Maternal Antenatal Depression Research Articles

Intimate partner violence across pregnancy and the postpartum and the relationship to depression and perinatal wellbeing: findings from a pregnancy cohort study.

To compare the prevalence of emotional and physical intimate partner violence (IPV) across pregnancy and the first year postpartum in those with and without clinical depression and assess the association between maternal childhood trauma, current stressful life events and depression and IPV over the perinatal period. Data were obtained from 505 pregnant women from the Mercy Pregnancy and Emotional Wellbeing Study (MPEWS), a cohort study with data collected across pregnancy until 12 months postpartum. Maternal antenatal depression was measured using the Structured Clinical Interview for DSM-IV (SCID-IV) with repeat measurement of perinatal depressive symptoms using the Edinburgh Postnatal Depression Scale (EPDS). Trauma was measured using the Childhood Trauma Questionnaire, and experiences of physical and emotional intimate partner violence using items in the Stressful Life Events Scale. Women experiencing IPV across the perinatal period were significantly more likely to score over 13 on the EPDS (p < .001) at each timepoint in pregnancy and the postpartum and physical IPV was associated with clinical depression. Further, a history of childhood trauma and current additional stressful life events were significantly associated with reporting current IPV in the perinatal period. This study confirmed the risk factors of childhood trauma and current stressful life events for reporting experiences of IPV in the perinatal period. Furthermore, women experiencing IPV reported higher depressive symptoms, providing evidence supporting the value of assessing those women who screen higher on the EPDS for IPV. Together these findings also support trauma informed care across pregnancy and the postpartum.

Path analysis of influencing factors for maternal antenatal depression in the third trimester.

Maternal antenatal depression (AD) is a nonpsychotic depressive episode during pregnancy that can harm both the pregnant woman and the fetus. This study aimed to investigate the intrinsic interrelationships between AD and its influencing factors by constructing a path model. This survey-based cross-sectional study included 1071 pregnant women who underwent pregnancy examinations in three hospitals in Nantong City, China, between February and June 2023. General information and information regarding maternal AD, pregnancy stress, prenatal anxiety, social support, marital satisfaction, sleep quality, and resilience were collected. Multiple linear regression analysis using SPSS 25.0 was employed to determine the factors influencing pregnancy depression, and Amos25.0 was used to construct a structural equation model. AD incidence was 19.4% (208/1071). The independent risk factors affecting AD in pregnant women have been integrated into the established path analysis model. The model demonstrated a good fit (χ2/DF = 1.238, comparative fit index = 0.999, goodness-of-fit index = 0.998, normed fit index = 0.996, adjusted goodness-of-fit index = 0.990, incremental fit index = 0.999, and root mean square error of approximation = 0.015). While prenatal anxiety (0.230) and hyperthyroidism (0.048) only had direct effects on AD, mental resilience was the biggest factor affecting AD, followed by pregnancy stress, marital satisfaction, prenatal anxiety, sleep quality, social support, and hyperthyroidism. Improved mental resilience, social support, sleep quality, and marital satisfaction; reduced pregnancy stress and prenatal anxiety; and effective hyperthyroidism treatment might reduce AD. This study underscored the significance of delivering actionable strategies and tangible assistance to pregnant women to reduce AD.

