Introduction

More youth use cannabis than smoke cigarettes in the United States 1, and in other parts of the world cannabis use has become almost as regular as tobacco use among adolescents and young adults 2. In the United States, many states and jurisdictions have relaxed laws against possession of small amounts of this drug, and more states are considering taking a similar course. One of the first meta‐analyses on the effects of these trends did not show that legalization of medical cannabis until 2014 in the United States increased the prevalence of adolescent cannabis use 3. However, the currently limited research is mixed on whether trends toward legalization of recreational cannabis lead to greater access to cannabis for youth, which could subsequently lead to greater use of this drug 4-7. This is an important question, as increased adolescent cannabis use could potentially have adverse consequences, considering that some adolescents are neurobiologically vulnerable to experimentation and subsequent addiction to such substances 8, 9. Hence, it is critical and timely to examine the precursors and potential adverse consequences associated with patterns of cannabis use among youth and whether these associations lead to cannabis use disorder (CUD).

One concern is that the use of cannabis might lead not only to CUD but to other unhealthy outcomes, such as conduct problems (CP) (e.g. school truancy, stealing), which typically peak during adolescence 10. It is well documented that substance use and conduct disorder (i.e. the clinical variant of CP) are interconnected 11, 12. In fact, substance use including cannabis use during adolescence is more strongly associated with conduct disorder than to any other psychiatric disorder 13. Even in community samples, a longitudinal link between cannabis use and CP has consistently been replicated 14, 15. However, the sequencing of this link is still debated, i.e. it remains unclear whether cannabis use predicts subsequent CP and/or whether CP predicts subsequent cannabis use.

When addressing the sequencing between youth cannabis use and CP, it is essential to consider the peer context. Similar to other substance use and problem behaviors, cannabis use during adolescence is primarily a social behavior 16, and peers can play a critical role in predicting such behaviors 17-21. Specifically, if adolescents affiliate with peers who use cannabis, this could increase their risk for both cannabis use and CP via social learning processes 16, 19, 22. However, most studies on the link between youth cannabis use and CP do not account for peer influences. In this study, we specifically test three ways in which peer cannabis use can explain the developmental associations between youth cannabis use and CP (Fig. 1).

Figure 1 Open in figure viewer PowerPoint Hypothesized interrelations between cannabis use, conduct problems and peer cannabis use and cannabis use disorder (CUD)

Table 1. Descriptive statistics of study variables per year. Minimum Maximum Mean (SD) T1 Cannabis use 0 3 0.10 (0.41) T2 Cannabis use 0 3 0.17 (0.54) T3 Cannabis use 0 3 0.44 (0.86) T4 Cannabis use 0 4 10.03 (10.16) T4 CUD 0 3 0.44 (89) T1 Conduct problems 0 1.40 0.22 (0.23) T2 Conduct problems 0 1.00 0.24 (0.21) T3 Conduct problems 0 1.27 0.27 (0.24) T4 Conduct problems 0 1 0.22 (0.19) T1 Peer cannabis use 1 4 10.26 (0.59) T2 Peer cannabis use 1 5 10.62 (0.94) T3 Peer cannabis use 1 5 20.13 (10.13) T4 Peer cannabis use 1 5 20.51 (10.15)

First, youth cannabis use could lead to CP either directly 17, 18, 23, 24 or via exposure to peer cannabis use (e.g. 19 (model A; Fig. 1). Such links have been observed even when accounting for effects of peers and other common confounding factors, such as socio‐economic status (SES) and gender 17-19, 24. Consistent with a ‘psychopharmacological model’, a direct link from cannabis use to CP could occur because cannabis use induces cognitive impairment that can affect judgment and decision‐making more broadly 2, 25, 26. We are not aware of studies that have found whether or not these cascading chain of events could predict later CUD, however.

