Whereas genetics plays a critical role in vulnerability and resilience to mental illness, the contribution of early-life experiences to these outcomes has been strongly suggested in humans and supported by studies in animal models [1]. Early-life adversity (ELA), including poverty, chaotic environment, and abuse, predicts vulnerability to depression as well as lower cognitive function [1, 2]. Yet, at the individual level it is not possible to predict which child exposed to ELA will be vulnerable later in life. Lacking are predictive biomarkers that enable early diagnosis, prevention, and intervention [1,2,3].

There is evidence that the mechanisms by which early-life experiences influence the function of neurons (and neuronal networks) underlying vulnerability or resilience involve alterations of the repertoire and levels of gene expression via epigenetic processes. Among those, changes in DNA methylation at the individual gene and genomic scale may partially govern gene expression. It is not possible to examine DNA from brain samples in children, so that current approaches have largely employed peripheral cells including white blood cells or buccal swabs (mixed epithelial/white blood cells). Numerous studies have compared DNA methylation profiles from individuals experiencing adversity to those raised in ‘typical’ environments; yet cross-sectional studies are challenged by the large inter-individual variance of DNA methylation profiles.

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