Maternal prenatal depression and epigenetic age deceleration: testing potentially confounding effects of prenatal stress and SSRI use

BG McKenna, CL Hendrix, PA Brennan, AK Smith… - Epigenetics, 2021 - Taylor & Francis
BG McKenna, CL Hendrix, PA Brennan, AK Smith, ZN Stowe, DJ Newport, AK Knight
Epigenetics, 2021Taylor & Francis
Previous studies suggest epigenetic alterations may contribute to the association between
maternal prenatal depression and adverse offspring outcomes. Developmental researchers
have recently begun to examine these associations in relation to epigenetic age
acceleration/deceleration, a biomarker of developmental risk that reflects the deviation
between epigenetic age and chronological age. In the perinatal period, preliminary studies
indicate that maternal prenatal depression may lead to epigenetic age deceleration in …
Abstract
Previous studies suggest epigenetic alterations may contribute to the association between maternal prenatal depression and adverse offspring outcomes. Developmental researchers have recently begun to examine these associations in relation to epigenetic age acceleration/deceleration, a biomarker of developmental risk that reflects the deviation between epigenetic age and chronological age. In the perinatal period, preliminary studies indicate that maternal prenatal depression may lead to epigenetic age deceleration in newborns, which may predict adverse developmental outcomes. The present study examined the relationship between maternal prenatal exposures (i.e., depression, stress, and SSRI use) and offspring epigenetic age deceleration in 303 mother-offspring dyads. Women were recruited in the first trimester of pregnancy and followed longitudinally until delivery. Maternal depression, perceived stress, and SSRI use were assessed at each prenatal visit. Newborn epigenetic age was determined via cord blood samples. Results indicated maternal prenatal stress was not associated with newborn epigenetic age deceleration (ΔR2 = 0.002; p = 0.37). Maternal prenatal depression was associated with decelerated epigenetic age (ΔR2 = 0.01, p = 0.04), but this relationship did not hold when accounting for maternal use of SSRIs (ΔR2 = 0.002, p = 0.43). Conversely, maternal SSRI use significantly predicted newborn epigenetic age deceleration over and above the influence of maternal depression (ΔR2 = 0.03, p = 0.001). These findings suggest maternal prenatal SSRI use may significantly contribute to the previously documented association between maternal prenatal depression and epigenetic age deceleration. Further studies are needed to examine how these epigenetic differences at birth may contribute to adverse outcomes in later development.
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