clinicaltrials.gov Identifier: NCT01243606.

This study further evaluates the efficacy of the Unified Protocol for Transdiagnostic Treatment of Emotional Disorders (UP). A diagnostically heterogeneous clinical sample of 37 patients with a principal anxiety disorder diagnosis was enrolled in a randomized controlled trial (RCT) involving up to 18 sessions of treatment and a 6-month follow-up period. Patients were randomly assigned to receive either immediate treatment with the UP (n=26) or delayed treatment, following a 16-week wait-list control period (WLC; n= 11). The UP resulted in significant improvement on measures of clinical severity, general symptoms of depression and anxiety, levels of negative and positive affect, and a measure of symptom interference in daily functioning across diagnoses. In comparison, participants in the WLC condition exhibited little to no change following the 16-week wait-list period. The effects of UP treatment were maintained over the 6-month follow-up period. Results from this RCT provide additional evidence for the efficacy of the UP in the treatment of anxiety and comorbid depressive disorders, and provide additional support for a transdiagnostic approach to the treatment of emotional disorders.

We highlight the role of neuroticism in the development and course of emotional disorders and make a case for shifting the focus of intervention to this higher-order dimension of personality. Recent decades have seen great emphasis placed on differentiating disorders into Diagnostic and Statistical Manual of Mental Disorders diagnoses; however, evidence has suggested that splitting disorders into such fine categories may be highlighting relatively trivial differences. Emerging research on the latent structure of anxiety and mood disorders has indicated that trait neuroticism, cultivated through genetic, neurobiological, and psychological factors, underscores the development of these disorders. We raise the possibility of a new approach for conceptualizing these disorders-as emotional disorders. From a service-delivery point of view, we explore the possibility that neuroticism may be more malleable than previously thought and may possibly be amenable to direct intervention. The public-health implications of directly treating and even preventing the development of neuroticism would be substantial.

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The need to capture severity and impairment of depressive symptomatology is widespread. Existing depression scales are lengthy and largely focus on individual symptoms rather than resulting impairment. The Overall Depression Severity and Impairment Scale (ODSIS) is a 5-item, continuous measure designed for use across heterogeneous mood disorders and with subthreshold depressive symptoms. This study examined the psychometric properties of the ODSIS in outpatients in a clinic for emotional disorders (N = 100), undergraduate students (N = 566), and community-based adults (N = 189). Internal consistency, latent structure, item response theory, classification accuracy, convergent and discriminant validity, and differential item functioning analyses were conducted. ODSIS scores exhibited excellent internal consistency, and confirmatory factor analyses supported a unidimensional structure. Item response theory results demonstrated that the ODSIS provides more information about individuals with high levels of depression than those with low levels of depression. Responses on the ODSIS discriminated well between individuals with and without a mood disorder and depression-related severity across clinical and subclinical levels. A cut score of 8 correctly classified 82% of outpatients as with or without a mood disorder; it evidenced a favorable balance of sensitivity and specificity and of positive and negative predictive values. The ODSIS demonstrated good convergent and discriminant validity, and results indicate that items function similarly across clinical and nonclinical samples. Overall, findings suggest that the ODSIS is a valid tool for measuring depression-related severity and impairment. The brevity and ease of use of the ODSIS support its utility for screening and monitoring treatment response across a variety of settings.

In this article, we provide a fresh perspective on the developmental origins of neuroticism--a dimension of temperament marked by elevated stress reactivity resulting in the frequent experience of negative emotions. This negative affectivity is accompanied by a pervasive perception that the world is a dangerous and threatening place, along with beliefs about one's inability to manage or cope with challenging events. Historically, neuroticism has been viewed as a stable, genetically based trait. However, recent understanding of ongoing gene-environment interactions that occur throughout the life span suggests there may be a more complex and dynamic etiology. Thus, the purpose of this article is to offer a theory for understanding the development of neuroticism that integrates genetic, neurobiological, and environmental contributions to this trait. Given the strong correlation between neuroticism and the development of negative health outcomes--most notably, the full range of anxiety and mood disorders--an enhanced understanding of how neuroticism originates has implications for the treatment and prevention of a broad range of pathologies and, perhaps, even for the prevention of neuroticism itself.

Non-human animal studies demonstrate relationships between stress and selective intake of palatable food. In humans, exposure to laboratory stressors and self-reported stress are associated with greater food intake. Large studies have yet to examine chronic stress exposure and eating behavior. The current study assessed the relationship between stress (perceived and chronic), drive to eat, and reported food frequency intake (nutritious food vs. palatable non-nutritious food) in women ranging from normal weight to obese (N = 457). Greater reported stress, both exposure and perception, was associated with indices of greater drive to eat— including feelings of disinhibited eating, binge eating, hunger, and more ineffective attempts to control eating (rigid restraint; r’s from .11 to .36, p ’s < .05). These data suggest that stress exposure may lead to a stronger drive to eat and may be one factor promoting excessive weight gain. Relationships between stress and eating behavior are of importance to public health given the concurrent increase in reported stress and obesity rates.