Robust research has established that preexisting physical and mental health conditions increase risk for adverse psychiatric outcomes after disasters. However, it is unclear if increased risk is independent of disaster exposure, and most studies have relied on retrospective reports of pre-disaster functioning.

In a pre-post sample of high-risk Puerto Rican adults (N = 361) who experienced Hurricanes Irma and Maria, we assessed: 1) whether indicators of pre-disaster depression and physical health conditions were associated with posttraumatic stress disorder (PTSD) and major depressive disorder (MDD) symptoms; and 2) whether the effects of pre-disaster depression and physical health conditions on PTSD and MDD symptoms were indirect via disaster exposure or had exacerbated the effects of disaster exposure on PTSD and MDD symptoms.

Pre-disaster depression and physical health problems were significantly associated with higher post-disaster MDD symptoms (B = 1.50, SE = 0.36, p < .001, and B = 0.21; SE = 0.09, P = 0.016), but not PTSD symptoms. Indirect effects of pre-disaster depression and physical health symptoms via disaster exposure were non-significant, and neither moderated the association of disaster exposure on PTSD and MDD symptoms.

Research is needed to understand other pathways through which pre-disaster health conditions predict post-disaster mental health.

Genetically informative twin studies have consistently found that individual differences in anxiety and depression symptoms are stable and primarily attributable to time-invariant genetic influences, with non-shared environmental influences accounting for transient effects.

We explored the etiology of psychological and somatic distress in 2279 Australian twins assessed up to six times between ages 12–35. We evaluated autoregressive, latent growth, dual-change, common, and independent pathway models to identify which, if any, best describes the observed longitudinal covariance and accounts for genetic and environmental influences over time.

An autoregression model best explained both psychological and somatic distress. Familial aggregation was entirely explained by additive genetic influences, which were largely stable from ages 12 to 35. However, small but significant age-dependent genetic influences were observed at ages 20–27 and 32–35 for psychological distress and at ages 16–19 and 24–27 for somatic distress. In contrast, environmental influences were predominantly transient and age-specific.

The longitudinal trajectory of psychological distress from ages 12 to 35 can thus be largely explained by forward transmission of a stable additive genetic influence, alongside smaller age-specific genetic innovations. This study addresses the limitation of previous research by exhaustively exploring alternative theoretical explanations for the observed patterns in distress symptoms over time, providing a more comprehensive understanding of the genetic and environmental factors influencing psychological and somatic distress across this age range.

Previous studies (various designs) present contradicting insights on the potential causal effects of diet/physical activity on depression/anxiety (and vice versa). To clarify this, we employed a triangulation framework including three methods with unique strengths/limitations/potential biases to examine possible bidirectional causal effects of diet/physical activity on depression/anxiety.

Study 1: 3-wave longitudinal study (n = 9,276 Dutch University students). Using random intercept cross-lagged panel models to study temporal associations. Study 2: cross-sectional study (n = 341 monozygotic and n = 415 dizygotic Australian adult twin pairs). Using a co-twin control design to separate genetic/environmental confounding. Study 3: Mendelian randomization utilizing data (European ancestry) from genome-wide association studies (n varied between 17,310 and 447,401). Using genetic variants as instrumental variables to study causal inference.

Study 1 did not provide support for bidirectional causal effects between diet/physical activity and symptoms of depression/anxiety. Study 2 did provide support for causal effects between fruit/vegetable intake and symptoms of depression/anxiety, mixed support for causal effects between physical activity and symptoms of depression/anxiety, and no support for causal effects between sweet/savoury snack intake and symptoms of depression/anxiety. Study 3 provides support for a causal effect from increased fruit intake to the increased likelihood of anxiety. No support was found for other pathways. Adjusting the analyses including diet for physical activity (and vice versa) did not change the conclusions in any study.

Triangulating the evidence across the studies did not provide compelling support for causal effects of diet/physical activity on depression/anxiety or vice versa.

Early pubertal timing is associated with depressive symptoms in girls, but studies in boys are limited and have yielded conflicting results.

