The foetal origins hypothesis suggests an association between low birth weight and later depression, yet evidence supporting this association has been inconsistent.

We systematically reviewed evidence for an association between low birth weight and adult depression or psychological distress in the general population by meta-analysis. We searched EMBASE, Medline, PsycINFO and ISI Web of Science for studies reporting observational data with low birth weight as the exposure and self- or clinician-rated depression or psychological distress measures as an outcome. Selective studies of exposures such as famine or outcomes such as severe illness only were excluded. Altogether,1454 studies were screened for relevance, 26 were included in the qualitative synthesis, 18 were included in the meta-analysis. A random effects meta-analysis method was used to obtain a pooled estimate of effect size.

The odds of depression or psychological distress was greater for those of low birth weight (<2500 g) compared to those of normal birth weight (>2500 g) or greater [odds ratio (OR) 1.15, 95% confidence intervals (CI) 1.00–1.32]. However, this association became non-significant after trim-and-fill correction for publication bias (OR 1.08, 95% CI 0.92–1.27). Using meta-regression, no differences in effect size were observed by gender, outcome measure of depression or psychological distress, or whether the effect size was adjusted for possible confounders.

We found evidence to support a weak association between low birth weight and later depression or psychological distress, which may be due to publication bias. It remains possible that the association may vary according to severity of symptoms or other factors.

It is unclear how the course of maternal depressive symptoms affects child development. We modelled trajectories of maternal depressive symptoms from mid-pregnancy to 3 years after childbirth to better determine their associations with child problem behaviour.

Mother–child dyads (n = 4167) participated in a population-based prospective cohort in The Netherlands. Depressive symptoms were assessed with the Brief Symptom Inventory during pregnancy and at 2, 6 and 36 months postnatally. When children were 3 years old, problem behaviour was assessed with the Child Behaviour Checklist completed by each parent. A group-based modelling technique was used to model trajectories of maternal depressive symptoms and to examine their association with child problem behaviour. The added value of trajectory modelling was determined with successive linear regressions.

We identified four trajectories of maternal depressive symptoms; ‘no’ (34%), ‘low’ (54%), ‘moderate’ (11%) and ‘high’ (1.5%). Child problem behaviour varied as a function of maternal trajectory membership. Whether rated by mother or father, children of mothers assigned to higher trajectories had significantly more problem behaviours than children of mothers assigned to lower trajectories. The model including trajectories had additive predictive value over a model relying only on a summed repeated measure of severity and a predefined chronicity variable.

Depending on their course, maternal depressive symptoms have different effects on child problem behaviour. More information is gained by studying trajectories of symptoms, than only predefined measures of severity and chronicity. Moreover, trajectories can help identifying clinically depressed mothers who are possible candidates for early interventions.

Alterations in reward processing may represent an early vulnerability factor for the development of depressive disorder. Depression in adults is associated with reward hyposensitivity and diminished reward seeking may also be a feature of depression in children and adolescents. We examined the role of reward responding in predicting depressive symptoms, functional impairment and new-onset depressive disorder over time in the adolescent offspring of depressed parents. In addition, we examined group differences in reward responding between currently depressed adolescents, psychiatric and healthy controls, and also cross-sectional associations between reward responding and measures of positive social/environmental functioning.

We conducted a 1-year longitudinal study of adolescents at familial risk for depression (n = 197; age range 10–18 years). Reward responding and self-reported social/environmental functioning were assessed at baseline. Clinical interviews determined diagnostic status at baseline and at follow-up. Reports of depressive symptoms and functional impairment were also obtained.

Low reward seeking predicted depressive symptoms and new-onset depressive disorder at the 1-year follow-up in individuals free from depressive disorder at baseline, independently of baseline depressive symptoms. Reduced reward seeking also predicted functional impairment. Adolescents with current depressive disorder were less reward seeking (i.e. bet less at favourable odds) than adolescents free from psychopathology and those with externalizing disorders. Reward seeking showed positive associations with social and environmental functioning (extra-curricular activities, humour, friendships) and was negatively associated with anhedonia. There were no group differences in impulsivity, decision making or psychomotor slowing.

