Revising a Self-Regulation Phenotype for Depression Through Individual Differences in Macroscale Brain Organization

Abstract

Self-regulation denotes the processes by which people initiate, maintain, and control their own thoughts, behaviors, or emotions to produce a desired outcome or avoid an undesired outcome. Self-regulation brings the influence of distal factors, such as biology, temperament, and socialization history, onto cognition, motivation, and behavior. Dysfunction in self-regulation represents a contributory causal factor for psychopathology. Accordingly, we previously proposed a risk phenotype model for depression drawing from regulatory focus theory and traditional studies using task-based functional magnetic resonance imaging. In this article, we revise and expand our risk phenotype model using insights from new methodologies allowing quantification of individual differences in task-free macroscale brain organization. We offer a set of hypotheses as examples of how examination of intrinsic macroscale brain organization can extend and enrich investigations of self-regulation and depression. In doing so, we hope to promote a useful heuristic for model development and for identifying transdiagnostic risk phenotypes in psychopathology.

Multiple paths to rumination within a network analytical framework

“…The RRST conceptualizes depressive rumination as a trait-like passive and unhelpful response style to negative mood, and its potential causes and consequences. Other major theories include the Habit-Goal Framework of Depressive Rumination 10 , the Self-Regulatory Executive Function model (S-REF) 11 , the Impaired Disengagement Hypothesis 12 , the Goal Progress Theory 13 , the Control Theory 14 , and the Self-Regulation Risk Phenotype hypothesis 15 . These theories capture different focal points within the cognitive architecture behind rumination, such as the emphasis on metacognitive factors (e.g.…”