As far as we know, only one study 19 has attempted to investigate the developmental cascades contained in model A. In a birth cohort of 935 adolescents who were born in New Zealand in 1977, a series of regression models with two waves of longitudinal data found support for the links in model A. However, that study 19 did not consider whether engaging in CP also potentially influences cannabis use and/or CUD (see model B; Fig. 1). Of note, that study 19 was based on self‐reports of property or violent offences, whereas other studies reviewed here investigated other types of conduct problems such as non‐violent offences. For the sake of consistency, we refer to all these externalizing behaviors as conduct problems.

In the alternative model B, CP could lead to cannabis use directly or via exposure to peers who use cannabis. Several studies have found a direct link from CP to cannabis use 27-29, even when controlling for common confounding factors 30-32. These findings suggest the often‐overlooked hypothesis that youth with CP might use cannabis as a coping mechanism to deal with disapproval of their CP 25 and perhaps to self‐medicate 31, 33. Indeed, recent research revealed that ‘feeling stressed out’ is the primary reason adolescents use cannabis 16. Alternatively, an ‘under‐control‐disinhibition’ hypothesis suggests that CP in childhood and preadolescence predicts substance use, because CP are manifestations of underlying behavioral under‐control that lead to problem behaviors such as drug use, and ultimately drug use disorders, as adolescents age 34-36. Additionally, an indirect pathway from CP to cannabis use could also emerge if youth with CP affiliate with other problem‐behavior peers who use cannabis, which could also induce cannabis use that potentially leads to CUD. We could not identify any empirical studies that have explicitly investigated such cascading developmental chains of events. Nevertheless, scholars have speculated that affiliation with delinquent and cannabis using peers could, in turn, cause heightened cannabis use in youth because these peers are likely to reinforce the use of such substances 16, 37. Prior clinical research also suggests that substance use develops later as a symptom of conduct disorder 38.

A combination of models A and B is also possible, which would constitute a bidirectional link between cannabis use and CP leading eventually to CUD, with peer cannabis use operating as an intervening factor. A direct bidirectional relation would be consistent with the ‘under‐control‐disinhibition’ hypothesis’ 34-36 as well as problem behavior theory (PBT; [38]), which postulates that problem behaviors such as cannabis use and CP are interrelated (suggesting bidirectional links) and predicted by a shared set of psychosocial risk factors in the personality, perceived environment and behavior systems 39. We could not locate any empirical studies that have explicitly investigated the cascading chain of events in model B. One study investigated bidirectional links between cannabis use and violence and found a bidirectional relationship in a UK young adult male sample 40. However, this study did not investigate CUD. There is no longitudinal adolescent study with at least four waves that employ sensitive analytical techniques to simultaneously test such bidirectional and cascading effects for cannabis use and CP.

In a third model (C), peer cannabis use could serve as a common confounding factor and fully account for any links between youth cannabis use and CP. Specifically, considering that peer cannabis use could lead to both youth CP and cannabis use, any links between cannabis use and CP would be spurious and no longer exist when peer cannabis use is controlled. This would be consistent with the hypothesis that adolescents experiment with CP and substance use because they are both manifestations of an underlying problem behavior syndrome (such as ‘deviant peer affiliation’ in the environment system) that predicts both of these behaviors 39, 41. However, specifically in relation to cannabis use and CP, studies show that the cannabis use–CP link does not (completely) vanish when accounting for common confounding factors, such as deviant peer influences 17-19, 31.

The current study was designed to investigate which of the above‐described models (or a combination thereof) provides the best explanation for the well‐documented link between youth cannabis use and CP, the potential role of peer cannabis use in this link and how these three variables could lead to subsequent CUD. To test the various links, we used a longitudinal design with four waves of observations of a US urban sample starting at age 13.5 in 2006 and approximately age 19 at the last wave. A recent and advanced version of the standard cross‐lagged panel model (CLPM) was utilized, which is often regarded as a stronger methodology for inferring causality 42, when experimental research is not possible. Whereas the standard CLPM confounds between‐ and within‐person associations, we used the random intercept cross‐lagged panel model (RI‐CLPM), which isolates changes within‐persons as predictors of subsequent within‐person changes 42, 43. When it is possible to identify such within‐person processes, it provides a more stringent test of potential causal relations between variables.