Prenatal Adversity Research Articles

Prenatal and Childhood Adverse Events and Child Brain Morphology: A Population-Based Study

Prenatal and childhood adverse events have been shown to be related to children’s cognitive and psychological development. However, the influence of early-life adversities on child brain morphology is not well understood, and most studies are based on small samples and often examine only one adversity. Thus, the goal of our study is to examine the relationship between cumulative exposures to prenatal and childhood adversities and brain morphology in a large population-based study. Participants included 2,993 children from the Generation R Study, a cohort of children growing up in Rotterdam, the Netherlands. Recruitment was initiated between 2002 and 2006, and the study is currently performing the 17- to 19-year follow-up wave. Prenatal adversities were reported by mothers at 20–25 weeks of pregnancy, and the child’s lifetime exposure to adversities was reported by mothers when the children were 10 years old. The total brain, gray and white matter volumes, and the volume of the cerebellum, amygdala, and hippocampus were assessed with magnetic resonance imaging when children were 10 years old. In total, 36% of children had mothers who were exposed to at least one adversity during pregnancy and 35% of children were exposed to adversities in childhood. In our study sample, the cumulative number of prenatal adversities was not related to any brain outcome. In contrast, per each additional childhood adverse event, the total brain volume was 0.07 standard deviations smaller (SE = 0.02, p = 0.001), with differences in both gray and white matter volumes. Childhood adversities were not related to the amygdala or hippocampal volumes. Additionally, the link between childhood events and the preadolescent brain was not modified by prenatal events and was not explained by maternal psychopathology. Our results suggest that childhood adversities, but not prenatal adverse events, are associated with smaller global brain volumes in preadolescence. Notably, this is the first large population-based study to prospectively assess the association between the cumulative number of prenatal adversities and the preadolescent brain morphology. The study findings extend the evidence from high-risk samples, providing support for a link between cumulative childhood adverse events and brain morphology in children from the general population.

Impact of prenatal and childhood adversity\xa0effects around World War II on multimorbidity: results from the KORA-Age study

BackgroundWhile risk factors for age-related diseases may increase multimorbidity (MM), early life deprivation may also accelerate the development of chronic diseases and MM.MethodsThis study explores the prevalence and pattern of MM in 65–71 year-old individuals born before, during, and after World War II in Southern Germany based on two large cross-sectional KORA (Cooperative Health Research in the Region of Augsburg) -Age studies in 2008/9 and 2016. MM was defined as having at least two chronic diseases, and birth periods were classified into five phases: pre-war, early war, late war, famine, and after the famine period. Logistic regression models were used to analyze the effect of the birth phases on MM with adjustment for sociodemographic and lifestyle risk factors. Furthermore, we used agglomerative hierarchical clustering to investigate the co-occurrence of diseases.ResultsParticipants born during the late war phase had the highest prevalence of MM (62.2%) and single chronic diseases compared to participants born during the other phases. Being born in the late war phase was significantly associated with a higher odds of MM (OR = 1.83, 95% CI: 1.15–2.91) after adjustment for sociodemographic and lifestyle factors. In women, the prevalence of joint, gastrointestinal, eye diseases, and anxiety was higher, while heart disease, stroke, and diabetes were more common in men. Moreover, three main chronic disease clusters responsible for the observed associations were identified as: joint and psychosomatic, cardiometabolic and, other internal organ diseases.ConclusionsOur findings imply that adverse early-life exposure may increase the risk of MM in adults aged 65–71 years. Moreover, identified disease clusters are not coincidental and require more investigation.

