Unlabelled

Studies examining the association between childhood trauma exposure and neuroendocrine functioning have returned inconsistent findings. To date, few studies have accounted for the role exposure to different types of childhood trauma may have on different neuroendocrine adaptations, and no study has examined this association using multiple indices of hypothalamic-pituitary-adrenal axis (HPA-axis) functioning. The purpose of this study was to characterize the unique associations between exposure to physical abuse, emotional abuse, and non-intentional trauma, and multiple indices of HPA-axis functioning.

Methods

A community sample of 138 youth (aged 9-16) completed the Socially Evaluated Cold Pressor Task (SE-CPT) while their parents completed the Early Trauma Inventory (ETI). All youth then collected 4 diurnal salivary cortisol samples at home across 2 consecutive weekdays.

Results

High reported exposure to non-intentional trauma was associated with intact diurnal regulation but elevated cortisol at bedtime, physical abuse was associated with faster reactivity to acute stress, and emotional abuse was associated with delayed recovery of cortisol following acute stress. Taken together, there was a heterogeneous relationship among different indices of HPA-axis functioning and trauma subtype.

Discussion

Different types of childhood trauma exposure are related to distinct anomalies in HPA-axis functioning. This study underscores the importance of research incorporating multiple indices of HPA-axis functioning to inform our understanding of the underlying neuroendocrine dysregulation that may later lead to stress-related psychopathology.

Research suggests that sleep preferentially consolidates the negative aspects of memories at the expense of the neutral aspects. However, the mechanisms by which sleep facilitates this emotional memory trade-off remain unknown. Although active processes associated with sleep-dependent memory consolidation have been proposed to underlie this effect, this trade-off may also be modulated by non-sleep-related processes, such as the circadian factors, stress-related factors, and/or mood congruent context effects involved in sleep deprivation. We sought to examine the potential role of these factors by randomizing 39 young adults into either a total sleep deprivation condition (26 consecutive hours awake) or a sleep condition (8 h sleep opportunity). Replicating the emotional memory trade-off effect, negative objects were better remembered than neutral objects or background images. However, in spite of generally worse memory performance (for neutral and background information), sleep-deprived participants showed similar recognition rates for negative emotional memories relative to participants who were given a full night of sleep.

Early life stress (ELS) is a well-established risk factor for psychopathology across the lifespan. Cognitive vulnerability to stress-induced cortisol may explain risk and resilience. The current study aimed to elucidate a psychobiological pathway linking stress to altered memory for affective words among youth with and without exposure to ELS. One hundred and fifteen youth (ages 9-16, 47% female) were randomized either to a psychosocial stressor or a control condition. Immediately following the stress or control condition, participants completed a memory task for affective words. Change in salivary cortisol from immediately before to 25 min after stress onset were used to predict memory for affective words. Exposure to the acute laboratory stressor led to activation of the HPA axis. Greater cortisol reactivity was associated with less accurate recognition of negative valence words. Among youth exposed to ELS, greater cortisol reactivity to acute stress was associated with poorer recognition of dysphoric and neutral words. Acute increases in cortisol may interfere with negatively-valenced information processing that has implications for memory. Youth exposed to high ELS may be particularly vulnerable to the effects of cortisol, which may explain one pathway through which stress leads to psychopathology among at-risk youth.