Postnatal Influences Research Articles

Prenatal influences across the life course: Biobehavioral mechanisms of development.

Despite the well-established importance of prenatal experiences for offspring health throughout the lifespan, our understanding of prenatal influences on psychological outcomes faces challenges due to a wide-ranging and somewhat fragmented literature. Here, we introduce the special issue of Developmental Psychology, "Prenatal Influences Across the Life Course: Biobehavioral Mechanisms of Development," which draws together a broad collection of 12 empirical studies and one review article. These studies illustrate the diversity in biobehavioral mechanisms and biopsychosocial processes that help explain the long-term impacts of prenatal experiences on human development. Collectively, these studies help to disentangle sources of influence across different life stages (e.g., prenatal from genetic, preconception, and/or postnatal influences) and fill key gaps in the literature, such as the inclusion of minoritized populations currently underrepresented in research, the role of fathers, and protective mechanisms. The research featured in this special issue underscores both the long reach of prenatal influences on child and adolescent development as well as the challenges in observing specific biological mediators given that prenatal risks are currently operationalized as specific or broad cumulative measures. In an effort to organize this complex literature, we propose a guiding framework for how to conceptualize the continued integration of the prenatal environment into the field of developmental psychology. This framework broadens the prevailing dichotomous view of prenatal mechanisms as cumulative or specific to articulate a dimensional approach focused on adaptation. We anticipate that such an approach may uncover meaningful and observable biobehavioral mechanisms of prenatal influence on offspring development in the future. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Trends in Amplitude-Integrated Electroencephalography in the Smallest Preterm Neonates.

Amplitude-integrated electroencephalography is increasingly used for the neuromonitoring of premature infants. However, it is still not clear how bioelectrical activity changes in the smallest gestational age newborns. The aim of our study was to evaluate the bioelectrical activity of amplitude-integrated electroencephalograms in premature newborns of different gestational age to assess how gestational age and postnatal age influence patterns of amplitude-integrated electroencephalograms and to test the hypothesis of whether the bioelectrical activity of the brain matures faster after the birth of premature newborns than in utero. We prospectively included infants born before 32 weeks of gestational age between June 2020 and July 2022. Serial recordings of amplitude-integrated electroencephalograms were performed at three time points of age (days 1-3, 13-15, and 27-29). Recordings were analyzed for background patterns, the onset and appearance of cyclicity, and lower amplitude border and bandwidth, which were used to derive a composite Burdjalov score. In total, 140 premature neonates were included in the study, and 112 of them completed the study. The median gestational age of the newborns enrolled in the study was 29 (27-30) weeks, and the mean weight was 1206 (350) g. Burdjalov scores increased with increasing gestational age. Higher scores were observed in every dimension of the amplitude-integrated electroencephalograms for newborns of lower gestational age when compared to newborns of higher gestational age of the same postmenstrual age. There was a significant correlation between gestational age and parameters of amplitude-integrated electroencephalograms at all time points. A higher gestational age has a positive effect on the bioelectrical activity of amplitude-integrated electroencephalograms. Increasing postnatal age affected amplitude-integrated electroencephalograms more than gestational age. Our hypothesis that the bioelectrical activity of the brain matures faster for premature newborns after birth than in the womb was confirmed.

Mode of birth and DNA methylation at birth, in childhood, and in adolescence: Uncovering the relationship using ALSPAC data.

Mode of birth has been linked to offspring health. Changes in DNA methylation (DNAm) may represent a potential mechanism; however, findings are heterogeneous and limited to early infancy. This preregistered study examined whether mode of birth (vaginal birth compared with elective or emergency cesarean section) affects DNAm at birth, in childhood, and adolescence and whether these effects are modified by the postnatal care environment, specifically by breastfeeding and mother-infant bonding. Using data from 876 mother-infant dyads from the U.K. Avon Longitudinal Study of Parents and Children, we examined differentially methylated cytosine-phosphate-guanine dinucleotides and regions associated with mode of birth. DNAm was quantified using Illumina Infinium Human Methylation 450 K BeadChip in cord blood (at birth) and in peripheral blood (at 7 and 15-17 years). Analyses controlled for maternal age, education, smoking during pregnancy, child sex, gestational week at birth, and batch effects. We also examined interactions of mode of birth with breastfeeding practices and mother-infant bonding. In cord blood, two cytosine-phosphate-guanine dinucleotides (cg05230316; cg13230077) were linked to mode of birth (pFDR < .050). DNAm in childhood or adolescence was not statistically associated with mode of birth (pFDR > .050), and breastfeeding and mother-infant bonding were not moderators (p > .050). Overall, findings suggest mode of birth may have a small effect on cord blood DNAm, but these effects may not persist into later developmental stages. Other postnatal influences should be considered, and further investigation is needed to address study limitations. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Prenatal and postnatal influences on behavioral development in a mouse model of preconceptional stress