N = 4,664 male participants from a UK birth cohort (Avon Longitudinal Study of Parents and Children – ALSPAC). Seven indicators of pubertal timing were measured repeatedly from 7 to 17 years (age at: peak height velocity, peak weight velocity, peak bone mineral content velocity, Tanner stage 3 pubic hair, Tanner stage 3 genitalia, axillary hair, and voice break), categorised into ‘early’, ‘on-time,’ and ‘late’ (mean ± 1 SD). Depressive symptoms (binary variable indicating higher versus lower levels) were assessed at 14 and 18 years, and depression (ICD-10 diagnosis) was assessed at 18 years. Multivariable logistic regression was used to examine associations between each indicator of pubertal timing and depressive symptoms/depression, adjusted for socioeconomic status (SES) and prepubertal body mass index (BMI).

Compared to males with normative pubertal development, the odds of depression at age 18 were higher in those with early age at peak height velocity (OR: 2.06; 95% CI 1.27–3.34), early age at peak weight velocity (OR: 2.10; 95% CI 1.16–3.79), and early age at Tanner genitalia stage 3 (OR: 1.81; 95% CI 1.01–3.26). There was no evidence for associations between pubertal timing and depressive symptoms at age 14 or 18.

We found evidence that males with an earlier pubertal timing had increased odds of depression at age 18. Early maturing boys could be targeted for interventions aimed at preventing depression.

The prevalence of youth anxiety and depression has increased globally, with limited causal explanations. Long-term physical health conditions (LTCs) affect 20–40% of youth, with rates also rising. LTCs are associated with higher rates of youth depression and anxiety; however, it is uncertain whether observed associations are causal or explained by unmeasured confounding or reverse causation.

Using data from the Norwegian Mother, Father, and Child Cohort Study (MoBa) and Norwegian National Patient Registry, we investigated phenotypic associations between childhood LTCs, and depression and anxiety diagnoses in youth (<19 years), defined using ICD-10 diagnoses and self-rated measures. We then conducted two-sample Mendelian Randomization (MR) analyses using SNPs associated with childhood LTCs from existing genome-wide association studies (GWAS) as instrumental variables. Outcomes were: (i) diagnoses of major depressive disorder (MDD) and anxiety disorders or elevated symptoms in MoBa, and (ii) youth-onset MDD using summary statistics from a GWAS in iPSYCH2015 cohort.

Having any childhood LTC phenotype was associated with elevated youth MDD (OR = 1.48 [95% CIs 1.19, 1.85], p = 4.2×10−4) and anxiety disorder risk (OR = 1.44 [1.20, 1.73], p = 7.9×10−5). Observational and MR analyses in MoBa were consistent with a causal relationship between migraine and depression (IVW OR = 1.38 [1.19, 1.60], pFDR = 1.8x10−4). MR analyses using iPSYCH2015 did not support a causal link between LTC genetic liabilities and youth-onset depression or in the reverse direction.

Childhood LTCs are associated with depression and anxiety in youth, however, little evidence of causation between LTCs genetic liability and youth depression/anxiety was identified from MR analyses, except for migraine.

Despite high levels of depression and anxiety, there is relatively little attention to psychological treatment approaches to mental health issues for older adults living in nursing homes. Recent studies support the use of cognitive behaviour therapy (CBT) in this population and here we aim to highlight how CBT can be successfully adapted and implemented with beneficial results. The ELders AT Ease (ELATE) program is a unique service delivery model illustrating delivery of CBT with older adults living in nursing homes. The six modules forming the program, based on CBT, are described. A systems wide approach to delivery is emphasised and illustrated through two clinical case descriptions. Innovative mental health programs can have positive benefits for both residents and staff and support the use of CBT in this vulnerable and under-served client group.

1. (1) Knowledge of the content and application of CBT for older adults living in nursing homes.

2. (2) Understanding of CBT session structure as applied to older adults living in nursing homes.

3. (3) Recognising and utilising specific strategies to highlight a systemic approach as central to implementing CBT strategies, such as behavioural activation and reminiscence, with considered involvement by staff and family.

