Jun 2026· International Journal of Epidemiology· Vol 55· 0 citations· 50 references
Medicine
TL;DR
It is suggested that acute maternal stress during pregnancy is associated with cardiovascular risk factors in offspring in adolescence and is modulated by the timing of the exposure.
Abstract
Abstract Background Cardiometabolic risk factors are major contributors to poor health outcomes and premature mortality. While the effect of prenatal exposure to stress on cardiometabolic outcomes has been examined, the findings remain inconsistent across studies, and even more so with regard to the timing of exposure. In the present study, we aimed to explore the association of short-term prenatal exposure to the acute stress of the 1967 Six-Day War with cardiovascular and anthropometric risk factors in adolescent offspring. Methods Using a population-based birth cohort, we examined data from 61 237 offspring born in Jerusalem during 1964–76, linked to their military-draft records at age 17 years. These provided information on those exposed to acute prenatal stress and the timing of exposure within the pregnancy (N = 2471) as well as on height, weight, heart rate (HR), and blood pressure (BP) in adolescence. Linear regression models estimated the associations between prenatal stress and measurements at age 17 years, controlling for potential confounders. Results Prenatal exposure to acute stress was associated with increased systolic blood pressure (SBP) and diastolic blood pressure (DBP) [SBP: B = 1.85, 95% confidence interval (CI): 1.15, 2.56; DBP: B = 1.89, 95% CI: 1.40, 2.38] and a decreased HR (B = –1.39, CI: –1.88, –0.91) but not with anthropometric outcomes. Furthermore, gestational age at exposure modified these associations: the associations with DBP and mean arterial pressure tended to increase and with HR to decrease the later the exposure occurred during the pregnancy. Conclusion Findings suggest that acute maternal stress during pregnancy is associated with cardiovascular risk factors in offspring in adolescence and is modulated by the timing of the exposure.
Cardiovascular disease (CVD) is the leading cause of death among women, yet how psychosocial experiences across the life course contribute to early maternal cardiovascular risk is not well-understood. Pregnancy and the years following childbirth represent a critical window for identifying emerging cardiometabolic vulnerability. The primary goals of this dissertation were to examine how childhood experiences and everyday discrimination during pregnancy are associated with maternal CVD risk factors assessed at 3-4 years postpartum.
This dissertation addressed these aims through two independent, prospective studies conducted using a longitudinal cohort of 223 individuals recruited during pregnancy and followed through 3-4 years postpartum. Study 1 examined whether everyday discrimination during pregnancy, often a chronic psychosocial stressor, was associated with maternal CVD risk factors (body mass index [BMI], waist circumference, body fat percentage, systolic and diastolic blood pressure, arterial stiffness, and a composite CVD risk index). Study 2 examined whether adverse childhood experiences (ACEs) and positive childhood experiences (PCEs) were associated with the same cardiovascular outcomes and tested whether obstetric complications (e.g., hypertensive disorders of pregnancy, preterm birth, etc.) mediated these associations.
In Study 1, linear regression analyses found that greater everyday discrimination during pregnancy was significantly associated with higher arterial stiffness at 3-4 years postpartum, even after controlling for sociodemographic factors and other stressful life events during pregnancy. Everyday discrimination was not associated with BMI, waist circumference, body fat percentage, blood pressure, or composite CVD risk. In Study 2, greater ACEs were consistently associated with higher composite CVD risk, BMI, waist circumference, body fat percentage, systolic blood pressure, and arterial stiffness in adjusted models. Greater PCEs were associated with lower arterial stiffness, but not other outcomes. Obstetric complications did not mediate associations between childhood experiences and cardiovascular risk, although they were independently associated with multiple CVD risk factors.
Together, these findings suggest that early experiences and psychosocial stressors during pregnancy are associated with maternal cardiovascular health in the years following childbirth through distinct patterns. ACEs were broadly linked to greater CVD risk, whereas everyday discrimination during pregnancy and PCEs were specifically associated with arterial stiffness in opposite directions. These results highlight the importance of a life course perspective for understanding maternal cardiovascular risk and highlight pregnancy and the years following childbirth as key windows for early identification and prevention.
Background: Prenatal maternal stress is increasingly recognized as a critical determinant of fetal programming, with potential consequences for early physical growth and neurodevelopment. Although a growing body of evidence links maternal psychological stress to adverse perinatal and developmental outcomes, most studies originate from high-income Western settings, rely predominantly on self-reported stress measures, and rarely incorporate biological stress markers. Evidence from post-Soviet regional contexts remains limited. Methods: A two-phase study was conducted in Tbilisi, Georgia. Phase I employed a cross-sectional observational design involving 398 pregnant women recruited from maternity homes and women’s consultations. Maternal psycho-emotional stress was assessed using a study-specific pregnancy stress questionnaire, and salivary cortisol was measured in a subsample of women reporting chronic stress (N = 95). Phase II used a prospective cohort design to follow infants born to stress-exposed mothers (N = 95) and non-stressed controls (N = 95) from birth to 12 months. Infant outcomes included anthropometric measurements evaluated using World Health Organization Child Growth Standards and neurodevelopmental screening using the Ages & Stages Questionnaires, Third Edition (ASQ-3), at 1–3, 5–7, and 11–13 months. Statistical analyses were made by SPSS 23.0. Results: Salivary cortisol assessment in the stress-exposed subsample provided supportive biological evidence of elevated stress levels but was not used for direct comparison with the control group. Children born to stress-exposed mothers showed significantly poorer physical growth and lower ASQ-3 scores across all developmental domains during the first year of life (all p < 0.05). Conclusions: This study provides novel evidence from an underrepresented regional context and supports early developmental surveillance and preventive strategies to improve maternal and child health outcomes.
