A proportion of ex-military personnel who develop mental health and social problems end up in the Criminal Justice System. A government review called for better understanding of pathways to offending among ex-military personnel to improve services and reduce reoffending. We utilised data linkage with criminal records to examine the patterns of offending among military personnel after they leave service and the associated risk (including mental health and alcohol problems) and socio-economic protective factors.

Questionnaire data from a cohort study of 13 856 randomly selected UK military personnel were linked with national criminal records to examine changes in the rates of offending after leaving service.

All types of offending increased after leaving service, with violent offending being the most prevalent. Offending was predicted by mental health and alcohol problems: probable PTSD, symptoms of common mental disorder and aggressive behaviour (verbal, property and threatened or actual physical aggression). Reduced risk of offending was associated with post-service socio-economic factors: absence of debt, stable housing and relationship satisfaction. These factors were associated with a reduced risk of offending in the presence of mental health risk factors.

Ex-military personnel are more likely to commit violent offences after leaving service than other offence-types. Mental health and alcohol problems are associated with increased risk of post-service offending, and socio-economic stability is associated with reduced risk of offending among military veterans with these problems. Efforts to reduce post-service offending should encompass management of socio-economic risk factors as well as mental health.

Given its diverse disease courses and symptom presentations, multiple phenotype dimensions with different biological underpinnings are expected with bipolar disorders (BPs). In this study, we aimed to identify lifetime BP psychopathology dimensions. We also explored the differing associations with bipolar I (BP-I) and bipolar II (BP-II) disorders.

We included a total of 307 subjects with BPs in the analysis. For the factor analysis, we chose six variables related to clinical courses, 29 indicators covering lifetime symptoms of mood episodes, and 6 specific comorbid conditions. To determine the relationships among the identified phenotypic dimensions and their effects on differentiating BP subtypes, we applied structural equation modeling.

We selected a six-factor solution through scree plot, Velicer's minimum average partial test, and face validity evaluations; the six factors were cyclicity, depression, atypical vegetative symptoms, elation, psychotic/irritable mania, and comorbidity. In the path analysis, five factors excluding atypical vegetative symptoms were associated with one another. Cyclicity, depression, and comorbidity had positive associations, and they correlated negatively with psychotic/irritable mania; elation showed positive correlations with cyclicity and psychotic/irritable mania. Depression, cyclicity, and comorbidity were stronger in BP-II than in BP-I, and they contributed significantly to the distinction between the two disorders.

We identified six phenotype dimensions; in addition to symptom features of manic and depressive episodes, various comorbidities and high cyclicity constructed separate dimensions. Except for atypical vegetative symptoms, all factors showed a complex interdependency and played roles in discriminating BP-II from BP-I.

We reanalyzed data from a previously published randomized component study that aimed to test the incremental effect of systematic exposure in an internet-delivered cognitive behavioral treatment (ICBT) for irritable bowel syndrome (IBS).

Three hundred and nine individuals with IBS were randomly assigned to either the full treatment protocol (experimental condition) or the same treatment protocol without systematic exposure (control). Participants were assessed weekly for IBS symptoms over the active treatment phase. We used a complier average causal effect (CACE) analysis, in the growth mixture modeling framework, to (1) examine the specific effect of exposure among those who received the intervention (i.e. compliers), and (2) explore the associations of pre-treatment patient characteristics with compliance status and outcome changes.

Fifty-five per cent of those assigned to the experimental condition were classified as compliers. The CACE analysis that took into account compliance status demonstrated that the magnitude of the incremental effect of systematic exposure on IBS symptoms was larger than the effect observed in an intention-to-treat analysis that ignored compliance status (d = 0.81 v. d = 0.44). Patients with university education showed more improvement during the exposure phase of the treatment. Pre-treatment patient characteristics did not predict compliance status.

The effect of systematic exposure on IBS symptoms is of substantial magnitude among those individuals who actually receive the intervention (CACE). Studying the subsample of individuals who discontinue treatment prematurely and tailoring interventions to improve compliance may increase overall improvement rates in ICBT for IBS.

