Genetic influences on alcohol involvement are likely to vary as a function of the ‘alcohol environment,’ given that exposure to alcohol is a necessary precondition for genetic risk to be expressed. However, few gene–environment interaction studies of alcohol involvement have focused on characteristics of the community-level alcohol environment. The goal of this study was to examine whether living in a community with more alcohol outlets would facilitate the expression of the genetic propensity to drink in a genetically-informed national survey of United States young adults.

The participants were 2434 18–26-year-old twin, full-, and half-sibling pairs from Wave III of the National Longitudinal Study of Adolescent to Adult Health. Participants completed in-home interviews in which alcohol use was assessed. Alcohol outlet densities were extracted from state-level liquor license databases aggregated at the census tract level to derive the density of outlets.

There was evidence that the estimates of genetic and environmental influences on alcohol use varied as a function of the density of alcohol outlets in the community. For example, the heritability of the frequency of alcohol use for those residing in a neighborhood with ten or more outlets was 74% (95% confidence limits = 55–94%), compared with 16% (95% confidence limits = 0–34%) for those in a neighborhood with zero outlets. This moderating effect of alcohol outlet density was not explained by the state of residence, population density, or neighborhood sociodemographic characteristics.

The results suggest that living in a neighborhood with many alcohol outlets may be especially high-risk for those individuals who are genetically predisposed to frequently drink.

Subgenual cingulate cortex (SCC) responses to self-blaming emotion-evoking stimuli were previously found in individuals prone to self-blame with and without a history of major depressive disorder (MDD). This suggested SCC activation reflects self-blaming emotions such as guilt, which are central to models of MDD vulnerability.

Here, we re-examined these hypotheses in an independent larger sample. A total of 109 medication-free participants (70 with remitted MDD and 39 healthy controls) underwent fMRI whilst judging self- and other-blaming emotion-evoking statements. They also completed validated questionnaires of proneness to self-blaming emotions including those related to internal (autonomy) and external (sociotropy) evaluation, which were subjected to factor analysis.

An interaction between group (remitted MDD v. Control) and condition (self- v. other-blame) was observed in the right SCC (BA24). This was due to higher SCC signal for self-blame in remitted MDD and higher other-blame-selective activation in Control participants. Across the whole sample, extracted SCC activation cluster averages for self- v. other-blame were predicted by a regression model which included the reliable components derived from our factor analysis of measures of proneness to self-blaming emotions. Interestingly, this prediction was solely driven by autonomy/self-criticism, and adaptive guilt factors, with no effect of sociotropy/dependency.

Despite confirming the prediction of SCC activation in self-blame-prone individuals and those vulnerable to MDD, our results suggest that SCC activation reflects blame irrespective of where it is directed rather than selective for self. We speculate that self-critical individuals have more extended SCC representations for blame in the context of self-agency.

The purpose of this study was to assess the associations of comorbid opioid use disorders and psychiatric disorders with suicide attempts among veterans seeking pain care.

The cohort (N = 226 444) was selected by identifying pain care initiation from 2012 to 2014 using national Veterans Health Administration (VHA) data. Data on opioid use disorders (OUD), psychiatric disorders, medical comorbidity, demographics at baseline, and suicide attempts in the year following the initiation of pain care were extracted from VHA databases. Relative excess risk due to interaction (RERI) was used to assess departure from additivity of effects.

Adjusted models indicated that both comorbid OUD and depression (RERI = 1.07) and comorbid OUD and AUD (RERI = 1.23) were significantly associated with additive risk of suicide attempt. In adjusted multiplicative interaction models, only comorbid OUD and bipolar disorder was significantly associated with suicide attempts; however, this association was protective (HR = 0.54).

The current findings highlight the importance of addressing opioid use disorders and alcohol use disorders and depression together to mitigate the risk of suicidal behavior.

Bipolar disorder (BD) is associated with cognitive and functional difficulties, persistent beyond mood episodes. Cognitive remediation (CR) is a psychological therapy targeting cognitive and functioning difficulties. Recent evidence suggests that CR may enhance long-term functioning but transfer mechanisms on functional outcomes have not been explored. We aim to investigate whether and how cognitive gains after CR transfer to functional improvement.

We considered data from a randomized controlled trial comparing CR (n = 40) to treatment-as-usual (TAU; n = 40) in euthymic people with BD. Treatment outcomes included individual cognitive domains and global cognition, psychosocial functioning, and goal attainment. Regression-based mediation and moderation modelling were used to assess whether and how post-treatment cognitive changes translate into functional improvement at follow-up, three months after treatment end.

