Goal-directed control guides optimal decision-making and it is an important cognitive faculty that protects against developing habits. Previous studies have found some evidence of goal-directed deficits when healthy individuals are stressed, and in psychiatric conditions characterised by compulsive behaviours and anxiety. Here, we tested if goal-directed control is affected by state anxiety, which might explain the former results.

We carried out a causal test of this hypothesis in two experiments (between-subject N = 88; within-subject N = 50) that used the inhalation of hypercapnic gas (7.5% CO2) to induce an acute state of anxiety in healthy volunteers. In a third experiment (N = 1413), we used a correlational design to test if real-life anxiety-provoking events (panic attacks, stressful events) are associated with impaired goal-directed control.

In the former two causal experiments, we induced a profoundly anxious state, both physiologically and psychologically, but this did not affect goal-directed performance. In the third, correlational, study, we found no evidence for an association between goal-directed control, panic attacks or stressful life eventsover and above variance accounted for by trait differences in compulsivity.

In sum, three complementary experiments found no evidence that anxiety impairs goal-directed control in human subjects.

Alterations in heart rate (HR) may provide new information about physiological signatures of depression severity. This 2-year study in individuals with a history of recurrent major depressive disorder (MDD) explored the intra-individual variations in HR parameters and their relationship with depression severity.

Data from 510 participants (Number of observations of the HR parameters = 6666) were collected from three centres in the Netherlands, Spain, and the UK, as a part of the remote assessment of disease and relapse-MDD study. We analysed the relationship between depression severity, assessed every 2 weeks with the Patient Health Questionnaire-8, with HR parameters in the week before the assessment, such as HR features during all day, resting periods during the day and at night, and activity periods during the day evaluated with a wrist-worn Fitbit device. Linear mixed models were used with random intercepts for participants and countries. Covariates included in the models were age, sex, BMI, smoking and alcohol consumption, antidepressant use and co-morbidities with other medical health conditions.

Decreases in HR variation during resting periods during the day were related with an increased severity of depression both in univariate and multivariate analyses. Mean HR during resting at night was higher in participants with more severe depressive symptoms.

Our findings demonstrate that alterations in resting HR during all day and night are associated with depression severity. These findings may provide an early warning of worsening depression symptoms which could allow clinicians to take responsive treatment measures promptly.

Complicated grief is a distinct psychological response of individuals facing the loss of a loved one and can lead to many types of adverse health outcomes. Although social support may be beneficial, few studies have examined the beneficial effects of helpful support on complicated grief following bereavement.

A randomized controlled trial was conducted. Bereaved participants and supporters were randomized to psychoeducation on complicated grief and helpful social support or psychoeducation on complicated grief. The primary outcome was the Inventory of Complicated Grief.

The results showed that psychoeducation of supporters of bereaved individuals has significant beneficial effects. Particularly, symptoms of complicated grief were decreased in bereaved individuals with supporters that received psychoeducation.

The results highlight the potential of psychoeducation to facilitate helpful social support and reduce complicated grief.

Prior work has robustly suggested that social processes in the neighborhood (i.e. informal social control, social cohesion, norms) influence child conduct problems (CP) and related outcomes, but has yet to consider how these community-level influences interact with individual-level genetic risk for CP. The current study sought to do just this, evaluating neighborhood-level social processes as etiologic moderators of child CP for the first time.

We made use of two nested samples of child and adolescent twins within the Michigan State University Twin Registry (MSUTR): 5649 families who participated in in the Michigan Twins Project (MTP) and 1013 families who participated in the Twin Study of Behavioral and Emotional Development (TBED-C). The neighborhood social processes of informal social control, social cohesion, and norms were assessed using neighborhood sampling techniques, in which residents of each twin family's neighborhood reported on the social processes in their neighborhood. Standard biometric GxE analyses evaluated the extent to which they moderated the etiology of CP.

The ‘no moderation’ model provided the best fit to the data in nearly all cases, arguing against neighborhood social processes as etiologic moderators of youth CP.

The neighborhood social processes evaluated here do not appear to exert their effects on child CP via etiologic moderation. The documented links between neighborhood social processes and child CP are thus likely to reflect a different etiologic process. Possibilities include environmental main effects of neighborhood social processes on child CP, or genotype-environment correlations.

Reduced P300 event-related potential (ERP) amplitude and latency prolongation have been reported in patients with schizophrenia compared to healthy controls. However, the influence of antipsychotics (and dopamine) on ERP measures are poorly understood and medication confounding remains a possibility.

We explored ERP differences between 36 drug-naive patients with schizophrenia and 138 healthy controls and examined whether P300 performance was related to dopamine transporter (DAT) availability, both without the confounding effects of medication. We also conducted a random effects meta-analysis of the available literature, synthesizing the results of three comparable published articles and our local study.

No overall significant difference was found in mean P300 ERP between patients and controls in latency or in amplitude. There was a significant gender effect, with females showing greater P300 amplitude than males. A difference between patients and controls in P300 latency was evident with ageing, with latency increasing faster in patients. No effect of DAT availability on P300 latency or amplitude was detected. The meta-analysis computed the latency pooled standardized effect size (PSES; Cohen's d) of −0.13 and the amplitude PSES (Cohen's d) of 0.48, with patients showing a significant reduction in amplitude.

