Explaining the covariance between attention-deficit hyperactivity disorder symptoms and depressive symptoms: the role of hedonic responsivity

Attention-deficit hyperactivity disorder (ADHD) is one of the most commonly occurring childhood disorders, affecting up to 9% of children (Centers for Disease Control, 2010). Though once considered solely a childhood disorder, ADHD has been found to persist into adolescence in 50%–80% of cases and into adulthood in 10%–50% of cases (Barkley, Murphy & Kwasnik, 1996; Klassen, Katzman, & Chokka, 2010). Recent data indicate a 6-month prevalence rate of 3.4% among adults (McIntosh et al., 2009). ADHD is associated with numerous detrimental outcomes in adolescence and early adulthood, including academic failure, delinquency, substance abuse, automobile accidents, and risky sexual behavior (Barkley et al., 1996; Barkley, 2006; Klassen et al., 2010). Additionally, college students with ADHD have been shown to have lower levels of college adjustment, academic achievement, self esteem, and social skills (Shaw-Zirt, Popali-Lehane, Chaplin, & Bergman, 2005; Frazier, Youngstrom, Glutting, & Watkins, 2007) compared with college students without ADHD. Individuals with ADHD also show higher rates of comorbid externalizing, anxiety, learning, and depressive disorders than individuals without a diagnosis of ADHD (Bagwell, Molina, Pelham, & Hoza, 2001; Biederman, Faraone, Mick, & Lelon, 1995; Flory, Molina, Pelham, Gnagy, & Smith, 2006; Hoza, Pelham, Waschbusch, Kipp, & Owens, 2001; Jensen et al., 2001; Meinzer et al., 2012; Milberger, Biederman, Faraone, & Murphy, 1995). For example, a recent report estimated that the prevalence of major depressive disorder (MDD) in the past year was 18.6% in adults with ADHD compared with 7.8% in non-ADHD adults (McIntosh et al., 2009). Similarly, the prevalence of dysthymia in the past year was 12.8% in adults with ADHD compared with 1.9% of non-ADHD adults (McIntosh et al., 2009). Research also indicates that individuals with comorbid ADHD-MDD experience higher levels of psychosocial impairment than individuals with either disorder in isolation (Biederman et al., 2008; Biederman, Mick, & Faraone, 1998; Biederman, Newcorn, & Sprich, 1991; Chronis-Tuscano et al., 2010). The high rates of comorbidity between ADHD and unipolar depressive disorders and the high level of impairment associated with their co-occurrence highlight the need to develop an understanding of the mechanisms underlying their relationship. One potential explanation for the covariance of depressive symptoms and ADHD symptoms is shared endophenotypes. Endophenotypes are constructs that underlie psychopathological symptoms and are more directly influenced by genes than the manifest symptoms (Rende & Waldman, 2006; Turetsky et al., 2008). Recent work from genetic, neurological, and behavior paradigms has drawn attention to the possible role of altered reward system functioning in both ADHD and major depressive disorder (MDD). For example, molecular genetic studies have linked several dopaminergic and serotonergic genes to both ADHD (Wood & Neale, 2010) and MDD (Kato, 2007), and evidence indicates that neural activity in dopamine-mediated reward circuitry is linked to negative affect, low motivation, inattention, and depression (Beauchaine, Neuhaus, Brenner, & Gatzke-Kopp, 2008; Durston, 2003; Epstein et al., 2006; Pizzagalli, Iosifescu, Hallet, Ratner, & Fava, 2009; Scheres, Milham, Knutson, & Castellanos, 2007). Given the moderate to high heritability estimates for ADHD and MDD and the overlapping neurotransmitter systems and neural circuitry involved in ADHD and MDD, it is possible that altered reward system functioning (i.e., hedonic capacity; Meehl, 1975) represents a common endophenotype for symptoms seen in both depression and ADHD. The purpose of the present study was to examine that possibility among college students who completed self-report measures of ADHD symptoms, depressive symptoms, and hedonic responsiveness. Hedonic responsivity, a feature of hedonic capacity, is a heritable individual difference in reactivity to pleasurable stimuli and reward (Bogdan & Pizzagalli, 2009). Hedonic responsiveness has often been studied in the context of the mesocortical dopamine system, where the role of dopamine has received the most focus as a neural substrate of reward processing (Naranjo, Tremblay, & Busto, 2001). Research has established elements of poor hedonic responsiveness as a feature of both depression and ADHD (Bogdan & Pizzagalli, 2006; Forbes & Dahl, 2005; Luman, Oosterlaan, & Sergeant, 2005; Pizzagalli, Jahn, & O’Shea, 2005; Pizzagalli et