Considering existing knowledge on the relationship between certain environmental factors and incidence rates of psychosis, we carried out a systematic review to provide a broad and updated picture of the incidences of different psychotic disorder subgroups worldwide and how some environmental factors influence these rates.

Studies with original data related to the incidence of psychosis (published between 2000 and 2015) were identified via searching electronic databases (CINAHL, MEDLINE, PSYCINFO, PUBMED, and SCOPUS). Data on the following risk factors were extracted: gender, urbanicity, immigration and socio-economic level. Descriptive appraisals of variation in incidence rates (IR) and incidence rate ratios (IRR), with a 95% confidence interval were calculated. In addition, a meta-analysis was performed to calculate IR pooled by diagnosis group and IRR pooled by diagnosis and gender, urbanity, immigration and socio-economic level, using a random effects model.

We identified 33 reports to analyse. Overall IR per 100 000 persons for non-affective psychoses (IR pooled = 22.53 (16.51–28.54)) were higher than affective psychoses (IR pooled = 7.12 (5.03–9.22)). There was an increase in rates of psychosis in men v. women (IRR pooled = 1.54 (1.37–1.72)), in urban v. rural areas (IRR pooled = 1.64 (1.38–1.95)), in immigrants v. natives (IRR pooled = 3.09 (2.74–3.49)), and in lower socio-economic level areas (IRR pooled = 1.78 (1.43–2.22)).

IR among different psychotic disorders was found to vary depending on gender, urbanicity, and immigration (as most of the previous literature focuses on non-affective psychosis or schizophrenia).

More than half of patients who present with depressive disorders also have elevated comorbid anxiety symptoms. Given the high comorbidity between these disorders, it is important to understand the extent that psychotherapies for depression additionally ameliorate symptoms of anxiety.

Systematic searches were conducted in PubMed, PSYCinfo, EMBASE, and the Cochrane Registry of Controlled Trials. Included studies were randomized controlled trials that compared psychotherapy compared with a control condition for the treatment of adults with a primary diagnosis or elevated symptoms of depression and that examined the effects of treatment on anxiety outcomes. Acute phase depression and anxiety (continuous measure) outcomes were extracted. Effect sizes were calculated by subtracting the average post-treatment scores of the psychotherapy group from the average post-treatment scores of the comparison group divided by the pooled standard deviation.

Fifty-two studies of varying quality met the inclusion criteria. Pooled effect sizes showed that anxiety outcomes were significantly lower in the psychotherapy conditions than in control conditions at post-treatment [g = 0.52; 95% confidence interval (CI) 0.44–0.60; NNT (numbers-needed-to-treat) = 3.50]. Moderate heterogeneity was observed (I2 = 55%, 95% CI 40–66). Bivariate metaregression analysis revealed a significant association between depression and anxiety effect sizes at post-treatment Longer-term follow-ups of up to 14 months post-baseline showed indications for a small lasting effect of psychotherapy on anxiety outcomes (g = 0.27).

This meta-analysis provides evidence that psychotherapy aimed at depression can also reduce anxiety symptoms in relation to control conditions.

Previous studies find that both schizophrenia and mood disorder risk alleles contribute to adult depression and anxiety. Emotional problems (depression or anxiety) begin in childhood and show strong continuities into adult life; this suggests that symptoms are the manifestation of the same underlying liability across different ages. However, other findings suggest that there are developmental differences in the etiology of emotional problems at different ages. To our knowledge, no study has prospectively examined the impact of psychiatric risk alleles on emotional problems at different ages in the same individuals.

Data were analyzed using regression-based analyses in a prospective, population-based UK cohort (the National Child Development Study). Schizophrenia and major depressive disorder (MDD) polygenic risk scores (PRS) were derived from published Psychiatric Genomics Consortium genome-wide association studies. Emotional problems were assessed prospectively at six time points from age 7 to 42 years.

