Longitudinal Association Between Depressive Symptoms and Multidimensional Sleep Health: The SWAN Sleep Study.

BACKGROUND: Depressive symptoms and sleep disturbances disproportionately affect midlife women. While there may be a bidirectional association, few studies have examined whether depressive symptoms are longitudinally associated with subsequent sleep. Sleep is typically considered unidimensional, despite emerging evidence that multidimensional sleep health provides novel information on the sleep-health link. PURPOSE: The current study examined whether higher depressive symptoms were longitudinally associated with poorer multidimensional sleep health. METHOD: Depressive symptoms were assessed with the Center for Epidemiologic Studies Depression Scale across six to nine annual assessments in 302 midlife women from the Study of Women's Health Across the Nation. Six months after their last assessment, actigraphy (mean ± standard deviation = 29.3 ± 6.9 days) and self-report were used to assess sleep health components: efficiency, duration, mid-sleep timing, regularity, alertness, and satisfaction, which were dichotomized and summed to create a composite multidimensional sleep health score. Mixed-effects models were used to evaluate the longitudinal associations between depressive symptoms and multidimensional sleep health, as well as individual sleep health components, adjusting for covariates. Exploratory analyses stratified models by race/ethnicity. RESULTS: Higher depressive symptoms were associated with subsequent poorer multidimensional sleep health (p < .0.001) and lower alertness (p < .0001) and satisfaction with sleep (p < .0001). CONCLUSIONS: Our finding that higher average depressive symptoms were associated longitudinally with actigraphy-measured poorer sleep health in midlife women is novel and converges with the larger body of evidence that these two common symptoms are strongly associated. The bidirectional relationship between these two prevalent symptoms needs to be studied in prospective longitudinal studies.

Evening chronotype, alcohol use disorder severity, and emotion regulation in college students.

The evening chronotype is strongly associated with greater alcohol use, though mechanisms underlying this association are not well understood. The current study evaluated emotion regulation as a potential mechanism linking evening chronotype and alcohol use. Participants were 81 undergraduate students. Chronotype was assessed using the Composite Scale of Morningness (CSM). Alcohol use disorder severity was assessed using the Alcohol Use Disorder Identification Test (AUDIT). Participants recorded daily sleep patterns using an online diary for seven days. Participants then completed a standardized laboratory emotion regulation task. Self-reported affect, high-frequency heart rate variability (HF-HRV), and pre-ejection period (PEP) were measured throughout the task. Sleep duration on non-free days (defined as days when sleep was restricted by morning obligations such as work or school) was evaluated as a moderator. Thirty-one evening chronotypes (CSM scores ≤ 26) were compared to 50 non-evening chronotypes (CSM scores >26). Evening chronotypes reported significantly greater symptoms of alcohol use disorder (F = 4.399, p = .039). In the full sample, emotion regulation was successful for altering affective but not autonomic reactivity to emotional stimuli. There were no chronotype differences in self-reported affect, HF-HRV, or PEP during the emotion regulation task. Longer sleep duration on non-free days was associated with increased HF-HRV during negative emotion regulation among non-evening chronotypes. Moderated mediation revealed that emotion regulation did not mediate the association between evening chronotype and alcohol use, irrespective of sleep duration on non-free days. This study is consistent with the literature on chronotype and substance use, demonstrating that undergraduate evening chronotypes endorse greater severity of alcohol use disorder. Given that emotion regulation did not successfully alter autonomic reactivity to emotional stimuli, emotion regulation as a potential mechanism linking chronotype and alcohol use remains inconclusive. Longer sleep duration appears to be protective for non-evening chronotypes in terms of parasympathetic control during the regulation of negative emotions.

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.

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.

Sleep's benefits to emotional processing emerge in the long term.

Sleep benefits the long-term preservation of emotional memories, making them accessible even years after the emotional episode has occurred. However, whether sleep also influences the emotional response that gets elicited while retrieving such memories (e.g., by increasing autonomic activity) remains unclear. Here, we demonstrate that sleep fosters a coherent decrease in both automatic (heart rate deceleration) and more cognitively controlled subjective measures (valence ratings) of the emotional tone associated with memories when they are retrieved after one week. Exploratory analyses suggest that sleep might initiate an enhancement of the neural representation of emotional compared to neutral memories (as reflected in the late positive potential of the electroencephalogram) that becomes pronounced after one week. These long-term effects are in contrast to sleep's immediate influence on the emotional response (i.e., 10 h after encoding), where heart rate deceleration was preserved and the late positive potential decreased when compared to the changes seen over a day of wake. Together, these results suggest that sleeping after an emotional experience has dynamic and protracted influences on the emotional tone associated with memories.

Disturbed Sleep as a Mechanism of Race Differences in Nocturnal Blood Pressure Non-Dipping.

PURPOSE OF REVIEW: Disturbed sleep may be a mechanism of race differences in nocturnal blood pressure non-dipping. In support of this proposal, we summarize recent research from three literatures: (1) race differences (Black compared with White individuals) in nocturnal blood pressure non-dipping, (2) the association between disturbed sleep and nocturnal blood pressure non-dipping, and (3) race differences in disturbed sleep. RECENT FINDINGS: Black individuals are nearly twice as likely to have blood pressure non-dipping profiles compared with White individuals. This may be explained, in part, by sleep; shorter sleep duration, greater sleep fragmentation, less slow-wave sleep, and obstructive sleep apnea have each been associated with nocturnal blood pressure non-dipping. These sleep disturbances, in turn, are more common in Black compared with White individuals. Studies focused on nocturnal blood pressure non-dipping rarely assess sleep, and experimental evidence linking disturbed sleep with nocturnal blood pressure non-dipping in Black individuals is lacking. While mounting evidence from independent literatures suggests that disturbed sleep is a plausible, modifiable mechanism of race differences in nocturnal blood pressure non-dipping, definitive conclusions are premature given the current state of science.

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.