Objectives: The purpose of this study was to determine the relationship between fetal exposure to maternal prenatal stressors and infant parasympathetic (PNS) and sympathetic (SNS) nervous function at 3 timepoints across the first year of life.
Background: Autonomic nervous system impairments may mediate associations between gestational exposure to stressors and later infant health problems. Heart rate variability (HRV) provides a sensitive index of PNS and SNS function. However, no studies have assessed longitudinal associations between prenatal stressors and infant HRV measures of both PNS and SNS over the first year of life.
Methods: During the third trimester of pregnancy, 233 women completed measures of life stressors and depression. At 1, 6 and 12 months of age, a stressor protocol was administered while infant electrocardiographic (ECG) data were collected from a baseline through a post-stressor period. HRV measures of PNS and SNS activity (HF, LF, LF/HF ratio) were generated from ECG data. We used multilevel regression to examine the aims, adjusting for maternal depression and neonatal morbidity.
Results: There were no associations between prenatal stressors and any baseline or reactivity HRV metric over the infant's first year of life. However, exposure to more stressors was associated with lower post-stressor LF HRV at both 6 (β = -.44, = .001) and 12 (β = -.37, = .005) months of age.
Conclusions: Findings suggest potential alterations in development of the vagally mediated baroreflex function as a result of exposure to prenatal stressors, with implications for the infants' ability to generate a resilient recovery in response to stressors.
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http://dx.doi.org/10.1080/10253890.2024.2327328 | DOI Listing |
Fam Pract
January 2025
Department of Public Health, Centre for General Practice, University of Copenhagen, Øster Farimagsgade 5 1353, København K, Denmark.
Background: Antenatal depression and anxiety are associated with preterm labour, low birth weight, and postpartum depression, and can impact the emotional and mental development of the child. Both adverse childhood experiences and recent stressful events are linked to negative health outcomes. However, certain events may be more impactful than others.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Laboratory of Comparative Developmental Physiology, Koltzov Institute of Developmental Biology of the Russian Academy of Sciences, 119334 Moscow, Russia.
Available evidence from animal studies suggests that placental serotonin plays an important role in proper fetal development and programming by altering brain circuit formation, which later translates into altered abnormal adult behaviors. Several environmental stimuli, including stress and maternal inflammation, affect placental and, hence, fetal serotonin levels and thus may disturb fetal brain development. We investigated the effect of prenatal stress of varying intensities on the formation of adaptive behaviors in mouse offspring and the role of placental serotonin in these processes.
View Article and Find Full Text PDFAnnu Rev Dev Psychol
December 2024
Department of Child and Adolescent Psychiatry, New York University Medical Center, New York, NY, USA.
This review summarizes recent findings on stress-related programming of brain development , with an emphasis on situating findings within the mothers' broader psychosocial experiences. Meta-analyses of observational studies on prenatal stress exposure indicate the direction and size of effects on child neurodevelopment are heterogeneous across studies. Inspired by lifespan and topological frameworks of adversity, we conceptualize individual variation in mothers' lived experience during and prior to pregnancy as a key determinant of these heterogeneous effects across populations.
View Article and Find Full Text PDFBrain Behav Immun Integr
December 2024
Biomedical Sciences, Colorado State University, Fort Collins, CO, United States.
Maternal immune activation (MIA), a maternal stressor, increases risk for neuropsychiatric diseases, such as Major Depressive Disorder in offspring. MIA of toll-like receptor 7 (TLR7) initiates an immune response in mother and fetuses in a sex-selective manner. The paraventricular nucleus of the hypothalamus (PVN), a brain region that is sexually dimorphic and regulates hypothalamic-pituitary-adrenal (HPA) stress responses, have been tied to stress-related behaviors (i.
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