Positron emission tomography and post-mortem studies of the number of somatodendritic 5-hydroxytryptamine1A (5-HT1A) autoreceptors in raphé nuclei have found both increases and decreases in depression. However, recent genetic studies suggest they may be increased in number and/or function. The current study examined the effect of buspirone on the electroencephalographic (EEG) centroid frequency, a putative index of somatodendritic 5-HT1A receptor functional status, in a cohort of medication-free depressed patients and controls.

A total of 15 depressed patients (nine male) and intelligence quotient (IQ)-, gender- and age-matched healthy controls had resting EEG recorded from 29 scalp electrodes prior to and 30, 60 and 90 min after oral buspirone (30 mg) administration. The effect of buspirone on somatodendritic 5-HT1A receptors was assessed by calculating the EEG centroid frequency between 6 and 10.5 Hz. The effect of buspirone on postsynaptic 5-HT1A receptors was assessed by measuring plasma growth hormone, prolactin and cortisol concentrations.

Analysis of variance revealed a significantly greater effect of buspirone on the EEG centroid frequency in patients compared with controls (F1,28 = 6.55, p = 0.016). There was no significant difference in the neuroendocrine responses between the two groups.

These findings are consistent with an increase in the functional status of somatodendritic, but not postsynaptic, 5-HT1A autoreceptors, in medication-free depressed patients in line with hypotheses based on genetic data. This increase in functional status would be hypothesized to lead to an increase in serotonergic negative feedback, and hence decreased release of 5-HT at raphé projection sites, in depressed patients.

Nonsuicidal self-injury (NSSI) is a risk factor for suicide, yet how changes in NSSI engagement relate to suicide ideation, planning, and attempts remains largely unknown. The current study aims to fill this gap by examining how changes in NSSI frequency over time related to concurrent changes in suicide thoughts and behaviors.

Data came from a sample of 403 self-injuring young adults who completed assessments of NSSI and suicide thoughts and behaviors at baseline, 6, and 12 months. Bivariate latent growth modeling, adjusting for covariates of lifetime NSSI frequency and treatment status, was used to examine the extent to which changes in NSSI frequency related to suicide ideation and suicide planning.

The frequency of NSSI declined across the study period. The slopes of NSSI and suicide ideation were significantly correlated, suggesting individuals with sharper declines in NSSI across time also showed sharper declines in suicide ideation. The intercepts between NSSI and suicide planning were significantly correlated, suggesting those with high NSSI frequency at baseline tended to report higher suicide planning across time. After covariate adjustment, the intercept of suicide planning marginally (p = 0.08) correlated with the slope of NSSI, tentatively suggesting that those who had less reductions in NSSI tended to have higher frequencies of suicide planning.

These results provide new evidence that changes in NSSI are related to subsequent changes in suicide thoughts and behaviors. Monitoring suicide risk among those with NSSI is important and treatment aiming to reduce NSSI may also reduce suicide risk.

Few studies have explored whether high-anticholinergic load may hamper rehabilitation in persons with schizophrenia. We aim to explore the associations between anticholinergic load of psychotropic treatment and functioning or cognitive performances of persons with psychosis engaged in psychosocial rehabilitation.

The study was performed using data collected at baseline assessment in the REHABase cohort including persons referred to a French network of psychosocial rehabilitation centers. The composite-rating scale developed by Salahudeen et al. was used to rate the anticholinergic load of psychotropic drugs prescribed at baseline assessment. The associations between total anticholinergic load score (categorized as ‘low’ <3 v. ‘high’ ⩾3) and functioning or cognitive characteristics were explored using multivariate analyses.

Of the 1012 participants with schizophrenia spectrum disorders identified in the REHABase, half used at least two psychotropic drugs with anticholinergic activity and one out of three was prescribed at least one psychotropic drug with high-anticholinergic activity. High-anticholinergic load was significantly associated with lower stage of recovery [odds ratio (OR) = 1.70, 95% confidence interval (CI) 1.05–2.76, p = 0.03], poor mental well-being (OR = 1.55, 95% CI 1.02–2.33, p = 0.04) and poor self-rated medication adherence (OR = 2.14, 95% CI 1.29–3.53, p = 0.003). Regarding cognition, a high-anticholinergic score was associated with poorer delayed-episodic memory (OR = 1.69, 95% CI 1.01–2.85, p = 0.05) and at the trend level with faster completion time on the test exploring executive performance (OR = 0.67, 95% CI 0.43–1.04, p = 0.07).

