Editorial: Understanding the Child at Risk for Substance Use Disorders: Neuroimaging Addiction Risk.

Recent surveys demonstrate skyrocketing rates of adolescent vaping,1 while the opioid epidemic, rightfully, is daily front page news. At the same time, the public perceives cannabis as a harmless source of recreation or even as cure-all therapy. Now more than ever, child and adolescent psychiatrists, politicians, policy leaders, and parents need empirical support to bolster the position that drugs of abuse should be avoided by young people. We have a robust literature connecting cannabis use to earlier and worse psychotic disorders,2 as well as strong longitudinal data implicating cannabis in various neuropsychological deficits.3 What our field lacks, however, are brain imaging studies that definitively document the negative neurobiological impact of substance use on the developing human brain. The key to appreciating why this research literature is so limited has to do with one of the core tenets of substance use disorder (SUD) etiology: SUDs do not emerge de novo in adulthood or late adolescence when people typically present with impairing symptoms. Decades of research now suggests that certain latent childhood traits predispose some youth to initiate and then escalate drug and alcohol use more often than is typical.4 Children born into families with SUDs are more likely to express these highly heritable traits and are additionally subject to environmental risk factors and adversity. Therefore, children born into families with SUDs are disproportionately laden with genetic and environmental factors that shape brain structure and function. In other words, before exposure to drugs of abuse (which themselves may influence the brain), some children's brains already differ from those of typically developing youth. This observation limits the usefulness of cross-sectional neuroimaging studies that compare youth who have used drugs to those who have not, because of the nonrandom interaction of latent traits, environmental factors, and pre-existing brain differences. This interaction likely accelerates these adolescents' propensity to initiate and continue to use drugs of abuse.