Putting feelings into words, or "affect labeling," can attenuate our emotional experiences. However, unlike explicit emotion regulation techniques, affect labeling may not even feel like a regulatory process as it occurs. Nevertheless, research investigating affect labeling has found it produces a pattern of effects like those seen during explicit emotion regulation, suggesting affect labeling is a form of implicit emotion regulation. In this review, we will outline research on affect labeling, comparing it to reappraisal, a form of explicit emotion regulation, along four major domains of effects-experiential, autonomic, neural, and behavioral-that establish it as a form of implicit emotion regulation. This review will then speculate on possible mechanisms driving affect labeling effects and other remaining unanswered questions.

Past research suggests that feeling understood enhances both personal and social well-being. However, little research has examined the neurobiological bases of feeling understood and not understood. We addressed these gaps by experimentally inducing felt understanding and not understanding as participants underwent functional magnetic resonance imaging. The results demonstrated that feeling understood activated neural regions previously associated with reward and social connection (i.e. ventral striatum and middle insula), while not feeling understood activated neural regions previously associated with negative affect (i.e. anterior insula). Both feeling understood and not feeling understood activated different components of the mentalizing system (feeling understood: precuneus and temporoparietal junction; not feeling understood: dorsomedial prefrontal cortex). Neural responses were associated with subsequent feelings of social connection and disconnection and were modulated by individual differences in rejection sensitivity. Thus, this study provides insight into the psychological processes underlying feeling understood (or not) and may suggest new avenues for targeted interventions that amplify the benefits of feeling understood or buffer individuals from the harmful consequences of not feeling understood.

Previous research has often highlighted hyperactivity in emotion regions to simple, static social threat cues in social anxiety disorder (SAD). Investigation of the neurobiology of SAD using more naturalistic paradigms can further reveal underlying mechanisms and how these relate to clinical outcomes. We used fMRI to investigate responses to novel dynamic rejection stimuli in individuals with SAD (N=70) and healthy controls (HC; N=17), and whether these responses predicted treatment outcomes following cognitive behavioral therapy (CBT) or acceptance and commitment therapy (ACT). Both HC and SAD groups reported greater distress to rejection compared to neutral social stimuli. At the neural level, HCs exhibited greater activations in social pain/rejection regions, including dorsal anterior cingulate cortex and anterior insula, to rejection stimuli. The SAD group evidenced a different pattern, with no differences in these rejection regions and relatively greater activations in the amygdala and other regions to neutral stimuli. Greater responses in anterior cingulate cortex and the amygdala to rejection vs. neutral stimuli predicted better CBT outcomes. In contrast, enhanced activity in sensory-focused posterior insula predicted ACT responses.

Social anxiety disorder (SAD) is characterized at a neurobiological level by disrupted activity in emotion regulation neural circuitry. Previous work has demonstrated amygdala hyperreactivity and disrupted prefrontal responses to social cues in individuals with SAD (Kim et al., 2011). While exposure-based psychological treatments effectively reduce SAD symptoms, not all individuals respond to treatment. Better understanding of the neural mechanisms involved offers the potential to improve treatment efficacy. In this study, we investigated functional connectivity in emotion regulation neural circuitry in a randomized controlled treatment trial for SAD. Participants with SAD underwent fMRI scanning while performing an implicit emotion regulation task prior to treatment (n=62). Following 12 weeks of cognitive behavioral therapy, acceptance and commitment therapy, or wait-list, participants completed a second scan (n=42). Psychophysiological interaction analyses using amygdala seed regions demonstrated differences between SAD and healthy control participants (HC; n=16) in right amygdala-vmPFC connectivity. SAD participants demonstrated more negative amygdala-to-vmPFC connectivity, compared to HC participants, an effect that was correlated with SAD symptom severity. Post-treatment symptom reduction was correlated with altered amygdala-to-vm/vlPFC connectivity, independent of treatment type. Greater symptom reduction was associated with more negative amygdala-to-vm/vlPFC connectivity. These findings suggest that effective psychological treatment for SAD enhances amygdala-prefrontal functional connectivity.

Background Exaggerated anticipatory anxiety is common in social anxiety disorder (SAD). Neuroimaging studies have revealed altered neural activity in response to social stimuli in SAD, but fewer studies have examined neural activity during anticipation of feared social stimuli in SAD. The current study examined the time course and magnitude of activity in threat processing brain regions during speech anticipation in socially anxious individuals and healthy controls (HC). Method Participants (SAD n = 58; HC n = 16) underwent functional magnetic resonance imaging (fMRI) during which they completed a 90s control anticipation task and 90s speech anticipation task. Repeated measures multi-level modeling analyses were used to examine group differences in time course activity during speech vs. control anticipation for regions of interest, including bilateral amygdala, insula, ventral striatum, and dorsal anterior cingulate cortex. Results The time course of amygdala activity was more prolonged and less variable throughout speech anticipation in SAD participants compared to HCs, whereas the overall magnitude of amygdala response did not differ between groups. Magnitude and time course of activity was largely similar between groups across other regions of interest. Limitations Analyses were restricted to regions of interest and task order was the same across participants due to the nature of deception instructions. Conclusions Sustained amygdala time course during anticipation may uniquely reflect heightened detection of threat or deficits in emotion regulation in socially anxious individuals. Findings highlight the importance of examining temporal dynamics of amygdala responding.

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CD38 genetic variation has been associated with autism spectrum disorders and social anxiety disorder, which may result from CD38's regulation of oxytocin secretion. Converging evidence has found that the rs3796863 A-allele contributes to increased social sensitivity compared to the CC genotype. The current study examined the moderating role of CD38 genetic variants (rs3796863 and rs6449182) that have been associated with enhanced (or reduced) social sensitivity on neural activation related to neuroticism, which is commonly elevated in individuals with social anxiety and depression. Adults (n = 72) with varying levels of social anxiety and depression provided biological samples for DNA extraction, completed a measure of neuroticism, and participated in a standardized emotion processing task (affect matching) while undergoing fMRI. A significant interaction effect was found for rs3796863 x neuroticism that predicted right amygdala-subgenual anterior cingulate cortex (sgACC) functional connectivity. Simple slopes analyses showed a positive association between neuroticism and right amygdala-sgACC connectivity among rs3796863 A-allele carriers. Findings suggest that the more socially sensitive rs3796863 A-allele may partially explain the relationship between a known risk factor (i.e., neuroticism) and promising biomarker (i.e., amygdala-sgACC connectivity) in the development and maintenance of social anxiety and depression.

Self-referential processing is critical to understanding social anxiety disorder (SAD). This study examined neural differences in self-referential processing in healthy controls (HC) and participants with SAD at pre-and post-treatment. Participants (n = 64) underwent fMRI scanning while