Fetal exposure to prenatal stress can increase risk for psychopathology but postnatal caregiving may offset risk. This study tests whether maternal sensitivity and the home environment during early childhood modify associations of prenatal stress with offspring behavior in a sample of 127 mother–child pairs (n = 127). Mothers reported on perceived stress during pregnancy. Maternal sensitivity was rated by coders during a parent–child free play task when children were 4 years old. One year later, mothers reported on the home environment, child internalizing and externalizing behaviors, and children completed an assessment of inhibitory control. As hypothesized, the early childhood caregiving environment modified associations of prenatal stress with child behavior. Specifically, prenatal stress was associated with more internalizing behaviors at lower levels of maternal sensitivity and in home environments that were lower in emotional support and cognitive stimulation, but not at mean or higher levels. Furthermore, prenatal stress was associated with lower inhibitory control only at lower levels of maternal sensitivity, but not at higher levels. Maternal sensitivity and an emotionally supportive and cognitively stimulating home environment in early childhood may be important factors that mitigate risk for mental health problems among children exposed to prenatal stress.

Prenatal stress has a significant, but small, negative effect on children’s executive function (EF) in middle and high socioeconomic status (SES) households. Importantly, rates and severity of prenatal stress are higher and protective factors are reduced in lower SES households, suggesting prenatal stress may be particularly detrimental for children’s EF in this population. This study examined whether prenatal stress was linked to 5-year-old’s EF in a predominantly low SES sample and child sex moderated this association, as males may be more vulnerable to adverse prenatal experiences. Participants were 132 mother-child dyads drawn from a prospective prenatal cohort. Mothers reported on their depression symptoms, trait anxiety, perceived stress, everyday discrimination, and sleep quality at enrollment and once each trimester, to form a composite prenatal stress measure. Children’s EF was assessed at age 5 years using the parent-report Behavior Rating Inventory of Executive Function - Preschool (BRIEF-P) Global Executive Composite subscale and neuropsychological tasks completed by the children. Mixed models revealed higher prenatal stress was associated with lower BRIEF-P scores, indicating better EF, for females only. Higher prenatal stress was associated with lower performance on neuropsychological EF measures for both males and females. Results add to the limited evidence about prenatal stress effects on children’s EF in low SES households.

Prenatal maternal stress and mental health problems are known to increase risk for developmental psychopathology in offspring, yet pathways leading to risk or resiliency are poorly understood. In a quasi-experimental design, we prospectively examined associations between disaster-related prenatal stress, maternal mental health symptoms, and infant temperament outcomes. Mothers who were pregnant during Hurricane Harvey (N = 527) reported on objective hardships (e.g., loss of belongings or income, evacuation, home flooding) related to the storm and subsequent mental health symptoms (anxiety/depression, posttraumatic stress) across time. At a postpartum assessment, mothers reported on their infant’s temperament (negative affect, positive affect, orienting/regulatory capacity). Greater objective hardship indirectly predicted higher levels of infant orienting/regulatory capacity through its association with increased maternal posttraumatic stress symptoms. Greater objective hardship also indirectly predicted higher levels of infant negative affect through its association with increased maternal anxiety/depression symptoms across time. Our findings suggest a psychological mechanism linking prenatal stress with specific temperamental characteristics via maternal mental health symptoms. Findings point to the importance of high-quality assessment and mental health services for vulnerable women and young children.

