Sleep health mediates the relationship between physical activity and depression symptoms.

PURPOSE: This study aimed to investigate cross-sectional associations between physical activity, sleep health, and depression symptoms using mediation models. METHODS: Participants (N = 1576, MAge = 39.3 years, 40% female) were recruited online from Amazon's Mechanical Turk crowd-sourcing service. Physical activity was measured using a single-item self-report measure and depression symptoms were reported using the Hospital Anxiety and Depression Scale. Sleep health was measured using the 6-question RUSATED Sleep Health survey V2.0. RESULTS: Good sleep health (direct effect: ß = - .273, t = - 13.87, p < .0001) and high levels of physical activity (direct effect: ß = - .092, t = - 4.73, p < .0001) were both individually associated with fewer depression symptoms. Sleep health significantly mediated 19% of the association between physical activity and depression symptoms (indirect effect: ß = - .022, 95% CI [- .036 to - .008]), while physical activity significantly mediated 3% of the relationship between sleep health and depression symptoms (indirect effect: ß = - .008, 95% CI [- .014 to - .003]). CONCLUSION: Physical activity and sleep health act as predictors and mediators of depression symptoms.

Heart Rate Reactivity to Acute Psychological Stress Predicts Higher Levels of Posttraumatic Stress Disorder Symptoms During the COVID-19 Pandemic.

OBJECTIVE: Increased autonomic arousal is a proposed risk factor for posttraumatic stress disorder (PTSD). Few studies have prospectively examined the association between physiological responses to acute psychological stress before a traumatic event and later PTSD symptoms. The present prospective study examined whether cardiovascular responses to an acute psychological stress task before the COVID-19 global pandemic predicted PTSD symptoms related to the ongoing pandemic. METHODS: Participants (n = 120) were a subsample of an ongoing research study. Phase 1 consisted of a 10-minute baseline and 4-minute acute psychological stress task with blood pressure and heart rate recorded throughout. Phase 2 was initiated 2 weeks after the COVID-19 pandemic declaration. Participants completed the Impact of Event Scale-Revised (IES-R) with respect to the ongoing pandemic. Hierarchical linear regression analyses were used to examine whether cardiovascular stress reactivity predicted COVID-19 PTSD symptoms. RESULTS: Heart rate reactivity significantly predicted IES intrusion (ß = -0.208, t = -2.28, p = .025, ΔR2 = 0.041, confidence interval = -0.021 to -0.001) and IES hyperarousal (ß = -0.224, t = -2.54, p = .012, ΔR2 = 0.047, confidence interval = -0.22 to - 0.003), but not IES avoidance (p = .077). These results remained statistically significant after adjustment for sex, socioeconomic status, baseline cardiovascular activity, neuroticism, race, ethnicity, body mass index, and adverse childhood experiences. There were no statistically significant associations between blood pressure and any of the Impact of Event Scale-Revised subscales (p values > .12). CONCLUSIONS: Diminished heart rate responses (i.e., lower physiological arousal) to acute psychological stress before the COVID-19 pandemic significantly predicted reported PTSD symptoms during the crisis.

The association between physical activity and a composite measure of sleep health.

