The influence of adversity and perceived social support on the outcome of major depressive disorder in subjects with different levels of depressive symptoms
ABSTRACT Adverse life events and social support may influence the outcome of major depressive disorder (MDD). We hypothesized that outcome would depend on the level of depressive symptoms present at the outset, with those in partial remission being particularly vulnerable.
In the Vantaa Depression Study (VDS), patients with DSM-IV MDD were interviewed at baseline, and at 6 and 18 months. Life events were investigated with the Interview for Recent Life Events (IRLE) and social support with the Interview Measure of Social Relationships (IMSR) and the Perceived Social Support Scale - Revised (PSSS-R). The patients were divided into three subgroups at 6 months, those in full remission (n = 68), partial remission (n = 75) or major depressive episode (MDE) (n = 50). The influence of social support and negative life events during the next 12 months on the level of depressive symptoms, measured by the Hamilton Rating Scale for Depression (HAMD), was investigated at endpoint.
The severity of life events and perceived social support influenced the outcome of depression overall, even after adjusting for baseline level of depression and neuroticism. In the full remission subgroup, both severity of life events and subjective social support significantly predicted outcome. However, in the partial remission group, only the severity of events, and in the MDE group, the level of social support were significant predictors.
Adverse life events and/or poor perceived social support influence the medium-term outcome of all psychiatric patients with MDD. These factors appear to have the strongest predictive value in the subgroup of patients currently in full remission.
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ABSTRACT: Depression is a significant public health problem, but its etiology and pathophysiology remain poorly understood. Such incomplete understanding likely arises from the fact that depression encompasses a heterogeneous set of disorders. To overcome these limitations, renewed interest in intermediate phenotypes (endophenotypes) has resurfaced, and anhedonia has emerged as one of the most promising endophenotypes of depression. Here, a heuristic model is presented postulating that anhedonia arises from dysfunctional interactions between stress and brain reward systems. To this end, we review and integrate three bodies of independent literature investigating the role of (a) anhedonia, (b) dopamine, and (c) stress in depression. In a fourth section, we summarize animal data indicating that stress negatively affects mesocorticolimbic dopaminergic pathways critically implicated in incentive motivation and reinforcement learning. In the last section, we provide a synthesis of these four literatures, present initial evidence consistent with our model, and discuss directions for future research. Expected final online publication date for the Annual Review of Clinical Psychology Volume 10 is March 20, 2014. Please see http://www.annualreviews.org/catalog/pubdates.aspx for revised estimates.Annual Review of Clinical Psychology 01/2014; DOI:10.1146/annurev-clinpsy-050212-185606 · 12.92 Impact Factor
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ABSTRACT: Recent neuroimaging studies support the contention that depression, pain distress, and rejection distress share the same neurobiological circuits. In two recently published studies we confirmed the hypothesis that the perception of increased pain during both treatment-refractory depression (predominantly unipolar) and difficult-to-treat bipolar depression was related to increased state rejection sensitivity (i.e., rejection sensitivity when depressed). In the present study, we aimed to compare the correlates of pain and rejection sensitivity in individuals with bipolar versus unipolar depression and test the hypothesis that bipolar disorder may be distinguished from unipolar depression both by an increased perception of pain and heightened rejection sensitivity during depression. We analyzed data from 113 bipolar and 146 unipolar depressed patients presenting to the Black Dog Institute, Sydney, Australia. The patients all met DSM-IV criteria for bipolar disorder or unipolar depression (major depressive disorder). Bipolar disorder predicted a major increase in state rejection sensitivity when depressed (p = 0.001), whereas trait rejection sensitivity (i.e., a long-standing pattern of rejection sensitivity) was not predicted by polarity. A major increase in the experience of headaches (p = 0.007), chest pain (p < 0.001), and body aches and pains (p = 0.02) during depression was predicted by a major increase in state rejection sensitivity for both bipolar and unipolar depression. State, but not trait, rejection sensitivity is significantly predicted by bipolar depression, suggesting that this might be considered as a state marker for bipolar depression and taken into account in the clinical differentiation of bipolar and unipolar depression.Bipolar Disorders 03/2014; 16:190-198. DOI:10.1111/bdi.12147 · 4.89 Impact Factor
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ABSTRACT: Adolescence is a peak period for the onset of depression, and it is also a time marked by substantial stress as well as neural development within the brain reward circuitry. In this review, we provide a selective overview of current animal and human research investigating the relationship among reward processes, stress, and depression. Three separate, but related, etiological models examine the differential roles that stress may play in relation to reward dysfunction and adolescent depression. First, the reward mediation model suggests that both acute and chronic stress contribute to reward deficits, which, in turn, potentiate depressive symptoms or increase the risk for depression. Second, in line with the stress generation perspective, it is plausible that premorbid reward-related dysfunction generates stress-in particular, interpersonal stress-which then leads to the manifestation of depressive symptoms. Third, consistent with a diathesis-stress model, the interaction between stress and premorbid reward dysfunction may contribute to the onset of depression. Given the equifinal nature of depression, these models could shed important light on different etiological pathways during adolescence, particularly as they may relate to understanding the heterogeneity of depression. To highlight the translational potential of these insights, a hypothetical case study is provided as a means of demonstrating the importance of targeting reward dysfunction in both assessment and treatment of adolescent depression.Harvard Review of Psychiatry 04/2014; DOI:10.1097/HRP.0000000000000034 · 2.49 Impact Factor