The deleterious effects of maternal adverse childhood events (ACE) and prenatal stress
(PNMS) are established and these experiences are likely biologically embedded in the
infant. The Mismatch hypothesis of the Developmental Origins of Health and Disease
model suggests that differential fetal development occurs based on expected postnatal
exposures and that adaptation to environmental changes is costly. One marker of biological
cost, linked to both transgenerational adversity and PNMS, is telomere length (TL).
This study examined the Mismatch hypothesis on infant TL.
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© 2018 Published by Elsevier Inc.
