Dr. Paul Lanier of the UNC School of Social Work presented on Adverse Childhood Experiences and Resiliency: Opportunities for Behavioral Health and Substance Use Disorders at the Governor’s Institute’s recent Addiction Medicine 2020 conference held May 1 and 2. Here he answers a question about the interaction between genetics and environment in the development of ACEs.
Q: Could you elaborate on evidence for an interaction between genetic susceptibility to SUD and ACES in relation to risk of developing an SUD? Do the genetically at-risk individuals account for a lot of the 12% who develop SUD among those with 5 ACES?
A: I don’t think we know as much about ACEs as an environmental factor specifically, but there is evidence about individual ACEs (maltreatment) or social stressors more broadly. For a review of GxE interactions in this context, I would refer people to two articles:
*Pasman, J.A., Verweij, K.J.H. & Vink, J.M. Systematic Review of Polygenic Gene–Environment Interaction in Tobacco, Alcohol, and Cannabis Use. Behav Genet 49, 349–365 (2019). https://doi.org/10.1007/s10519-019-09958-7
*Kirsch, D., Nemeroff, C.M. & Lippard, E.T.C. Early Life Stress and Substance Use Disorders: Underlying Neurobiology and Pathways to Adverse Outcomes. ADV RES SCI 1, 29–47 (2020). https://doi.org/10.1007/s42844-020-00005-7
Q: I have always wondered how they determined the adverse outcome from ACEs from other risk factors like smoking. How do they parse that out in the research? Especially since ACEs increase risk of substance use.
A: Most studies control for other risk factors in statistical models. However, the order of events, and the dynamic interaction of risk factors is rarely considered.