Breaking the Rhythm of Depression: Cognitive Behavior Therapy and Relapse Prevention for Depression

A crucial part of the treatment of depression is the prevention of relapse and recurrence. Psychological interventions, especially cognitive behavior therapy (CBT) are helpful in preventing relapse and recurrence in depression. The effectivity of four types of relapse prevention cognitive behavior therapy strategies will be addressed, i.e. acute prophylactic cognitive behavior therapy, continuation cognitive behavior therapy, sequential cognitive behavior therapy and cognitive behavior therapy in partial remission. Specific ingredients of three sequential cognitive behavior therapy programs (well-being cognitive therapy, preventive cognitive therapy, and mindfulness-based cognitive therapy) will be discussed as applied after remission in patients that experienced previous depressive episodes. Sequential preventive cognitive behavior therapy after acute treatment may be an attractive alternative treatment for many patients who currently use antidepressants for years and years to prevent relapse and recurrence. This is an extremely challenging issue to research thoroughly. Future studies must rule out what intervention for whom is the best protection against relapse and recurrence in depression

Explaining the Efficacy of an Internet-Based Behavioral Activation Intervention for Major Depression:A Mechanistic Study of a Randomized-Controlled Trial

Background: Behavioral activation is an effective treatment for depression that is theorized to facilitate structured increases in enjoyable activities that increase opportunities for contact with positive reinforcement; to date, however, only few mechanistic studies focused on a standalone intervention. Method: Interventions using internet-based behavioral activation or psychoeducation were compared based on data from a randomized-controlled trial of 313 patients with major depressive disorder. Activation level and depression were measured fortnightly (baseline, Weeks 2, 4, 6, 8, 10), using the Patient Health Questionnaire-9 and the Behavioral Activation for Depression Scale-Short Form, respectively. Analysis was performed to determine if a change in activation level mediated treatment efficacy. Results: Latent growth modeling showed that internet-based behavioral activation treatment significantly reduced depressive symptoms from baseline to the end of treatment (standardized coefficient = −.13, p = .017) by increasing the rate of growth in the activation level (mediated effect)

For whom are internet-based occupational mental health interventions effective? Moderators of internet-based problem-solving training outcome

AbstractInternet-based problem-solving training (IPST) effectively reduces depressive symptoms in employees. Yet, it is unknown which employees benefit most from this particular treatment. The study aimed to identify predictors and moderators of treatment outcome in IPST offered to employees with depressive symptoms. Within a randomized controlled trial (N=150), designed to test the effectiveness of IPST, variables that predict and moderate the effects of IPST when compared with a waitlist control group (WLC) were explored. The outcome was change in depression severity, assessed using the Center for Epidemiological Studies Depression Scale (CES-D). Both depression severity and other psychopathological symptoms and potential predictors/moderators were assessed as self-reports at baseline (t1) and in follow-up assessments after seven weeks (t2), three months (t3) and six months (t4). Higher depression severity at baseline predicted improvement in depressive symptomology in follow-up assessments after seven weeks, and three- and six months. Depression severity moderated the effectiveness of IPST assessed at six-month follow-up. Simple slope analyses revealed that the long-term effectiveness of the intervention was more pronounced among participants with high (CES-D range: 33–44, M=37.0, SD=3.2) and moderate (CES-D range: 14–32, M=23.1, SD=5.6) depression baseline scores, compared to participants displaying low depression baseline scores (CES-D range: 5–13, M=9.0, SD=2.2). No indication was found that participants presenting low depression severity at baseline significantly benefitted from IPST in the long-term. IPST might be appropriate for employees with a wide range of different characteristics. While there appears to be no reason to exclude employees with severe depression from Internet-based occupational mental health interventions, for employees low in depression severity, watchful waiting or potentially no intervention should be considered. These findings may not apply to other low-intensity interventions and/or target groups

Preventive cognitive therapy versus treatment as usual in preventing recurrence of depression:Protocol of a multi-centered randomized controlled trial

Background Major depressive disorder (MDD) is projected to rank second on a list of 15 major diseases in terms of burden in 2030. The contribution of MDD to disability and health care costs is largely due to its highly recurrent nature. Therefore, part of the efforts to reduce the disabling effects of depression should focus on preventing recurrence, especially in patients at high risk of recurrence. The best established effective psychological intervention is cognitive therapy, with indications for prophylactic effects after remission. Methods/Design In this randomized controlled trial (cost-) effectiveness of Preventive Cognitive Therapy (PCT) after response to Acute Cognitive Therapy (A-CT) will be evaluated in comparison with Treatment As Usual (TAU). Remitted patients that responded to A-CT treatment with at least two previous depressive episodes will be recruited. Randomization will be stratified for number of previous episodes. Follow-ups are at 3, 6, 12 and 15 months. The primary outcome measure will be the time to relapse or recurrence of depression meeting DSM-IV criteria for a major depressive episode on the Structured Clinical Interview for DSM-VI Axis I Disorders (SCID-I). Costs will be measured from a societal perspective. Discussion This study is the first to examine the addition of PCT to TAU, compared to TAU alone in patients that recovered from depressive disorder with A-CT. Alongside this effect study a cost effectiveness analysis will be conducted. Furthermore, the study explores potential moderators to examine what works for whom. Trial registration Netherlands Trial Register (NTR): 2599, date of registration: 11-11-2010. Keywords Depression Relapse Recurrence Cognitive Therapy Preventio