In support of the placental programming hypothesis: Placental endocrine insufficiency programs atypical behaviour in mothers and their offspring

New Findings What is the topic of this review? More than half of all pregnancies in the UK are exposed to adversity linked to increased problems in pregnancy for mothers and adverse outcomes for their children, but we do not know the mechanism(s) underpinning these relationships. What advances does it highlight? Studies in mice prove that placental endocrine insufficiency driven by genetic manipulation of imprinted genes in the offspring can concurrently drive fetal growth restriction, alterations in maternal caregiving and aberrant behaviour in wild‐type offspring exposed to an adverse environment. This suggests that placental endocrine insufficiency might contribute to the co‐morbidity of low birth weight, maternal depression and neurodevelopmental disorders observed in human populations. Prenatal adversity, which is estimated to impact more than half of all pregnancies in the UK, compromises fetal growth and increases the chances of stillbirth, prematurity and infant mortality. Beyond these immediate and highly visible problems, infants that survive carry the invisible burden of increased risk of some of the most common and pervasive diseases that impact human populations. In utero exposure to depression and anxiety is one adversity that has been linked to these poorer outcomes, suggesting that maternal mood disorders drive the outcomes. However, recent studies in animal models suggest that both the maternal mood disorders and the detrimental outcomes for children could be the result of the same underlying placental pathology. In these studies, genetically wild‐type rodent mothers exposed to placental endocrine insufficiency engaged in less pup‐focused behaviours and less self‐care. Genetically wild‐type rodent offspring raised in this abnormal environment exhibited increased anxiety‐like behaviours, with male offspring additionally exhibiting deficits in cognition and atypical social behaviour, with some evidence of depressive‐like symptoms. This work establishes experimentally that placental endocrine insufficiency alone is sufficient to drive atypical behaviour in both mothers and their offspring. Although there are some data to suggest that this phenomenon is relevant to human pregnancy, considerably more work is required.

Supplemental Material for Prenatal Distress Links Maternal Early Life Adversity to Infant Stress Functioning in the Next Generation

Supplemental Material for Prenatal Distress Links Maternal Early Life Adversity to Infant Stress Functioning in the Next Generation

Cognitive Development and Brain Gray Matter Susceptibility to Prenatal Adversities: Moderation by the Prefrontal Cortex Brain-Derived Neurotrophic Factor Gene Co-expression Network.

Background: Previous studies focused on the relationship between prenatal conditions and neurodevelopmental outcomes later in life, but few have explored the interplay between gene co-expression networks and prenatal adversity conditions on cognitive development trajectories and gray matter density.Methods: We analyzed the moderation effects of an expression polygenic score (ePRS) for the Brain-derived Neurotrophic Factor gene network (BDNF ePRS) on the association between prenatal adversity and child cognitive development. A score based on genes co-expressed with the prefrontal cortex (PFC) BDNF was created, using the effect size of the association between the individual single nucleotide polymorphisms (SNP) and the BDNF expression in the PFC. Cognitive development trajectories of 157 young children from the Maternal Adversity, Vulnerability and Neurodevelopment (MAVAN) cohort were assessed longitudinally in 4-time points (6, 12, 18, and 36 months) using the Bayley-II mental scales.Results: Linear mixed-effects modeling indicated that BDNF ePRS moderates the effects of prenatal adversity on cognitive growth. In children with high BDNF ePRS, higher prenatal adversity was associated with slower cognitive development in comparison with those exposed to lower prenatal adversity. Parallel-Independent Component Analysis (pICA) suggested that associations of expression-based SNPs and gray matter density significantly differed between low and high prenatal adversity groups. The brain IC included areas involved in visual association processes (Brodmann area 19 and 18), reallocation of attention, and integration of information across the supramodal cortex (Brodmann area 10).Conclusion: Cognitive development trajectories and brain gray matter seem to be influenced by the interplay of prenatal environmental conditions and the expression of an important BDNF gene network that guides the growth and plasticity of neurons and synapses.

Prenatal Adversity Alters the Epigenetic Profile of the Prefrontal Cortex: Sexually Dimorphic Effects of Prenatal Alcohol Exposure and Food-Related Stress.

