Combat exposure is associated with elevated risk for post-traumatic stress disorder (PTSD). Despite considerable research on PTSD symptom clustering, it remains unknown how symptoms of PTSD re-organize following combat. Network analysis provides a powerful tool to examine such changes.

A network analysis approach was taken to examine how symptom networks change from pre- to post-combat using longitudinal prospective data from a cohort of infantry male soldiers (Mage = 18.8 years). PTSD symptoms measured using the PTSD Checklist (PCL) were assessed after 6 months of combat training but before deployment and again after 6 months of combat (Ns = 910 and 725 at pre-deployment and post-combat, respectively)

Stronger connectivity between PTSD symptoms was observed post-combat relative to pre-deployment (global strength values of the networks were 7.54 pre v. 7.92 post; S = .38, p < 0.05). Both the re-experiencing symptoms cluster (1.92 v. 2.12; S = .20, p < 0.03) and the avoidance symptoms cluster (2.61 v. 2.96; S = .35, p < 0.005) became more strongly inter-correlated post-combat. Centrality estimation analyses revealed that psychological reaction to triggers was central and linked the intrusion and avoidance sub-clusters at post-combat. The strength of associations between the arousal and reactivity symptoms cluster remained stable over time (1.85 v. 1.83; S = .02, p = .92).

Following combat, PTSD symptoms and particularly the re-experiencing and avoidance clusters become more strongly inter-correlated, indicating high centrality of trigger-reactivity symptoms.

Few studies have examined the latent construct of psychotic symptoms or distinguished between the latent construct and its manifest indicators. The current study aimed to investigate the latent structure of psychotic symptoms using factor mixture modeling (FMM) and to use the best-fitting model to examine its sociodemographic and clinical correlates.

The Singapore Mental Health Study (SMHS) was based on an adult representative sample of the Singapore population. Psychotic symptoms were assessed by using the Psychosis Screen section of the Composite International Diagnostic Interview version 3.0 (CIDI 3.0). FMM analyses were applied to determine the latent construct of psychotic symptoms. Sociodemographic and clinical correlates of the latent structure of psychosis symptoms were examined using multiple linear and logistic regression analyses.

The overall weighted lifetime prevalence of any psychotic experience was 3.8% in the SMHS after excluding subthreshold experiences. The FMM analysis clearly supported the dimensional model of the latent structure of psychotic symptoms. On deriving the total score for ‘psychosis symptoms’ in accordance with the one latent trait model, and correlating it with sociodemographic factors, we found that female gender, vocational education, current and past smokers were positively associated with the ‘psychosis’ total score.

There is a need for an increased understanding of, and research into, this intermediate state of ‘psychosis symptoms’ that do not meet diagnostic criteria for psychosis. It is also important to learn more about the group of individuals in the community who may have preserved functioning to elucidate the protective factors that prevent transition to psychosis.

Evidence shows that cognitive deficits and white matter (WM) dysconnectivity can independently be associated with clinical manifestations in schizophrenia. It is important to explore this triadic relationship in order to investigate whether the triplet could serve as potential extended endophenotypes of schizophrenia.

Diffusion tensor images and clinical performances were evaluated in 122 individuals with first-episode schizophrenia and 122 age- and gender-matched controls. In addition, 65 of 122 of the patient group and 40 of 122 controls were measured using intelligence quotient (IQ) testing.

The schizophrenia group showed lower fractional anisotropy (FA) values than controls in the right cerebral frontal lobar sub-gyral (RFSG) WM. The schizophrenia group also showed a significant positive correlation between FA in the RFSG and performance IQ (PIQ); in turn, their PIQ score showed a significant negative correlation with negative syndromes.

Overall, these findings support the hypothesis that WM deficits may be a core deficit that contributes to cognitive deficits as well as to negative symptoms.

There is an established relationship between depression and sexual functioning in women. However, there is limited research examining the relationship between perinatal depression and sexual functioning.

This study draws on the Mercy Pregnancy and Emotional Wellbeing Study and reports on 211 women recruited in early pregnancy and followed to 12 months postpartum. Women were assessed for depression using the Structured Clinical Interview for the DSM-IV, repeated measurement of depressive symptoms using the Edinburgh Postnatal Depression Scale and sexual functioning using the Female Sexual Functioning Inventory. Data were also collected on antidepressant use, mode of delivery, history of childhood trauma, breastfeeding and partner support.

Women showed a decline in sexual functioning over pregnancy and the first 6 months postpartum, which recovered by 12 months. For women with depression, sexual functioning was lower throughout pregnancy and continued to be lower at 6 months postpartum than those without depression. Ongoing depressive symptoms at 12 months were also associated with lower sexual functioning. Sexual functioning was not predicted by mode of delivery, antidepressant use or childhood trauma. Breastfeeding predicted lower sexual functioning only at 6 months. Higher partner support predicted higher female sexual functioning.

Pregnancy and the postpartum are a time of reduced sexual functioning for women; however, women with depression are more likely to have lower levels of sexual functioning and this was not predicted by antidepressant use. In women with perinatal depression, consideration of the impact on sexual functioning should be an integral part of care.

Childhood adversity (CA) is commonly associated with an increased risk of subsequent psychopathology. It is important to identify potential mediators of this relationship which can allow for the development of interventions. In a large population-based cohort study we investigated the relationship between CA and late adolescent psychopathology and early adolescent candidate mediators of this relationship.

