Previous studies have suggested that physical activity may have antidepressant and/or anti-anxiety effects.

To examine the bidirectional relationship between physical activity and common mental disorders and establish the importance of context, type and intensity of activity undertaken.

A clinical examination of 40 401 residents of Norway was undertaken. Participants answered questions relating to the frequency and intensity of both leisure-time and workplace activity. Depression and anxiety were measured using the Hospital Anxiety and Depression Scale (HADS). Biological and social data were also collected.

There was an inverse relationship between the amount of leisure-time physical activity and case-level symptoms of depression. This cross-sectional association was only present with leisure-time (as opposed to workplace) activity and was not dependent on the intensity of activities undertaken. Higher levels of social support and social engagement were important in explaining the relationship between leisure activity and depression. Biological changes such as alterations to parasympathetic vagal tone (resting pulse) and changes to metabolic markers had a less important role.

Individuals who engage in regular leisure-time activity of any intensity are less likely to have symptoms of depression. The context and social benefits of exercise are important in explaining this relationship.

Antisocial personality disorder and psychopathy have been hypothesised to have a neurodevelopmental basis, but this proposition has not been formally tested.

This study tests the hypothesis that individuals with cavum septum pellucidum (CSP), a marker of limbic neural maldevelopment, will show higher levels of psychopathy and antisocial personality.

Cavum septum pellucidum was assessed using anatomical magnetic resonance imaging in a community sample. Those with CSP (n = 19) were compared with those lacking CSP (n = 68) on antisocial personality, psychopathy and criminal offending.

Those with CSP had significantly higher levels of antisocial personality, psychopathy, arrests and convictions compared with controls. The pervasiveness of this association was indicated by the fact that those lacking a diagnosis of antisocial personality disorder, but who were charged or convicted for an offence, had a more extensive CSP than non-antisocial controls. Results could not be attributed to prior trauma exposure, head injury, demographic factors or comorbid psychiatric conditions.

Our findings appear to be the first to provide evidence for a neurodevelopmental brain abnormality in those with antisocial personality disorder and psychopathy, and support the hypothesis that early maldevelopment of limbic and septal structures predisposes to the spectrum of antisocial behaviours.

Familial co-occurrence of frontotemporal dementia and schizophrenia has never been investigated.

To test the hypothesis that frontotemporal dementia and schizophrenia might have a common aetiology in some families in which both syndromes coexist (mixed families).

The morbid risk for schizophrenia, calculated in first-degree relatives of 100 frontotemporal dementia probands, was compared with that calculated in first-degree relatives of 100 Alzheimer's disease probands. In mixed families, sequencing analysis of known frontotemporal dementia genes and detailed phenotype characterisation of individuals with frontotemporal dementia and schizophrenia were performed.

The morbid risk for schizophrenia was significantly higher in relatives of frontotemporal dementia probands (1.35, s.e. = 0.45) than in relatives of Alzheimer's disease probands (0.32, s.e. = 0.22). Ten mixed families were characterised. In three of them a frontotemporal dementia causal mutation was identified that was present in individuals with schizophrenia. Several specific clinical features were noted in people with schizophrenia and frontotemporal dementia in mixed families.

Co-occurrence of schizophrenia and frontotemporal dementia could indicate, in some families, a common aetiology for both conditions.

Fatigue is a common symptom in Western high-income countries but is often medically unexplained and little is known about its presentation in other populations.

To explore the epidemiology and aetiology of fatigue in Sri Lanka, and of its overlap with depression.

A total of 4024 randomly selected twins from a population-based register in Sri Lanka (Colombo district) completed home interviews including the Chalder Fatigue Questionnaire.

The prevalence of fatigue was similar to that in other countries, although prolonged fatigue may be less common. There was substantial comorbidity with a screen for lifetime depression. Non-shared environmental factors made the largest contributions, although genetic/family factors also contributed. The aetiology appeared consistent across the spectrum of severity.