PURPOSE: Physical activity has been associated with several individual dimensions of sleep. However, the association between physical activity and sleep health, a construct that emphasizes the multidimensional nature of sleep, has not been explored. This analysis examined the relationship between physical activity and a composite measure of sleep health. METHODS: A total of 114 adults (66% female, 60.3 ± 9.2 years) were included in the analyses. Participants reported daily light-intensity physical activity (LPA) and moderate- and vigorous-intensity physical activity (MVPA) via diary, while wearing a pedometer (Omron HJ-720ITC) to measure daily steps. Sleep health was measured using the RU_SATED questionnaire, which addresses regularity of sleep patterns, satisfaction with sleep, daytime alertness, and sleep timing, efficiency, and duration. Multiple linear regression, binary logistic regression, and analysis of covariance (ANCOVA) were utilized for analyses. RESULTS: Mean sleep health score was 9.6 ± 2.4 (0 [poor]-12 [good]). Participants reported 62.9 ± 66.0 and 51.2 ± 51.2 min/day of LPA and MVPA, respectively, and took 5585.5 ± 2806.7 steps/day. Greater MVPA was associated with better sleep health (ß = 0.27, P = 0.005) and sleep health scores differed between those reporting < 30 min/day and ≥ 60 min/day of MVPA (P = 0.004). Greater MVPA was associated with higher odds of having good sleep satisfaction (OR = 1.58 [1.14-2.20], P < 0.01), timing (OR = 2.07 [1.24-3.46], P < 0.01), and duration (OR = 1.48 [1.02-2.18], P = 0.04). Pedometer-based physical activity and LPA were not related to sleep health or its individual dimensions. CONCLUSIONS: In middle- to older-aged adults, higher-intensity activity, but not lower-intensity or volume of activity, was associated with greater sleep health. These data suggest that physical activity intensity may be important for sleep health.

Cardiovascular Stress Reactivity and Carotid Intima-Media Thickness: The Buffering Role of Slow-Wave Sleep.

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.

The Relationship Between Childhood Trauma and Poor Sleep Health in Adulthood.

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: ß = -0.20, ΔR = 0.032; actigraphy: ß = -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.

Testing adverse childhood experiences (ACEs) as a potential moderator of the association between current chronic stress and cardiovascular reactivity.

Motivated by mixed findings regarding the relationship between chronic stress and cardiovascular reactivity, the current study aimed to investigate whether adverse childhood experiences (ACEs) serve as a potential moderator of the association between current chronic stress and cardiovascular reactivity. Incidence of ACEs, levels of current chronic stress, and heart rate (HR) reactivity to a mental arithmetic stress task were measured in 111 participants (age = 20.83, 76 % female, 66 % White). ACEs were measured using the Childhood Trauma Questionnaire and current chronic stress was measured using the Perceived Stress Scale. Moderation analyses were conducted with HR reactivity as the outcome and ACEs as the moderator. Results indicated that a greater amount of current chronic stress was significantly associated with relatively blunted HR reactivity (ß = -0.25, p = 0.03) even after controlling for sociodemographic variables. Exposure to ACEs was not significantly related to HR reactivity, (all p ≥ 0.66), and there was no significant interaction between current chronic stress and ACE exposure in predicting HR reactivity, (all p ≥ 0.44). These results show that current chronic stress is associated with relatively blunted HR reactivity and that exposure to ACEs does not moderate the relationship between chronic stress and cardiac stress reactivity.

Physical activity and sleep relate to antibody maintenance following naturalistic infection and/or vaccination in older adults.

Health behaviours such as being physically active and having good quality sleep have been associated with decreased susceptibility to infection and stronger antibody responses to vaccination. Less is known about how such factors might influence the maintenance of immunity following naturalistic infection and/or prior vaccination, particularly among older adults who may have formed initial antibodies some time ago. This analysis explored antibody levels against a range of common infectious diseases in 104 older adults (60 women) aged 65+ years, and whether these relate to self-reported physical activity (PA) and sleep. PA and sleep were measured subjectively through standardized questions. Antibody levels to a range of common pathogens, including pneumococcal (Pn) and meningococcal (Men) serotypes, Haemophilus influenza type b, diphtheria, and tetanus were assayed using Multiplex technology. Higher PA at baseline related to higher antibody levels against three Pn serotypes and MenY, and higher PA at one month with higher levels against six Pn serotypes. Longer time in bed related to higher antibody levels against Pn4, and longer sleep related to higher levels against Pn19f. More difficulty staying awake in the day related to lower antibodies against Pn19a, Pn19f, MenA and MenY, and more frequent daytime napping related to lower levels against three Pn serotypes and MenY. Using clinically protective antibody thresholds as an outcome showed similar results for PA, but effects for sleep became non-significant, with the exception of time in bed. This extends beyond existing literature demonstrating associations between PA and sleep and peak antibody response to vaccination to antibody maintenance. Longitudinal research with objective measures of health behaviours is warranted.