Prenatal adversity has been linked to later psychopathology. Yet, research on cumulative prenatal adversity, as well as its interaction with offspring genotype, on brain and behavioral development is scarce. With this study, we aimed to address this gap. In Finnish mother–infant dyads, we investigated the association of a cumulative prenatal adversity sum score (PRE-AS) with (a) child emotional and behavioral problems assessed with the Strengths and Difficulties Questionnaire at 4 and 5 years (N = 1568, 45.3% female), (b) infant amygdalar and hippocampal volumes (subsample N = 122), and (c) its moderation by a hippocampal-specific coexpression polygenic risk score based on the serotonin transporter (SLC6A4) gene. We found that higher PRE-AS was linked to greater child emotional and behavioral problems at both time points, with partly stronger associations in boys than in girls. Higher PRE-AS was associated with larger bilateral infant amygdalar volumes in girls compared to boys, while no associations were found for hippocampal volumes. Further, hyperactivity/inattention in 4-year-old girls was related to both genotype and PRE-AS, the latter partially mediated by right amygdalar volumes as preliminary evidence suggests. Our study is the first to demonstrate a dose-dependent sexually dimorphic relationship between cumulative prenatal adversity and infant amygdalar volumes.

For mother-infant health especially, the pandemic has brought multiple stressors inside a susceptible psychobiological system. We study the longitudinal associations between maternal prenatal and postpartum: (a) COVID-19 stressful events exposure, (b) pandemic psychological stress, and (c) mental health and infants’ negative affect. A sample of 643 Italian pregnant women completed a web-based survey from April 8th to May 4th, 2020 and a follow-up at 6 months after delivery. Maternal assessment covered prenatal and postpartum measures for: COVID-19 stressful events exposure, pandemic psychological stress, mental health symptoms (i.e., depression, anxiety, posttraumatic stress disorder) and postpartum, social support and report of infants’ negative affect. Maternal mental health symptoms during pregnancy, at the peak of pandemic, is longitudinally associated with infant negative affect, with postpartum mental health mediating this association. Also, maternal COVID-19 stressful events exposure in postpartum is associated with negative affect at 6 months mediated by postpartum mental health symptoms. Maternal pandemic psychological stress during pregnancy predicted mental health symptoms in postpartum. The study supports the association between pandemic-related maternal health across pregnancy and postpartum and offspring’s development (i.e., negative affect). It also puts the spotlight on mental health risk in women experiencing lockdown during pregnancy, especially when feeling high psychological stress in pregnancy or when directly exposed to COVID-19 stressful events postpartum.

In Canada, the 2014 Code of Practice for the Care and Handling of Pigs proposed the continued operation of existing stall barns after 2024 on condition that bred sows be given access to periodic exercise. Therefore, this study evaluated the effects of periodic exercise on sow welfare. Sows (n = 180) were assigned to one of three treatments: stall-housed (Control: C); stall-housed and exercised weekly for 10 min (Exercise: E); and group-housed (Group: G). Sow postures and stereotypies were recorded once per week in early, mid and late gestation before (AM) and after (PM) exercise. Female piglets (n = 168 from C, E and G sows) underwent isolation and novel object tests at 19-22 days of age. Postures differed by treatment in AM with G sows lying more and sitting less than C and E sows, which did not differ. In PM, E sows sat more than G sows, with C sows being intermediate. In early gestation, G sows performed fewer stereotypies than E sows, with C sows being intermediate. In mid gestation, G sows performed fewer stereotypies than C and E sows, which did not differ. Piglets from C sows were more active in the novel object test than E and G piglets, which did not differ. Group housing improved sow comfort (indicated by postures) and reduced sow stress (indicated by stereotypies), but periodic exercise did not. Decreased activity level in piglets from sows given greater freedom of movement indicates that gestation housing can influence the behaviour of offspring.

In summer 2014, southern Israel experienced rocket attacks from the Hamas-ruled Gaza strip on a nearly daily basis for over 50 consecutive days. We exploit this unexpected escalation in the Israeli-Palestinian conflict and variation across localities in Israel in the amount of sirens that warned of rocket attacks to measure the effect of conflict intensity on birth weight and gestation length among pregnant women during this period. In addition to the common notion that conflict intensity induces stress and anxiety, we show changes in prenatal care in response to sirens. This maternal behavioral response varies based on socioeconomic status, which ultimately differentially affected birth outcomes. While mothers ranked high socioeconomically likely had the resources to increase their prenatal care and shield their fetuses from the negative shock of sirens, mothers ranked low socioeconomically did not have these resources and even decreased prenatal care.