Placental accelerated aging in antenatal depression

Antenatal maternal depression is associated with poor pregnancy outcomes and long-term effects on the offspring. Previous studies have identified links between antenatal depression and placental DNA methylation and between placental epigenetic aging and poor pregnancy outcomes, such as preterm labor and preeclampsia. The relationship between antenatal depression and poor pregnancy outcomes may be partly mediated via placental aging. This study aimed to investigate whether antenatal depressive symptoms are associated with placental epigenetic age acceleration, an epigenetic aging clock measure derived from the difference between methylation age and gestational age at delivery. The study included 301 women who provided placenta samples at delivery as part of the Eunice Kennedy Shriver National Institute of Child Health and Human Development Fetal Growth Studies - Singletons that recruited participants from diverse race and ethnic groups at 12 US clinical sites (2009-2013). Women underwent depression screening using the Edinburgh Postnatal Depression Scale up to 6 times across the 3 trimesters of pregnancy. Depressive symptoms status was determined for each pregnancy trimester using an Edinburgh Postnatal Depression Scale score, in which a score of ≥10 was defined as having depressive symptoms and a score of <10 was defined as not having depressive symptoms. Placental DNA methylation was profiled from placenta samples. Placental epigenetic age was estimated using a methylation-based age estimator (placental "epigenetic clock") that has previously been found to have high placental gestational age prediction accuracy for uncomplicated term pregnancies. Placental age acceleration was defined to be the residual upon regressing the estimated epigenetic age on gestational age at delivery. Associations between an Edinburgh Postnatal Depression Scale score of ≥10 and an Edinburgh Postnatal Depression Scale score of <10 in the first, second, and third trimesters of pregnancy (ie, depressive symptoms vs none in each trimester) and placental age acceleration were tested using multivariable linear regression adjusting for maternal age, parity, race and ethnicity, and employment. There were 31 (10.3%), 48 (16%), and 49 (16.4%) women with depressive symptoms (ie, Edinburgh Postnatal Depression Scale score of ≥10) in the first, second, and third trimesters of pregnancy, respectively. Of these women, 21 (7.2%) had sustained first- and second-trimester depressive symptoms, 19 (7%) had sustained second- and third-trimester depressive symptoms, and 12 (4.8%) had sustained depressive symptoms throughout pregnancy. Women with depressive symptoms in the second trimester of pregnancy had 0.41 weeks higher placental age acceleration than women without depressive symptoms during the second trimester of pregnancy (β=0.21 weeks [95% confidence interval, -0.17 to 0.58; P=.28] during the first trimester of pregnancy; β=0.41 weeks [95% confidence interval, 0.10-0.71; P=.009] during the second trimester of pregnancy; β=0.17 weeks [95% confidence interval, -0.14 to 0.47; P=.29] during the third trimester of pregnancy). Sustained first- and second-trimester depressive symptoms were associated with 0.72 weeks higher placental age acceleration (95% confidence interval, 0.29-1.15; P=.001) than no depressive symptom in the 2 trimesters. The association between second-trimester depressive symptoms and higher placental epigenetic age acceleration strengthened in the analysis of pregnancies with male fetuses (β=0.53 weeks; 95% confidence interval, 0.06-1.08; P=.03) but was not significant in pregnancies with female fetuses. Antenatal depressive symptoms during the second trimester of pregnancy were associated with an average of 0.41 weeks of increased placental age acceleration. Accelerated placental aging may play an important role in the underlying mechanism linking antenatal depression to pregnancy complications related to placental dysfunction.

Antenatal predictors of postnatal maternal attachment and competence after assisted conception-a prospective cohort study in South India.

The aim of this study is to examine the influence of antenatal factors suchas anxiety, depression, perceived stress, marital satisfaction, maternal antenatal attachment, and social support on postnatal maternal attachment and competence in women whoreceived assisted reproductive treatment. A prospective longitudinal cohort design was adopted with two groups-50 women who received assisted reproductive treatment and 50 women who had natural conception. Both the groups were assessed using self-report measures over three time points: T1, 7th month of pregnancy; T2, 2weeks postpartum; and T3, 3months postpartum.Afinal sample of44 women who had assisted conception and 47 women who had natural conception completed assessments across all three time points. Descriptive, bivariate analyses, and stepwise multiple linear regression analyseswerecarried out.In the assisted conception group, maternal antenatal attachment, depression, and marital satisfaction significantly predicted postnatal maternal-infant attachment. Perceived social support, depression, and duration of marriage significantly predicted postnatal maternal competence. In the naturally conceived group, maternal antenatal attachment and social support significantly predicted postnatal maternal-infant attachment;perceived stresssignificantly predicted postnatal maternal competence. Antenatal depressive symptoms and relational factors significantly influenced postnatal maternal attachment and competence highlighting the need for screening and targeted psychological interventions during pregnancy.