Daytime sleep accelerates cardiovascular recovery after psychological stress.

BACKGROUND: Sleep restriction and poor sleep quality is linked with cardiovascular morbidity. PURPOSE: The present study aimed to explore the influence of daytime sleep supplementation on cardiovascular reactivity. METHOD: Participants (N = 85) were generally healthy young adults and were randomized to a 60-min polysomnographically-monitored sleep condition or to a no-sleep condition. Participants then completed a standard three-phase mental stress reactivity task. RESULTS: Significantly lower mean arterial pressure means were found in the recovery phase of the stress reactivity task among participants that accrued more than 45 min of daytime sleep. CONCLUSION: These findings suggest daytime sleep may offer cardiovascular benefit in the form of greater cardiovascular recovery from psychological stress. Further research should assess daytime sleep characteristics (time of day, length, and architecture) on cardiovascular response, in an effort to better understand its role as a possible recuperative agent against suboptimal nocturnal sleep patterns.

Adverse childhood experiences (ACEs) relate to blunted cardiovascular and cortisol reactivity to acute laboratory stress: A systematic review and meta-analysis.

Adverse childhood experiences (ACEs) are associated with poor future mental and physical health. Altered biological reactivity to mental stress may be a possible mechanism linking ACEs to poor health. However, it is not clear if ACEs relate to blunted or exaggerated stress reactivity. This meta-analysis aimed to determine whether exposure to ACEs is associated with cardiovascular and cortisol stress reactivity. A systematic review yielded 37 sources. Random-effects modelling tested the aggregate effects of 83 studies of the association between ACEs and stress reactivity. Exposure to ACEs was associated with relatively blunted cardiovascular and cortisol stress reactivity. Effect sizes did not vary as a function of sample sex or reactivity measure (e.g., heart rate, blood pressure, or cortisol). Meta-regression revealed preliminary evidence of greater blunting in samples of a younger age and samples reporting greater ACE exposure. Subgroup analyses for stress task, ACE measurement instrument, and sample race were not conducted because of a lack of between-study variability. Exposure to ACEs is associated with dysregulation of multiple components of the human stress response system.

Cardiovascular reactions to acute psychological stress and academic achievement.

Cardiovascular reactions to acute psychological stress have been associated with cognitive function. However, previous work has assessed cardiovascular reactions and cognitive function in the laboratory at the same time. The present study examined the association between cardiovascular reactions to acute psychological stress in the laboratory and academic performance in final year high school students. Heart rate, blood pressure, stroke volume, and cardiac output reactions to an acute psychological stress task were measured in 131 participants during their final year of high school. Performance on high school A-levels were obtained the following year. Higher heart rate and cardiac output reactivity were associated with better A-level performance. These associations were still statistically significant after adjusting for a wide range of potentially confounding variables. The present results are consistent with a body of literature suggesting that higher heart rate reactions to acute psychological stress are associated with better cognitive performance across a variety of domains.

Trait neuroticism does not relate to cardiovascular reactivity or habituation to repeated acute psychosocial stress.

