There is evidence to suggest that cognitive deficits might persist beyond the acute stages of illness in major depressive disorder (MDD). However, the findings are somewhat inconsistent across the individual studies conducted to date. Our aim was to conduct a systematic review and meta-analysis of existing studies that have examined cognition in euthymic MDD patients.

Following a systematic search across several publication databases, meta-analyses were conducted for 27 empirical studies that compared euthymic adult MDD patients (895 participants) and healthy controls (997 participants) across a range of cognitive domains. The influence of demographic variables and confounding factors, including age of onset and recurrent episodes, was examined.

Compared with healthy controls, euthymic MDD patients were characterized by significantly poorer cognitive functions. However, the magnitude of observed deficits, with the exception of inhibitory control, were generally modest when late-onset cases were excuded. Late-onset cases demonstrated significantly more pronounced deficits in verbal memory, speed of information processing and some executive functions.

Cognitive deficits, especially poor response inhibition, are likely to be persistent features, at least of some forms, of adult-onset MDD. More studies are necessary to examine cognitive dysfunction in remitted psychotic, melancholic and bipolar spectrum MDD. Cognitive deficits overall appear to be more common among patients with late-onset depression, supporting the theories suggesting that possible vascular and neurodegenerative factors play a role in a substantial number of these patients.

Ageing is an important factor in the development of mental health problems and their treatment. We assessed age trajectories of common mental disorders (CMDs) and psychotherapy utilization from adolescence to old age, and examined whether these trajectories were modified by time period or birth cohort effects.

British Household Panel Survey (BHPS) with an 18-year follow-up between 1991 and 2009 (n = 30 224 participants, aged 15–100 years, with an average 7.3 person-observations per person). CMDs were assessed with the 12-item version of the General Health Questionnaire (GHQ). Psychotherapy treatment utilization during the past year was self-reported by the participants. The modifying influences of time period and cohort effects were assessed in a cohort-sequential longitudinal setting.

Following a moderate decrease after age 50, the prevalence of GHQ caseness increased steeply from age 75. This increase was more marked in the 2000s (GHQ prevalence increasing from 24% to 43%) than in the 1990s (from 22% to 34%). Psychotherapy utilization decreased after age 55, with no time period or cohort effects modifying the age trajectory. These ageing patterns were replicated in within-individual longitudinal analysis.

Old age is associated with higher risk of CMDs, and this association has become more marked during the past two decades. Ageing is also associated with an increasing discrepancy between prevalence of mental disorders and provision of treatment, as indicated by lower use of psychotherapy in older individuals.

Evidence shows that cognitive deficits and white matter (WM) dysconnectivity can independently be associated with clinical manifestations in schizophrenia. It is important to explore this triadic relationship in order to investigate whether the triplet could serve as potential extended endophenotypes of schizophrenia.

Diffusion tensor images and clinical performances were evaluated in 122 individuals with first-episode schizophrenia and 122 age- and gender-matched controls. In addition, 65 of 122 of the patient group and 40 of 122 controls were measured using intelligence quotient (IQ) testing.

The schizophrenia group showed lower fractional anisotropy (FA) values than controls in the right cerebral frontal lobar sub-gyral (RFSG) WM. The schizophrenia group also showed a significant positive correlation between FA in the RFSG and performance IQ (PIQ); in turn, their PIQ score showed a significant negative correlation with negative syndromes.

Overall, these findings support the hypothesis that WM deficits may be a core deficit that contributes to cognitive deficits as well as to negative symptoms.

Accumulating evidence suggests that fetal growth restriction may increase risk of later schizophrenia but this issue has not been addressed directly in previous studies. We examined whether the degree of fetal growth restriction was linearly related to risk of schizophrenia, and also whether maternal pre-eclampsia, associated with both placental dysfunction and poor fetal growth, was related to risk of schizophrenia.

