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Associations between different dimensions of prenatal distress, neonatal hippocampal connectivity, and infant memory.

ABSTRACT: Prenatal maternal distress-an umbrella concept encompassing multiple negative psychological states including stress, anxiety, and depression-is a substantial prenatal exposure. Consistent across preclinical and human studies, the hippocampus displays alterations due to prenatal distress. Nevertheless, most prenatal distress studies do not focus on multiple dimensions of, have not examined hippocampal functional connectivity in association with, and do not consider observer-based functional outcomes related to distress. We investigated the effects of different dimensions of prenatal distress in pregnant adolescents, a population at high risk for distress, in association with neonatal hippocampal connectivity and infant memory. In pregnant adolescents (n = 42), we collected four measures of distress (perceived stress, depression, pregnancy-specific distress, and 24-h ambulatory salivary cortisol) during the 2nd and 3rd trimesters. Resting-state imaging data were acquired in their infants at 40-44 weeks post-menstrual age. Functional connectivity was measured from hippocampal seeds. Memory abilities were obtained at 4 months using the mobile conjugate reinforcement task. Shared across different dimensions of maternal distress, increased 3rd trimester maternal distress associated with weaker hippocampal-cingulate cortex connectivity and stronger hippocampal-temporal lobe connectivity. Perceived stress inversely correlated while hippocampal-cingulate cortex connectivity positively correlated with infant memory. Increased cortisol-collected during the 2nd, but not the 3rd, trimester-associated with weaker hippocampal-cingulate cortex connectivity and stronger hippocampal-temporal lobe connectivity. Different dimensions of prenatal maternal distress likely contribute shared and unique effects to shaping infant brain and behavior.

SUBMITTER: Scheinost D

PROVIDER: S-EPMC7297970 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundThe COVID-19 pandemic has caused substantially elevated distress in pregnant individuals, which has the potential to affect the developing infant brain. Our main objective was to understand how prenatal distress was related to infant brain structure and function and whether social support moderated the associations.MethodsThe Pregnancy during the COVID-19 Pandemic (PdP) cohort study collected Patient-Reported Outcomes Measurement Information System Anxiety scale, Edinburgh Postnatal Depression Scale, and Social Support Effectiveness Questionnaire data from a population-based sample of pregnant individuals living in Canada (N = 8602). For a subsample of participants, their infants (n = 75) underwent magnetic resonance imaging at 3 months of age to examine whether prenatal maternal distress was associated with infant brain architecture, including the role of social support as a potential protective factor.ResultsOverall, 33.4% of participants demonstrated clinically elevated depression symptoms and 47.1% of participants demonstrated clinically elevated anxiety symptoms. We identified lower social support as a significant predictor of clinically elevated prenatal maternal distress (t8598 = -22.3, p < .001). Fifty-eight diffusion image datasets (20 female/38 male, 92 ± 14 days old) and 41 functional datasets (13 female/28 male, 92 ± 14 days old) were included in our analysis after removal of poor-quality images and infants without postpartum maternal distress scores. We found significant relationships between prenatal maternal distress and infant amygdala-prefrontal microstructural and functional connectivity measures, and we demonstrate for the first time that social support moderates these relationships.ConclusionsOur findings suggest a potentially long-lasting impact of the COVID-19 pandemic on children and show that social support acts as a possible mediator not just for pregnant individuals but also developing infants. These findings provide timely evidence to inform clinical practice and policy surrounding the care of pregnant individuals and highlight the importance of social support.

Project description:BackgroundPrenatal alcohol exposure (PAE) is associated with postnatal iron deficiency (ID), which has been shown to exacerbate deficits in growth, cognition, and behavior seen in fetal alcohol spectrum disorders. However, the mechanisms underlying PAE-related ID remain unknown.ObjectivesWe aimed to examine biochemical measures of iron homeostasis in the mother, placenta, neonate, and 6.5-month-old infant.MethodsIn a prenatally recruited, prospective longitudinal birth cohort in South Africa, 206 gravidas (126 heavy drinkers and 80 controls) were interviewed regarding alcohol, cigarette, and drug use and diet at 3 prenatal visits. Hemoglobin, ferritin, and soluble transferrin receptor (sTfR) were assayed twice during pregnancy and urinary hepcidin:creatinine was assayed once. Infant ferritin and hemoglobin were measured at 2 weeks and 6.5 months and sTfR was measured at 6.5 months. Histopathological examinations were conducted on 125 placentas and iron transport assays (iron regulatory protein-2, transferrin receptor-1, divalent metal transporter-1, ferroportin-1, and iron concentrations) were conducted on 63.ResultsIn multivariable regression models, prenatal drinking frequency (days/week) was related to higher maternal hepcidin and to sequestration of iron into storage at the expense of erythropoiesis in mothers and neonates, as evidenced by a lower hemoglobin (g/dL)-to-log(ferritin) (ug/L) ratio [mothers: raw regression coefficient (β) = -0.21 (95% CI: -0.35 to -0.07); neonates: β = -0.15 (95% CI: -0.24 to -0.06)]. Drinking frequency was also related to decreased placental ferroportin-1:transferrin receptor-1 (β = -0.57 for logged values; 95% CI: -1.03 to -0.10), indicating iron-restricted placental iron transport. At 6.5 months, drinking frequency was associated with lower hemoglobin (β = -0.18; 95% CI: -0.33 to -0.02), and increased prevalences of ID (β = 0.09; 95% CI: 0.02-0.17) and ID anemia (IDA) (β = 0.13; 95% CI: 0.04-0.23). In causal inference analyses, the PAE-related increase in IDA was partially mediated by decreased neonatal hemoglobin:log(ferritin), and the decrease in neonatal hemoglobin:log(ferritin) was partially mediated by decreased maternal hemoglobin:log(ferritin).ConclusionsIn this study, greater PAE was associated with an unfavorable profile of maternal-fetal iron homeostasis, which may play mechanistic roles in PAE-related ID later in infancy.

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Associations between different dimensions of prenatal distress, neonatal hippocampal connectivity, and infant memory.

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