Prenatal Maternal Depressive Symptoms Research Articles

Microglial function interacts with the environment to affect sex-specific depression risk

There is a two-fold higher incidence of depression in females compared to men with recent studies suggesting a role for microglia in conferring this sex-dependent depression risk. In this study we investigated the nature of this relation. Using GWAS enrichment, gene-set enrichment analysis and Mendelian randomization, we found minimal evidence for a direct relation between genes functionally related to microglia and sex-dependent genetic risk for depression. We then used expression quantitative trait loci and single nucleus RNA-sequencing resources to generate polygenic scores (PGS) representative of individual variation in microglial function in the adult (UK Biobank; N = 54753–72682) and fetal (ALSPAC; N = 1452) periods. The adult microglial PGS moderated the association between BMI (UK Biobank; beta = 0.001, 95 %CI 0.0009 to 0.003, P = 7.74E-6) and financial insecurity (UK Biobank; beta = 0.001, 95 %CI 0.005 to 0.015, P = 2E-4) with depressive symptoms in females. The fetal microglia PGS moderated the association between maternal prenatal depressive symptoms and offspring depressive symptoms at 24 years in females (ALSPAC; beta = 0.04, 95 %CI 0.004 to 0.07, P = 0.03). We found no evidence for an interaction between the microglial PGS and depression risk factors in males. Our results illustrate a role for microglial function in the conferral of sex-dependent depression risk following exposure to a depression risk factor.

Maternal prenatal depressive symptoms and child brain responses to affective touch at two years of age

BackgroundTouch is an essential form of mother-child interaction, instigating better social bonding and emotional stability. MethodsWe used diffuse optical tomography to explore the relationship between total haemoglobin (HbT) responses to affective touch in the child's brain at two years of age and maternal self-reported prenatal depressive symptoms (EPDS). Affective touch was implemented via slow brushing of the child's right forearm at 3 cm/s and non-affective touch via fast brushing at 30 cm/s and HbT responses were recorded on the left hemisphere. ResultsWe discovered a cluster in the postcentral gyrus exhibiting a negative correlation (Pearson's r = −0.84, p = 0.015 corrected for multiple comparisons) between child HbT response to affective touch and EPDS at gestational week 34. Based on region of interest (ROI) analysis, we found negative correlations between child responses to affective touch and maternal prenatal EPDS at gestational week 14 in the precentral gyrus, Rolandic operculum and secondary somatosensory cortex. The responses to non-affective touch did not correlate with EPDS in these regions. LimitationsThe number of mother-child dyads was 16. However, by utilising high-density optode arrangements, individualised anatomical models, and video and accelerometry to monitor movement, we were able to minimize methodological sources of variability in the data. ConclusionsThe results show that maternal depressive symptoms during pregnancy may be associated with reduced child responses to affective touch in the temporoparietal cortex. Responses to affective touch may be considered as potential biomarkers for psychosocial development in children. Early identification of and intervention in maternal depression may be important already during early pregnancy.

Association between maternal prenatal depressive symptoms and offspring epigenetic aging at 3-5 weeks

Epigenetic clocks are emerging as tools for assessing acceleration and deceleration of biological age during childhood. Maternal depression during pregnancy may affect the biological aging of offspring and related development. In a low-income cohort of mother-child dyads, we investigated the relationship between prenatal maternal depressive symptoms and infant epigenetic age residuals, which represent the deviation (acceleration or deceleration) that exists between predicted biological age and chronological age. The epigenetic age residuals were derived from a pediatric-specific buccal epithelial clock. We hypothesized that maternal depressive symptoms, both sub-clinical and elevated (clinical level), would be associated with estimated biological age deceleration in offspring during early infancy. We analyzed data from 94 mother-child dyads using the Edinburgh Postnatal Depression Scale (EPDS) and DNA methylation derived from offspring buccal cells collected at 3–5 weeks of age. There was a significant non-linear association between the EPDS score and epigenetic age residual (β = −0.017, 95% confidence interval: −0.03,−0.01, P = <0.01). The results indicated that infants of mothers with sub-clinical depressive symptoms had the lowest infant epigenetic age residuals while infants of mothers with no-to-low depressive symptoms had the highest and experienced biological age acceleration. Maternal depressive symptoms may influence the biological aging of offspring living in poverty.

