Christopher P. Fairholme

Unified protocol for transdiagnostic treatment of emotional disorders: a randomized controlled trial.

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.

Sleep disturbance and emotion dysregulation as transdiagnostic processes in a comorbid sample

Sleep disturbance and emotion dysregulation have been identified as etiologic and maintaining factors for a range of psychopathology and separate literatures support their relationships to anxiety, depression, PTSD, and alcohol dependence (AD) symptom severity. Previous studies have examined these relationships in isolation, failing to account for the high rates of comorbidity among disorders. It is not yet known whether these processes uniquely predict symptom severity in each of these domains. Participants were 220 patients in residential substance abuse treatment, who had experienced a potentially traumatic event and exceeded screening cutoffs for probable PTSD and problematic alcohol use. Controlling for emotion dysregulation and the interrelationships among the outcome variables, insomnia was uniquely associated with anxiety (B = .27, p < .001), depression (B = .25, p < .001), PTSD (B = .22, p < .001), and AD (B = .17, p = .01) symptom severity. Similarly, controlling for insomnia, emotion dysregulation was uniquely associated with anxiety (B = .40, p < .001), depression (B = .47, p < .001), PTSD (B = .38, p < .001), and AD (B = .26, p < .001) symptom severity. Insomnia and emotion dysregulation appear to be transdiagnostic processes uniquely associated with symptom severity across a number of different domains and might be important treatment targets for individuals with PTSD and AD.

Who is at risk for having persistent insomnia symptoms? A longitudinal study in the general population in Korea☆

OBJECTIVES Our study had three goals: (1) to investigate the longitudinal course of insomnia symptoms over 4 years (3 time points) by analyzing the trajectory of insomnia symptoms for all participants, (2) to compare persistent insomnia symptom to nonpersistent insomnia symptom groups on mental health and quality of life (QoL), and (3) to conduct exploratory analyses on the relative contribution of multiple factors to persistence of insomnia symptoms. METHODS Our population-based longitudinal study utilized a community-based sample from the Korean Genome and Epidemiology study (KoGES). Participants were 1247 individuals (40.1% men; mean age, 54.3±7.1 years). Insomnia, QoL (measured by 12-item Short-Form health survey [SF-12]), sleep-interfering behaviors, and depression (measured by the Beck Depression Inventory [BDI]) were followed with biennial examinations at 3 data points spaced 2 years apart (baseline, time 1, and time 2). RESULTS Among individuals experiencing insomnia symptoms at baseline, the most common trajectory was to experience persistent nocturnal insomnia symptoms across all 3 time points. Those with persistent insomnia symptoms had significantly lower physical and mental QoL (measured by SF-12) and higher depression (measured by BDI) at time points compared to those without persistent nocturnal insomnia symptoms. A follow-up exploratory receiver operating characteristic curve (ROC) analysis identified poor sleep quality, frequent sleep-interfering behaviors, and low mental health QoL as the strongest predictors of persistent insomnia symptoms above other well-known risk factors. CONCLUSIONS In particular, an interaction between poor sleep quality, sleep-interfering behaviors, and mental health QoL appeared to be the strongest risk factor for persistent insomnia symptoms.

Transdiagnostic processes in emotional disorders and insomnia: results from a sample of adult outpatients with anxiety and mood disorders.

Conceptual similarities between recent models of insomnia and emotional disorders suggest there may be common factors that underlie or maintain these difficulties. Maladaptive cognitive and behavioral processes similar to those described in connection with emotional disorders have been cited as key mechanisms in the maintenance of primary insomnia. Unfortunately, research on this potential overlap is lacking. The present study examined the relationship among anxiety sensitivity (AS), dysfunctional beliefs, fatigue, safety behaviors, and insomnia severity in 59 outpatients with anxiety and mood disorders. Key insomnia processes (dysfunctional beliefs, fatigue, safety behaviors) were all related to insomnia severity in the comorbid sample, although AS was not. However, as hypothesized, AS did moderate the relationship of both dysfunctional beliefs and fatigue with insomnia severity. The relationships between key insomnia processes and insomnia severity was strongest among individuals high in AS. Results support the hypothesis that common mechanisms are involved for insomnia and emotional disorders. AS might function as a mechanism for the maintenance of sleep disturbance in the context of anxiety and mood disorders, suggesting a promising avenue for future research.