Reward seeking predicts depression severity and onset in adolescents at elevated risk of depression. Adaptive reward responses may be amenable to change through modification of existing preventive psychological interventions.

Knowledge of the risk of recurrence after recovery from major depressive disorder (MDD) in the general population is scarce.

Data were derived from 687 subjects in the general population with a lifetime DSM-III-R diagnosis of MDD but without a current major depressive episode (MDE) or dysthymia. Participants had to be at least 6 months in remission, and were recruited from The Netherlands Mental Health Survey and Incidence Study (NEMESIS), using the Composite International Diagnostic Interview (CIDI). Recency and severity of the last MDE were assessed retrospectively at baseline. Recurrence of MDD was measured prospectively during the 3-year follow-up. Kaplan–Meier survival curves were used to measure time to recurrence. Determinants of time to recurrence were analyzed using proportional hazard models.

The estimated cumulative recurrence of MDD was 13.2% at 5 years, 23.2% at 10 years and 42.0% at 20 years. In bivariate analysis, the following variables predicted a shorter time to recurrence: younger age, younger age of onset, higher number of previous episodes, a severe last depressive episode, negative youth experiences, ongoing difficulties before recurrence and high neuroticism. Multivariably, younger age, a higher number of previous episodes, a severe last depressive episode, negative youth experiences and ongoing difficulties remained significant.

In this community sample, the long-term risk of recurrence was high, but lower than that found in clinical samples. Subjects who had had an MDE had a long-term vulnerability for recurrence. Factors predicting recurrence included illness- and stress-related factors.

Cognitive ability/intelligence quotient (IQ) in youth has previously been associated with subsequent completed and attempted suicide, but little is known about the mechanisms underlying the associations. This study aims to assess the roles of various risk factors over the life course in explaining the observed relationships.

The present investigation is a cohort study based on data on IQ test performance and covariates, recorded on 49 321 Swedish men conscripted in 1969–1970, at ages 18–20 years. Information on suicides and hospital admissions for suicide attempt up to the age of 57 years, childhood and adult socio-economic position, and adult family formation, was obtained from linkage to national registers.

Lower IQ was associated with increased risks of both suicide and suicide attempt during the 36 years of follow-up. The associations followed a dose–response pattern. They were attenuated by approximately 45% in models controlling for social background, mental ill-health, aspects of personality and behavior, adult socio-economic position and family formation. Based on one-unit decreases in IQ test performance on a nine-point scale, the hazard ratios between ages 35 and 57 years were: for suicide 1.19 [95% confidence interval (CI) 1.13–1.25], fully adjusted 1.10 (95% CI 1.04–1.18); and for suicide attempt 1.25 (95% CI 1.20–1.31), fully adjusted 1.14 (95% CI 1.09–1.20).

Cognitive ability was found to be associated with subsequent completed and attempted suicide. The associations were attenuated by 45% after controlling for risk factors measured over the life course. Psychiatric diagnosis, maladjustment and aspects of personality in young adulthood, and social circumstances in later adulthood, contributed in attenuating the associations.

Psychiatric in-patients are at high risk of suicide. Recent reductions in bed numbers in many countries may have affected this risk but few studies have specifically investigated temporal trends. We aimed to explore trends in psychiatric in-patient suicide over time.

A prospective study of all patients admitted to National Health Service (NHS) in-patient psychiatric care in England (1997–2008). Suicide rates were determined using National Confidential Inquiry and Hospital Episode Statistics (HES) data.

Over the study period there were 1942 psychiatric in-patient suicides. Between the first 2 years of the study (1997, 1998) and the last 2 years (2007, 2008) the rate of in-patient suicide fell by nearly one-third from 2.45 to 1.68 per 100 000 bed days. This fall in rate was observed for males and females, across ethnicities and diagnoses. It was most marked for patients aged 15–44 years. Rates also fell for the most common suicide methods, particularly suicide by hanging on the ward (a 59% reduction). Although the number of post-discharge suicides fell, the rate of post-discharge suicide may have increased by 19%. The number of suicide deaths in those under the care of crisis resolution/home treatment teams has increased in recent years to approximately 160 annually.