Maternal Prenatal Depressive Symptoms and Fetal Growth During the Critical Rapid Growth Stage

Fetal growth in the critical rapid growth stage (CRGS) before delivery, approximately between 30 to 37 gestational weeks, carries significant implications for subsequent overweight, obesity, and arterial health. Previous evidence has demonstrated the association between maternal depressive symptoms and fetal growth trajectories from early to late pregnancy, but there remains limited understanding of the association of these symptoms with the longitudinal fetal growth change within the CRGS. To investigate the association between maternal depressive symptoms and fetal growth during the CRGS before delivery. This prospective birth cohort study was conducted from January 2018 to December 2020. Volunteer pregnant women were enrolled in their first trimester of prenatal visits. Women with severe disease before pregnancy and multiple births, fetuses with congenital anomalies, and preterm or postterm births were excluded. This multicenter study was based in 13 hospitals covering 81 counties across 12 cities in Sichuan Province, China. Follow-up visits were performed at the second trimester, the third trimester, and 24 hours after delivery. The analysis was conducted from January to May 2023. Maternal depressive symptoms, as a continuous variable, measured by the Edinburgh Postpartum Depression Scale (EPDS) at a median gestational week of 24 (range, 14 to 27) weeks of gestation. A higher score on the EPDS indicates worse depressive symptoms. The main outcomes included ultrasonography-measured biparietal diameter (BPD), femur length (FL), and abdominal circumference (AC), along with calculated estimated fetal weight (EFW). These parameters were evaluated longitudinally at a median gestational week of 30 (range, 28 to 32) and 37 (range, 35 to 39) weeks. Linear mixed models were used to estimate the associations between maternal depressive symptoms and fetal growth parameters. A total of 2676 mother-offspring dyads were included, in which the mean (SD) age of mothers was 28.0 (4.4) years, and 1294 (48.4%) of the offspring were female. The median (IQR) maternal EPDS score was 5.0 (4.0 to 9.0). After adjustment for confounders, a significant correlation was found between a higher score of depressive symptoms in mothers and a slower rate of fetal growth across FL (β = -0.40; 95% CI, -0.58 to -0.22), AC (β = -1.97; 95% CI, -2.90 to -1.03), and EFW (β = -50.11; 95% CI, -68.46 to -31.75). These associations were stronger in female fetuses or those with better family socioeconomic conditions. In this prospective cohort study, maternal depressive symptoms were associated with slower fetal growth rate in the CRGS before delivery. Early screening for depressive disorders in pregnant women appears to be essential for fetal growth and later health.

Associations of maternal prenatal psychological symptoms and saliva cortisol with neonatal meconium microbiota: A cross-sectional study

Alterations in the diversity and relative abundances of the gut microbiome have been associated with a broad spectrum of medical conditions. Maternal psychological symptoms during pregnancy may impact on offspring development by altering the maternal and the foetal gut microbiome. We aimed to investigate whether self-reported maternal anxiety, depressive symptoms, and distress as well as saliva cortisol levels in late pregnancy alter the bacterial composition of the infant's meconium. MethodsA total of N = 100 mother-infant pairs were included. Maternal psychological symptoms were measured using psychological questionnaires (EPDS, PSS-10, STAI) at 34–36 weeks gestation and salivary cortisol was measured at 34–36 and 38 weeks gestation. Infant meconium samples were collected in the first five days postpartum and analysed using 16S rRNA amplicon sequencing. ResultsCorrelations showed that lower alpha diversity of the meconium microbiome was significantly associated with increased maternal prenatal depressive symptoms in late gestation (τ = −0.15, p = .04). Increased saliva cortisol AUCg at T2 was significantly related to higher beta diversity of the meconium samples (Pr(>F) = 0.003*). Pseudomonas was the most abundant phylum and was associated with maternal saliva cortisol total decline. No other associations were found. ConclusionsMaternal prenatal depressive symptoms are associated with infant faecal microbiome alpha diversity, whereas maternal saliva cortisol AUCg is linked to increased beta diversity and total decline related to increased Psuedomonas. Future studies are warranted to understand how these microbiota community alterations are linked to child health outcomes.