The course of depression is heterogeneous. The employed treatment is a key element in the impact of the course of depression over the time. However, there is currently a gap of knowledge about the trajectories per treatment and related baseline factors. We aimed to identify trajectories of depressive symptoms and associated baseline characteristics for two treatment arms in a randomized clinical trial: treatment as usual (TAU) or TAU plus transdiagnostic group cognitive behavioral therapy (TAU + TDG-CBT).

Growth mixture modeling (GMM) was used to identify trajectories of depressive symptoms over 12 months post-treatment. Logistic regression models were used to examine associations between baseline characteristics and trajectory class membership in 483 patients (TAU: 231; TAU + TDG-CBT: 251).

We identified different patterns of symptom change in the randomized groups: two trajectories in TAU (‘improvement’ (71.4%) and ‘no improvement’ (28.6%)), and four trajectories in TAU + TDG-CBT (‘recovery’ (69.8%), ‘late recovery’ (5.95%), ‘chronicity’ (4.77%), and ‘relapse’ (19.44%)). Higher baseline symptom severity and comorbidity were associated with poorer treatment outcomes in both treatment groups and worse emotional regulation strategies were linked to the ‘no improvement trajectory’ in TAU. The TAU + TDG-CBT group demonstrated greater symptom reduction compared to TAU alone.

There is heterogeneity in treatment outcomes. Integration of TDG-CBT with TAU significantly improves symptom reduction compared to TAU alone. Patients with higher baseline severity and comorbidities show poorer outcomes. Identification of trajectories and related factors could assist clinicians in tailoring treatment strategies to optimize outcomes, particularly for patients with a worse prognosis.

Ultrasonic vocalisations (USVs) emitted by rats may reflect affective states. Specifically, 50 kHz calls emitted during juvenile playing are associated with positive affect. Given that depression is characterised by profound alterations in this domain, we proposed that USV calls may configure a suitable tool for assessing depressive-like states. Utilising the Flinders Sensitive Line (FSL), a well-established animal model of depression, we assessed USV calls emitted by rats during tickling, a procedure based on juvenile rats’ rough-and-tumble play.

Juvenile FSL rats and their control counterparts, the Flinders Resistant Line (FRL) and Sprague Dawley, were submitted to tickling sessions to imitate rats playing behaviour. The rats were tickled daily for 6 weeks starting at PND21. Tickling sessions were recorded for further acoustic analysis of 50 kHz calls.

Tickling increased 50 kHz calls in all the strains. FSL rats emitted more calls than control strains and exhibited a higher number of flat-trill combination calls.

Tickling is a robust method for inducing 50 kHz USV calls. Analysing USV calls emitted during tickling configurates a suitable method for studying affective states relevant to depression. FSL rats did not present anhedonia but rather higher reward sensitivity, which may underlie their stress vulnerability.

Time distortions characterise severe mental disorders, exhibiting different clinical and neurobiological manifestations. This systematic review aims to explore the existing literature encompassing experimental studies on time perception in patients with bipolar disorder (BD), considering psychopathological and cognitive correlates.

Studies using an experimental paradigm to objectively measure the capacity to judge time have been searched for. Selected studies have been described based on whether i) explicit or implicit time perception was investigated, ii) the temporal intervals involved were sub-second or supra-second, and iii) a perceptual or motor timing paradigm was used.

Only 11 met the criteria for inclusion in the review. The available literature shows that the performance of BD patients mostly aligns with controls within sub-second timeframes (six articles), while a different pattern emerges within supra-second intervals based on the clinical phase of the disease (seven articles). Specifically, for longer temporal spans, BD patients tend to overestimate the duration during manic states and underestimate it during depressive states. Notably, no studies have directly investigated the neurobiological mechanisms associated with time perception.

This review indicates that BD patients exhibit time perception similar to controls within sub-second intervals, but tend to overestimate time and underestimate it based on the clinical phase within supra-second intervals. Expanding the understanding of time perception in BD, particularly in relation to clinical phases and cognitive function, is of great importance. Such insights could deepen our understanding of the disorder, refine diagnostic processes, and guide the development of innovative therapeutic interventions.

