Maternal Prenatal Psychosocial Stress Research Articles

Maternal stressful life events during pregnancy and childhood asthma and wheeze

BackgroundStudies have linked prenatal maternal psychosocial stress to childhood wheeze/asthma but have rarely investigated factors that may mitigate risks. ObjectiveTo investigate associations between prenatal stress and childhood wheeze/asthma, evaluating factors that may modify stress effects. MethodsParticipants included 2056 mother-child dyads from Environmental influences on Child Health Outcomes (ECHO)-PATHWAYS, a consortium of 3 prospective pregnancy cohorts (the Conditions Affecting Neurocognitive Development and Learning in Early Childhood study, The Infant Development and Environment Study, and a subset of the Global Alliance to Prevent Prematurity and Stillbirth study) from 6 cities. Maternal stressful life events experienced during pregnancy (PSLEs) were reported using the Pregnancy Risk Assessment Monitoring System Stressful Life Events questionnaire. Parents reported child wheeze/asthma outcomes at age 4 to 6 years using standardized questionnaires. We defined outcomes as ever asthma, current wheeze, current asthma, and strict asthma. We used modified Poisson regression with robust standard errors (SEs) to estimate risk ratios (RRs) and 95% CI per 1-unit increase in PSLE, adjusting for confounders. We evaluated effect modification by child sex, maternal history of asthma, maternal childhood traumatic life events, neighborhood-level resources, and breastfeeding. ResultsOverall, we observed significantly elevated risk for current wheeze with increasing PSLE (RR, 1.09 [95% CI, 1.03-1.14]), but not for other outcomes. We observed significant effect modification by child sex for strict asthma (P interaction = .03), in which risks were elevated in boys (RR, 1.10 [95% CI, 1.02-1.19]) but not in girls. For all other outcomes, risks were significantly elevated in boys and not in girls, although there was no statistically significant evidence of effect modification. We observed no evidence of effect modification by other factors (P interactions > .05). ConclusionRisk of adverse childhood respiratory outcomes is higher with increasing maternal PSLEs, particularly in boys.

Maternal distress, DNA methylation, and fetal programing of stress physiology in Brazilian mother-infant pairs.

Maternal prenatal psychosocial stress is associated with adverse hypothalamic-pituitary-adrenal axis (HPAA) function among infants. Although the biological mechanisms influencing this process remain unknown, altered DNA methylation is considered to be one potential mechanism. We investigated associations between maternal prenatal psychological distress, infant salivary DNA methylation, and stress physiology at 12 months. Mother's distress was measured via depression and anxiety in early and late pregnancy in a cohort of 80 pregnant adolescents. Maternal hair cortisol was collected during pregnancy. Saliva samples were collected from infants at 12 months to quantify DNA methylation of three stress-related genes (FKBP5, NR3C1, OXTR) (n=62) and diurnal cortisol (n=29). Multivariable linear regression was used to test for associations between prenatal psychological distress, and infant DNA methylation and cortisol. Hair cortisol concentrations in late pregnancy were negatively associated with two sites of FKBP5 (site 1: B=-22.33, p=.003; site 2: B=-15.60, p=.012). Infants of mothers with elevated anxiety symptoms in late pregnancy had lower levels of OXTR2 CpG2 methylation (B=-2.17, p=.03) and higher evening salivary cortisol (B=0.41, p=.03). Furthermore, OXTR2 methylation was inversely associated with evening cortisol (B=-0.14, p-value≤.001). Our results are, to our knowledge, the first evidence that the methylation of the oxytocin receptor may contribute to the regulation of HPAA during infancy.

