Later transitions to adult roles and responsibilities have been linked with better psychological well-being yet psychological distress has risen despite young people making the transition to adulthood at older ages over recent years.

We examine the role of structural constraints and adolescent resources in the relationship between the timing of transitions and psychological distress in early adult life in the 1958 National Child Development Study and the 1970 British Cohort Study. Graphical chain models were used to examine the influences on timing of four key transitions and their relationship with psychological distress (Malaise Inventory). The role of structural factors at birth (gender, social class) and adolescent resources (psychosocial problems, exam grades) were modelled.

An earlier transition to adult roles was associated with an increased risk for psychological distress but so was failing to make some key transitions. Structural constraints had negative effects on successful development. Persistent social class and gender inequalities in psychological distress were evident in both cohorts. Social class constraints were mediated by educational resources whereas gender constraints were mediated by psychosocial resources. The influence of structural constraints on the timing of transitions to adult roles was more complex with evidence of positive and negative mediation and moderation effects.

Delaying transition to adulthood promotes psychological health but failure of transition to independent living is associated with psychological distress. Life-course transitions are constrained by social origin and gender and possibly economic environment. Adolescent resources help young adults to make timely transitions to adult roles.

Patients with anorexia nervosa (AN) overestimate their size despite being severely underweight. Whether this misperception echoes an underlying emotional disturbance or also reflects a genuine body-representation deficit is debatable. Current measures inquire directly about subjective perception of body image, thus distinguishing poorly between top-down effects of emotions/attitudes towards the body and disturbances due to proprioceptive disorders/distorted body schema. Disorders of body representation also emerge following damage to the right parietal lobe. The possibility that parietal dysfunction might contribute to AN is suspected, based on the demonstrated association of spatial impairments, comparable to those found after parietal lesion, with this syndrome.

We used a behavioral task to compare body knowledge in severe anorexics (n=8), healthy volunteers (n=11) and stroke patients with focal damage to the left/right parietal lobe (n=4). We applied a psychophysical procedure based on the perception, in the dark, of an approaching visual stimulus that was turned off before reaching the observer. Participants had to predict whether the stimulus would have hit/missed their body, had it continued its linear motion.

Healthy volunteers and left parietal patients estimated body boundaries very close to the real ones. Conversely, anorexics and right parietal patients underestimated eccentricity of their left body boundary.

These findings are in line with the role the parietal cortex plays in developing and maintaining body representation, and support the possibility for a neuropsychological component in the pathogenesis of anorexia, offering alternative approaches to treatment of the disorder.

Gender is known to modulate the clinical course and severity of bipolar disorder (BD). Although cognitive abnormalities are an established feature of BD, there is limited information regarding whether gender also influences the pattern and severity of cognitive impairment.

We evaluated the performance of 86 remitted patients with BD, type 1, (BD-I) (36 male and 50 female) and 46 healthy participants (21 male and 25 female) on tasks of general intellectual ability, memory encoding, recognition and retrieval, response inhibition and executive function (abstraction and perseveration). The impact of illness severity in patients was assessed using the global assessment of functioning (GAF).

We found a gender effect and an interaction between diagnosis and gender on immediate memory, implicating encoding and retrieval processes, both showing male BD-I patients being disadvantaged compared with female patients and healthy controls. Immediate memory correlated with GAF scores and this association was statistically significant for male BD-I patients.

Our findings suggest that gender differences in BD-I are associated with memory function, particularly processes relating to encoding and retrieval, and may contribute to poor functional outcome particularly in men.

Childbirth has been linked to postpartum impairment. However, controversy exists regarding the onset and prevalence of post-traumatic stress disorder (PTSD) after childbirth, with seminal studies being limited by methodological issues. This longitudinal prospective study examined the prevalence of PTSD following childbirth in a large sample while controlling for pre-existing PTSD and affective symptomatology.

Pregnant women in their third trimester were recruited over a 12-month period and interviewed to identify PTSD and anxiety and depressive symptoms during the last trimester of pregnancy, 4–6 weeks postpartum, 12 weeks postpartum and 24 weeks postpartum.

