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Paternal adverse childhood experiences: Associations with infant DNA methylation
Author(s) -
Merrill Sarah M.,
Moore Sarah R.,
Gladish Nicole,
Giesbrecht Gerald F.,
Dewey Deborah,
Konwar Chaini,
MacIssac Julia L.,
Kobor Michael S.,
Letourneau Nicole L.
Publication year - 2021
Publication title -
developmental psychobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 93
eISSN - 1098-2302
pISSN - 0012-1630
DOI - 10.1002/dev.22174
Subject(s) - dnam , offspring , dna methylation , psychology , epigenetics , pregnancy , demography , medicine , genetics , biology , gene expression , sociology , gene
Abstract Adverse childhood experiences (ACEs), or cumulative childhood stress exposures, such as abuse, neglect, and household dysfunction, predict later health problems in both the exposed individuals and their offspring. One potential explanation suggests exposure to early adversity predicts epigenetic modification, especially DNA methylation (DNAm), linked to later health. Stress experienced preconception by mothers may associate with DNAm in the next generation. We hypothesized that fathers’ exposure to ACEs also associates with their offspring DNAm, which, to our knowledge, has not been previously explored. An epigenome‐wide association study (EWAS) of blood DNAm (n = 45) from 3‐month‐old infants was regressed onto fathers’ retrospective ACEs at multiple Cytosine‐phosphate‐Guanosine (CpG) sites to discover associations. This accounted for infants’ sex, age, ethnicity, cell type proportion, and genetic variability. Higher ACE scores associated with methylation values at eight CpGs. Post‐hoc analysis found no contribution of paternal education, income, marital status, and parental postpartum depression, but did with paternal smoking and BMI along with infant sleep latency. These same CpGs also contributed to the association between paternal ACEs and offspring attention problems at 3 years. Collectively, these findings suggested there were biological associations with paternal early life adversity and offspring DNAm in infancy, potentially affecting offspring later childhood outcomes.