Prospective association of maternal psychosocial stress in pregnancy with newborn hippocampal volume and implications for infant social-emotional development

Maternal psychosocial stress during pregnancy can impact the developing fetal brain and influence offspring mental health. In this context, animal studies have identified the hippocampus and amygdala as key brain regions of interest, however, evidence in humans is sparse. We, therefore, examined the associations between maternal prenatal psychosocial stress, newborn hippocampal and amygdala volumes, and child social-emotional development.In a sample of 86 mother-child dyads, maternal perceived stress was assessed serially in early, mid and late pregnancy. Following birth, newborn (aged 5–64 postnatal days, mean: 25.8 ± 12.9) hippocampal and amygdala volume was assessed using structural magnetic resonance imaging. Infant social-emotional developmental milestones were assessed at 6- and 12-months age using the Bayley-III.After adjusting for covariates, maternal perceived stress during pregnancy was inversely associated with newborn left hippocampal volume (β = −0.26, p = .019), but not with right hippocampal (β = −0.170, p = .121) or bilateral amygdala volumes (ps > .5). Furthermore, newborn left hippocampal volume was positively associated with infant social-emotional development across the first year of postnatal life (B = 0.01, p = .011). Maternal perceived stress was indirectly associated with infant social-emotional development via newborn left hippocampal volume (B = −0.34, 95% CIBC [-0.97, −0.01]), suggesting mediation.This study provides prospective evidence in humans linking maternal psychosocial stress in pregnancy with newborn hippocampal volume and subsequent infant social-emotional development across the first year of life. These findings highlight the importance of maternal psychosocial state during pregnancy as a target amenable to interventions to prevent or attenuate its potentially unfavorable neural and behavioral consequences in the offspring.

Maternal Prenatal Psychosocial Stress and Prepregnancy BMI Associations with Fetal Iron Status.

ABSTRACTBackgroundIron accrued in utero is critical for fetal and infant neurocognitive development. Psychosocial stress and obesity can each suppress fetal iron accrual. Their combined effects and differences by fetal sex are not known. In an observational pregnancy cohort study in Mexico City, we investigated associations of maternal prenatal life stressors, psychological dysfunction, and prepregnancy BMI with fetal iron status at delivery.ObjectivesWe hypothesized that greater maternal prenatal psychosocial stress and prepregnancy overweight and obesity are associated with lower cord blood ferritin and hemoglobin (Hb), with stronger associations in boys than girls.MethodsPsychosocial stress in multiple domains of life stress (negative life events, perceived stress, exposure to violence) and psychological dysfunction symptoms (depression, generalized anxiety, and pregnancy-specific anxiety) were assessed with validated questionnaires during pregnancy. Prepregnancy BMI was predicted with a validated equation and categorized as normal/overweight/obese. Cord blood ferritin and Hb associations with prenatal psychosocial stress and BMI were modeled in multivariable linear regressions adjusted for maternal age, socioeconomic status, child sex, and prenatal iron supplementation. Interactions with child sex and 3-way stress-overweight/obesity-sex interactions were tested with product terms and likelihood ratio tests.ResultsIn 493 dyads, median (IQR) cord blood ferritin and Hb concentrations were 185 µg/L (126–263 g/dL) and 16 g/dL (14.7–17.1 g/dL), respectively. Ferritin was lower in infants of mothers with higher prenatal perceived stress (−23%; 95% CI: −35%, −9%), violence exposure (−28%; 95% CI: −42%, −12%), anxiety symptoms (−16%; 95% CI: −27%, −4%), and obesity (−17%; 95% CI: −31%, 0.2%). Interaction models suggested sex differences and synergism between maternal stress and overweight/obesity. No associations were observed between stress or BMI and Hb.ConclusionsMultiple prenatal psychosocial stressors and excess prepregnancy BMI were each inversely associated with fetal iron status at birth. Pregnancies and infants at elevated risk of impaired fetal iron accrual may be identifiable according to observed synergism between maternal stress and obesity and differential associations with fetal iron status by infant sex.