Associations of prenatal maternal depressive symptoms with cord blood glucocorticoids and child hair cortisol levels in the project viva and the generation R cohorts: a prospective cohort study

BackgroundPrior studies have reported conflicting results regarding the association of prenatal maternal depression with offspring cortisol levels. We examined associations of high levels of prenatal depressive symptoms with child cortisol biomarkers.MethodsIn Project Viva (n = 925, Massachusetts USA), mothers reported their depressive symptoms using the Edinburgh Postnatal Depression Scale (EPDS) during pregnancy, cord blood glucocorticoids were measured at delivery, and child hair cortisol levels were measured in mid-childhood (mean (SD) age: 7.8 (0.8) years) and early adolescence (mean (SD) age: 13.2 (0.9) years). In the Generation R Study (n = 1644, Rotterdam, The Netherlands), mothers reported depressive symptoms using the Brief Symptom Inventory (BSI) during pregnancy, and child hair cortisol was measured at a mean (SD) age of 6.0 (0.5) years. We used cutoffs of ≥ 13 for the EPDS and > 0.75 for the BSI to indicate high levels of prenatal depressive symptoms. We used multivariable linear regression models adjusted for child sex and age (at outcome), and maternal pre-pregnancy BMI, education, social support from friends/family, pregnancy smoking status, marital status, and household income to assess associations separately in each cohort. We also meta-analyzed childhood hair cortisol results from both cohorts.Results8.0% and 5.1% of women respectively experienced high levels of prenatal depressive symptoms in Project Viva and the Generation R Study. We found no associations between high levels of maternal depressive symptoms during pregnancy and child cortisol biomarkers in either cohort.ConclusionsThe present study does not find support for the direct link between high levels of maternal depressive symptoms and offspring cortisol levels.

Maternal prenatal social contact during the COVID-19 pandemic predicts infant birth weight

BackgroundSocial connectedness and mental health have been associated with infant birth weight, and both were compromised by the COVID-19 pandemic. AimsWe sought to examine whether changes in maternal prenatal social contact due to the COVID-19 pandemic were associated with infant birth weight and if maternal prenatal mental health mediated this association. Study designA longitudinal study of mothers and their infants born during the first wave of the COVID-19 pandemic. SubjectsThe sample consisted of 282 United States-based mother-infant dyads. Outcome measuresDepressive symptoms were measured with the Beck Depression Inventory-II, anxiety was measured with the State Anxiety Inventory, and stress was measured using the Perceived Stress Scale 14. We also asked participants about pandemic-related changes in social contact across various domains. Adjusted birth weight was calculated from birth records or participant-report when birth records were unavailable. ResultsDecreases in social contact during the pandemic were associated with lower adjusted infant birth weight (B = 76.82, SE = 35.82, p = .035). This association was mediated by maternal prenatal depressive symptoms [Effect = 15.06, 95 % CI (0.19, 35.58)] but not by prenatal anxiety [95 % CI (−0.02, 32.38)] or stress [95 % CI (−0.31, 26.19)]. ConclusionThese findings highlight concerns for both mothers and infants in the wake of the COVID-19 pandemic, since birth weight can have long-term health implications and the social restructuring occasioned by the pandemic may lead to lasting changes in social behavior.