Children exposed to prenatal maternal psychological distress are at elevated risk for a range of adverse outcomes; however, it remains poorly understood whether postnatal influences can ameliorate impairments related to prenatal distress. The current study evaluated if sensitivematernal care during the first postnatal year could mitigate child cognitive and emotional impairments associated with prenatal psychological distress. Prenatal maternal psychological distress was assessed via self-reports of anxiety, depression, and perceived stress for 136 mothers at five prenatal and four postpartum time points. Quality of maternal care (sensitivity to nondistress, positive regard, and intrusiveness reverse-scored) were assessed during a mother–child play interaction at 6 and 12 months. Child cognitive function and negative emotionality were assessed at 2 years, using The Bayley Scales and the Early Childhood Behavior Questionnaire. Elevated prenatal distress was associated with poorer child cognitive function and elevated negative emotionality. Children exposed to elevated prenatal maternal distress did not, however, display these outcomes if they received high-quality caregiving. Specifically, maternal care moderated the relation between prenatal psychological distress and child cognitive function and negative emotionality. This association remained after consideration of postnatal maternal psychological distress and relevant covariates. Sensitive maternal care was associated with altered offspring developmental trajectories, supporting child resilience following prenatal distress exposure.

The COVID-19 pandemic is a global traumatic experience for citizens, especially during sensitive time windows of heightened plasticity such as pregnancy and neonatal life. Pandemic-related stress experienced by mothers during pregnancy may act as an early risk factor for infants’ regulatory capacity development by altering maternal psychosocial well-being (e.g., increased anxiety, reduced social support) and caregiving environment (e.g., greater parenting stress, impaired mother–infant bonding). The aim of the present longitudinal study was to assess the consequences of pandemic-related prenatal stress on infants’ regulatory capacity. A sample of 163 mother–infant dyads was enrolled at eight maternity units in northern Italy. They provided complete data about prenatal stress, perceived social support, postnatal anxiety symptoms, parenting stress, mother–infant bonding, and infants’ regulatory capacity at 3 months of age. Women who experienced emotional stress and received partial social support during pregnancy reported higher anxious symptoms. Moreover, maternal postnatal anxiety was indirectly linked to the infants’ regulatory capacity at 3 months, mediated by parenting stress and mother–infant bonding. Dedicated preventive interventions should be delivered to mothers and should be focused on protecting the mother–infant dyad from the detrimental effects of pandemic-related stress during the COVID-19 healthcare emergency.

Prenatal insults during fetal development result in increased likelihood of developing chronic disease. Obesity, the biggest risk factor for the development of metabolic disease, is affected by several genetic and environmental factors. High-fat diet (HFD) consumption is usually linked with the development of obesity. The main goal of this study was to analyze the impact of the exposure to a HFD in prenatally stressed animals. For this purpose, we subjected pregnant BALB/c mice to restraint stress for 2 h a day between gestational day (GD) 14 and GD 21. Prenatally stressed and control offspring of both sexes were postnatally exposed to a HFD for 24 weeks. We found that prenatal stress (PS) per se produced disturbances in males such as increased total blood cholesterol and triglycerides, with a decrease in mRNA expression of sirtuin-1. When these animals were fed a HFD, we observed a rise in glucose and insulin levels and an increase in visceral adipose tissue gene expression of leptin, resistin, and interleukin-1 beta. Although females proved to be more resilient to PS consequences, when they were fed a HFD, they showed significant metabolic impairment. In addition to the changes observed in males, females also presented an increase in body weight and adiposity and a rise in cholesterol levels.