Our findings suggest the P300 ERP is not altered in the early stages of schizophrenia before medication is introduced, and the DAT availability does not influence the P300 ERP amplitude or latency. P300 ERP amplitude reduction could be an indicator of the progression of illness and chronicity.

Does the genetic aptitude for educational attainment (GAEA) moderate the genetic risk for alcohol use disorder (AUD) and drug use disorder (DUD)?

In the native Swedish population, born 1960–1980 and followed through 2017 (n = 1 862 435), the family genetic risk score (FGRS) for AUD and DUD and GAEA were calculated from, respectively, the educational attainment and risk for AUD and DUD, of 1st through 5th degree relatives from Swedish national registers. Analyses utilized Aalen's linear hazards models.

Risk for AUD was robustly predicted by the main effects of FGRSAUD [b = 6.32 (95% CI 6.21–6.43), z = 64.9, p < 0.001) and GAEA [b = −2.90 (2.83–2.97), z = 44.1, p < 0.001] and their interaction [b = −1.93 (1.83–2.03), z = 32.9, p < 0.001]. Results were similar for the prediction of DUD by the main effects of FGRSDUD [b = 4.65 (CI 4.56–4.74), z = 59.4, p < 0.001] and GAEA [−2.08 (2.03–2.13), z = 46.4, p < 0.001] and their interaction [b = −1.58 (1.50–1.66)), z = 30.2, p < 0.001]. The magnitude of the interactions between GAEA and FGRSAUD and FGRSDUD in the prediction of, respectively, AUD and DUD was attenuated only slightly by the addition of educational attainment to the model.

The genetic propensity to high educational attainment robustly moderates the genetic risk for both AUD and DUD such that the impact of the genetic liability to AUD and DUD on the risk of illness is substantially attenuated in those with high v. low GAEA. This effect is not appreciably mediated by the actual level of educational attainment. These naturalistic findings could form the basis of prevention efforts in high-risk youth.

Over the past two decades, early detection and early intervention in psychosis have become essential goals of psychiatry. However, clinical impressions are insufficient for predicting psychosis outcomes in clinical high-risk (CHR) individuals; a more rigorous and objective model is needed. This study aims to develop and internally validate a model for predicting the transition to psychosis within 10 years.

Two hundred and eight help-seeking individuals who fulfilled the CHR criteria were enrolled from the prospective, naturalistic cohort program for CHR at the Seoul Youth Clinic (SYC). The least absolute shrinkage and selection operator (LASSO)-penalized Cox regression was used to develop a predictive model for a psychotic transition. We performed k-means clustering and survival analysis to stratify the risk of psychosis.

The predictive model, which includes clinical and cognitive variables, identified the following six baseline variables as important predictors: 1-year percentage decrease in the Global Assessment of Functioning score, IQ, California Verbal Learning Test score, Strange Stories test score, and scores in two domains of the Social Functioning Scale. The predictive model showed a cross-validated Harrell's C-index of 0.78 and identified three subclusters with significantly different risk levels.

Overall, our predictive model showed a predictive ability and could facilitate a personalized therapeutic approach to different risks in high-risk individuals.

Little is known about the mental health of partners of survivors of high levels of trauma in post-conflict countries.

We studied 677 spouse dyads (n = 1354) drawn from a community survey (response 82.4%) in post-conflict Timor-Leste. We used culturally adapted measures of post-traumatic stress disorder (PTSD), psychological distress, explosive anger and grief.

Latent class analysis identified three classes of couples: class 1, comprising women with higher trauma events (TEs), men with intermediate TEs (19%); class 2, including men with higher TEs, women with lower TEs (23%); and class 3, comprising couples in which men and women had lower TE exposure (58%) (the reference group). Men and women partners of survivors of higher TE exposure (classes 1 and 2) had increased symptoms of explosive anger and grief compared with the reference class (class 3). Women partners of survivors of higher TE exposure (class 2) had a 20-fold increased rate of PTSD symptoms compared with the reference class, a pattern that was not evident for men living with women exposed to higher levels of trauma (class 1).

Men and women living with survivors of higher levels of trauma showed an increase in symptoms of grief and explosive anger. The manifold higher rate of PTSD symptoms amongst women living with men exposed to high levels of trauma requires replication. It is important to assess the mental health of partners when treating survivors of high levels of trauma in post-conflict settings.

The genetic component of Cannabis Use Disorder may overlap with influences acting more generally on early stages of cannabis use. This paper aims to determine the extent to which genetic influences on the development of cannabis abuse/dependence are correlated with those acting on the opportunity to use cannabis and frequency of use.

A cross-sectional study of 3303 Australian twins, measuring age of onset of cannabis use opportunity, lifetime frequency of cannabis use, and lifetime DSM-IV cannabis abuse/dependence. A trivariate Cholesky decomposition estimated additive genetic (A), shared environment (C) and unique environment (E) contributions to the opportunity to use cannabis, the frequency of cannabis use, cannabis abuse/dependence, and the extent of overlap between genetic and environmental factors associated with each phenotype.