A population-based cohort of single live births in the Medical Birth Registry of Norway (MBRN) between 1967 and 1982 was followed to adulthood (n = 873 612). The outcome was schizophrenia (n=2207) registered in the National Insurance Scheme (NIS). The degree of growth restriction was assessed by computing sex-specific z scores (standard deviation units) of ‘birth weight for gestational age’ and ‘birth length for gestational age’. Analyses were adjusted for potential confounders. Maternal pre-eclampsia was recorded in the Medical Birth Registry by midwives or obstetricians using strictly defined criteria.

The odds ratio (OR) for schizophrenia increased linearly with decreasing birth weight for gestational age z scores (p value for trend = 0.005). Compared with the reference group (z scores 0.01–1.00), the adjusted OR [95% confidence interval (CI)] for the lowest z-score category (< − 3.00) was 2.0 (95% CI 1.2–3.5). A similar pattern was observed for birth length for gestational age z scores. Forty-nine individuals with schizophrenia were identified among 15 622 births with pre-eclampsia. The adjusted OR for schizophrenia following maternal pre-eclampsia was 1.3 (95% CI 1.0–1.8).

Associations of schizophrenia risk with degree of fetal growth restriction and pre-eclampsia suggest future research into schizophrenia etiology focusing on mechanisms that influence fetal growth, including placental function.

Schizophrenia often becomes manifest in late adolescence and young adulthood but deviations in physical and behavioural development may already be present in childhood. We investigated the relationship between hearing impairment (measured with audiometry) and speech impairment (broadly defined) at age 4 years and adult risk of non-affective psychosis.

We performed a population-based, case–control study in Sweden with 105 cases of schizophrenia or other non-affective psychoses and 213 controls matched for sex, date and place of birth. Information on hearing and speech impairment at age 4, along with potential confounding factors, was retrieved from Well Baby Clinic (WBC) records.

Hearing impairment [odds ratio (OR) 6.0, 95% confidence interval (CI) 1.6–23.2] and speech impairment (OR 2.6, 95% CI 1.4–4.9) at age 4 were associated with an increased risk of non-affective psychotic illness. These associations were mutually independent and not explained by parental psychiatric history, occupational class or obstetric complications.

These results support the hypothesis that psychosis has a developmental aspect with presentation of antecedent markers early in childhood, long before the disease becomes manifest. Our findings add to the growing evidence that early hearing impairment and speech impairment are risk indicators for later non-affective psychosis and possibly represent aetiological clues and potentially modifiable risk factors. Notably, speech impairment and language impairment are both detectable with inexpensive, easily accessible screening.

Childhood psychotic symptoms have been used as a subclinical phenotype of schizophrenia in etiological research and as a target for preventative interventions. However, recent studies have cast doubt on the specificity of these symptoms for schizophrenia, suggesting alternative outcomes such as anxiety and depression. Using a prospective longitudinal birth cohort we investigated whether childhood psychotic symptoms predicted a diagnosis of schizophrenia or other psychiatric disorders by 38 years of age.

Participants were drawn from a birth cohort of 1037 children from Dunedin, New Zealand, who were followed prospectively to 38 years of age (96% retention rate). Structured clinical interviews were administered at age 11 to assess psychotic symptoms and study members underwent psychiatric assessments at ages 18, 21, 26, 32 and 38 to obtain past-year DSM-III-R/IV diagnoses and self-reports of attempted suicides since adolescence.

Psychotic symptoms at age 11 predicted elevated rates of research diagnoses of schizophrenia and post-traumatic stress disorder (PTSD) and also suicide attempts by age 38, even when controlling for gender, social class and childhood psychopathology. No significant associations were found for persistent anxiety, persistent depression, mania or persistent substance dependence. Very few of the children presenting with age-11 psychotic symptoms were free from disorder by age 38.

Childhood psychotic symptoms were not specific to a diagnosis of schizophrenia in adulthood and thus future studies of early symptoms should be cautious in extrapolating findings only to this clinical disorder. However, these symptoms may be useful as a marker of adult mental health problems more broadly.

Schizophrenia is associated with various brain structural abnormalities, including reduced volume of the hippocampi, prefrontal lobes and thalami. Cannabis use increases the risk of schizophrenia but reports of brain structural abnormalities in the cannabis-using population have not been consistent. We used automated image analysis to compare brain structural changes over time in people at elevated risk of schizophrenia for familial reasons who did and did not use cannabis.

