Sleep health as a predictor of the course of depressed mood and loss of interest in individuals with depression

Tracking the course of depressive and anxiety symptoms across adolescence (the CATS study): a population-based cohort study in Australia

As suggested by previous research, sleep health is assumed to be a key determinant of future morbidity and mortality. In line with this, recent studies have found that poor sleep is associated with impaired cognitive function. However, to date, little is known about brain structural abnormalities underlying this association. Although recent findings link sleep health deficits to specific alterations in grey matter volume, evidence remains inconsistent and reliant on small sample sizes. Addressing this problem, the current preregistered study investigated associations between sleep health and grey matter volume (139 imaging-derived phenotypes) in the UK Biobank cohort (33 356 participants). Drawing on a large sample size and consistent data acquisition, sleep duration, insomnia symptoms, daytime sleepiness, chronotype, sleep medication and sleep apnoea were examined. Our main analyses revealed that long sleep duration was systematically associated with larger grey matter volume of basal ganglia substructures. Insomnia symptoms, sleep medication and sleep apnoea were not associated with any of the 139 imaging-derived phenotypes. Short sleep duration, daytime sleepiness as well as late and early chronotype were associated with solitary imaging-derived phenotypes (no recognizable pattern, small effect sizes). To our knowledge, this is the largest study to test associations between sleep health and grey matter volume. Clinical implications of the association between long sleep duration and larger grey matter volume of basal ganglia are discussed. Insomnia symptoms as operationalized in the UK Biobank do not translate into grey matter volume findings.

Lacunar Infarcts in Deep White Matter Are Associated with Higher and More Fluctuating Depressive Symptoms During Three Years Follow-up

The clinical course of depressive symptoms in schizophrenia

Children with overweight or obesity are more likely to experience sleep disorders, although the role of weight in pediatric insomnia treatment has not been examined. The current study examined the relationships of high body mass with pretreatment insomnia severity and global sleep problems and the potential moderating impact of weight on changes in insomnia severity following insomnia treatment. Participants included 1,133 youth ages 2-18 years clinically referred for insomnia treatment. The Pediatric Insomnia Severity Index was collected at the initial assessment and throughout treatment as part of routine clinical care. Treatment status was coded as no treatment, early termination, and completed treatment. Secondary measures of global sleep problems at the initial assessment included the Adolescent Sleep Wake Scale, Adolescent Sleep Hygiene Scale, and Children's Sleep Habits Questionnaire. Medical chart review of visits within ± 3 months of baseline was used to obtain age-adjusted and sex-adjusted body mass index Z-score. Among adolescents, regression analyses found that higher body mass index Z-score modestly predicted baseline insomnia severity (P = .021) and worse sleep hygiene (P < .001). For children, higher body mass index Z-score was modestly associated with baseline total sleep problems (P = .006) but not insomnia severity (P = .792). Across ages, body mass index Z-score predicted neither treatment status nor insomnia improvement (P > .05). Findings were similar in categorical analyses comparing patients with overweight/obesity to healthy weight. Although there is evidence that children of higher body mass present for insomnia treatment with greater sleep concerns, body mass does not predict treatment completion or insomnia improvement. Data suggest insomnia treatment is effective irrespective of weight status. Duraccio KM, Simmons DM, Beebe DW, Byars KC. Relationship of overweight and obesity to insomnia severity, sleep quality, and insomnia improvement in a clinically referred pediatric sample. J Clin Sleep Med. 2022;18(4):1083-1091.

The study aimed: (1) to describe the 12-month course of depressive symptoms among medical inpatients aged 65+, and (2) to investigate predictors of a more severe course that could be identified easily by non-psychiatric staff. Patients were recruited at two Montreal hospitals. Inclusion criteria were: aged 65+, admitted to medical service, at most mild cognitive impairment. Patients were screened for major and minor depression (DSM-IV criteria). All depressed patients and a random sample of non-depressed patients were invited to participate in the prospective study. The Hamilton Depression Scale (HAMD) was administered at admission, 3, 6, and 12 months. Individual patient trajectories of depressive symptoms over time were grouped using hierarchical clustering into three patient groups with a minimal, mild, and moderate/severe course of symptoms, respectively. The baseline predictors of a more severe clinical course were identified using ordinal logistic regression. Two hundred and thirty-two patients completed baseline and one or more follow-up interviews. Baseline patient characteristics that independently predicted a more severe symptom course included higher initial HAMD score, depressive core symptoms lasting 6 months or more, and female sex. The 12-month course of depression symptoms in this medically ill older sample was generally stable. Patients who will experience a more severe course can be identified by non-psychiatric staff at admission to hospital.

