Behavioral activation system moderates self-referent processing following recovery from depression.

Depressed mood and loss of interest or pleasure are hallmark symptoms of Major Depressive Disorder (MDD; American Psychiatric Association, 2000). Biopsychological models of emotion postulate a behavioral activation system (BAS) that regulates reward sensitivity and behavioral approach (e.g., Fowles, 1988; Depue & Iacono, 1989; Gray, 1994), which, when underactive, manifests as the diminished positive affect and goal motivation that characterizes MDD (e.g., Davidson, 1992; Mineka et al. 1998). These models also postulate a behavioral inhibition system (BIS) that regulates sensitivity to threat and behavioral avoidance; higher levels of BIS functioning have been associated with both depression and anxiety disorders (see Zinbarg & Yoon, 2008; and Bijttebier et al. 2009, for reviews of this literature). Investigators have reliably documented a relation between diminished BAS functioning and unipolar depression (e.g., Henriques et al. 1994; Harmon-Jones & Allen, 1997). Based on Davidson’s (1992) proposal that electrophysiological activity in the left hemisphere is positively associated with BAS functioning, researchers have used electroencephalography (EEG) to demonstrate that depressed individuals are characterized by left relative to right frontal hypoactivation (e.g., Henriques & Davidson, 1991; Gotlib et al.1998). Carver and White (1994) developed the commonly used self-report BIS/BAS scales, in which the BIS scale measures sensitivity to experiencing fear and anxiety in response to imminent punishment, and the BAS scales measure sensitivity to experiencing positive emotions such as happiness, excitement, and hope in response to imminent reward. Researchers using these measures have found that depressed individuals report lower levels of BAS functioning than do nondepressed controls (e.g., Kasch et al. 2002), and that in unselected samples, lower levels of BAS functioning are associated with more severe depressive symptoms (e.g., Beevers & Meyer, 2002; Spielberg et al. 2011). Importantly, individuals who have recovered from depression have been found to exhibit the same patterns of frontal cortical asymmetry (Henriques & Davidson, 1990; Gotlib et al. 1998; reviewed in Thibodeau et al. 2006) and self-reported levels of BAS functioning (Pinto-Meza et al. 2006) that have been documented in depressed individuals. Furthermore, in a recent study of individuals with no history of depression, Nusslock et al. (2011) found that left frontal hypoactivation predicted the subsequent onset of a first depressive episode, suggesting that reductions in BAS sensitivity are not simply a consequence or scar of previous depressive episodes. In sum, the results of cross-sectional and longitudinal research converge on the formulation that BAS functioning is related to vulnerability to depression (Carver & White, 1994; Gray, 1994; Campbell-Sills et al. 2004). Carver and White’s (1994) BAS scale is composed of three subscales: BAS-Reward Responsiveness (BAS-RR), BAS-Drive, and BAS-Fun-Seeking (BAS-Fun) (e.g., Huebeck et al. 1998; Jorm et al. 1999; Ross et al. 2002; Campbell-Sills et al. 2004; Levinson et al. 2011). BAS-RR measures affective responding, BAS-Drive assesses behavioral responding, and BAS-Fun measures affective and behavioral responding (Carver & White, 1994; Campbell-Sills et al. 2004). Interestingly, within samples diagnosed with MDD, BAS-RR most consistently predicts the general course of the disorder, whereas BAS-Drive predicts specific aspects of disorder course. For example, Kasch and colleagues (2002) found that in participants with MDD, lower BAS-RR and BAS-Drive scores predicted the subsequent persistence of the diagnosis and a higher number of depressive symptoms at an eight-month follow-up assessment; lower baseline BAS-RR scores also predicted greater severity of depressive symptoms. Similarly, McFarland and colleagues (2006) found that after controlling for baseline clinical variables, lower BAS-RR and BAS-Drive scores predicted the maintenance of MDD at a six-month follow-up assessment; lower BAS-RR scores also predicted a higher number of subsequent depressive symptoms and poorer psychiatric status. These findings indicate that, even within depressed groups, variation in BAS functioning may be a marker for disorder persistence and subsequent symptomatology. Indeed, BAS sensitivity may be a particularly potent risk factor for depression in persons who are already vulnerable to MDD because of having experienced prior episodes. The precise mechanisms explaining the association between reductions in BAS functioning and risk for depression are not yet known. Theorists have proposed that because persons with diminished BAS sensitivity are less responsive to positive stimuli, they have a lower likelihood of exerting effort toward or engaging in potentially rewarding experiences, which thereby increases their risk for depression (e.g., Depue & Iacono, 1989; Fritzsche et al. 2010). It is also possible that BAS functioning is related to aspects of cognitive vulnerability to depression. Spurred by Beck’s (1967) concept of negative cognitive schemas as risk factors for depression, a large body of research has demonstrated that depression is associated with negative biases in the processing of self-referent information, as one such facet of cognitive vulnerability (reviewed in Beevers, 2005, and Gotlib & Joormann, 2010). In this context, investigators have used the self-referential encoding task (SRET; Derry & Kuiper, 1981), an information-processing task that assesses self-schema function, to examine the processing of valenced stimuli in depressed, recovered depressed, and nondepressed participants. Depressed individuals have been shown to endorse and recall more negative and/or less positive self-referent information than do their nondepressed counterparts. Findings for persons who have recovered from MDD are less consistent; an initial negative mood induction appears necessary to detect negatively biased self-referent processing in this group (e.g., Dobson & Shaw, 1987; Fritzsche et al. 2010). Researchers have recently begun to explore the relations between BAS functioning and different facets of cognitive vulnerability to depression, although they have not yet examined self-referent processing. Beevers and Meyer (2002) found in an unselected sample of participants that positive experiences and expectancies mediated the relation between self-reported level of BAS functioning and anhedonic symptoms of depression. Similarly, Nusslock et al. (2011) found that left frontal hypoactivation in their sample of currently nondepressed participants was associated with the extent to which the participants attributed negative events to stable and global causes and endorsed likely negative consequences of the events. The present study is the first to examine associations among BAS functioning and one aspect of cognitive vulnerability to depression in both a clinical sample (participants with a history of recurrent major depression [RMD]) and in never-depressed control (CTL) participants. As we noted above, BAS sensitivity has been found to be related to risk for depression in both clinical and non-clinical samples; therefore, we hypothesized that lower self-reported level of BAS functioning would be associated with less positive and more negative self-referent processing across both groups. Given the particularly striking relation of BAS sensitivity to risk for future depression within samples of individuals who are already vulnerable to MDD, however, we hypothesized that these associations between BAS functioning and self-referent processing would be stronger in the RMD group than in the CTL group. In the present study we focused on level of BAS-RR because it is the BAS subscale that has been found most consistently to predict depression course. To assess the specificity and robustness of the association of BAS-RR with self-referent processing, we controlled for current levels of depressive and anxiety symptoms (e.g., Kasch et al. 2002) and also assessed the relation between BIS functioning and self-referent processing.