Depression during pregnancy is detrimental for the wellbeing of the expectant mother and can exert long-term consequences on the offspring's development and mental health. In this context, both the gestational environment and the postpartum milieu may be negatively affected by the depressive pathology. It is, however, challenging to assess whether the contributions of prenatal and postnatal depression exposure are distinct, interactive, or cumulative, as it is unclear whether antenatal effects are due to direct effects on fetal development or because antenatal symptoms continue postnatally. Preclinical models have sought to answer this question by implementing stressors that induce a depressive-like state in the dams during pregnancy and studying the effects on the offspring. The aim of our present study was to disentangle the contribution of direct stress in utero from possible changes in maternal behavior in a novel model of preconceptional stress based on social isolation rearing (SIR). Using a cross-fostering paradigm in this model, we show that while SIR leads to subtle changes in maternal behavior, the behavioral changes observed in the offspring are driven by a complex interaction between sex, and prenatal and postnatal maternal factors. Indeed, male offspring are more sensitive to the prenatal environment, as demonstrated by behavioral and transcriptional changes driven by their birth mother, while females are likely affected by more complex interactions between the pre and the postpartum milieu, as suggested by the important impact of their surrogate foster mother. Taken together, our findings suggest that male and female offspring have different time-windows and behavioral domains of susceptibility to maternal preconceptional stress, and thus underscore the importance of including both sexes when investigating the mechanisms that mediate the negative consequences of exposure to such stressor.

The role of fathers in child development from preconception to postnatal influences: Opportunities for the National Institutes of Health Environmental influences on Child Health Outcomes (ECHO) program.

A growing body of literature highlights the important role of paternal health and socioemotional characteristics in child development, from preconception through adolescence. Much of this research addresses the indirect effects of fathers, for instance, their influence on maternal behaviors during the prenatal period or via the relationship with their partner. However, emerging evidence also recognizes the direct role of paternal health and behavior for child health and adjustment across development. This critical review presents evidence of biological and sociocultural influences of fathers on preconception, prenatal, and postnatal contributions to child development. The National Institutes of Health Environmental influences on Child Health Outcomes (ECHO) program incorporates in its central conceptualization the impact of fathers on family and child outcomes. This critical synthesis of the literature focuses on three specific child outcomes in the ECHO program: health outcomes (e.g., obesity), neurodevelopmental outcomes (e.g., emotional, behavioral, psychopathological development), and positive health. We highlight the unique insights gained from the literature to date and provide next steps for future studies on paternal influences.

The inflammatory response to birth requires MyD88 and is driven by both mother and offspring

Birth is an inflammatory event for the newborn, characterized by elevations in interleukin (IL)-6, IL-10, and tumor necrosis factor (TNF)-α peripherally and/or centrally, as well as changes in brain microglia. However, the mechanism(s) underlying these responses is unknown. Toll-like receptors (TLRs) play crucial roles in innate immunity and initiate inflammatory cascades upon recognition of endogenous or exogenous antigens. Most TLR signaling depends on the adaptor molecule myeloid differentiation primary response 88 (MyD88). We independently varied MyD88 gene status in mouse dams and their offspring to determine whether the inflammatory response to birth depends on MyD88 signaling and, if so, whether that signaling occurs in the offspring, the mother, or both. We find that the perinatal surges in plasma IL-6 and brain expression of TNF-α depend solely on MyD88 gene status of the offspring, whereas postnatal increases in plasma IL-10 and TNF-α depend on MyD88 in both the pup and dam. Interestingly, MyD88 genotype of the dam primarily drives differences in offspring brain microglial density and has robust effects on developmental neuronal cell death. Milk cytokines were evaluated as a possible source of postnatal maternal influence; although we found high levels of CXCL1/GROα and several other cytokines in ingested post-partum milk, their presence did not require MyD88. Thus, the inflammatory response previously described in the late-term fetus and newborn depends on MyD88 (and, by extension, TLRs), with signaling in both the dam and offspring contributing. Unexpectedly, naturally-occuring neuronal cell death in the newborn is modulated primarily by maternal MyD88 gene status.