Online cognitive behaviour therapy for maternal antenatal and postnatal anxiety and depression in routine care

BackgroundPerinatal depression and anxiety are associated with significant adverse effects for the mother and child. Online cognitive behavioural therapy (iCBT) can provide scalable access to psychological interventions to improve perinatal depression and anxiety, however, few studies have examined the effectiveness of these interventions in routine care. This study investigated the uptake and treatment outcomes of women living in the Australian community who enrolled in a pregnancy or postnatal iCBT program for their symptoms of depression and anxiety. Methods1502 women commenced iCBT (529 pregnancy and 973 postnatal) and completed measures of anxiety and depression symptom severity, and psychological distress pre- and post-treatment. Results35.0 % of women in the pregnancy program and 41.6 % in the postnatal program completed all 3 lessons, with lower pre-treatment depression symptom severity significantly associated with increased likelihood of perinatal program completion. Both iCBT programs were associated with medium pre- to post-treatment effect size reductions in generalised anxiety symptom severity (gs = 0.63 and 0.71), depression symptom severity (gs = 0.58 and 0.64), and psychological distress (gs = 0.52 and 0.60). LimitationsLack of control group and long-term follow-up, as well as detailed information on nature of the sample (e.g., health status, relationship status). Additionally, the sample was limited to Australian residents. ConclusioniCBT for perinatal anxiety and depression was associated with significant symptom improvement. Current findings support the use of iCBT in perinatal populations and its integration within routine healthcare provision.

Associations Between Social Support and Symptoms of Antenatal Depression with Infant Growth and Development Among Mothers Living with HIV in Tanzania.

Children born to mothers living with HIV may experience greater risk of poor growth and development outcomes than their HIV-unexposed peers. Few studies have examined the relationship between maternal depression and social support with infant growth and development in the context of HIV. We conducted a prospective cohort study of 2,298 pregnant women living with HIV in Dar es Salaam, Tanzania, assessing antenatal depression (Hopkins Symptoms Checklist-25) and social support (Duke-UNC Functional Social Support Questionnaire) at 12-27 weeks of gestation. At one-year age, infant anthropometry and caregiver-reported infant development were assessed. Generalized estimating equations were used to assess mean differences (MD) and relative risks (RR) for growth and developmental outcomes. Symptoms consistent with maternal antenatal depression had 67% prevalence and were associated with infant wasting (RR 2.61; 95% confidence interval (CI) 1.03-6.65; z = 2.02; p = 0.04), but no other growth or developmental outcomes. Greater maternal social support was not associated with infant growth outcomes. Greater affective support was associated with better cognitive (MD 0.18; CI 0.01-0.35; z = 2.14; p = 0.03) and motor (MD 0.16; CI 0.01-0.31; z = 2.04; p = 0.04) development scores. Greater instrumental support was associated with better cognitive (MD 0.26; CI 0.10-0.42; z = 3.15; p < 0.01), motor (MD 0.17; CI 0.02-0.33; z = 2.22; p = 0.03), and overall (MD 0.19; CI 0.03-0.35; z = 2.35; p = 0.02) development scores. Depressive symptoms were associated with greater risk of wasting, while social support was associated with better infant development scores. Strategies to improve mental health and social support for mothers living with HIV during the antenatal period may benefit infant growth and development.

Maternal antenatal depression's effects on child developmental delays: Gestational age, postnatal depressive symptoms, and breastfeeding as mediators

BackgroundMaternal antenatal depression experienced around conception or during pregnancy may adversely affect child development. This study explores three potential mechanisms of the effects of antenatal depression on children's developmental delays at 2–3 years: gestational age of the child, continued depressive symptoms postnatally, and interrupted breastfeeding practices. MethodsMothers (N = 2888) of 3450 children, including 2303 singletons and 1147 multiples from the Upstate KIDS cohort provided data. Linked hospital discharge data was combined with mothers' reports to identify women with moderate to severe antenatal depression. Gestational age was extracted from birth certificates. Mothers completed a depression screener at 4 months postpartum, reported about their breastfeeding practices from 4 to 12 months postpartum, and completed a developmental delay screener when children were 24, 30, and 36 months. ResultsIn unadjusted path analysis models, mothers with antenatal depression had more postnatal depressive symptoms and breastfed fewer months, which translated into children being more likely to have developmental delays. Gestational age was not a mediator. Effects were similar across girls and boys and singletons and twins, and largely held when adjusting for covariates. LimitationsMain limitations were the relatively advantaged sample and reliance on maternal report. ConclusionsMaternal antenatal depression may impact child development through continued depressive symptoms in the postpartum period and through reduced breastfeeding duration suggesting additional targets for intervention.