Maternal Prenatal Psychosocial Stress and BMI Predict Lower Fetal Iron Status in a Mexico City Cohort (FS01-07-19)

ObjectivesInsufficient iron in utero may impair neurocognitive development. Prenatal physiological stress, as in obesity, inhibits fetal iron accumulation. Emerging evidence suggests prenatal psychosocial stress may similarly suppress fetal iron, a novel potential mechanism linking prenatal stress and child neuro-cognition. In a pregnancy cohort in Mexico City, Mexico, we investigated associations between maternal prenatal stress and psychological function, pre-pregnancy BMI and fetal iron at delivery. We hypothesized that maternal prenatal psychosocial stress and psychological dysfunction and pre-pregnancy BMI would be associated with lower cord blood Hb and ferritin. MethodsPsychosocial stress and psychological function were assessed with validated questionnaires in mid-pregnancy: depression symptoms (CES-D), trait anxiety (STI), perceived stress (PSS-4), lifetime exposure to violence (ETV), and negative life events (NLEs, CRISYS). Pre-pregnancy BMI was calculated from self-reported height and weight. Cord blood was collected at delivery and ferritin (ferr.) and hemoglobin (Hb) measured. Regression models were developed for Hb and log-transformed ferr. as functions of dichotomized stress scores (CES-D ≥ 13, STI > median, PSS-4 > 4th quartile, ETV > 0.5, CRISYS > 1st quartile) and pre-pregnancy overweight and obesity in separate models, each adjusted for maternal age, SES, child sex and maternal prenatal iron supplementation (yes/no). ResultsIn 455 dyads with complete data, median (IQR) ferr. and Hb were 186 μg/L (125, 265) and 16 g/dL (14.7, 17), respectively. In adjusted models, lower ferr. was associated with prenatal depression symptoms (11%, 95% CI: –0.26, 0.01), elevated perceived stress (23%, –0.35, –0.09), high lifetime violence (21%, –0.33, –0.06) and high NLEs count (10%, –0.22, 0.02), as well as maternal pre-pregnancy obesity (17%, –0.31, –0.00). Interaction models suggested possible stronger prenatal stressor effects among overweight and obese mothers. No associations with cord blood Hb were observed. ConclusionsIn Mexico City pregnant women, excess pre-pregnancy BMI and multiple prenatal psychosocial stressors were each associated with fetal iron stores at birth. Insufficient fetal iron accrual may explain links between maternal prenatal stress and child neurocognitive development, but more research is needed. Funding SourcesNational Institutes of Health, Office of the Director; National Institute of Environmental Health Sciences.

Maternal Prenatal Psychosocial Stress and BMI Predict Lower Fetal Iron Status in a Mexico City Cohort (FS01-07-19)

ObjectivesInsufficient iron in utero may impair neurocognitive development. Prenatal physiological stress, as in obesity, inhibits fetal iron accumulation. Emerging evidence suggests prenatal psychosocial stress may similarly suppress fetal iron, a novel potential mechanism linking prenatal stress and child neuro-cognition. In a pregnancy cohort in Mexico City, Mexico, we investigated associations between maternal prenatal stress and psychological function, pre-pregnancy BMI and fetal iron at delivery. We hypothesized that maternal prenatal psychosocial stress and psychological dysfunction and pre-pregnancy BMI would be associated with lower cord blood Hb and ferritin. MethodsPsychosocial stress and psychological function were assessed with validated questionnaires in mid-pregnancy: depression symptoms (CES-D), trait anxiety (STI), perceived stress (PSS-4), lifetime exposure to violence (ETV), and negative life events (NLEs, CRISYS). Pre-pregnancy BMI was calculated from self-reported height and weight. Cord blood was collected at delivery and ferritin (ferr.) and hemoglobin (Hb) measured. Regression models were developed for Hb and log-transformed ferr. as functions of dichotomized stress scores (CES-D ≥ 13, STI > median, PSS-4 >4th quartile, ETV >0.5, CRISYS >1st quartile) and pre-pregnancy overweight and obesity in separate models, each adjusted for maternal age, SES, child sex and maternal prenatal iron supplementation (yes/no). ResultsIn 455 dyads with complete data, median (IQR) ferr. and Hb were 186 μg/L (125, 265) and 16 g/dL (14.7, 17), respectively. In adjusted models, lower ferr. was associated with prenatal depression symptoms (11%, 95% CI: -0.26, 0.01), elevated perceived stress (23%, -0.35, -0.09), high lifetime violence (21%, -0.33, -0.06) and high NLEs count (10%, -0.22, 0.02), as well as maternal pre-pregnancy obesity (17%, -0.31, -0.00). Interaction models suggested possible stronger prenatal stressor effects among overweight and obese mothers. No associations with cord blood Hb were observed. ConclusionsIn Mexico City pregnant women, excess pre-pregnancy BMI and multiple prenatal psychosocial stressors were each associated with fetal iron stores at birth. Insufficient fetal iron accrual may explain links between maternal prenatal stress and child neurocognitive development, but more research is needed. Funding SourcesNational Institutes of Health, Office of the Director; National Institute of Environmental Health Sciences.

