Homelessness is a major public health problem among U.S. military veterans. However, contemporary, population-based data on the prevalence, correlates, and mental health burden of homelessness among veterans are lacking.

Data were analyzed from the 2019–2020 National Health and Resilience in Veterans Study, a nationally representative survey of veterans (n = 4069). Analyses examined the prevalence and correlates of homelessness, as well as the independent associations between homelessness and current probable psychiatric conditions, suicidality, and functioning.

The lifetime prevalence of homelessness was 10.2% (95% confidence interval 9.3–11.2). More than 8-of-10 veterans reported experiencing their first episode of homelessness following military service, with a mean of 10.6 years post-discharge until onset (s.d. = 12.6). Adverse childhood experiences (ACEs), cumulative trauma burden, current household income, younger age, and drug use disorder emerged as the strongest correlates of homelessness (49% of total explained variance). Veterans with a history of homelessness had elevated odds of lifetime suicide attempt, attempting suicide two or more times, and past-year suicide ideation [odd ratios (ORs) 1.3–3.1]. They also had higher rates of current probable posttraumatic stress disorder, major depressive, generalized anxiety, and drug use disorders (ORs 1.7–2.4); and scored lower on measures of mental, physical, cognitive, psychosocial functioning (d = 0.11–0.15).

One in ten U.S. veterans has experienced homelessness, and these veterans represent a subpopulation at substantially heightened risk for poor mental health and suicide. ACEs were the strongest factor associated with homelessness, thus underscoring the importance of targeting early childhood adversities and their mental health consequences in prevention efforts for homelessness in this population.

This study examined the efficacy of attention bias modification training (ABMT) for the treatment of depression.

In this randomized clinical trial, 145 adults (77% female, 62% white) with at least moderate depression severity [i.e. self-reported Quick Inventory of Depressive Symptomatology (QIDS-SR) ⩾13] and a negative attention bias were randomized to active ABMT, sham ABMT, or assessments only. The training consisted of two in-clinic and three (brief) at-home ABMT sessions per week for 4 weeks (2224 training trials total). The pre-registered primary outcome was change in QIDS-SR. Secondary outcomes were the 17-item Hamilton Depression Rating Scale (HRSD) and anhedonic depression and anxious arousal from the Mood and Anxiety Symptom Questionnaire (MASQ). Primary and secondary outcomes were administered at baseline and four weekly assessments during ABMT.

Intent-to-treat analyses indicated that, relative to assessment-only, active ABMT significantly reduced QIDS-SR and HRSD scores by an additional 0.62 ± 0.23 (p = 0.008, d = −0.57) and 0.74 ± 0.31 (p = 0.021, d = −0.49) points per week. Similar results were observed for active v. sham ABMT: a greater symptom reduction of 0.44 ± 0.24 QIDS-SR (p = 0.067, d = −0.41) and 0.69 ± 0.32 HRSD (p = 0.033, d = −0.42) points per week. Sham ABMT did not significantly differ from the assessment-only condition. No significant differences were observed for the MASQ scales.

Depressed individuals with at least modest negative attentional bias benefitted from active ABMT.

Major depressive disorder (MDD) is associated with increased allostatic load (AL; a measure of physiological costs of repeated/chronic stress-responding) and metabolic dysregulation (MetD; a measure of metabolic health and precursor to many medical illnesses). Though AL and MetD are associated with poor somatic health outcomes, little is known regarding their relationship with antidepressant-treatment outcomes.

We determined pre-treatment AL and MetD in 67 healthy controls and 34 unmedicated, medically healthy MDD subjects. Following this, MDD subjects completed 8-weeks of open-label selective serotonin reuptake inhibitor (SSRI) antidepressant treatment and were categorized as ‘Responders’ (⩾50% improvement in depression severity ratings) or ‘Non-responders’ (<50% improvement). Logistic and linear regressions were performed to determine if pre-treatment AL or MetD scores predicted SSRI-response. Secondary analyses examined cross-sectional differences between MDD and control groups.

Pre-treatment AL and MetD scores significantly predicted continuous antidepressant response (i.e. absolute decreases in depression severity ratings) (p = 0.012 and 0.014, respectively), as well as post-treatment status as a Responder or Non-responder (p = 0.022 and 0.040, respectively), such that higher pre-treatment AL and MetD were associated with poorer SSRI-treatment outcomes. Pre-treatment AL and MetD of Responders were similar to Controls, while those of Non-responders were significantly higher than both Responders (p = 0.025 and 0.033, respectively) and Controls (p = 0.039 and 0.001, respectively).