N. Masiukovichi, W. M. Caudle, T. Masiukovichi et al.· Healthcare· 0 citations
Hypertensive disorders of pregnancy (HDP) affect 5–10% of pregnancies globally and are a leading cause of maternal and fetal morbidity and mortality. Beyond their acute obstetrics impact, HDP unmask a lifelong cardiovascular (CV) vulnerability in affected women and confer intergenerational risk to their offspring. In this review, we discuss the latest evidence regarding the CV risk profiles following HDP in the mothers and their offspring. In mothers, HDP is associated with a 7.29-fold increased risk of new chronic hypertension (HTN) within 24 months postpartum and long-term risks of heart failure, coronary heart disease and stroke. Offspring exposed carry a 1.5-fold increased risk for adult HTN and increased risks for ischemic heart disease and stroke. We review evidence on potential pathophysiologic mechanisms including shared genetic, epigenetic programming and persistent immune dysregulation that contribute to the CV risk. We make recommendations on surveillance strategies in mothers and their offspring beginning in the immediate postpartum period and for lifelong follow-up. Management strategies of the CV risk factors, using latest guidelines are discussed. We suggest future directions for research and intervention. Integrated maternal-offspring CV care, women-specific risk prediction tools and equity focused research are needed to reduce the intergenerational burden of HDP.
Abstract Background Maternal perinatal stress links to developmental delay and later vulnerability to psychiatric disease in the offspring. Low social support in pregnancy relates to anxiety and attention deficit hyperactivity disorder in 8 year old offspring. The biological mechanisms remain unclear and may involve early alterations of fetal growth factors such as brain-derived neurotrophic factor (BDNF) and insulin-like growth factor (IGF)-1. Aims & Objectives We aimed to analyze the link between maternal stress and fetal growth factors (IGF-1, BDNF) in amniotic fluid in mid-pregnancy and at birth. The association of fetal growth factors with anthropometrics at birth was assessed. Method In two prospective cohorts of women undergoing amniocentesis at 15.9 ± 0.9 weeks (n=79), and women undergoing elective cesarean section at 39.5 ± 1.5 weeks (n=41), maternal stress (childhood trauma, psychiatric symptoms including depressive symptoms, anxiety, social support, socioeconomic status and glucocorticoids in amniotic fluid) was assessed and related to fetal IGF-1 in amniotic fluid in mid-pregnancy and at birth and to BDNF in cord blood and in amniotic fluid at birth. Results Presence of maternal childhood trauma was linked to lower fetal IGF-1 in mid-pregnancy in amniotic fluid (M=3.48 vs. 2.98, p=0.012), with the sexual abuse subscale linked to lower IGF-1 in mid-pregnancy (p=0.006) and at birth (p=0.049). Fetal IGF-1 in mid-pregnancy showed a trend-level association with newborn weight at birth (p=0.096). Higher maternal depressive symptoms and lower socioeconomic status at birth were associated with higher fetal BDNF in cord blood at birth (p=0.002; p=0.002). Increased glucocorticoids in amniotic fluid at birth were linked to higher fetal BDNF in amniotic fluid at birth (p<0.001), and fetal BDNF in amniotic fluid at birth was further related to newborn weight adjusted for gestational age (p<0.001). Discussion & Conclusions Higher maternal stress was associated with altered levels of fetal growth factors, underlying that specific aspects of maternal stress can influence fetal neurodevelopmental markers. Additionally, IGF-1 and BDNF levels were linked to newborn weight. Birth weight is a known predictor for later somatic and psychiatric disorders. These results may reflect a potential early biological pathway to long-term vulnerability. These findings show that maternal stress can impact fetal endocrine regulation as early as in mid-pregnancy and at birth.
E. K. Lamadé, F. Hendlmeier, P. Meininger et al.· International Journal of Neu...· 0 citations
Pregnancy provides a unique physiological stress test for the cardiovascular system, during which, adverse pregnancy outcomes (APOs) can unmask latent susceptibility to future disease. Common complications, including hypertensive disorders of pregnancy (HDP), gestational diabetes, and preterm birth (delivery before 37 weeks' gestation), identify women at substantially higher long-term risk of cardiovascular morbidity and mortality compared with women without a history of APOs. These excess risks likely reflect the combined effects of pre-existing cardiometabolic and genetic susceptibility, as well as the haemodynamic and metabolic stressors of pregnancy, heralding accelerated risk factor trajectories, relative impairment in endothelial and microvascular function, and early disease onset. This final Review in the Series extends the focus from cardiovascular disease during pregnancy and HDP to the long-term cardiovascular implications of APOs after delivery. We synthesise epidemiological data quantifying cardiovascular risk across major APO phenotypes and emerging evidence linking maternal APO history with cardiometabolic risk trajectories in offspring. We also delineate putative mechanistic pathways and summarise guidelines and consensus-informed recommendations for short-term and long-term follow-up after APOs. Finally, we propose practical approaches for integrating APO history into cardiovascular disease risk assessment and guideline-directed prevention across the female life course. We highlight key knowledge gaps, including uncertainty about optimal follow-up models, the limitations of current risk-stratification tools, and the absence of APO-specific prevention trials. We also outline priorities for mechanistic and implementation research. Positioning APOs as early, sex-specific indicators of cardiovascular risk offers a key window of opportunity to shift prevention upstream and improve cardiovascular health outcomes for women.
M. A. Pabón, Graeme N. Smith, Garima Sharma et al.· The Lancet· 2 citations
Little evidence that maternal smoking initiation affected WHR is found, and little evidence that maternal smoking heaviness affected the remaining cardiometabolic risk factors; paternal smoking showed no clear effect on any outcome.
G. Power, T. Bond, L. Bhatta et al.· BMC Medicine· 0 citations
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