Reprint of "Epigenetics, maternal prenatal psychosocial stress, and infant mental health"

This paper provides a summary of literature on epigenetic effects and infant health outcomes of maternal psychosocial stress during pregnancy. A search of literature yielded a large body of publications between 2008 and 2018. Relevant articles were selected, and additional sources were located from ancestry searches of reference lists. Results implicate maternal prenatal stress as a source of epigenetic mechanisms that affect fetal brain development and program risk for emotional dysregulation and mental disorders over a lifetime and across generations. Implications for nursing practice are explored at multiple levels of policy advocacy, public education, primary prevention, screening and intervention.

Association between Psychosocial Stress and Fecal Microbiota in Pregnant Women

Maternal prenatal psychosocial stress is associated with altered child emotional and behavioral development. One potential underlying mechanism is that prenatal psychosocial stress affects child outcomes via the mother’s, and in turn the child’s, intestinal microbiota. This study investigates the first step of this mechanism: the relation between psychosocial stress and fecal microbiota in pregnant mothers. Mothers (N = 70) provided a late pregnancy stool sample and filled in questionnaires on general and pregnancy-specific stress and anxiety. Bacterial DNA was extracted and analysed by Illumina HiSeq sequencing of PCR-amplified 16 S ribosomal RNA gene fragments. Associations between maternal general anxiety and microbial composition were found. No associations between the other measured psychosocial stress variables and the relative abundance of microbial groups were detected. This study shows associations between maternal pregnancy general anxiety and microbial composition, providing first evidence of a mechanism through which psychological symptoms in pregnancy may affect the offspring.

Epigenetics, maternal prenatal psychosocial stress, and infant mental health

This paper provides a summary of literature on epigenetic effects and infant health outcomes of maternal psychosocial stress during pregnancy. A search of literature yielded a large body of publications between 2008 and 2018. Relevant articles were selected, and additional sources were located from ancestry searches of reference lists. Results implicate maternal prenatal stress as a source of epigenetic mechanisms that affect fetal brain development and program risk for emotional dysregulation and mental disorders over a lifetime and across generations. Implications for nursing practice are explored at multiple levels of policy advocacy, public education, primary prevention, screening and intervention.

Prenatal maternal psychosocial stress and offspring's asthma and allergic disease: A systematic review and meta-analysis.