Prenatal adversity or stress can have long-term consequences on developmental trajectories and health outcomes. Although the biological mechanisms underlying these effects are poorly understood, epigenetic modifications, such as DNA methylation, have the potential to link early-life environments to alterations in physiological systems, with long-term functional implications. We investigated the consequences of two prenatal insults, prenatal alcohol exposure (PAE) and food-related stress, on DNA methylation profiles of the rat brain during early development. As these insults can have sex-specific effects on biological outcomes, we analyzed epigenome-wide DNA methylation patterns in prefrontal cortex, a key brain region involved in cognition, executive function, and behavior, of both males and females. We found sex-dependent and sex-concordant influences of these insults on epigenetic patterns. These alterations occurred in genes and pathways related to brain development and immune function, suggesting that PAE and food-related stress may reprogram neurobiological/physiological systems partly through central epigenetic changes, and may do so in a sex-dependent manner. Such epigenetic changes may reflect the sex-specific effects of prenatal insults on long-term functional and health outcomes and have important implications for understanding possible mechanisms underlying fetal alcohol spectrum disorder and other neurodevelopmental disorders.

Prenatal adversity drives placental endocrine insufficiency impacting maternal caregiving and offspring behaviour

Prenatal adversity drives placental endocrine insufficiency impacting maternal caregiving and offspring behaviour

Maternal Prenatal Anxiety and the Fetal Origins of Epigenetic Aging

BackgroundThe fetal origins of mental health is a well-established framework that currently lacks a robust index of the biological embedding of prenatal adversity. The Pediatric-Buccal-Epigenetic (PedBE) clock is a novel epigenetic tool that associates with aspects of the prenatal environment, but additional validation in longitudinal datasets is required. Likewise, the relationship between prenatal maternal mental health and the PedBE clock has not been described. MethodsLongitudinal cohorts from the Netherlands (Basal Influences on Baby Development [BIBO] n = 165) and Singapore (Growing Up in Singapore Towards Healthy Outcomes [GUSTO] n = 340) provided data on prenatal maternal anxiety and longitudinal assessments of buccal cell–derived genome-wide DNA methylation assessed at 6 and 10 years of age in BIBO, and at 3, 9, and 48 months of age in GUSTO. Measures of epigenetic age acceleration were calculated using the PedBE clock and benchmarked against an established multi-tissue epigenetic predictor. ResultsPrenatal maternal anxiety predicted child PedBE epigenetic age acceleration in both cohorts, with effects largely restricted to males and not females. These results were independent of obstetric, socioeconomic, and genetic risk factors, with a larger effect size for prenatal anxiety than depression. PedBE age acceleration predicted increased externalizing symptoms in males from mid- to late childhood in the BIBO cohort only. ConclusionsThese findings point to the fetal origins of epigenetic age acceleration and reveal an increased sensitivity in males. Convergent evidence underscores the societal importance of providing timely and effective mental health support to pregnant individuals, which may have lasting consequences for both mother and child.

The Interplay Between Prenatal Adversity, Offspring Dopaminergic Genes, and Early Parenting on Toddler Attentional Function.

Background: Few studies have explored the complex gene-by-prenatal environment-by-early postnatal environment interactions that underlie the development of attentional competence. Here, we examined if variation in dopamine-related genes interacts with prenatal adversity to influence toddler attentional competence and whether this influence is buffered by early positive maternal behavior.Methods: From the Maternal Adversity, Vulnerability and Neurodevelopment cohort, 134 participants (197 when imputing missing data) had information on prenatal adversity (prenatal stressful life events, prenatal maternal depressive symptoms, and birth weight), five dopamine-related genes (DAT1, DRD4, DRD2, COMT, BDNF), observed maternal parenting behavior at 6 months and parent-rated toddler attentional competence at 18 and 24 months. The Latent Environmental and Genetic Interaction (LEGIT) approach was used to examine genes-by-prenatal environment-by-postnatal environment interactions while controlling for sociodemographic factors and postnatal depression.Results: Our hypothesis of a three-way interaction between prenatal adversity, dopamine-related genes, and early maternal parenting behavior was not confirmed. However, consistent two-way interactions emerged between prenatal adversity and dopamine-related genes; prenatal adversity and maternal parenting behavior, and dopamine-related genes and maternal parenting behavior in relation to toddler attentional competence. Significant interaction effects were driven by the DAT1, COMT, and BDNF genotypes; prenatal stressful life events; maternal sensitivity, tactile stimulation, vocalization, and infant-related activities.Conclusions: Multiple dopamine-related genes affected toddler attentional competence and they did so in interaction with prenatal adversity and the early rearing environment, separately. Effects were already visible in young children. Several aspects of early maternal parenting have been identified as potential targets for intervention.