Impact of postnatal weight gain on brain white matter maturation in very preterm infants.

Very preterm infants (VPIs, <32 weeks gestational age at birth) are prone to long-term neurological deficits. While the effects of birth weight and postnatal growth on VPIs' neurological outcome are well established, the neurobiological mechanism behind these associations remains elusive. In this study, we utilized diffusion tensor imaging (DTI) to characterize how birth weight and postnatal weight gain influence VPIs' white matter (WM) maturation. We included VPIs with complete birth and postnatal weight data in their health record, and DTI scan as part of their predischarge Magnetic Resonance Imaging (MRI). We conducted voxel-wise general linear model and tract-based regression analyses to explore the impact of birth weight and postnatal weight gain on WM maturation. We included 91 VPIs in our analysis. After controlling for gestational age at birth and time between birth and scan, higher birth weight Z-scores were associated with DTI markers of more mature WM tracts, most prominently in the corpus callosum and sagittal striatum. The postnatal weight Z-score changes over the first 4 weeks of life were also associated with increased maturity in these WM tracts, when controlling for gestational age at birth, birth weight Z-score, and time between birth and scan. In VPIs, birth weight and post-natal weight gain are associated with markers of brain WM maturation, particularly in the corpus callosum, which can be captured on discharge MRI. These neuroimaging metrics can serve as potential biomarkers for the early effects of nutritional interventions on VPIs' brain development.

Causes of obesity: a review

Obesity research is advancing swiftly, but the increase in obesity prevalence is faster. Over the past three decades, researchers have found that biopsychosocial factors determine weight gain much more than personal choices and responsibility. Various genes have found to predispose people to obesity by interacting with our obesogenic environment. In this review, we discuss the impact of physical inactivity, excessive caloric intake, intrauterine environment, postnatal influences, insufficient sleep, drugs, medical conditions, socioeconomic status, ethnicity, psychosocial stress, endocrine disrupting chemicals and the gastrointestinal microbiome, on the occurrence of obesity.

Intergenerational Transmission of Maternal Childhood Maltreatment Prior to Birth: Effects on Human Fetal Amygdala Functional Connectivity

Childhood maltreatment (CM) is a potent risk factor for developing psychopathology later in life. Accumulating research suggests that the influence is not limited to the exposed individual but may also be transmitted across generations. In this study, we examine the effect of CM in pregnant women on fetal amygdala-cortical function, prior to postnatal influences. Healthy pregnant women (N= 89) completed fetal resting-state functional magnetic resonance imaging (rsfMRI) scans between the late second trimester and birth. Women were primarily from low socioeconomic status households with relatively high CM. Mothers completed questionnaires prospectively evaluating prenatal psychosocial health and retrospectively evaluating trauma from their own childhood. Voxelwise functional connectivity was calculated from bilateral amygdala masks. Connectivity of the amygdala network was relatively higher to left frontal areas (prefrontal cortex and premotor) and relatively lower to right premotor area and brainstem areas in fetuses of mothers exposed to higher CM. These associations persisted after controlling for maternal socioeconomic status, maternal prenatal distress, measures of fetal motion, and gestational age at the time of scan and at birth. Pregnant women's experiences of CM are associated with offspring brain development in utero. The strongest effects were found in the left hemisphere, potentially indicating lateralization of the effects of maternal CM on the fetal brain. This study suggests that the time frame of the Developmental Origins of Health and Disease research should be extended to exposures from mothers' childhood, and indicates that the intergenerational transmission of trauma may occur prior to birth.

Maternal separation increased memory function and anxiety without effects of environmental enrichment in male rats

Maternal separation is a detrimental postnatal influence, whereas environmental enrichment is a therapeutic and protective agent. It is unclear if long-term environmental enrichment can compensate for the effects of maternal separation stress on memory-related alterations. This study examined how environmental enrichment affected memory functions, anxiety level, Grin2a, Grin2b, BDNF, and cFos expressions in the maternally separated rats. There are seven groups in this study: control (C), maternal separation+standard cage (MS), maternal separation + enriched cage (MSE), enriched cage (E), the maternal separation that decapitated at postnatal 21 (MS21) and standard cage that decapitated at PN21 (C21) for hormone and gene expression analysis. The maternal separation procedure consisted of postnatal 21 days. Learning and memory performance were determined with the Morris water tank test; anxiety and locomotor activity were examined with the open field and elevated plus-maze test. The expression levels of genes were measured by the RT-PCR method. Blood corticosterone level was evaluated by the ELISA method. Results showed that MS increased memory performance, locomotor activity, and anxiety, but it did not change gene expression levels. An enriched environment did not change the memory performance, locomotor activity, and related gene expression levels. MSE group increased their memory performance, but the anxiety, locomotor activity, and gene expression level did not change. Grin2a, Grin2b, and BDNF gene expression and corticosterone levels increased in the MS21 group. Maternal separation increased memory performance, but it also increased anxiety. Environmental enrichment alone was insufficient to cause alterations in the memory performance.