Prenatal maternal stress may influence offspring's atopic risk through sustained cortisol secretion resulting from activation of the hypothalamic-pituitary axis (HPA), leading to Th2-biased cell differentiation in the foetus. We undertook a systematic review and meta-analysis investigating the relationship between prenatal maternal psychosocial stress and risk of asthma and allergy in the offspring. We searched 11 electronic databases from 1960 to 2016, searched the grey literature and contacted experts in the field. Type of stress indicator included mood disorders, anxiety, exposure to violence, bereavement and socio-economic problems occurring during pregnancy, both objectively and subjectively measured. We included all possible asthma and IgE-mediated allergy outcomes. We conducted random-effects meta-analyses to synthesize the data. We identified 9779 papers of which 30 studies (enrolling >6 million participants) satisfied inclusion criteria. The quality of 25 studies was moderate, 4 were strong, and one was weak. Maternal exposure to any type of stressors was associated with an increased risk of offspring atopic eczema/dermatitis (OR 1.34, 95% CI 1.22-1.47), allergic rhinitis (OR 1.30, 95% CI 1.04-1.62), wheeze (OR 1.34, 95% CI 1.16-1.54) and asthma (OR 1.15, 95% CI 1.04-1.27). Exposure to anxiety and depression had strongest effect compared to other stressors. Exposure during the third trimester had the greatest impact compared to first and second trimesters. The increased risk was stronger for early-onset and persistent than for late-onset wheeze. Bereavement of a child (HR 1.28, 95% CI 1.10-1.48) or a spouse (HR 1.40, 95% CI 1.03-1.90) increased the risk of offspring asthma. Exposure to prenatal maternal psychosocial stress was associated with increased risk, albeit modestly, of asthma and allergy in the offspring. The pronounced risk during the third trimester may represent cumulative stress exposure throughout pregnancy rather than trimester-specific effect. Our findings may represent a causal effect or a result of inherent biases in studies, particularly residual confounding.

Association of Maternal Psychosocial Stress With Increased Risk of Asthma Development in Offspring.

Prenatal maternal psychosocial stress might influence the development of childhood asthma. Evaluating paternal psychosocial stress and conducting a sibling comparison could provide further insight into the role of unmeasured confounding. We examined the associations of parental psychosocial stress during and after pregnancy with asthma at age 7 years in the Norwegian Mother and Child Cohort Study (n = 63,626; children born in 2000–2007). Measures of psychosocial stress included lifetime major depressive symptoms, current anxiety/depression symptoms, use of antidepressants, anxiolytics, and/or hypnotics, life satisfaction, relationship satisfaction, work stress, and social support. Childhood asthma was associated with maternal lifetime major depressive symptoms (adjusted relative risk (aRR) = 1.19, 95% confidence interval (CI): 1.09, 1.30), in addition to symptoms of anxiety/depression during pregnancy (aRR = 1.17, 95% CI: 1.06, 1.29) and 6 months after delivery (aRR = 1.17, 95% CI: 1.07, 1.28). Maternal negative life events during pregnancy (aRR = 1.10, 95% CI: 1.06, 1.13) and 6 months after delivery (aRR = 1.14, 95% CI: 1.11, 1.18) were also associated with asthma. These associations were not replicated when evaluated within sibling groups. There were no associations with paternal psychosocial stress. In conclusion, maternal anxiety/depression and negative life events were associated with offspring asthma, but this might be explained by unmeasured maternal background characteristics that remain stable across deliveries.

Prenatal maternal psychosocial stress and risk of asthma and allergy in their offspring: protocol for a systematic review and meta-analysis.

Prenatal maternal psychosocial stress and risk of asthma and allergy in their offspring: protocol for a systematic review and meta-analysis.

The Cohort for Childhood Origin of Asthma and allergic diseases (COCOA) study: design, rationale and methods.

