Associations between maternal prenatal stress and children’s socioemotional development have varied widely in the literature. The main objectives of the current study were as follows: 1) to provide a synthesis of studies examining the association between maternal prenatal depression and their children’s socioemotional development; and 2) to examine potential moderators of this association.
AIM:A systematic review and meta-analysis was conducted to examine the relationship between KMC and infant/toddler biopsychosocial outcomes.METHOD:PubMed, MEDLINE (OvidSP), MEDLINE in Process (OvidSP), Embase (OvidSP), PsycINFO (OvidSP), and AMED (OvidSP) were searched. Observational studies and randomized control trials through October 2015 that investigated the association between KMC intervention and infant/toddler biopsychosocial outcomes were included. Studies with <10 participants, those using skin-to-skin only during painful procedures or only on the day of birth, and those that did not report quantitative outcomes were excluded. Data were extracted by two coders and estimates were examined using random-effects.RESULTS:3177 studies were screened with 13 meeting inclusion criteria and representing 5 child outcomes (cognitive, motor, self-regulation, socio-emotional and temperament). Among LBW/premature neonates, KMC compared to conventional care was associated with improved infant self-regulation. Moderated effects were identified for cognitive (duration of KMC) and motor development (duration of KMC, country-level mortality ratio, and infant gender).INTERPRETATIONS:KMC administered to vulnerable neonates during a sensitive period of brain development has a lasting impact on self-regulation skills later in infancy. Further research examining the longer-term effect of KMC on cognitive and motor development, socioemotional skills, and temperament is needed.
Objective: Observed associations between maternal prenatal stress and children's socioemotional development have varied widely in the literature. The objective of the current study was to provide a synthesis of studies examining maternal prenatal anxiety and depression and the socioemotional development of their children. Method: Eligible studies through to February 2018 were identified using a comprehensive search strategy. Included studies examined the association between maternal prenatal depression or anxiety and the future development of their children's socioemotional development (eg, difficult temperament, behavioral dysregulation) up to 18 years later. Two independent coders extracted all relevant data. Random-effects meta-analyses were used to derive mean effect sizes and test for potential moderators. Results: A total of 71 studies met full inclusion criteria for data analysis. The weighted average effect size for the association between prenatal stress and child socioemotional problems was as follows: odds ratio (OR) = 1.66 (95% CI = 1.54-1.79). Effect sizes were stronger for depression (OR = 1.79; 95% CI = 1.61-1.99) compared to anxiety (OR = 1.50; 95% CI = 1.36-1.64). Moderator analyses indicated that effect sizes were stronger when depression was more severe and when socio-demographic risk was heightened. Conclusion: Findings suggest that maternal prenatal stress is associated with offspring socioemotional development, with the effect size for prenatal depression being more robust than for anxiety. Mitigating stress and mental health difficulties in mothers during pregnancy may be an effective strategy for reducing offspring behavioral difficulties, especially in groups with social disadvantage and greater severity of mental health difficulties.
At 18 months, children show marked variability in their social-cognitive skill development, and the preponderance of past research has focused on constitutional and contextual factors in explaining this variability. Extending this literature, the current study examined whether cumulative biomedical risk represents another source of variability in social cognition at 18 months. Further, we aimed to determine whether responsive parenting moderated the association between biomedical risk and social cognition. A prospective community birth cohort of 501 families was recruited at the time of the child's birth. Cumulative biomedical risk was measured as a count of 10 prenatal/birth complications. Families were followed up at 18 months, at which point socialcognitive data was collected on children's joint attention, empathy, cooperation, and self recognition using previously validated tasks. Concurrently, responsive maternal behavior was assessed through observational coding of mother-child interactions. After controlling for covariates (e.g., age, gender, child language, socioeconomic variables), both cumulative biomedical risk and maternal responsivity significantly predicted social cognition at 18 months. Above and beyond these main effects, there was also a significant interaction between biomedical risk and maternal responsivity, such that higher biomedical risk was significantly associated with compromised social cognition at 18 months, but only in children who experienced low levels of responsive parenting. For those receiving comparatively high levels of responsive parenting, there was no apparent effect of biomedical risk on social cognition. This study shows that cumulative biomedical risk may be one source of inter-individual variability in social cognition at 18 months. However, positive postnatal experiences, particularly high levels of responsive parenting, may protect children against the deleterious effects of these risks on social cognition.