Improving translational relevance: The need for combined exposure models for studying prenatal adversity

Prenatal environmental adversity is a risk factor for neurodevelopmental disorders (NDDs), with the neuroimmune environment proposed to play a role in this risk. Adverse maternal exposures are associated with cognitive consequences in the offspring that are characteristics of NDDs and simultaneous neuroimmune changes that may underlie NDD risk. In both animal models and human studies the association between prenatal environmental exposure and NDD risk has been shown to be complex. Maternal overnutrition/obesity and opioid use are two different examples of complex exposure epidemics, each with their own unique comorbidities. This review will examine maternal obesity and maternal opioid use separately, illustrating the pervasive comorbidities with each exposure to argue a need for animal models of compound prenatal exposures. Many of these comorbidities can impact neuroimmune function, warranting systematic investigation of combined exposures to begin to understand this complexity. While traditional approaches in animal models have focused on modeling a single prenatal exposure or second exposure later in life, a translational approach would begin to incorporate the most prevalent co-occurring prenatal exposures. Long term follow-up in humans is extremely challenging, so animal models can provide timely insight into neurodevelopmental consequences of complex prenatal exposures. Animal models that represent this translational context of comorbid exposures behind maternal obesity or comorbid exposures behind maternal opioid use may reveal potential synergistic neuroimmune interactions that contribute to cognitive consequences and NDD risk. Finally, translational co-exposure models can identify concerning exposure combinations to guide treatment in complex cases, and identify high risk children starting in the prenatal period where early interventions improve prognosis.

Neonatal Abstinence Syndrome in Rural Appalachia.

As the United States faces the repercussions of the current opioid epidemic, it is important for social workers to be able to identify risks for poor birth outcomes in infants with neonatal abstinence syndrome (NAS). Although some studies have identified single risk factors, no studies have tested associations between total amount of risk (that is, cumulative risk) and birth outcomes in infants with NAS. Authors examined 318 mothers who used opioids during pregnancy and their infants' birthweight, length, head circumference, and Apgar scores (which measure overall infant health after birth). All infants were admitted to a neonatal intensive care unit in Appalachia and were diagnosed with NAS. Authors found that high cumulative risk during pregnancy was associated with lower birthweight and Apgar scores one and five minutes after birth as well as shorter length and smaller head circumference at birth. Social workers are encouraged to assess for the quantity of prenatal adversity experienced by the mothers they serve and to consider multicomponent, comprehensive community-based interventions to reduce cumulative risk.

Liver Proteome Profile of Growth Restricted and Appropriately Grown Newborn Wistar Rats Associated With Maternal Undernutrition.