The aetiology of fatigue is broadly similar in Sri Lanka and Western high-income countries. Abnormal experiences of fatigue appear to be the extreme form of more common fatigue, rather than representing independent entities with different genetic or environmental risk factors.

Children with Tourette syndrome generally experience improvement of tics by age 18 years, but psychosocial and comorbidity outcomes at this age are unclear.

To compare psychosocial outcomes and lifetime comorbidity rates in older adolescents with Tourette syndrome and controls. We hypothesised a priori that individuals with Tourette syndrome would have lower Children's Global Assessment Scale (CGAS) scores.

A total of 65 individuals with Tourette syndrome, identified in childhood, and 65 matched community controls without tic or obsessive–compulsive disorder (OCD) symptoms were assessed around 18 years of age regarding psychosocial functioning and lifetime psychiatric disorders.

Compared with controls, individuals with Tourette syndrome had substantially lower CGAS scores (P=10−8) and higher rates of attention-deficit hyperactivity disorder (ADHD), major depression, learning disorder and conduct disorder (P⩽0.01). In the participants with Tourette syndrome, poorer psychosocial outcomes were associated with greater ADHD, OCD and tic severity.

Clinically ascertained children with Tourette syndrome typically have impaired psychosocial functioning and high comorbidity rates in late adolescence.

Interventions to improve adherence to treatment in people with psychotic disorders have produced inconclusive results. We developed a new treatment, treatment adherence therapy (TAT), whose intervention modules are tailored to the reasons for an individual's non-adherence.

To examine the effectiveness of TAT with regard to service engagement and medication adherence in out-patients with psychotic disorders who engage poorly.

Randomised controlled study of TAT v. treatment as usual (TAU) in 109 out-patients. Most outcome measurements were performed by masked assessors. We used intention-to-treat multivariate analyses (Dutch Trial Registry: NTR1159).

Treatment adherence therapy v. TAU significantly benefited service engagement (Cohen's d = 0.48) and medication adherence (Cohen's d = 0.43). Results remained significant at 6-month follow-up for medication adherence. Near-significant effects were also found regarding involuntary readmissions (1.9% v. 11.8%, P = 0.053). Symptoms and quality of life did not improve.

Treatment adherence therapy helps improve engagement and adherence, and may prevent involuntary admission.

There is increasing evidence for genetic effects on the hypothalamic–pituitary axis system. More than one gene is likely to moderate corticoid-mediated activity.

To investigate whether the brain-derived neurotrophic factor (BDNF) polymorphism (rs6265, Val66Met) is associated with morning waking salivary cortisol and moderates the corticoid-mediated risk for subsequent depressive episode onset independently of the known effects of 5-HTTLPR (the serotonin transporter gene promoter).

High-risk adolescents (n = 401) were genotyped for Val66Met BDNF and 5-HTTLPR. Salivary samples were obtained on four consecutive school days within 1 h of waking. There were 365 (91%) remaining participants reassessed at 12 months for episodes of psychiatric disorder in the follow-up period. Of these, 357 (89%) had complete data for multivariate modelling.

There were 41 (11.2%) individuals who reported a new episode of clinical depression over the follow-up period. Increased risk for subsequent depression was found in carriers of the Val66Val genotype in BDNF with higher morning waking cortisol. This remained present when the known interaction between carriers of a short allele of 5-HTTLPR with higher morning salivary cortisol was taken into account.

Both BDNF and 5-HTTLPR genes show evidence of modifying the risk of a subsequent new depressive episode associated with elevated morning salivary cortisol. In adolescents morning salivary cortisol levels may constitute a biomarker for some forms of unipolar depression.

Current classifications of personality disorders do not classify severity despite clinical practice favouring such descriptions.

To assess whether an existing measure of severity of personality disorder predicted clinical pathology and societal dysfunction in a community sample.

UK national epidemiological study in which personality status was measured using the screening version of the Structured Clinical Interview for DSM–IV Personality Disorders (SCID–II) and reclassified to five levels using a modified severity index. Associations between levels of severity of personality pathology and social, demographic and clinical variables were measured.