Prenatal Antidepressant Exposure and Offspring Brain Morphologic Trajectory

Clinical decision-making on antidepressant treatment during pregnancy, particularly selective serotonin reuptake inhibitors (SSRIs), is challenging, as both prenatal SSRI exposure and maternal depressive symptoms may be associated with negative outcomes in offspring. To investigate the association between intrauterine SSRI exposure and maternal depressive symptoms and structural brain development in offspring from mid-childhood to early puberty. This prospective, population-based cohort study was embedded in the Generation R Study in Rotterdam, the Netherlands. All pregnant individuals with an expected delivery date between April 1, 2002, and January 31, 2006, were invited to participate. Data were analyzed from February 1 to September 30, 2022. Maternal-reported SSRI use verified by pharmacy records. In mid-pregnancy and 2 and 6 months after delivery, participants reported depressive symptoms using the Brief Symptom Inventory and were divided into 5 groups: SSRI use during pregnancy (n = 41; 80 scans), SSRI use only before pregnancy (n = 77; 126 scans), prenatal depressive symptoms without prenatal SSRI use (n = 257; 477 scans), postnatal depressive symptoms only (n = 74; 128 scans), and nonexposed control individuals (n = 2749; 4813 scans). The main outcome was brain morphometry in offspring, including global and cortical brain volumes, measured at 3 magnetic resonance imaging assessments from 7 to 15 years of age. The study included 3198 mother-child dyads. A total of 3198 mothers (100%) identified as women; mean (SD) age at intake was 31.1 (4.7) years. Children (1670 [52.2%] female) underwent brain imaging assessment from 7 to 15 years of age with 5624 total scans. Most brain gray matter volumes showed an inverted U-shaped trajectory. Compared with nonexposed controls, children prenatally exposed to SSRIs had less cerebral gray matter (β [SE], -20 212.2 [7285.6] mm3; P = .006), particularly within the corticolimbic circuit, which persisted up to 15 years of age. Children exposed to SSRIs prenatally showed a steeper increase in volumes of the amygdala (age interaction: β [SE], 43.3 [13.4] mm3; P = .006) and fusiform gyrus (age interaction: β [SE], 168.3 [51.4] mm3; P = .003) from 7 to 15 years of age. These volumetric differences in the amygdala and fusiform observed in childhood did not persist until early adolescence. Prenatal depression was associated with a smaller volume in the rostral anterior cingulate gyrus (β [SE], -166.3 [65.1] mm3; P = .006), and postnatal depression was associated with a reduced fusiform gyrus (β [SE], -480.5 [189.2] mm3; P = .002). No association of SSRI use before pregnancy with brain outcomes was observed. The results of this cohort study suggest that prenatal SSRI exposure may be associated with altered developmental trajectories of brain regions involved in emotional regulation in offspring. Further research on the functional implications of these findings is needed.

Prenatal depressive symptoms are associated with altered structural brain networks in infants and moderated by infant sleep

BackgroundThe prevalence of prenatal depressive symptoms has more than doubled during the COVID-19 pandemic, raising substantial concerns about child outcomes including sleep problems and altered brain development. The objective of this work was to determine relationships between prenatal depressive symptoms, infant brain network structure, and infant sleep. MethodsPregnant individuals were recruited as part of the Pregnancy during the Pandemic (PdP) study. Maternal depressive symptoms were measured in pregnancy and postpartum. When infants of those participants were 3 months of age (n=66; 26 females), infants underwent diffusion magnetic resonance imaging and infant sleep was evaluated. Using tractography, we calculated structural connectivity matrices for the default mode (DMN) and limbic networks. We examined associations between graph theory metrics of infant brain networks and prenatal maternal depressive symptoms, with infant sleep as a moderator. ResultsPrenatal depressive symptoms were negatively related to average DMN clustering coefficient and local efficiency in infant brains. Infant sleep duration was related to DMN global efficiency and moderated the relationship between prenatal depressive symptoms and density of limbic connections such that infants who slept less had a more negative relationship between prenatal depressive symptoms and local brain connectivity. ConclusionsPrenatal depressive symptoms appear to impact early topological development in brain networks important for emotion regulation. In the limbic network, sleep duration moderated this relationship, suggesting sleep may play a role in infant brain network development.

Maternal Diet Quality and Prenatal Depressive Symptoms: The Moderating Role of Economic Well-Being.

