Cortisol responses to psychosocial stress predict depression trajectories: Social-evaluative threat and prior depressive episodes as moderators

Abstract

Background Alterations of hypothalamic-pituitary-adrenal (HPA) function are well-established in adults with current depression. HPA alterations may persist into remission and confer increased risk for recurrence. Methods A modified version of the Trier Social Stress Test (TSST) was administered at baseline to 32 young adults with remitted major depressive disorder and 36 never-depressed controls. Participants were randomly assigned to either a ‘high–stress’ condition involving social evaluation or a ‘low-stress’ control condition. Cortisol concentrations were measured in saliva samples throughout the TSST. Participants were assessed again after 6 months for the occurrence of stressful life events and depressive symptoms/disorders during the follow-up period. Results Participants who exhibited enhanced cortisol reactivity in the low-stress condition showed increases in depressive symptoms over follow-up, after controlling for stressful life events during the follow-up period. Anticipatory stress cortisol and cortisol reactivity each interacted with history of depressive episodes to predict depression trajectories. Limitations The single TSST administration limits conclusions about whether alterations of cortisol reactivity represent trait-like vulnerability factors or consequences (“scars’) of past depression. Conclusions These results extend previous findings on stress sensitivity in depression and suggest that altered HPA function during remission could reflect an endophenotype for vulnerability to depression recurrence. Findings support interactive models of risk for depression recurrence implicating HPA function, depression history, and sensitivity to minor stressors. Results may have implications for interventions that match treatment approaches to profiles of HPA function.

Cognitive–behavioural group therapy improves a psychophysiological marker of stress in caregivers of patients with Alzheimer's disease

“…The significant correlations observed between salivary cortisol levels and perceived stress, anxiety and depression are in line with previous findings (Morris, Rao, & Garber, 2012) and reinforce the knowledge of the association between psychological and psychophysiological activities. However, while we observed significant changes in cortisol release following CBT, there were no corresponding changes in psychometric scores.…”

Anxious attachment style predicts an enhanced cortisol response to group psychosocial stress

“…For example an enhanced cortisol response to the TSST has been shown to predict depressive symptoms in young adults (Morris et al, 2012) and suicidal ideation in female adolescents with a history of mental health concerns (Giletta et al, 2014). The results are also consistent with evidence showing greater cortisol reactivity to the TSST in older adults subjected to separation from both parents during childhood (Pesonen et al, 2010) and in young adults exposed to severe pre-natal stress (Entringer et al, 2009).…”

“…This may provide an eventual route to allostatic overload and negative physical and mental health outcomes (McEwen, 2000;Morris et al, 2012). It may also underpin observed aberrant diurnal profiles of cortisol secretion in anxious attachment style (Oskis et al, 2011;Quirin et al, 2008).…”

Comorbid alcohol and mental health disorders: a longitudinal analysis of development to young adulthood

“…These stress-responses may have less to do with learned reactions to stress and coping styles than with genetically determined biochemical responses which describe a stress-sensitivity (109,180,181). It has been suggested that exposure to major negative life events can activate genetic risks for child and adolescent depression (182).…”

“…However, contrary to the evidence above about conflict, a recent analysis of data from the Minnesota Twin study suggested that life stressors outside the family (so excluding divorce) were more likely to be associated with internalising disorders at age 17 than were problematic parent relationships (178). Similarly, other studies have associated stressful life events beyond the family with drinking among adolescents with depression (179), and childhood trauma appears to account at least partially for comorbid anxiety and alcohol problems in adolescence (155).These stress-responses may have less to do with learned reactions to stress and coping styles than with genetically determined biochemical responses which describe a stress-sensitivity (109,180,181). It has been suggested that exposure to major negative life events can activate genetic risks for child and adolescent depression (182).…”