The temporal course of anxiety sensitivity in outpatients with anxiety and mood disorders: Relationships with behavioral inhibition and depression

The present study evaluated the temporal course of three dimensions of anxiety sensitivity (AS; concerns over physical symptoms, mental incapacitation, and social embarrassment) and their relationships with behavioral inhibition (BI) and depression (DEP) in 606 outpatients with anxiety and mood disorders. A semi-structured interview and self-report questionnaires were administered on three occasions over a two-year period. All three constructs decreased over the study period and AS temporally functioned more similar to DEP than BI. Cross-sectional and temporal correlations supported the discriminant validity of AS from BI. As expected, initial levels of BI predicted less improvement in all AS dimensions. In contrast, higher initial levels of mental incapacitation AS were associated with greater improvement in DEP. Our results are discussed in regard to the measurement of AS in clinical samples, conceptualizations of AS as a lower-order vulnerability, and prognostic implications of directional paths between BI and AS and AS and DEP.

Sleep, Emotions, and Emotion Regulation: An Overview

Abstract This chapter discusses the relationship between sleep and emotional functioning in the absence of psychopathology. Research evaluating the impact of sleep on emotional functioning supports associations between deficient sleep and reduced positive affect, increased negative affect, and increased difficulties with emotion regulation. Research evaluating the impact of emotions on sleep suggests that the negative valence and high arousal dimensions of emotion are similarly associated with increased sleep latency and fragmentation and decreased sleep quality and total sleep time. However, negative valence and high arousal potentially have unique effects on sleep architecture, with high arousal being associated with reductions in slow-wave sleep and negative valence being associated with disruptions to REM sleep. Moreover, individual differences in emotion regulation also impact sleep parameters, above and beyond the influence of current emotions. The chapter discusses implications of this research, highlighting future directions for improving our understanding of the dynamic relationship between sleep and emotional functioning.This chapter discusses the relationship between sleep and emotional functioning in the absence of psychopathology. Research evaluating the impact of sleep on emotional functioning supports associations between deficient sleep and reduced positive affect, increased negative affect, and increased difficulties with emotion regulation. Research evaluating the impact of emotions on sleep suggests that the negative valence and high arousal dimensions of emotion are similarly associated with increased sleep latency and fragmentation and decreased sleep quality and total sleep time. However, negative valence and high arousal potentially have unique effects on sleep architecture, with high arousal being associated with reductions in slow-wave sleep and negative valence being associated with disruptions to REM sleep. Moreover, individual differences in emotion regulation also impact sleep parameters, above and beyond the influence of current emotions. The chapter discusses implications of this research, highlighting future directions for improving our understanding of the dynamic relationship between sleep and emotional functioning.

Safety behaviors and sleep effort predict sleep disturbance and fatigue in an outpatient sample with anxiety and depressive disorders