Neuroticism has been associated with adverse cardiovascular health. Adverse cardiovascular health outcomes have also been linked to cardiovascular reactivity and cardiovascular reactivity habituation to acute psychosocial stress. As such, cardiovascular stress reactivity and habituation may be a factor in the association between neuroticism and disease risk. However, studies of the relationship between neuroticism and cardiovascular reactivity have produced mixed results. Moreover, the relationships between neuroticism, cardiovascular reactivity habituation, and general affect across a repeated stress paradigm have not been examined. The present study aimed to assess the relationships between neuroticism, positive and negative affect, and cardiovascular reactivity and habituation to acute psychosocial stress in a large, demographically diverse sample. Participants (N = 426) completed two 4-min mental arithmetic stressors, each with a separate baseline, in a single laboratory session while having discrete blood pressure and heart rate measurements taken. State positive and negative affect were measured immediately following informed consent, after receiving task instructions, and after each stress task. Trait neuroticism was measured using the Big Five Inventory. Each stress task elicited significant cardiovascular changes. Trait neuroticism was not significantly associated with cardiovascular reactivity or cardiovascular reactivity habituation, within or across stress tasks (all p's > 0.12). Across the entire study protocol, neuroticism was significantly related to lower positive affect and higher negative affect (both p's < 0.001). Trait neuroticism did not relate to stress-related cardiovascular adjustments but might confer a predisposition toward high negative affect.

Multidimensional Sleep Health and Physical Functioning in Older Adults.

Objective: To examine the association between multidimensional sleep health and objective measures of physical functioning in older adults. Method: We conducted a secondary analysis of 158 adults ≥65 years who participated in Midlife in the United States (MIDUS) 2 and MIDUS Refresher studies. Physical functioning was assessed using gait speed during a 50-foot timed walk, lower extremity strength via chair stand test, and grip strength via hand-held dynamometers. Composite multidimensional sleep health scores were derived from 1 week of sleep diaries and wrist actigraphy. Results: Multiple linear regression was used to examine the associations between multidimensional sleep health and physical functioning measures. In adjusted regression analyses, multidimensional sleep health was significantly positively associated with gait speed but not lower extremity strength or grip strength. Discussion: These findings suggest multidimensional sleep health may contribute to physical functioning in older adults. Longitudinal examinations are needed to determine the value of multidimensional sleep health as a therapeutic target to optimize physical functioning.

Cynical hostility relates to a lack of habituation of the cardiovascular response to repeated acute stress.

Hostility is associated with increased risk for cardiovascular disease. Heightened cardiovascular reactivity to psychological stress has been proposed as a potential mechanism. Recent work has emphasized a need to measure cardiovascular reactivity across multiple stress exposures to assess potential habituation over time. The aims of the current study were (a) to examine the relationship between each of the three main components of hostility (i.e., emotional, cognitive, and behavioral) and cardiovascular reactivity at two separate stress testing visits and (b) to examine the relationship between hostility components and cardiovascular reactivity habituation. This study utilized previously collected data from the Pittsburgh Cold Study 3. One hundred and ninety-six participants (Mean (SD)[range] age = 29.9 (10.8)[18-55] years, 42.9% female, 67.3% Caucasian) completed 2 separate, identical laboratory sessions, consisting of a 20-min baseline and 15-min stress (Trier Social Stress Test). Heart rate and systolic/diastolic blood pressure were recorded throughout. Reactivity was calculated separately for heart rate, systolic, and diastolic blood pressure (stress-baseline). Participants also completed a modified version of the Cook-Medley Hostility Scale. Results indicated that greater cognitive hostility (i.e., cynicism) was associated with blunted cardiovascular reactivity at Visit 1 and less cardiovascular reactivity habituation between visits, even when controlling for confounding variables. No significant relationships to cardiovascular reactivity or habituation were found for emotional (i.e., hostile affect) or behavioral (i.e., aggressive responding) components. Outcomes for total hostility did not survive adjustment for confounders. These results identify a potential pathway through which hostility, particularly cynicism, contributes to disease risk.

Does objectively-assessed sleep moderate the association between history of major depressive disorder and task-switching?

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.

Multidimensional sleep health is not cross-sectionally or longitudinally associated with adiposity in the Study of Women's Health Across the Nation (SWAN).