Magnetic resonance imaging (MRI) scans were obtained from subjects at high familial risk of schizophrenia at entry to the Edinburgh High Risk Study (EHRS) and approximately 2 years later. Differential grey matter (GM) loss in those exposed (n = 23) and not exposed to cannabis (n = 32) in the intervening period was compared using tensor-based morphometry (TBM).

Cannabis exposure was associated with significantly greater loss of right anterior hippocampal (pcorrected = 0.029, t = 3.88) and left superior frontal lobe GM (pcorrected = 0.026, t = 4.68). The former finding remained significant even after the exclusion of individuals who had used other drugs during the inter-scan interval.

Using an automated analysis of longitudinal data, we demonstrate an association between cannabis use and GM loss in currently well people at familial risk of developing schizophrenia. This observation may be important in understanding the link between cannabis exposure and the subsequent development of schizophrenia.

People with psychosis demonstrate impaired response inhibition on the Stop Signal Task (SST). It is less clear if this impairment extends to reflection impulsivity, a form of impulsivity that has been linked to substance use in non-psychotic samples.

We compared 49 patients with first-episode psychosis (FEP) and 30 healthy control participants on two forms of impulsivity measured using the Information Sampling Test (IST) and the SST, along with clinical and IQ assessments. We also compared those patients who used cannabis with those who had either given up or never used.

Patients with FEP had significantly greater impairment in response inhibition but not in reflection impulsivity compared with healthy controls. By contrast, patients who reported current cannabis use demonstrated greater reflection impulsivity than those that had either given up or never used, whereas there were no differences in response inhibition.

These data suggest that abnormal reflection impulsivity is associated with substance use in psychosis but not psychosis itself; the opposite relationship may hold for response inhibition.

Several studies have reported weak associations between religious or spiritual belief and psychological health. However, most have been cross-sectional surveys in the USA, limiting inference about generalizability. An international longitudinal study of incidence of major depression gave us the opportunity to investigate this relationship further.

Data were collected in a prospective cohort study of adult general practice attendees across seven countries. Participants were followed at 6 and 12 months. Spiritual and religious beliefs were assessed using a standardized questionnaire, and DSM-IV diagnosis of major depression was made using the Composite International Diagnostic Interview (CIDI). Logistic regression was used to estimate incidence rates and odds ratios (ORs), after multiple imputation of missing data.

The analyses included 8318 attendees. Of participants reporting a spiritual understanding of life at baseline, 10.5% had an episode of depression in the following year compared to 10.3% of religious participants and 7.0% of the secular group (p < 0.001). However, the findings varied significantly across countries, with the difference being significant only in the UK, where spiritual participants were nearly three times more likely to experience an episode of depression than the secular group [OR 2.73, 95% confidence interval (CI) 1.59–4.68]. The strength of belief also had an effect, with participants with strong belief having twice the risk of participants with weak belief. There was no evidence of religion acting as a buffer to prevent depression after a serious life event.

These results do not support the notion that religious and spiritual life views enhance psychological well-being.

Medical patients are often screened for distress in the clinic using a questionnaire such as the Hospital Anxiety and Depression Scale (HADS) while awaiting their consultation. However, might the context of the clinic artificially inflate the distress score? To address this question we aimed to determine whether those who scored high on the HADS in the clinic remained high scorers when reassessed later at home.

We analysed data collected by a distress and depression screening service for cancer out-patients. All patients had completed the HADS in the clinic (on computer or on paper) prior to their consultation. For a period, patients with a high score (total of ⩾15) also completed the HADS again at home (over the telephone) 1 week later. We used these data to determine what proportion remained high scorers and the mean change in their scores. We estimated the effect of ‘regression to the mean’ on the observed change.

Of the 218 high scorers in the clinic, most [158 (72.5%), 95% confidence interval (CI) 66.6–78.4] scored high at reassessment. The mean fall in the HADS total score was 1.74 (95% CI 1.09–2.39), much of which could be attributed to the estimated change over time (regression to the mean) rather than the context.