The social predictors of paternal antenatal mental health and their associations with maternal mental health in the Queensland Family Cohort prospective study

Antenatal depression (AND) affects 1 in 10 fathers, potentially negatively impacting maternal mental health and well-being during and after the transition to parenthood. However, few studies have assessed the social predictors of paternal AND or their possible associations with maternal mental health. We analysed data from 180 couples participating in the Queensland Family Cohort longitudinal study. Both parents completed surveys measuring mental health, relationship quality, social support, and sleep quality at 24 weeks of pregnancy. Mothers also completed the same surveys 6 weeks’ postpartum. Antenatal depression, stress, and anxiety were highest among fathers reporting lower social support and higher sleep impairment. Maternal AND, stress, and anxiety were higher among mothers reporting higher physical pain and poor sleep quality. Postnatally, mothers reporting lower social support also reported higher depression, anxiety, stress, and psycho-social well-being. While there were no significant associations between AND among fathers and maternal antenatal or postnatal depression, an exploratory analysis revealed that mothers whose partners reported lower antenatal social support also reported lower postnatal social support and higher postnatal depression. Our findings highlight the importance of including data among fathers to achieve a whole family approach to well-being during the transition to parenthood.

Antenatal maternal depression, early life inflammation and neurodevelopment in a South African birth cohort

BackgroundAntenatal exposure to maternal psychological adversity, including depression, increases the risk of impaired neurodevelopment in children. The underlying biological mechanisms remain unclear, especially in early life during critical windows of development and maturation. This study investigated the association of antenatal maternal depression, maternal and early life inflammatory markers and neurodevelopmental outcomes in children at 2 years of age. MethodsA subgroup of mothers and their children (n = 255) that were enrolled in a South African birth cohort study, the Drakenstein Child Health Study, were followed from the antenatal period through to 2 years of child age. Maternal depressive symptoms were measured by the Beck Depression Inventory (BDI-II) at 26 weeks gestation. Serum inflammatory markers [granulocyte–macrophage colony-stimulating factor (GM-CSF), interferon-γ (IFN-γ), interleukin IL-1β, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12p70, IL-13, tumour necrosis factor-α (TNF-α), neutrophil gelatinase-associated lipocalin (NGAL) and metalloproteinase-9 (MMP-9)] were measured in mothers at enrolment and in their children at 6–10 weeks and at 2 years. Neurodevelopment was assessed at 2 years using the Bayley Scales of Infant and Toddler Development III. ResultsAntenatal depressive symptoms (present in 25% of the mothers) were significantly associated with higher levels of IL-7 (p = 0.008), IL-8 (p = 0.019) and TNF-α (p = 0.031) in the mothers after correcting for sociodemographic and lifestyle factors. Serum IL-1β and NGAL levels were significantly elevated over time in children born to mothers with depressive symptoms compared to those without depression, after controlling for maternal and child health and sociodemographic factors. Elevated infant IL-1β at 6–10 weeks of age partially mediated the association of maternal depressive symptoms with poorer language scores at 2 years. ConclusionAlterations in early life immunity, as reflected by elevated IL-1β, is a potential pathway through which antenatal maternal depressive symptoms may impact language development in young children.

Longitudinal phenotyping of maternal antenatal depression in obese pregnant women supports multiple-hit hypothesis for fetal brain development, a secondary analysis of the UPBEAT study.