Of the 1067 women approached, 933 were recruited into the study. In total, 866 (93%) were retained to 4–6 weeks, 826 (89%) were retained to 12 weeks and 776 (83%) were retained to 24 weeks. Results indicated that, uncontrolled, 3.6% of women met PTSD criteria at 4–6 weeks postpartum, 6.3% at 12 weeks postpartum and 5.8% at 24 weeks postpartum. When controlling for PTSD and partial PTSD due to previous traumatic events as well as clinically significant anxiety and depression during pregnancy, PTSD rates were less at 1.2% at 4–6 weeks, 3.1% at 12 weeks and 3.1% at 24 weeks postpartum.

This is the first study to demonstrate the occurrence of full criteria PTSD resulting from childbirth after controlling for pre-existing PTSD and partial PTSD and clinically significant depression and anxiety in pregnancy. The findings indicate that PTSD can result from a traumatic birth experience, though this is not the normative response.

Previous cross-diagnosis studies of interaction between mothers with severe mental illness and their babies have concluded that mothers with schizophrenia have deficits in interaction, but these studies have not included healthy controls.

In-patients on a mother and baby unit, with diagnoses of schizophrenia (n=15), depressive mood disorders with or without psychosis (n=23), or mood disorders where mania was the predominant feature, with or without psychosis (n=12), were observed interacting with their infants on admission and discharge. Mothers' mind-mindedness and other measures of the quality of maternal and infant behaviour were coded. Findings from this sample were compared with those from healthy mothers and their infants (n=49).

Compared with healthy controls, on admission depressed mothers were marginally less likely to comment appropriately on their infants' mental states. Both the depressed and mania groups were more likely to touch their babies and engage in attention-seeking behaviours. Interactional behaviours of mothers in the schizophrenia group were not markedly different from healthy controls. On discharge there were fewer differences between the clinical and healthy groups, although the depressed group continued to engage in more attention-seeking and touching behaviour and the mania group continued to touch their infants more. Only mothers in the schizophrenia group showed changes in interactional behaviours between admission and discharge, talking more to their infants.

The findings challenge previous conclusions that mothers with schizophrenia have deficits in their interactions with their babies, and demonstrate that mothers with severe mental illness are able to respond appropriately to their infants' cues.

Certain personality traits have long been suspected to reflect an enduring vulnerability to major depression (MD) in part because of shared genetic risk factors. Although many have agreed that normative personality is well captured by the ‘Big-Five’ personality traits of Openness (O), Conscientiousness (C), Extraversion (E), Agreeableness (A) and Neuroticism (N), to date genetically informative studies have only examined the relationship between MD and N and E.

Questionnaires were completed on a website, yielding a sample of 44 112 subjects including both members of 542 same-sex twin pairs. Personality was measured by the Big Five Inventory. Structural modeling was performed by Mx.

Three of the big-five personality traits – O, E and A – had small phenotypic associations with risk for MD and small genetic correlations. Two traits – N and C – had stronger phenotypic associations (positive for N and negative for C) with the following estimates of the genetic correlation with MD: +0.43 for N and −0.36 for C. N and C were moderately negatively correlated. Controlling for N reduced the genetic correlation between C and MD more than controlling for C reduced the genetic correlation between N and MD.

A large proportion of the genetic risk for MD that is expressed via personality is captured by N, with a modest amount due to C, and small amounts from O, E and A.

Anxiety disorders are the most prevalent mental health disorders and are associated with substantial disability and reduced well-being. It is unknown whether the relative impact of different anxiety disorders is due to the anxiety disorder itself or to the co-occurrence with other anxiety disorders. This study compared the functional impact of combinations of anxiety disorders in primary care out-patients.

A total of 1004 patients with panic disorder (PD), generalized anxiety disorder (GAD), social anxiety disorder (SAD) or post-traumatic stress disorder (PTSD) provided data on their mental and physical functioning, and disability. Multivariate regressions compared functional levels for patients with different numbers and combinations of disorders.