Seminal and vagino-uterine microbiome and their individual and interactive effects on cattle fertility.

Reproductive failure is a major economical drain on cow-calf operations across the globe. It can occur in both males and females and stem from prenatal and postnatal influences. Therefore, the cattle industry has been making efforts to improve fertility and the pregnancy rate in cattle herds as an attempt to maintain sustainability and profitability of cattle production. Despite the advancements made in genetic selection, nutrition, and the implementation of various reproductive technologies, fertility rates have not significantly improved in the past 50 years. This signifies a missing factor or factors in current reproductive management practices that influence successful fertilization and pregnancy. Emerging lines of evidence derived from human and other animals including cattle suggest that the microbial continuum along the male and female reproductive tracts are associated with male and female fertility-that is, fertilization, implantation, and pregnancy success-highlighting the potential for harnessing the male and female reproductive microbiome to improve fertility in cattle. The objective of this narrative review is to provide an overview of the recent studies on the bovine seminal and vagino-uterine microbiome and discuss individual and interactive roles of these microbial communities in defining cattle fertility.

Prenatal Bisphenol S and Postnatal High-Fat Diet Influence DNA Methylation of the Mest Gene in F1 Male Mice

Prenatal Bisphenol S and Postnatal High-Fat Diet Influence DNA Methylation of the Mest Gene in F1 Male Mice

Maternal depressive symptoms, neonatal white matter, and toddler social-emotional development

Maternal prenatal depression is associated with increased likelihood of neurodevelopmental and psychiatric conditions in offspring. The relationship between maternal depression and offspring outcome may be mediated by in-utero changes in brain development. Recent advances in magnetic resonance imaging (MRI) have enabled in vivo investigations of neonatal brains, minimising the effect of postnatal influences. The aim of this study was to examine associations between maternal prenatal depressive symptoms, infant white matter, and toddler behaviour. 413 mother-infant dyads enrolled in the developing Human Connectome Project. Mothers completed the Edinburgh Postnatal Depression Scale (median = 5, range = 0–28, n = 52 scores ≥ 11). Infants (n = 223 male) (median gestational age at birth = 40 weeks, range 32.14–42.29) underwent MRI (median postmenstrual age at scan = 41.29 weeks, range 36.57–44.71). Fixel-based fibre metrics (mean fibre density, fibre cross-section, and fibre density modulated by cross-section) were calculated from diffusion imaging data in the left and right uncinate fasciculi and cingulum bundle. For n = 311, internalising and externalising behaviour, and social-emotional abilities were reported at a median corrected age of 18 months (range 17–24). Statistical analysis used multiple linear regression and mediation analysis with bootstrapping. Maternal depressive symptoms were positively associated with infant fibre density in the left (B = 0.0005, p = 0.003, q = 0.027) and right (B = 0.0006, p = 0.003, q = 0.027) uncinate fasciculus, with left uncinate fasciculus fibre density, in turn, positively associated with social-emotional abilities in toddlerhood (B = 105.70, p = 0.0007, q = 0.004). In a mediation analysis, higher maternal depressive symptoms predicted toddler social-emotional difficulties (B = 0.342, t(307) = 3.003, p = 0.003), but this relationship was not mediated by fibre density in the left uncinate fasciculus (Sobel test p = 0.143, bootstrapped indirect effect = 0.035, SE = 0.02, 95% CI: [−0.01, 0.08]). There was no evidence of an association between maternal depressive and cingulum fibre properties. These findings suggest that maternal perinatal depressive symptoms are associated with neonatal uncinate fasciculi microstructure, but not fibre bundle size, and toddler behaviour.

Fetal Hippocampal Connectivity Shows Dissociable Associations with Maternal Cortisol and Self-Reported Distress during Pregnancy.