OBJECTIVES: The association between sleep and adiposity (indexed by body mass index or waist-to-hip ratio) has typically been evaluated using a single dimension of self-reported sleep. However, other dimensions and behavioral measures of sleep may also be associated with adiposity. This study evaluated whether multidimensional sleep health calculated from actigraphy and self-report was longitudinally associated with adiposity in a sample of midlife women who have a high prevalence of sleep disturbances and adiposity. DESIGN: Longitudinal study with 11-14 years of follow-up time between the sleep health assessment and body mass index / waist-to-hip ratio measurements. PARTICIPANTS: Two hundred and twenty-one midlife women enrolled in the Study of Women's Health Across the Nation Sleep Study. MEASUREMENTS: Multidimensional sleep health was quantified using actigraphy (M[SD] = 29.1[7.2] nights) measures of sleep efficiency, midpoint, duration, regularity, and self-report measures of alertness and satisfaction. Each component was dichotomized and summed; higher values indicated better sleep health. Height, body weight, and waist and hip circumference were measured at the sleep study and at follow-up. Linear regression models were used to assess associations between sleep health and adiposity, adjusting for demographic and menopausal covariates. RESULTS: There was no substantial within-person change in adiposity over time. Better sleep health was cross-sectionally and longitudinally associated with lower adiposity in unadjusted, but not in adjusted, models. Individual sleep health components were not associated with adiposity after adjustment. CONCLUSION: We did not observe cross-sectional or longitudinal associations between multidimensional sleep health and adiposity. The sleep-adiposity link may be weaker in midlife adults than in other age groups.

Empirical derivation of cutoff values for the sleep health metric and its relationship to cardiometabolic morbidity: results from the Midlife in the United States (MIDUS) study.

STUDY OBJECTIVES: Emerging evidence supports a multidimensional perspective of sleep in the context of health. The sleep health model, and composite sleep health score, are increasingly used in research. However, specific cutoff values that differentiate "good" from "poor" sleep, have not been empirically derived and its relationship to cardiometabolic health is less-well understood. We empirically derived cutoff values for sleep health dimensions and examined the relationship between sleep health and cardiometabolic morbidity. METHODS: Participants from two independent Biomarker Studies in the MIDUS II (N = 432, 39.8% male, age = 56.92 ± 11.45) and MIDUS Refresher (N = 268, 43.7% male, age = 51.68 ± 12.70) cohorts completed a 1-week study where sleep was assessed with daily diaries and wrist actigraphy. Self-reported physician diagnoses, medication use, and blood values were used to calculate total cardiometabolic morbidity. Receiver operating characteristic (ROC) curves were generated in the MIDUS II cohort for each sleep health dimension to determine cutoff values. Using derived cutoff values, logistic regression was used to examine the relationship between sleep health scores and cardiometabolic morbidity in the MIDUS Refresher cohort, controlling for traditional risk factors. RESULTS: Empirically derived sleep health cutoff values aligned reasonably well to cutoff values previously published in the sleep health literature and remained robust across physical and mental health outcomes. Better sleep health was significantly associated with a lower odds of cardiometabolic morbidity (OR [95% CI] = 0.901 [0.814-0.997], p = .044). CONCLUSIONS: These results contribute to the ongoing development of the sleep health model and add to the emerging research supporting a multidimensional perspective of sleep and health.

Should heart rate variability be "corrected" for heart rate? Biological, quantitative, and interpretive considerations.

Metrics of heart period variability are widely used in the behavioral and biomedical sciences, although somewhat confusingly labeled as heart rate variability (HRV). Despite their wide use, HRV metrics are usually analyzed and interpreted without reference to prevailing levels of cardiac chronotropic state (i.e., mean heart rate or mean heart period). This isolated treatment of HRV metrics is nontrivial. All HRV metrics routinely used in the literature exhibit a known and positive relationship with the mean duration of the interval between two beats (heart period): as the heart period increases, so does its variability. This raises the question of whether HRV metrics should be "corrected" for the mean heart period (or its inverse, the heart rate). Here, we outline biological, quantitative, and interpretive issues engendered by this question. We provide arguments that HRV is neither uniformly nor simply a surrogate for heart period. We also identify knowledge gaps that remain to be satisfactorily addressed with respect to assumptions underlying existing HRV correction approaches. In doing so, we aim to stimulate further progress toward the rigorous use and disciplined interpretation of HRV. We close with provisional guidance on HRV reporting that acknowledges the complex interplay between the mean and variability of the heart period.