Variance components estimates were A = 0.64 [95% confidence interval (CI) 0.58–0.70] and E = 0.36 (95% CI 0.29–0.42) for age of opportunity to use cannabis, A = 0.74 (95% CI 0.66–0.80) and E = 0.26 (95% CI 0.20–0.34) for cannabis use frequency, and A = 0.78 (95% CI 0.65–0.88) and E = 0.22 (95% CI 0.12–0.35) for cannabis abuse/dependence. Opportunity shares 45% of genetic influences with the frequency of use, and only 17% of additive genetic influences are unique to abuse/dependence from those acting on opportunity and frequency.

There are significant genetic contributions to lifetime cannabis abuse/dependence, but a large proportion of this overlaps with influences acting on opportunity and frequency of use. Individuals without drug use opportunity are uninformative, and studies of drug use disorders must incorporate individual exposure to accurately identify aetiology.

Alterations in self-monitoring have been reported in patients with psychotic disorders, but it remains unclear to what degree they represent true indicators of familial vulnerability for psychosis.

An error-correction action-monitoring task was used to examine self-monitoring in 42 patients with schizophrenia, 32 of their unaffected siblings and 41 healthy controls.

Significant between-group differences in self-monitoring accuracy were found (χ2=29.3, p<0.0001), patients performing worst and unaffected siblings performing at an intermediate level compared to controls (all between-group differences p<0.05). In the combined group of healthy controls and unaffected siblings, detection accuracy was associated with positive schizotypy as measured by the Structured Interview for Schizotypy – Revised (SIS-R) (β=−0.16, s.e.=0.07, p=0.026), but not with negative schizotypy (β=−0.05, s.e.=0.12, p=0.694). In patients, psychotic symptoms were not robustly associated with detection accuracy (β=−0.01, s.e.=0.01, p=0.094), although stratified analysis revealed suggestive evidence for association in patients not currently using antipsychotic medication (β=−0.03, s.e.=0.01, p=0.052), whereas no association was found in patients on antipsychotic medication (β=−0.01, s.e.=0.01, p=0.426). A similar pattern of associations was found for negative symptoms.

Alterations in self-monitoring may be associated with familial risk and expression of psychosis. The association between psychotic symptoms and self-monitoring in patients may be affected by antipsychotic medication, which may explain previous inconsistencies in the literature.

Catechol-O-methyltransferase (COMT) Val158Met has been associated with activity of the mesial temporal lobe during episodic memory and it may weakly increase risk for schizophrenia. However, how this variant affects parahippocampal and hippocampal physiology when dopamine transmission is perturbed is unclear. The aim of the present study was to compare the effects of the COMT Val158Met genotype on parahippocampal and hippocampal physiology during encoding of recognition memory in patients with schizophrenia and in healthy subjects.

Using blood oxygen level-dependent (BOLD) functional magnetic resonance imaging (fMRI), we studied 28 patients with schizophrenia and 33 healthy subjects matched for a series of sociodemographic and genetic variables while they performed a recognition memory task.

We found that healthy subjects had greater parahippocampal and hippocampal activity during memory encoding compared to patients with schizophrenia. We also found different activity of the parahippocampal region between healthy subjects and patients with schizophrenia as a function of the COMT genotype, in that the predicted COMT Met allele dose effect had an opposite direction in controls and patients.

Our results demonstrate a COMT Val158Met genotype by diagnosis interaction in parahippocampal activity during memory encoding and may suggest that modulation of dopamine signaling interacts with other disease-related processes in determining the phenotype of parahippocampal physiology in schizophrenia.

Cognitive behaviour therapy (CBT) for chronic fatigue syndrome (CFS) leads to a significant decrease in CFS-related symptoms and disability. The primary objective of this study was to explore whether partners’ solicitous responses and patients’ and partners’ perceived relationship satisfaction had an effect on treatment outcome.

The treatment outcome of a cohort of 204 consecutively referred patients treated with CBT was analysed. At baseline, CFS patients completed the Maudsley Marital Questionnaire. The Checklist Individual Strength subscale Fatigue and the Sickness Impact Profile total scores completed by CFS patients post-treatment were used as measures of clinically significant improvement. Partners completed the Family Response Questionnaire, the Maudsley Marital Questionnaire, the Brief Illness Perception Questionnaire, and the Causal Attribution List. Logistic regression analyses were performed with clinically significant improvement in fatigue and disability as dependent variables and scores on questionnaires at baseline as predictors.

Solicitous responses of the partner were associated with less clinically significant improvement in fatigue and disability. Partners more often reported solicitous responses when they perceived CFS as a severe condition. Patients’ relationship dissatisfaction was negatively associated with clinically significant improvement in fatigue.

Partners’ solicitous responses and illness perceptions at the start of the therapy can negatively affect the outcome of CBT for CFS. We emphasize the importance of addressing this in therapy.