The rate of suicide among psychiatric in-patients in England has fallen considerably. Possible explanations include falling general population rates, changes in the at-risk population or improved in-patient safety. However, a transfer of risk to the period after discharge or other clinical settings such as crisis resolution teams cannot be ruled out.

Although it has been posited that exposure to adverse childhood experiences (ACEs) increases vulnerability to deployment stress, previous literature in this area has demonstrated conflicting results. Using a cross-sectional population-based sample of active military personnel, the present study examined the relationship between ACEs, deployment related stressors and mood and anxiety disorders.

Data were analyzed from the 2002 Canadian Community Health Survey – Canadian Forces Supplement (CCHS-CFS; n = 8340, age 18–54 years, response rate 81%). The following ACEs were self-reported retrospectively: childhood physical abuse, childhood sexual abuse, economic deprivation, exposure to domestic violence, parental divorce/separation, parental substance abuse problems, hospitalization as a child, and apprehension by a child protection service. DSM-IV mood and anxiety disorders [major depressive disorder, post-traumatic stress disorder (PTSD), generalized anxiety disorder (GAD), panic attacks/disorder and social phobia] were assessed using the Composite International Diagnostic Interview (CIDI).

Even after adjusting for the effects of deployment-related traumatic exposures (DRTEs), exposure to ACEs was significantly associated with past-year mood or anxiety disorder among men [adjusted odds ratio (aOR) 1.34, 99% confidence interval (CI) 1.03–1.73, p < 0.01] and women [aOR 1.37, 99% CI 1.00–1.89, p = 0.01]. Participants exposed to both ACEs and DRTEs had the highest prevalence of past-year mood or anxiety disorder in comparison to those who were exposed to either ACEs alone, DRTEs alone, or no exposure.

ACEs are associated with several mood and anxiety disorders among active military personnel. Intervention strategies to prevent mental health problems should consider the utility of targeting soldiers with exposure to ACEs.

This study aimed to determine whether patients with post-traumatic stress disorder (PTSD) show difficulty in recruitment of the regions of the frontal and parietal cortex implicated in top-down attentional control in the presence and absence of emotional distracters.

Unmedicated individuals with PTSD (n = 14), and age-, IQ- and gender-matched individuals exposed to trauma (n = 15) and healthy controls (n = 19) were tested on the affective number Stroop task. In addition, blood oxygen level-dependent responses, as measured via functional magnetic resonance imaging, were recorded.

Patients with PTSD showed disrupted recruitment of lateral regions of the superior and inferior frontal cortex as well as the parietal cortex in the presence of negative distracters. Trauma-comparison individuals showed indications of a heightened ability to recruit fronto-parietal regions implicated in top-down attentional control across distracter conditions.

These results are consistent with suggestions that emotional responsiveness can interfere with the recruitment of regions implicated in top-down attentional control; the heightened emotional responding of patients with PTSD may lead to the heightened interference in the recruitment of these regions.

Co-morbidity patterns in epidemiological studies of mental illness consistently demonstrate that a latent internalizing factor accounts for co-morbidity patterns among unipolar mood and anxiety disorders, whereas a latent externalizing factor underlies the covariation of substance-use disorders and antisocial behaviors. However, this structure needs to be extended to include a broader range of disorders.

Exploratory and confirmatory factor analyses were used to examine the structure of co-morbidity using data from the Collaborative Psychiatric Epidemiological Surveys (n = 16 233).

In the best-fitting model, eating and bipolar disorders formed subfactors within internalizing, impulse control disorders were indicators of externalizing, and factor-analytically derived personality disorder scales split between internalizing and externalizing.

This was the first large-scale nationally representative study that has included uncommon mental disorders with sufficient power to examine their fit within a structural model of psychopathology. The results of this study have important implications for conceptualizing myriad mental disorders.

