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Changing Emotions

Self-regulation as a mediator of change in psychotherapy

Publication ,  Chapter
Strauman, TJ; Klenk, MM; Eddington, KM
January 1, 2013

Regulatory focus and depression Individual differences in regulatory focus develop primarily from differential exposure to positive-outcome-focused vs. negative-outcome-focused parenting, with temperament manifesting an indirect influence by sensitizing or buffering children to the reward and punishment contingencies from their interactions with parents. Affective responses to ideal or ought goal pursuit feedback are moderated by individual differences in strength of orientation to promotion and prevention goals. People’s fundamental needs for promotion and prevention have significant implications relating to the behaviors, evaluations, and experiences that characterize our social identities, the nature of our social perceptions and appraisals, and our reactions to social feedback. Although regulatory focus was originally conceptualized at the psychological level of analysis, EEG and FMRI studies have begun to identify its neurobiological correlates. These findings provide an important conceptual bridge to understanding how individual differences in regulatory focus, as a cognitive/ motivational orientation, might be implicated in vulnerability to psychopathology. Eddington, Dolcos, Cabeza, Krishnan, and Strauman (2007) found that priming of promotion goals was associated with activation in left orbitofrontal cortex (LOFC), whereas priming of prevention goals was associated with activation in right OFC. In addition, individual differences in promotion focus correlated significantly with magnitude of LOFC response to promotion goal priming. Thus, individuals whose socialization history shaped a dominant orientation toward promotion goals-that is, a characteristic world view in which social interactions are typically viewed as opportunities to “make good things happen”-manifested a characteristic neural activation pattern when incidentally exposed to social stimuli relevant to their own promotion goals. The Eddington et al. study was the first to use FMRI to link idiographicallyassessed personal goal priming with changes in OFC activation-a region implicated in representing the hedonic value of primary as well as abstract (secondary) reinforcers in decision making, and in performance monitoring (Ramnani and Owen, 2004). Furthermore, the left OFC activation following promotion goal priming was detected while participants were performing a task unrelated to goal pursuit, suggesting that promotion and prevention goals, as highly accessible knowledge structures, can be activated implicitly and still have a pervasive influence on the interpretation of social stimuli. Chronic perceived failure to attain promotion versus prevention goals is associated with symptoms of depression vs. anxiety respectively. Strauman (2002) proposed a model in which individuals whose socialization histories led them to acquire a strong orientation toward promotion goals were more vulnerable to depression when exposed to chronic failure feedback. Whereas under normal circumstances these individuals self-regulate effectively toward their goals and respond to acute failure feedback adaptively, they would become vulnerable to depression if they experience chronic or catastrophic goal pursuit failure. If promotion goal priming is associated with left OFC activation, and individuals experiencing chronic failure to attain promotion goals are vulnerable to depression, then among such individuals depression should be characterized by a dysfunction in left OFC activation following promotion goal priming. Given the evidence for a bidirectional functional link between OFC and limbic structures regulating affect and motivation, changes in OFC activation driven by perceived failure in self-regulation could feed back directly to the amygdala and related limbic structures. Consistent with this hypothesized pathway, Eddington, Dolcos, McLean, Cabeza, Krishnan, and Strauman (2009) found that clinically depressed individuals showed attenuated left OFC activation following promotion goal priming. Depressed participants who also reported significant levels of anxiety symptoms likewise manifested a significant increase in right OFC activation following prevention goal priming. This combination of left OFC hypoactivation (representing a deficit in promotion goal pursuit motivation) with right OFC hyperactivation (representing a vigilant and ruminative response to cues for prevention goals) was consistent with the high degree of comorbidity between unipolar depression and generalized anxiety disorder. In addition to the prediction that promotion goal pursuit failure will be associated with dysphoric affect and (if sufficiently chronic) depressive symptoms, there are other characteristics of the promotion