SummaryBackgroundMaternal antenatal depression is associated with offspring psychological disorders, but obesity is also widely implicated in maternal depression and neurodevelopment. In pregnant women with obesity we explored interrelationships between antenatal depressive symptom trajectories and multiple exposures implicated in fetal neurodevelopment which could explain these associations, as a prelude to exploring associations with infant mental health.MethodsThe UK Pregnancies Better Eating and Activity Trial (UPBEAT) recruited multi-ethnic pregnant women with obesity (BMI >= 30kg/m2) between March 2009 and June 2014 from 8 UK sites and 1369 were included to model longitudinal antenatal depressive symptoms from Edinburgh Postnatal Depression Scale (EPDS) scores using Latent Class Growth Analysis. Classes were compared on maternal baseline demography, biomarkers of metabolism, inflammation and placental function, infection, diet and by pregnancy and birth outcomes. Odds ratios, mean differences and 95% Confidence Intervals were calculated using robust auxiliary modelling techniques.FindingsThe chosen model produced four classes: “Not Depressed” (n=575 [42%], “reference”), “Mild” (n=523 [37·5%]), “Moderate” (n=219 [16%]) and “Severe” (n=62 [4·5%]) symptom trajectories. Socio-economic deprivation and ethnic diversity were greater in Severe and Moderate classes. Dietary glycaemic load and saturated fat intake were higher in Severe and Moderate classes (at 17 and 27 weeks). Higher Interleukin-6, glycoprotein acetyls (17 weeks), glucose (34 weeks) and lower placental growth factor (PlGF, 17 and 27 weeks) was found in the Severe class. PlGF was lower in the Moderate class (27 weeks). Infection was least likely in the Not Depressed class across gestation. Risks of preterm birth were associated with Severe depressive symptoms (aOR 3·05[1·11 to 8·36]).InterpretationComprehensive phenotyping exposes important fetal exposures implicated in adverse neurodevelopment, differing by depression class. This study expands substantially on causal models of suboptimal fetal neurodevelopment and offers potential new targets for intervention in obese pregnant women.FundingJNS was funded by a PhD studentship from the National Institute for Health Research (NIHR) Biomedical Research Centre based at Guy's and St Thomas’ NHS Foundation Trust and King's College London. UPBEAT was supported by the European Union's 7th Framework Programme (FP7/2007-2013), project EarlyNutrition; grant agreement no. 289346 and the National Institute for Health Research (NIHR) (UK) Programme Grants for Applied Research Programme (RP-0407-10452), Medical Research Council UK Project Grant (MR/L002477/1). Support was also provided by the Chief Scientist Office Scotland, Guy's and St Thomas’ Charity and Tommy's Charity (Registered charity no. 1060508). LP and SLW are funded by Tommy's Charity.

Special Report: Stress and Distress During Pregnancy—How to Protect Both Mother and Child

Special Report: Stress and Distress During Pregnancy—How to Protect Both Mother and Child

Burden and risk factors for antenatal depression and its effect on preterm birth in South Asia: A population-based cohort study.

IntroductionWomen experience high rates of depression, particularly during pregnancy and the postpartum periods. Using population-based data from Bangladesh and Pakistan, we estimated the burden of antenatal depression, its risk factors, and its effect on preterm birth.MethodsThe study uses the following data: maternal depression measured between 24 and 28 weeks of gestation using the 9–question Patient Health Questionnaire (PHQ-9); data on pregnancy including an ultrasound before 19 weeks of gestation; data on pregnancy outcomes; and data on woman’s age, education, parity, weight, height, history of previous illness, prior miscarriage, stillbirth, husband’s education, and household socioeconomic data collected during early pregnancy. Using PHQ-9 cutoff score of ≥12, women were categorized into none to mild depression or moderate to moderately severe depression. Using ultrasound data, preterm birth was defined as babies born <37 weeks of gestation. To identify risk ratios (RR) for antenatal depression, unadjusted and adjusted RR and 95% confidence intervals (CI) were calculated using log- binomial model. Log-binomial models were also used for determining the effect of antenatal depression on preterm birth adjusting for potential confounders. Data were analyzed using Stata version 16 (StataCorp LP).ResultsAbout 6% of the women reported moderate to moderately severe depressive symptoms during the antenatal period. A parity of ≥2 and the highest household wealth status were associated with an increased risk of depression. The overall incidence of preterm birth was 13.4%. Maternal antenatal depression was significantly associated with the risk of preterm birth (ARR, 95% CI: 1.34, 1.02–1.74).ConclusionThe increased risk of preterm birth in women with antenatal depression in conjunction with other significant risk factors suggests that depression likely occurs within a constellation of other risk factors. Thus, to effectively address the burden of preterm birth, programs require developing and providing integrated care addressing multiple risk factors.

