ADHD Medication and Substance-Related Problems

population of 7% (male/female ratio of 3:1) (Owens, Cardoos, & Hinshaw, 2015; Thomas, Sanders, Doust, Beller, & Glasziou, 2015), is the diagnosis given to individuals who present with childhood onset of significant, impairing symptoms of inattention, impulsivity, and hyperactivity (American Psychiatric Association, 2013). These symptoms and impairments persist into adolescence and adulthood for a majority of individuals (Asherson, Buitelaar, Faraone, & Rohde. 2016; Barkley, 2016; Hechtman, 2017). Reviews of numerous prospective studies have found that children with ADHD (combined type) are at heightened risk for substance abuse (SA) (Patrick, Foell, Venables, & Worthy, 2016; Wilens, & Morrison, 2015). This increased risk is reflected in prevalence rates of ADHD among adolescents and adults with substance abuse ranging from 24% to 50% (Wilens & Morrison, 2015). Of the several possible mechanisms that might explain how ADHD increases risk for SA, the predominant mechanism involves a deviance-proneness pathway that begins with ADHDin childhood followed by oppositional/defiant behaviors, culminating in more severe conduct problem behavior (Beauchaine, Zisner, & Sauder, 2017). It is these latter behaviors that markedly elevate the risk for developing an SA in adolescence as they not only promote risky, sensation seeking behaviors that can result in experimentation with substances of abuse but also promote associating with substance abusing peers (Molina, & Pelham, 2014). Hence, given the risk ADHD poses for the development of SA, its successful treatment should make a significant contribution to reducing the risk of SA. However, despite the copious evidence attesting to the remarkable efficacy of short-term treatment of ADHD (e.g., up to 2 years) with stimulant medication (Connor, 2015; Hinshaw & Ellison, 2016), there has been a long-standing concern stimulant treatment might result in an increased response to addictive substances. This concern derives from the fact that stimulant medications increase dopamine concentration in the nucleus accumbens which is a brain region implicated in SA (Koob & Volkow, 2016) and the putative neural mechanism for ADHD treatment (Faraone et al., 2015). This concern has been addressed in two meta-analyses. A 2013 meta-analysis of 15 longitudinal studies (published between January 1980 and February 2012) with a total of 2565 individuals found that stimulant treatment for ADHD posed no increased risk for lifetime use or abuse/ dependence for alcohol, marijuana, nicotine and nonspecific drugs (Humphreys, Eng, & Lee, 2013). A second meta-analysis in 2014 confirmed the findings for nicotine and suggested that stimulant treatment might even reduce the likelihood of cigarette smoking (Schoenfelder, Faraone, & Kollins, 2014). However,the studies that comprise these meta-analyses suffer from a major limitation of small, non-random samples (McCabe, Dickinson, West, & Wilens, 2016). This limitation has been overcome in three recent studies. The purpose of this brief communication is to provide the readers of this journal with a detailed review of these studies, concluding with what the best evidence-based answer is to the concern that stimulant treatment for ADHD might increase risk for SA.