The psychosocial rehabilitation plan of persons with psychosis should integrate optimization of psychotropic treatment in order to lessen the functional and cognitive impact of high-anticholinergic load.

Early irritability predicts a broad spectrum of psychopathology spanning both internalizing and externalizing disorders, rather than any particular disorder or group of disorders (i.e. multifinality). Very few studies, however, have examined the developmental mechanisms by which it leads to such phenotypically diverse outcomes. We examined whether variation in the diurnal pattern of cortisol moderates developmental pathways between preschool irritability and the subsequent emergence of internalizing and externalizing symptoms 9 years later.

When children were 3 years old, mothers were interviewed about children's irritability and completed questionnaires about their children's psychopathology. Six years later, children collected saliva samples at wake-up and bedtime on three consecutive days. Diurnal cortisol patterns were modeled as latent difference scores between evening and morning samples. When children were approximately 12 years old, mothers again completed questionnaires about their children's psychopathology.

Among children with higher levels of irritability at age 3, a steeper diurnal cortisol slope at age 9 predicted greater internalizing symptoms and irritability at age 12, whereas a blunted slope at age 9 predicted greater externalizing symptoms at age 12, adjusting for baseline and concurrent symptoms.

Our results suggest that variation in stress system functioning can predict and differentiate developmental trajectories of early irritability that are relatively more internalizing v. those in which externalizing symptoms dominate in pre-adolescence.

Cannabis and its main psychoactive ingredient δ-9-tetrahydrocannibidiol (THC) can induce transient psychotic symptoms in healthy individuals and exacerbate them in those with established psychosis. However, not everyone experience these effects, suggesting that certain individuals are particularly susceptible. The neural basis of this sensitivity to the psychotomimetic effects of THC is unclear.

We investigated whether individuals who are sensitive to the psychotomimetic effects of THC (TP) under experimental conditions would show differential hippocampal activation compared with those who are not (NP). We studied 36 healthy males under identical conditions under the influence of placebo or THC (10 mg) given orally, on two separate occasions, in a pseudo-randomized, double-blind, repeated measures, within-subject, cross-over design, using psychopathological assessments and functional MRI while they performed a verbal learning task. They were classified into those who experienced transient psychotic symptoms (TP; n = 14) following THC administration and those who did not (NP; n = 22).

Under placebo conditions, there was significantly greater engagement of the left hippocampus (p < 0.001) in the TP group compared with the NP group during verbal encoding, which survived leave-one-out analysis. The level of hippocampal activation was directly correlated (Spearman's ρ = 0.44, p = 0.008) with the severity of transient psychotic symptoms induced by THC. This difference was not present when we compared two subgroups from the same sample that were defined by sensitivity to anxiogenic effects of THC.

These results suggest that altered hippocampal activation during verbal encoding may serve as a marker of sensitivity to the acute psychotomimetic effects of THC.

Previous literature supports exercise as a preventative agent for prenatal depression; however, treatment effects for women at risk for prenatal depression remain unexplored. The purpose of the study was to examine whether exercise can lower depressive symptoms among women who began pregnancy at risk for depression using both a statistical significance and reliable and clinically significant change criteria.

This study is a secondary analysis of two randomized controlled trials that followed the same exercise protocol. Pregnant women were allocated to an exercise intervention group (IG) or control group (CG). All participants completed the Center for Epidemiological Depression (CES-D) scale at gestational week 9–16 and 36–38. Women with a baseline score ⩾16 were included. A clinically reliable cut-off was calculated as a 7-point change in scores from pre- to post-intervention.

Thirty-six women in the IG and 25 women in the CG scored ⩾16 on the CES-D at baseline. At week 36–38 the IG had a statistically significant lower CES-D score (14.4 ± 8.6) than the CG (19.4 ± 11.1; p < 0.05). Twenty-two women in the IG (61%) had a clinically reliable decrease in their post-intervention score compared to eight women in the CG (32%; p < 0.05). Among the women who met the reliable change criteria, 18 (81%) in the IG and 7 (88%) in the CG had a score <16 post-intervention, with no difference between groups (p > 0.05).

A structured exercise program might be a useful treatment option for women at risk for prenatal depression.

Cohort studies of the long-term outcome of anxiety, depression and personality status rarely join together.

