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. 2016 Dec 6;6(12):e976. doi: 10.1038/tp.2016.247

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Copyright © 2016 The Author(s)

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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Indirect effect of prenatal smoking on adolescent substance use via neonatal DNA methylation. (a) Path analytic indirect effects model. Dotted arrowed lines indicate non-significant paths. Single arrowed lines indicate standardized path coefficients that survived bootstrap-corrected confidence intervals (i.e., significant path). Red arrows show significant indirect path. Population effect sizes are interpreted using the standardized estimates (Std. B) following Cohen's guidelines: an effect of 0.10 is small effect, an effect of 0.24 is a medium effect, and an effect of 0.37 is a large effect. (b) Graphical representation of the indirect effect, where prenatal smoking associates with higher cumulative DNA methylation risk at birth (top panel), which in turn associates with higher substance use in adolescence (bottom panel). DNAm, DNA methylation.