Coping and the Course of Mother's Depressive Symptoms During and After Pediatric Bone Marrow Transplantation

BackgroundLow-grade inflammation (LGI) and endothelial dysfunction (ED) might play a key role in the development of depression. We investigated the associations and mediation of LGI and ED with four-year incidence and course of depressive symptoms (remitted, recurrent or persistent). Design, setting, participants, measurementsIn this prospective cohort study (mean age 59.6 ± 8.2 years, 48.9% women, 26.6% diabetes by design), Cox and multinomial regression analyses, adjusted for age, sex, educational level and diabetes status were used to investigate the associations of LGI and ED with onset and course of depressive symptoms as assessed by the PHQ-9 questionnaire. ResultsDuring 10,847 person-years of follow-up, 264 participants developed incident depression. Higher levels of LGI (OR [95%CI] per SD 1.32[1.16–1.49], p < 0.001) and ED (1.26[1.11–1.43], p < 0.001) were associated with incident depressive symptoms. In mediation analysis, 60% of the total effect of ED with incident depressive symptoms could be attributed to LGI. 76 out of 2637 participants had a persistent course of depressive symptoms. Higher levels of LGI (1.75[1.40–2.19], p < 0.001) and ED (1.33[1.04–1.71], p = 0.021) were associated with a persistent course of depressive symptoms. Higher ED was more strongly associated with persistent depressive symptoms (1.33[1.04–1.71], p = 0.021), while LGI was associated with remission of depression symptoms. ConclusionsLGI and ED were both associated with incident depressive symptoms, where the latter association was substantially mediated by LGI. ED was further associated with a persistent course of depressive symptoms, while LGI was not. These results suggest a temporal, vascular contribution of both LGI and ED to the etiology and chronicity of depressive symptoms.

Poor sleep quality during pregnancy is associated with both antepartum and postpartum depression and adverse birth outcomes. This study evaluated both objective and subjective sleep quality and the effects on the subsequent course of antepartum depressive symptoms in psychiatric patients. This observational explorative study was embedded in an ongoing study focusing on pregnant women with a mental disorder and was performed in 18 patients (24–29 weeks pregnant). Depressive symptoms were assessed throughout pregnancy using the Edinburgh Postnatal Depression Scale (EPDS) with 5-week intervals. Sleep was assessed with actigraphy, the Pittsburgh Sleep Quality Index (PSQI) and sleep diaries at the start of the study. We studied correlations between sleep parameters and EPDS scores cross-sectionally using Spearman correlation. Next, we studied the course of antepartum EPDS scores over time per sleep parameter using generalized linear mixed modelling analysis. Objectively measured fragmentation index, total PSQI score and 4 PSQI subscales (sleep quality, sleep duration, sleep disturbances and daytime dysfunctions) were significantly correlated with EPDS scores when measured cross-sectionally at the start. Six objectively and subjectively measured sleep parameters had moderate to large effects on the course of depressive symptoms through the third trimester, but these effects were not statistically significant. More research is necessary to explore the causality of the direction between sleep problems and antepartum depressive symptoms we found in psychiatric patients.

To estimate the association between hippocampal and total brain volume and the course of depressive symptoms over eight years of follow-up in patients with a history of vascular disease. Within the SMART-Medea study, 636 participants (62 ± 10 years) had a 1.5-tesla brain MRI obtaining hippocampal and total brain volumes. Depressive symptoms were assessed with the Patient Health Questionnaire-9 biannually during eight-year follow-up. Generalized estimating equation models with robust standard errors were used to assess the associations of hippocampal and total brain volumes with depressive symptoms during follow-up adjusting for age, sex, education, and intracranial volume. An interaction term between volume and time (6-month intervals) was included to examine whether the course of depressive symptoms differed according to hippocampal and total brain volume. The mean PHQ-9 score was 2.8 ± 3.5. Smaller hippocampal volumes were associated with an increasing course of depressive symptom levels, while larger volumes were associated with decreasing levels (P-value interaction = 0.07). Smaller total brain volume was associated with consistently higher levels of depressive symptoms, but not with change in course of depressive symptoms (P-value interaction = 0.45). Smaller hippocampal volume but not total brain volume is associated with poorer course of depressive symptoms over eight years of follow-up.

Using data from the Netherlands Study of Depression and Anxiety, we examined among 1322 participants with a DSM–IV diagnosis of depression or anxiety: (i) whether positive and negative life events influence 1–year course of anxiety and depressive symptoms; (ii) whether personality traits (neuroticism and extraversion) predict symptom course and moderate the impact of life events on symptom course; and (iii) whether life events mediate relationships of neuroticism and extraversion with symptom course. Negative life events were predictive of both anxiety and depressive symptoms, while positive life events predicted the course of depressive symptoms only. Personality traits had significant predictive and moderating effects on symptom course, though these effects were rather small. Copyright © 2011 John Wiley &amp; Sons, Ltd.