Two hundred and ten patients recruited with anxiety and depression to a randomised controlled trial between 1983 and 1987 (Nottingham Study of Neurotic Disorder) were followed up over 30 years. At trial entry personality status was assessed, together with the general neurotic syndrome, a combined diagnosis of mixed anxiety–depression (cothymia) linked to neurotic personality traits. Personality assessment used a procedure allowing conversion of data to the ICD-11 severity classification of personality disorder. After the original trial, seven further assessments were made. Observer and self-ratings of psychopathology and global outcome were also made. The primary outcome at 30 years was the proportion of those with no Diagnostic and Statistical Manual of Mental Disorders (DSM) diagnosis.

Data were analysed using multilevel repeated measures models that adjusted for age and gender. Missing data were assumed to be missing at random, and the models allowed all subjects to be included in the analysis with missing data automatically handled in the model estimation.

At 30 years, 69% of those with a baseline diagnosis of panic disorder had no DSM diagnosis compared to 37–47% of those with generalised anxiety disorder, dysthymia or mixed symptoms (cothymia) (p = 0.027). Apart from those with no personality dysfunction at entry all patients had worse outcomes after 30 years with regard to total psychopathology, anxiety and depression, social function and global outcome.

The long-term outcome of disorders formerly called ‘neurotic’ is poor with the exception of panic disorder. Personality dysfunction accentuates poor recovery.

Various studies support the inclusion of cannabis withdrawal in the diagnosis of cannabis use disorder (CUD) in the upcoming DSM-5. The aims of the current study were to (1) estimate the prevalence of DSM-5 cannabis withdrawal (criterion B), (2) estimate the role of genetic and environmental influences on individual differences in cannabis withdrawal and (3) determine the extent to which genetic and environmental influences on cannabis withdrawal overlap with those on DSM-IV-defined abuse/dependence.

The sample included 2276 lifetime cannabis-using adult Australian twins. Cannabis withdrawal was defined in accordance with criterion B of the proposed DSM-5 revisions. Cannabis abuse/dependence was defined as endorsing one or more DSM-IV criteria of abuse or three or more dependence criteria. The classical twin model was used to estimate the genetic and environmental influences on variation in cannabis withdrawal, along with its covariation with abuse/dependence.

Of all the cannabis users, 11.9% met criteria for cannabis withdrawal. Around 50% of between-individual variation in withdrawal could be attributed to additive genetic variation, and the rest of the variation was mostly due to non-shared environmental influences. Importantly, the genetic influences on cannabis withdrawal almost completely (99%) overlapped with those on abuse/dependence.

We have shown that cannabis withdrawal symptoms exist among cannabis users, and that cannabis withdrawal is moderately heritable. Genetic influences on cannabis withdrawal are the same as those affecting abuse/dependence. These results add to the wealth of literature that recommends the addition of cannabis withdrawal to the diagnosis of DSM-5 CUD.

Childhood adversity is associated with mental disorder following military deployment. However, it is unclear how different childhood trauma profiles relate to developing a post-deployment disorder. We investigated childhood trauma prospectively in determining new post-deployment probable disorder.

In total, 1009 Regular male ADF personnel from the Australian Defence Force (ADF) Middle East Area of Operations (MEAO) Prospective Study provided pre- and post-deployment self-report data. Logistic regression and generalised structural equation modelling were utilised to examine associations between childhood trauma and new post-deployment probable disorder and possible mediator pathways through pre-deployment symptoms.

There were low rates of pre-deployment probable disorder. New post-deployment probable disorder was associated with childhood trauma, index deployment factors (combat role and deployment trauma) and pre-deployment symptoms but not with demographic, service or adult factors prior to the index deployment (including trauma, combat or previous deployment). Even after controlling for demographic, service and adult factors prior to the index deployment as well as index deployment trauma, childhood trauma was still a significant determinant of new post-deployment probable disorder. GSEM demonstrated that the association between interpersonal childhood trauma and new post-deployment probable disorder was fully mediated by pre-deployment symptoms. This was not the case for those who experienced childhood trauma that was not interpersonal in nature.

To determine the risk of developing a post-deployment disorder an understanding of the types of childhood trauma encountered is essential, and pre-deployment symptom screening alone is insufficient