Revising the Intolerance of Uncertainty Model of Generalized Anxiety Disorder: Evidence from UK and Italian Undergraduate Samples

The Intolerance of Uncertainty Model (IUM) of Generalized Anxiety Disorder (GAD) attributes a key role to Intolerance of Uncertainty (IU), and additional roles to Positive Beliefs about Worry (PBW), Negative Problem Orientation (NPO), and Cognitive Avoidance (CA), in the development and maintenance of worry, the core feature of GAD. Despite the role of the IUM components in worry and GAD has been considerably demonstrated, to date no studies have explicitly assessed whether and how PBW, NPO, and CA might turn IU into worry and somatic anxiety. The current studies sought to re-examine the IUM by assessing the relationships between the model’s components on two different non-clinical samples made up of UK and Italian undergraduate students. One-hundred and seventy UK undergraduates and 488 Italian undergraduates completed measures assessing IU, worry, somatic anxiety, depression, and refined measures of PBW, NPO, and CA. In each sample, two mediation models were conducted in order to test whether PBW, NPO, and CA differentially mediate the path from IU to worry and the path from IU to somatic anxiety. Secondly, it was tested whether IU also moderates the mediations. Main findings showed that, in the UK sample, only NPO mediated the path from IU to worry; as far as concern the path to anxiety, none of the putative mediators was significant. Differently, in the Italian sample PBW and NPO were mediators in the path from IU to worry, whereas only CA played a mediational role in the path from IU to somatic anxiety. Lastly, IU was observed to moderate only the association between NPO and worry, and only in the Italian sample. Some important cross-cultural, conceptual, and methodological issues raised from main results are discussed

Anxiety: An Evolutionary Approach

Anxiety disorders are among the most common mental illnesses, with huge attendant suffering. Current treatments are not universally effective, suggesting that a deeper understanding of the causes of anxiety is needed. To understand anxiety disorders better, it is first necessary to understand the normal anxiety response. This entails considering its evolutionary function as well as the mechanisms underlying it. We argue that the function of the human anxiety response, and homologues in other species, is to prepare the individual to detect and deal with threats. We use a signal detection framework to show that the threshold for expressing the anxiety response ought to vary with the probability of threats occurring, and the individual's vulnerability to them if they do occur. These predictions are consistent with major patterns in the epidemiology of anxiety. Implications for research and treatment are discussed

Anger: the unrecognized emotion in emotional disorders

Anger plays a prominent definitional role in some psychological disorders currently widely scattered across DSM‐5 categories (e.g., intermittent explosive disorder, borderline personality disorder). But the presence and consequences of anger in the emotional disorders (e.g., anxiety disorders, depressive disorders) remain sparsely examined. In this review, we examine the presence of anger in the emotional disorders and find that anger is elevated across these disorders and, when it is present, is associated with negative consequences, including greater symptom severity and worse treatment response. Based on this evidence, anger appears to be an important and understudied emotion in the development, maintenance, and treatment of emotional disorders.First author draf

Addressing neuroticism in psychological treatment

Neuroticism has long been associated with psychopathology and there is increasing evidence that this trait represents a shared vulnerability responsible for the development and maintenance of a range of common mental disorders. Given that neuroticism may be more malleable than previously thought, targeting this trait in treatment, rather than its specific manifestations (e.g., anxiety, mood, and personality disorders), may represent a more efficient and cost-effective approach to psychological treatment. The goals of the current manuscript are to (a) review the role of neuroticism in the development of common mental disorders, (b) describe the evidence of its malleability, and (c) review interventions that have been explicitly developed to target this trait in treatment. Implications for shifting the focus of psychological treatment to underlying vulnerabilities, such as neuroticism, rather than on the manifest symptoms of mental health conditions, are also discussed.First author draf

Error-related brain activity as a transdiagnostic endophenotype for obsessive-compulsive disorder, anxiety and substance use disorder

Background Increased neural error-signals have been observed in obsessive-compulsive disorder (OCD), anxiety disorders, and inconsistently in depression. Reduced neural error-signals have been observed in substance use disorders (SUD). Thus, alterations in error-monitoring are proposed as a transdiagnostic endophenotype. To strengthen this notion, data from unaffected individuals with a family history for the respective disorders are needed. Methods The error-related negativity (ERN) as a neural indicator of error-monitoring was measured during a flanker task from 117 OCD patients, 50 unaffected first-degree relatives of OCD patients, and 130 healthy comparison participants. Family history information indicated, that 76 healthy controls were free of a family history for psychopathology, whereas the remaining had first-degree relatives with depression (n = 28), anxiety (n = 27), and/or SUD (n = 27). Results Increased ERN amplitudes were found in OCD patients and unaffected first-degree relatives of OCD patients. In addition, unaffected first-degree relatives of individuals with anxiety disorders were also characterized by increased ERN amplitudes, whereas relatives of individuals with SUD showed reduced amplitudes. Conclusions Alterations in neural error-signals in unaffected first-degree relatives with a family history of OCD, anxiety, or SUD support the utility of the ERN as a transdiagnostic endophenotype. Reduced neural error-signals may indicate vulnerability for under-controlled behavior and risk for substance use, whereas a harm- or error-avoidant response style and vulnerability for OCD and anxiety appears to be associated with increased ERN. This adds to findings suggesting a common neurobiological substrate across psychiatric disorders involving the anterior cingulate cortex and deficits in cognitive control