Maternal stress can shape long-term child neurodevelopment beginning in utero. One mechanism by which stress is transmitted from mothers to their offspring is via alterations in maternal cortisol, which can cross the placenta and bind to glucocorticoid receptor-rich regions in the fetal brain, such as the hippocampus. Although prior studies have demonstrated associations between maternal prenatal stress and cortisol levels with child brain development, we lack information about the extent to which these associations originate prior to birth and prior to confounding postnatal influences. Pregnant mothers (n = 77) completed questionnaires about current perceived stress, depressive symptoms, and anxiety symptoms, provided three to four salivary cortisol samples, and completed a fetal resting-state functional MRI scan during their second or third trimester of pregnancy (mean gestational age = 32.8 weeks). Voxelwise seed-based connectivity analyses revealed that higher prenatal self-reported distress and higher maternal cortisol levels corresponded to dissociable differences in fetal hippocampal functional connectivity. Specifically, self-reported distress was correlated with increased positive functional coupling between the hippocampus and right posterior parietal association cortex, while higher maternal cortisol was associated with stronger positive hippocampal coupling with the dorsal anterior cingulate cortex and left medial prefrontal cortex. Moreover, the association between maternal distress, but not maternal cortisol, on fetal hippocampal connectivity was moderated by fetal sex. These results suggest that prenatal stress and peripheral cortisol levels may shape fetal hippocampal development through unique mechanisms.

Pregnant women with bipolar disorder who have a history of childhood maltreatment: Intergenerational effects of trauma on fetal neurodevelopment and birth outcomes.

Intergenerational transmission of trauma occurs when the effects of childhood maltreatment (CM) influence the next generation's development and health; prenatal programming via maternal mood symptoms is a potential pathway. CM is a risk factor for bipolar disorder which is present in 1.8% of pregnant women. Mood symptoms are likely to increase during pregnancy, particularly for those with a history of CM. We examined whether there was evidence for intergenerational transmission of trauma in utero in this population, and whether maternal mood was a transmission pathway. CM and maternal mood were self-reported by N=82 pregnant women in treatment for bipolar disorder. Fetal heart rate variability (FHRV) was measured at 24, 30, and 36 weeks' gestation. Gestational age at birth and birth weight were obtained from medical charts. A cluster analysis yielded two groups, Symptom+ (18.29%) and Euthymic (81.71%), who differed on severe mood symptoms (p < 0.001) but not on medication use. The Symptom+ group had more CM exposures (p < 0.001), a trend of lower FHRV (p=0.077), and greater birth complications (33.3% vs. 6.07% born preterm p < 0.01). Maternal prenatal mood mediated the association between maternal CM and birth weight in both sexes and at trend level for gestational age at birth in females. This is the first study to identify intergenerational effects of maternal CM prior to postnatal influences in a sample of pregnant women with bipolar disorder. These findings underscore the potential enduring impact of CM for women with severe psychiatric illness and their children.

Unique Contributions of Maternal Prenatal and Postnatal Emotion Dysregulation on Infant Respiratory Sinus Arrhythmia.

Prenatal intrauterine exposures and postnatal caregiving environments may both shape the development of infant parasympathetic nervous system (PNS) activity. However, the relative contributions of prenatal and postnatal influences on infant respiratory sinus arrhythmia (RSA)-an index of PNS functioning-are relatively unknown. We examined whether prenatal and postnatal maternal emotion dysregulation, a transdiagnostic construct that spans mental health diagnoses, were independently related to infant RSA trajectories during a social stressor, the still-face paradigm. Our sample included 104 mothers and their 7-month-old infants. Maternal emotion dysregulation was measured with the Difficulties in Emotion Regulation Scale during the 3rd trimester of pregnancy and again at a 7-month postpartum laboratory visit. Infant RSA was recorded during the still-face paradigm. Only postnatal maternal emotion dysregulation was associated with infant RSA. Specifically, high postnatal emotion dysregulation was associated with a blunted (i.e., dampened reactivity and recovery) infant RSA response profile. Infant sex did not moderate the associations between maternal emotion dysregulation and infant RSA. Findings suggest that postnatal interventions to promote effective maternal emotion regulation may reduce risk for infants' dysregulated psychophysiological stress responses.

No effects of siblings and twin testosterone transfer on autistic traits.