Cognitive gains after CR transferred to functional changes three months later: improvement in post-treatment global cognition partially mediated the effect of CR on psychosocial functioning (standardized indirect effect: −0.23, 95% CI −0.51 to −0.04). Goal attainment was not significantly mediated by changes in cognition, but post-treatment cognitive performance moderated the effect of CR on the GAS at follow-up (interaction effect: 0.78, 95% CI 0.08–1.55).

Our findings suggest that cognitive improvements contribute to functional improvement but transfer mechanisms differ between psychosocial functioning and idiosyncratic recovery goals. Cognition accounted for only a proportion of the total CR effect on functional outcomes. Future studies should consider other variables, such as metacognition, that may drive the transfer of CR effects to functional outcomes.

Maternal stress during pregnancy is associated with a modestly increased risk of fetal growth restriction and pre-eclampsia. Since placental abruption shares similar pathophysiological mechanisms and risk factors with fetal growth restriction and pre-eclampsia, we hypothesized that maternal stress may be implicated in abruption risk. We investigated the association between maternal bereavement during pregnancy and placental abruption.

We studied singleton births in Denmark (1978–2008) and Sweden (1973–2006) (n = 5 103 272). In nationwide registries, we obtained data on death of women's close family members (older children, siblings, parents, and partners), abruption and potential confounders.

A total of 30 312 (6/1000) pregnancies in the cohort were diagnosed with placental abruption. Among normotensive women, death of a child the year before or during pregnancy was associated with a 54% increased odds of abruption [95% confidence interval (CI) 1.30–1.82]; the increased odds were restricted to women who lost a child the year before or during the first trimester in pregnancy. In the group with chronic hypertension, death of a child the year before or in the first trimester of pregnancy was associated with eight-fold increased odds of abruption (odds ratio 8.17, 95% CI 3.17–21.10). Death of other relatives was not associated with abruption risk.

Loss of a child the year before or in the first trimester of pregnancy was associated with an increased risk of abruption, especially among women with chronic hypertension. Studies are needed to investigate the effect of less severe, but more frequent, sources of stress on placental abruption risk.

Anxiety disorders are very common and increase risk for suicide attempts. Little is known about predictors of increased risk specifically among individuals with anxiety disorders. The purpose of this study was to investigate whether specific anxiety disorders and other co-morbid psychiatric disorders, physical health, or work or social functioning increased the future likelihood of a suicide attempts among individuals with anxiety disorders.

In this prospective study, 676 individuals with an anxiety disorder were followed for an average of 12 years.

As hypothesized, we found that post-traumatic stress disorder, major depressive disorder (MDD), intermittent depressive disorder (IDD), epilepsy, pain, and poor work and social functioning all predicted a shorter time to a suicide attempt in univariate analyses. In multivariate analyses, baseline MDD and IDD were independent predictors of time to suicide attempt, even when controlling for a past history of suicide attempt. No specific anxiety disorder was an independent predictor of time to attempt in this anxiety-disordered sample. Adding baseline physical health variables and social functioning did not improve the ability of the model to predict time to suicide attempt.

Mood disorders and past history of suicide attempts are the most powerful predictors of a future suicide attempt in this sample of individuals, all of whom have an anxiety disorder.

Major depression and anxiety disorders are known to negatively influence cognitive performance. Moreover, there is evidence for greater cognitive decline in older adults with generalized anxiety disorder. Except for clinical studies, complex executive planning functions and subclinical levels of anxiety have not been examined in a population-based sample with a broad age range.

Planning performance was assessed using the Tower of London task in a population-based sample of 4240 participants aged 40–80 years from the Gutenberg Health Study (GHS) and related to self-reported anxiety and depression by means of multiple linear regression analysis.

Higher anxiety ratings were associated with lower planning performance (β = −0.20; p < 0.0001) independent of age (β = 0.03; p = 0.47). When directly comparing the predictive value of depression and anxiety on cognition, only anxiety attained significance (β = −0.19; p = 0.0047), whereas depression did not (β = −0.01; p = 0.71).

Subclinical levels of anxiety but not of depression showed negative associations with cognitive functioning independent of age. Our results demonstrate that associations observed in clinical groups might differ from those in population-based samples, also with regard to the trajectory across the life span. Further studies are needed to uncover causal interrelations of anxiety and cognition, which have been proposed in the literature, in order to develop interventions aimed at reducing this negative affective state and to improve executive functioning.

