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F47. Infant Telomere Length Differs in Matched and Mismatched Postnatal Expectancy

      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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