Of the patients, 42% had one anxiety disorder only, 38% two, 16% three and 3% all four. There were few relative differences in functioning among patients with only one anxiety disorder, although those with SAD were most restricted in their work, social and home activities and those with GAD were the least impaired. Functioning levels tended to deteriorate as co-morbidity increased.

Of the four anxiety disorders examined, GAD appears to be the least disabling, although they all have more in common than in distinction when it comes to functional impairment. A focus on unique effects of specific anxiety disorders is inadequate, as it fails to address the more pervasive impairment associated with multiple anxiety disorders, which is the modal presentation in primary care.

Affective symptoms are common in subjects with mild cognitive impairment (MCI), but there is disagreement whether these symptoms are predictive for Alzheimer's disease (AD). We investigated the predictive accuracy of affective symptoms for AD during a follow-up study in subjects with MCI, and whether the predictive accuracy was modified by age, the presence of amnestic MCI or the length of follow-up.

Newly referred subjects (n=263) with MCI older than 55 years were selected from a memory clinic and followed up after 2, 5 and 10 years. Predictors investigated were: symptoms of depression, anxiety, apathy and sleeping problems.

Affective symptoms were present in 50–70% of the subjects. The average follow-up period was 5.4 years and 79 subjects (29%) developed AD. Sleeping problems were associated with a decreased risk for AD [odds ratio (OR) 0.35, p<0.001]. Symptoms of depression (OR 0.61, p=0.059) and anxiety (OR 0.58, p=0.051) showed a trend in the same direction. The OR of apathy for AD was 0.67 (p=0.14). Depression was associated with a decreased risk for AD only in subjects without amnestic MCI, but not in subjects with amnestic MCI. Moreover, anxiety was related to the risk for AD differently between subjects diagnosed with AD at the 5-year follow-up (OR 0.23) and subjects diagnosed with AD at the 10-year follow-up (OR 1.7).

Affective symptoms are associated with a decreased risk for AD. The risk may be dependent on MCI subtype or length of follow-up, but it does not depend on age.

Communication skills are considered ‘core skills’ in the curriculum of psychiatry but studies evaluating the effectiveness of a time-limited training course in interviewing skills in psychiatry have remained rare. The aim was to assess the effectiveness of training in patient-centred interviewing on the interview performance of psychiatric residents.

Psychiatric residents (n=10) each interviewed 12 different anonymized standardized patients (SPs), eight before and another four after training. SPs simulated psychiatric out-patients who attended for a first visit to the psychiatric out-patient clinic. The consultations were videotaped, transcribed and coded with a classification scheme developed for psychiatric consultations from which an interview performance index was derived. An interrupted time-series design and a segmented regression analysis with multilevel analysis explored the performance trend within the series of consultations.

The regression model evidenced a horizontal slope at pre- and post-training, with a significant level change. These findings excluded the presence of a practice effect and indicated a significant effect of training. Performance variability between and within residents over the series of consultations increased at post-training.

The training improved patient-centred interviewing performance. More post-training exercise time and supervised practice are necessary to establish consistent performance patterns at a higher skill level.

It is not known whether social support modifies the association between depression and impairment or disability in older people from developing countries in Asia.

We used a Thai version of the EURO-D scale to measure depression in 1104 Thai rural community-dwelling parents aged ⩾60 years. These were all those providing data on depression who were recruited as part of a study of older adults with at least one living child (biological, stepchild or adopted child). Logistic regression modelling was used to determine: (a) whether impairment, disability and social support deficits were associated with depression; (b) whether social support modified this association.

There were strong graded relationships between impairment, disability, social support deficits and EURO-D caseness. Level of impairment, but not disability, interacted with poor social support in that depression was especially likely in those who had more physical impairments as well as one or more social support deficits (p value for interaction=0.018), even after full adjustment.

Social support is important in reducing the association between physical impairment and depression in Thai older adults, especially for those with a large number of impairments. Enhancing social support as well as improving healthcare and disability facilities should be emphasized in interventions to prevent depression in older adults.

A significant gap in the literature on risk factors for psychopathy is the relative lack of research on parental bonding.