These preliminary findings suggest that indices of metabolic and hypothalamic-pituitary-adrenal-axis dysregulation are associated with poorer SSRI-treatment response. To our knowledge, this is the first study to demonstrate that these markers of medical disease risk also predict poorer antidepressant outcomes.

U.S. veterans report high rates of traumatic experiences and mental health symptomology [e.g. posttraumatic stress disorder (PTSD)]. The stress sensitization hypothesis posits experiences of adversity sensitize individuals to stress reactions which can lead to greater psychiatric problems. We extend this hypothesis by exploring how multiple adversities such as early childhood adversity, combat-related trauma, and military sexual trauma related to heterogeneity in stress over time and, subsequently, greater risk for PTSD.

1230 veterans were recruited for an observational, longitudinal study. Veterans responded to questionnaires on PTSD, stress, and traumatic experiences five times over an 18-month study period. We used latent transition analysis to understand how heterogeneity in adverse experiences is related to transition into stress trajectory classes. We also explored how transition patterns related to PTSD symptomology.

Across all models, we found support for stress sensitization. In general, combat trauma in combinations with other types of adverse experiences, namely early childhood adversity and military sexual trauma, imposed a greater probability of transitioning into higher risk stress profiles. We also showed differential effects of early childhood and military-specific adversity on PTSD symptomology.

The present study rigorously integrates both military-specific and early life adversity into analysis on stress sensitivity, and is the first to examine how sensitivity might affect trajectories of stress over time. Our study provides a nuanced, and specific, look at who is risk for sensitization to stress based on previous traumatic experiences as well as what transition patterns are associated with greater PTSD symptomology.

Unpaid carers who look after another member of their household (home-carers) have poorer mental health than the general population. The first COVID-19 national lockdown led to an increasing reliance on home-carers and we investigate the short- and longer-term impacts of lockdown on their mental health.

Data from 9737 adult participants (aged 16+) from the UK Household Longitudinal Study (Understanding Society) were used to explore changes in 12-item General Health Questionnaire (GHQ-12) score between (a) pre-pandemic (2019) and early lockdowns (April 2020) and (b) early and later (July 2020) lockdowns.

GHQ-12 scores among home-carers were higher pre-lockdown and increased more than for non-carers from 2019 to April 2020 with further increases for home-carers compared with non-carers between April and July. Compared with respondents caring for a spouse/partner, those caring for a child under 18 had a particularly marked increase in GHQ-12 score between 2019 and April, as did those caring for someone with a learning disability. Home-carers of children under 18 improved from April to July while those caring for adult children saw a marked worsening of their mental health. Home-carers with greater care burden saw larger increases in GHQ-12 score from 2019 to April and from April to July, and increases through both periods were greater for home-carers who had formal help prior to lockdown but then lost it.

The mental health of home-carers deteriorated more during lockdown than non-carers. Policies that reinstate support for them and their care-recipients will benefit the health of both vulnerable groups.

Openness on one's health condition or (stigmatized) identity generally improves mental health. Intersex or differences of sex development (DSD) conditions have long been kept concealed and high levels of (internalizing) mental health problems are reported. This study examines the effects of condition openness on anxiety and depression and the role of mediating concepts in this population.

Cross-sectional data of individuals of 16 years and older with an intersex/DSD condition was collected in 14 specialized European clinics as part of the dsd-LIFE study. Patient-reported measures were taken on openness and shame (Coping with DSD), self-esteem (Rosenberg Self-Esteem Scale), satisfaction with care (CSQ4), anxiety and depression (HADS). Scores were compared per clinical group and data were analyzed via structural equation modeling (SEM) to calculate prediction and mediation models.

Data of 903 individuals were included in this study (Turner syndrome (n = 284), 46, XY DSD (n = 233), CAH (n = 206) and Klinefelter syndrome (n = 180)). Participants were moderately open on their condition. High levels of both anxiety and depression were observed across the sample. In SEM analysis, the tested models predicted 25% of openness, 31% of anxiety and 48% of depression. More condition openness directly predicted lower anxiety and depression symptoms, as well as indirectly through increased self-esteem, self-satisfaction and satisfaction with social support.

Condition openness is associated with lower anxiety and depression in individuals with an intersex/DSD condition. Healthcare may provide the necessary knowledge and skills to employ one's optimal level of self-disclosure in order to improve mental health.