Exposure to adverse childhood experiences (ACEs) is not only associated with one's adverse health outcomes in adulthood but also increases the risk of child developmental problems in offspring. However, the mechanisms involved in the transmission of the effects of maternal ACEs to the offspring largely remain unexplored. This study sought to identify possible psychosocial pathways of intergenerational effects of maternal ACEs on child development at 6 months. Data from a longitudinal study on maternal childhood adversity and maternal psychosocial risk during pregnancy as well as maternal mental health problems and child development at 6 months postnatal were used. Structural equation modeling with bootstrapping was used to estimate the indirect effects of maternal ACEs on child development at 6 months. The model showed that maternal ACEs indirectly influenced offspring's development via maternal stressful events during pregnancy and pre- and postnatal mental health problems. This finding highlights the possible interventions at the prenatal and postnatal periods. Early identification of women who have ACEs or who are at psychosocial risk during pre- and postnatal periods is critical to provide interventions to buffer those negative effects on offspring's development. Future studies are needed to longitudinally assess the effects of maternal ACEs on child development over time.

Very little work has examined potential moderating effects in the link between prenatal intimate partner violence (IPV) and infant adjustment, especially in the first critical weeks following delivery. The current study evaluated the protective role of breastfeeding in the relationship between prenatal IPV and infant temperament at 4 months. Pregnant women (n = 82) were interviewed during pregnancy and at 6 weeks and 4 months postpartum. It was hypothesized that (a) prenatal IPV would predict infant temperament outcomes at the 4-month postpartum visit, and (b) breastfeeding continuation at 6 weeks acts as a protective factor such that breastfed infants will be less affected by the risk posed by prenatal IPV. Results indicated direct and negative effects of prenatal IPV on positive affectivity/surgency and orienting/regulatory capacity at 4 months. A significant moderating effect of breastfeeding at 6 weeks postpartum was identified. Mothers who were not breastfeeding at 6 weeks postpartum demonstrated the expected negative relationship between prenatal IPV exposure and infant adjustment, but if mothers were breastfeeding at 6 weeks postpartum, the relationship between IPV exposure and infant positive affectivity/surgency and orienting/regulatory capacity was not significantly different from zero. Results indicate a significant protective effect of breastfeeding in the intergenerational transmission of risk for infants born to mothers exposed to IPV.

Recent findings highlight that there are prenatal risks for affective disorders that are mediated by glucocorticoid mechanisms, and may be specific to females. There is also evidence of sex differences in prenatal programming mechanisms and developmental psychopathology, whereby effects are in opposite directions in males and females. As birth weight is a risk for affective disorders, we sought to investigate whether maternal prenatal cortisol may have sex-specific effects on fetal growth. Participants were 241 mothers selected from the Wirral Child Health and Development Study (WCHADS) cohort (n=1233) using a psychosocial risk stratifier, so that responses could be weighted back to the general population. Mothers provided saliva samples, which were assayed for cortisol, at home over 2 days at 32 weeks gestation (on waking, 30-min post-waking and during the evening). Measures of infant birth weight (corrected for gestational age) were taken from hospital records. General population estimates of associations between variables were obtained using inverse probability weights. Maternal log of the area under the curve cortisol predicted infant birth weight in a sex-dependent manner (interaction term P=0.029). There was a positive and statistically significant association between prenatal cortisol in males, and a negative association in females that was not statistically significant. A sex interaction in the same direction was evident when using the waking (P=0.015), and 30-min post-waking (P=0.013) cortisol, but not the evening measure. There was no interaction between prenatal cortisol and sex to predict gestational age. Our findings add to an emerging literature that suggests that there may be sex-specific mechanisms that underpin fetal programming.

