Jutta Joormann

Cognition and Depression: Current Status and Future Directions

Cognitive theories of depression posit that peoples thoughts, inferences, attitudes, and interpretations, and the way in which they attend to and recall information, can increase their risk for depression. Three mechanisms have been implicated in the relation between biased cognitive processing and the dysregulation of emotion in depression: inhibitory processes and deficits in working memory, ruminative responses to negative mood states and negative life events, and the inability to use positive and rewarding stimuli to regulate negative mood. In this review, we present a contemporary characterization of depressive cognition and discuss how different cognitive processes are related not only to each other, but also to emotion dysregulation, the hallmark feature of depression. We conclude that depression is characterized by increased elaboration of negative information, by difficulties disengaging from negative material, and by deficits in cognitive control when processing negative information. We discuss treatment implications of these conclusions and argue that the study of cognitive aspects of depression must be broadened by investigating neural and genetic factors that are related to cognitive dysfunction in this disorder. Such integrative investigations should help us gain a more comprehensive understanding of how cognitive and biological factors interact to affect the onset, maintenance, and course of depression.

Attentional Biases for Negative Interpersonal Stimuli in Clinical Depression

An information-processing paradigm was used to examine attentional biases in clinically depressed participants, participants with generalized anxiety disorder (GAD), and nonpsychiatric control participants for faces expressing sadness, anger, and happiness. Faces were presented for 1000 ms, at which point depressed participants had directed their attention selectively to depression-relevant (i.e., sad) faces. This attentional bias was specific to the emotion of sadness; the depressed participants did not exhibit attentional biases to the angry or happy faces. This bias was also specific to depression; at 1000 ms, participants with GAD were not attending selectively to sad, happy, or anxiety-relevant (i.e., angry) faces. Implications of these findings for both the cognitive and the interpersonal functioning of depressed individuals are discussed and directions for future research are advanced.

Emotion regulation in depression: relation to cognitive inhibition.

Depression is a disorder of impaired emotion regulation. Consequently, examining individual differences in the habitual use of emotion-regulation strategies has considerable potential to inform models of this debilitating disorder. The aim of the current study was to identify cognitive processes that may be associated with the use of emotion-regulation strategies and to elucidate their relation to depression. Depression has been found to be associated with difficulties in cognitive control and, more specifically, with difficulties inhibiting the processing of negative material. We used a negative affective priming task to assess the relations among inhibition and individual differences in the habitual use of rumination, reappraisal, and expressive suppression in clinically depressed, formerly depressed, and never-depressed participants. We found that depressed participants exhibited the predicted lack of inhibition when processing negative material. Moreover, within the group of depressed participants, reduced inhibition of negative material was associated with greater rumination. Across the entire sample, reduced inhibition of negative material was related to less use of reappraisal and more use of expressive suppression. Finally, within the formerly depressed group, less use of reappraisal, more use of rumination, and greater expressive suppression were related to higher levels of depressive symptoms. These findings suggest that individual differences in the use of emotion-regulation strategies play an important role in depression, and that deficits in cognitive control are related to the use of maladaptive emotion-regulation strategies in this disorder.

HPA-Axis Reactivity: A Mechanism Underlying the Associations Among 5-HTTLPR, Stress, and Depression

BACKGROUND Recent evidence indicates that individuals who are homozygous for the short (s) allele in the promoter region of the serotonin transporter gene have higher rates of depression and other psychiatric disorders as a function of exposure to increasing levels of stressful life events than do individuals who have one or two copies of the long (l) allele. Despite the reliability of this association, the mechanism by which this polymorphism confers risk for psychopathology in the presence of stress is not understood. This study was designed to examine the formulation that individuals who are homozygous for the s allele are characterized by a greater biological reactivity to stress than are their counterparts who have one or two copies of the l allele. METHODS Girls at high (n = 25) and low (n = 42) risk for depression by virtue of the presence or absence of a family history of this disorder were genotyped and exposed to a standardized laboratory stress task. Cortisol levels were assessed before the stressor, after the stressor, and during an extended recovery period. RESULTS Girls who were homozygous for the s allele produced higher and more prolonged levels of cortisol in response to the stressor than did girls with an l allele. CONCLUSIONS These findings indicate that the 5-HTTLPR polymorphism is associated with biological stress reactivity, which may increase susceptibility to depression in the face of stressful life events.

Selective Attention to Emotional Faces Following Recovery From Depression

This study was designed to examine attentional biases in the processing of emotional faces in currently and formerly depressed participants and healthy controls. Using a dot-probe task, the authors presented faces expressing happy or sad emotions paired with emotionally neutral faces. Whereas both currently and formerly depressed participants selectively attended to the sad faces, the control participants selectively avoided the sad faces and oriented toward the happy faces, a positive bias that was not observed for either of the depressed groups. These results indicate that attentional biases in the processing of emotional faces are evident even after individuals have recovered from a depressive episode. Implications of these findings for understanding the roles of cognitive and interpersonal functioning in depression are discussed.