Prenatal depression is prevalent and adversely impacts maternal and infant health. This study addresses a critical literature gap and investigates the association between maternal diet quality and prenatal depressive symptoms, as well as the moderating effect of economic well-being on this link. A cross-sectional design was used, including 43 healthy pregnant women in the second trimester aggregated from two research projects. Prenatal depressive symptoms were assessed using the Edinburgh Postnatal Depression Scale. Dietary quality was evaluated using two non-consecutive 24 h dietary recalls, from which the Adapted Dietary Inflammatory Index (ADII) and the Healthy Eating Index (HEI)-2015 were derived. Economic well-being was indicated by the income-to-poverty ratio. A higher HEI-2015 (adherence to dietary guidelines; β = -0.53, p = 0.01) and negative ADII (anti-inflammatory diet; β = 0.40, p = 0.06) were associated with fewer prenatal depressive symp-toms. Among pregnant women with worse economic well-being, a pro-inflammatory diet was as-sociated with more prenatal depressive symptoms (b = 1.69, p = 0.004), but among those with better economic well-being, the association was not significant (b = 0.51, p = 0.09). Dietary interventions aimed at reducing dietary inflammation might hold some promise for improving mental health among pregnant women who are economically vulnerable.

Investigating the role of relationship satisfaction and paternal psychological distress during pregnancy on offspring health in early life.

The research on the role of father in the foetal programming of health and behaviour has received increasing attention. However, the influences of paternal depressive symptoms and couple relationship satisfaction during pregnancy - potentially mediated via maternal well-being - on the offspring's risk of infections in early life is still seldom assessed. The aim was to investigate if paternal psychological distress during pregnancy is associated with elevated risk of recurrent respiratory infections (RRIs) for offspring at 12 months of age, and whether maternal distress mediates the association between paternal distress and offspring RRIs. The study population was drawn from the nested case-control cohort of the FinnBrain Birth Cohort Study. Children with RRIs (n = 50) were identified by maternal reports at the age of 12 months, whereas mothers did not report RRIs for the comparison group (n = 716). Parental depressive symptoms were measured with the Edinburgh Postnatal Depression Scale and couple relationship satisfaction was measured with the Revised Dyadic Adjustment Scale. The association between paternal depressive symptoms during pregnancy and offspring RRIs was mediated by maternal prenatal depressive symptoms. Additionally, paternal poorer relationship satisfaction was associated with child RRIs independently of maternal distress. The results suggest different pathways through which paternal distress during pregnancy may contribute to elevated risk of offspring RRIs, and more research is needed to study their underlying mechanisms. Paternal distress and couple relationship satisfaction during pregnancy should be assessed and screened as a contributor to offspring health.

Differences in infant negative affectivity during the COVID-19 pandemic.

This longitudinal study compared infant temperament rated at 3 months postpartum by 263 United-States-based women who gave birth during the COVID-19 pandemic and 72 who gave birth prior to the pandemic. All women completed questionnaires assessing perinatal mental health, social contact, and infant temperament. Mothers whose infants were born during the pandemic reported higher levels of infant negative affectivity as compared with mothers whose infants were born earlier (F(1, 324)=18.28, p<.001), but did not differ in their ratings of surgency or effortful control. Maternal prenatal depressive symptoms, prenatal stress, and postpartum stressmediated differences in infant negative affectivity between pandemic and pre-pandemic groups. Within the pandemic group, decreased postpartum social contact was associated with higher ratings of infant negative affectivity. These findings suggest that the pandemic has affected maternal perceptions of infant temperament, perinatal mental health, and social contact.