Of 8391 individuals interviewed and their personality status assessed, only a minority (n = 1933, 23%) had no personality pathology. The results supported the hypothesis. More severe personality pathology was associated incrementally with younger age, childhood institutional care, expulsion from school, contacts with the criminal justice system, economic inactivity, more Axis I pathology and greater service contact (primary care and secondary care, all P<0.001). Significant handicap was noted among people with even low levels of personality pathology. No differences contradicted the main hypothesis.

A simple reconstruction of the existing classification of personality disorder is a good predictor of social dysfunction and supports the development of severity measures as a critical requirement in both DSM–V and ICD–11 classifications.

The two main constituents of cannabis, cannabidiol and δ9-tetrahydrocannabinol (THC), have opposing effects both pharmacologically and behaviourally when administered in the laboratory. Street cannabis is known to contain varying levels of each cannabinoid.

To study how the varying levels of cannabidiol and THC have an impact on the acute effects of the drug in naturalistic settings.

Cannabis users (n = 134) were tested 7 days apart on measures of memory and psychotomimetic symptoms, once while they were drug free and once while acutely intoxicated by their own chosen smoked cannabis. Using an unprecedented methodology, a sample of cannabis (as well as saliva) was collected from each user and analysed for levels of cannabinoids. On the basis of highest and lowest cannabidiol content of cannabis, two groups of individuals were directly compared.

Groups did not differ in the THC content of the cannabis they smoked. Unlike the marked impairment in prose recall of individuals who smoked cannabis low in cannabidiol, participants smoking cannabis high in cannabidiol showed no memory impairment. Cannabidiol content did not affect psychotomimetic symptoms, which were elevated in both groups when intoxicated.

The antagonistic effects of cannabidiol at the CB1 receptor are probably responsible for its profile in smoked cannabis, attenuating the memory-impairing effects of THC. In terms of harm reduction, users should be made aware of the higher risk of memory impairment associated with smoking low-cannabidiol strains of cannabis like ‘skunk’ and encouraged to use strains containing higher levels of cannabidiol.

Epidemiological data on alcohol-induced psychotic disorder and delirium (alcohol-induced psychotic syndrome, AIPS) are scarce.

To investigate the epidemiology of AIPS, the risk factors for developing AIPS among people with alcohol dependence, and mortality associated with alcohol dependence with or without AIPS, in a sample drawn from the general population of Finland.

A general population sample of 8028 persons were interviewed with the Composite International Diagnostic Interview and screened for psychotic disorders using multiple sources. Best-estimate diagnoses of psychotic disorders were made using the Structured Clinical Interview for DSM–IV Axis I Disorders and case notes. Data on hospital treatments and deaths were collected from national registers.

The lifetime prevalence was 0.5% for AIPS and was highest (1.8%) among men of working age. Younger age at onset of alcohol dependence, low socioeconomic status, father's mental health or alcohol problems and multiple hospital treatments were associated with increased risk of AIPS. Participants with a history of AIPS had considerable medical comorbidity, and 37% of them died during the 8-year follow-up.

Alcohol-induced psychotic disorder is a severe mental disorder with poor outcome.

Burden-of-illness data, which are often used in setting healthcare policy-spending priorities, are unavailable for mental disorders in most countries.

To examine one central aspect of illness burden, the association of serious mental illness with earnings, in the World Health Organization (WHO) World Mental Health (WMH) Surveys.

The WMH Surveys were carried out in 10 high-income and 9 low- and middle-income countries. The associations of personal earnings with serious mental illness were estimated.

Respondents with serious mental illness earned on average a third less than median earnings, with no significant between-country differences (χ2(9) = 5.5–8.1, P = 0.52–0.79). These losses are equivalent to 0.3–0.8% of total national earnings. Reduced earnings among those with earnings and the increased probability of not earning are both important components of these associations.

These results add to a growing body of evidence that mental disorders have high societal costs. Decisions about healthcare resource allocation should take these costs into consideration.

Few randomised controlled trials (RCTs) have examined potential preventive agents in high-risk community populations.