This study examines the cross-sectional relationship between maternal and paternal bonding, childhood physical abuse and psychopathic personality at age 28 years in a community sample of 333 males and females. It also assesses prospectively whether children separated from their parents in the first 3 years of life are more likely to have a psychopathic-like personality 25 years later.

Hierarchical regression analyses indicated that: (1) poor parental bonding (lack of maternal care and low paternal overprotection) and childhood physical abuse were both associated with a psychopathic personality; (2) parental bonding was significantly associated with psychopathic personality after taking into account sex, social adversity, ethnicity and abuse; (3) those separated from parents in the first 3 years of life were particularly characterized by low parental bonding and a psychopathic personality in adulthood; and (4) the deviant behavior factor of psychopathy was more related to lack of maternal care whereas the emotional detachment factor was related to both lack of maternal care and paternal overprotection.

Findings draw attention to the importance of different components of early bonding in relation to adult psychopathy, and may have potential implications for early intervention and prevention of psychopathy.

Prior studies suggest that certain types of personality are at higher risk for developing depressive disorders. This study examined the relationship between old age depressive symptoms and two middle-age personality dimensions, neuroticism and extraversion.

The present study is part of the Finnish Twin Study on Aging, where altogether 409 female twins who had completed the Eysenck Personality Inventory at the age of 38–51 years were studied for depressive symptoms 28 years later using Center for the Epidemiologic Studies Depression Scale. Logistic regression analysis suitable for dependent data and univariate and Cholesky models for decomposing the genetic and environmental factor were used.

Middle age extraversion protected from later depressive symptoms while neuroticism increased the risk. Twin modeling indicated that the association between neuroticism and depressive symptoms resulted from shared genetic risk factors common to both traits. However, a substantial proportion of the genetic vulnerability was specific to old age depressive symptoms and was not shared with neuroticism. Middle age extraversion had no genetic relationship with old age depressive symptoms.

The relationship between middle age neuroticism and old age depressive symptoms is strong but only partly the result of genetic factors that predispose to both neuroticism and depressive symptoms. Extraversion, by contrast, has no genetic relationship with depressive symptoms experienced in old age.

Worry is considered a key feature of generalized anxiety disorder (GAD), whose neural correlates are poorly understood. It is not known whether the brain regions involved in pathological worry are similar to those involved in worry-like mental activity in normal subjects or whether brain areas associated with worry are the same for different triggers such as verbal stimuli or faces. This study was designed to clarify these issues.

Eight subjects with GAD and 12 normal controls underwent functional magnetic resonance imaging (fMRI) mood induction paradigms based on spoken sentences or faces. Sentences were either neutral or designed to induce worry. Faces conveyed a sad or a neutral mood and subjects were instructed to empathize with those moods.

We found that the anterior cingulate and dorsal medial prefrontal cortex [Brodmann area (BA) 32/23 and BA 10/11] were associated with worry triggered by sentences in both subjects with GAD and normal controls. However, GAD subjects showed a persistent activation of these areas even during resting state scans that followed the worrying phase, activation that correlated with scores on the Penn State Worry Questionnaire (PSWQ). This region was activated during the empathy experiment for sad faces.

The results show that worry in normal subjects and in subjects with GAD is based on activation of the medial prefrontal and anterior cingulate regions, known to be involved in mentalization and introspective thinking. A dysregulation of the activity of this region and its circuitry may underpin the inability of GAD patients to stop worrying.

Perinatal factors seem to be implicated in the pathogenesis of anorexia nervosa (AN) and may be involved in the programming of stress response systems in humans. Our aim was to explore one of the possible pathways to explain the association between perinatal complications and a psychiatric disorder. In particular, we tested the hypothesis that neonatal immaturity may confer an enhanced vulnerability to AN after exposure to a severe stressful event, such as childhood abuse.

The sample was composed of subjects who took part in a prevalence study carried out on a representative sample of the general population and cases of AN referred to an out-patient specialist unit. All subjects (n=663) were born in the two obstetric wards of Padua Hospital between 1971 and 1979. We analysed data using both a case-control and a cohort design.