goal system that help to explain how, under specific conditions, certain individuals might become vulnerable to depression when they experience chronic promotion goal failure. Individuals with a characteristic promotion orientation will be more likely to construe goals in promotion (gain/non-gain) terms and will be more committed to goals that are framed in promotion terms. For these individuals, there will be more opportunity for promotion success (“gain”), but also more opportunities for promotion failure (“non-gain”). Also, failure to attain a specific promotion goal increases the importance of promotion goals in general as well as the individual’s motivation to pursue them, because promotion goals are more interconnected than prevention goals. And in addition, even a small actual-ideal discrepancy (promotion failure) is highly motivationally significant, due to the greater degree of interconnectedness among promotion goals. Thus, for individuals with a dominant promotion orientation, promotion failure feedback takes precedence in social information processing and drives affective reactions to subsequent goal pursuit. Finally, promotion goals are also more substitutable than prevention goals, but only if the individual can effectively disengage from pursuing one promotion goal and engage in a substitute goal. Otherwise, individuals will become trapped by unsuccessful pursuit of a goal they are failing to attain and experience more intense and chronic dysphoric affect. Although the data are consistent with this hypothesized pathway to depression, social-cognitive mechanisms alone cannot provide a sufficient account either for normal variability in affective and motivational responses to goal pursuit failure or for vulnerability to depression associated with maladaptive self-regulation. Nonetheless, cross-disciplinary research linking genetic, neurobiological, and behavioral levels of analysis is beginning to identify how variability in brain function contributes to individual differences in complex behavioral traits and how such diatheses interact with environmental factors to precipitate psychiatric disorders (e.g., Hariri, 2009). For example, research indicates that genetic and neurobiological factors interact with socialization patterns to influence the development of individual differences in self-regulation of goal pursuit. In turn, the cognitive-motivational systems postulated by RFT are largely responsible for affective responses to socially-embedded goal pursuit feedback, and therefore represent potential sources of vulnerability to mood disorders via their interactions with neural mechanisms that underlie incentive motivation, approach behavior, and affective responses to goal-relevant feedback. We hypothesize that a combination of three contributory factors-individual differences in regulatory focus, genetically determined individual differences in goal-specific information processing and the intensity and duration of affective responses to goal-relevant feedback, and the experience of chronic failure to attain a particular kind of personal goal-creates a self-regulation pathway to depression. A critical feature of the proposed phenotype is the conditional nature of its relation to depressive vulnerability. Because individual differences in regulatory focus involve both costs and benefits, vulnerability to depression will depend upon the individual’s social context. Under circumstances of chronic perceived promotion goal pursuit failure, such individuals would be more vulnerable to intense, prolonged dysphoric affect, would perseverate on failure feedback, would have greater difficulty objectively evaluating their progress and, if needed, disengaging from promotion goal pursuit, and could ultimately “spiral down” into a state of diminished appetitive motivation, anhedonia, and hopelessness.

Duke Scholars

DOI

ISBN

9781848720909

Publication Date

January 1, 2013

Start / End Page

209 / 216
 

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Strauman, T. J., Klenk, M. M., & Eddington, K. M. (2013). Self-regulation as a mediator of change in psychotherapy. In Changing Emotions (pp. 209–216). https://doi.org/10.4324/9780203075630-38
Strauman, T. J., M. M. Klenk, and K. M. Eddington. “Self-regulation as a mediator of change in psychotherapy.” In Changing Emotions, 209–16, 2013. https://doi.org/10.4324/9780203075630-38.
Strauman TJ, Klenk MM, Eddington KM. Self-regulation as a mediator of change in psychotherapy. In: Changing Emotions. 2013. p. 209–16.
Strauman, T. J., et al. “Self-regulation as a mediator of change in psychotherapy.” Changing Emotions, 2013, pp. 209–16. Scopus, doi:10.4324/9780203075630-38.
Strauman TJ, Klenk MM, Eddington KM. Self-regulation as a mediator of change in psychotherapy. Changing Emotions. 2013. p. 209–216.
Journal cover image

DOI

ISBN

9781848720909

Publication Date

January 1, 2013

Start / End Page

209 / 216