Previous studies suggest that offspring of mothers with psychotic disorders have an almost two-fold higher mortality risk from birth until early adulthood. We investigated predictors of mortality from late adolescence until middle age in offspring of mothers with psychotic disorders.

The Helsinki High-Risk Study follows up offspring (n=337) of women treated for schizophrenia spectrum disorders in mental hospitals in Helsinki before 1975. Factors related to mortality up to 2005 among offspring of these mothers was investigated with a survival model. Hazard rate ratios (HRR) were calculated using sex, diagnosis of psychotic disorder, childhood socio-economic status, maternal diagnosis, and maternal suicide attempts and aggressive symptoms as explanatory variables. The effect of family was investigated by including a frailty term in the model. We also compared mortality between the high-risk group and the Finnish general population.

Within the high-risk group, females had lower all-cause mortality (HRR 0.43, p=0.05) and mortality from unnatural causes (HRR 0.24, p=0.03) than males. Having themselves been diagnosed with a psychotic disorder was associated with higher mortality from unnatural causes (HRR 4.76, p=0.01), while maternal suicide attempts were associated with higher suicide mortality (HRR 8.64, p=0.03). Mortality in the high-risk group was over two-fold higher (HRR 2.44, p<0.0001) than in the general population, and remained significantly higher when high-risk offspring who later developed psychotic disorders were excluded from the study sample (HRR 2.30, p<0.0001).

Offspring of mothers with psychotic disorder are at increased risk of several adverse outcomes, including premature death.

A variety of methodologies and techniques converge on the notion that adults and children with attention deficit hyperactivity disorder (ADHD) have similar deficits, but there is limited knowledge about whether adult retrospective reports reflect similar genetic and environmental influences implicated in childhood ADHD.

DSM-IV ADHD symptoms were collected retrospectively from 3896 young adults participating in the National Longitudinal Study of Adolescent Health. Responses from this genetically informative sample of same- and opposite-sex twins and siblings were used to determine the magnitude of genetic and environmental influences. Possible gender differences in these effects were also examined. The degree of familial specificity of the genetic and environmental influences on the Inattentive and Hyperactive-Impulsive symptom dimensions was also determined.

Additive genetic effects contributed moderately to DSM-IV Inattentive, Hyperactive-Impulsive and Combined ADHD subtypes (heritability estimates of 0.30–0.38). Individual-specific influences accounted for the remaining proportion of the variance. Both genetic and individual-specific environmental effects contributed to the covariation of Inattentive and Hyperactive-Impulsive symptomologies.

Results from our genetic analyses agree with previous findings based on self-assessment of current and retrospectively reported ADHD symptoms in adolescents and adults. Large individual-specific environmental influences as identified here suggest that current questionnaires used for retrospective diagnoses may not provide the most accurate reconstruction of the etiological influences on childhood ADHD in general population samples.

The DSM-IV-R classification Pervasive Developmental Disorder – Not otherwise Specified (PDD-NOS) is based on the symptoms for autism and includes a wide variety of phenotypes that do not meet full criteria for autism. As such, PDD-NOS is a broad and poorly defined residual category of the autism spectrum disorders. In order to address the heterogeneity in this residual category it may be helpful to define clinical and neurobiological subtypes. Multiple complex developmental disorder (MCDD) may constitute such a subtype. In order to study the neurobiological specificity of MCDD in comparison with other autism spectrum disorders, we investigated brain morphology in children (age 7–15 years) with MCDD compared to children with autism and typically developing controls.

Structural MRI measures were compared between 22 high-functioning subjects with MCDD and 21 high-functioning subjects with autism, and 21 matched controls.

Subjects with MCDD showed an enlarged cerebellum and a trend towards larger grey-matter volume compared to control subjects. Compared to subjects with autism, subjects with MCDD had smaller intracranial volume.

We report a pattern of volumetric changes in the brains of subjects with MCDD, similar to that seen in autism. However, no enlargement in head size was found. This suggests that although some of the neurobiological changes associated with MCDD overlap with those in autism, others do not. These neurobiological changes may reflect differences in the developmental trajectories associated with these two subtypes of autism spectrum disorders.

Patients with schizophrenia have been found to display abnormalities in social cognition. The aim of the study was to test whether patients with schizophrenia and unaffected first-degree relatives of schizophrenic patients display behavioural signs of social brain dysfunction when making social judgements.