We hypothesize that the tumor necrosis factor-α (TNF-α) may play a role in disturbing the effect of selective serotonin reuptake inhibitor (SSRI) on the striatal connectivity in patients with major depressive disorder (MDD).

We performed a longitudinal observation by combining resting-state functional magnetic resonance imaging (rs-fMRI) and biochemical analyses to identify the abnormal striatal connectivity in MDD patients, and to evaluate the effect of TNF-α level on these abnormal connectivities during SSRI treatment. Eighty-five rs-fMRI scans were collected from 25 MDD patients and 35 healthy controls, and the scans were repeated for all the patients before and after a 6-week SSRI treatment. Whole-brain voxel-wise functional connectivity (FC) was calculated by correlating the rs-fMRI time courses between each voxel and the striatal seeds (i.e. spherical regions placed at the striatums). The level of TNF-α in serum was evaluated by Milliplex assay. Factorial analysis was performed to assess the interaction effects of ‘TNF-α × treatment’ in the regions with between-group FC difference.

Compared with controls, MDD patients showed significantly higher striatal FC in the medial prefrontal cortex (MPFC) and bilateral middle/superior temporal cortices before SSRI treatment (p < 0.001, uncorrected). Moreover, a significant interaction effect of ‘TNF-α × treatment’ was found in MPFC-striatum FC in MDD patients (p = 0.002), and the significance remained after adjusted for age, gender, head motion, and episode of disease.

These findings provide evidence that treatment-related brain connectivity change is dependent on the TNF-α level in MDD patients, and the MPFC-striatum connectivities possibly serve as an important target in the brain.

The association between schizophrenia and decreased vitamin D levels is well documented. Low maternal and postnatal vitamin D levels suggest a possible etiological mechanism. Alternatively, vitamin D deficiency in patients with schizophrenia is presumably (also) the result of disease-related factors or demographic risk factors such as urbanicity.

In a study population of 347 patients with psychotic disorder and 282 controls, group differences in vitamin D concentration were examined. Within the patient group, associations between vitamin D, symptom levels and clinical variables were analyzed. Group × urbanicity interactions in the model of vitamin D concentration were examined. Both current urbanicity and urbanicity at birth were assessed.

Vitamin D concentrations were significantly lower in patients (B = −8.05; 95% confidence interval (CI) −13.68 to −2.42; p = 0.005). In patients, higher vitamin D concentration was associated with lower positive (B = −0.02; 95% CI −0.04 to 0.00; p = 0.049) and negative symptom levels (B = −0.03; 95% CI −0.05 to −0.01; p = 0.008). Group differences were moderated by urbanicity at birth (χ2 = 6.76 and p = 0.001), but not by current urbanicity (χ2 = 1.50 and p = 0.224). Urbanicity at birth was negatively associated with vitamin D concentration in patients (B = −5.11; 95% CI −9.41 to −0.81; p = 0.020), but not in controls (B = 0.72; 95% CI −4.02 to 5.46; p = 0.765).

Lower vitamin D levels in patients with psychotic disorder may in part reflect the effect of psychosis risk mediated by early environmental adversity. The data also suggest that lower vitamin D and psychopathology may be related through direct or indirect mechanisms.

Genome-wide association studies (GWAS) have consistently revealed that a variant of microRNA 137 (MIR137) shows a quite significant association with schizophrenia. Identifying the network of genes regulated by MIR137 could provide insights into the biological processes underlying schizophrenia. In addition, DLPFC functional connectivity, a robust correlate of MIR137, may provide plausible endophenotypes. However, the regulatory role of the MIR137 gene network in the disrupted functional connectivity remains unclear. Here, we tested the effects of the MIR137 regulated genes on the risk for schizophrenia and DLPFC functional connectivity.

To evaluate the additive effects of the MIR137 regulated genes (N = 1274), we calculated a MIR137 polygenic risk score (PRS) for schizophrenia and tested its association with the risk for schizophrenia in the genomic data of a Han Chinese population that included schizophrenia patients (N = 589) and normal controls (N = 575). We then investigated the association between MIR137 PRS and DLPFC functional connectivity in two independent young healthy cohorts (N = 356 and N = 314).

We found that the MIR137 PRS successfully captured the differences in genetic structure between the patients and controls, but the single gene MIR137 did not. We then consistently found that a higher MIR137 PRS was correlated with lower functional connectivities between the DLPFC and both the superior parietal cortex and the inferior temporal cortex in two independent cohorts.