Patients with bipolar disorder exhibit consistent deficits in facial affect identification at both behavioral and neural levels. However, little is known about which stages of facial affect processing are dysfunctional.

Event-related potentials (ERPs), including amplitude and latency, were used to evaluate two stages of facial affect processing: N170 to examine structural encoding of facial features and N250 to examine decoding of facial features in 57 bipolar disorder patients, 30 schizophrenia patients and 30 healthy controls. Three conditions were administered: participants were asked to identify the emotion of a face, the gender of a face, or whether a building was one or two stories tall.

Schizophrenia patients' emotion identification accuracy was lower than that of bipolar patients and healthy controls. N170 amplitude was significantly smaller in schizophrenia patients compared to bipolar patients and healthy controls, which did not differ from each other. Both patient groups had significantly longer N170 latency compared to healthy controls. For N250, both patient groups showed significantly smaller amplitudes compared with controls, but did not differ from each other. Bipolar patients showed longer N250 latency than healthy controls; patient groups did not differ from each other.

Bipolar disorder patients have relatively intact structural encoding of faces (N170) but are impaired when decoding facial features for complex judgments about faces (N250 latency and amplitude), such as identifying emotion or gender.

Persons developing schizophrenia (SCZ) manifest various pre-morbid neuropsychological deficits, studied most often by measures of IQ. Far less is known about pre-morbid neuropsychological functioning in individuals who later develop bipolar psychoses (BP). We evaluated the specificity and impact of family history (FH) of psychosis on pre-morbid neuropsychological functioning.

We conducted a nested case-control study investigating the associations of neuropsychological data collected systematically at age 7 years for 99 adults with psychotic diagnoses (including 45 SCZ and 35 BP) and 101 controls, drawn from the New England cohort of the Collaborative Perinatal Project (CPP). A mixed-model approach evaluated full-scale IQ, four neuropsychological factors derived from principal components analysis (PCA), and the profile of 10 intelligence and achievement tests, controlling for maternal education, race and intra-familial correlation. We used a deviant responder approach (<10th percentile) to calculate rates of impairment.

There was a significant linear trend, with the SCZ group performing worst. The profile of childhood deficits for persons with SCZ did not differ significantly from BP. Neuropsychological impairment was identified in 42.2% of SCZ, 22.9% of BP and 7% of controls. The presence of psychosis in first-degree relatives (FH+) significantly increased the severity of childhood impairment for SCZ but not for BP.

Pre-morbid neuropsychological deficits are found in a substantial proportion of children who later develop SCZ, especially in the SCZ FH+ subgroup, but less so in BP, suggesting especially impaired neurodevelopment underlying cognition in pre-SCZ children. Future work should assess genetic and environmental factors that explain this FH effect.

Social anxiety disorder (SAD) is surprisingly prevalent among people with psychosis and exerts significant impact on social disability. The processes that underlie its development remain unclear. The aim of this study was to investigate the relationship between shame cognitions arising from a stigmatizing psychosis illness and perceived loss of social status in co-morbid SAD in psychosis.

This was a cross-sectional study. A sample of individuals with SAD (with or without psychosis) was compared with a sample with psychosis only and healthy controls on shame proneness, shame cognitions linked to psychosis and perceived social status.

Shame proneness (p < 0.01) and loss of social status (p < 0.01) were significantly elevated in those with SAD (with or without psychosis) compared to those with psychosis only and healthy controls. Individuals with psychosis and social anxiety expressed significantly greater levels of shame (p < 0.05), rejection (p < 0.01) and appraisals of entrapment (p < 0.01) linked to their diagnosis and associated stigma, compared to those without social anxiety.

These findings suggest that shame cognitions arising from a stigmatizing illness play a significant role in social anxiety in psychosis. Psychological interventions could be enhanced by taking into consideration these idiosyncratic shame appraisals when addressing symptoms of social anxiety and associated distress in psychosis. Further investigation into the content of shame cognitions and their role in motivating concealment of the stigmatized identity of being ‘ill’ is needed.