We found that functional signs of neonatal dysmaturity, but not a low birthweight or prematurity, had a significant additive interaction with childhood abuse in determining the risk for this illness. In normal subjects, but not in subjects with AN, neonatal dysmaturity was associated with being small, short or thin for gestational age at birth.

The synergistic effect of neonatal dysmaturity and childhood abuse in increasing the risk for AN provides evidence for the hypothesis that a prenatal programming of stress response systems can result in an impairment of the individual's resilience to severe stressful events.

Increased psychiatric morbidity has been widely reported among non-heterosexual individuals (defined as reporting a homosexual/bisexual identity and/or same-sex sexual partners). However, the causes of this psychiatric ill-health are mostly unknown.

We attempted to estimate the influence of minority stress and familial factors on psychiatric disorder among adults with same-sex sexual partners. Self-report data from a 2005 survey of adults (age 20–47 years, n=17 379) in the population-based Swedish Twin Registry were analysed with regression modelling and co-twin control methodology.

Rates of depression, generalized anxiety disorder (GAD), eating disorders, alcohol dependence and attention deficit hyperactivity disorder (ADHD) were increased among men and women with same-sex sexual experiences. Adjusting for perceived discrimination and hate crime victimization lowered this risk whereas controlling for familial (genetic or environmental) factors in within-twin pair comparisons further reduced or eliminated it.

Components of minority stress influence the risk of psychiatric ill-health among individuals with any same-sex sexual partner. However, substantial confounding by familial factors suggests a common genetic and/or environmental liability for same-sex sexual behaviour and psychiatric morbidity.

Body dysmorphic disorder (BDD) is a poorly understood disorder that involves a preoccupation with imagined or minor bodily defects. Only a few studies of neuropsychological function have been conducted. Two previous studies have indicated executive dysfunction in BDD. The current study sought to further define these executive deficits.

Fourteen DSM-IV BDD patients and 14 age- and sex-matched control participants took part. Because of the high incidence of co-morbidity in BDD, patients with co-morbid Axis I disorders were not excluded. Control participants had no history of psychiatric illness. All participants completed the following executive function (EF) tests: Spatial Span (SS), Spatial Working Memory (SWM) and the Stockings of Cambridge (SOC) task. They also completed the Pattern Recognition (PR) test, a test of visual memory (VM).

BDD participants made significantly more between-search errors on the SWM task, an effect that increased with task difficulty. Between-search errors are an example of poor maintenance and manipulation of information. SOC results indicated slower subsequent thinking times (i.e. the time taken to plan) in BDD participants. There were no group differences in SS or PR scores. The severity of BDD, depressive or anxiety symptoms was not correlated with performance on any of the cognitive tasks.

The results of this study indicate that BDD patients have EF deficits in on-line manipulation, planning and organization of information. By contrast, spatial memory capacity, motor speed and visual memory were intact. Considered with evidence from lesion and neuroimaging studies, these results suggest frontal lobe dysfunction in BDD.

The impact of different levels of depression severity on quality of life (QoL) is not well studied, particularly regarding ICD-10 criteria. The ICD classification of depressive episodes in three levels of severity is also controversial and the less severe category, mild, has been considered as unnecessary and not clearly distinguishable from non-clinical states. The present work aimed to test the relationship between depression severity according to ICD-10 criteria and several dimensions of functioning as assessed by Medical Outcome Study (MOS) 36-item Short Form general health survey (SF-36) at the population level.

A sample of 551 participants from the second phase of the Outcome of Depression International Network (ODIN) study (228 controls without depression and 313 persons fulfilling ICD criteria for depressive episode) was selected for a further assessment of several variables, including QoL related to physical and mental health as measured with the SF-36.

Statistically significant differences between controls and the depression group were found in both physical and mental markers of health, regardless of the level of depression severity; however, there were very few differences in QoL between levels of depression as defined by ICD-10. Regardless of the presence of depression, disability, widowed status, being a woman and older age were associated with worse QoL in a structural equation analysis with covariates. Likewise, there were no differences according to the type of depression (single-episode versus recurrent).

These results cast doubt on the adequacy of the current ICD classification of depression in three levels of severity.

