Socially explosive minds: the triple imbalance hypothesis of reactive aggression.
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.
van Honk
Jack
J
Department of Psychology, Experimental Psychology, Utrecht University, Heidelberglaan2, 3584 CS Utrecht, The Netherlands. J.vanHonk@uu.nl
Harmon-Jones
Eddie
E
Morgan
Barak E
BE
Schutter
Dennis J L G
DJ
D000374:Aggression / Q000523:psychology*; D001921:Brain / Q000378:metabolism / Q000503:physiopathology; D003071:Cognition; D019955:Conduct Disorder / Q000453:epidemiology / Q000378:metabolism; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism*; D007398:Interpersonal Relations; D008297:Male; D009415:Nerve Net / Q000503:physiopathology; D015588:Observer Variation; D011582:Psychological Theory; D012701:Serotonin / Q000378:metabolism*; D012919:Social Behavior; D013739:Testosterone / Q000378:metabolism*
D012701:Serotonin; D013739:Testosterone; D006854:Hydrocortisone