Cardiovascular effects of prenatal stress-Are there implications for cerebrovascular, cognitive and mental health
Julia J Müller1, Iwa Antonow-Schlorke1, Nasim Kroegel1
1Hans Berger Department of Neurology, Jena University Hospital, Jena, Germany.
Insights
Prenatal stress, especially maternal anxiety, can negatively impact fetal circulation and neurodevelopment, potentially leading to cardiovascular issues. More research is needed on long-term effects on brain health and cognition.
Area of Science:
- Neuroscience
- Cardiovascular Science
- Developmental Biology
Background:
- Prenatal stress is known to affect offspring cognitive and mental health.
- The impact of prenatal stress on cardiovascular dysfunction and its link to cerebrovascular, cognitive, and mental health disorders requires further investigation.
- Maternal stress and prenatal glucocorticoid (GC) exposure have distinct programming effects due to placental differences in cortisol inactivation and GC permeability.
Purpose of the Study:
- To review the programming effects of prenatal stress and glucocorticoid exposure on cardiovascular dysfunction.
- To explore the potential modulation of cerebrovascular, cognitive, and mental health disorders by prenatal stress-induced cardiovascular changes.
- To differentiate the programming effects of maternal stress versus direct GC exposure during gestation.
Main Methods:
- Review of experimental data on maternal stress and prenatal GC exposure in early and mid-gestation.
- Analysis of potential programming mechanisms including cardiac and kidney development, the renin-angiotensin-aldosterone system, stress axis, and vasculature.
- Identification of gaps in human studies, particularly concerning older age and cerebrovascular/cognitive/mental health outcomes.
Main Results:
- Maternal stress, particularly anxiety, adversely affects maternal-fetal circulation via sympathetic nervous system activation and increased fetal catecholamines, potentially impairing neurodevelopment.
- Unlike maternal stress, GC exposure has different programming effects, with synthetic GCs crossing the placenta more readily.
- Experimental data suggest severe maternal stress and GC exposure may increase cardiovascular disorder risk, with programming mechanisms involving developmental aberrations and functional vascular changes.
Conclusions:
- Prenatal stress, especially maternal anxiety, can initiate cardiovascular programming with potential long-term health consequences.
- While experimental data exist, human studies on the long-term cardiovascular, cerebrovascular, cognitive, and mental health consequences of prenatal stress are scarce, particularly in older populations.
- Further research is crucial to fully understand the complex interplay between prenatal stress, cardiovascular health, and neurodevelopmental outcomes across the lifespan.
Abstract:
Prenatal stress programs offspring cognitive and mental health outcome. We reviewed whether prenatal stress also programs cardiovascular dysfunction which potentially modulates cerebrovascular, cognitive and mental health disorders. We focused on maternal stress and prenatal glucocorticoid (GC) exposure which have different programming effects. While maternal stress induced cortisol is mostly inactivated by the placenta, synthetic GCs freely cross the placenta and have different receptor-binding characteristics. Maternal stress, particularly anxiety, but not GC exposure, has adverse effects on maternal-fetal circulation throughout pregnancy, probably by co-activation of the maternal sympathetic nervous system, and by raising fetal catecholamines. Both effects may impair neurodevelopment. Experimental data also suggest that severe maternal stress and GC exposure during early and mid-gestation may increase the risk for cardiovascular disorders. Human data are scarce and especially lacking for older age. Programming mechanisms include aberrations in cardiac and kidney development, and functional changes in the renin-angiotensin-aldosterone-system, stress axis and peripheral and coronary vasculature. Adequate experimental or human studies examining the consequences for cerebrovascular, cognitive and mental disorders are unavailable.
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