Jack van Honk was supported by a High Potential Grant from Utrecht University, The Netherlands. The research of Eddie Harmon discussed in this article was supported by the National Science Foundation (BCS-0552152 and BCS-0643348). Barak Morgan was supported by a Professional Development Program grant from the Medical Research Council of South Africa. Dennis J.L.G. Schutter was supported by an Innovational Research Grant (452-07-012) from the Netherlands Organization for Scientific Research (NWO).
Socially Explosive Minds: The Triple Imbalance Hypothesis of Reactive Aggression
Article first published online: 20 JAN 2010
© 2010, Copyright the Authors. Journal compilation © 2010, Wiley Periodicals, Inc.
Journal of Personality
Special Issue: Trait Anger and Reactive Aggression: Edited by: Michael D. Robinson and Benjamin M. Wilkowski
Volume 78, Issue 1, pages 67–94, February 2010
How to Cite
Van Honk, J., Harmon-Jones, E., Morgan, B. E. and Schutter, D. J. L. G. (2010), Socially Explosive Minds: The Triple Imbalance Hypothesis of Reactive Aggression. Journal of Personality, 78: 67–94. doi: 10.1111/j.1467-6494.2009.00609.x
- Issue published online: 20 JAN 2010
- Article first published online: 20 JAN 2010
ABSTRACT The psychobiological basis of reactive aggression, a condition characterized by uncontrolled outbursts of socially violent behavior, is unclear. Nonetheless, several theoretical models have been proposed that may have complementary views about the psychobiological mechanisms involved. In this review, we attempt to unite these models and theorize further on the basis of recent data from psychological and neuroscientific research to propose a comprehensive neuro-evolutionary framework: The Triple Imbalance Hypothesis (TIH) of reactive aggression. According to this model, reactive aggression is essentially subcortically motivated by an imbalance in the levels of the steroid hormones cortisol and testosterone (Subcortical Imbalance Hypothesis). This imbalance not only sets a primal predisposition for social aggression, but also down-regulates cortical–subcortical communication (Cortical-Subcortical Imbalance Hypothesis), hence diminishing control by cortical regions that regulate socially aggressive inclinations. However, these bottom-up hormonally mediated imbalances can drive both instrumental and reactive social aggression. The TIH suggests that reactive aggression is differentiated from proactive aggression by low brain serotonergic function and that reactive aggression is associated with left-sided frontal brain asymmetry (Cortical Imbalance Hypothesis), especially observed when the individual is socially threatened or provoked. This triple biobehavioral imbalance mirrors an evolutionary relapse into violently aggressive motivational drives that are adaptive among many reptilian and mammalian species, but may have become socially maladaptive in modern humans.