Objective: The impact of postpartum depression on mother-infant interaction, affective responses to infant cries, as well as hormonal and autonomic responses to infant stimuli were examined in a sample of primiparous and multiparous women. Methods: A sample of 140 depressed and non-depressed women where randomly assigned to one of two conditions: 1) cry (pain; hunger); and 2) neutral (female neutral voice). Emotional response scores, salivary cortisol, and heart rate were collected. Depression was designated if women scored 12 or above on the Edinburgh Postpartum Depression Scale (EPDS). Results: Depressed mothers reported feeling more anxious and negative when listening to infant cries and responded more strongly to the pain as opposed to the hunger cries compared to non-depressed mothers. Depressed mothers also showed higher overall cortisol levels compared to non-depressed mothers, with non-depressed mothers demonstrating a slight increase in response to the cries, while depressed mothers had a blunted response to the cries. No differences were reported in maternal heart-rate. Conclusions: PPD has a clear impact on a mother’s interaction with her infant which in turn, can have substantial effects on the infant’s social and emotional development.
Introduction: Experimental evidence in rodents shows that maternal stress during pregnancy (MSDP) negatively impacts spatial learning and memory in the offspring. We aim to investigate the association between MSDP (i.e., life events) and spatial working memory, as well as attention skills (attention shifting and attention focusing), in humans. The moderating roles of child sex, maternal anxiety during pregnancy and postnatal care are also investigated.Methods: Participants were 236 mother-child dyads that were followed from the second trimester of pregnancy until 4 years postpartum. Measurements included questionnaires and independent observations.Results: MSDP was negatively associated with attention shifting at 18 months when concurrent maternal anxiety was low. MSDP was associated with poorer spatial working memory at 4 years of age, but only for boys who experienced poorer postnatal care.Conclusion: Consistent with results observed in rodents, MSDP was found to be associated with spatial working memory and attention skills. These results point to postnatal care and maternal anxiety during pregnancy as potential targets for interventions that aim to buffer children from the detrimental effects of MSDP. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
BACKGROUNDParental responsivity is important to children's cognitive and socioemotional development, yet is under-represented in primary healthcare, because the measurement is specialized and time-consuming.METHODSThe current study developed a measure of maternal cognitive sensitivity (CS), which uses impressionistic ratings based on brief observations of parent-child interaction when children are 3 years old.RESULTSUsing data from a longitudinal cohort (Time 1, N = 501), the CS measure had good psychometric properties, was significantly related to a gold-standard maternal responsivity measure, and was predicted by the same socio-demographic factors predictive of other measures of parental responsivity. Finally, a well-established pathway from socioeconomic risk (child age 2 months) to compromised parenting (child age 3 years) to negative child outcome (child age 4.5 years) was demonstrated with CS as the mediator.CONCLUSIONThe maternal CS measure is brief, can be easily trained, and takes 8 min to administer and code, making it potentially useful in primary healthcare settings.
To determine the pattern of gene expression in brains associated with mothering during the postpartum period, in the present study we assessed gene expression through microarrays in four groups of female rats: two groups of new mothers that were experiencing the hormonal and neurochemical changes associated with pregnancy and parturition, and two groups of virgin females that were not. Within each of these parity groups we assessed one group of animals that was exposed to and responded to pups and engaged in maternal behavior, and one group left without any exposure to pups and therefore had no maternal experience. We explored the pattern of expression of genes related to the hormones, neurotransmitters, and modulatory neuropeptides associated with maternal behavior within the medial preoptic area (MPOA) and the medial amygdala (MeA) in the rat. Within the MPOA there were significant main effects of pup exposure for the dopamine-related genes (DRD4 and dopamine transporter, DAT), the glucocorticoid-related gene (CYPX1B1a), the opioid receptor μ-1 gene (OPRM1) and the gamma-aminobutyric acid (GABA) receptor gene (GABAbRid). OPRM1 and the serotonin-related gene that regulates biosynthesis of serotonin (5HTR2A) showed a main effect of parity. For both sets of analyses, higher gene expression was associated with pup exposure and parity. Genes expressed in the MeA tended to reside in the glucocorticoid family. The microarrays were able to identify, on a transcriptional level, a list of candidate genes involved in maternal behavior and the factors that surround it.