Understanding vulnerability for depression from a cognitive neuroscience perspective: a reappraisal of attentional factors and a new conceptual framework

We propose a framework to understand increases in vulnerability for depression after recurrent episodes that links attention processes and schema activation to negative mood states, by integrating cognitive and neurobiological findings. Depression is characterized by a mood-congruent attentional bias at later stages of information processing. The basic idea of our framework is that decreased activity in prefrontal areas, mediated by the serotonin metabolism which the HPA axis controls, is associated with an impaired attenuation of subcortical regions, resulting in prolonged activation of the amygdala in response to stressors in the environment. Reduced prefrontal control in interaction with depressogenic schemas leads to impaired ability to exert attentional inhibitory control over negative elaborative processes such as rumination, leading in turn to sustained negative affect. These elaborative processes are triggered by the activation of negative schemas after confrontation with stressors. In our framework, attentional impairments are postulated as a crucial process in explaining the increasing vulnerability after depressive episodes, linking cognitive and biological vulnerability factors. We review the empirical data on the biological factors associated with the attentional impairments and detail how they are associated with rumination and mood regulation. The aim of our framework is to stimulate translational research

Examining hope as a transdiagnostic mechanism of change across anxiety disorders and CBT treatment protocols.

Hope is a trait that represents the capacity to identify strategies or pathways to achieve goals and the motivation or agency to effectively pursue those pathways. Hope has been demonstrated to be a robust source of resilience to anxiety and stress and there is limited evidence that, as has been suggested for decades, hope may function as a core process or transdiagnostic mechanism of change in psychotherapy. The current study examined the role of hope in predicting recovery in a clinical trial in which 223 individuals with 1 of 4 anxiety disorders were randomized to transdiagnostic cognitive behavior therapy (CBT), disorder-specific CBT, or a waitlist controlled condition. Effect size results indicated moderate to large intraindividual increases in hope, that changes in hope were consistent across the five CBT treatment protocols, that changes in hope were significantly greater in CBT relative to waitlist, and that changes in hope began early in treatment. Results of growth curve analyses indicated that CBT was a robust predictor of trajectories of change in hope compared to waitlist, and that changes in hope predicted changes in both self-reported and clinician-rated anxiety. Finally, a statistically significant indirect effect was found indicating that the effects of treatment on changes in anxiety were mediated by treatment effects on hope. Together, these results suggest that hope may be a promising transdiagnostic mechanism of change that is relevant across anxiety disorders and treatment protocols.R01 MH090053 - NIMH NIH HHSAccepted manuscrip

Resting state correlates of subdimensions of anxious affect

Resting state fMRI may help identify markers of risk for affective disorder. Given the comorbidity of anxiety and depressive disorders and the heterogeneity of these disorders as defined by DSM, an important challenge is to identify alterations in resting state brain connectivity uniquely associated with distinct profiles of negative affect. The current study aimed to address this by identifying differences in brain connectivity specifically linked to cognitive and physiological profiles of anxiety, controlling for depressed affect. We adopted a two-stage multivariate approach. Hierarchical clustering was used to independently identify dimensions of negative affective style and resting state brain networks. Combining the clustering results, we examined individual differences in resting state connectivity uniquely associated with subdimensions of anxious affect, controlling for depressed affect. Physiological and cognitive subdimensions of anxious affect were identified. Physiological anxiety was associated with widespread alterations in insula connectivity, including decreased connectivity between insula subregions and between the insula and other medial frontal and subcortical networks. This is consistent with the insula facilitating communication between medial frontal and subcortical regions to enable control of physiological affective states. Meanwhile, increased connectivity within a frontoparietal-posterior cingulate cortex-precunous network was specifically associated with cognitive anxiety, potentially reflecting increased spontaneous negative cognition (e.g., worry). These findings suggest that physiological and cognitive anxiety comprise subdimensions of anxiety-related affect and reveal associated alterations in brain connectivity