The Effects of Rumination on Psychological and Biological Recovery from Stress in Depression

Diathesis-stress models of depression highlight that stress triggers the onset of a depressive episode. Increasing evidence, however, suggest that increased risk comes not from the initial response to stress, but rather from difficulty regulating emotions in a way that facilitates recovery. Rumination is a maladaptive emotion regulation strategy shown to prolong negative affect in response to distress. The current study extends past research by comparing the effects of a rumination versus distraction induction on biological and psychological recovery from stress among individuals with major depressive disorder (MDD) and healthy controls (CTLs). Participants were exposed to a psychosocial stressor and then randomly assigned to either the rumination or distraction condition. Self-reported affect and markers of biological arousal (salivary cortisol and respiratory sinus arrhythmia; RSA) were assessed before, during, and after the stressor. Participants demonstrated significant reactivity to stress, evidenced by an increase in self-reported negative affect and decrease in RSA. In contrast, participants did not demonstrate the expected significant cortisol reactivity to stress. Also unexpected was a significant increase in RSA during the latter-half of the stressor, suggesting spontaneous parasympathetic recovery. Although no group differences were seen in stress reactivity, significant time by group by condition interactions were seen in stress recovery. Within the CTL group, participants in the rumination and distraction conditions did not differ in their psychological or biological recovery from stress. Within the MDD group, however, participants in the rumination condition demonstrated higher negative affect and salivary cortisol during the recovery period than participants in the distraction condition. Evidence therefore suggests that rumination affects neuroendocrine and psychological recovery from stress in depression. Moreover, depressed participants in the distraction condition demonstrated significantly greater RSA withdrawal during the ER induction compared to control participants in the distraction condition, potentially suggesting that distraction was more effortful for the MDD versus CTL group. During the subsequent nature video, RSA recovery was greater in the MDD versus CTL group. Results from this study provide important insights into the effect of rumination on psychological and biological recovery from stress in MDD

Co-rumination via communication domains across time

This study is a long-term longitudinal study investigating co-rumination across time, and predicting various outcomes (e.g., internalizing symptoms, friendship quality)

Cognitive Disengagement and Biological Stress Responses in Early Adolescence

Individual differences in biological responses to stress increase risk for the onset and exacerbation of health and psychiatric conditions. Biases in cognitive disengagement are hypothesized to underlie these individual differences in biological responses to stress. However, no studies have examined which cognitive disengagement bias has the strongest relation with biological responses to stress, and no studies have examined this relation during early adolescence, despite evidence that this is a critical developmental window in which patterns of cognition and biological responses to stress influence trajectories of health throughout life. The current study is the first to test whether difficulty disengaging attention versus working memory from valenced stimuli is associated with biological responses to stress in early adolescence. Youth between 11 and 13 years of age completed two computer-based tasks to assess biases in attention and working memory disengagement to valenced stimuli, and then completed a standardized psychosocial stressor. Consistent with expectations, attention and working memory disengagement biases were associated with stress responses of both the neuroendocrine and autonomic nervous systems, but bias valence and cognitive system influenced the directionality of results. These findings inform our understanding of cognitive mechanisms that influence biological stress reactivity.Arts, Faculty ofPsychology, Department ofReviewedFacultyGraduat

Childhood Maltreatment, Negative Self-Referential Processing, and Depressive Symptoms During Stress

Introduction: Researchers have documented that the impact of childhood maltreatment on later symptoms of depression differs depending on the type(s) of maltreatment experienced, with emotional abuse and neglect being more likely than other forms of childhood maltreatment to increase the risk for depression. It is possible that emotional abuse and neglect are more likely to increase the risk for depression because they promote the development of negative selfreferential processing (SRP), but this has not yet been tested empirically. The current study was designed to examine whether negative SRP mediated the association between different forms of childhood maltreatment and symptoms of depression during a time of stress. Methods: We assessed the experience of different forms of childhood maltreatment (ie, emotional neglect, physical neglect, emotional abuse, physical abuse, and sexual abuse) and negatively biased self-schemas early on in the university semester, among a sample of undergraduate students. We then assessed levels of depressive symptoms 2 months later during a naturalistic stressor (ie, university students’ first final exams). Results: As expected, negative SRP mediated the relation between both neglect and emotional abuse, but not physical and sexual abuse, and later symptoms of depression. Discussion: This is the first study to examine SRP as a mechanism underlying the association between forms of childhood maltreatment and symptoms of depression during a time of stress. Results suggest that the development of negative SRP biases may explain why some types of childhood maltreatment are more likely than others to increase an individual’s risk for depression during stressful developmental periods.Arts, Faculty ofPsychology, Department ofReviewedFacultyGraduat

