Addiction

We study the development of addiction in a variety of domains: alcohol, tobacco, marijuana, and food. We’re interested in how parents and peers influence these addictive behaviours, how genes and risky environments interact to predispose adolescents to addiction and how we can prevent these problems in the first place. In addition, we study neurocognitive aspects of addiction to unravel important mechanism contributing to the continuation of substance use.

We study how children and adolescents begin to use substances such as alcohol, marijuana and tobacco. Some highlights of our research: Our longitudinal research showed strong effects of alcohol rule setting on the development of adolescent drinking in general (Van der Vorst et al., 2006a, 2006b, 2007), and in genetically vulnerable adolescents specifically (Van der Zwaluw et al., 2010). Further, studies on smoking revealed that parental anti-smoking socialization efforts affect the likelihood that adolescents will engage in smoking themselves (Harakeh et al., 2005, 2008; Huver et al., 2006, 2007), their motivation to quit after they have started (Van Zundert et al., 2006), and the extent to which they progress to later smoking stages (De Leeuw et al., 2009, 2010; Otten et al., 2006). Importantly, in two papers of Kleinjanet al. (2007, 2008), we found no support for the impact of the Transtheoretical model in predicting juvenile smoking cessation. Instead, our data have repeatedly shown that parental socialization efforts influence the onset of smoking indirectly through youths’ explicit cognitions (De Leeuw et al., 2010; Otten et al., 2009) and implicit associations (Pieters et al., 2010; Van der Vorst et al., 2010). We have also tested and further refined dual process models of addiction with our adolescent samples (e.g., Wiers et al., 2007). Both prospective gene-environment studies as well as fMRI and EEG studies (Luijten et al. 2011; Luijten et al. 2013) have fueled the development of these models (Van der Zwaluw & Engels, 2009; Van der Zwaluw et al., 2010a, 2010b).

Our observational bar lab studies on social modeling and imitation show that people are 1) strongly affected by their peers’ behaviour when they are in an alcohol drinking context; potential moderators such as group status differences (Bot et al., 2007) and outcome expectancies for alcohol use have proven to be poor predictors of actual drinking behaviour (Bot et al., 2005; Larsen et al., 2010), and 2) people strongly imitate smoking of complete strangers (Harakeh et al., 2005). Our experimental research has revealed that adolescents imitate other people ́s drinking (Larsen et al., 2009; 2010) and food intake (Hermans et al., 2009, 2010), and that adolescents imitate the behaviour of people they do not even interact with (actors on the screen; Engels et al., 2009; Koordeman et al., 2010). These results are consistent with our research on food commercials as well and how these affect children’s (Anschutz et al., 2008) and adults’ (Anschutz et al., 2009) immediate imitative behaviour. Support for unconscious imitation of alcohol consumption (Larsen et al., 2009) and even spontaneous synchronization of food intake (Hermans et al., 2010) has also been found. Taken together, this set of studies are pointing us away from conventional social reinforcement models of risky development and increasingly supporting a dynamic phase-dependent model that incorporates both cue-reactivity and mimicry processes of influence (Engels et al., 2008; Lochbuehler et al., 2010).