Subcortical brain volumes in young infants exposed to antenatal maternal depression: Findings from a South African birth cohort

BackgroundSeveral studies have reported enlarged amygdala and smaller hippocampus volumes in children and adolescents exposed to maternal depression. It is unclear whether similar volumetric differences are detectable in the infants’ first weeks of life, following exposure in utero. We investigated subcortical volumes in 2-to-6 week old infants exposed to antenatal maternal depression (AMD) from a South African birth cohort. MethodsAMD was measured with the Beck Depression Inventory 2nd edition (BDI-II) at 28–32 weeks gestation. T2-weighted structural images were acquired during natural sleep on a 3T Siemens Allegra scanner. Subcortical regions were segmented based on the University of North Carolina neonatal brain atlas. Volumetric estimates were compared between AMD-exposed (BDI-II ⩾ 20) and unexposed (BDI-II < 14) infants, adjusted for age, sex and total intracranial volume using analysis of covariance. ResultsLarger volumes were observed in AMD-exposed (N = 49) compared to unexposed infants (N = 75) for the right amygdala (1.93% difference, p = 0.039) and bilateral caudate nucleus (left: 5.79% difference, p = 0.001; right: 6.09% difference, p < 0.001). A significant AMD-by-sex interaction was found for the hippocampus (left: F(1,118) = 4.80, p = 0.030; right: F(1,118) = 5.16, p = 0.025), reflecting greater volume in AMD-exposed females (left: 5.09% difference, p = 0.001, right: 3.54% difference, p = 0.010), but not males. ConclusionsVolumetric differences in subcortical regions can be detected in AMD-exposed infants soon after birth, suggesting structural changes may occur in utero. Female infants might exhibit volumetric changes that are not observed in male infants. The potential mechanisms underlying these early volumetric differences, and their significance for long-term child mental health, require further investigation.

Predictors of Antenatal Depression in Pregnant Couples.

Pregnant women and their partners are at an increased risk of antenatal depression. Therefore, this cross-sectional study of data from 116 couples investigated predictors of maternal and paternal antenatal depression using sociodemographic data, women's risk factors for depression during the antenatal period, women's perceived stress, and antenatal depression in the other partner. Pregnant women had higher depression scores (7.4 ± 4.7) and a higher frequency of being at high risk for depression (25.9%) than their spouses (4.6 ± 3.5, 9.5%). Multiple linear regression analysis revealed that the statistically significant predictors of antenatal depression in pregnant women were perceived stress (β = .45, p < .001) and antenatal depression risk factors (β = .30, p = .002) and in spouses, women's antenatal depression risk factors (β = .29, p = .013). The present findings suggest that nurses should intervene to mitigate the risk of maternal antenatal depression and perceived stress to prevent depression in pregnant couples.

Prenatal predictors of childhood anxiety disorders: An exploratory study of the role of attachment organization.

Childhood anxiety disorders (CAD) are a common childhood mental disorder and understanding early developmental pathways is key to prevention and early intervention. What is not understood is whether early life stress predictors of CAD might be both mediated by infant cortisol reactivity and moderated by infant attachment status. To address this question, this exploratory study draws on 190 women recruited in early pregnancy and followed together with their children until 4 years of age. Early life stress is operationalized as maternal depression measured using the Structured Clinical Interview for the DSM, Childhood Trauma Questionnaire, Parenting Stress Index, and antenatal maternal hair cortisol concentrations. Infant cortisol reactivity was measured at 12 months together with the Strange Situation Procedure and CAD assessed at 4 years of age using the Preschool Age Psychiatric Assessment. There was no direct association between attachment classification and CAD. Furthermore, infant cortisol reactivity neither mediated nor attachment moderated the association of early life stress predictors and CAD. However, only for infants with organized attachment classifications, higher maternal antenatal depression, and hair cortisol were associated with a higher risk of CAD.