al., 2009). A substantial body of research has documented impaired hedonic responsivity in depression and has demonstrated that the failure to respond to rewarding stimuli maps onto the severity of anhedonic symptoms (Bogdan & Pizzagalli, 2006; Forbes, 2009; Pizzagalli et al., 2005; Pizzagalli et al., 2009; Shankman, Klein, Tenke, & Bruder, 2007). Furthermore, comparative research has replicated this general deficit in hedonic responsivity, as well as a blunted dopaminergic reward system, among animals bred to display depressive behaviors (Naranjo et al., 2001). Neurological studies have revealed that depressed individuals display decreased activity in the striatum in response to rewarding stimuli, specifically in the region associated with the detection of rewards and the representation of reward-related goals (Forbes, 2009; Forbes & Dahl, 2005). Additionally, Heller and colleagues (2009) reported that compared with nondepressed controls, individuals with MDD displayed a decrease in activation over time in the nucleus accumbens, a region associated with motivation and reward processing. This may reflect difficulty sustaining positive affect following reward (Heller et al., 2009). Research also supports impaired hedonic responsivity in ADHD. Scheres and colleagues (2007) reported reduced ventral striatal activation during anticipation of reward among adolescents with ADHD as compared with healthy controls. Similarly, neural activation during dopaminergic-driven reward tasks was negatively correlated with severity of ADHD symptoms among individuals with ADHD (Stark et al., 2011). In behavioral paradigms, children with ADHD show less response to both positive and negative reinforcement as well as reward and extinction conditions (Luman et al., 2005). Furthermore, research has suggested that children with ADHD have a tendency to choose smaller rewards sooner rather than delay gratification for a larger reward, which may represent an impulsive drive for immediate rewards and a delay aversion (Marco et al., 2009). However, research regarding responsiveness to reward incentives has received far less attention and it remains unclear whether children with ADHD show hyper- or hypo-responsiveness to rewarding incentives (Scheres et al., 2007). Additionally, prior research has indicated that reward preferences and inhibitory deficits were not significantly correlated (Solanto et al., 2001), which suggests that the poor impulse inhibition often seen in individuals with ADHD is distinct from their responsiveness to rewards. Though little research has examined reward processing across ADHD subtypes, the inattentive subtype of ADHD may relate to dysfunctional reward patterns through its association with sluggish cognitive tempo, or marked drowsiness, lethargy, passivity, and forgetfulness, a key feature in ADHD-Inattentive subtype (Derefinko et al., 2008). Given that a tendency to automatically attend to reward-related stimuli is an important aspect of appraising the incentive salience of cues (Berridge, Robinson, & Aldrige, 2009), it is also possible that inattention may disrupt one’s ability to process the incentive properties of reward-related stimuli, which could in turn result in impaired reward responsiveness. Even though evidence suggests dysregulated hedonic responsiveness in both depression and ADHD, prior research has not examined it as an explanation for the covariation between depression and ADHD symptoms. Given the overlap in neural circuitry affected in regards to reward processing in ADHD and MDD as well as similar findings of irregular reward processing, the current cross-sectional study examined the role of hedonic responsiveness in accounting for the relationship between ADHD symptoms and depressive symptoms. In this initial investigation, these associations were studied in a sample of college students. Examining factors that explain depression-ADHD relationships among college students is important because this is a high-risk period for depression, ADHD symptoms, and their co-occurrence (Kisch, Leino, & Silverman, 2005; Weyendat & Dupal, 2006). Based on prior research and theory, we expected that ADHD symptoms would be significantly and positively associated with depressive symptoms, and that ADHD symptoms and depressive symptoms each would be significantly and negatively associated with hedonic responsivity. Finally, we hypothesized that hedonic responsivity would significantly account for the covariation between ADHD symptoms and depressive symptoms, such that there would be a significant indirect effect of ADHD symptoms on depressive symptoms via hedonic responsiveness.