Prenatal and Postnatal Maternal Depressive Symptoms Are Associated With White Matter Integrity in 5-Year-Olds in a Sex-Specific Manner

BackgroundPrenatal and postnatal maternal psychological distress predicts various detrimental consequences on social, behavioral, and cognitive development of offspring, especially in girls. Maturation of white matter (WM) continues from prenatal development into adulthood and is thus susceptible to exposures both before and after birth. MethodsWM microstructural features of 130 children (mean age, 5.36 years; range, 5.04–5.79 years; 63 girls) and their association with maternal prenatal and postnatal depressive and anxiety symptoms were investigated with diffusion tensor imaging, tract-based spatial statistics, and regression analyses. Maternal questionnaires were collected during first, second, and third trimesters and at 3, 6, and 12 months postpartum with the Edinburgh Postnatal Depression Scale (EPDS) for depressive symptoms and Symptom Checklist-90 for general anxiety. Covariates included child’s sex; child’s age; maternal prepregnancy body mass index; maternal age; socioeconomic status; and exposures to smoking, selective serotonin reuptake inhibitors, and synthetic glucocorticoids during pregnancy. ResultsPrenatal second-trimester EPDS scores were positively associated with fractional anisotropy in boys (p < .05, 5000 permutations) after controlling for EPDS scores 3 months postpartum. In contrast, postpartum EPDS scores at 3 months correlated negatively with fractional anisotropy (p < .01, 5000 permutations) in widespread areas only in girls after controlling for prenatal second-trimester EPDS scores. Perinatal anxiety was not associated with WM structure. ConclusionsThese results suggest that prenatal and postnatal maternal psychological distress is associated with brain WM tract developmental alterations in a sex- and timing-dependent manner. Future studies including behavioral data are required to consolidate associative outcomes for these alterations.

Association of Gestational Diabetes Mellitus and Perinatal Maternal Depression with Early Childhood Behavioral Problems: An Environmental Influences on Child Health Outcomes (ECHO) Study.

This study examined the association of gestational diabetes mellitus (GDM), prenatal, and postnatal maternal depressive symptoms with externalizing, internalizing, and autism spectrum problems on the Preschool Child Behavior Checklist in 2379 children aged 4.12 ± 0.60 (48% female; 47% White, 32% Black, 15% Mixed Race, 4% Asian, <2% American Indian/Alaskan Native, <2% Native Hawaiian; 23% Hispanic). Data were collected from the NIH Environmental influences on Child Health Outcomes (ECHO) Program from 2009-2021. GDM, prenatal, and postnatal maternal depressive symptoms were each associated with increased child externalizing and internalizing problems. GDM was associated with increased autism behaviors only among children exposed to perinatal maternal depressive symptoms above the median level. Stratified analyses revealed a relation between GDM and child outcomes in males only.

Prenatal maternal depressive symptoms are associated with neonatal left amygdala microstructure in a sex-dependent way.

Exposures to prenatal maternal depressive symptoms (PMDS) may lead to neurodevelopmental changes in the offspring in a sex-dependent way. Although a connection between PMDS and infant brain development has been established by earlier studies, the relationship between PMDS exposures measured at various prenatal stages and microstructural alterations in fundamental subcortical structures such as the amygdala remains unknown. In this study, we investigated the associations between PMDS measured during gestational weeks 14, 24 and 34 and infant amygdala microstructural properties using diffusion tensor imaging. We explored amygdala mean diffusivity (MD) alterations in response to PMDS in infants aged 11 to 54 days from birth. PMDS had no significant main effect on the amygdala MD metrics. However, there was a significant interaction effect for PMDS and infant sex in the left amygdala MD. Compared with girls, boys exposed to greater PMDS during gestational week 14 showed significantly higher left amygdala MD. These results indicate that PMDS are linked to infants' amygdala microstructure in boys. These associations may be relevant to later neuropsychiatric outcomes in the offspring. Further research is required to better understand the mechanisms underlying these associations and to develop effective interventions to counteract any potential adverse consequences.

Self-objectification during the perinatal period: The role of body surveillance in maternal and infant wellbeing.