We used data from three waves (n = 6039) of Cohort 98′ of the Growing up in Ireland Study (age 9, 13 and 17). We used doubly robust counterfactual analyses to investigate the relationship between CA (reported at age-9) with psychopathology (internalizing and externalizing problems), measured using the Strengths and Difficulties Questionnaire at age-17. Counterfactual and traditional mediation was used to investigate the mediating effects of the parent-child relationship, peer relations, self-concept, computer usage and physical activity.

CA was associated with an increased risk of internalizing and externalizing problems at age-17. Parent-child conflict mediated 35 and 42% of the relationship between CA and late adolescent externalizing problems and internalizing problems, respectively. Self-concept and physical activity mediated an additional proportion of the relationship between CA and internalizing problems. These results were robust to unmeasured confounding.

Parent-child conflict explains more than a third of the relationship between CA and later psychopathology. Self-concept and physical activity explain the additional proportion of the relationship between CA and internalizing problems. This suggests that these factors may be good targets for intervention in young people who have experienced CA to prevent subsequent psychopathology.

A history of childhood adversity is associated with psychotic disorder, with an increase in risk according to the number of exposures. However, it is not known why only some exposed individuals go on to develop psychosis. One possibility is pre-existing polygenic vulnerability. Here, we investigated, in the largest sample of first-episode psychosis (FEP) cases to date, whether childhood adversity and high polygenic risk scores for schizophrenia (SZ-PRS) combine synergistically to increase the risk of psychosis, over and above the effect of each alone.

We assigned a schizophrenia-polygenic risk score (SZ-PRS), calculated from the Psychiatric Genomics Consortium (PGC2), to all participants in a sample of 384 FEP patients and 690 controls from the case–control component of the EU-GEI study. Only participants of European ancestry were included in the study. A history of childhood adversity was collected using the Childhood Trauma Questionnaire (CTQ). Synergistic effects were estimated using the interaction contrast ratio (ICR) [odds ratio (OR)exposure and PRS − ORexposure − ORPRS + 1] with adjustment for potential confounders.

There was some evidence that the combined effect of childhood adversities and polygenic risk was greater than the sum of each alone, as indicated by an ICR greater than zero [i.e. ICR 1.28, 95% confidence interval (CI) −1.29 to 3.85]. Examining subtypes of childhood adversities, the strongest synergetic effect was observed for physical abuse (ICR 6.25, 95% CI −6.25 to 20.88).

Our findings suggest possible synergistic effects of genetic liability and childhood adversity experiences in the onset of FEP, but larger samples are needed to increase precision of estimates.

While drug abuse (DA) is strongly familial, we still have limited knowledge about the causes of its cross-generational transmission.

We examined DA ascertained from national registers in offspring of three family types from the Swedish population [intact (n = 2 111 074), ‘not-lived-with’ (n = 165 315, where biological parents never lived with their offspring) and ‘step’ (n = 124 800 offspring)], which reflected, respectively, the effects of genes + rearing, genes only and rearing only. We replicated these results in three high-risk co-relative designs.

Combined across mothers and fathers, the hazard ratio (HR) for DA in offspring given DA in parents was 3.52 in intact, 2.73 in ‘not-lived-with’ and 1.79 in stepfamilies. In 968 biological full or half-sibling pairs one of whom was reared by and the other never lived with their parent with DA, the HR for DA was greater in the reared than ‘not-lived-with’ child (HR 1.57). In 64 offspring pairs of a parent with DA, the HR for DA was greater in a reared biological v. step-parented non-biological child (HR 3.33). In 321 pairs of offspring of a parent with DA one of whom was a not-lived-with biological child and the second a step-parented non-biological child, the HR for DA was greater in the biological v. stepchild (HR 1.80).

Both genetic and environmental factors contribute substantially to parent–offspring resemblance for DA. The general population contains informative family constellations that can complement more traditional adoption designs in clarifying the sources of parent–offspring resemblance.

Cognitive impairment is a core feature of psychotic disorders, but the profile of impairment across adulthood, particularly in African-American populations, remains unclear.

Using cross-sectional data from a case–control study of African-American adults with affective (n = 59) and nonaffective (n = 68) psychotic disorders, we examined cognitive functioning between early and middle adulthood (ages 20–60) on measures of general cognitive ability, language, abstract reasoning, processing speed, executive function, verbal memory, and working memory.

Both affective and nonaffective psychosis patients showed substantial and widespread cognitive impairments. However, comparison of cognitive functioning between controls and psychosis groups throughout early (ages 20–40) and middle (ages 40–60) adulthood also revealed age-associated group differences. During early adulthood, the nonaffective psychosis group showed increasing impairments with age on measures of general cognitive ability and executive function, while the affective psychosis group showed increasing impairment on a measure of language ability. Impairments on other cognitive measures remained mostly stable, although decreasing impairments on measures of processing speed, memory and working memory were also observed.

These findings suggest similarities, but also differences in the profile of cognitive dysfunction in adults with affective and nonaffective psychotic disorders. Both affective and nonaffective patients showed substantial and relatively stable impairments across adulthood. The nonaffective group also showed increasing impairments with age in general and executive functions, and the affective group showed an increasing impairment in verbal functions, possibly suggesting different underlying etiopathogenic mechanisms.