BackgroundFetal growth restriction (FGR) has been associated with adverse perinatal outcomes and epigenetic modifications that impact gene expression leading to permanent changes of fetal metabolic pathways and thereby influence development of disease in childhood and adult life. In this study, we investigated the result of maternal food restriction on liver protein expression in Wistar male newborn pups.Materials & MethodsTen (n = 10) timed pregnant Wistar rats on their 14th day of gestation were randomly assigned to either control (n = 4) or food restricted group (n = 6). The control group had ad libitum access to food. In the food restricted group, maternal diet was limited in a moderate fashion (50%) from day 15 of pregnancy until delivery. All rats delivered spontaneously on day 21 and newborn pups were immediately weighed. Pups born to normally nourished mothers were considered as controls, while pups born to food restricted mothers were subdivided into two groups, based on their birth weight: growth restricted (FGR) and appropriately grown (non-FGR). Rats were euthanized immediately after birth and liver tissues of 11 randomly selected male offspring (FGR n = 4, non-FGR n = 4, control n = 3) were collected and analyzed using quantitative proteomics.ResultsIn total 6,665 proteins were profiled. Of these, 451 and 751 were differentially expressed in FGR and non-FGR vs. control, respectively, whereas 229 proteins were commonly expressed. Bioinformatics analysis of the differentially expressed proteins (DEPs) in FGR vs. control revealed induction of the super-pathway of cholesterol biosynthesis and inhibition of thyroid hormone metabolism, fatty acid beta oxidation and apelin liver signaling pathway. Analysis of DEPs in non-FGR vs. control groups showed inhibition of thyroid hormone metabolism, fatty acid beta oxidation, and apelin liver signaling pathway.ConclusionThis study demonstrates the impact of prenatal food restriction on the proteomic liver profile of FGR and non-FGR offspring underlying the importance of both prenatal adversities and birth weight on liver-dependent postnatal disease.

Prenatal programming of depression: cumulative risk or mismatch in the Ontario Child Health Study?

Consistent with cumulative risk hypotheses of psychopathology, studies examining prenatal adversity and later mental health largely suggest that pre and postnatal stress exposures have summative effects. Fewer data support that a mismatch in stress levels between pre- and postnatal life increases risk (the mismatch hypothesis). In this retrospective cohort study using data from the 1983 Ontario Child Health Study (OCHS), we examined interactions between birth weight status and childhood/adolescent stress to predict major depression in adulthood. Ninety-five participants born at low birth weight (LBW; <2500 g) and 972 normal birth weight (NBW) control participants completed the Composite International Diagnostic Interview Short-Form Major Depression module at 21-34 years of age. A youth risk scale consisting of five stressful exposures (family dysfunction, socioeconomic disadvantage, parental criminality, maternal mental illness, exposure to other life stresses) indexed child/adolescent adversity. Birth weight groups did not differ by childhood risk score nor depression levels. A significant interaction was observed between birth weight and the youth risk scale whereby exposure to increasing levels of exposure to childhood/adolescent adversity predicted increased levels of depression in the NBW group, but lower rates in those born at LBW. Consistent with the mismatch hypothesis, data from a large, longitudinally followed cohort suggest that the mental health of adults born LBW may be more resilient to the adverse effects of childhood/adolescent stress. Taken in the context of previous studies of low birth weight infants, these findings suggest that the nature of associations between gestational stress and later mental health may depend on the magnitude of prenatal stress exposure, as well as the degree of resilience and/or plasticity conferred by their early-life environment.

Fetal-Derived Immune Cells at the Roots of Lifelong Pathophysiology.

Tissue-resident innate immune cells exert a wide range of functions in both adult homeostasis and pathology. Our understanding of when and how these cellular networks are established has dramatically changed with the recognition that many lineages originate at least in part from fetal sources and self-maintain independently from hematopoietic stem cells. Indeed, fetal-derived immune cells are found in most organs and serous cavities of our body, where they reside throughout the entire lifespan. At the same time, there is a growing appreciation that pathologies manifesting in adulthood may be caused by adverse early life events, a concept known as “developmental origins of health and disease” (DOHaD). Yet, whether fetal-derived immune cells are mechanistically involved in DOHaD remains elusive. In this review, we summarize our knowledge of fetal hematopoiesis and its contribution to adult immune compartments, which results in a “layered immune system.” Based on their ontogeny, we argue that fetal-derived immune cells are prime transmitters of long-term consequences of prenatal adversities. In addition to increasing disease susceptibility, these may also directly cause inflammatory, degenerative, and metabolic disorders. We explore this notion for cells generated from erythro-myeloid progenitors (EMP) produced in the extra-embryonic yolk sac. Focusing on macrophages and mast cells, we present emerging evidence implicating them in lifelong disease by either somatic mutations or developmental programming events resulting from maternal and early environmental perturbations.