The findings suggested that these two functional connectivities of the DLPFC could be important endophenotypes linking the MIR137-regulated genetic structure to schizophrenia.

The 2004 tsunami, the civil conflict until 2009 and the youth insurrection in the late 1980s in Sri Lanka resulted in many persons being classified as ‘missing’ as they disappeared and were unaccounted for. Our aim was to compare the prevalence of major depressive disorder (MDD) and prolonged grief disorder (PGD) in families of disappeared individuals, who eventually received the mortal remains and those who did not.

An ethically approved cross sectional study was conducted in a purposively selected sample after informed consent. Information on the circumstances of the family member going missing was gathered. Culturally adapted versions of the General Health Questionnaire and the Beck Depression Scale were administered. Those who screened positive were assessed by a psychiatrist on Diagnostic and Statistical Manual of Mental Disorders-5 criteria to arrive at a diagnosis.

Of 391 cases of disappearances studied, MDD (17.5% v. 6%) and PGD (22% v. 7%) were significantly higher in those who did not eventually receive the mortal remains of the disappeared person. Among those who did not receive the mortal remains, being unsure whether the disappeared person was dead or alive was highly predictive of MDD and PGD. Mothers and wives, older family members and those with a family history of mental illness were more vulnerable.

Family members of missing individuals unsure whether their loved one was alive or dead have higher psychological morbidity in the form of MDD and PGD.

Little is known about suicide risk among offspring of parents hospitalized for schizophrenia and the mechanisms behind this association.

We applied a nested case–control design based on linkage of Swedish population-based registers. Among 12- to 30-year-old offspring, we identified 68 318 offspring with suicidal behavior (attempted and completed suicide) and their parents. Five healthy control–parent pairs were matched to each suicidal case–parent pair and conditional logistic regression used to obtain odds ratios (ORs). Further, to disentangle familial confounding from causal environmental mechanisms, we compared the population-based suicide risk with the risk found within full-cousins and half-cousins differentially exposed to parental schizophrenia.

Offspring of parents with schizophrenia had significantly increased suicide risk after accounting for socio-economic status, parental suicidal behavior and offspring mental illness [OR 1.68, 95% confidence interval (CI) 1.53–1.85]. Suicide risks in offspring of schizophrenic mothers and fathers were similar in magnitude; so were risks across different developmental periods. Importantly, offspring suicide risk remained essentially unchanged across genetically different relationships; offspring of siblings discordant for schizophrenia had equivalent risk increases within full-cousins (OR 1.96, 95% CI 1.66–2.31) and half-cousins (OR 1.69, 95% CI 1.17–2.44).

Parental schizophrenia was associated with increased risk of offspring suicidal behavior, independent of gender of the schizophrenic parent, and persisting into adulthood. The suicide risk in offspring remained at a similar level when comparing genetically different relationships, which suggests that at least part of the association is due to environmental mechanisms. These findings should inspire increased attention to suicidal ideation and prevention efforts in offspring of parents with schizophrenia.

Cognitive mechanisms that characterize or precede depressive symptoms are poorly understood. We investigated cross-sectional and longitudinal associations between risk taking to obtain reward and adolescent depressive symptoms in a large prospective cohort, using the Cambridge Gambling Task (CGT). We also explored sex differences.

The Millennium Cohort Study (MCS) is an ongoing UK study, following the lives of 19 000 individuals born 2000/02. The CGT was completed at ages 11 (n = 12 355) and 14 (n = 10 578). Our main exposure was the proportion of points gambled, when the odds of winning were above chance (risk-taking to obtain reward). Outcomes were emotional symptoms (Strengths and Difficulties Questionnaire, SDQ) at age 11 and depressive symptoms (short Mood and Feelings Questionnaire, sMFQ) at age 14. We calculated cross-sectional and longitudinal associations, using linear regressions.

In univariable models, there was evidence of cross-sectional associations between risk-taking and SDQ/sMFQ scores, but these associations disappeared after we adjusted for sex. Longitudinally, there was weak evidence of an association between risk-taking and depressive symptoms in females only [a 20-point increase in risk-taking at age 11 was associated with a reduction of 0.31 sMFQ points at age 14 (95% CI −0.60 to −0.02)]. At both time-points, females were less risk-taking than males.

We found no convincing evidence of a relationship between risk-taking to obtain reward and depressive symptoms. There were large sex differences in risk-taking, but these do not appear to contribute to the female preponderance of depressive symptoms in adolescence.