Predicting change in symptoms of depression during the transition to university: The roles of BDNF and working memory capacity

Studies on depression risk emphasize the importance of both cognitive and genetic vulnerability factors. The present study has provided the first examination of whether working memory capacity, the BDNF Val66Met polymorphism, and their interaction predict changes in symptoms of depression during the transition to university. Early in the semester, students completed a self-report measure of depressive symptoms and a modified version of the reading span task to assess working memory capacity in the presence of both neutral and negative distractors. Whole blood was genotyped for the BDNF Val66Met polymorphism. Students returned at the end of the semester to complete additional self-report questionnaires. Neither working memory capacity nor the BDNF Val66Met polymorphism predicted change in depressive symptoms either independently or in interaction with self-reported semester difficulty. The BDNF Val66Met polymorphism, however, moderated the association between working memory capacity and symptom change. Among met carriers, lower working memory capacity in the presence of negative—but not neutral—distractors was associated with increased symptoms of depression over the semester. For the val/val group, working memory capacity did not predict symptom change. These findings contribute directly to biological and cognitive models of depression and highlight the importance of examining Gene × Cognition interactions when investigating risk for depression

Predicting change in symptoms of depression during the transition to university: The roles of BDNF and working memory capacity

Studies on depression risk emphasize the importance of both cognitive and genetic vulnerability factors. The present study has provided the first examination of whether working memory capacity, the BDNF Val66Met polymorphism, and their interaction predict changes in symptoms of depression during the transition to university. Early in the semester, students completed a self-report measure of depressive symptoms and a modified version of the reading span task to assess working memory capacity in the presence of both neutral and negative distractors. Whole blood was genotyped for the BDNF Val66Met polymorphism. Students returned at the end of the semester to complete additional self-report questionnaires. Neither working memory capacity nor the BDNF Val66Met polymorphism predicted change in depressive symptoms either independently or in interaction with self-reported semester difficulty. The BDNF Val66Met polymorphism, however, moderated the association between working memory capacity and symptom change. Among met carriers, lower working memory capacity in the presence of negative-but not neutral-distractors was associated with increased symptoms of depression over the semester. For the val/val group, working memory capacity did not predict symptom change. These findings contribute directly to biological and cognitive models of depression and highlight the importance of examining Gene × Cognition interactions when investigating risk for depression

Gene Effects and G × E Interactions in the Differential Prediction of Three Aspects of Impulsiveness

Several polymorphisms relevant to dopamine and serotonin have been identified as potential contributors to individual differences in impulsivity versus self-control. Because impulsivity is a multifaceted construct, a need remains to examine more closely how various genes relate to different aspects of impulsivity. We examined four dopamine-related polymorphisms and the serotonin transporter as predictors of three aspects of impulsivity, two bearing on impulsive reactions to emotions and one on difficulty in completing intended actions. Early adversity was also examined as a potentiator of genetic effects. Undergraduates completed measures of impulsivity and early adversity and were genotyped. COMT, BDNF, DRD4, and 5HTTLPR (the latter two in interaction with early adversity) made independent contributions to prediction of Pervasive Influence of Feelings. BDNF made a contribution to Lack of Follow-Through. ANKK1 and 5HTTLPR (both in interaction with early adversity) made independent contributions to Feelings Trigger Action. Thus, five polymorphisms contributed to predicting impulsivity, but different polymorphisms related to different aspects