Schizo-affective disorder has not been studied to any significant extent using functional imaging. The aim of this study was to examine patterns of brain activation and deactivation in patients meeting strict diagnostic criteria for the disorder.

Thirty-two patients meeting Research Diagnostic Criteria (RDC) for schizo-affective disorder (16 schizomanic and 16 schizodepressive) and 32 matched healthy controls underwent functional magnetic resonance imaging (fMRI) during performance of the n-back task. Linear models were used to obtain maps of activations and deactivations in the groups.

Controls showed activation in a network of frontal and other areas and also deactivation in the medial frontal cortex, the precuneus and the parietal cortex. Schizo-affective patients activated significantly less in prefrontal, parietal and temporal regions than the controls, and also showed failure of deactivation in the medial frontal cortex. When task performance was controlled for, the reduced activation in the dorsolateral prefrontal cortex (DLPFC) and the failure of deactivation of the medial frontal cortex remained significant.

Schizo-affective disorder shows a similar pattern of reduced frontal activation to schizophrenia. The disorder is also characterized by failure of deactivation suggestive of default mode network dysfunction.

Most studies reporting the gender difference in age at onset of schizophrenia show an earlier onset in males, but vary considerably in their estimates of the difference. This may be due to variations in study design, setting and diagnostic criteria. In particular, several studies conducted in developing countries have found no difference or a reversed effect whereby females have an earlier onset. The aim of the study was to investigate gender differences in age of onset, and the impact of study design and setting on estimates thereof.

Study methods were a systematic literature search, meta-analysis and meta-regression.

A total of 46 studies with 29218 males and 19402 females fulfilled the inclusion criteria and were entered into a meta-analysis. A random-effects model gave a pooled estimate of the gender difference of 1.07 years (95% confidence interval 0.21–1.93) for age at first admission of schizophrenia, with males having earlier onset. The gender difference in age at onset was not significantly different between developed and developing countries. Studies using Diagnostic and Statistical Manual of Mental Disorders (DSM) criteria showed a significantly greater gender difference in age at onset than studies using International Classification of Diseases (ICD) criteria, the latter showing no difference.

The gender difference in age of onset in schizophrenia is smaller than previously thought, and appears absent in studies using ICD. There is no evidence that the gender difference differs between developed and developing countries.

Patients with schizophrenia and their first-degree relatives exhibit both abnormally diminished and increased neural activation during cognitive tasks. In particular, excessive task-related activity is often observed when tasks are easy, suggesting that inefficient cerebral recruitment may be a marker of vulnerability for schizophrenia. This hypothesis might best be tested using a very easy task, thus avoiding confounding by individual differences in task difficulty.

Eighteen people with schizophrenia, 18 unaffected full siblings of patients with schizophrenia and 26 healthy controls performed an easy auditory target-detection task in a 3-T magnetic resonance imaging (MRI) scanner. Groups were matched for accuracy on the task. Blood oxygen level-dependent (BOLD) responses to non-target stimuli in participants with vulnerability for schizophrenia (siblings and patients) were compared with those of healthy controls, and those of patients with those of unaffected siblings. BOLD responses to targets were compared with baseline, across groups.

Subjects with vulnerability for schizophrenia showed significant hyperactivation to non-targets in brain areas activated by targets in all groups, in addition to reduced deactivation to non-targets in areas suppressed by targets in all groups. Siblings showed greater activation than patients to non-targets in the medial frontal cortex. Patients exhibited significantly longer reaction times (RTs) than unaffected siblings and healthy controls.

Inefficient cerebral recruitment is a vulnerability marker for schizophrenia, marked by reduced suppression of brain areas normally deactivated in response to task stimuli, and increased activation of areas normally activated in response to task stimuli. Moreover, siblings show additional activation in the medial frontal cortex that may be protective.

Very preterm (VP) children are at particular risk for attention deficit/hyperactivity disorder (ADHD) of the inattentive subtype. It is unknown whether the neurodevelopmental pathways to academic underachievement are the same as in the general population. This study investigated whether middle childhood attention or hyperactivity/impulsivity problems are better predictors of VP adolescents' academic achievement.