Exploring Links Between Prenatal Adversity and Adolescent Psychiatric Risk in a Canadian Population-Based Sample.

Adverse prenatal and postnatal exposures may have long-lasting effects on health and development. However, it remains unclear whether being exposed to a greater number of prenatal adversities affects mental health risk. The current study examined whether exposure to maternal health problems prenatally is associated with an increasing risk of psychiatric morbidity in adolescents. Using data from the 2014 Ontario Child Health Study (OCHS), we examined associations between a count of 7 prenatal risk factors (maternal hypertension, diabetes mellitus, bleeding during pregnancy, influenza, urinary tract infection, thyroid disease, and depression/anxiety) and adolescent psychiatric morbidity. Adolescents (N = 2219) aged 12 to 17 years were assessed using the Mini-International Neuropsychiatric Interview for Children and Adolescents. Exposure to each additional prenatal adversity was correlated with increased odds of attention-deficit/hyperactivity disorder (odds ratio [OR] = 1.29, 95% confidence interval [CI] = 1.03-1.60), generalized anxiety disorder (OR = 1.27, 95% CI = 1.05-1.55), and social anxiety disorder (OR = 1.35, 95% CI = 1.01-1.80) after adjustment for confounding variables. Exposure to prenatal adversity in the form of maternal health problems was correlated with an increased risk of attention deficit hyperactivity disorder and anxiety disorders in adolescence. Future studies should further investigate the effects of antenatal environmental exposures on these associations to determine the potential value of close monitoring of those exposed to prenatal risks.

Impact of Maternal Food Restriction on Heart Proteome in Appropriately Grown and Growth-Restricted Wistar-Rat Offspring.

Objective: Fetal growth restriction is associated with increased postnatal cardiovascular morbidity. The alterations in heart physiology and structure caused by in utero nutrient deprivation have not been extensively studied. We aim to investigate the impact of maternal food restriction on the cardiac proteome of newborn rats with normal (non-fetal growth-restricted (FGR)) and reduced (FGR) birth weight. Methods: On day 14 of gestation, 10 timed pregnant rats were randomized into two nutritional groups: (a) Standard laboratory diet and (b) 50% global food restriction. Pups born to food-restricted mothers were subdivided, based on birthweight, into fetal growth-restricted (FGR) and non-FGR, while pups born from normally nourished mothers were considered controls. Rat neonates were euthanized immediately after birth and the hearts of 11 randomly selected male offspring (n = 4 FGR, n = 4 non-FGR, n = 3 control group) were analyzed using quantitative proteomics. Results: In total, 7422 proteins were quantified (q < 0.05). Of these, 1175 were differentially expressed in FGR and 231 in non-FGR offspring vs. control with 151 common differentially expressed proteins (DEPs) between the two groups. Bioinformatics analysis of DEPs in FGR vs. control showed decreased integrin and apelin cardiac fibroblast signaling, decreased muscle contraction and glycolysis, and over-representation of a protein network related to embryonic development, and cell death and survival. Conclusion: Our study illustrates the distinct proteomic profile of FGR and non-FGR offspring of food-restricted dams underlying the importance of both prenatal adversities and birth weight in cardiac physiology and development.

Sex differences in the associations between maternal prenatal distress and infant cortisol reactivity and recovery

