Search

Application of emotion regulation strategies might be susceptible to the context of social rejection for individuals with borderline personality disorder (BPD). This study compared the ability of 27 outpatient youths (15-25 years old) with early-stage BPD and 37 healthy controls (HC) to apply expressive suppression and cognitive reappraisal in standard and socially rejecting laboratory contexts. BPD youths were largely as able as HCs to regulate negative affect across instruction and contexts. However, cognitive reappraisal in the context of social rejection heightened BPD negative facial expression relative to HCs. Thus, while BPD emotion regulation ability was largely normative, cognitive reappraisal might be ineffective in the context of social rejection for this group, with social rejection acting as an accelerant that heightens the expression of negative affect. Given the common experience of perceived and actual social rejection for this group, clinicians should carefully consider treatments that include cognitive reappraisal strategies because they might be contraindicated.

Background: Alcohol intoxication disrupts many aspects of cognition, including the generation of phenomenological characteristics of future events (a component of episodic foresight), and the execution of directed preparatory behaviours (a component of prospective memory). However, no study has tested whether alcohol intoxication is also associated with deficits engaging episodic foresight to guide future-directed behaviour. Aims: This study was designed to provide the first test of how alcohol intoxication influences the functional application of episodic foresight. The secondary aim was to establish the degree to which any observed episodic foresight difficulties associated with alcohol use might reflect broader problems in retrospective memory and executive control. Sex differences were also examined. Methods: Healthy adult social drinkers randomly received either a moderate dose of 0.6 g/kg alcohol ( n = 61) or a matched placebo drink ( n = 63) and then completed a validated measure that met strict criteria for assessing the functional application of episodic foresight as well as a broader cognitive test battery. Results: Relative to the placebo condition, episodic foresight was impaired by acute alcohol consumption, with this impairment related to poorer retrospective memory, but not executive control. The negative effects of alcohol intoxication on episodic foresight did not differ as a function of sex. Conclusions: Even a moderate level of intoxication impairs the ability to use episodic foresight in a functionally adaptive way. These findings have implications for understanding many of the maladaptive behaviours that are often associated with acute alcohol use.

Rationale Acute alcohol consumption adversely affects many cognitive abilities, including episodic memory and executive functioning. However, no study to date has tested whether these acute effects of alcohol also extend to episodic future thinking (EFT). This is a surprising omission given that EFT refers to the ability to imagine oneself experiencing the future, a highly adaptive ability that has been implicated in many important functional behaviours. EFT is also thought to impose demands on episodic memory and executive control. Objectives The current study was designed to provide the first test of whether a moderate dose of alcohol influences EFT and whether any observed EFT difficulties are secondary to broader problems in episodic memory and executive functioning. Sex differences in EFT following acute alcohol consumption were also examined. Methods One hundred and twenty-four healthy adult social drinkers were recruited and randomly assigned to either the alcohol (n = 61) or placebo (n = 63) condition. Participants were administered a dose of 0.6 g/kg alcohol or a matched placebo drink. Results Relative to the placebo condition, EFT was impaired by acute alcohol consumption. This impairment was underpinned by broader difficulties with episodic memory, but not executive functioning. There were no sex differences in EFT performance following acute alcohol use. Conclusion These data provide novel insights into the effects of acute alcohol consumption on EFT and the broader cognitive mechanisms that contribute to these difficulties. The results are discussed in relation to their implications for understanding many of the maladaptive behaviours commonly associated with acute alcohol use.

BackgroundSocial anxiety disorder (SAD) is a prevalent and disabling mental health condition, characterized by excessive fear and anxiety in social situations. Resting-state functional magnetic resonance imaging (fMRI) paradigms have been increasingly used to understand the neurobiological underpinnings of SAD in the absence of threat-related stimuli. Previous studies have primarily focused on the role of the amygdala in SAD. However, the amygdala consists of functionally and structurally distinct subregions, and recent studies have highlighted the importance of investigating the role of these subregions independently.MethodUsing multiband fMRI, we analyzed resting-state data from 135 participants (42 SAD, 93 healthy controls). By employing voxel-wise permutation testing, we examined group differences of fMRI connectivity and associations between fMRI connectivity and social anxiety symptoms to further investigate the classification of SAD as a categorical or dimensional construct.ResultsSeed-to-whole brain functional connectivity analysis using multiple ‘seeds’ including the amygdala and its subregions and the precuneus, revealed no statistically significant group differences. However, social anxiety severity was significantly negatively correlated with functional connectivity of the precuneus - perigenual anterior cingulate cortex and positively correlated with functional connectivity of the amygdala (specifically the superficial subregion) - parietal/cerebellar areas.ConclusionOur findings demonstrate clear links between symptomatology and brain connectivity in the absence of diagnostic differences, with evidence of amygdala subregion-specific alterations. The observed brain-symptom associations did not include disturbances in the brain’s fear circuitry (i.e., disturbances in connectivity between amygdala - prefrontal regions) likely due to the absence of threat-related stimuli.