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.

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.

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.

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.

Anxiety symptoms are elevated among people with joint hypermobility. The underlying neural mechanisms are attributed theoretically to effects of variant connective tissue on the precision of interoceptive representations contributing to emotions.

To investigate the neural correlates of anxiety and hypermobility using functional neuroimaging.

We used functional magnetic resonance neuroimaging to quantify regional brain responses to emotional stimuli (facial expressions) in people with generalised anxiety disorder (GAD) (N = 30) and a non-anxious comparison group (N = 33). All participants were assessed for joint laxity and were classified (using Brighton Criteria) for the presence and absence of hypermobility syndrome (HMS: now considered hypermobility spectrum disorder).

Participants with HMS showed attenuated neural reactivity to emotional faces in specific frontal (inferior frontal gyrus, pre-supplementary motor area), midline (anterior mid and posterior cingulate cortices) and parietal (precuneus and supramarginal gyrus) regions. Notably, interaction between HMS and anxiety was expressed in reactivity of the left amygdala (a region implicated in threat processing) and mid insula (primary interoceptive cortex) where activity was amplified in people with HMS with GAD. Severity of hypermobility in anxious, compared with non-anxious, individuals correlated with activity within the anterior insula (implicated as the neural substrate linking anxious feelings to physiological state). Amygdala-precuneus functional connectivity was stronger in participants with HMS, compared with non-HMS participants.

The predisposition to anxiety in people with variant connective tissue reflects dynamic interactions between neural centres processing threat (amygdala) and representing bodily state (insular and parietal cortices). Correspondingly, interventions to regulate amygdala reactivity while enhancing interoceptive precision may have therapeutic benefit for symptomatic hypermobile individuals.

Evidence suggests that death anxiety is a transdiagnostic construct underlying numerous anxiety-related conditions. A previous phase I trial of Overcome Death Anxiety (ODA), a novel online stand-alone psychological intervention to reduce death anxiety, demonstrated preliminary evidence of efficacy and acceptability in a clinical population. However, this trial was limited by a small sample size (n=20).

To further evaluate the efficacy of this intervention in reducing death anxiety in a clinical population, compared with a waitlist control.

This paper describes the protocol of a phase II randomized controlled, unblinded trial of ODA. A total sample of 256 adults living in Australia, diagnosed with an anxiety-related condition, will be recruited. These participants will be randomised to ODA or a waitlist control. Primary outcomes will be measured as changes in scores on death anxiety questionnaires, reflecting treatment efficacy. The secondary outcomes to be measured are depression, anxiety, stress, suicidality, insomnia, and meaning of life, as well as feedback about treatment program acceptability. This trial will assess the efficacy of ODA for reducing death anxiety in a population diagnosed with various anxiety-related conditions, as well as the overall acceptability and tolerability of the intervention.

This study will provide evidence to evaluate the efficacy of ODA in people diagnosed with an anxiety-related condition.

There have been inconsistent findings for an association between assisted reproductive technology (ART) and poorer perinatal emotional wellbeing. This study is to explore whether ART is associated with increased depression and depressive symptoms, anxiety symptoms and parenting stress, and poorer antenatal attachment, over the perinatal period from pregnancy to 12 months postpartum.

This study drew on data collected within an ongoing cohort from 806 women including 42 who had conceived using ART, and all recruited in early pregnancy and followed to 12 months postpartum. Measures included the Structured Clinical Interview for the DSM, Edinburgh Postnatal Depression Scale, State and Trait Anxiety Inventory, Maternal Antenatal Attachment Scale and Parenting Stress Index.

Women who conceived with ART were no more likely to be depressed. They had lower depressive and anxiety symptoms in early pregnancy, higher antenatal attachment and lower parenting stress. However, women who conceived with ART had a significant increase in depressive and anxiety symptoms in late pregnancy which reduced in the postpartum and showed a distinct pattern compared to those who conceived naturally.

This study found that women who conceived with ART did not have poorer emotional wellbeing across the perinatal period. However, in late pregnancy depressive and anxiety symptoms did rise and consideration of this clinically and in future research is warranted.

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.

Transcranial direct current stimulation (tDCS) is a promising treatment for major depressive disorder (MDD). This study evaluated its antidepressant and cognitive effects as a safe, effective, home-based therapy for MDD.

This double-blind, sham-controlled, randomized trial divided participants into low-intensity (1 mA, n = 47), high-intensity (2 mA, n = 49), and sham (n = 45) groups, receiving 42 daily tDCS sessions, including weekends and holidays, targeting the dorsolateral prefrontal cortex for 30 minutes. Assessments were conducted at baseline and weeks 2, 4, and 6. The primary outcome was cognitive improvement assessed by changes in total accuracy on the 2-back test from baseline to week 6. Secondary outcomes included changes in depressive symptoms (HAM-D), anxiety (HAM-A), and quality of life (QLES). Adverse events were monitored. This trial was registered with ClinicalTrials.gov (NCT04709952).

In the tDCS study, of 141 participants (102 [72.3%] women; mean age 35.7 years, standard deviation 12.7), 95 completed the trial. Mean changes in the total accuracy scores from baseline to week 6 were compared across the three groups using an F-test. Linear mixed-effects models examined the interaction of group and time. Results showed no significant differences among groups in cognitive or depressive outcomes at week 6. Active groups experienced more mild adverse events compared to sham but had similar rates of severe adverse events and dropout.

Home-based tDCS for MDD demonstrated no evidence of effectiveness but was safe and well-tolerated. Further research is needed to address the technical limitations, evaluate broader cognitive functions, and extend durations to evaluate its therapeutic potential.