Updating the Contents of Working Memory in Depression: Interference From Irrelevant Negative Material

This study was designed to assess the effects of irrelevant emotional material on the ability to update the contents of working memory in depression. For each trial, participants were required to memorize 2 lists of emotional words and subsequently to ignore 1 of the lists. The impact of irrelevant emotional material on the ability to update the contents of working memory was indexed by response latencies on a recognition task in which the participants decided whether or not a probe was a member of the relevant list. The authors compared response latencies to probes from the irrelevant list to response latencies to novel probes of the same valence (intrusion effect). The results indicate that, compared to control participants in both neutral and sad mood states, depressed participants showed greater intrusion effects when presented with negative words. In an important finding, intrusion effects for negative words were correlated with self-reported rumination. These findings indicate that depression is associated with difficulties removing irrelevant negative material from working memory. Results also indicate that the increased interference from irrelevant negative material is associated with rumination.

Is this happiness I see? Biases in the identification of emotional facial expressions in depression and social phobia

The present study was designed to examine the operation of depression-specific biases in the identification or labeling of facial expression of emotions. Participants diagnosed with major depression and social phobia and control participants were presented with faces that expressed increasing degrees of emotional intensity, slowly changing from a neutral to a full-intensity happy, sad, or angry expression. The authors assessed individual differences in the intensity of facial expression of emotion that was required for the participants to accurately identify the emotion being expressed. The depressed participants required significantly greater intensity of emotion than did the social phobic and the control participants to correctly identify happy expressions and less intensity to identify sad than angry expressions. In contrast, social phobic participants needed less intensity to correctly identify the angry expressions than did the depressed and control participants and less intensity to identify angry than sad expressions. Implications of these results for interpersonal functioning in depression and social phobia are discussed.

Coherence and Specificity of Information-Processing Biases in Depression and Social Phobia

Research has not resolved whether depression is associated with a distinct information-processing bias, whether the content of the information-processing bias in depression is specific to themes of loss and sadness, or whether biases are consistent across the tasks most commonly used to assess attention and memory processing. In the present study, participants diagnosed with major depression, social phobia, or no Axis I disorder, completed several information-processing tasks assessing attention and memory for sad, socially threatening, physically threatening, and positive stimuli. As predicted, depressed participants exhibited specific biases for stimuli connoting sadness; social phobic participants did not evidence such specificity for threat stimuli. It is important to note that the different measures of bias in memory and attention were not systematically intercorrelated. Implications for the study of cognitive bias in depression, and for cognitive theory more broadly, are discussed.

Serotonergic Function, Two-Mode Models of Self-Regulation, and Vulnerability to Depression: What Depression Has in Common With Impulsive Aggression

Evidence from diverse literatures supports the viewpoint that two modes of self-regulation exist, a lower-order system that responds quickly to associative cues of the moment and a higher-order system that responds more reflectively and planfully; that low serotonergic function is linked to relative dominance of the lower-order system; that how dominance of the lower-order system is manifested depends on additional variables; and that low serotonergic function therefore can promote behavioral patterns as divergent as impulsive aggression and lethargic depression. Literatures reviewed include work on two-mode models; studies of brain function supporting the biological plausibility of the two-mode view and the involvement of serotonergic pathways in functions pertaining to it; and studies relating low serotonergic function to impulsiveness, aggression (including extreme violence), aspects of personality, and depression vulnerability. Substantial differences between depression and other phenomena reviewed are interpreted by proposing that depression reflects both low serotonergic function and low reward sensitivity. The article closes with brief consideration of the idea that low serotonergic function relates to even more diverse phenomena, whose natures depend in part on sensitivities of other systems.

Attentional bias in dysphoria: The role of inhibitory processes

This study investigates inhibitory dysfunctions in the processing of emotional material and their relation to depressive symptomatology and vulnerability. In a series of three experiments, a negative priming task with positive and negative distractor and target words was presented. The negative priming task makes it possible to assess the degree of inhibition of activated but nongoal‐relevant stimulus representations. Results indicate that participants with elevated depression scores fail to show negative priming in affective evaluation and self‐reference tasks. Moreover, participants reporting a history of major depressive episodes fail to show negative priming when asked to respond to the valence or self‐descriptiveness of emotional stimuli. The obtained results are in line with the hypothesis that depression is associated with an inhibitory deficit for negative information. Implications of these results for research on selective attention in depression are discussed.