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Background: Prenatal stress is associated with altered fetal and infant development. Previous studies have suggested that these effects may be mediated in part via altered functioning of placental enzymes and receptors involved in the HPA-axis, including the glucocorticoid receptor (NR3C1) and HSD11B2, the enzyme which metabolises cortisol. However, previous studies have not examined the potential ethnicity effects on these associations. This study aimed to characterise the association between maternal prenatal stress and placental genes expression and subsequently, any potential effect of maternal ethnicity., Method: Pregnant women(n=83) were recruited prior to elective caesarean section and assessed for trait anxiety, depression and life events. Placentas were collected and placental gene expression of NR3C1 and HSD11B2 were analysed. We examined associations between maternal prenatal stress and placental gene expression, and the tested for a possible moderating effect of maternal ethnicity(59.0% Caucasian;41.0% non-Caucasian:12.0% South Asian;6.0% African/African-American;14.4% Other;8.4% Mixed)., Results: Analyses demonstrated a trend in the association between both maternal trait anxiety and depression symptoms with placental gene expression of NR3C1(adj.β=0.220,p=0.067;adj.β=0.212,p=0.064 respectively). We found a significant interaction with maternal ethnicity(β=0.249;p=0.033). In Caucasian women only prenatal trait anxiety and depressive symptoms were associated with an increase in placental NR3C1 expression(adj.β=0.389,p=0.010;adj.β=0.294;p=0.047 respectively). Prenatal life events were associated with a down regulation of HSD11B2(adj.β=0.381;p=0.008), but only in Caucasians., Conclusion: These results support previous findings of an association between maternal prenatal stress and the expression of placental genes associated with the HPA-axis, but only in Caucasians. These ethnic specific findings are novel and require replication in different populations., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Domestic violence and abuse is a considerable international public health problem, which is associated with mental disorders in both women and men. Nevertheless, victimization and perpetration remain undetected by mental health services. This paper reviews the evidence on mental health service responses to domestic violence, including identifying, referring, and providing care for people experiencing or perpetrating violence. The review highlights the need for mental health services to improve rates of identification and responses to domestic violence and abuse, through the provision of specific training on domestic violence and abuse, the implementation of clear information sharing protocols and evidence-based interventions, and the establishment of care referral pathways. This review also highlights the need for further research into mental health service users who perpetrate domestic violence and abuse.

Background: Maternal prenatal stress during pregnancy is associated with fetal growth restriction and adverse neurodevelopmental outcomes, which may be mediated by impaired placental function. Imprinted genes control fetal growth, placental development, adult behaviour (including maternal behaviour) and placental lactogen production. This study examined whether maternal prenatal depression was associated with aberrant placental expression of the imprinted genes paternally expressed gene 3 (PEG3), paternally expressed gene 10 (PEG10), pleckstrin homology-like domain family a member 2 (PHLDA2) and cyclin-dependent kinase inhibitor 1C (CDKN1C), and resulting impaired placental human placental lactogen (hPL) expression., Method: A diagnosis of depression during pregnancy was recorded from Manchester cohort participants' medical notes (n = 75). Queen Charlotte's (n = 40) and My Baby and Me study (MBAM) (n = 81) cohort participants completed the Edinburgh Postnatal Depression Scale self-rating psychometric questionnaire. Villous trophoblast tissue samples were analysed for gene expression., Results: In a pilot study, diagnosed depression during pregnancy was associated with a significant reduction in placental PEG3 expression (41%, p = 0.02). In two further independent cohorts, the Queen Charlotte's and MBAM cohorts, placental PEG3 expression was also inversely associated with maternal depression scores, an association that was significant in male but not female placentas. Finally, hPL expression was significantly decreased in women with clinically diagnosed depression (44%, p < 0.05) and in those with high depression scores (31% and 21%, respectively)., Conclusions: This study provides the first evidence that maternal prenatal depression is associated with changes in the placental expression of PEG3, co-incident with decreased expression of hPL. This aberrant placental gene expression could provide a possible mechanistic explanation for the co-occurrence of maternal depression, fetal growth restriction, impaired maternal behaviour and poorer offspring outcomes.

Objective: Maternal antenatal depression and anxiety are associated with increased risk of childhood behavioural and emotional problems in offspring; it remains unclear to what extent this is due to a maternal biological impact on foetal development. Here, we compare associations between maternal and paternal antenatal depression and anxiety with offspring anxiety disorders, thus controlling for some genetic and shared environmental factors., Methods: We used data from the ALSPAC population cohort including measures of antenatal parental depression and anxiety. At 18 years, offspring completed the CIS-R interview, yielding diagnoses for anxiety disorders. Results were adjusted for confounding variables including parental postnatal depression and anxiety., Results: Children of women with antenatal depression (18 weeks gestation), had an increased risk of anxiety disorders at 18 years of age (11.1% vs. 6.2%; adj. OR 1.75 (1.19, 2.58); p=0.01). Children of women with antenatal anxiety had increased risk of co-morbid anxiety and depression (adj. OR 1.39 (1.06, 1.82); p=0.02). No such associations were found with paternal antenatal depression or anxiety., Limitations: There was a high attrition rate from the original cohort to the CIS-R completion at 18 years postpartum. Parental mood was only assessed together at one time point during the antenatal period., Conclusions: The differences in the association between maternal and paternal mood during pregnancy and child outcomes supports the hypothesis that foetal programming may account, at least in part, for this association. We highlight the potential opportunity for preventative intervention by optimising antenatal mental health., (Copyright © 2015 The Authors. Published by Elsevier B.V. All rights reserved.)

Objective: Maternal prenatal symptoms of depression and anxiety have been associated with altered neurodevelopmental outcomes in the child. These effects may be mediated in part by altered placental function, with increased fetal 5-hydroxytryptamine (5-HT) exposure being one possible mechanism. The current study aimed to determine whether maternal symptoms of depression or anxiety were associated with decreased placental expression of monoamine oxidase A (MAO A), the enzyme which metabolises 5-HT into 5-hydroxyindoleacetic acid. The localisation of MAO A in the placenta was also investigated., Methods: Pregnant women were recruited one day prior to elective caesarean and assessed using psychometric tests for symptoms of depression (Edinburgh Depression Scale) and anxiety (Spielberger State/Trait Index). Villous trophoblast tissue was extracted from each placenta and used for subsequent gene expression analysis (N=62). Localisation was studied using immunohistochemistry, with a specific polyclonal antibody., Results: Increasing symptoms of maternal depression were associated with a reduction in placental MAO A expression (r=-0.339, p=0.007, N=62). There was a trend for a similar correlation with symptoms of maternal trait anxiety, but not with state anxiety. MAO A was localised to the syncytiotrophoblast, the tissue between maternal and fetal blood., Conclusions: These findings support the hypothesis that maternal mood is associated with altered placental function. A reduction in placental MAO A expression is consistent with a subsequent increase in fetal exposure to 5-HT., (© 2013.)