Negative feedback-seeking in depression: The moderating roles of rumination and interpersonal life stress.

OBJECTIVES: Swann's self-verification theory proposes that negative feedback seeking (NFS)-the solicitation of negative feedback from others that confirms one's self-views-works in a negative cycle to maintain and exacerbate depression in the face of interpersonal stress. We propose a cognitive-interpersonal integration account of NFS such that this maladaptive behavior prospectively predicts depression only among those with a trait tendency to ruminate on the causes and consequences of depressed mood and stress. METHOD: Participants included 91 young adults who were over-sampled for a lifetime history of a unipolar depressive disorder (age 17-33; 69% women; 67% lifetime depressive disorder). At baseline, participants completed a structured diagnostic interview and self-report measures of NFS, rumination, and depression symptoms. In addition, participants engaged in an interpersonal rejection task (the Yale Interpersonal Stressor) followed by a behavioral measure of NFS. At a 3-month follow-up, depression symptoms were again assessed by self-report and exposure to stressful interpersonal life events in the intervening period were assessed with a rigorous contextual interview and independent rating system. RESULTS: Controlling for baseline depression severity, greater self-reported, and behaviorally assessed NFS predicted greater follow-up depression severity, but only among those with higher trait tendency to ruminate. For self-reported NFS, this association was further moderated by level of interpersonal, but not noninterpersonal, life events experienced over follow-up. CONCLUSION: These findings suggest that rumination may represent a modifiable intervention target that could break the vicious interpersonal cycle of depression and, thus, mitigate the depressogenic effects of NFS.

Maternal history of depression is associated with enhanced theory of mind in depressed and nondepressed adult women.

Theory of mind forms the basis of social cognition and develops on a stereotyped ontogenetic timetable. Yet, there are individual differences in theory of mind that may be transmitted through genetic and/or environmental mechanisms. In the current study we examined the relation of maternal history of depression to individual differences in theory of mind in a sample of adult women. Sixty-one depressed women (23% with a positive maternal history of depression) and 30 non-depressed women (33% with a positive maternal history of depression) completed the 'Reading the Mind in the Eyes task', a test of theory of mind decoding. Women with a maternal history of depression performed better on the Eyes task than those without. Further, the younger the mother's onset of depression, the better the current probands' Eyes task performance. These results are consistent with a broader literature linking hypersensitive social cognition and depression risk. We discuss the potential clinical implications of our results.

Childhood emotional abuse, physical abuse, and neglect are associated with theory of mind decoding accuracy in young adults with depression.

The current study is the first to examine the relation of childhood abuse and neglect history to theory of mind decoding accuracy as moderated by depression. Fifty-five young adults with current or lifetime unipolar depression diagnosis and 70 never-depressed young adults completed the 'Reading the Mind in the Eyes task,' (RMET). Childhood emotional abuse, physical abuse, and neglect were assessed with a gold-standard contextual interview with standardized, independent ratings. Poorer RMET accuracy was associated with a history of emotional abuse in the depressed group and a history of physical abuse in the non-depressed group. In contrast, across both groups, those with a history of neglect showed significantly enhanced theory of mind decoding accuracy compared to those without. Further, differential accuracy across positive, negative, and neutral valenced stimuli in the RMET was observed in each model. These findings indicate that distinct theory of mind performance results from early experiences of threat versus deprivation, and suggest that early intervention may be most successful in preventing negative interpersonal outcomes of maltreatment by focusing on remediating theory of mind deficits resulting from abuse, and tempering heightened sensitivity in those exposed to neglect.

Theory of mind in social anxiety disorder, depression, and comorbid conditions.

Social anxiety disorder is characterized by marked interpersonal impairment, particularly when presenting with comorbid major depression. However, the foundational social-cognitive skills that underlie interpersonal impairment in comorbid and non-comorbid manifestations of SAD has to date received very little empirical investigation. In a sample of 119 young adults, the current study examined differences in theory of mind (ToM), defined as the ability to decode and reason about others' mental states, across four groups: (a) non-comorbid SAD; (b) non-comorbid Lifetime MDD; (c) comorbid SAD and Lifetime MDD; and (d) healthy control. The non-comorbid SAD group was significantly less accurate at decoding mental states than the non-comorbid MDD and control groups. Further, both the comorbid and non-comorbid SAD groups made significantly more 'excessive' ToM reasoning errors than the non-comorbid MDD group, suggesting a pattern of over-mentalizing. Findings are discussed in terms of their implications for understanding the social cognitive foundations of social anxiety.

Serotonin and Dopamine Gene Variation and Theory of Mind Decoding Accuracy in Major Depression: A Preliminary Investigation.

Theory of mind-the ability to decode and reason about others' mental states-is a universal human skill and forms the basis of social cognition. Theory of mind accuracy is impaired in clinical conditions evidencing social impairment, including major depressive disorder. The current study is a preliminary investigation of the association of polymorphisms of the serotonin transporter (SLC6A4), dopamine transporter (DAT1), dopamine receptor D4 (DRD4), and catechol-O-methyl transferase (COMT) genes with theory of mind decoding in a sample of adults with major depression. Ninety-six young adults (38 depressed, 58 non-depressed) completed the 'Reading the Mind in the Eyes task' and a non-mentalistic control task. Genetic associations were only found for the depressed group. Specifically, superior accuracy in decoding mental states of a positive valence was seen in those homozygous for the long allele of the serotonin transporter gene, 9-allele carriers of DAT1, and long-allele carriers of DRD4. In contrast, superior accuracy in decoding mental states of a negative valence was seen in short-allele carriers of the serotonin transporter gene and 10/10 homozygotes of DAT1. Results are discussed in terms of their implications for integrating social cognitive and neurobiological models of etiology in major depression.

The effects of glucocorticoids on the inhibition of emotional information: A dose-response study.

There is evidence that cortisol influences cognitive and affective processes such as selective attention and memory for emotional events, yet the effects of glucocorticoids on attentional inhibition in humans remain unknown. Consequently, this double-blind study examined dose-dependent effects of exogenous glucocorticoids on the inhibition of emotional information. Sixty-three university students (14 male, 49 female) ingested either a placebo pill or hydrocortisone (10mg or 40mg), and completed a negative priming task assessing the inhibition of pictures depicting angry, sad, and happy faces. The 10mg, but not the 40mg hydrocortisone dose elicited increased inhibition for angry faces relative to placebo. Thus, moderate glucocorticoid elevations may have adaptive effects on emotional information processing, whereas high glucocorticoid elevations appear to attenuate this effect, consistent with the view that there are dose-dependent effects of glucocorticoids on cognition.