The behavioral activation and inhibition systems have been theorized to explain both mania and depression (Depue & Zald, 1993
; Gray, 1990
). This study was the first direct examination of the relation between BIS/BAS levels and symptoms among individuals diagnosed with bipolar I disorder. It was hypothesized that BAS scores would associate positively with mania and inversely with depression. The opposite pattern was expected for BIS.
Support for these hypotheses was generally weak, although evidence was obtained for a hypothesized link between BAS and manic symptom intensification over time. Although the primary analyses focused on longitudinal patterns, cross-sectional correlations were considered first. These analyses generally failed to support state-dependent links between symptoms and BIS/BAS levels. The observed pattern was somewhat incongruent with results from a previous study of undergraduates at risk for mood disorders, in that BAS did not correlate with concurrently assessed symptom severity (Meyer et al., 1999
Cross-sectional analyses did reveal one significant link—BIS self-reports correlated with higher depressive symptoms. This finding is consistent with a broad literature that links threat responsiveness or neuroticism with depression (Clark, Watson, & Mineka, 1994
; Mineka, Watson, & Clark, 1993
; Watson, Clark, & Harkness, 1994
). In contrast to this scarcity of findings, stronger and more consistent links were observed for all three BAS scales with current levels of both mania and depression in an at-risk undergraduate sample (Meyer et al., 1999
). Two obvious reasons may account for this difference: (1) The earlier findings relied on BIS/BAS self-report–mania and depression symptoms self-report correlations, whereas in the present study clinician-administered interviews were used as symptom measures; (2) In the earlier study, BIS/BAS and symptom measures were collected at exactly the same time, whereas time was not as closely matched in the present study.
In addition to examining cross-sectional associations, analyses were conducted that specifically disentangle the longitudinal links between BIS/BAS levels and symptoms: (1) the random effects regression models, indexing how BIS/BAS levels fluctuated with symptom changes within individuals and (2) the partial correlation coefficients, indexing how BIS/BAS levels at recovery predicted changes in symptoms over time.
As hypothesized, BIS levels fluctuated with depressive symptoms. However, BIS levels after recovery did not predict increased depression over time. In short, BIS reports appeared to function as a state-dependent characteristic of depression, but there was little evidence that BIS operated as a vulnerability characteristic. Although it seems plausible to assume that threat responsiveness (BIS) places people at risk for future distress or depression, no evidence was found in support of such a link. In preliminary work, however, the interaction of BIS at baseline and subsequent stressful experience was associated with relative intensification of depressive symptoms over time (Meyer, Johnson, & Blaney, 2000
). Thus, high levels of threat responsiveness may constitute a vulnerability in combination with aversive experience, but not as a “main effect” predictor of symptom intensification.
BAS appeared unrelated to depression in the present analyses. This was surprising, given that BAS inactivity appears to be a marker of unipolar depression (Gotlib, Ranganath, & Rosenfeld, 1998
; Harmon-Jones & Allen, 1997
; Henriques et al., 1994
; Mineka et al., 1998). Indeed, a correlation of −.53(p
< .01) between the total BAS scale and a depression self-report was observed in an undergraduate at-risk sample (Meyer et al., 1999
). In another recent study, low BAS appeared to be relevant specifically for the anhedonic but not the negative affect components of depression (Beevers & Meyer, in press
). Comparisons among these studies are limited, however, by the differences in measurement and design, as well as the fact that many previous studies focused on unipolar depression. The role of the BAS in bipolar depression certainly seems worthy of further study, despite the null findings reported here.
Although some have suggested that low BIS strength might be associated with manic disinhibition (Fowles, 1993
; Gray, 1994
), self-reported BIS strength did not correlate with or predict manic symptoms. This lack of association was also observed in an at-risk student sample (Meyer et al., 1999
). Further study is needed to test whether these null findings are limited to BIS self-reports but can perhaps be detected with biochemical or behavioral indexes of BIS strength.
