Prompt initial contact with a treatment provider is a critical first step in seeking help for a mental or substance use disorders (SUDs). The aim of the current study was to provide estimates of patterns and predictors of delay in making initial treatment contact based on the recently completed Australian National Survey of Mental Health and Wellbeing.

Data came a nationally representative epidemiological survey of n = 15,893 Australians. Measures included DSM-IV lifetime diagnoses of mood (MD), anxiety (AD) and SUDs; age of disorder onset; and age of first treatment contact. Correlates of treatment delay were examined.

SUDs exhibited the lowest lifetime treatment rate (27%), compared to MD (94%) and ADs (85%). Individuals with AD experienced the longest delay in seeking treatment (Mdn = 11 years), followed by those with SUDs (Mdn = 8 years) and MDs (Mdn = 3 years). Females had higher odds of seeking treatment for MD and AD but lower odds for SUDs. Recent birth cohorts showed increased treatment seeking across disorders, and higher education was associated with increased treatment seeking for MD and AD. Age of onset, country of birth and co-occurring disorders had mixed associations with treatment seeking.

The study reveals stark disparities in treatment-seeking behaviour and delays across mental and substance use disorders, with a pronounced underutilization of services for SUDs. Additionally, attention should be directed towards early intervention for individuals with earlier symptom onset, those from earlier cohorts and those with co-occurring SUDs.

Cannabis is one of the most commonly used drugs globally, although its legal status varies across regions. Public support for its decriminalization has increased, but gaps in our understanding of the health consequences of cannabis use remain, particularly related to its impact on mental health. This article provides an updated systematic review and meta-analysis (previous being Lev-Ran et al., 2014) looking at the relationship between cannabis and depression.

Literature available before March 2023 was screened for longitudinal studies that included cannabis use and depression. Cross-sectional studies and those only looking at special populations were excluded. Studies must have also controlled for depression at baseline to allow for investigation of a temporal relationship. Extracted data included cannabis measures, depression outcomes, adjusted odds ratios, and study settings. Meta-analysis employed a random effects model with multilevel meta-regression for effect size moderators.

The search yielded 1,599 titles from various databases, resulting in 22 studies for meta-analysis, including 14 from Lev-Ran et al. Eleven studies were US-based, with participants mostly under 18. Meta-analysis showed a higher risk of depression among cannabis users (OR: 1.29, 95% CI: 1.13–1.46). Risk of bias assessment showed medium risk across studies with exposure measurement being a key bias area. The funnel plot and Egger’s Sandwich test did not suggest publication bias.

This study underscores the association between cannabis use and depression but also emphasizes the need for further research, especially in understanding usage patterns, heavy use definitions, and long-term effects on depression risk amidst changing cannabis trends.

Traumatic brain injury (TBI) can alter day-to-day life. While changes in cognition and physical function are most often cited, emotional disturbances, notably depression, are also common. For individuals who experience depression symptoms, mindfulness-based cognitive therapy (MBCT) may afford the opportunity to address these symptoms by teaching skills to mitigate negative thought patterns and foster acceptance. Yet, as with any treatment for depression, MBCT may not be the best fit for everyone. According to the literature, characteristics such as age, gender, and baseline mindfulness or pain levels have the potential to affect treatment response. While these factors have yet to be explored within a TBI sample, we must additionally consider whether possible cognitive impairment due to TBI plays a role in treatment response. Drawing from an earlier multi-site randomized controlled trial to explore the efficacy of MBCT for depression in a TBI sample, the current study examined the associations between a number of baseline factors (demographic, emotional, physical, and cognitive) and decreased depression scores post-intervention. Partial correlations adjusted for gender. Findings indicated that only higher levels of pain at baseline were associated with lesser effectiveness of the intervention. MBCT offers a good treatment option for most individuals experiencing depression following TBI.

1. (1) To explore factors associated with treatment response to MBCT for depression after TBI.

2. (2) To understand how cognitive impairment resulting from TBI need not preclude treatment response.

3. (3) To reflect on the role of pain in treatment response.

Adverse childhood experiences (ACEs) have been associated with increased risks of autoimmune diseases. However, data are scarce on the role of specific ACEs as well as the potential mediating role of adverse mental health symptoms in this association.

A cohort study using the nationwide Icelandic Stress-And-Gene-Analysis (SAGA, 22,423 women) cohort and the UK Biobank (UKB, 86,492 women) was conducted. Participants self-reported on five ACEs. Twelve autoimmune diseases were self-reported in SAGA and identified via hospital records in UKB. Poisson regression was used to assess the cross-sectional association between ACEs and autoimmune diseases in both cohorts. Using longitudinal data on self-reported mental health symptoms in the UKB, we used causal mediation analyses to study potential mediation by depressive, anxiety, and PTSD symptoms in the association between ACEs and autoimmune diseases.

The prevalence of ACEs was 50% in SAGA and 35% in UKB, while the prevalence of autoimmune diseases was 29% (self-reported) and 14% (clinically confirmed), respectively. In both cohorts, ACEs were associated with an increased prevalence ratio (PR) of any studied autoimmune disease in a dose–response manner (PR = 1.10 (95%CI = 1.08–1.12) per ACE), particularly for Sjögrens (PR = 1.34), polymyalgia rheumatica (PR = 1.20), rheumatoid arthritis (PR = 1.14), systemic lupus erythematosus (PR = 1.13), and thyroid disease (PR = 1.11). Sexual abuse and physical and emotional neglect were consistently associated with an elevated prevalence of autoimmune diseases when including all ACEs in the model. Approximately one fourth of the association was mediated through depression, anxiety, and PTSD.

These findings based on two large cohorts indicate a role of ACEs and corresponding mental health distress in autoimmune diseases among adult women.

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.