BackgroundThis paper describes the background, aim, and design of a prospective birth-cohort study in Korea called the COhort for Childhood Origin of Asthma and allergic diseases (COCOA). COCOA objectives are to investigate the individual and interactive effects of genetics, perinatal environment, maternal lifestyle, and psychosocial stress of mother and child on pediatric susceptibility to allergic diseases.Methods/DesignThe participants in COCOA represents a Korean inner-city population. Recruitment started on 19 November, 2007 and will continue until 31 December, 2015. Recruitment is performed at five medical centers and eight public-health centers for antenatal care located in Seoul. Participating mother-baby pairs are followed from before birth to adolescents. COCOA investigates whether the following five environmental variables contribute causally to the development and natural course of allergic diseases: (1) perinatal indoor factors (i.e. house-dust mite, bacterial endotoxin, tobacco smoking, and particulate matters 2.5 and 10), (2) perinatal outdoor pollutants, (3) maternal prenatal psychosocial stress and the child’s neurodevelopment, (4) perinatal nutrition, and (5) perinatal microbiome. Cord blood and blood samples from the child are used to assess whether the child’s genes and epigenetic changes influence allergic-disease susceptibility. Thus, COCOA aims to investigate the contributions of genetics, epigenetics, and various environmental factors in early life to allergic-disease susceptibility in later life. How these variables interact to shape allergic-disease susceptibility is also a key aim.The COCOA data collection schedule includes 11 routine standardized follow-up assessments of all children at 6 months and every year until 10 years of age, regardless of allergic-disease development. The mothers will complete multiple questionnaires to assess the baseline characteristics, the child’s exposure to environmental factors, maternal pre- and post-natal psychological stress, and the child’s neurodevelopment, nutritional status, and development of allergic and respiratory illnesses. The child’s microbiome, genes, epigenetics, plasma cytokine levels, and neuropsychological status, the microbiome of the residence, and the levels of indoor and outdoor pollutants are measured by standard procedures.DiscussionThe COCOA study will improve our understanding of how individual genetic or environmental risk factors influence susceptibility to allergic disease and how these variables interact to shape the phenotype of allergic diseases.

No associations of prenatal maternal psychosocial stress with fasting glucose metabolism in offspring at 5-6 years of age.

Highly prevalent maternal psychosocial complaints are accompanied by increases in glucocorticoid stress hormones, which may predispose the offspring for type 2 diabetes and cardiovascular disease later in adulthood. The aim of the current research is to study whether prenatal maternal psychosocial stress is associated with parameters of blood glucose metabolism in their children aged 5-6 years. The study design was a prospective birth cohort (the Amsterdam Born Children and their Development study, the Netherlands). Depressive symptoms, pregnancy-related anxiety, parenting daily hassles and job strain were recorded by questionnaire (gestational week 16). A cumulative score was also calculated. Possible sex differences in the associations were considered. The subjects were 1952 mother-child pairs. Outcome measures were fasting glucose (n=1952), C-peptide and insulin resistance (HOMA2-IR) (n=1478) in the children at the age of 5-6 years. The stress scales, single and cumulative, were not associated with glucose/C-peptide/insulin resistance (all P>0.05). We did not find evidence for sex differences. In conclusion, we did not find evidence for an association between psychosocial stress during early pregnancy and parameters of glucose metabolism in offspring at the age of 5-6 years. Differences emerging later in life or in response to a metabolic challenge should not be ruled out.

Mechanisms underlying the effects of prenatal psychosocial stress on child outcomes: beyond the HPA axis.

Accumulating evidence from preclinical and clinical studies indicates that maternal psychosocial stress and anxiety during pregnancy adversely affect child outcomes. However, knowledge on the possible mechanisms underlying these relations is limited. In the present paper, we review the most often proposed mechanism, namely that involving the HPA axis and cortisol, as well as other less well-studied but possibly relevant and complementary mechanisms. We present evidence for a role of the following mechanisms: compromised placental functioning, including the 11β-HSD2 enzyme, increased catecholamines, compromised maternal immune system and intestinal microbiota, and altered health behaviors including eating, sleep, and exercise. The roles of (epi)genetics, the postnatal environment and the fetus are also discussed. We conclude that maternal prenatal psychosocial stress is a complex phenomenon that affects maternal emotions, behavior and physiology in many ways, and may influence the physiology and functioning of the fetus through a network of different pathways. The review concludes with recommendations for future research that helps our understanding of the mechanisms by which maternal prenatal stress exerts its effect on the fetus.