Previous research suggests that maternal prenatal psychological distress (PPD) is related to altered cortisol reactivity in the exposed child. There are indications for the sex differences in vulnerability for prenatal adversities that depend on the exposure and child outcome. Still, it is not known whether the association between maternal PPD and infant cortisol stress response is moderated by sex. In addition, the recovery phase of the cortisol stress response has not been given as much attention as reactivity. Our aim was to study the sex differences in the associations between self-reported maternal prenatal depressive-, anxiety- and pregnancy-related anxiety symptoms through gestational weeks 14, 24 and 34 and the saliva cortisol reactivity to and recovery from the acute stress among 10-week-old infants. The study population comprised of 363 mother-infant pairs from the FinnBrain Birth Cohort Study. We found evidence for sex-dependent associations between PPD exposure and infant cortisol response. A less steep recovery slope (-10 % per one SD increase in PPD [95 % CI = -18 to -2 %] and -8 % [-16 to 0 %] depending on the exposure) and a possibly less steep reactivity slope (-14 % [95 % CI = -25 to 0 %] and -10 % [-21 to 3 %]) were associated with higher PPD exposure in females. Of the PPD measures, the strongly intercorrelated, and thus combined, depressive and anxiety symptom score provided the most robust prediction of infant cortisol recovery. Our results demonstrate sexually dimorphic alterations in the functioning of the infant hypothalamus-pituitary-adrenal axis and especially in the functioning of the negative feedback loop of the axis after prenatal PPD exposure among healthy babies.

DNA methylation profiles in adults born at extremely low birth weight.

Effects of stresses associated with extremely preterm birth may be biologically "recorded" in the genomes of individuals born preterm via changes in DNA methylation (DNAm) patterns. Genome-wide DNAm profiles were examined in buccal epithelial cells from 45 adults born at extremely low birth weight (ELBW; ≤1000 g) in the oldest known cohort of prospectively followed ELBW survivors (Mage = 32.35 years, 17 male), and 47 normal birth weight (NBW; ≥2500 g) control adults (Mage = 32.43 years, 20 male). Sex differences in DNAm profiles were found in both birth weight groups, but they were greatly enhanced in the ELBW group (77,895 loci) versus the NBW group (3,424 loci), suggesting synergistic effects of extreme prenatal adversity and sex on adult DNAm profiles. In men, DNAm profiles differed by birth weight group at 1,354 loci on 694 unique genes. Only two loci on two genes distinguished between ELBW and NBW women. Gene ontology (GO) and network analyses indicated that loci differentiating between ELBW and NBW men were abundant in genes within biological pathways related to neuronal development, synaptic transportation, metabolic regulation, and cellular regulation. Findings suggest increased sensitivity of males to long-term epigenetic effects of extremely preterm birth. Group differences are discussed in relation to particular gene functions.

Brain, interrupted: alpha/delta EEG ratio in survivors of pre- and post-natal adversity

Objective: Does exposure to prenatal and postnatal adversity have the same long-term effects on brain development in humans? Methods: We examined whether these two types of exposures differed from their demographically matched controls on a frontal EEG alpha/delta ratio score, a proxy of brain maturation. Results Young adults born at extremely low birth weight (prenatal adversity; N = 64, M age = 23.14 years, SD age = 1.26 years) had a lower alpha/delta ratio score compared to normal birth weight controls (N = 76, M age = 23.60 years, SD age = 1.09 years), while youth exposed to child maltreatment (postnatal adversity; N = 39, M age = 16.18 years, SD age = 1.15) had a higher alpha/delta ratio compared to controls (N = 23, M age = 16.00 years, SD age = 1.50 years). Conclusions Our results suggest that being exposed to pre- and post-natal adversity may have different long-term consequences on brain development. We speculate that these differences might be associated with some of the different functional outcomes known to characterize each type of adverse experience.

The effect of prenatal adversity on externalizing behaviors at 24 months of age in a high-risk sample: Maternal sensitivity as a moderator.

The purpose of this study was to examine the moderating role of maternal sensitivity on the association between prenatal adversity and externalizing behaviors at 24 months of age in a diverse, high-risk sample. We hypothesized that among children with higher prenatal adversity, high maternal sensitivity would serve as a protective factor. Participants were 247 primarily low-income, diverse dyads. Results indicated a significant interaction effect of maternal sensitivity and prenatal adversity on externalizing problems. The association between prenatal adversity and externalizing behaviors was significant only among children who experienced low prenatal adversity, with higher maternal sensitivity associated with lower externalizing behaviors. These findings indicate that, in the absence of high prenatal risk, responsive and sensitive parenting can buffer children in an otherwise high-risk sample from the development of externalizing behaviors.