiety. To study this, we assessed 42 healthy participants with the State-Trait Anxiety Inventory and then investigated with MRI to characterize structural grey matter covariance and resting-state functional connectivity (rs-FC). We found several differences in the structural–functional patterns across anxiety types: (1) trait anxiety was associated to both structural covariance of Default Mode Network (DMN), with an increase in dorsal nodes and a decrease in its ventral part, and to rs-FC of DMN within frontal regions; (2) state anxiety, instead, was widely related to rs-FC of Salience Network and of DMN, specifically in its ventral nodes, but not associated with any structural pattern. In conclusion, our study provides evidence of a neuroanatomical and functional distinction between state and trait anxiety. These neural features may be additional markers in future studies evaluating early diagnosis or treatment effects.

The purpose of this paper is to review some of the psychological and neural mechanisms behind mindfulness practice in order to explore the unique factors that account for its positive impact on emotional regulation and health. After reviewing the mechanisms of mindfulness and its effects on clinical populations we will consider how the practice of mindfulness contributes to the regulation of emotions. We argue that mindfulness has achieved effective outcomes in the treatment of anxiety, depression, and other psychopathologies through the contribution of mindfulness to emotional regulation. We consider the unique factors that mindfulness meditation brings to the process of emotion regulation that may account for its effectiveness. We review experimental evidence that points towards the unique effects of mindfulness specifically operating over and above the regulatory effects of cognitive reappraisal mechanisms. A neuroanatomical circuit that leads to mindful emotion regulation is also suggested. This paper thereby aims to contribute to proposed models of mindfulness for research and theory building by proposing a specific model for the unique psychological and neural processes involved in mindful detachment that account for the effects of mindfulness over and above the effects accounted for by other well-established emotional regulation processes such as cognitive reappraisal.

Affect can have a significant influence on decision-making processes and subsequent choice. One particularly relevant type of negative affect is anxiety, which serves to enhance responses to threatening stimuli or situations. In its exaggerated form, it can lead to psychiatric disorders, with detrimental consequences for quality of life, including the ability to make choices. This study investigated, for the first time, how pathological anxiety affects risk-taking behavior. In this study, 20 anxious participants meeting Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, criteria for either generalized anxiety disorder (n = 10) and for panic attack disorder (n = 10), as well as 20 matched nonanxious controls, performed a gambling task. To investigate the tendency toward either a risk-seeking or a risk-averse behavior, we employed a task that did not allow for learning from outcomes. Anxious participants made significantly fewer risky choices than matched nonanxious participants. Specifically, they become risk-avoidant after gains. Moreover, anxious participants not only were less happy after gains but were also less sad after losses, and they also evinced less desire to change their choices after losses than did nonanxious participants. Importantly, whereas the desire to switch choice was followed by actual choice switch for all participants, happiness directly predicted subsequent risky choices, particularly in the nonanxious participants. Further analyses revealed that the anxious participants' risk-avoidance behavior was independent of different types of anxiety disorder (panic attack disorder and generalized anxiety disorder) as well as of the effects of psychotropic drugs treatment. This study demonstrates a specific role for anxiety in individual decision making. In particular, hypersensitivity to potential threats and pessimistic evaluation of future events reduced risk-taking behavior.

The term emotional dysregulation refers to an impaired ability to regulate unwanted emotional states. Scientific evidence supports the idea that emotional dysregulation underlies several psychological disorders as, for example: personality disorders, bipolar disorder type II, interpersonal trauma, anxiety disorders, mood disorders and post-traumatic stress disorder. Emotional dysregulation may derive from early interpersonal traumas in childhood. These early traumatic events create a persistent sensitization of the central nervous system in relation to early life stressing events. For this reason, some authors suggest a common endophenotypical origin across psychopathologies. In the last 20 years, cognitive behavioral therapy has increasingly adopted an interactive-ontogenetic view to explain the development of disorders associated to emotional dysregulation. Unfortunately, standard Cognitive Behavior Therapy (CBT) methods are not useful in treating emotional dysregulation. A CBT-derived new approach called Schema Therapy (ST), that integrates theory and techniques from psychodynamic and emotion focused therapy, holds the promise to fill this gap in cognitive literature. In this model, psychopathology is viewed as the interaction between the innate temperament of the child and the early experiences of deprivation or frustration of the subject’s basic needs. This deprivation may lead to develop early maladaptive schemas (EMS), and maladaptive Modes. In the present paper we point out that EMSs and Modes are associated with either dysregulated emotions or with dysregulatory strategies that produce and maintain problematic emotional responses. Thanks to a special focus on the therapeutic relationship and emotion focused-experiential techniques, this approach successfully treats severe emotional dysregulation. In this paper, we make several comparisons between the main ideas of ST and the science of emotion regulation, and we present how to conceptualize pathological phenomena in terms of failed regulation and some of the ST strategies and techniques to foster successful regulation in patients.

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Autism is a neurodevelopmental disorder that mainly affects social interaction and communication. Evidence from behavioral and functional MRI studies supports the hypothesis that dysfunctional mechanisms involving social brain structures play a major role in autistic symptomatology. However, the investigation of anatomical abnormalities in the brain of people with autism has led to inconsistent results. We investigated whether specific brain regions, known to display functional abnormalities in autism, may exhibit mutual and peculiar patterns of covariance in their gray-matter concentrations. We analyzed structural MRI images of 32 young men affected by autistic disorder (AD) and 50 healthy controls. Controls were matched for sex, age, handedness. IQ scores were also monitored to avoid confounding. A multivariate Source-Based Morphometry (SBM) was applied for the first time on AD and controls to detect maximally independent networks of gray matter. Group comparison revealed a gray-matter source that showed differences in AD compared to controls. This network includes broad temporal regions involved in social cognition and high-level visual processing, but also motor and executive areas of the frontal lobe. Notably, we found that gray matter differences, as reflected by SBM, significantly correlated with social and behavioral deficits displayed by AD individuals and encoded via the Autism Diagnostic Observation Schedule scores. These findings provide support for current hypotheses about the neural basis of atypical social and mental states information processing in autism.