Migration has been implicated as a risk factor for autism, but evidence is limited and inconsistent.

To investigate the relationship between parental migration status and risk of autism spectrum disorder, taking into consideration the importance of region of origin, timing of migration and possible discrepancies in associations between autism subtypes.

Record-linkage study within the total child population of Stockholm County between 2001 and 2007. Individuals with high- and low-functioning autism were defined as having autism spectrum disorder with and without comorbid intellectual disability, and ascertained via health and habilitation service registers.

In total, 4952 individuals with autism spectrum disorder were identified, comprising 2855 children with high-functioning autism and 2097 children with low-functioning autism. Children of migrant parents were at increased risk of low-functioning autism (odds ratio (OR) = 1.5, 95% CI 1.3–1.7); this risk was highest when parents migrated from regions with a low human development index, and peaked when migration occurred around pregnancy (OR = 2.3, 95% CI 1.7–3.0). A decreased risk of high-functioning autism was observed in children of migrant parents, regardless of area of origin or timing of migration. Parental age, income or obstetric complications did not fully explain any of these associations.

Environmental factors associated with migration may contribute to the development of autism presenting with comorbid intellectual disability, especially when acting in utero. High- and low-functioning autism may have partly different aetiologies, and should be studied separately.

Aetiological mechanisms underlying ethnic density associations with psychosis remain unclear.

To assess potential mechanisms underlying the observation that minority ethnic groups experience an increased risk of psychosis when living in neighbourhoods of lower own-group density.

Multilevel analysis of nationally representative community-level data (from the Ethnic Minorities Psychiatric Illness Rates in the Community survey), which included the main minority ethnic groups living in England, and a White British group. Structured instruments assessed discrimination, chronic strains and social support. The Psychosis Screening Questionnaire ascertained psychotic experiences.

For every ten percentage point reduction in own-group density, the relative odds of reporting psychotic experiences increased 1.07 times (95% CI 1.01–1.14, P = 0.03 (trend)) for the total minority ethnic sample. In general, people living in areas of lower own-group density experienced greater social adversity that was in turn associated with reporting psychotic experiences.

People resident in neighbourhoods of higher own-group density experience ‘buffering’ effects from the social risk factors for psychosis.

Poverty may moderate the effect of treatment of depression in low-income countries.

To assess poverty and lack of empowerment as moderators of a cognitive-behavioural therapy (CBT)-based intervention for perinatal depression in rural Pakistan.

Using secondary analysis of data from a randomised controlled trial (trial registration: ISRCTN65316374) we identified predictors of depression at 1-year follow-up and moderators of the intervention (n=791).

Predictors of follow-up depression included household debt, the participant not being empowered to manage household finance and the interaction terms for these variables with the trial arm. Effect sizes for women with and without household debt were 0.80 and 0.55 respectively. The effect size for women in debt and not empowered financially was 0.94 compared with 0.50 for women with neither of these factors.

Our findings demonstrate the importance of household debt and lack of financial empowerment of women as important maintaining factors of depression in low-income countries and our locally developed intervention tackled these problems successfully.

Most studies of the mental health of UK armed forces focus on retrospective accounts of deployment and few sample personnel while they are deployed.

This study reports the results of a survey of deployed personnel, examining the perceived impact of events at home and military support for the family on current mental health during the deployment.

Surveys were conducted with 2042 British forces personnel serving in Iraq and Afghanistan. Prevalence of common mental disorders was assessed with the 12-item General Health Questionnaire (GHQ-12) and post-traumatic stress disorder (PTSD) was assessed with the PTSD Checklist – Civilian version (PCL-C).

The prevalence of common mental disorders was 17.8% and of probable PTSD was 2.8%. Perceived home difficulties significantly influenced the mental health of deployed personnel; the greater the perception of negative events in the home environment, the greater the reporting of adverse mental health effects. This finding was independent of combat exposure and was only partially mitigated by being well led and reporting subjectively good unit cohesion; however, the effect of the totality of home-front events was not improved by the latter. Poor perceived military support for the family had a detrimental impact on deployment mental health.

The armed forces offer many support services to the partners and families of deployed personnel and ensuring that the efforts being made on their behalf are well communicated might improve the mental health of deployed personnel.

Studies suggest a role for cardiovascular fitness in the prevention of affective disorders.

To determine whether cardiovascular fitness at age 18 is associated with future risk of serious affective illness.

Population-based Swedish cohort study of male conscripts (n = 1 117 292) born in 1950–1987 with no history of mental illness who were followed for 3–40 years. Data on cardiovascular fitness at conscription were linked with national hospital registers to calculate future risk of depression (requiring in-patient care) and bipolar disorder.

In fully adjusted models low cardiovascular fitness was associated with increased risk for serious depression (hazard ratios (HR)=1.96, 95%, CI 1.71–2.23). No such association could be shown for bipolar disorder (HR=1.11, 95% CI 0.84–1.47).

Lower cardiovascular fitness at age 18 was associated with increased risk of serious depression in adulthood. These results strengthen the theory of a cardiovascular contribution to the aetiology of depression.