To determine whether a mental health literacy intervention, the promotion of physical activity, or folic acid plus vitamin B12 reduce depression symptoms in community-dwelling older adults with elevated psychological distress.

An RCT with a completely crossed 2 × 2 × 2 factorial design: (400 mcg/d folic acid + 100 mcg/d vitamin B12v. placebo)×(physical activity v. nutrition promotion control) × (mental health literacy v. pain information control). The initial target sample size was 2000; however, only 909 adults (60–74 years) met the study criteria. Interventions were delivered by mail with telephone calls. The main outcome was depressive symptoms on the Patient Health Questionnaire (PHQ–9) at 6 weeks, 6, 12 and 24 months. The Clinicaltrials.gov registration number is NCT00214682.

The drop-out rate was low (13.5%) from randomisation to 24-month assessment. Neither folic acid + B12 (F(3,856) = 0.83, P = 0.476) nor physical activity (F(3,856) = 1.65, P = 0.177) reduced depressive symptoms at any time point. At 6 weeks, depressive symptoms were lower for the mental health literacy intervention compared with its control condition (t(895) = 2.04, P = 0.042).

Mental health literacy had a transient effect on depressive symptoms. Other than this, none of the interventions significantly reduced symptoms relative to their comparator at 6 weeks or subsequently. Neither folic acid plus B12 nor physical activity were effective in reducing depressive symptoms.

Longer-term follow-up of patients with borderline personality disorder have found favourable clinical outcomes, with long-term reduction in symptoms and diagnosis.

We examined the 6-year outcome of patients with borderline personality disorder who were randomised to 1 year of cognitive–behavioural therapy for personality disorders (CBT–PD) or treatment as usual (TAU) in the BOSCOT trial, in three centres across the UK (trial registration: ISRCTN86177428).

In total, 106 participants met criteria for borderline personality disorder in the original trial. Patients were interviewed at follow-up by research assistants masked to the patient's original treatment group, CBT–PD or TAU, using the same measures as in the original randomised trial. Statistical analyses of data for the group as a whole are based on generalised linear models with repeated measures analysis of variance type models to examine group differences.

Follow-up data were obtained for 82% of patients at 6 years. Over half the patients meeting criteria for borderline personality disorder at entry into the study no longer did so 6 years later. The gains of CBT–PD over TAU in reduction of suicidal behaviour seen after 1-year follow-up were maintained. Length of hospitalisation and cost of services were lower in the CBT–PD group compared with the TAU group.

Although the use of CBT–PD did not demonstrate a statistically significant cost-effective advantage, the findings indicate the potential for continued long-term cost-offsets that accrue following the initial provision of 1 year of CBT–PD. However, the quality of life and affective disturbance remained poor.

Although there is cross-sectional evidence that changes in the immune system contribute to the pathophysiology of depression, longitudinal data capable of elucidating cause and effect relationships are lacking.

We aimed to determine whether subclinical systemic inflammation, as measured by serum high-sensitivity C-reactive protein (hsCRP) concentration, is associated with an increased risk of de novo major depressive disorder.

Major depressive disorder was diagnosed using a clinical interview (SCID–I/NP). This is a retrospective cohort study; from a population-based sample of 1494 randomly selected women recruited at baseline during the period 1994–7, 822 were followed for a decade and provided measures of both exposure and outcome. Of these women, 644 (aged 20–84 years) had no prior history of depression at baseline and were eligible for analysis.

During 5827 person-years of follow-up, 48 cases of de novo major depressive disorder were identified. The hazard ratio (HR) for depression increased by 44% for each standard deviation increase in log-transformed hsCRP (ln-hsCRP) (HR = 1.44, 95% CI 1.04–1.99), after adjusting for weight, smoking and use of non-steroidal anti-inflammatory drugs. Further adjustment for other lifestyle factors, medications and comorbidity failed to explain the observed increased risk for depression.

Serum hsCRP is an independent risk marker for de novo major depressive disorder in women. This supports an aetiological role for inflammatory activity in the pathophysiology of depression.