Abstract
To test alterations in placental cellular aging as one pathway by which maternal early adversity influences physiologic development in her offspring.Maternal report of her adverse childhood experiences (ACE) was obtained prenatally along with measures of prenatal stress and demographic information. Placentas (N = 67) were collected at birth and telomere length (TL) was measured in four separate fetally-derived placental tissues: amnion, chorion, villus, and umbilical cord. At four months of age, infants completed the still-face paradigm (SFP) during which respiratory sinus arrhythmia (RSA) data were collected; RSA reactivity and RSA recovery was available from 44 and 41 infants respectively. Multi-level mixed effects models examined the impact of maternal ACE score on placental TL. Generalized linear models tested the relation between composite placental TL and infant RSA, as well as the moderation of maternal ACE score and infant RSA by composite placental TL.Higher maternal ACE score significantly predicted shorter placental TL across tissues (β = −0.015; P = 0.036) and infant RSA across the SFP. No direct relation was found between placental TL and RSA, however composite placental TL moderated the relation between ACE score and both infant RSA reactivity (β = 0.025; P = 0.005) and RSA recovery (β = −0.028; P = 0.032). In infants with shorter composite placental TL, higher ACE score predicted greater RSA suppression during the still-face epoch relative to play period 1 and greater RSA augmentation during play period 2 relative to the still-face epoch.These data are the first, to our knowledge, to report that changes in placental TL influence the transgenerational impact of maternal early life adversity on the development of her offspring’s autonomic nervous system.
Published Version
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