Attention-deficit hyperactivity disorder (ADHD) has been associated with socioeconomic difficulties later in life. Little research in this area has been based on longitudinal and community studies.

To examine the relationship between childhood attention problems and socioeconomic status 18 years later.

Using a French community sample of 1103 youths followed from 1991 to 2009, we tested associations between childhood attention problems and socioeconomic status between ages 22 and 35 years, adjusting for potential childhood and family confounders.

Individuals with high levels of childhood attention problems were three times more likely to experience subsequent socioeconomic disadvantage than those with low levels of attention problems (odds ratio 3.44, 95% CI 1.72–6.92). This association remained statistically significant even after adjusting for childhood externalising problems, low family income, parental divorce and parental alcohol problems.

This longitudinal community-based study shows an association between childhood attention problems and socioeconomic disadvantage in adulthood. Taking into account ADHD and associated difficulties could help reduce the long-term socioeconomic burden of the disorder.

The ‘extreme male brain’ theory suggests that autism spectrum disorder (ASD) is an extreme variant of male intelligence. However, somewhat paradoxically, many individuals with ASD display androgynous physical features regardless of gender.

To assess physical measures, supposedly related to androgen influence, in adults with and without ASD.

Serum hormone levels, anthropometry, the ratio of 2nd to 4th digit length (2D:4D) and psychiatric symptomatology were measured in 50 adults with high-functioning ASD and age- and gender-matched neurotypical controls. Photographs of face and body, as well as voice recordings, were obtained and assessed with respect to gender coherence, blindly and independently, by eight assessors.

Women with ASD had higher total and bioactive testosterone levels, less feminine facial features and a larger head circumference than female controls. Men in the ASD group were assessed as having less masculine body characteristics and voice quality, and displayed higher (i.e. less masculine) 2D:4D ratios, but similar testosterone levels to controls. Androgynous facial features correlated strongly and positively with autistic traits measured with the Autism-Spectrum Quotient in the total sample. In males and females with ASD dehydroepiandrosterone sulfate did not decrease with age, in contrast to the control group.

Women with ASD had elevated testosterone levels and several masculinised characteristics compared with controls, whereas men with ASD displayed several feminised characteristics. Our findings suggest that ASD, rather than being characterised by masculinisation in both genders, may constitute a gender defiant disorder.

Little is known about the impact of different types of stressful events (for example divorce v. bereavement) on unipolar depression compared with bipolar disorder. Inconsistencies exist concerning the association between independent events (beyond an individual's control, such as bereavement) and bipolar disorder.

To examine the role of specific, independent and dependent events in mood disorders.

Life-event information was collected from 512 people with bipolar disorder, 1448 people with unipolar depression and over 600 controls.

Various events were associated with unipolar depression and bipolar disorder, but some event specificity was detected. For example, financial crisis was more strongly related to bipolar disorder rather than unipolar depression. Independent events were only related to unipolar depression and not bipolar disorder.

The events that were linked to bipolar disorder and unipolar depression were similar. Independent events were not associated with bipolar episodes, suggesting that life stress may be a consequence of, rather than a trigger for, bipolar episodes.

Harsh parenting practices and negative parental feelings may be environmental risk factors for low self-control in children. Children may also evoke certain parenting reactions.

To investigate the longitudinal relationship between parenting and self-control, as well as associated outcomes within the monozygotic (MZ) twin differences framework.

Longitudinal MZ twin differences analysis was conducted on a community sample of 5184 twins using data from ages 3, 4, 7 and 9 years. Outcomes related to self-control and parenting were analysed at age 12 years.

Non-shared environmental effects of parenting on the development of self-control and an evocative effect of child self-control on parenting were found. Harsh parenting predicted conduct problems for both boys and girls. Self-control at age 9 predicted conduct problems and emotional difficulties at age 12.

Parenting and child self-control affect one another, highlighting the potential of early interventions that target parents and children simultaneously.

Cortisol levels may be altered in childhood in association with maltreatment (neglect, abuse and witnessing abuse) and other adversities, yet little is known about whether effects on cortisol persist into later life.

To establish whether childhood psychosocial adversities predict cortisol levels in mid-adulthood.

Childhood psychosocial adversities were ascertained in the 1958 British birth cohort and cortisol was measured in two saliva samples, one 45 min after awaking (T1) and the other 3 h later the same day (T2), from 6524 participants aged 45 years.

No association was seen for abuse or household dysfunction in childhood and adult cortisol levels. In women but not men, T1 cortisol was lowered by 7.9% per unit increase in childhood neglect score (range 0–3); T1 to T2 cortisol decline was less steep. High levels of maltreatment (abuse, neglect, witnessed abuse) were associated with >25% lower T1 cortisol in both men and women, and 24% higher T2 cortisol for men after adjustment for concurrent depressive/anxiety symptoms.

In a non-clinical population, cumulative maltreatments in childhood were associated with flattened morning cortisol secretion in mid-adult life.