Aberrations in reward and penalty processing are implicated in depression and putatively reflect altered dopamine signalling. This study exploits the advantages of a placebo-controlled design to examine how a novel D2 antagonist with adjunctive antidepressant properties modifies activity in the brain's reward network in depression.

We recruited 43 medication-naïve subjects across the range of depression severity (Beck's Depression Inventory-II score range: 0–43), including healthy volunteers, as well as people meeting full-criteria for major depressive disorder. In a double-blind placebo-controlled cross-over design, all subjects received either placebo or lurasidone (20 mg) across two visits separated by 1 week. Functional magnetic resonance imaging with the Monetary Incentive Delay (MID) task assessed reward functions via neural responses during anticipation and receipt of gains and losses. Arterial spin labelling measured cerebral blood flow (CBF) at rest.

Lurasidone altered fronto-striatal activity during anticipation and outcome phases of the MID task. A significant three-way Medication-by-Depression severity-by-Outcome interaction emerged in the anterior cingulate cortex (ACC) after correction for multiple comparisons. Follow-up analyses revealed significantly higher ACC activation to losses in high- v. low depression participants in the placebo condition, with a normalisation by lurasidone. This effect could not be accounted for by shifts in resting CBF.

Lurasidone acutely normalises reward processing signals in individuals with depressive symptoms. Lurasidone's antidepressant effects may arise from reducing responses to penalty outcomes in individuals with depressive symptoms.

Perceived loneliness, an increasingly prevalent social issue, is closely associated with major depressive disorder (MDD). However, the neural mechanisms previously implicated in key cognitive and affective processes in loneliness and MDD still remain unclear. Such understanding is critical for delineating the psychobiological basis of the relationship between loneliness and MDD.

We isolated the unique and interactive cognitive and neural substrates of loneliness and MDD among 27 MDD patients (mean age = 51.85 years, 20 females), and 25 matched healthy controls (HCs; mean age = 48.72 years, 19 females). We assessed participants' behavioral performance and neural regional and network functions on a Stroop color-word task, and their resting-state neural connectivity.

Behaviorally, we found greater incongruence-related accuracy cost in MDD patients, but reduced incongruence effect on reaction time in lonelier individuals. When performing the Stroop task, loneliness positively predicted prefrontal-anterior cingulate-parietal connectivity across all participants, whereas MDD patients showed a decrease in connectivity compared to controls. Furthermore, loneliness negatively predicted parietal and cerebellar activities in MDD patients, but positively predicted the same activities in HCs. During resting state, MDD patients showed reduced parietal-anterior cingulate connectivity, which again positively correlated with loneliness in this group.

We speculate the distinct neurocognitive profile of loneliness might indicate increase in both bottom-up attention and top-down executive control functions. However, the upregulated cognitive control processes in lonely individuals may eventually become exhausted, which may in turn predispose to MDD onset.

Appraisals are suggested to play a determining role in the clinical outcome of psychotic experiences (PEs). We used experimental tasks that mimic PEs to investigate appraisals in individuals with PEs with and without a ‘need-for-clinical-care’, and psychosis patients whose symptoms have remitted. We predicted that patients would appraise the tasks as threatening regardless of current symptom level, while non-clinical and control groups would appraise them as non-threatening.

Appraisals following three anomalous experiences-inducing tasks [Telepath, Cards task, Virtual acoustic space paradigm (VASP)] were examined in 71 individuals: symptomatic (n = 18) and remitted (n = 16) psychosis patients; non-clinical group with PEs (n = 16); controls without PEs (n = 21).

As predicted, symptomatic patients endorsed more threatening appraisals for all tasks than non-clinical and control groups, who did not differ from each other. However, remitted patients were less likely to endorse threatening appraisals of the Cards and Telepath than their symptomatic counterparts, although they did not differ in global ratings of how striking, threatening and distressing they found the tasks. Moreover, remitted participants endorsed more threatening appraisals of the Telepath and VASP than non-clinical participants, and of the VASP than controls. Remitted participants also rated all three tasks as globally more threatening than the non-clinical group and controls.

Clinical outcome may not necessarily be driven by the presence of symptoms, with threatening appraisals of PEs representing a key factor. The remitted group's intermediate appraisal scores imply that the relationship between appraisal and clinical outcome is not straightforward, and potential mediating factors need to be determined.

Insomnia symptoms are common during the postpartum period, yet interventions remain scarce. This trial aimed to simultaneously examine the efficacy of cognitive behavioural therapy (CBT) and light dark therapy (LDT), targeting different mechanisms, against treatment-as-usual (TAU), in reducing maternal postpartum insomnia symptoms.

