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Epigenetic correlates of neonatal contact in humans

Published online by Cambridge University Press:  22 November 2017

Sarah R. Moore*
Affiliation:
British Columbia Children's Hospital University of British Columbia
Lisa M. McEwen
Affiliation:
British Columbia Children's Hospital University of British Columbia
Jill Quirt
Affiliation:
British Columbia Children's Hospital
Alex Morin
Affiliation:
British Columbia Children's Hospital
Sarah M. Mah
Affiliation:
British Columbia Children's Hospital
Ronald G. Barr
Affiliation:
British Columbia Children's Hospital Canadian Institute for Advanced Research
W. Thomas Boyce
Affiliation:
University of British Columbia University of California, San Francisco Canadian Institute for Advanced Research
Michael S. Kobor
Affiliation:
British Columbia Children's Hospital University of British Columbia Canadian Institute for Advanced Research
*
Address correspondence and reprint requests to: Sarah R. Moore, Centre for Molecular Medicine and Therapeutics, British Columbia Children's Hospital, Department of Medical Genetics, University of British Columbia, 950 West 28th Avenue, Vancouver, British Columbia V5Z 4H4, Canada; E-mail: smoore@cmmt.ubc.ca.

Abstract

Animal models of early postnatal mother–infant interactions have highlighted the importance of tactile contact for biobehavioral outcomes via the modification of DNA methylation (DNAm). The role of normative variation in contact in early human development has yet to be explored. In an effort to translate the animal work on tactile contact to humans, we applied a naturalistic daily diary strategy to assess the link between maternal contact with infants and epigenetic signatures in children 4–5 years later, with respect to multiple levels of child-level factors, including genetic variation and infant distress. We first investigated DNAm at four candidate genes: the glucocorticoid receptor gene, nuclear receptor subfamily 3, group C, member 1 (NR3C1), μ-opioid receptor M1 (OPRM1) and oxytocin receptor (OXTR; related to the neurobiology of social bonds), and brain-derived neurotrophic factor (BDNF; involved in postnatal plasticity). Although no candidate gene DNAm sites significantly associated with early postnatal contact, when we next examined DNAm across the genome, differentially methylated regions were identified between high and low contact groups. Using a different application of epigenomic information, we also quantified epigenetic age, and report that for infants who received low contact from caregivers, greater infant distress was associated with younger epigenetic age. These results suggested that early postnatal contact has lasting associations with child biology.

Type
Special Issue Articles
Copyright
Copyright © Cambridge University Press 2017 

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Footnotes

We express our deepest gratitude to Dr. Meaghan Jones and Dr. Nicole Bush for their helpful feedback on earlier versions of this manuscript.

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