In a geographically defined prospective whole-population sample of VP (<32 weeks gestation) and/or very low birth weight (<1500 g birth weight) (VLBW/VP; n = 281) and full-term control children (n = 286) in South Germany, ADHD subtypes were assessed at 6 years 3 months and 8 years 5 months using multiple data sources. Academic achievement was assessed at 13 years of age.

Compared with full-term controls, VLBW/VP children were at higher risk for ADHD inattentive subtype [6 years 3 months: odds ratio (OR) 2.8, p < 0.001; 8 years 5 months: OR 1.7, p = 0.020] but not for ADHD hyperactive-impulsive subtype (6 years 3 months: OR 1.4, p = 0.396; 8 years 5 months: OR 0.9, p = 0.820). Childhood attention measures predicted academic achievement in VLBW/VP and also full-term adolescents, whereas hyperactive/impulsive behaviour did not.

Attention is an important prerequisite for learning and predicts long-term academic underachievement. As ADHD inattentive subtype and cognitive impairments are frequent in VLBW/VP children, their study may help to identify the neurofunctional pathways from early brain development and dysfunction to attention problems and academic underachievement.

Attention deficit hyperactivity disorder (ADHD) frequently persists into adulthood. Family and twin studies delineate a disorder with strong genetic influences among children and adolescents based on parent- and teacher-reported data but little is known about the genetic and environmental contribution to DSM-IV ADHD symptoms in adulthood. We therefore aimed to investigate the impact of genetic and environmental influences on the inattentive and hyperactive–impulsive symptoms of ADHD in adults.

Twin methods were applied to self-reported assessments of ADHD symptoms from a large population-based Swedish twin study that included data from 15 198 Swedish male and female twins aged 20 to 46 years.

The broad heritability [i.e. A + D, where A is an additive genetic factor and D (dominance) a non-additive genetic factor] was 37% (A = 11%, D = 26%) for inattention and 38% (A = 18%, D = 20%) for hyperactivity–impulsivity. The results also indicate that 52% of the phenotypic correlation between inattention and hyperactivity–impulsivity (r = 0.43) was explained by genetic influences whereas the remaining part of the covariance was explained by non-shared environmental influences. These results were replicated across age strata.

Our findings of moderate broad heritability estimates are consistent with previous literature on self-rated ADHD symptoms in older children, adolescents and adults and retrospective reports of self-rated childhood ADHD by adults but differ from studies of younger children with informant ratings. Future research needs to clarify whether our data indicate a true decrease in the heritability of ADHD in adults compared to children, or whether this relates to the use of self-ratings in contrast to informant data.

We examined the cross-sectional relationship between environmental tobacco smoke exposure, continuous performance test (CPT) measures, and attention deficit hyperactivity disorder (ADHD) or learning disability symptoms in school-aged children.

In total, 989 children (526 boys, mean age 9.1 ± 0.7 years), recruited from five South Korean cities participated in this study. We used urine cotinine as a biomarker for environmental tobacco smoke exposure, and obtained the children's scores on a CPT. Parents completed the Korean versions of the ADHD Rating Scale – IV (ADHD-RS) and Learning Disability Evaluation Scale (LDES). Using generalized linear mixed model (GLMM), we assessed the associations between urine cotinine concentrations, neuropsychological variables, and symptoms of ADHD and learning disabilities. Additionally, we conducted structural equation models to explore the effects' pathways.

After adjusting for a range of relevant covariates, GLMM showed urinary cotinine levels were significantly and positively associated with CPT scores on omission errors, commission errors, response time, and response time variability, and with parent- and teacher-rated ADHD-RS scores. In addition, urine cotinine levels were negatively associated with LDES scores on spelling and mathematical calculations. The structural equation model revealed that CPT variables mediated the association between urine cotinine levels and parental reports of symptoms of ADHD and learning disabilities.

Our data indicate that environmental exposure to tobacco smoke is associated with ADHD and learning disabilities in children, and that impairments in attention and inhibitory control probably mediate the effect.