J.C. has no financial interest in the use of, or reproduction of, the EPDS.

None.

T.A. is a paid consultant for Boston Scientific, Medtronic and St. Jude Medical. He has received honoraria from Abbott, Boston and Medtronics and served as consultant to all three.

Heritability of antisocial behaviour is estimated at approximately 50% and involves multiple genes.

To investigate the cumulative genetic effects of 116 single nucleotide polymorphisms mapping to 11 candidate serotonergic genes and antisocial behaviours, in adolescence and in early adulthood.

Participants were 410 male members of the Quebec Longitudinal Study of Kindergarten Children, a population-based cohort followed up prospectively from age 6 to age 23. The serotonergic genes were selected based on known physiological processes and prior associations with antisocial behaviours. Antisocial behaviours were self-reported and assessed by using semi-structured interviews in adolescence and in adulthood.

Cumulative, haplotype-based contributions of serotonergic genes conferring risk and protection for antisocial behaviours were detected by using multilocus genetic profile risk scores (MGPRSs) and multilocus genetic profile protection scores (MGPPSs). Cumulatively, haplotype-based MGPRSs and MGPPSs contributed to 9.6, 8.5 and 15.2% of the variance in general delinquency in adolescence, property/violent crimes in early adulthood and physical partner violence in early adulthood, respectively.

This study extends previous research by showing a cumulative effect of multiple haplotypes conferring risk and protection to antisocial behaviours in adolescence and early adulthood. The findings further support the relevance of concomitantly considering multiple serotonergic polymorphisms to better understand the genetic aetiology of antisocial behaviours. Future studies should investigate the interplay between risk and protective haplotype-based multilocus genetic profile scores with the environment.

I.O.-M. holds a Canada Research Chair in the developmental origins of vulnerability and resilience.

There is little investigation on the interaction effects of adverse childhood experiences (ACEs) and social support on non-suicidal self-injury (NSSI), suicidal ideation and suicide attempt in community adolescent populations, or gender differences in these effects.

To examine the individual and interaction effects of ACEs and social support on NSSI, suicidal ideation and suicide attempt in adolescents, and explore gender differences.

A school-based health survey was conducted in three provinces in China between 2013–2014. A total of 14 820 students aged 10–20 years completed standard questionnaires, to record details of ACEs, social support, NSSI, suicidal ideation and suicide attempt.

Of included participants, 89.4% reported one or more category of ACEs. The 12-month prevalence of NSSI, suicidal ideation and suicide attempt was 26.1%, 17.5% and 4.4%, respectively; all were significantly associated with increased ACEs and lower social support. The multiple adjusted odds ratio of NSSI in low versus high social support was 2.27 (95% CI 1.85–2.67) for girls and 1.81 (95% CI 1.53–2.14) for boys, and their ratio (Ratio of two odds ratios, ROR) was 1.25 (P = 0.037). Girls with high ACEs scores (5–6) and moderate or low social support also had a higher risk of suicide attempt than boys (RORs: 2.34, 1.84 and 2.02, respectively; all P < 0.05).

ACEs and low social support are associated with increased risk of NSSI and suicidality in Chinese adolescents. Strategies to improve social support, particularly among female adolescents with a high number of ACEs, should be an integral component of targeted mental health interventions.

None.

The extent to which exposure to childhood sexual and physical abuse increases the risk of psychotic experiences in adulthood is currently unclear.

To examine the relationship between childhood sexual and physical abuse and psychotic experiences in adulthood taking into account potential confounding and time-dynamic covariate factors.

Data were from a cohort of 1265 participants studied from birth to 35 years. At ages 18 and 21, cohort members were questioned about childhood sexual and physical abuse. At ages 30 and 35, they were questioned about psychotic experiences (symptoms of abnormal thought and perception). Generalised estimating equation models investigated covariation of the association between abuse exposure and psychotic experiences including potential confounding factors in childhood (socioeconomic disadvantage, adverse family functioning) and time-dynamic covariate factors (mental health, substance use and life stress).

Data were available for 962 participants; 6.3% had been exposed to severe sexual abuse and 6.4% to severe physical abuse in childhood. After adjustment for confounding and time-dynamic covariate factors, those exposed to severe sexual abuse had rates of abnormal thought and abnormal perception symptoms that were 2.25 and 4.08 times higher, respectively than the ‘no exposure’ group. There were no significant associations between exposure to severe physical abuse and psychotic experiences.

Findings indicate that exposure to severe childhood sexual (but not physical) abuse is independently associated with an increased risk of psychotic experiences in adulthood (particularly symptoms of abnormal perception) and this association could not be fully accounted for by confounding or time-dynamic covariate factors.

None.

Electroconvulsive therapy (ECT) is the treatment of choice for severe mental illness including treatment-resistant depression (TRD). Increases in volume of the hippocampus and amygdala following ECT have consistently been reported.

To investigate neuroplastic changes after ECT in specific hippocampal subfields and amygdala nuclei using high-resolution structural magnetic resonance imaging (MRI) (trial registration: clinicaltrials.gov – NCT02379767).

MRI scans were carried out in 14 patients (11 women, 46.9 years (s.d. = 8.1)) with unipolar TRD twice before and once after a series of right unilateral ECT in a pre–post study design. Volumes of subcortical structures, including subfields of the hippocampus and amygdala, and cortical thickness were extracted using FreeSurfer. The effect of ECT was tested using repeated-measures ANOVA. Correlations of imaging and clinical parameters were explored.

Increases in volume of the right hippocampus by 139.4 mm3 (s.d. = 34.9), right amygdala by 82.3 mm3 (s.d. = 43.9) and right putamen by 73.9 mm3 (s.d. = 77.0) were observed. These changes were localised in the basal and lateral nuclei, and the corticoamygdaloid transition area of the amygdala, the hippocampal–amygdaloid transition area and the granule cell and molecular layer of the dentate gyrus. Cortical thickness increased in the temporal, parietal and insular cortices of the right hemisphere.

Following ECT structural changes were observed in hippocampal subfields and amygdala nuclei that are specifically implicated in the pathophysiology of depression and stress-related disorders and retain a high potential for neuroplasticity in adulthood.

S.K. has received grants/research support, consulting fees and/or honoraria within the past 3 years from Angelini, AOP Orphan Pharmaceuticals AG, AstraZeneca, Celegne GmbH, Eli Lilly, Janssen-Cilag Pharma GmbH, KRKA-Pharma, Lundbeck A/S, Neuraxpharm, Pfizer, Pierre Fabre, Schwabe and Servier. R.L. received travel grants and/or conference speaker honoraria from Shire, AstraZeneca, Lundbeck A/S, Dr. Willmar Schwabe GmbH, Orphan Pharmaceuticals AG, Janssen-Cilag Pharma GmbH, and Roche Austria GmbH.

None.