Non-fatal disease burden for subtypes of depressive disorder: population-based epidemiological study

Background: Major depression is the leading cause of non-fatal disease burden. Because major depression is not a homogeneous condition, this study estimated the non-fatal disease burden for mild, moderate and severe depression in both single episode and recurrent depression. All estimates were assessed from an individual and a population perspective and presented as unadjusted, raw estimates and as estimates adjusted for comorbidity. Methods: We used data from the first wave of the second Netherlands-Mental-Health-Survey-and-Incidence-Study (NEMESIS-2, n = 6646; single episode Diagnostic and Statistical Manual (DSM)-IV depression, n = 115; recurrent depression, n = 246). Disease burden from an individual perspective was assessed as 'disability weight * time spent in depression' for each person in the dataset. From a population perspective it was assessed as 'disability weight * time spent in depression *number of people affected'. The presence of mental disorders was assessed with the Composite International Diagnostic Interview (CIDI) 3.0. Results: Single depressive episodes emerged as a key driver of disease burden from an individual perspective. From a population perspective, recurrent depressions emerged as a key driver. These findings remained unaltered after adjusting for comorbidity. Conclusions: The burden of disease differs between the subtype of depression and depends much on the choice of perspective. The distinction between an individual and a population perspective may help to avoid misunderstandings between policy makers and clinicians. © 2016 Biesheuvel-Leliefeld et al

Emotion regulation mediates the effect of childhood trauma on depression

Background Childhood trauma increases the risks of both depression and dysfunctional emotion regulation, which is a factor that has been strongly linked to depression. Because of these demonstrated relationships, it can be hypothesized that dysfunctional emotion regulation is a mediator of the association between childhood trauma and depression. Methods To test this hypothesis, we assessed the indirect effect of emotion regulation (Emotion Regulation Skills Questionnaire) on the relationship between childhood trauma (Childhood Trauma Questionnaire) and depression severity (24-item Hamilton Rating Scale for Depression) as well as depression lifetime persistency (i.e., lifetime percentage spent in major depressive episodes; assessed via SCID and Life Chart Interviews) in 269 patients with major depressive disorder (MDD). Results Bootstrapping-enhanced mediation analyses indicated that deficits in general emotion regulation mediated the association of childhood trauma to both depression severity and depression lifetime persistency. Further exploratory analyses indicated that specific emotion regulation skills (such as the ability to mindfully observe, accept, and tolerate undesired emotions or the willingness to voluntarily confront situations that prompt negative emotions in order to attain personally relevant goals) significantly mediated the association between childhood trauma and depression severity. Willingness to confront was a mediator for both depression outcomes (depression severity and lifetime persistency). Limitations The employed mediation analyses are cross-sectional in nature, which limits any firm conclusions regarding causality. Conclusions The findings support the assumption that a sophisticated emotion regulation may help prevent the onset or unfavorable course of depression in individuals who have experienced childhood trauma

A hot-cold cognitive model of depression: Integrating the neuropsychological approach into the cognitive theory framework

Background: In the 50 years following Beck’s cognitive theory, empirical research has consistently supported the role of dysfunctional, ‘hot’ cognition in the onset and maintenance of major depressive disorder. Compromised ‘cold’ cognition in attention, memory, and executive control abilities, independent of the affective state, has attracted much clinical interest for its role throughout the course of illness and into remission. We propose integrating cold cognition into Beck’s cognitive theory framework to account for the complementary roles of both hot and cold cognition in depression onset and maintenance. Method: A critical review of cognitive research was conducted to inform an integrated hot-cold cognitive model of depression. Results: Cold cognitive deficits likely act as a gateway to facilitate the activation and expression of the hot cognitive biases through a weakened ability to attend, retrieve, and critically assess information. Cold deficits become exacerbated by the negative mood state, essentially ‘becoming hot’, lending to maladaptive emotion regulation through ruminative processes. Depleted cognitive resources contribute to the manifestation of further deficit in problem-solving ability in everyday life, which in itself, may act as a stressor for the onset of recurrent episodes, perpetuating the depressive cycle. Conclusion: We discuss the interaction between hot and cold cognition within the cognitive theory framework and the potential of complementary hot-cold pathways to elucidate novel means of prevention and treatment for depression