Eighteen patients with schizophrenia, 24 first-degree unaffected relatives and 28 healthy comparison subjects completed a task which involves trustworthiness judgements of faces. A second task was completed to measure the general ability to recognize faces.

Patients with schizophrenia rated faces as more trustworthy, especially those that were judged to be untrustworthy by healthy comparison subjects. Siblings of schizophrenia patients display the same bias, albeit to a lesser degree.

The pattern of more positive trustworthiness judgements parallels the results from studies of patients with abnormalities in brain areas involved in social cognition. Because patients and siblings did not differ significantly from controls in their general ability to recognize faces, these findings cannot be dismissed as abnormalities in face perception by itself.

Inter-country adoptees run risks of developmental and health-related problems. Cognitive ability is one important indicator of adoptees' development, both as an outcome measure itself and as a potential mediator between early adversities and ill-health. The aim of this study was to analyse relations between proxies for adoption-related circumstances and cognitive development.

Results from global and verbal scores of cognitive tests at military conscription (mandatory for all Swedish men during these years) were compared between three groups (born 1968–1976): 746 adoptees born in South Korea, 1548 adoptees born in other non-Western countries and 330 986 non-adopted comparisons in the same birth cohort. Information about age at adoption and parental education was collected from Swedish national registers.

South Korean adoptees had higher global and verbal test scores compared to adoptees from other non-European donor countries. Adoptees adopted after age 4 years had lower test scores if they were not of Korean ethnicity, while age did not influence test scores in South Koreans or those adopted from other non-European countries before the age of 4 years. Parental education had minor effects on the test performance of the adoptees – statistically significant only for non-Korean adoptees' verbal test scores – but was prominently influential for non-adoptees.

Negative pre-adoption circumstances may have persistent influences on cognitive development. The prognosis from a cognitive perspective may still be good regardless of age at adoption if the quality of care before adoption has been ‘good enough’ and the adoption selection mechanisms do not reflect an overrepresentation of risk factors – both requirements probably fulfilled in South Korea.

Major depressive disorder (MDD) and alcohol use disorders (AUDs) are among the most prevalent psychiatric disorders and are frequently co-morbid. However, some component of this co-morbidity may be artifactual and arise from the influence of current mental state on self-reports of AUD.

This study examined whether past-year MDD is associated with differential criterion functioning (DCF) in reports of AUD symptomatology in male and female participants in the National Epidemiological Survey on Alcohol and Related Conditions (NEASRC).

Reports of past-year AUD symptomatology were adequately summarized by a single-factor model in which each of the 11 abuse and dependence criteria had high factor loadings (0.71–0.93) and did not vary between men and women after allowing for threshold differences. Co-morbid MDD was associated with higher AUD mean scores. There was some evidence for DCF with past-year MDD being associated with a lower endorsement of use in hazardous situations among men whereas women with MDD were more likely to endorse both social/interpersonal problems and emotional/physical problems.

Several items assessing AUD display DCF in the presence of MDD. While these findings highlight the need to consider the possibility that mental state can influence reporting of psychiatric symptoms and potentially inflate estimates of co-morbidity, they suggest that only a negligible component of the co-morbidity between MDD and AUDs can be attributed to over-reporting of alcohol symptomatology conditional on current MDD.

Alcohol is commonly considered to be associated with persistence of common mental disorder (CMD; anxiety/depression). However no community-based longitudinal studies have investigated the direction of causality.

We examined the association between alcohol consumption and recovery from CMD using data on 706 community-based subjects with CMD who were followed for 18 months. Alcohol consumption at baseline was defined as hazardous drinking [Alcohol Use Disorders Identification Test (AUDIT) ⩾8], binge drinking (defined as six or more units of alcohol on one occasion, approximately two to three pints of commercially sold beer) and dependence.

When compared with a non-binge-drinking group, non-recovery at follow-up was associated with binge drinking on at least a monthly basis at baseline, although the confidence interval (CI) included unity [adjusted odds ratio (OR) 1.47, 95% CI 0.89–2.45]. There was also weak evidence that alcohol dependence was associated with non-recovery (adjusted OR 1.37, 95% CI 0.67–2.81). There was little evidence to support hazardous drinking as a risk factor for non-recovery (adjusted OR 1.12, 95% CI 0.67–1.88).

Binge drinking may be a potential risk factor for non-recovery from CMD, although the possibility of no effect cannot be excluded. Larger studies are required to refute or confirm this finding.