Previous research has made significant progress elucidating the nature of cognitive biases in emotional disorders. However, less work has focused on the relation among cognitive biases and emotional responding in clinical samples. This study uses eye-tracking to examine difficulties disengaging attention from emotional material in depressed participants and to test its relation with mood reactivity and recovery during and after a stress induction. Participants diagnosed with Major Depressive Disorder (MDD) and never-disordered control participants (CTL) completed a novel eye-tracking paradigm in which participants had to disengage their attention from emotional material to attend to a neutral stimulus. Time to disengage attention was computed using a direct recording of eye movements. Participants then completed a stress induction and mood reactivity and recovery were assessed. MDD compared with CTL participants took significantly longer to disengage from depression-related stimuli (i.e., sad faces). Individual differences in disengagement predicted lower recovery from sad mood in response to the stress induction in the MDD group. These results suggest that difficulties in attentional disengagement may contribute to the sustained negative affect that characterizes depressive disorders.

A growing body of research demonstrates that individuals diagnosed with major depressive disorder (MDD) are characterized by shortened telomere length, which has been posited to underlie the association between depression and increased instances of medical illness. The temporal nature of the relation between MDD and shortened telomere length, however, is not clear. Importantly, both MDD and telomere length have been associated independently with high levels of stress, implicating dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis and anomalous levels of cortisol secretion in this relation. Despite these associations, no study has assessed telomere length or its relation with HPA-axis activity in individuals at risk for depression, before the onset of disorder. In the present study, we assessed cortisol levels in response to a laboratory stressor and telomere length in 97 healthy young daughters of mothers either with recurrent episodes of depression (i.e., daughters at familial risk for depression) or with no history of psychopathology. We found that daughters of depressed mothers had shorter telomeres than did daughters of never-depressed mothers and, further, that shorter telomeres were associated with greater cortisol reactivity to stress. This study is the first to demonstrate that children at familial risk of developing MDD are characterized by accelerated biological aging, operationalized as shortened telomere length, before they had experienced an onset of depression; this may predispose them to develop not only MDD but also other age-related medical illnesses. It is critical, therefore, that we attempt to identify and distinguish genetic and environmental mechanisms that contribute to telomere shortening.