Schizophrenia PRS were associated with emotional problems from childhood [age 7, OR 1.09 (1.03–1.15), p = 0.003] to mid-life [age 42, OR 1.10 (1.05–1.17), p < 0.001], while MDD PRS were associated with emotional problems only in adulthood [age 42, OR 1.06 (1.00–1.11), p = 0.034; age 7, OR 1.03 (0.98–1.09), p = 0.228].

Our prospective investigation suggests that early (childhood) emotional problems in the general population share genetic risk with schizophrenia, while later (adult) emotional problems also share genetic risk with MDD. The results suggest that the genetic architecture of depression/anxiety is not static across development.

Many preschool-age children meet criteria for psychiatric disorders, and rates approach those observed in later childhood and adolescence. However, there is a paucity of longitudinal research examining the outcomes of preschool diagnoses.

Families with a 3-year-old child (N = 559) were recruited from the community. Primary caregivers were interviewed using the Preschool Age Psychiatric Assessment when children were 3 years old (n = 541), and, along with children, using the Schedule for Affective Disorders and Schizophrenia for School-Age Children Present and Lifetime Version when children were 9 and 12 years old.

Rates of disruptive behavior disorders (DBD) decreased from preschool to middle childhood and early adolescence, whereas rates of attention-deficit/hyperactivity disorder (ADHD) increased. Rates of any psychiatric disorder and depression increased from preschool to early adolescence only. Preschoolers with a diagnosis were over twice as likely to have a diagnosis during later periods. Homotypic continuity was present for anxiety disorders from preschool to middle childhood, for ADHD from preschool to early adolescence, and for DBD through both later time points. There was heterotypic continuity between preschool anxiety and early adolescent depression, and between preschool ADHD and early adolescent DBD. Dimensional symptom scores showed homotypic continuity for all diagnostic categories and showed a number of heterotypic associations as well.

Results provide moderate support for the predictive validity of psychiatric disorders in preschoolers. Psychopathology in preschool is a significant risk factor for future psychiatric disorders during middle childhood and early adolescence.

Evidence regarding the association between cannabis use and depression remain conflicting, especially as studies have not typically adopted a longitudinal design with a follow-up period that was long enough to adequately cover the risk period for onset of depression.

Males from the Cambridge Study in Delinquent Development (CSDD) (N = 285) were assessed seven times from age 8 to 48 years to prospectively investigate the association between cannabis use and risk of major depressive disorder (MDD). A combination of multiple analyses (logistic regression, Cox regression, fixed-effects analysis) was employed to explore the strength and direction of effect within different developmental stages.

Multiple regression analyses revealed that early-onset cannabis use (before age 18) but not late-onset cannabis use (after age 27) was associated with a higher risk and shorter time until a subsequent MDD diagnosis. This effect was present in high-frequency [(odds ratio (OR) 8.83, 95% confidence interval (CI) 1.29–70.79]; [hazard ratio (HR) 8.69, 95% CI 2.07–36.52)] and low-frequency early-onset users (OR 2.41, 95% CI 1.22–4.76; HR 2.09, 95% CI 1.16–3.74). Effect of increased frequency of cannabis use on increased risk of subsequent MDD was observed only for use during adolescence (age 14–18) but not at later life stages, while controlling for observed and non-unobserved time-invariant factors. Conversely, MDD in adulthood (age 18–32) was linked to a reduction in subsequent cannabis use (age 32–48).

The present findings provide evidence implicating frequent cannabis use during adolescence as a risk factor for later life depression. Future studies should further examine causality of effects in larger samples.

Cognitive–behavioral group therapy (CBGT) is a first-line treatment for social anxiety disorder (SAD). However, since many patients remain symptomatic post-treatment, there is a need for augmenting procedures. This randomized controlled trial (RCT) examined the potential augmentation effect of attention bias modification (ABM) for CBGT.

Fifty patients with SAD from three therapy groups were randomized to receive an 18-week standard CBGT with either ABM designed to shift attention away from threat (CBGT + ABM), or a placebo protocol not designed to modify threat-related attention (CBGT + placebo). Therapy groups took place in a large mental health center. Clinician and self-report measures of social anxiety and depression were acquired pre-treatment, post-treatment, and at 3-month follow-up. Attention bias was assessed at pre- and post-treatment.