Prolactin (PRL), an anterior pituitary hormone with neurogenic properties associated with pregnancy, has been implicated in oligodendrocyte proliferation during gestation, contributing to increased myelination in the maternal brain. However, PRL is elevated during lactation as well, suggesting that the postpartum (PP) period may contribute to additional gliogenesis in lactating females. In the present study, we assessed oligodendrocyte number in the corpus callosum (CC) of female Sprague-Dawley rats near the end of gestation, and at two weeks postpartum in both lactating and non-lactating dams, and in virgins. Though pregnant females did not differ significantly from any other group, lactating females had significantly more oligodendrocytes in the CC than virgins (p=.01), and in medial regions of the CC than non-lactating dams (p<.02). Oligodendrocyte number in the CC of pregnant and PP females correlated positively with the number of pups in their litter (r(2)=.68, p<.005). These results suggest that the gestational period contributes to oligodendrocyte proliferation or survival, likely mediated by an endocrine hormone whose concentration varies with the size of the litter. The PP period also contributes to increases in CC oligodendrocyte number, though it is unclear whether endocrine influences and/or pup-interaction underlie the differences in myelination between lactating and non-lactating groups. Further investigation is required in order to confirm whether the effects observed are mediated by members of the PRL-family, experience, and/or other gestational/PP endocrine hormones.
Juvenile female rats show maternal-like behavior toward pups. The purpose of the following experiment was to investigate whether the HPA axis, through the use of early separation manipulations that alter HPA functioning in rats, plays a role in the juvenile response to foster pups. Female rats were early deprived or maternally separated for 5 hours daily from PND 2 to 14 and compared to animal facility-reared rats. Deprivation or separation increased CRH-R1 IR in the juvenile PVN, but had no other effects on other HPA measures or on maternal behavior. Pup-exposure during the juvenile period blunted corticosterone levels after acute and repeated pup-exposures when compared to exposure to novelty and conspecifics respectively. Repeated exposures to pups also increased CRH-R1 IR relative to isolation during the juvenile period. Overall, the data suggest that although pup-exposure affects corticosterone levels, the HPA axis does not relate to juvenile maternal behavior in the present experiments.
Previous findings have demonstrated that the maternal environment is important for the development of male sexual behavior. The present study examined the effects of complete early life isolation and replacement 'stroking' stimulation on male sexual behavior and neural activation as seen by Fos immunoreactivity (Fos-IR). Animals were either artificially reared (AR) with minimal (AR-MIN) or maximal (AR-MAX) body simulation, or maternally reared (MR). In adulthood, animals were either given an exposure to an estrous female (EXP) or left undisturbed (NoEXP). No significant effects of early development were found in sexual behavior; however differences in activation in response to this exposure were observed. AR-MIN animals showed lower Fos-IR in the medial preoptic area and the ventromedial hypothalamus compared to MR animals. AR-MAX animals were not significantly different from either condition. These findings demonstrate that although there are no differences in the quality of the first copulatory exposure between AR and MR animals, the brain's response to this exposure differs in sites within the brain that subserve sexual behavior.
Postpartum maternal experience produces long-lasting changes in maternal behavior in the mother rat, which can be altered by early-life isolation. Postpartum experience also affects the regulation of adult neurogenesis in the neural circuit underlying maternal behavior, in a region-specific manner. Female rats were reared either with their mothers (MR) or in isolation in an artificial rearing (AR) paradigm. In adulthood, rats were mated and separated from their pups at birth. The following day, dams were injected with a mitotic marker and either allowed to interact with pups (maternal experience) or left alone. Results show that MR rats that acquire a later maternal experience show increases in cell survival in parts of the excitatory limb of the maternal neural network (bed nucleus of the stria terminalis and nucleus accumbens), but no changes in the inhibitory limb (amygdala). In comparison to AR inexperienced rats, AR maternally experienced rats show no increases in cell survival in the excitatory limb, but a striking reduction in cell survival in the inhibitory limb. The results suggest that early preweaning maternal isolation alters the structural plasticity that occurs following a postpartum maternal experience.