24.6 EVALUATING THE GENOMIC CONTRIBUTION TO THE FETAL ORIGINS OF MENTAL HEALTH: A TEST USING POLYGENIC RISK SCORES

The fetal origins hypothesis, which emphasizes adaptations to in utero exposures with long-term implications for brain and behavior, has emerged as a leading conceptual model for mental health research. One potentially major factor that has not been given significant attention in existing studies is child genomic risk for mental health disorders, which may confound or modify the association between prenatal exposures and child mental health. We capitalize on recent advances in population genetics, specifically polygenic risk scores, to test if child polygenic risk for major mental health disorders confounds or modifies the relationship between maternal antenatal depression and child psychopathology. The Avon Longitudinal Study of Parents and Children (ALSPAC) provided measures of maternal antenatal mood and child mental health data from 4 to 16 years of age. We used polygenic risk scores to derive measures of child genomic risk for ADHD, schizophrenia, and depression. Child outcomes included internalizing, externalizing, and total emotional/behavioral difficulties from childhood to midadolescence. Our primary analysis focuses on longitudinal symptom data from the ALSPAC cohort (n = 5237) with secondary analyses in an independent cohort of children from the PREDO (Prediction and Prevention of Preeclampsia and Intrauterine Growth Restriction) cohort (n = 514). There was a robust prediction of child and adolescent mental health from maternal antenatal depression, or maternal anxiety, independent of child polygenic risk for ADHD, schizophrenia, or depression; there were similar independent effects of maternal depression on child mental health in an independent cohort. These findings provide the most direct test to date of the genomic contribution to the fetal origins of mental health hypothesis and indicate a modest influence of polygenic risk scores on the emergence of symptoms from early childhood through adolescence. Our findings further underscore the potential value of investing in mental health supports in pregnancy for the benefit of both mother and child.

Child Cortisol Output During Cold Pressor Task is Associated with Trait Anxiety, but Not Maternal Antenatal Depression

Child Cortisol Output During Cold Pressor Task is Associated with Trait Anxiety, but Not Maternal Antenatal Depression

Maternal depression during pregnancy alters infant subcortical and midbrain volumes.

BackgroundMaternal depression in pregnancy increases the risk for adverse neurodevelopmental outcomes in the offspring. The reason for this is unknown, however, one plausible mechanism may include the impact of maternal antenatal depression on infant brain. Nevertheless, relatively few studies have examined the brain anatomy of infants born to clinically diagnosed mothers. MethodsA legacy magnetic resonance imaging (MRI) dataset was used to compare regional brain volumes in 3-to-6-month-old infants born to women with a clinically confirmed diagnosis of major depressive disorder (MDD) during pregnancy (n = 31) and a reference sample of infants born to women without a current or past psychiatric diagnosis (n = 33). A method designed for analysis of low-resolution scans enabled examination of subcortical and midbrain regions previously found to be sensitive to the parent-child environment. ResultsCompared with infants of non-depressed mothers, infants exposed to maternal antenatal depression had significantly larger subcortical grey matter volumes and smaller midbrain volumes. There was no association between gestational medication exposure and the infant regional brain volumes examined in our sample. LimitationsOur scanning approach did not allow for an examination of fine-grained structural differences, and without repeated measures of brain volume, it is unknown whether the direction of reported associations are dependent on developmental stage. ConclusionsMaternal antenatal depression is associated with an alteration in infant brain anatomy in early postnatal life; and that this is not accounted for by medication exposure. However, our study cannot address whether anatomical differences impact on future outcomes of the offspring.

