Association of Comorbid Psychopathology with the Duration of Cannabis Use Disorders

Cannabis abuse and dependence disorders (or, collectively, cannabis use disorders; CUDs) are often age limited. By age 35, most individuals with prior CUD diagnoses no longer meet diagnostic criteria or have ceased cannabis use altogether (Farmer et al., 2015a; Newcomb, Galaif, & Locke, 2001; Perkonigg et al., 2008). For others, however, CUDs are persistent conditions that extend 5 to 10 years or longer following the baseline diagnosis (Farmer et al., 2015a; Lopez-Quintero et al., 2011; Lynskey et al., 2006; Newcomb et al., 2001; Perkonigg et al., 2008). Among those who regularly use or abuse cannabis, concurrent and lifetime comorbid psychiatric disorders are common (Armstrong & Costello, 2002; Costello, Erkanli, Federman, & Angold, 1999; Roberts, Roberts, & Xing, 2007). The influence that other disorders have on CUDs is important for understanding processes that contribute to the etiology and course of CUDs, as well as for the development of interventions that seek to reduce or eliminate cannabis use (Angold, Costello, & Erkanli, 1999; Armstrong & Costello, 2002). The present research explores the temporal sequencing of CUDs with other psychiatric disorders and the associations that comorbidity patterns have with the persistence of the index CUD episode. Common psychiatric disorders can be subsumed under two broad and moderately related superordinate psychopathology domains: internalizing and externalizing. These domains of psychopathology account well for patterns of psychiatric symptom and disorder covariation among children and adults in cross-sectional and longitudinal studies (e.g., Achenbach, 1966; Farmer, Seeley, Kosty, Olino, & Lewinsohn, 2013b; Kessler et al., 2011; Krueger & Markon, 2006; Lahey et al., 2008), and have been proposed as a guiding framework for research on common causal pathways that account for disorder comorbidity (Kessler et al., 2011; Krueger, 1999). Internalizing (e.g., mood and anxiety disorders) and externalizing psychopathology (e.g., disruptive behavior and substance use disorders [SUDs]) have been associated with the persistence of cannabis use over time (Chen & Kandel, 1998; Florez-Salamanca et al., 2013; Perkonigg et al., 2008; van den Bree & Pickworth, 2005), although the temporal sequencing of these problems in relation to the onset of CUDs remains uncertain. Several motivational models of addiction highlight the relevance of comorbid conditions and their temporal sequencing for ongoing drug use. The tension reduction model (Conger, 1956) and the more contemporary self-medication model (Khantzian, 1985; Quitkin, Rifkin, Kaplan, & Klein, 1972), for example, assume that problems with mood or anxiety are primary conditions and that substance use is a secondary condition whereby substances are used as a means of providing temporary relief from persistent negative moods. In contrast, the substance-induced enhancement model suggests that multiple intoxication and withdrawal experiences increase susceptibility to anxious and depressed moods that, in turn, occasion subsequent substance use due to the temporary relieving effects from negative moods that substance use affords (Kushner, Sher, & Beitman, 1990; Zvolensky, Schmidt, & Stewart, 2003). Whereas the tension reduction/self-medication and substance-induced enhancement frameworks imply different directional temporal relations between problematic cannabis use and internalizing features, reward processing dysfunction models suggest temporal continuity between cannabis misuse and other forms of externalizing psychopathology due to common causal factors. The reward deficiency hypothesis (Blum et al., 2000; Blum, Gardner, Oscar-Berman, & Gold, 2012; Comings & Blum, 2000), for example, attributes substance use initiation, persistent substance use, and habitual reward-seeking, risk-taking, and impulsive behaviors to a hypo-responsive reward processing system whereby aberrant reward-seeking behavior is regarded as a compensatory response to a reward-deficiency state. The impulsivity hypothesis conversely suggests that individuals with externalizing tendencies have an overly-sensitive or hyper-responsive reward system that produces a behavioral bias toward the active pursuit of immediate rewards, including substance-seeking behavior (Finn, Mazas, Justus, Steinmetz, 2002; Hariri et al., 2006; Hommer, Bjork, & Gilman, 2011; Jager, Block, Luijten, & Ramsey, 2013; Joseph, Liu, Jiang, Lynam, & Kelly, 2009). Despite differences in presumed underlying mechanisms among these theories, they each propose that externalizing tendencies signal dysfunctional reward processing that, in turn, enhances risk for substance initiation, SUDs, and the persistence of SUDs over time. Whereas the reward deficiency and impulsivity hypotheses posit reward processing dysfunctions that precede the onset of SUDs that subsequently influence their course, the allostatic hypothesis (Koob & Le Moal, 2005; 2008; see also Koob et al., 2014) emphasizes the motivational aspects of ongoing drug use. In this model, responses to drug administration among drug-naive individuals are initially experienced as positively rewarding or reinforcing. Repeated drug exposures over time, however, are thought to result in a degradation of reward system functioning, leading to a progressively decreasing sensitivity to positive reward cues unrelated to substance use and an enduring reliance on substances to produce positive hedonic responses. Among heavier or chronic cannabis users, periods of acute drug abstinence also occasion negative emotional states (e.g., irritability, dysphoria, malaise, anhedonia) that, in turn, establish a motivation for drug use as a means for gaining relief from these aversive states. The progression from occasional user to chronic user, then, is one in which there is a corresponding shift from substance use as a positively reinforced reward-seeking behavior to a negatively reinforced compulsive behavior. With respect to comorbid psychopathology, this model suggests that negative mood states related to frequent intoxication/withdrawal cycles evolve into more protracted or chronic conditions (i.e., internalizing psychopathology). Because the allostatic theory is not drug specific, the emergence of non-cannabis SUDs following the onset of the index CUD episode is also anticipated and thought to reflect expanded efforts to gain relief from reward deficient states and acute negative moods stemming from prolonged heavy cannabis use.