Maternal stress has been linked to low birth weight in newborns. One potential pathway involves epigenetic changes at candidate genes that may mediate the effects of prenatal maternal stress on birth weight. This relationship has been documented in stress-related genes, such as NR3C1. There is less literature exploring the effect of stress on growth-related genes. IGF1 and IGF2 have been implicated in fetal growth and development, though via different mechanisms as IGF2 is under imprinting control. In this study, we tested for associations between prenatal stress, methylation of IGF1 and IGF2, and birth weight. A total of 24 mother–newborn dyads in the Democratic Republic of Congo were enrolled. Ethnographic interviews were conducted with mothers at delivery to gather culturally relevant war-related and chronic stressors. DNA methylation data were generated from maternal venous, cord blood and placental tissue samples. Multivariate regressions were used to test for associations between stress measures, DNA methylation and birth weight in each of the three tissue types. We found an association between IGF2 methylation in maternal blood and birth weight. Previous literature on the relationship between IGF2 methylation and birth weight has focused on methylation at known differentially methylated regions in cord blood or placental samples. Our findings indicate there may be links between the maternal epigenome and low birth weight that rely on mechanisms outside known imprinting pathways. It thus may be important to consider the effect of maternal exposures and epigenetic profiles on birth weight even in the setting of maternally imprinted genes such as IGF2.

Prenatal stress and prenatal nutrition each have demonstrable impact on fetal development, with implications for child neurodevelopment and behavior. However, few studies have examined their joint influences despite evidence of potential interactive effects. We examined associations among prenatal stress, prenatal antioxidant intakes, and child temperament in a sociodemographically diverse pregnancy cohort (N=137 mother–child dyads). In mid-pregnancy, mothers completed an assessment of recent negative life events as a measure of prenatal stress and an assessment of prenatal diet. When the children were 30 months of age, mothers completed the Early Childhood Behavior Questionnaire-Very Short form, which provides scores on child Negative Affectivity, Effortful Control, and Surgency/Extraversion. Linear regressions tested associations between maternal prenatal negative life events and child temperament, and effect modification by maternal prenatal antioxidant intakes (vitamins A, C, and E, magnesium, zinc, selenium, β-carotene). Analyses revealed that increased maternal prenatal negative life events were associated with higher child Negative Affectivity (β=0.08, P=0.009) but not with child Effortful Control (β=−0.03, P=0.39) or Surgency/Extraversion (β=0.04, P=0.14). Prenatal intakes of zinc and selenium modified this effect: Maternal exposure to prenatal negative life events was associated with higher child Negative Affectivity in the presence of lower intakes of zinc and selenium. Modification effects approached significance for vitamins A and C. The results suggest that the combination of elevated stress exposures and lower antioxidant intakes in pregnancy increases the likelihood of heightened child temperamental negative affectivity. Increased antioxidant intakes during pregnancy may protect against influences of prenatal stress on child temperament.

Intrauterine growth restriction (IUGR) and maternal stress during pregnancy are two compromises that negatively impact neurodevelopment and increase the risk of developing later life neuropsychiatric disorders such as schizophrenia, depression and behavioural disorders. Neurosteroids, particularly allopregnanolone, are important in protecting the developing brain and promoting many essential neurodevelopmental processes. Individually, IUGR and prenatal stress (PS) reduce myelination and neurogenesis within affected fetal brains, however less information is available on the combined effects of these two disorders on the term fetal brain. This study aimed to investigate how IUGR and PS impairs the neurosteroid pathway when combined using a guinea pig model, and how these then disrupt the neurodevelopment of the fetus. Uterine artery blood flow restriction was performed at GA30-35 to induce growth restriction, whilst PS was induced by exposure of the dam to a strobe light during gestation commencing GA40 and repeated every 5 days. Exposure in this model caused reductions in hippocampal CA1 MBP immunostaining of male fetuses in both IUGR alone and IUGR+PS paradigms but only by IUGR in the subcortical white mater, compared with control males. Plasma allopregnanolone was reduced by both stressors irrespective of sex, whereas GFAP or MAP2 expression were not affected by either stressor. Female neurodevelopment, as assessed by these markers, was unimpeded by these compromises. The addition of prenatal stress did not further compound these deficits.