OBJECTIVE: Exaggerated cardiovascular reactivity to acute psychological stress has been associated with increased carotid intima-media thickness (IMT). However, interstudy variability in this relationship suggests the presence of moderating factors. The current study aimed to test the hypothesis that poor nocturnal sleep, defined as short total sleep time or low slow-wave sleep, would moderate the relationship between cardiovascular reactivity and IMT. METHODS: Participants (N = 99, 65.7% female, age = 59.3 ± 9.3 years) completed a two-night laboratory sleep study and cardiovascular examination where sleep and IMT were measured. The multisource interference task was used to induce acute psychological stress, while systolic and diastolic blood pressure and heart rate were monitored. Moderation was tested using the PROCESS framework in SPSS. RESULTS: Slow-wave sleep significantly moderated the relationship between all cardiovascular stress reactivity variables and IMT (all pinteraction ≤ .048, all ΔRinteraction ≥ .027). Greater stress reactivity was associated with higher IMT values in the low slow-wave sleep group and lower IMT values in the high slow-wave sleep group. No moderating effects of total sleep time were observed. CONCLUSIONS: The results provide evidence that nocturnal slow-wave sleep moderates the relationship between cardiovascular stress reactivity and IMT and may buffer the effect of daytime stress-related disease processes.

BACKGROUND: Executive function and psychomotor speed are consistently impaired in patients with major depressive disorder (MDD). Persistent cognitive impairments after depression remission are thought to reflect scarring from the neurotoxic effects of hypothalamic-pituitary-adrenal axis activity during a depressive episode. As sleep also deteriorates with depression and restores daytime executive functions, we examined whether adequate sleep could be protective against task-switching and psychomotor impairments associated with a history of MDD. METHODS: This cross-sectional study tested task-switching associations with MDD history, sleep, and their interaction to determine whether sleep continuity and sleep duration moderate the relationship between MDD history and task-switching performance. RESULTS: After adjusting for age, sex, education, current depressive symptoms, and use of anti-depressants, a history of MDD, particularly recurrent MDD, was associated with slower response speed and disproportionately lower accuracy on repetition trials compared to switch trials, reflecting impaired adoption of a task-set. Regardless of MDD history, higher wake after sleep onset and shorter total sleep time were associated with slower response times, but neither sleep measure moderated the association between depression history and task-switching performance. LIMITATIONS: This cross-sectional study cannot assess the causal direction of associations. One night of sleep in the laboratory was used to assess sleep and a single task-switching paradigm was used to assess executive function. CONCLUSIONS: These results suggest that longer, more continuous sleep is associated with greater psychomotor speed across healthy controls and those with a history of MDD, but MDD-task-switching associations are not mitigated by longer or more continuous sleep.

OBJECTIVE: Childhood trauma has been related to adverse behavioral, mental, and health outcomes later in life. Sleep may be a potential mechanism through which childhood trauma is related to adverse health. The current retrospective study aimed to characterize the relationship between childhood trauma exposure and sleep health, a novel multidimensional measure of sleep. METHODS: Participants (N = 161; mean [standard deviation] age = 59.85 [9.06] years; 67.7% female) retrospectively reported trauma exposure using the Trauma History Questionnaire. Childhood trauma was defined as the number of reported traumatic events before 18 years of age. Trauma exposure after 18 years of age and across the life-span was also recorded. Sleep health was derived both from diary- and actigraphy-assessed measures of sleep regularity, timing, efficiency, and duration, subjective sleep satisfaction, and daytime sleepiness from the Epworth Sleepiness Scale. The relationships between childhood trauma exposure and sleep health were examined using hierarchical linear regression, controlling for relevant covariates. RESULTS: In unadjusted models, a greater number of childhood trauma exposures were associated with poorer diary- and actigraphy-measured sleep health in adulthood. After adjustment for current stress, depression history, and other sociodemographic covariates, greater childhood trauma remained significantly associated with poorer sleep health (diary: β = -0.20, ΔR = 0.032; actigraphy: β = -0.19, ΔR = 0.027). Trauma exposure after 18 years of age and across the life-span did not relate to diary- or actigraphy-based sleep health. CONCLUSIONS: Childhood trauma may affect sleep health in adulthood. These findings align with the growing body of evidence linking childhood trauma to adverse health outcomes later in life.