Infant cortisol and behavioral habituation to weekly maternal separations: Links with maternal prenatal cortisol and psychosocial stress

Our aim was to examine infants' behavioral and physiological stress responses to three weekly maternal separations, in relation to maternal prenatal psychosocial stress and cortisol. The hypothesis was that more prenatal stress and higher cortisol concentrations would predict smaller decreases in negative behavior and cortisol responses over the separations (i.e. less habituation). General and pregnancy-related feelings of stress and anxiety, as well as circadian cortisol levels, were measured in 107 mothers in the third trimester of pregnancy. At 9 months of age, infants were subjected to three weekly 1-h maternal separations in their homes. Salivary cortisol was obtained from the infants prior to the separation and at 35, 75, and 90 min after the mother had left. For each separation, the area under the curve to the ground (AUCg) was calculated to measure the infants' cortisol response, and the sum of the time spent crying and fussing was calculated to measure the infants' behavioral response. Maternal pregnancy cortisol awakening response (CAR) significantly predicted infants' cortisol and behavioral responses. A lower CAR was related to a decreasing cortisol response, while a higher CAR was related to a stable cortisol response over all separations, as well as to less crying and fussing over all separations. Increased maternal prenatal stress, as measured by the CAR, is related to altered behavioral and cortisol responses to a repeated stressor in the 9-month-old infant. These responses might result in prolonged periods with high cortisol levels that may affect the child's development.

The association of maternal prenatal psychosocial stress with vascular function in the child at age 10–11 years: findings from the Avon longitudinal study of parents and children

ObjectiveTo investigate whether (1) maternal psychosocial stress (depression/anxiety) during pregnancy is associated with offspring vascular function and (2) whether any association differs depending on the gestational timing of exposure to stress. We also investigated whether any association is likely to be due to intrauterine mechanisms by (3) comparing with the association of paternal stress with offspring vascular function and (4) examining whether any prenatal association is explained by maternal postnatal stress.Methods and resultsAssociations were examined in a UK birth cohort, with offspring outcomes (systolic and diastolic blood pressure, SBP and DBP, endothelial function assessed by brachial artery flow-mediated dilatation (FMD); arterial stiffness assessed by carotid to radial pulse wave velocity (PWV), brachial artery distensibility (DC), and brachial artery diameter (BD) assessed at age 10–11 years (n = 4318). Maternal depressive symptoms and anxiety were assessed at 18 and 32 weeks gestation and 8 months postnatally. Paternal symptoms were assessed at week 19. With the exception of DBP and BD, there were no associations of maternal depressive symptoms with any of the vascular outcomes. Maternal depressive and anxiety symptoms were associated with lower offspring DBP and wider BD, though the latter attenuated to the null with adjustment for confounding factors. Paternal symptoms were not associated with offspring outcomes. Maternal postnatal depressive symptoms were associated with lower offspring SBP.ConclusionsWe found no evidence to support the hypothesis that maternal stress during pregnancy adversely affects offspring vascular function at age 10–12 years via intrauterine mechanisms.

Prenatal stress and balance of the child's cardiac autonomic nervous system at age 5-6 years.

ObjectiveAutonomic nervous system (ANS) misbalance is a potential causal factor in the development of cardiovascular disease. The ANS may be programmed during pregnancy due to various maternal factors. Our aim is to study maternal prenatal psychosocial stress as a potential disruptor of cardiac ANS balance in the child.MethodsMothers from a prospective birth cohort (ABCD study) filled out a questionnaire at gestational week 16 [IQR 12–20], that included validated instruments for state anxiety, depressive symptoms, pregnancy-related anxiety, parenting daily hassles and job strain. A cumulative stress score was also calculated (based on 80th percentiles). Indicators of cardiac ANS in the offspring at age 5–6 years are: pre-ejection period (PEP), heart rate (HR), respiratory sinus arrhythmia (RSA) and cardiac autonomic balance (CAB), measured with electrocardiography and impedance cardiography in resting supine and sitting positions.Results2,624 mother-child pairs, only single births, were available for analysis. The stress scales were not significantly associated with HR, PEP, RSA and CAB (p≥0.17). Accumulation of maternal stress was also not associated with HR, PEP, RSA and CAB (p≥0.07).Conclusion Results did not support the hypothesis that prenatal maternal psychosocial stress deregulates cardiac ANS balance in the offspring, at least in rest, and at the age of five-six years.

