- University of Leeds
- University of Nottingham
- University of Stirling
- University of Glasgow
Research output: Contribution to journal › Article › peer-review
Suicide is a leading cause of mortality worldwide. Dysregulated hypothalamic-pituitary-adrenal (HPA) axis activity, as measured by cortisol levels, has been identified as 1 potential risk factor. Evidence has indicated that childhood trauma is associated with dysregulated cortisol reactivity to stress in adulthood. The current study investigated for the first time whether childhood trauma and daily stressors and emotions were associated with diurnal cortisol levels over a 7-day study in individuals vulnerable to suicide. One hundred and forty-two participants were categorized according to their suicidal history into 3 groups: suicide attempt, suicidal ideation, or control group. Participants completed questionnaires before commencing a 7-day study. Cortisol samples were provided immediately upon waking, at 15 min, 30 min, 45 min, 3 hr, 6 hr, 9 hr, and 12 hr on 7 consecutive days. Measures of daily stressors, mood, defeat, and entrapment were completed at the end of each day. Participants in the suicide attempt and ideation groups released significantly lower cortisol upon awakening (CAR) and had a tendency toward flatter wake-peak to 12 hr (WP-12) cortisol slopes compared to controls. Childhood trauma was found to be associated with significantly lower CAR and a tendency toward flatter WP-12 cortisol slope. Childhood trauma also had an indirect effect on suicide vulnerability group membership via lower daily CAR levels. Lower CAR was associated with increased suicide ideation at 1 month but not 6 months. Daily stress and emotion measures were not associated with cortisol levels. This is the first 7-day daily diary investigation of naturally fluctuating cortisol levels in individuals vulnerable to suicide. The results indicate that dysregulated HPA axis activity is associated with suicidal ideation and behavior. Childhood trauma appears to be an important distal factor associated with HPA-axis dysregulation.