Having twin and non-twin siblings might influence autistic traits both prenatally and postnatally. The twin testosterone transfer hypothesis suggests that girls with a twin brother are exposed to higher levels of prenatal testosterone than girls with a twin sister, and that increased testosterone exposure masculinizes neural development and increases autistic traits. Postnatally, siblings may provide example behaviour, which could reduce autistic traits. We studied pre- and postnatal influences of twin and non-twin siblings on mother and teacher-reported autistic traits in 7714 dizygotic twins. We examined the effect of sex of the proband child and of the siblings. We fitted regression models (for boys and girls separately) with sex of co-twin and having older and/or younger siblings of each sex as predictors. Girls' mother-reported autistic traits were slightly lower for those with a twin brother than those with a twin sister (β=-.08, p = .001, Cohen's d=-.13). This difference was not replicated in teacher-reported autistic traits (β = .01, p=.734). Boys' (mother and teacher-reported) autistic traits were not related to the sex of their co-twin (ps>0.50). Teacher-reported autistic traits were slightly higher if girls had an older brother (β = .07, p = .013, Cohen's d=.12). Other than this small effect, we found no effect of non-twin siblings on autistic traits in either girls or boys (ps>.18). We did not find increased autistic traits in girls with a twin brother compared to girls with a twin sister. This finding contributes to a body of literature that rejects the twin testosterone transfer hypothesis. In addition, we found little evidence for pre- and postnatal sibling influences. Our findings align with high heritability and absence of shared-environmental influences inASD.

Early life adoption shows rearing environment supersedes transgenerational effects of paternal stress on aggressive temperament in the offspring

Prenatal experience and transgenerational influences are increasingly recognized as critical for defining the socio-emotional system, through the development of social competences and of their underlying neural circuitries. Here, we used an established rat model of social stress resulting from male partner aggression induced by peripubertal (P28-42) exposure to unpredictable fearful experiences. Using this model, we aimed to first, characterize adult emotionality in terms of the breadth of the socio-emotional symptoms and second, to determine the relative impact of prenatal vs postnatal influences. For this purpose, male offspring of pairs comprising a control or a peripubertally stressed male were cross-fostered at birth and tested at adulthood on a series of socio-emotional tests. In the offspring of peripubertally stressed males, the expected antisocial phenotype was observed, as manifested by increased aggression towards a female partner and a threatening intruder, accompanied by lower sociability. This negative outcome was yet accompanied by better social memory as well as enhanced active coping, based on more swimming and longer latency to immobility in the forced swim test, and less immobility in the shock probe test. Furthermore, the cross-fostering manipulation revealed that these adult behaviors were largely influenced by the post- but not the prenatal environment, an observation contrasting with both pre- and postnatal effects on attacks during juvenile play behavior. Adult aggression, other active coping behaviors, and social memory were determined by the predominance at this developmental stage of postnatal over prenatal influences. Together, our data highlight the relative persistence of early life influences.

Maternal caregiving ameliorates the consequences of prenatal maternal psychological distress on child development.

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.

Ante-Natal and Post-Natal Influences on Neonatal Immunity, Growth and Puberty of Calves-A Review.

Simple SummaryThe objective of this review is to give the reader an overview of interactions between immunity, growth and puberty in calves and highlight how these influence future performances. The risk of morbidity and mortality is high during the first four weeks of age. Adaption to extra-uterine life starts early during embryonic development and is underpinned by optimal maternal nutrition. It is known that colostrum is paramount to neonate nutrition and passive immunity. Good colostrum management allows the calf to develop coping mechanisms to efficiently utilize feed resources for optimal growth. A deeper understanding of these interactions paves the way for developing strategies to improve immune responses to environmental pathogens, optimal growth and timely attainment of puberty in calves. The literature reviewed here shows that there are opportunities to enhance future performance of cattle paying attention to the interaction of nutrition and immunity at early developmental stages. This then guarantees efficient neonate nutrition and profitable cattle production.Calf immunity, growth and puberty are important factors affecting heifer productivity. The first four weeks of age are critical for reducing calf morbidity and mortality. It is well documented that colostrum is paramount to neonatal nutrition and passive immunity, however, adaptation to extra-uterine life starts early during embryonic development. Therefore, successful calf rearing strategies are underpinned by adequate maternal nutrition during gestation, and good colostrum management. A deeper understanding of these interactions paves the way for developing strategies to improve immune responses to environmental pathogens, optimal growth and timely attainment of puberty in calves. The literature reviewed here shows that there are opportunities to enhance the future performance of cattle paying attention to the interaction of nutrition and immunity at each developmental stage. Therefore, the objective of this review is to give the reader an overview of interactions between immunity, growth and puberty in dairy calves and highlight how these influence future performances.