Prospective associations among objectively and subjectively assessed sleep and the metabolic syndrome.

OBJECTIVE: Subjective sleep disturbances have been associated with greater risk for concurrent and incident metabolic syndrome (MetS). Previous studies have not examined prospective associations among polysomnography-assessed sleep and the MetS, despite knowledge that self-reported sleep is subject to reporting bias, and that subjectively and objectively assessed sleep are weakly correlated. METHOD: In the current study, objectively-assessed (polysomnography) and subjectively-assessed (Pittsburgh Sleep Quality Index, PSQI) sleep was measured in 145 adults at two timepoints, separated by 12-30 years. A continuous measure of the MetS was assessed at the second time point. Statistical analyses were adjusted for age, sex, lifetime history of major depressive disorder, follow-up time, and apnea-hypopnea index. RESULTS: Polysomnography-assessed sleep duration, latency, efficiency, and slow wave sleep were not significantly prospectively associated with the MetS (ps ≥ 0.16). Self-reported longer sleep latency was prospectively associated with higher MetS scores in unadjusted (ß = 0.29, p = 0.002) and adjusted models (ß = 0.25, p = 0.009). Longer sleep latency was associated with higher fasting glucose levels (ß = 0.47, p < 0.001). CONCLUSION: Our study provides evidence that subjective and objective measures of sleep may differ in their ability to prospectively predict MetS.

Sleep and cardiovascular disease: Emerging opportunities for psychology.

Sleep disturbances and disorders have been implicated in cardiovascular morbidity and mortality. Converging evidence suggests that psychosocial factors that confer risk or resilience to cardiovascular disease (CVD) are also related to sleep. Profound differences in sleep among racial/ethnic minorities compared with non-Hispanic Whites in the United States suggest that sleep, and its interplay with psychosocial factors, may contribute to observed disparities in CVD and in health and functioning more broadly. Less understood is the extent to which sleep and psychosocial factors interact to influence the pathophysiology and clinical course of CVD. This article reviews observational and experimental evidence linking short sleep duration and insomnia, both modifiable sleep disturbances, to CVD, including key physiological mechanisms. Also reviewed is evidence of significant interrelationships among sleep, race/ethnicity, and psychosocial factors known to confer risk or resilience to CVD, including depression, psychological stress, and close interpersonal relationships. It is proposed that a transdisciplinary research framework that integrates knowledge, methods, and measures from the fields of psychology and sleep research may be used to catalyze advances in the prevention and treatment of CVD. Also discussed are promising new directions, expected challenges, and the importance of training in transdisciplinary science and research approaches. (PsycINFO Database Record (c) 2018 APA, all rights reserved).

Childhood Trauma and Sleep Among Young Adults With a History of Depression: A Daily Diary Study.

Child maltreatment and sleep disturbances are particularly prevalent among individuals with a history of depression. However, the precise relation between child maltreatment and sleep within this population is unclear. The present study evaluated childhood maltreatment and trauma as a predictor of sleep duration and insomnia symptoms among young adults with prior depression. A total of 102 young adults (18-22; 78% female) with a history of clinical or subclinical depression completed an in-person visit with diagnostic interviews and questionnaires of childhood trauma (maltreatment and general trauma), and 2 weeks of daily assessments of sleep and depressive symptoms using internet-capable devices. Using multilevel modeling, we found that only childhood emotional neglect significantly predicted higher levels of insomnia symptoms over the 2 weeks, controlling for daily depression. Neither childhood maltreatment nor trauma predicted sleep duration. Our findings highlight a unique relationship between emotional neglect and insomnia symptoms among individuals with a depression history that, given prior research, may potentially play a role in depression recurrence and represent a potential treatment target.