Patients randomized to the CBGT + ABM group, relative to those randomized to the CBGT + placebo group, showed greater reductions in clinician-rated SAD symptoms post-treatment, with effects maintained at 3-month follow-up. Group differences were not evident for self-report or attention-bias measures, with similar reductions in both groups. Finally, reduction in attention bias did not mediate the association between group and reduction in Liebowitz Social Anxiety Scale Structured Interview (LSAS) scores.

This is the first RCT to examine the possible augmenting effect of ABM added to group-based cognitive–behavioral therapy for adult SAD. Training patients’ attention away from threat might augment the treatment response to standard CBGT in SAD, a possibility that could be further evaluated in large-scale RCTs.

Childhood adversity is associated with cognitive impairments in schizophrenia. However, findings to date are inconsistent and little is known about the relationship between social cognition and childhood trauma. We investigated the relationship between childhood abuse and neglect and cognitive function in patients with a first-episode of schizophrenia or schizophreniform disorder (n = 56) and matched healthy controls (n = 52). To the best of our knowledge, this is the first study assessing this relationship in patients and controls exposed to similarly high levels of trauma.

Pearson correlational coefficients were used to assess correlations between Childhood Trauma Questionnaire abuse and neglect scores and cognition. For the MCCB domains displaying significant (p < 0.05) correlations, within group hierarchical linear regression, was done to assess whether abuse and neglect were significant predictors of cognition after controlling for the effect of education.

Patients and controls reported similarly high levels of abuse and neglect. Cognitive performance was poorer for patients compared with controls for all cognitive domains except working memory and social cognition. After controlling for education, exposure to childhood neglect remained a significant predictor of impairment in social cognition in both patients and controls. Neglect was also a significant predictor of poorer verbal learning in patients and of attention/vigilance in controls. However, childhood abuse did not significantly predict cognitive impairments in either patients or controls.

These findings are cross sectional and do not infer causality. Nonetheless, they indicate that associations between one type of childhood adversity (i.e. neglect) and social cognition are present and are not illness-specific.

Low resting heart rate (RHR) is a consistent biological correlate of antisocial behaviour (ASB), however potential mechanisms have been largely unexplored. We hypothesise that lower RHR will be associated with higher ASB levels in mid-adolescence and persistence into adulthood, and that these associations will be explained, in part, by sensation seeking and callous-unemotional traits.

ASB was assessed repeatedly with young people from ages 15 to 21 years in a population-based birth cohort (ALSPAC). A longitudinal trajectory was derived and showed ASB decreasing across adolescence before stabilising in early adulthood. RHR was recorded at age 12 years, and mediators were assessed at age 14 years.

After adjusting for socio-demographic confounders, there was evidence for a total effect of RHR on ASB levels in mid-adolescence [b(95% CI) = −0.08 (−0.14 to −0.02)], reflecting 0.08 more types of antisocial activity in the last year per 10 fewer heart beats per minute. This effect was almost entirely explained through sensation seeking [b(95% CI) = −0.06 (−0.08 to −0.04)]. After additionally adjusting for child and parent-related confounders, all effects weakened; however, there was still evidence of an indirect effect of RHR, via sensation seeking, on ASB levels in mid-adolescence [b(95% CI) = −0.01 (−0.03 to −0.003)]. There was no evidence for a total effect of RHR on ASB levels in early adulthood, and weak evidence of an indirect effect, via sensation seeking [b(95% CI) = −0.01 (−0.01 to −0.00)].

Lower RHR in childhood was associated with higher ASB levels in mid-adolescence, indirectly via sensation seeking.

Research into violence among military personnel has not differentiated between stranger- and family-directed violence. While military factors (combat exposure and post-deployment mental health problems) are risk factors for general violence, there has been limited research on their impact on violence within the family environment. This study aims to compare the prevalence of family-directed and stranger-directed violence among a deployed sample of UK military personnel and to explore risk factors associated with both family- and stranger-directed violence.

