Impulse and Constraint, Two-Mode Models and Depression
I have become very interested in the question of what processes underlie behavioral impulsiveness and constraint. I was first led to this question by the process of revising our textbook in personality, where such issues seemed to be very important. More recently, however, the interest has taken on a life of its own, and has led in several directions.
One direction is an increased awareness of, and appreciation of, the emergence throughout psychology of models of cognition and behavior that assume two parallel modes of functioning, one more basic (evolutionarily primitive) than the other. The two processing modes appear to use different aspects of available information, learn in different ways, and create competing paths to action. The more primitive mode is largely outside consciousness. The other is the familiar symbolic processor of the rational mind. This general theme has now appeared in a number of places. The two-mode (dual process) idea, in and of itself, seems very interesting and useful. (How the two-mode idea helps deal with some questions in personality is addressed here.)
A second direction this interest in impulse has led is more biological. It happens that research on the behavioral manifestations of serotonergic function contains conclusions that have more than a slight resemblance to ideas that connect to the two-mode models. Specifically, a good deal of evidence links low serotonergic function to an impulsive pattern of behavior that often results in aggression or emotional outbursts (a somewhat selective review of that evidence is here). It seems very much as though low serotonergic function allows the more primitive system to be in charge more of the time. Alternatively, high serotonergic function allows the higher-level system to keep the lower level under control more of the time.
More or less by accident, I stumbled across the fact that low serotonergic function also relates to a vulnerability to depression. This was a real puzzle. Depression does not look much like impulsive aggression. How could they both follow from the same genetically-based, biological risk factor? Trying to solve that puzzle led me and my colleagues to the view that risk of depression follows from a combination of low serotonergic function and low incentive sensitivity (or low approach motivation). We are now exploring these ideas more deeply, and hope to have evidence on some of these questions before too long.
The article in which these ideas are addressed most explicitly will appear sometime in 2009:
Carver, C. S., Johnson, S. L., & Joormann, J. (in press). Serotonergic function, two-mode models of self-regulation, and vulnerability to depression: What depression has in common with impulsive aggression. Psychological Bulletin. [abstract]
Carver Home Research Interests