Pre-consultation distress screening in clinic is widely used. Reassuringly, it only modestly overestimates distress measured later at home and consequently would result in a small proportion of unnecessary further assessments. We conclude it is a reasonable and convenient strategy.

Neural substrates of emotion dysregulation in adolescent suicide attempters remain unexamined.

We used functional magnetic resonance imaging to measure neural activity to neutral, mild or intense (i.e. 0%, 50% or 100% intensity) emotion face morphs in two separate emotion-processing runs (angry and happy) in three adolescent groups: (1) history of suicide attempt and depression (ATT, n = 14); (2) history of depression alone (NAT, n = 15); and (3) healthy controls (HC, n = 15). Post-hoc analyses were conducted on interactions from 3 group × 3 condition (intensities) whole-brain analyses (p < 0.05, corrected) for each emotion run.

To 50% intensity angry faces, ATT showed significantly greater activity than NAT in anterior cingulate gyral–dorsolateral prefrontal cortical attentional control circuitry, primary sensory and temporal cortices; and significantly greater activity than HC in the primary sensory cortex, while NAT had significantly lower activity than HC in the anterior cingulate gyrus and ventromedial prefrontal cortex. To neutral faces during the angry emotion-processing run, ATT had significantly lower activity than NAT in the fusiform gyrus. ATT also showed significantly lower activity than HC to 100% intensity happy faces in the primary sensory cortex, and to neutral faces in the happy run in the anterior cingulate and left medial frontal gyri (all p < 0.006,corrected). Psychophysiological interaction analyses revealed significantly reduced anterior cingulate gyral–insula functional connectivity to 50% intensity angry faces in ATT v. NAT or HC.

Elevated activity in attention control circuitry, and reduced anterior cingulate gyral–insula functional connectivity, to 50% intensity angry faces in ATT than other groups suggest that ATT may show inefficient recruitment of attentional control neural circuitry when regulating attention to mild intensity angry faces, which may represent a potential biological marker for suicide risk.

Overweight/obesity and depression are both major public health problems among adolescents. However, the question of a link between overweight/obesity and depression remains unresolved in this age group. We examined whether obesity increases risk of depression, or depression increases risk of obesity, or whether there is a reciprocal effect.

A two-wave prospective cohort study of adolescents aged 11–17 years at baseline (n = 4175) followed up a year later (n = 3134) sampled from the Houston metropolitan area. Overweight was defined as 95th percentile >body mass index (BMI) ⩽85th percentile and obese as BMI >95th percentile. Three indicators of depression were examined: any DSM-IV mood disorder, major depression, and symptoms of depression.

Data for the two-wave cohort indicated no evidence of reciprocal effects between weight and depression. Weight status predicted neither major depression nor depressive symptoms. However, mood disorders generally and major depression in particular increased risk of future obesity more than twofold. Depressed males had a sixfold increased risk of obesity. Females with depressive symptoms had a marginally increased risk of being overweight but not obese.

Our findings, combined with those of recent meta-analyses, suggest that obese youths are not more likely to become depressed but that depressed youths are more likely to become obese.

Many patients do not adhere to or benefit from cognitive behaviour therapy (CBT) for post-traumatic stress disorder (PTSD). This randomized controlled trial evaluates the extent to which preparing patients with emotion regulation skills prior to CBT enhances treatment outcome.

A total of 70 adult civilian patients with PTSD were randomized to 12 sessions of either supportive counselling followed by CBT (Support/CBT) or emotion regulation training followed by CBT (Skills/CBT).

Skills/CBT resulted in fewer treatment drop-outs, less PTSD and anxiety, and fewer negative appraisals at 6 months follow-up than Support/CBT. Between-condition effect size was moderate for PTSD severity (0.43, 95% confidence interval −0.04 to 0.90). More Skills/CBT (31%) patients achieved high end-state functioning at follow-up than patients in Support/CBT (12%) [χ2(n = 70) = 3.67, p < 0.05].