This study utilised data from a large cohort study which collected information by questionnaire from a representative sample of randomly selected deployed UK military personnel (n = 6711).

The prevalence of family violence immediately following return from deployment was 3.6% and 7.8% for stranger violence. Family violence was significantly associated with having left service, while stranger violence was associated with younger age, male gender, being single, having a history of antisocial behaviour as well as having left service. Deployment in a combat role was significantly associated with both family and stranger violence after adjustment for confounders [adjusted odds ratio (aOR) = 1.92 (1.25–2.94), p = 0.003 and aOR = 1.77 (1.31–2.40), p < 0.001, respectively], as was the presence of symptoms of post-traumatic stress disorder, common mental disorders and aggression.

Exposure to combat and post-deployment mental health problems are risk factors for violence both inside and outside the family environment and should be considered in violence reduction programmes for military personnel. Further research using a validated measurement tool for family violence would improve comparability with other research.

The course of illness in obsessive–compulsive disorder (OCD) varies significantly between patients. Little is known about factors predicting a chronic course of illness. The aim of this study is to identify factors involved in inducing and in maintaining chronicity in OCD.

The present study is embedded within the Netherlands Obsessive Compulsive Disorder Association (NOCDA) study, an ongoing multicenter naturalistic cohort study designed to identify predictors of long-term course and outcome in OCD. For this study, 270 subjects with a current diagnosis of OCD were included. Chronicity status at 2-year follow-up was regressed on a selection of baseline predictors related to OCD, to comorbidity and to stress and support.

Psychotrauma [odds ratio (OR) 1.98, confidence interval (CI) 1.22–3.22, p = 0.006], recent negative life events (OR 1.42, CI 1.01–2.01, p = 0.043), and presence of a partner (OR 0.28, CI 0.09–0.85, p = 0.025) influenced the risk of becoming chronic. Longer illness duration (OR 1.46, CI 1.08–1.96, p = 0.013) and higher illness severity (OR 1.09, CI 1.03–1.16, p = 0.003) increased the risk of remaining chronic.

External influences increase the risk of becoming chronic, whereas the factors involved in maintaining chronicity are illness-related. As the latter are potentially difficult to modify, treatment should be devoted to prevent chronicity from occurring in the first place. Therapeutic strategies aimed at alleviating stress and at boosting social support might aid in achieving this goal.

Fear responses are particularly intense and persistent in post-traumatic stress disorder (PTSD), and can be evoked by unspecific cues that resemble the original traumatic event. Overgeneralisation of fear might be one of the underlying mechanisms. We investigated the generalisation and discrimination of fear in individuals with and without PTSD related to prolonged childhood maltreatment.

Sixty trauma-exposed women with (N = 30) and without (N = 30) PTSD and 30 healthy control participants (HC) underwent a fear conditioning and generalisation paradigm. In a contingency learning procedure, one of two circles of different sizes was associated with an electrical shock (danger cue), while the other circle represented a safety cue. During generalisation testing, online risk ratings, reaction times and fear-potentiated startle were measured in response to safety and danger cues as well as to eight generalisation stimuli, i.e. circles of parametrically varying size creating a continuum of similarity between the danger and safety cue.

The increase in reaction times from the safety cue across the different generalisation classes to the danger cue was less pronounced in PTSD compared with HC. Moreover, PTSD participants expected higher risk of an aversive event independent of stimulus types and task.

Alterations in generalisation constitute one part of fear memory alterations in PTSD. Neither the accuracy of a risk judgement nor the strength of the induced fear was affected. Instead, processing times as an index of uncertainty during risk judgements suggested a reduced differentiation between safety and threat in PTSD.

Previous work showed traumatic life events (TLE) with intention to harm, like bullying and abuse, to be more strongly associated with psychotic experiences (PE) than other types of trauma, like accidents. However, this association is subject to reporting bias and can be confounded by demographic characteristics and by differences in dose of exposure across different trauma categories. We studied the association between TLE with and without intention to harm and PE, taking into account potential confounders and biases.