Prenatal maternal stress programs infant stress regulation

Prenatal exposure to inappropriate levels of glucocorticoids (GCs) and maternal stress are putative mechanisms for the fetal programming of later health outcomes. The current investigation examined the influence of prenatal maternal cortisol and maternal psychosocial stress on infant physiological and behavioral responses to stress. The study sample comprised 116 women and their full term infants. Maternal plasma cortisol and report of stress, anxiety and depression were assessed at 15, 19, 25, 31 and 36 + weeks' gestational age. Infant cortisol and behavioral responses to the painful stress of a heel-stick blood draw were evaluated at 24 hours after birth. The association between prenatal maternal measures and infant cortisol and behavioral stress responses was examined using hierarchical linear growth curve modeling. A larger infant cortisol response to the heel-stick procedure was associated with exposure to elevated concentrations of maternal cortisol during the late second and third trimesters. Additionally, a slower rate of behavioral recovery from the painful stress of a heel-stick blood draw was predicted by elevated levels of maternal cortisol early in pregnancy as well as prenatal maternal psychosocial stress throughout gestation. These associations could not be explained by mode of delivery, prenatal medical history, socioeconomic status or child race, sex or birth order. These data suggest that exposure to maternal cortisol and psychosocial stress exerts programming influences on the developing fetus with consequences for infant stress regulation.

Cardio-metabolic risk in 5-year-old children prenatally exposed to maternal psychosocial stress: the ABCD study.

BackgroundRecent evidence, both animal and human, suggests that modifiable factors during fetal and infant development predispose for cardiovascular disease in adult life and that they may become possible future targets for prevention. One of these factors is maternal psychosocial stress, but so far, few prospective studies have been able to investigate the longer-term effects of stress in detail, i.e. effects in childhood. Therefore, our general aim is to study whether prenatal maternal psychosocial stress is associated with an adverse cardio-metabolic risk profile in the child at age five.Methods/designData are available from the Amsterdam Born Children and their Development (ABCD) study, a prospective birth cohort in the Netherlands. Between 2003-2004, 8,266 pregnant women filled out a questionnaire including instruments to determine anxiety (STAI), pregnancy related anxiety (PRAQ), depressive symptoms (CES-D), parenting stress (PDH scale) and work stress (Job Content Questionnaire).Outcome measures in the offspring (age 5-7) are currently collected. These include lipid profile, blood glucose, insulin sensitivity, body composition (body mass index, waist circumference and bioelectrical impedance analysis), autonomic nervous system activity (parasympathetic and sympathetic measures) and blood pressure.Potential mediators are maternal serum cortisol, gestational age and birth weight for gestational age (intrauterine growth restriction). Possible gender differences in programming are also studied.DiscussionMain strengths of the proposed study are the longitudinal measurements during three important periods (pregnancy, infancy and childhood), the extensive measurement of maternal psychosocial stress with validated questionnaires and the thorough measurement of the children's cardio-metabolic profile. The availability of several confounding factors will give us the opportunity to quantify the independent contribution of maternal stress during pregnancy to the cardio-metabolic risk profile of her offspring. Moreover, the mediating role of maternal cortisol, intrauterine growth, gestational age and potential gender differences can be explored extensively. If prenatal psychosocial stress is indeed found to be associated with the offspring's cardio-metabolic risk, these results support the statement that primary prevention of cardiovascular disease may start even before birth by reducing maternal stress during pregnancy.