This three-arm randomised controlled trial recruited from the general community in Australia. Nulliparous females 4–12 months postpartum with self-reported insomnia symptoms [Insomnia Severity Index (ISI) scores >7] were included; severe medical/psychiatric conditions were excluded. Participants were randomised 1:1:1 to CBT, LDT, or TAU stratified by ISI (< or ⩾14) and infant age (< or ⩾8 months). Participants and principal investigators were unblinded. Six-week interventions were delivered via digital materials and telephone. The primary outcome was insomnia symptoms (ISI), assessed pre-, midpoint-, post- (primary endpoint), and one-month post-intervention. Analyses were intention-to-treat using latent growth models.

114 participants (CBT = 39, LDT = 36, TAU = 39; Mage = 32.20 ± 4.62 years) were randomised. There were significantly greater reductions in ISI scores in CBT and LDT (effect sizes −2.01 and −1.52 respectively, p < 0.001) from baseline to post-intervention compared to TAU; improvements were maintained at follow-up. Similar effects were observed for self-reported sleep disturbance. There were greater reductions in fatigue in CBT (effect size = 0.85, p < 0.001) but not LDT (p = 0.11) compared to TAU. Changes in sleepiness, depression, and anxiety were non-significant compared to TAU (all p > 0.08). Four participants (11%) in the LDT group reported headaches, dizziness, or nausea; no others reported adverse events.

Therapist-assisted CBT and LDT were feasible during the first postpartum year; data at post-intervention and 1-month follow-up support their safety and efficacy in reducing postpartum insomnia symptoms.

Psychotic experiences (PEs) frequently occur and are associated with a range of negative health outcomes. Prospective studies on PEs are scarce, and to date no study investigated PE prevalence, incidence, persistence, their risk indicators, and psychiatric comorbidity, in one dataset. Furthermore, most studies are based on self-report, and it is unclear how this compares to clinical interviews.

Data are used from the Netherlands Mental Health Survey and Incidence Study-2 (NEMESIS-2), a psychiatric cohort study among a representative sample of adults (baseline characteristics: N = 6646; 49.6% female; 18–64 years). Results are presented for self-reported and clinically validated PEs. Associations are assessed for mental disorders, socio-demographic, vulnerability, physical health, and substance use factors.

Based on self-report, at baseline 16.5% of respondents had at least one PE in their lifetime, of those, 30.1% also reported a PE at 3-year follow-up. 4.8% had a first PE at 3-year follow up. The 3-year prevalence of PE was associated with almost all studied risk indicators. Generally, the strongest associations were found for mental health disorders. Prevalence and incidence rates were two to three times higher in self-report than in clinical interview but results on associated factors were similar.

Validated prevalence and incidence estimates of PE are substantially lower than self-reported figures but results on associated factors were similar. Therefore, future studies on associations of PEs can rely on relatively inexpensive self-reports of PEs. The associations between PE and mental disorders underline the importance of assessment of PE in general practice.

Leptin is thought to act as an important mediator in stress reactions. To date, no study has examined the association between psychological stress and leptin levels in children. This study aimed to assess the association between emotional symptoms and peer problems and serum leptin levels in children aged 10 years of the two population-based GINI-plus and LISA-plus birth cohorts.

Cross-sectional data from 2827 children aged 10 years were assessed with regard to leptin concentrations in serum and behavioral problems using the parent-reported Strengths and Difficulties Questionnaire (SDQ). Linear regression modeling was applied to determine the likelihood of elevated leptin levels in children with emotional symptoms and peer problems, controlling for socio-economic status (SES), body mass index (BMI), fasting serum leptin levels, pubertal development and sex hormones.

We found that increases in emotional symptoms (exp βadj = 1.03, s.e. = 0.02, p < 0.04) and peer problems (exp βadj = 1.05, s.e. = 0.01, p = 0.0001) were significantly associated with higher serum leptin levels controlled for BMI and sociodemographic factors. Similar results were found when the fasting serum leptin sample was examined (exp βadj = 1.08, s.e. = 0.04, p = 0.0294). Gender-stratified analyses showed a significant relationship between serum leptin and peer problems in girls (exp βadj = 1.05, s.e. = 0.02, p = 0.03), and a borderline significant association in boys (exp βadj = 1.04, s.e. = 0.02, p = 0.05).

Children with peer problems have higher stress and eat more, acquire a higher body fat mass and thus, through increased leptin resistance, exhibit higher leptin levels.