Treatment-resistant depression (TRD) affects 10–30% of patients with major depressive disorder, leading to increased comorbidities, higher mortality, and significant economic and social burdens. This study aimed to compare the efficacy and safety of bupropion and aripiprazole as augmentation therapies for TRD.

This population-based, retrospective cohort study included adults aged ≥18 years with a diagnosis of depressive disorder who met the criteria for TRD. Data were collected from a nationwide claims database in South Korea. Patients prescribed bupropion were matched 1:1 with those prescribed aripiprazole. Subgroup analyses were performed according to age. An as-treated analysis was performed as the primary analysis, and an intention-to-treat analysis was performed to identify different risk windows. The primary outcome was depression-related hospitalization, and the secondary outcomes were first-time diagnoses of movement disorder and seizure.

A total of 5,619 patients (bupropion: n = 1,568; aripiprazole: n = 4,051) were included in this study. Bupropion was associated with lower risks of hospitalization (hazard ratio [HR]: 0.51; 95% confidence interval [CI] 0.29–0.86) and movement disorders (HR: 0.56; 95% CI 0.36–0.85) than aripiprazole. No significant difference in seizure risk (HR: 0.65; 95% CI 0.30–1.31) was observed between the two treatments. The subgroup analysis of participants aged ≥60 years revealed no significant differences in the three outcomes between the two medications.

Bupropion augmentation is associated with a significantly lower risk of depression-related re-hospitalization and movement disorders in patients with TRD. Therefore, bupropion augmentation can be a comprehensive treatment strategy for TRD.

Depressive symptoms remaining after antidepressant treatment increase the risk of relapse and recurrence. We aimed to analyze the distribution and main drivers of remaining symptoms in patients with a major depressive episode.

Two independent samples of 8,229 and 5,926 patients from two large naturalistic studies were retrospectively analyzed. DSM-IV criteria for major depressive episodes were assessed during two face-to-face visits with clinicians: before the prescription of a new antidepressant, and after 6 weeks of treatment. The Hospital Anxiety and Depression Scale (HADS) was used to assess baseline severity of anxiety and depression.

In both samples, two clusters of remaining symptoms were observed. The first cluster encompassed symptoms related to a negative emotional and cognitive bias and was specifically driven by the baseline severity of depression. The second cluster encompassed neurovegetative symptoms and was specifically driven by the baseline severity of anxiety.

The baseline anxiety-depressive balance of patients could be considered to adapt the treatment, focusing on emotional and cognitive symptoms with patients with high baseline severity of depression, and neurovegetative symptoms with patients with high baseline anxiety severity.

The school–vacation cycle may have impacts on the psychological states of adolescents. However, little evidence illustrates how transition from school to vacation impacts students’ psychological states (e.g. depression and anxiety).

To explore the changing patterns of depression and anxiety symptoms among adolescent students within a school–vacation transition and to provide insights for prevention or intervention targets.

Social demographic data and depression and anxiety symptoms were measured from 1380 adolescent students during the school year (age: 13.8 ± 0.88) and 1100 students during the summer vacation (age: 14.2 ± 0.93) in China. Multilevel mixed-effect models were used to examine the changes in depression and anxiety levels and the associated influencing factors. Network analysis was used to explore the symptom network structures of depression and anxiety during school and vacation.

Depression and anxiety symptoms significantly decreased during the vacation compared to the school period. Being female, higher age and with lower mother's educational level were identified as longitudinal risk factors. Interaction effects were found between group (school versus vacation) and the father's educational level as well as grade. Network analyses demonstrated that the anxiety symptoms, including ‘Nervous’, ‘Control worry’ and ‘Relax’ were the most central symptoms at both times. Psychomotor disturbance, including ‘Restless’, ‘Nervous’ and ‘Motor’, bridged depression and anxiety symptoms. The central and bridge symptoms showed variation across the school vacation.

The school–vacation transition had an impact on students’ depression and anxiety symptoms. Prevention and intervention strategies for adolescents’ depression and anxiety during school and vacation periods should be differentially developed.