Neurobehavioral Risk From Fetal Exposure to Stress Hormones
Neurobehavioral Risk From Fetal Exposure to Stress Hormones
In a previous study of 158 newborns within 24 h after birth, the authors found that fetal exposure to increased levels of maternal cortisol at 15 and 19 weeks gestation and increased levels of placental CRH at 31-weeks gestation were associated with significant decreases in newborn physical and neuromuscular maturation. These effects were observed after adjusting for length of gestation, indicating that fetal exposure to stress hormones programs neonatal neuromuscular maturation independent of GA. These observations in the neonate provide strong support for fetal programming because the consequences of gestational exposures cannot be explained by postnatal influences such as quality of maternal care.
In a large study (125 subjects) of the cognitive consequences of fetal exposures to stress hormones, the authors reported that high levels of maternal cortisol early in pregnancy resulted in significantly lower scores on measures of mental development at 12 months of age. Elevated maternal cortisol late in gestation, however, was associated with significantly better scores on measures of mental development. It is important to remember that the human fetus is partially protected from elevations of maternal cortisol early in pregnancy because it is oxidized and inactivated by the enzyme 11β-HSD2. However, 11β-HSD2 is only a partial barrier, which explains why maternal and fetal cortisol levels are correlated. Thus, synthesis and release of elevated levels of maternal cortisol exposes the fetus to concentrations that may have detrimental neurological consequences, especially when these exposures occur early in gestation. As described earlier, fetal exposure to elevated cortisol is necessary for maturation of the fetal nervous system and lungs as pregnancy advances towards term. Fetal exposure to cortisol during the third trimester is ensured by the sharp drop in 11β-HSD2, which allows a greater proportion of maternal cortisol to cross the placental barrier. These results indicate that gestational exposure to maternal stress hormones has a significant influence on the fetal nervous system with potentially long-term consequences for mental processes such as memory and attention and that these consequences are determined by the timing of exposure. Maternal psychological distress signals early in gestation were also associated with delays in mental development. Consistent with the observations for stress and emotional regulation, the consequences of psychological distress were independent from the effects of maternal cortisol. These data indicate that exposure to maternal psychobiological distress early in gestation is associated with an increased risk for cognitive impairments.
The authors report new findings that fetal exposure to maternal anxiety exerts persisting consequences on child cognition. High levels of maternal pregnancy-specific anxiety over the course of gestation were associated with lower inhibitory control in 6–9-year-old girls and poorer visuospatial working memory performance in both girls and boys. The findings are highly consistent with the observations during infancy and contribute to the literature supporting an association between prenatal anxiety and cognitive development. This study provides evidence about the persistence of this effect until middle childhood.
The authors have shown that fetal exposure to maternal anxiety was related to specific changes in brain morphology of children independent of birth phenotype. Specifically, maternal reports of anxiety about pregnancy early in gestation were associated with gray matter volume reductions in many areas of the brain that are associated with a variety of cognitive abilities. Specifically, prefrontal cortical areas that are responsible for executive functions such as reasoning, planning, attention, working memory and some aspects of language were reduced. Moreover, structures in the medial temporal lobe were reduced, including areas connected to the hippocampus that constitute a medial temporal lobe memory system. Reduced volume was observed in children whose mothers reported high levels of anxiety in the temporal polar cortex that is associated with social and emotional processing, including recognition and semantic memory. Reduction of volume in an auditory network and in brain systems involved in language learning was observed in children whose mothers reported high levels of anxiety early in gestation. The prospective longitudinal studies provide evidence that exposures to both maternal cortisol and maternal psychological distress early in gestation alter trajectories of brain development and increase risk for cognitive impairments, and that these effects persist at least into pre-adolescence.
Maternal Fight or Flight System Influences Cognition & Brain Development
Neonates
In a previous study of 158 newborns within 24 h after birth, the authors found that fetal exposure to increased levels of maternal cortisol at 15 and 19 weeks gestation and increased levels of placental CRH at 31-weeks gestation were associated with significant decreases in newborn physical and neuromuscular maturation. These effects were observed after adjusting for length of gestation, indicating that fetal exposure to stress hormones programs neonatal neuromuscular maturation independent of GA. These observations in the neonate provide strong support for fetal programming because the consequences of gestational exposures cannot be explained by postnatal influences such as quality of maternal care.
Infants
In a large study (125 subjects) of the cognitive consequences of fetal exposures to stress hormones, the authors reported that high levels of maternal cortisol early in pregnancy resulted in significantly lower scores on measures of mental development at 12 months of age. Elevated maternal cortisol late in gestation, however, was associated with significantly better scores on measures of mental development. It is important to remember that the human fetus is partially protected from elevations of maternal cortisol early in pregnancy because it is oxidized and inactivated by the enzyme 11β-HSD2. However, 11β-HSD2 is only a partial barrier, which explains why maternal and fetal cortisol levels are correlated. Thus, synthesis and release of elevated levels of maternal cortisol exposes the fetus to concentrations that may have detrimental neurological consequences, especially when these exposures occur early in gestation. As described earlier, fetal exposure to elevated cortisol is necessary for maturation of the fetal nervous system and lungs as pregnancy advances towards term. Fetal exposure to cortisol during the third trimester is ensured by the sharp drop in 11β-HSD2, which allows a greater proportion of maternal cortisol to cross the placental barrier. These results indicate that gestational exposure to maternal stress hormones has a significant influence on the fetal nervous system with potentially long-term consequences for mental processes such as memory and attention and that these consequences are determined by the timing of exposure. Maternal psychological distress signals early in gestation were also associated with delays in mental development. Consistent with the observations for stress and emotional regulation, the consequences of psychological distress were independent from the effects of maternal cortisol. These data indicate that exposure to maternal psychobiological distress early in gestation is associated with an increased risk for cognitive impairments.
Children
The authors report new findings that fetal exposure to maternal anxiety exerts persisting consequences on child cognition. High levels of maternal pregnancy-specific anxiety over the course of gestation were associated with lower inhibitory control in 6–9-year-old girls and poorer visuospatial working memory performance in both girls and boys. The findings are highly consistent with the observations during infancy and contribute to the literature supporting an association between prenatal anxiety and cognitive development. This study provides evidence about the persistence of this effect until middle childhood.
The authors have shown that fetal exposure to maternal anxiety was related to specific changes in brain morphology of children independent of birth phenotype. Specifically, maternal reports of anxiety about pregnancy early in gestation were associated with gray matter volume reductions in many areas of the brain that are associated with a variety of cognitive abilities. Specifically, prefrontal cortical areas that are responsible for executive functions such as reasoning, planning, attention, working memory and some aspects of language were reduced. Moreover, structures in the medial temporal lobe were reduced, including areas connected to the hippocampus that constitute a medial temporal lobe memory system. Reduced volume was observed in children whose mothers reported high levels of anxiety in the temporal polar cortex that is associated with social and emotional processing, including recognition and semantic memory. Reduction of volume in an auditory network and in brain systems involved in language learning was observed in children whose mothers reported high levels of anxiety early in gestation. The prospective longitudinal studies provide evidence that exposures to both maternal cortisol and maternal psychological distress early in gestation alter trajectories of brain development and increase risk for cognitive impairments, and that these effects persist at least into pre-adolescence.
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