Transdiagnostic phenotypes of compulsive behavior and associations with psychological, cognitive, and neurobiological affective processing

Compulsivity is a poorly understood transdiagnostic construct thought to underlie multiple disorders, including obsessive-compulsive disorder, addictions, and binge eating. Our current understanding of the causes of compulsive behavior remains primarily based on investigations into specific diagnostic categories or findings relying on one or two laboratory measures to explain complex phenotypic variance. This proof-of-concept study drew on a heterogeneous sample of community-based individuals (N = 45; 18–45 years; 25 female) exhibiting compulsive behavioral patterns in alcohol use, eating, cleaning, checking, or symmetry. Data-driven statistical modeling of multidimensional markers was utilized to identify homogeneous subtypes that were independent of traditional clinical phenomenology. Markers were based on well-defined measures of affective processing and included psychological assessment of compulsivity, behavioral avoidance, and stress, neurocognitive assessment of reward vs. punishment learning, and biological assessment of the cortisol awakening response. The neurobiological validity of the subtypes was assessed using functional magnetic resonance imaging. Statistical modeling identified three stable, distinct subtypes of compulsivity and affective processing, which we labeled “Compulsive Non-Avoidant”, “Compulsive Reactive” and “Compulsive Stressed”. They differed meaningfully on validation measures of mood, intolerance of uncertainty, and urgency. Most importantly, subtypes captured neurobiological variance on amygdala-based resting-state functional connectivity, suggesting they were valid representations of underlying neurobiology and highlighting the relevance of emotion-related brain networks in compulsive behavior. Although independent larger samples are needed to confirm the stability of subtypes, these data offer an integrated understanding of how different systems may interact in compulsive behavior and provide new considerations for guiding tailored intervention decisions.

How to Catch Customers’ Attention? A Study on the Effectiveness of Brand Social Media Strategies in Digital Customer Engagement

Enterprises often post branded content on social media and adopt a proactive response approach to improve digital customer engagement to gain a competitive advantage. However, there are many brands which fail to operate social media as effectively as expected. The effective use of brand social media strategies to improve digital customer engagement remains an ongoing challenge for the enterprises. Based on firm-generated content theory and social presence theory, this study aims to identify the impact of brand social media strategies on different levels of digital customer engagement, including positive filtering, cognitive and affective processing as well as advocacy from content strategy and response strategy. Based on 1,519 brand posts on the official Weibo pages of eight of the top 500 Chinese brands in 2021, this study uses a multiple linear regression model to examine the impact of brand social media strategies on digital customer engagement and the moderating effects of brand image and discretionary purchases. The findings show that, on the one hand, among the brand social media content strategies, action content strategy is associated with higher levels of digital customer engagement. On the other hand, different brand social media response strategies have a differential impact on digital customer engagement levels, with cohesive response being the best strategy for increasing digital customer engagement level. In addition, the effectiveness of brand social media response strategy in digital customer engagement is further moderated by the brand image and discretionary purchases. In contrast, the effectiveness of brand social media response strategy in digital customer engagement is stronger when the brand image emphasizes its “competence” or the discretionary purchases focus on “material purchases.” This study not only enriches the research on digital customer engagement but also provides a reference for the brand strategy selection, design and management based on social media.

Alcohol and the dysregulation of cognitive control: Exploring the role of emotion

<p>Alcohol consumption attenuates both the behavioural adjustments and the heightened activity in the anterior cingulate cortex (ACC) which are normally observed following errors, leading to the hypothesis that alcohol disrupts the ability to effectively regulate the use of cognitive control. It has furthermore been theorized that these deficits may occur because alcohol reduces the negative affect elicited by unfavourable events, such as errors, thereby weakening the motivation to utilize cognitive control to improve performance. The aim of the current thesis was to provide an empirical test of this model. I carried out two studies in which I examined changes in two physiological indices of affective processing, skin conductance and heart rate, as well as behavioural and EEG responses, following errors on a flanker task. The first study was conducted on sober participants, in order to validate my experimental paradigm, while the second compared the physiological and behavioural effects of errors in participants given either alcohol or a placebo. In both experiments in both experiments, errors produced increased skin conductance responses and heart rate deceleration, and a typical error-related negativity in EEG. However, contrary to what would be expected if alcohol reduced the negative affect generated by errors, no difference in skin conductance or heart rate responses to errors were observed between alcohol and placebo participants in the second study. Furthermore, although intoxicated participants displayed an overall reduction in the use of cognitive control, based on both behavioural (flanker interference) and EEG (occipital alpha power) measures, groups did not differ in the degree to which this control was upregulated immediately after task errors. However, exploratory analyses of EEG indices (the feedback-related negativity and midfrontal theta power) of ACC activity following errors were significantly diminished in intoxicated participants. Overall, these findings suggest that alcohol does not reduce the immediate negative emotional consequences of errors but may instead disrupt brain networks needed for the sustained engagement of cognitive control and attention to task performance.</p>

Alcohol and the dysregulation of cognitive control: Exploring the role of emotion

