Depression and obesity are highly prevalent, and major impacts on public health frequently co-occur. Recently, we reported that having depression moderates the effect of the FTO gene, suggesting its implication in the association between depression and obesity.

To confirm these findings by investigating the FTO polymorphism rs9939609 in new cohorts, and subsequently in a meta-analysis.

The sample consists of 6902 individuals with depression and 6799 controls from three replication cohorts and two original discovery cohorts. Linear regression models were performed to test for association between rs9939609 and body mass index (BMI), and for the interaction between rs9939609 and depression status for an effect on BMI. Fixed and random effects meta-analyses were performed using METASOFT.

In the replication cohorts, we observed a significant interaction between FTO, BMI and depression with fixed effects meta-analysis (β=0.12, P = 2.7 × 10−4) and with the Han/Eskin random effects method (P = 1.4 × 10−7) but not with traditional random effects (β = 0.1, P = 0.35). When combined with the discovery cohorts, random effects meta-analysis also supports the interaction (β = 0.12, P = 0.027) being highly significant based on the Han/Eskin model (P = 6.9 × 10−8). On average, carriers of the risk allele who have depression have a 2.2% higher BMI for each risk allele, over and above the main effect of FTO.

This meta-analysis provides additional support for a significant interaction between FTO, depression and BMI, indicating that depression increases the effect of FTO on BMI. The findings provide a useful starting point in understanding the biological mechanism involved in the association between obesity and depression.

To investigate scanpath abnormalities during the encoding of static stimuli in schizophrenia and their interaction with visuospatial working memory (VSWM) dysfunction.

Outpatients with schizophrenia and control subjects were asked to encode a static pattern for subsequent recognition after a short delay. We measured the number of correct and incorrect choices. We also assessed the number and the distribution of fixations, the scanning time in specific regions of interest (ROIs) and the head movements during the encoding of the stimuli. The distributions of fixations and scanning time in definite ROIs during the discrimination of the correct pattern from the foils were also measured.

Patients recognised fewer correct patterns than controls. Correct trials in patients were characterised by a specific exploration of the central part of the stimulus during its presentation, whereas this feature was absent in incorrect trials. However, the scanning time and the numbers of fixations and head movements during encoding were similar in both groups and unrelated to recognition accuracy. In both groups, correct trials were associated with a selective exploration of the correct pattern amongst the six possibilities during recognition. Furthermore, patients gave more attention to incorrect patterns with a leftmost element identical to that of the correct response and also those approximating its global structure.

Patients showed a VSWM deficit independent of oculomotor dysfunctions and head movements during encoding. Patients’ correct trials were related to specific scanning during encoding and discrimination phases. Analysis of these patterns suggests that patients try to compensate for reduced VSWM ability by using specific encoding strategies.

Although usually thought of as external environmental stressors, a significant heritable component has been reported for measures of stressful life events (SLEs) in twin studies.

We examined the variance in SLEs captured by common genetic variants from a genome-wide association study (GWAS) of 2578 individuals. Genome-wide complex trait analysis (GCTA) was used to estimate the phenotypic variance tagged by single nucleotide polymorphisms (SNPs). We also performed a GWAS on the number of SLEs, and looked at correlations between siblings.

A significant proportion of variance in SLEs was captured by SNPs (30%, p = 0.04). When events were divided into those considered to be dependent or independent, an equal amount of variance was explained for both. This ‘heritability’ was in part confounded by personality measures of neuroticism and psychoticism. A GWAS for the total number of SLEs revealed one SNP that reached genome-wide significance (p = 4 × 10−8), although this association was not replicated in separate samples. Using available sibling data for 744 individuals, we also found a significant positive correlation of R2 = 0.08 in SLEs (p = 0.03).

These results provide independent validation from molecular data for the heritability of reporting environmental measures, and show that this heritability is in part due to both common variants and the confounding effect of personality.