The presence of depressive symptoms after myocardial infarction (MI) is a risk factor for new cardiovascular events. The importance of the course of post-MI depressive symptoms for cardiac prognosis is not clear. We therefore set out to investigate whether different courses of post-MI depressive symptoms can be identified and determine their associations with cardiac events. Data were derived from the Depression after Myocardial Infarction (DepreMI) study, a naturalistic follow-up study of patients admitted for an MI in four hospitals in The Netherlands (N = 475). Scores on the Beck Depression Inventory (BDI) during hospitalization and at 3, 6, and 12 months post-MI were analyzed. Using latent class analysis (LCA), we identified classes characterized by distinctive courses of depressive symptoms and then examined their link to cardiac prognosis. The prevalence of significant depressive symptoms ranged from 22.7% to 25.5% throughout the post-MI year. Five distinct courses were found: no depressive symptoms (56.4%), mild depressive symptoms (25.7%), moderate and increasing depressive symptoms (9.3%), significant but decreasing depressive symptoms (4.6%), and significant and increasing depressive symptoms (4.0%). Subjects in this last class had, statistically, a significantly higher risk for a new cardiovascular event compared with subjects without depressive symptoms (hazard ratio (HR) = 2.73; p = .01). Controlling for baseline cardiac status and sociodemographic data did not alter the association (HR = 2.46; p = .03). Post-MI depressed subjects with significant and increasing depressive symptoms are at particular risk of new cardiac events. This subgroup may be most suited for evaluation of the effects of antidepressant treatment on cardiac prognosis.

It is well-established that depression is common after stroke. Much less is known about the longitudinal course of depressive symptoms in stroke survivors. Data for this study came from the DESERVE trial of a skills-based intervention to reduce vascular risk in mild/moderate stroke/TIA patients. Depressive symptoms were assessed at baseline (pre-discharge), 6 months and 1 year post-discharge using the Center for Epidemiologic Studies - Depression (CES-D) scale. Discrete mixture models identified distinct trajectories of depressive symptom severity over time and assigned patients to trajectory groups. We ran Poisson models using linear and quadratic parameters and chose the best-fitting model based on Bayesian information criterion and interpretability. Associations between baseline characteristics and trajectory group membership were examined using ANOVA and bivariable multinomial logistic regression. So far, 285 patients completed all three study waves and ≥ 1 depression assessment. A four-group model was selected: 1) resistance - low depressive symptom level at all waves (50% of patients); 2) delayed - low baseline symptom level, increasing to clinically significant levels (CES-D &gt; 16) by 6 months, remaining high at 1 year (18%); 3) recovery - clinically significant baseline symptom levels, dropping to low levels by 6 months, remaining low at 1 year (22%); 4) chronic - severe symptoms at all waves (10%). Hispanic patients had greater odds of delayed symptoms vs. resistance compared to non-Hispanics. Moderate stroke patients had greater odds of delayed and chronic symptoms vs. resistance compared to mild stroke patients. Patients with stroke history had greater odds of delayed symptoms and recovery vs. resistance compared to those without; those with psychiatric history had greater odds of recovery and chronic symptoms vs. resistance compared to those without. Those with chronic symptoms had significantly greater baseline disability compared to other groups. The course of post-stroke depressive symptoms is heterogeneous and associated with race/ethnicity and several clinical factors. Targeted interventions may be required to prevent the development of depression and address chronic symptoms that may interfere with stroke recovery.

Depressive symptoms and cognitive impairment often co-occur, but their interactive relationship is complex and the direction of causation is still a topic of research. We examined the influence of cognitive performance on the course of depressive symptoms during 7 years of follow-up in patients with vascular disease. Within the SMART-MR study, 736 patients (mean age 62 ± 10 years) had neuropsychological assessment on four cognitive domains at baseline [memory (MEM), working memory (WMEM), executive functioning (EXEC), and information processing speed (SPEED)]. Depressive symptoms were assessed with the Patient Health Questionnaire-9 (PHQ-9) at baseline and every 6 months during 7 years of follow-up. Generalized Estimating Equation (GEE) models were used to assess the association between cognitive performance with depressive symptoms at multiple time points during follow-up. Interaction terms between the respective cognitive domains and time was included to examine if the course of depressive symptoms differed according to baseline cognitive performance. The GEE analyses showed no significant interactions between the respective cognitive domains and time indicating no different course of depressive symptoms according to baseline cognitive performance. Lower MEM, EXEC or SPEED, but not WMEM performance, was significantly associated with more depressive symptoms during follow-up per z score decrease: MEM [B = 0.70, 95% confidence interval (CI) 0.35-1.05]; EXEC (B = 0.88, 95% CI 0.41-1.36), and SPEED (B = 0.57, 95% CI 0.21-0.92). Poorer cognitive performance on the domains MEM, EXEC and SPEED, but not WMEM, was associated with higher levels of depressive symptoms over 7 years of follow-up, but not with a different course of depressive symptoms over time.

The course of depressive symptoms as measured by the Cornell scale for depression in dementia over 74 months in 1158 nursing home residents