<p>Alcohol consumption attenuates both the behavioural adjustments and the heightened activity in the anterior cingulate cortex (ACC) which are normally observed following errors, leading to the hypothesis that alcohol disrupts the ability to effectively regulate the use of cognitive control. It has furthermore been theorized that these deficits may occur because alcohol reduces the negative affect elicited by unfavourable events, such as errors, thereby weakening the motivation to utilize cognitive control to improve performance. The aim of the current thesis was to provide an empirical test of this model. I carried out two studies in which I examined changes in two physiological indices of affective processing, skin conductance and heart rate, as well as behavioural and EEG responses, following errors on a flanker task. The first study was conducted on sober participants, in order to validate my experimental paradigm, while the second compared the physiological and behavioural effects of errors in participants given either alcohol or a placebo. In both experiments in both experiments, errors produced increased skin conductance responses and heart rate deceleration, and a typical error-related negativity in EEG. However, contrary to what would be expected if alcohol reduced the negative affect generated by errors, no difference in skin conductance or heart rate responses to errors were observed between alcohol and placebo participants in the second study. Furthermore, although intoxicated participants displayed an overall reduction in the use of cognitive control, based on both behavioural (flanker interference) and EEG (occipital alpha power) measures, groups did not differ in the degree to which this control was upregulated immediately after task errors. However, exploratory analyses of EEG indices (the feedback-related negativity and midfrontal theta power) of ACC activity following errors were significantly diminished in intoxicated participants. Overall, these findings suggest that alcohol does not reduce the immediate negative emotional consequences of errors but may instead disrupt brain networks needed for the sustained engagement of cognitive control and attention to task performance.</p>

The role of the SLC6A3 3’ UTR VNTR in nicotine effects on cognitive, affective, and motor function

Rationale Nicotine has been widely studied for its pro-dopaminergic effects. However, at the behavioural level, past investigations have yielded heterogeneous results concerning effects on cognitive, affective, and motor outcomes, possibly linked to individual differences at the level of genetics. A candidate polymorphism is the 40-base-pair variable number of tandem repeats polymorphism (rs28363170) in the SLC6A3 gene coding for the dopamine transporter (DAT). The polymorphism has been associated with striatal DAT availability (9R-carriers > 10R-homozygotes), and 9R-carriers have been shown to react more strongly to dopamine agonistic pharmacological challenges than 10R-homozygotes. Objectives In this preregistered study, we hypothesized that 9R-carriers would be more responsive to nicotine due to genotype-related differences in DAT availability and resulting dopamine activity. Methods N=194 non-smokers were grouped according to their genotype (9R-carriers, 10R-homozygotes) and received either 2-mg nicotine or placebo gum in a between-subject design. Spontaneous blink rate (SBR) was obtained as an indirect measure of striatal dopamine activity and smooth pursuit, stop signal, simple choice and affective processing tasks were carried out in randomized order. Results Reaction times were decreased under nicotine compared to placebo in the simple choice and stop signal tasks, but nicotine and genotype had no effects on any of the other task outcomes. Conditional process analyses testing the mediating effect of SBR on performance and how this is affected by genotype yielded no significant results. Conclusions Overall, we could not confirm our main hypothesis. Individual differences in nicotine response could not be explained by rs28363170 genotype.

The Interplay Between Affective Processing and Sense of Agency During Action Regulation: A Review

Sense of agency is the feeling of being in control of one's actions and their perceivable effects. Most previous research identified cognitive or sensory determinants of agency experience. However, it has been proposed that sense of agency is also bound to the processing of affective information. For example, during goal-directed actions or instrumental learning we often rely on positive feedback (e.g., rewards) or negative feedback (e.g., error messages) to determine our level of control over the current task. Nevertheless, we still lack a scientific model which adequately explains the relation between affective processing and sense of agency. In this article, we review current empirical findings on how affective information modulates agency experience, and, conversely, how sense of agency changes the processing of affective action outcomes. Furthermore, we discuss in how far agency-related changes in affective processing might influence the ability to enact cognitive control and action regulation during goal-directed behavior. A preliminary model is presented for describing the interplay between sense of agency, affective processing, and action regulation. We propose that affective processing could play a role in mediating the influence between subjective sense of agency and the objective ability to regulate one's behavior. Thus, determining the interrelation between affective processing and sense of agency will help us to understand the potential mechanistic basis of agency experience, as well as its functional significance for goal-directed behavior.

The development of depressogenic self-schemas: Associations with children's regional grey matter volume in ventrolateral prefrontal cortex

Cognitive theories of depression contend that biased cognitive information processing plays a causal role in the development of depression. Extensive research shows that deeper processing of negative and/or shallower processing of positive self-descriptors (i.e., negative and positive self-schemas) predicts current and future depression in adults and children. However, the neural correlates of the development of self-referent encoding are poorly understood. We examined children's self-referential processing using the self-referent encoding task (SRET) collected from 74 children at ages 6, 9, and 12; around age 10, these children also contributed structural magnetic resonance imaging data. From age 6 to age 12, both positive and negative self-referential processing showed mean-level growth, with positive self-schemas increasing relatively faster than negative ones. Further, voxel-based morphometry showed that slower growth in positive self-schemas was associated with lower regional gray matter volume (GMV) in ventrolateral prefrontal cortex (vlPFC). Our results suggest that smaller regional GMV within vlPFC, a critical region for regulatory control in affective processing and emotion development, may have implications for the development of depressogenic self-referential processing in mid-to-late childhood.