Child Polygenic Risk for Psychiatric Disorders Does Not Explain the Association Between Antenatal Maternal Symptoms of Depression and Child Mental Health

Background: There is considerable evidence for an association between antenatal maternal symptoms of depression and anxiety and an increased risk for child mental health problems. One possible major factor that has not been given significant attention is the genomic risk for psychiatric disorders, which may confound (e.g., vertical transmission of genetic risk factors from mother to child) or modify the impact of prenatal exposures on symptom development. Using recent advances in polygenic risk scores, we tested the hypothesis that child genomic risk is a confounder or effect modifier of antenatal maternal symptoms of depression or anxiety on child psychopathology. Methods: We used data from the Avon Longitudinal Study of Parents and Children (ALSPAC), a large prospective cohort from the United Kingdom with measures of antenatal maternal mood and child mental health data from 4–16 years. We quantified child genomic risk for ADHD, schizophrenia, and depression using established polygenic risk scores. Outcomes were internalising, externalising, and total emotional/behavioural difficulties from childhood to mid-adolescence. We analysed the data longitudinally with generalized estimating equations (n=5,237) with secondary analyses in an independent prospective cohort of children from the Finnish PREDO study (n=514). Findings: Maternal mood and child genomic risk additively predicted mental health symptoms across childhood and into mid-adolescence. There was a robust prediction of child and adolescent mental health from both antenatal maternal depression (Estimate=0·024, 95% CI: 0·019–0·029, p<0·001) and anxiety (Est.=0·029, CI: 0·022–0·036, p<0·001) independent of multiple measures of child genomic risk for mental disorders with a similar independent effect of maternal depression (B=0·156, CI: 0·067–0·244, p=0·001) on child symptoms in an independent cohort. Interpretation: These findings provide the most direct test to date of the genomic contribution to the in utero origins of mental health hypothesis. Results indicate a modest influence of PRS on the emergence of symptoms from early childhood through adolescence. The findings also further evidence that antenatal maternal distress independently constitutes a distinct risk for child psychiatric symptoms into adolescence. Funding Statement: UK Medical Research Council, CIFAR Child and Brain Development Program, Canada First Research Excellence Fund: Healthy Brains for Healthy Lives initiative at McGill University, the JPB Foundation through a grant to the JPB Research Network on Toxic Stress: A Project of the Center on the Developing Child at Harvard University, Jacobs Foundation, Fonds de recherche du Quebec-Sante, Brain and Behavior Research Foundation, Pfeil Foundation and National Institutes of Health (R01 MH073842 and UG3/UH3 OD023349), Academy of Finland. Declaration of Interests: None to declare. Ethics Approval Statement: Informed consent for the use of data collected via questionnaires and clinics was obtained from participants following the recommendations of the ALSPAC Ethics and Law Committee at the time. Consent for biological samples has been collected in accordance with the Human Tissue Act (2004). Ethical approval for the study was obtained from the ALSPAC Ethics and Law Committee and the Local Research Ethics Committees.

Antenatal maternal anxiety, maternal sensitivity and toddlers' behavioral problems: An investigation of possible pathways

BackgroundWhile evidence exists of an association between maternal antenatal anxiety and offspring's behavioral outcomes, the role played by maternal care in explaining this link has been poorly investigated. AimThe current study aimed to investigate the mediating/moderating role of maternal sensitivity in the association between maternal antenatal trait anxiety and toddlers' behavioral problems and temperament, taking also into account potential confounders. Analyses were also replicated for maternal antenatal state anxiety and depression. MethodsNinety women filled in the State-Trait Anxiety Questionnaire and the Edinburgh Postnatal Depression Scale to assess anxiety/depressive symptoms during the third trimester of pregnancy (34–36 weeks of gestation) and 14 months post-partum. They also filled in the Child Behavior Checklist and the Infant Behavior Questionnaire to evaluate their 14-month-olds' behavioral problems and negative affectivity, respectively. Maternal sensitivity was assessed through the Emotional Availability Scales. ResultsMaternal antenatal trait anxiety was associated with internalizing, but not externalizing, problems. Interestingly, maternal sensitivity moderated the association between antenatal trait anxiety and externalizing problems. Conversely, antenatal maternal depression was significantly associated with toddlers' negative affectivity. ConclusionsOur findings contribute to shed light on the association between maternal antenatal anxiety and child behaviors, as well as on the role played by parenting in moderating this link, with promising implications for targeted interventions.