OBJECTIVE Theoretical and empirical support for the role of dysfunctional beliefs, safety behaviors, and increased sleep effort in the maintenance of insomnia has begun to accumulate. It is not yet known how these factors predict sleep disturbance and fatigue occurring in the context of anxiety and mood disorders. It was hypothesized that these three insomnia-specific cognitive-behavioral factors would be uniquely associated with insomnia and fatigue among patients with emotional disorders after adjusting for current symptoms of anxiety and depression and trait levels of neuroticism and extraversion. METHODS Outpatients with a current anxiety or mood disorder (N = 63) completed self-report measures including the Dysfunctional Beliefs About Sleep Scale (DBAS), Sleep-Related Safety Behaviors Questionnaire (SRBQ), Glasgow Sleep Effort Scale (GSES), Pittsburgh Sleep Quality Index (PSQI), NEO Five-Factor Inventory (FFI), and the 21-item Depression Anxiety and Stress Scale (DASS). Multivariate path analysis was used to evaluate study hypotheses. RESULTS SRBQ (B = .60, p < .001, 95% CI [.34, .86]) and GSES (B = .31, p < .01, 95% CI [.07, .55]) were both significantly associated with PSQI. There was a significant interaction between SRBQ and DBAS (B = .25, p < .05, 95% CI [.04, .47]) such that the relationship between safety behaviors and fatigue was strongest among individuals with greater levels of dysfunctional beliefs. CONCLUSION Findings are consistent with cognitive behavioral models of insomnia and suggest that sleep-specific factors might be important treatment targets among patients with anxiety and depressive disorders with disturbed sleep.

Are Patients with Childhood Onset of Insomnia and Depression More Difficult to Treat Than Are Those with Adult Onsets of These Disorders? A Report from the TRIAD Study

STUDY OBJECTIVES To determine if patients with childhood onsets (CO) of both major depression and insomnia disorder show blunted depression and insomnia treatment responses to concurrent interventions for both disorders compared to those with adult onsets (AO) of both conditions. METHODS This study was a secondary analysis of data obtained from a multisite randomized clinical trial designed to test the efficacy of combining a psychological/behavior insomnia therapy with antidepressant medication to enhance depression treatment outcomes in patients with comorbid major depression and insomnia. This study included 27 adults with CO of depression and insomnia and 77 adults with AO of both conditions. They underwent a 16-week treatment including: (1) a standardized two-step pharmacotherapy for depression algorithm, consisting of escitalopram, sertraline, and desvenlafaxine in a prescribed sequence; and (2) either cognitive behavioral insomnia therapy (CBT-I) or a quasi-desensitization control (CTRL) therapy. Main outcome measures were the 17-item Hamilton Rating Scale for Depression (HRSD-17) and the Insomnia Severity Index (ISI) completed pre-treatment and every 2 weeks thereafter. RESULTS The AO and CO groups did not differ significantly in regard to their pre-treatment HRSD-17 and ISI scores. Mixed model analyses that adjusted for the number of insomnia treatment sessions attended showed that the AO group achieved significantly lower, subclinical scores on the HRSD-17 and ISI than did the CO group by the time of study exit. Moreover, a significant group by treatment arm interaction suggested that HRSD-17 scores at study exit remained significantly higher in the CO group receiving the CTRL therapy than was the case for the participants in the CO group receiving CBT-I. Greater proportions of the AO group achieved a priori criteria for remission of insomnia (49.3% vs. 29.2%, p = 0.04) and depression (45.5% vs. 29.6%, p = 0.07) than did those in the CO group. CONCLUSIONS Patients with comorbid depression and insomnia who experienced the first onset of both disorders in childhood are less responsive to the treatments offered herein than are those with adult onsets of these comorbid disorders. Further research is needed to identify therapies that enhance the depression and insomnia treatment responses of those with childhood onsets of these two conditions.

Sleep, Sadness, and Depression

Abstract: This chapter discusses the bidirectional association between sleep duration or quality and sadness, which is broadly defined as low positive affect. Regarding the impact of sleep on sadness and depression, observational and experimental studies suggest that poor sleep quality and insufficient sleep lead to low positive affect among depression-free individuals, but individuals with depression respond to the challenge of sleep deprivation with transient mood elevation. Regarding the impact of low mood on sleep, studies generally find little to no evidence supporting the hypothesis that, among people without depression, a low arousal negative affect, such as sadness, predicts poor sleep the next night. On the other hand, people with depression experience greater sleep abnormalities than do people without depression, including difficulties initiating and maintaining sleep and disturbances in rapid eye movement (REM) sleep. The chapter also discusses how depression and sad mood could contribute to the severity of insomnia, circadian rhythm sleep-wake disorders, and sleep apnea.