Evidence suggests sex differences in schizophrenia reflect differences in both neurodevelopmental processes and social effects on disease risk and course. Male:female incidence approximates 1.4:1 but at older onset women predominate. Prevalence differences appear smaller. Men have poorer premorbid adjustment and present with worse negative and less depressive symptoms than women, which may explain their worse medium term outcome according to a range of measures. Substance abuse is a predominantly male activity in this group, as elsewhere. Findings of sex differences in brain morphology are inconsistent but occur in areas that normally show sexual dimorphism, implying that the same factors are important drivers of sex differences in both normal neurodevelopmental processes and those associated with schizophrenia. There are sex differences in antipsychotic responses but sex-specific endocrine effects on illness and response to antipsychotics are potentially complex. Oestrogen's role as an adjunctive medication is not yet clear due to methodological differences between the few randomized controlled trials. Services that are sensitive to differences in gender can better meet their patients’ specific needs and potentially improve outcome.

The common conception that a mother's psychological state can influence her unborn baby is to some extent substantiated by the literature.¹ Severe life events during pregnancy are consistently associated with an elevated risk of low birth weight² and prematurity.³ Recently, Hansen et al⁴ reported specific effects of severe life events on neurodevelopment in exposed offspring. They found an increased risk of cranial neural crest malformations in offspring of mothers exposed to death of an older child during the first trimester. Other studies have also attempted to find evidence of a positive association between antenatal maternal stress and an increased risk of adult schizophrenia in exposed offspring.^5,6

Background: Preconception, prenatal and postnatal maternal stress is associated with increased offspring psychopathology, but findings are inconsistent and need replication. We estimated associations between maternal bereavement stress and offspring autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD), bipolar disorder, schizophrenia, suicide attempt and completed suicide.Method: Using Swedish registers, we conducted the largest population-based study to date examining associations between stress exposure in 738 144 offspring born 1992–2000 for childhood outcomes and 2 155 221 offspring born 1973–1997 for adult outcomes with follow-up to 2009. Maternal stress was defined as death of a first-degree relative during (a) the 6 months before conception, (b) pregnancy or (c) the first two postnatal years. Cox proportional survival analyses were used to obtain hazard ratios (HRs) in unadjusted and adjusted analyses.Results: Marginal increased risk of bipolar disorder and schizophrenia following preconception bereavement stress was not significant. Third-trimester prenatal stress increased the risk of ASD [adjusted HR (aHR) 1.58, 95% confidence interval (CI) 1.15–2.17] and ADHD (aHR 1.31, 95% CI 1.04–1.66). First postnatal year stress increased the risk of offspring suicide attempt (aHR 1.13, 95% CI 1.02–1.25) and completed suicide (aHR 1.51, 95% CI 1.08–2.11). Bereavement stress during the second postnatal year increased the risk of ASD (aHR 1.30, 95% CI 1.09–1.55).Conclusions: Further research is needed regarding associations between preconception stress and psychopathological outcomes. Prenatal bereavement stress increases the risk of offspring ASD and ADHD. Postnatal bereavement stress moderately increases the risk of offspring suicide attempt, completed suicide and ASD. Smaller previous studies may have overestimated associations between early stress and psychopathological outcomes.

The birth weight of an infant provides little information about the path of its growth in utero in either an adverse or favorable maternal environment. Nonetheless, low birth weight (defined by the World Health Organization as < 2500 g) has been shown to be an important marker of vulnerability to infant and child morbidity and mortality. Increasingly, studies have examined associations between low birth weight and various adult outcomes such as cardiovascular disease¹ and cognition.² Many of these studies have gone beyond the examination of low birth weight per se and have explored whether there is an inverse gradient between birth weight and risk of adult outcomes.^3-5

Purpose To conduct a systematic review and meta-analysis to examine the strength of associations between social network size and clinical and functional outcomes in schizophrenia. Method Studies were identified from a systematic search of electronic databases (EMBASE, Medline, PsycINFO, and Web of Science) from January 1970 to June 2016. Eligible studies included peer-reviewed English language articles that examined associations between a quantitative measure of network size and symptomatic and/or functional outcome in schizophrenia-spectrum diagnoses. Results Our search yielded 16 studies with 1,929 participants. Meta-analyses using random effects models to calculate pooled effect sizes (Hedge’s g) found that smaller social network size was moderately associated with more severe overall psychiatric symptoms (N = 5, n = 467, g = − 0.53, 95% confidence interval (CI) = − 0.875, − 0.184, p = 0.003) and negative symptoms (N = 8, n = 577, g = − 0.75, 95% CI = − 0.997, − 0.512, p = 0.000). Statistical heterogeneity was observed I² = 63.04%; I² = 35.75%,) which could not be explained by low-quality network measures or sample heterogeneity in sensitivity analyses. There was no effect for positive symptoms (N = 7, n = 405, g = − 0.19, 95% CI = 0.494, 0.110, p = 0.213) or social functioning (N = 3, n = 209, g = 0.36, 95% CI = − 0.078, 0.801, p = 0.107). Narrative synthesis suggested that larger network size was associated with improved global functioning, but findings for affective symptoms and quality of life were mixed. Conclusion Psychosocial interventions which support individuals to build and maintain social networks may improve outcomes in schizophrenia. The review findings are cross-sectional and thus causal direction cannot be inferred. Further research is required to examine temporal associations between network characteristics and outcomes in schizophrenia and to test theoretical models relating to explanatory or mediating mechanisms.