Depression (Major Depressive Disorder; MDD) has been dubbed "the common cold among the mental illnesses" and it is also a highly recurrent disorder. Secondary prevention has been identified as a key goal in the long-term management of depression. High recurrence rate suggests that there are specific vulnerability factors that increase people's risk for developing repeated episodes of the disorder. Preventive strategies should identify and ameliorate these factors to reduce the individual's risk of subsequent episodes. Biased attention for emotional stimuli is central to the cognitive model where increased sensitivity to negative cues is believed to fuel the negative thoughts and feelings in depression and play a key role in maintaining the illness. Selective biases in attention can be modified by a simple computerized technique; The Attention Bias Modification Task (ABM). This project aims to investigate whether ABM can reduce surrogate and clinical markers of relapse in a large group highly vulnerable to depressive episodes. The effects of ABM, immediately after the two weeks intervention, on three key risk factors for depression will be studied: Residual symptoms, cortisol awakening response and emotion regulation strategies. The participants will be followed up after 1 month, 6 months and 12 months. The hypothesis that ABM will reduce subsequent episodes of low mood over the following 12 months in this group in a manner predicted by early changes in these risk factors will be investigated. It will also be tested if such effects in the lab may be dependent on candidate genes which affect serotonin reuptake and which have been implicated in malleability and emotional learning. Effects on underlying neural correlates of emotion regulation will be studied in an fMRI experiment in a sub-sample and which will also be stratified by serotonin transporter genotype (see also NCT02931487). The predictive value of meta cognitions related to rumination and the possible mediating effects of automatic thoughts and perceived stress will also be investigated in a sub group (see also NCT02648165). The characterization of the cognitive, genetic and neural mechanisms underlying the ABM effect will have key implications for future treatment development and combination with other treatment modalities like pharmacotherapy.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
PREVENTION
Masking
TRIPLE
Enrollment
350
Computer based Attention Bias Modification
Computer based Sham Attention Bias Modification
Sørlandet Hospital, Department of Psychiatry
Arendal, Aust-Agder, Norway
University of Oslo, Department of Psychology
Oslo, Norway
Change in residual symptoms of depression. Self report.
Beck Depression Inventory
Time frame: At baseline and immediately after ABM intervention (during first week after ABM).
Change in residual symptoms of depression. Clinician rating
Hamilton Depression Rating Scale
Time frame: At baseline and immediately after ABM intervention (during first week after ABM).
Recurrence of major depressive episodes
Measured by the MINI structured interview
Time frame: Will be measured 12 month after baseline
Changes in Emotion Regulation
Emotion Regulation Questionnaire (ERQ).
Time frame: At baseline.
Changes in Rumination
The Rumination Response Scale
Time frame: At baseline and 12 months after intervention
Changes in cortisol response.
Cortisol samples from saliva measured by diural variation (6 samples).
Time frame: At baseline, immediately after ABM intervention and one month after intervention.
Changes in symptoms of anxiety
Beck Anxiety Inventory
Time frame: At baseline, immediately after ABM intervention (during first week after ABM intervention), 1 month after intervention, 6 months after intervention and 12 months after intervention
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