Pregnancy represents a unique time during which women's bodies undergo significant physical changes (e.g., expanding belly, larger breasts, weight gain) that can elicit increased objectification. Experiences of objectification set the stage for women to view themselves as sexual objects (i.e., self-objectification) and is associated with adverse mental health outcomes. Although women may experience heightened self-objectification and behavioral consequences (such as body surveillance) due to the objectification of pregnant bodies in Western cultures, there are remarkably few studies examining objectification theory among women during the perinatal period. The present study investigated the impact of body surveillance, a consequence of self-objectification, on maternal mental health, mother-infant bonding, and infant socioemotional outcomes in a sample of 159 women navigating pregnancy and postpartum. Utilizing a serial mediation model, we found that mothers who endorsed higher levels of body surveillance during pregnancy reported more depressive symptoms and body dissatisfaction, which were associated with greater impairments in mother-infant bonding following childbirth and more infant socioemotional dysfunction at 1-year postpartum. Maternal prenatal depressive symptoms emerged as a unique mechanism through which body surveillance predicted bonding impairments and subsequent infant outcomes. Results highlight the critical need for early intervention efforts that not only target general depression, but also promote body functionality and acceptance over the Western "thin ideal" of attractiveness among expecting mothers.

Maternal Prenatal Distress, Maternal Pre- and Postnatal Bonding and Behavioral and Emotional Problems in Toddlers. A Secondary Analysis of the IRIS Study

Maternal prenatal distress (i.e., anxiety and depressive symptoms) increases the risk for childhood behavioral and emotional problems. So far, the potential role of maternal bonding in this association still needs further study. Maternal prenatal distress can affect the development of maternal bonding from pregnancy onwards. Maternal prenatal and postnatal bonding in turn have been shown to predict child behavioral functioning. We aimed to investigate whether maternal prenatal and postnatal bonding mediate the association between maternal prenatal distress and toddlers’ internalizing and externalizing problems. Data from a Dutch prospective longitudinal sample (N = 666) were used to conduct single and multiple mediation models. Mothers reported prenatal anxiety (State Anxiety Inventory) and prenatal depressive symptoms (Edinburgh Postnatal Depression Scale) at 24 weeks’ gestation and maternal prenatal bonding (Maternal Antenatal Attachment Scale) at 32 weeks’ gestation. At 6 weeks and 6 months postpartum mothers completed questionnaires to assess maternal postnatal bonding (Maternal Postnatal Attachment Scale). Mothers reported child internalizing and externalizing problems (Child Behavior Checklist) at 28 months postpartum. Maternal prenatal and postnatal bonding mediated the link between maternal prenatal anxiety and child externalizing problems but not internalizing problems. Only maternal bonding 6 months postpartum mediated the link between maternal prenatal depressive symptoms and child internalizing problems but not externalizing problems. Our study showed that maternal postnatal bonding more consistently mediated links between measures of maternal prenatal distress and child behavioral and emotional problems than maternal prenatal bonding. Interventions reducing maternal prenatal distress and promoting maternal bonding should be developed.

Maternal Pre-Pregnancy BMI and Gestational Weight Gain Modified the Association between Prenatal Depressive Symptoms and Toddler's Emotional and Behavioral Problems: A Prospective Cohort Study.

