Self-efficacy in depression: Bridging the gap between competence and real-world functioning

Background: Depression is the largest contributing factor to years lost to disability, and symptom remission does not always result in functional improvement. Comprehensive analysis of functioning requires investigation both of the competence to perform behaviours, as well as actual performance in the real world. Further, two independent domains of functioning have been proposed: adaptive (behaviours conducive to daily living skills and independent functioning) and interpersonal (behaviours conducive to the successful initiation and maintenance of social relationships). To date, very little is known about the relationship between these constructs in depression, and the factors that may play a key role in the disparity between competence and real-world performance in adaptive and interpersonal functioning. Purpose: This study used a multidimensional (adaptive and interpersonal functioning), multi-level (competence and performance) approach to explore the potential discrepancy between competence and real-world performance in depression, specifically investigating whether self-efficacy (one’s beliefs of their capability to perform particular actions) predicts depressed individuals’ underperformance in the real world relative to their ability. A comparison sample of healthy participants was included to investigate the level of depressed individuals’ impairment, across variables, relative to healthy individuals. Method: Forty-two participants with depression and twenty healthy participants without history of, or current, psychiatric illness were recruited in the Kingston, Ontario community. Competence, self-efficacy, and real-world functioning all in both adaptive and interpersonal domains, and symptoms were assessed during a single-visit assessment. Results: Relative to healthy individuals, depressed individuals showed significantly poorer adaptive and interpersonal competence, adaptive and interpersonal functioning, and significantly lower self-efficacy for adaptive and interpersonal behaviours. Self-efficacy significantly predicted functional disability both in the domain of adaptive and interpersonal functioning. Interpersonal self-efficacy accounted for significant variance in the discrepancy between interpersonal competence and functioning. Conclusions: The current study provides the first data regarding relationships among competence, functioning, and self-efficacy in depression. Self-efficacy may play an important role in the deployment of functional skills in everyday life. This has implications for therapeutic interventions aimed at enhancing depressed individuals’ engagement in functional activities. There may be additional intrinsic or extrinsic factors that influence the relationships among competence and functioning in depression.

ENVIRONMENTAL INFLUENCES AND EPIGENETIC MECHANISMS IN RISK FOR DEPRESSION

Genetic and environmental factors interact to influence vulnerability for internalizing psychopathology, including Major Depressive Disorder (MDD). The mechanisms that account for how environmental stress can alter biological systems are not yet well understood yet are critical to develop more accurate models of vulnerability and targeted interventions. Epigenetic influences, and more specifically, DNA methylation, may provide a mechanism by which stress could program gene expression, thereby altering key systems implicated in depression, such as frontal-limbic circuitry and its critical role in emotion regulation. This thesis investigated the role of environmental factors from infancy and throughout the lifespan affecting the serotonergic (5-HT) system in the vulnerability to and treatment of depression and anxiety and potential underlying DNA methylation processes. First, we investigated the contributions of additive genetic vs. environmental factors on an early trait phenotype for depression (negative emotionality) in infants and their stability over time in the first 2 years of life. We provided evidence of the substantial contributions of both genetic and shared environmental factors to this trait, as well as genetically- and environmentally- mediated stability and innovation. Second, we studied how childhood environmental stress is associated with peripheral DNA methylation of the serotonin transporter gene, SLC6A4, as well as long-term trajectories of internalizing behaviours. There was a relationship between childhood psychosocial adversity and SLC6A4 methylation in males, as well as between SLC6A4 methylation and internalizing trajectory in both sexes. Third, we investigated changes in emotion processing and epigenetic modification of the SLC6A4 gene in depressed adolescents before and after Mindfulness-Based Cognitive Therapy (MBCT). The alterations from pre- to post-treatment in connectivity between the ACC and other network regions and SLC6A4 methylation suggested that MBCT may work to optimize the connectivity of brain networks involved in cognitive control of emotion as well as also normalize the relationship between SLC6A4 methylation and activation patterns in frontal-limbic circuitry. Our results from these three studies strengthen the theory that environmental influences are critical in establishing early vulnerability factors for MDD, driving epigenetic processes, and altering brain processes as an individual undergoes treatment, or experiences relapse.