Epidemiological research has shown that hallucinations and delusions, the classic symptoms of psychosis, are far more prevalent in the population than actual psychotic disorder. These symptoms are especially prevalent in childhood and adolescence. Longitudinal research has demonstrated that psychotic symptoms in adolescence increase the risk of psychotic disorder in adulthood. There has been a lack of research, however, on the immediate clinicopathological significance of psychotic symptoms in adolescence.

To investigate the relationship between psychotic symptoms and non-psychotic psychopathology in community samples of adolescents in terms of prevalence, co-occurring disorders, comorbid (multiple) psychopathology and variation across early v. middle adolescence.

Data from four population studies were used: two early adolescence studies (ages 11–13 years) and two mid-adolescence studies (ages 13–16 years). Studies 1 and 2 involved school-based surveys of 2243 children aged 11–16 years for psychotic symptoms and for emotional and behavioural symptoms of psychopathology. Studies 3 and 4 involved in-depth diagnostic interview assessments of psychotic symptoms and lifetime psychiatric disorders in community samples of 423 children aged 11–15 years.

Younger adolescents had a higher prevalence (21–23%) of psychotic symptoms than older adolescents (7%). In both age groups the majority of adolescents who reported psychotic symptoms had at least one diagnosable non-psychotic psychiatric disorder, although associations with psychopathology increased with age: nearly 80% of the mid-adolescence sample who reported psychotic symptoms had at least one diagnosis, compared with 57% of the early adolescence sample. Adolescents who reported psychotic symptoms were at particularly high risk of having multiple co-occurring diagnoses.

Psychotic symptoms are important risk markers for a wide range of non-psychotic psychopathological disorders, in particular for severe psychopathology characterised by multiple co-occurring diagnoses. These symptoms should be carefully assessed in all patients.

Lower cognitive ability in childhood is associated with increased risk of future schizophrenia, but its relationship with adult psychotic-like experiences and other psychopathology is less understood.

To investigate whether this childhood risk factor is shared with adult subclinical psychiatric phenotypes including psychotic-like experiences and general psychiatric morbidity.

A population-based sample of participants born in Great Britain during 1 week in March 1946 was contacted up to 20 times between ages 6 weeks and 53 years. Cognition was assessed at ages 8, 11 and 15 years using a composite of age-appropriate verbal and non-verbal cognitive tests. At age 53 years, psychotic-like experiences were self-reported by 2918 participants using four items from the Psychosis Screening Questionnaire and general psychiatric morbidity was assessed using the scaled version of the General Health Questionnaire (GHQ-28).

Psychotic-like experiences were reported by 22% of participants, and were highly comorbid with other psychopathology. Their presence in adults was significantly associated with poorer childhood cognitive test scores at ages 8 and 15 years, and marginally so at age 11 years. In contrast, high GHQ scores were not associated with poorer childhood cognition after adjustment for the presence of psychotic-like experiences.

Psychotic and non-psychotic psychopathologic symptoms are highly comorbid in the general population. Lower childhood cognitive ability is a risk factor for psychotic-like experiences in mid-life; these phenomena may be one end of a continuum of phenotypic expression driven by variation in early neurodevelopment.

To compare depressive symptoms in participants with low and high serum 25-hydroxyvitamin D (25(OH)D) levels and to examine whether supplementation with vitamin D3 would improve symptoms in those with low serum 25(OH)D levels.

Participants with low 25(OH)D levels were randomised to either placebo or 40 000 IU vitamin D3 per week for 6 months. Individuals with high serum 25(OH)D levels were used as nested controls. Depressive symptoms were evaluated with the Beck Depression Inventory, Hospital Anxiety and Depression Scale, Seasonal Pattern Assessment Scale and Montgomery-Åsberg Depression Rating Scale. The study was registered at ClinicalTrials.gov (NCT00960232).

Participants with low 25(OH)D levels (n=230) at baseline were more depressed (P<0.05) than participants with high 25(OH)D levels (n=114). In the intervention study no significant effect of high-dose vitamin D was found on depressive symptom scores when compared with placebo.

Low levels of serum 25(OH)D are associated with depressive symptoms, but no effect was found with vitamin D supplementation.

White matter abnormalities have been implicated in the aetiology of major depressive disorder; however, the relationship between the severity of symptoms and white matter integrity is currently unclear.

To investigate white matter integrity in people with major depression and healthy controls, and to assess its relationship with depressive symptom severity.

Diffusion tensor imaging data were acquired from 66 patients with recurrent major depression and a control group of 66 healthy individuals matched for age, gender and IQ score, and analysed with tract-based spatial statistics. The relationship between white matter integrity and severity of depression as measured by the Beck Depression Inventory was examined.

Depressive illness was associated with widespread regions of decreased white matter integrity, including regions in the corpus callosum, superior longitudinal fasciculus and anterior corona radiata, compared with the control group. Increasing symptom severity was negatively correlated with white matter integrity, predominantly in the corpus callosum.

Widespread alterations in white matter integrity are evident in major depressive disorder. These abnormalities are heightened with increasing severity of depressive symptoms.