Background: Maternal prenatal depressive symptoms and abnormal pre-pregnancy BMI have been scarcely reported to play interactive effects on child health. In this prospective cohort, we aimed to examine the interactive effects of maternal prenatal depressive symptoms and pre-pregnancy BMI as well as gestational weight gain (GWG) on offspring emotional and behavioral problems (EPBs). Methods: The study samples comprised 1216 mother−child pairs from Shanghai Maternal−Child Pairs Cohort recruited from 2016 to 2018. Maternal pre-pregnancy BMI and GWG were obtained from medical records, and maternal depressive symptoms were assessed via the Center for Epidemiological Studies Depression Scale (CES-D) at 32−36 gestational weeks. The child completed the behavioral measurement via the Strengths and Difficulties Questionnaire (SDQ) at 24 months postpartum. Results: There were 12.01% and 38.65% women with prenatal depressive symptoms and sub-threshold depressive symptoms during late pregnancy. Both maternal depressive symptoms and prenatal sub-threshold depressive symptoms were associated with higher internalizing (OR = 1.69, 95% CI, 1.05−2.72; OR = 1.48, 95% CI, 1.06−2.07) and externalizing (OR = 2.06, 95% CI, 1.30−3.25; OR = 1.42, 95% CI, 1.02−1.99) problems in children. Maternal pre-pregnancy BMI and GWG modified the association between prenatal depressive symptoms and child externalizing or total difficulties problems (p < 0.10 for interaction). Among the overweight/obese pregnant women, maternal prenatal depressive symptoms were associated with a higher risk of externalizing problems (OR = 2.75, 95% CI, 1.06−7.11) in children. Among the women who gained inadequate GWG, maternal prenatal sub-threshold depressive symptoms were associated with 2.85-fold (95% CI 1.48−5.48) risks for child externalizing problems, and maternal depressive symptoms were associated with higher externalizing and total difficulties problems (OR = 4.87, 95% CI, 2.03−11.70 and OR = 2.94, 95% CI, 1.28−6.74, respectively), but these associations were not significant in the appropriate or excessive GWG group. Conclusions: Both maternal prenatal sub-threshold depressive symptoms and depressive symptoms increased the risks of child internalizing and externalizing problems at 24 months of age, while the effects on child externalizing problems were stronger among overweight/obese or inadequate GWG pregnant women. Our study highlights the importance of simultaneously controlling the weight of pregnant women before and throughout pregnancy and prompting mental health in pregnant women, which might benefit their offspring’s EBPs.

Maternal Prenatal Depressive Symptoms and Infant Sleep Problems: The Role of Infant Temperament and Sex

ABSTRACT Objectives We aimed to analyze whether (1) infant temperament mediates the impact of maternal prenatal depressive symptoms on infant sleep problems and (2) the mediation role of infant temperament was moderated by the infant’s sex. Methods The sample was comprised of 172 mother-infant dyads. Mothers completed self-reported measures of prenatal and postnatal depressive symptoms, infant temperament (negative affectivity, surgency/extraversion, and orienting regulation), and sleep problems. Results While controlling for maternal postnatal depressive symptoms, our results revealed that (1) infant negative affectivity at two weeks partially mediated the impact of maternal prenatal depressive symptoms on sleep anxiety at six months, and (2) this mediation is independent of the infant’s sex. Conclusions Our findings provided evidence that negative affectivity can be an early specific marker of sleep anxiety and can partially explain the negative impact of maternal prenatal depressive symptoms on further sleep problems in the infant.

Maternal Early Life Adversity and Infant Stress Regulation: Intergenerational Associations and Mediation by Maternal Prenatal Mental Health

Early life adversity is a potent risk factor for poor mental health outcomes across the lifespan, including offspring vulnerability to psychopathology. Developmentally, the prenatal period is a sensitive window in which maternal early life experiences may influence offspring outcomes and demarcates a time when expectant mothers and offspring are more susceptible to stressful and salutary influences. This prenatal plasticity constituted the focus of the current study where we tested the association of maternal early life adversity with infant stress regulation through maternal prenatal internalizing symptoms and moderation by prenatal social support. Mother-infant dyads (n = 162) were followed prospectively and mothers completed assessments of social support and depressive and anxiety symptoms across pregnancy. Infants completed standardized stress paradigms at one month and six months. There were several key findings. First, maternal prenatal depressive symptoms significantly mediated predictions of infant cortisol reactivity to the heel stick at one month from maternal early life adversity: specifically, maternal early life adversity positively predicted depressive symptoms in pregnancy, which in turn predicted dampened infant cortisol reactivity. Second, prenatal social support did not significantly moderate predictions of depressive or anxiety symptoms in pregnancy from maternal early life adversity nor did it alter the associations of maternal depressive or anxiety symptoms with infant stress regulation. These results suggest that maternal prenatal mental health is a key mechanism by which maternal early life adverse experiences affect offspring risk for psychopathology. We discuss potential clinical and health implications of dysregulated infant cortisol reactivity with respect to lifespan development.