A consistent association between paternal age and their offspring's risk of schizophrenia has been observed, with no independent association with maternal age. The relationship of paternal and maternal ages with risk of bipolar affective disorders (BPAD) in the offspring is less clear. The present study aimed at testing the hypothesis that paternal age is associated with their offspring's risk of BPAD, whereas maternal age is not.

This population-based cohort study was conducted with individuals born in Sweden during 1973–1980 and still resident there at age 16 years. Outcome was first hospital admission with a diagnosis of BPAD. Hazard ratios (HRs) were calculated using Cox's proportional hazard regression.

After adjustment for all potential confounding variables except maternal age, the HR for risk of BPAD for each 10-year increase in paternal age was 1.28 [95% confidence interval (CI) 1.11–1.48], but this fell to 1.20 (95% CI 0.97–1.48) after adjusting for maternal age. A similar result was found for maternal age and risk of BPAD [HR 1.30 (95% CI 1.08–1.56) before adjustment for paternal age, HR 1.12 (95% CI 0.86–1.45) after adjustment]. The HR associated with having either parent aged 30 years or over was 1.26 (95% CI 1.01–1.57) and it was 1.45 (95% CI 1.16–1.81) if both parents were >30 years.

Unlike schizophrenia, the risk of BPAD seems to be associated with both paternal and maternal ages.

Recent research suggests the utility of distinguishing temperamental and acute symptoms of borderline personality disorder (BPD). Temperamental symptoms, such as chronic anger and odd thinking, remit relatively slowly and have been hypothesized to reflect a hyperbolic predisposition to emotional pain and negativistic cognitions, whereas acute symptoms, such as substance abuse and chaotic relationships, remit relatively quickly and have been hypothesized to represent the consequences of maladaptations to triggering environmental events.

The relationships of temperamental and acute BPD symptoms with normal personality traits and stability and dynamic associations over time across these symptom sets were tested in a 10-year longitudinal study of 362 patients with personality disorders.

Temperamental symptoms were associated with high neuroticism, whereas acute symptoms were associated with low agreeableness. These symptoms had similar rank-order stabilities and relative changes in symptom sets were reciprocally linked in a cross-lagged path model suggesting dynamic associations between temperamental and acute symptoms over time.

The distinction between temperamental and acute BPD symptoms is supported by differential relations of these symptom sets to normal personality traits. Moreover, these symptoms appear to be linked in a mutually reinforcing dynamic over time. This distinction should be kept in mind in future studies of the aetiology of BPD and in diagnostic and treatment considerations.

Individual symptoms of post-myocardial infarction (MI) depression may be differentially associated with cardiac prognosis, in which somatic/affective symptoms appear to be associated with a worse cardiovascular prognosis than cognitive/affective symptoms. These findings hold important implications for treatment but need to be replicated before conclusions regarding treatment can be drawn. We therefore examined the relationship between depressive symptom dimensions following MI and both disease severity and prospective cardiac prognosis.

Patients (n=473) were assessed on demographic and clinical variables and completed the Beck Depression Inventory (BDI) within the first week of hospital admission for acute MI. Depressive symptom dimensions were associated with baseline left ventricular ejection fraction (LVEF) and prospective cardiac death and/or recurrent MI. The average follow-up period was 2.8 years.

Factor analysis revealed two symptom dimensions – somatic/affective and cognitive/affective – in the underlying structure of the BDI, identical to previous results. There were 49 events attributable to cardiac death (n=23) or recurrent MI (n=26). Somatic/affective (p=0.010) but not cognitive/affective (p=0.153) symptoms were associated with LVEF and cardiac death/recurrent MI. When controlling for the effects of previous MI and LVEF, somatic/affective symptoms remained significantly predictive of cardiac death/recurrent MI (hazard ratio 1.31, 95% confidence interval 1.02–1.69, p=0.038). Previous MI was also an independent predictor of cardiac death/recurrent MI.

We confirmed that somatic/affective, rather than cognitive/affective, symptoms of depression are associated with MI severity and cardiovascular prognosis. Interventions to improve cardiovascular prognosis by treating depression should be targeted at somatic aspects of depression.