A total of 2245 children and adolescents aged 6–14 years were interviewed by psychologists. The interview included the presence of 20 PE (both self-report and psychologist evaluation). In addition, parents provided information on child exposure to trauma, mental health and PE.

Results showed no significant association between TLE without intention to harm only and PE for the three methods of assessment of PE (self-report, parent report and psychologist rating). On the other hand, there was a positive association between PE and TLE in groups exposed to traumatic experiences with intention to harm (with intention to harm only and with and without intention to harm). Results remained significant after controlling for demographic and clinical confounders, but this positive association was no longer significant after adjusting for the number of TLE.

TLE with intention to harm display a stronger association with PE than TLE without intention to harm, and this difference is likely reducible to a greater level of traumatic exposure associated with TLE with intention to harm.

Cognitive deficits are a core feature of early stages in schizophrenia. However, the extent to which antipsychotic (AP) have a deleterious effect on cognitive performance remains under debate. We aim to investigate whether anticholinergic loadings and dose of AP drugs in first episode of psychosis (FEP) in advanced phase of remission are associated with cognitive impairment and the differences between premorbid intellectual quotient (IQ) subgroups.

Two hundred and sixty-six patients participated. The primary outcomes were cognitive dimensions, dopaminergic/anticholinergic load of AP [in chlorpromazine equivalents (Eq-CPZ) and the Anticholinergic Risk Scale (ARS), respectively].

Impairments in processing speed, verbal memory and global cognition were significantly associated with high Eq-CPZ and verbal impairment with high ARS score. Moreover, this effect was higher in the low IQ subgroup.

Clinicians should be aware of the potential cognitive impairment associated with AP in advanced remission FEP, particularly in lower premorbid IQ patients.

The intergenerational risk for mental illness is well established within diagnostic categories, but the risk is unlikely to respect diagnostic boundaries and may be reflected more broadly in early life vulnerabilities. We aimed to establish patterns of association between externalising and internalising vulnerabilities in early childhood and parental mental disorder across the full spectrum of diagnoses.

A cohort of Australian children (n = 69 116) entering the first year of school in 2009 were assessed using the Australian Early Development Census, providing measures of externalising and internalising vulnerability. Parental psychiatric diagnostic status was determined utilising record-linkage to administrative health datasets.

Parental mental illness, across diagnostic categories, was associated with all child externalising and internalising domains of vulnerability. There was little evidence to support interaction by parental or offspring sex.

These findings have important implications for informing early identification and intervention strategies in high-risk offspring and for research into the causes of mental illness. There may be benefits to focusing less on diagnostic categories in both cases.

The vulnerability hypothesis suggests that impairments after remission of depressive episodes reflect a pre-existing vulnerability, while the scar hypothesis proposes that depression leaves residual impairments that confer risk of subsequent episodes. We prospectively examined vulnerability and scar effects in mental and physical functioning in a representative Dutch population sample.

Three waves were used from the Netherlands Mental Health Survey and Incidence Study-2, a population-based study with a 6-years follow-up. Mental and physical functioning were assessed with the Medical Outcomes Study Short Form (SF-36). Major depressive disorder (MDD) was assessed with the Composite International Diagnostic Interview 3.0. Vulnerability effects were examined by comparing healthy controls (n = 2826) with individuals who developed a first-onset depressive episode during first follow-up but did not have a lifetime diagnosis of MDD at baseline (n = 181). Scarring effects were examined by comparing pre- and post-morbid functioning in individuals who developed a depressive episode after baseline that was remitted at the third wave (n = 108).

Both mental (B = −5.4, s.e. = 0.9, p < 0.001) and physical functioning (B = −8.2, s.e. = 1.1, p < 0.001) at baseline were lower in individuals who developed a first depressive episode after baseline compared with healthy controls. This effect was most pronounced in people who developed a severe episode. No firm evidence of scarring in mental or physical functioning was found. In unadjusted analyses, physical functioning was still lowered post-morbidly (B = −5.1, s.e. = 2.1, p = 0.014), but this effect disappeared in adjusted analyses.

Functional impairments after remission of depression seem to reflect a pre-existing vulnerability rather than a scar.