This evidence suggests that response to CBT may be enhanced in PTSD patients by preparing them with emotion regulation skills. High attrition of participants during the study limits conclusions from this study.

Externalizing traits or behaviors are typically assessed by self-report scales or criminal records. Few genetically informative studies have used both methods to determine whether they assess the same genetic or environmental risk factors.

We examined 442 male Swedish twin pairs with self-reported externalizing behaviors at age 16–17 years [externalizing traits (EXT), self-reported delinquency (SRD), impulsivity (IMP), grandiosity (GRD) and callousness (CLS)] and criminal behavior (CB) from the National Suspect Registry from age 13 to 25 years. Multivariate structural equation modeling was conducted with Mx.

The best-fit model contained one genetic, one shared environmental and two non-shared environmental common factors, and variable specific genetic and non-shared environmental factors. The risk for CB was influenced substantially by both genetic (a2 = 0.48) and familial–environmental factors (c2 = 0.22). About one-third of the genetic risk for CB but all of the shared environmental risk was indexed by the self-report measures. The degree to which the individual measures reflected genetic versus familial–environmental risks for CB varied widely. GRD and CLS were correlated with CB mainly through common genetic risk factors. SRD and CB covaried largely because of shared familial–environmental factors. For EXT and IMP, observed correlations with CB resulted in about equal parts from shared genetic and shared familial–environmental factors.

In adolescence, measures of grandiose and callous temperament best tap the genetic liability to CB. Measures of antisocial behaviors better index familial–environmental risks for CB. A substantial proportion of the genetic risk to CB was not well reflected in any of the self-report measures.

Drug abuse (DA) is a clinically heterogeneous syndrome. Using medical, legal, death and pharmacy records covering the entire population of Sweden, could we uncover meaningful subtypes of DA?

We performed a latent class analysis (LCA) on all individuals in Sweden born 1950–1993 who were registered with DA or its consequences (n=192 501) and then validated these classes using demographics, patterns of co-morbidity with alcohol use disorder (AUD), non-DA crime and psychiatric illness, and the pattern of aggregation and co-aggregation in sibling pairs.

The best-fit LCA had six classes: (1) low-frequency pure criminal, (2) high-frequency medical criminal, (3) low-frequency pure medical, (4) high-frequency medical, (5) prescription and (6) death. Each class had a distinct pattern of demographic features and co-morbidity and aggregated within sibling pairs with at least moderate specificity. For example, class 2 was characterized by early age at registration, low educational attainment, high male preponderance, high rates of AUDs, strong resemblance within sibling pairs [odds ratio (OR) 12.6] and crime and the highest risk for DA in siblings (20.0%). By contrast, class 5 had a female preponderance, late age at registration, low rates of crime and AUDs, high rates of psychiatric illness, high familiality within sibling pairs (OR 14.7) but the lowest observed risk for DA in siblings (8.9%).

DA as assessed by public records is a heterogeneous syndrome. Familial factors contribute substantially to this heterogeneity. Advances in our understanding of etiological processes leading to DA will be aided by a consideration of this heterogeneity.

The fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) proposes aligning nicotine use disorder (NUD) criteria with those for other substances, by including the current DSM fourth edition (DSM-IV) nicotine dependence (ND) criteria, three abuse criteria (neglect roles, hazardous use, interpersonal problems) and craving. Although NUD criteria indicate one latent trait, evidence is lacking on: (1) validity of each criterion; (2) validity of the criteria as a set; (3) comparative validity between DSM-5 NUD and DSM-IV ND criterion sets; and (4) NUD prevalence.

Nicotine criteria (DSM-IV ND, abuse and craving) and external validators (e.g. smoking soon after awakening, number of cigarettes per day) were assessed with a structured interview in 734 lifetime smokers from an Israeli household sample. Regression analysis evaluated the association between validators and each criterion. Receiver operating characteristic analysis assessed the association of the validators with the DSM-5 NUD set (number of criteria endorsed) and tested whether DSM-5 or DSM-IV provided the most discriminating criterion set. Changes in prevalence were examined.