Additionally, no evidence was obtained to support the hypothesis that BAS scales would relate to concurrently assessed symptoms of mania. This null finding was surprising, given the theoretical plausibility of a BAS–mania link (Depue & Iacono, 1989
; Depue & Zald, 1993
; Fowles, 1993
) as well as earlier findings in an undergraduate sample (Meyer et al., 1999
). Again, methodological differences between the present study and the earlier study (e.g., reliance on self-report, time interval differences between BIS/BAS and symptom measures) may account for some of these discrepancies. On the other hand, there may be other reasons for this null finding. For example, the BAS scales were developed in an undergraduate sample, and item content may not capture adequately the construct of incentive responsiveness in clinical populations. The BAS scales were also developed to assess trait-like differences in threat and incentive responsiveness, but it was hypothesized here that these tendencies might fluctuate in tandem with symptoms. Thus, the BIS/BAS scales may not be suited to capture variability in threat- and incentive-responsiveness over time among patients with bipolar disorder. New measure development efforts may therefore be appropriate. One other possibility is that BAS sensitivity levels remain fairly stable as manic symptoms fluctuate—a model that is congruent with conceptualizing BAS as a vulnerability factor for manic symptoms.
Indeed, a significant relation was observed between BAS (total and reward responsiveness scales) and manic symptom intensification over time. Reward Responsiveness—the only BAS scale that was significantly linked with manic symptom intensification—appears to be a particularly good conceptual fit with Depue’s (Depue & Zald, 1993
) and Gray’s (Gray, 1990
) models. Partial correlations for the other two BAS subscales were also in predicted directions but did not attain significance. Thus, there was some evidence suggesting that heightened responsiveness to incentives places bipolar disordered persons at risk for mania. This is consistent with other recent findings. For example, bipolar individuals who experienced incentive-related events (e.g., receiving a promotion) were more likely to develop manic symptoms in subsequent months (Johnson et al., 2000
). Presumably, the perception of goal-attainment-related events constitutes an input to the BAS. Given such input, a “malfunctioning” BAS in bipolar disorder may produce the output of excessive positive affect and unrestrained activity.
Although no previous research has directly examined BAS sensitivity and clinical levels of mania, other literature is congruent with a role for BAS in manic symptoms. Several models of the neural pathways involved in bipolar disorder emphasize dysregulation of the dopaminergic projections from the ventral tegmentum, which are involved in sensitivity to reward and incentive (Depue & Iacono, 1989
; Depue & Zald, 1993
). High levels of achievement striving among individuals with bipolar disorder and their family members have been noted in clinical lore and empirical findings (Coryell et al., 1989
), and personality theorists have suggested that such traits are risk factors for mania (Plutchik, Platman, & Fieve, 1970
). In sum, an emergent empirical literature suggests that BAS functioning and related constructs have potentially important implications for understanding mania. It is also important to note that mania is predicted not only by BAS, but by a range of other, independent variables, including medication and sleep changes (Johnson, Winett, & Mellman, 1998
; Wehr, 1990
; Wehr, Sack, & Rosenthal, 1987
Several important limitations must be kept in mind when interpreting these findings, including the naturalistic design, limited power, and sample heterogeneity. One additional caveat concerns the content overlap between the items on the BAS scale and manic symptoms. The overlap between BAS Fun Seeking items such as “I crave excitement and new sensations” and manic symptoms such as “excessive involvement in pleasurable activities” cannot be denied, and indeed, such items appear to be a state marker of symptoms. However, items from the Reward Responsiveness scale (e.g., “It would excite me to win a contest”) appear to have less content overlap. It should be noted, however, that the strong conceptual overlap was an original influence on the development of the BAS model of bipolar disorder (e.g., Depue & Zald, 1993
These results may be viewed as a first step of model testing. A fundamental goal will be to test this bipolar model using BIS and BAS measures that have less direct overlap with symptoms, including indexes of cortical asymmetry (e.g., EEG measures), reinforcement sensitivity tasks, and extinction paradigms. Although these indices have received attention in the literature relating BIS/BAS to personality and to other psychopathologies (e.g., Milich, Hartung, Martin, & Haigler, 1994
; Newman, Patterson, & Kosson, 1987
), the field of bipolar disorder has not yet used such indices. The present findings point to the utility of the BIS and BAS constructs in the integration of psychosocial and biological research on bipolar disorder, but further empirical inquiry will certainly be needed.