Each DSM-5 NUD criterion was significantly associated with the validators, with strength of associations similar across the criteria. As a set, DSM-5 criteria were significantly associated with the validators, were significantly more discriminating than DSM-IV ND criteria, and led to increased prevalence of binary NUD (two or more criteria) over ND.

All findings address previous concerns about the DSM-IV nicotine diagnosis and its criteria and support the proposed changes for DSM-5 NUD, which should result in improved diagnosis of nicotine disorders.

In this global study we sought to estimate the degree to which a family member might feel embarrassed when a close relative is suffering from an alcohol, drug, or mental health condition (ADMC) versus a general medical condition (GMC). To date, most studies have considered embarrassment and stigma in society and internalized by the afflicted individual but have not assessed family embarrassment in a large-scale study.

In 16 sites of the World Mental Health Surveys (WMHS), standardized assessments were completed including items on family embarrassment. Site matching was used to constrain local socially shared determinants of stigma-related feelings, enabling a conditional logistic regression model that estimates the embarrassment close relatives may hold in relation to family members affected by an ADMC, a GMC, or both conditions.

There was a statistically robust association such that subgroups with an ADMC-affected relative were more likely to feel embarrassed compared to subgroups with a relative affected by a GMC (p < 0.001), even with covariate adjustments for age and sex.

The pattern of evidence from this research is consistent with conceptual models for interventions that target individual- and family-level stigma-related feelings of embarrassment as possible obstacles to effective early intervention and treatment for an ADMC. Macro-level interventions are under way but micro-level interventions may also be required among family members, along with care for each person with an ADMC.

Detailed population-based survey information on the relationship between the severity of common mental disorders (CMDs) and treatment for mental health problems is heavily based on North American research. The aim of this study was to replicate and expand existing knowledge by studying CMD severity and its association with treatment contact and treatment intensity in The Netherlands.

Data were obtained from the Netherlands Mental Health Survey and Incidence Study-2 (NEMESIS-2), a nationally representative face-to-face survey of the general population aged 18–64 years (n = 6646, response rate = 65.1%). DSM-IV diagnoses and disorder severity were assessed with the Composite International Diagnostic Interview Version 3.0 (CIDI 3.0). Treatment contact refers to at least one contact for mental health problems made in the general medical care (GMC) or mental health care (MHC) sector. Four levels of treatment intensity were assessed, based on type and duration of therapy received.

Although CMD severity was related to treatment contact, only 39.0% of severe cases received MHC. At the same time, 40.3% of MHC users did not have a 12-month disorder. Increasing levels of treatment intensity ranged from 51.6% to 13.0% in GMC and from 81.4% to 51.1% in MHC. CMD severity was related to treatment intensity in MHC but not in GMC. Sociodemographic characteristics were not significantly related to having experienced the highest level of treatment intensity in MHC.

Mental health treatment in the GMC sector should be improved, especially when policy is aimed at increasing the role of primary care in the management of mental health problems.

Sleep loss produces abnormal increases in reward seeking but the mechanisms underlying this phenomenon are poorly understood. The present study examined the influence of one night of sleep deprivation on neural responses to a monetary reward task in a sample of late adolescents/young adults.

Using a within-subjects crossover design, 27 healthy, right-handed late adolescents/young adults (16 females, 11 males; mean age 23.1 years) underwent functional magnetic resonance imaging (fMRI) following a night of sleep deprivation and following a night of normal sleep. Participants' recent sleep history was monitored using actigraphy for 1 week prior to each sleep condition.

Following sleep deprivation, participants exhibited increased activity in the ventral striatum (VS) and reduced deactivation in the medial prefrontal cortex (mPFC) during the winning of monetary reward, relative to the same task following normal sleep conditions. Shorter total sleep time over the five nights before the sleep-deprived testing condition was associated with reduced deactivation in the mPFC during reward.

These findings support the hypothesis that sleep loss produces aberrant functioning in reward neural circuitry, increasing the salience of positively reinforcing stimuli. Aberrant reward functioning related to insufficient sleep may contribute to the development and maintenance of reward dysfunction-related disorders, such as compulsive gambling, eating, substance abuse and mood disorders.