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Relationship Between Biochemistry and Aggression (Conclusion)

© Michael Decaire

Norepinephrine.

A second neurochemical-aggression relationship appears to exist within the chemical actions of norepinephrine. Evaluations of the norepinephrine levels of violent populations have shown increased norepinephrine metabolites when compared to controls (Lavine, 1997). Tricyclic antidepressants, which increase norepinephrine levels, tend to exacerbate aggressive behavior, suggesting a causal effect rather then covariation (Rampling, 1978). Psychopharmacological interventions that decrease norepinephrine levels have proven to be successful in decreasing aggressive behavior. Beta-adrenergic blockers have proven to be continuously effective at decreasing both norepinephrine levels and aggressive acts (Lavine, 1997). Similar effects have been found with a number of additional norepinephrine regulating agents (e.g., reserpine) with similar aggression inhibitory effects (Eichelman, 1986).

Dopamine. A final neurochemical correlate that has been proposed to have a role in aggression is dopamine. The increased rates of violence in schizophrenia, which is believed to be the result of dopamine dysfunction, have encouraged this hypothesis. Outside of psychotic populations, increases of dopaminergic activity via the usage of amphetamines have also been associated with aggressive behavior (Lavine, 1997). As a result anti-psychotics, which reduce dopamine levels, have been suggested as a potential aggression intervention. As predicted, anti- psychotics have been effective in decreasing violence in both psychotic populations (Eichelman, 1986; Glazer & Dickson, 1998; Yesavage, 1984) and non-psychotic delinquents (Molling, Lockner, Sauls, & Eisenberg, 1962).

Raine (1993) preformed an extremely in-depth meta-analysis that has statistically evaluated 79 neurotransmitter-effect reports. These reports examined the relationships between serotonin, norepinephrine, dopamine, and aggression. The sample for these studies were predominantly non-psychotic violent adults, and therefore are a good representation of violent correctional populations. A strong effect was consistently found between serotonin levels and aggression. Violent populations had significantly lower serotonin levels then their non-violent counterparts. The main effects for norepinephrine and dopamine were not significant. Subgroup analysis within the samples showed even greater effect sizes for serotonin and also found a significant relationship with norepinephrine level and aggression. Overall, the negative relationship between serotonin and aggression appears to be the only strong and consistent finding across studies. Scerbo (1991) predictions regarding neurotransmitter functioning in violent anti-socials is consistent with Raine's meta-analysis. Scerbo hypothesized that serotonin levels would be reduced in violent antisocials. His assumptions were based profoundly on the psychobiological theories of Gray (1975) and Fowles (1988). Gray (1976, 1981) proposed a two-factor learning theory that was driven by two competing behavioral systems. The first system, the Behavioral Activation System (BAS), is responsible for the activation of behavior as a result of reward and nonpunishment. Competing with BAS is the Behavioral Inhibition System (BIS), which inhibits behavior when faced with nonreward-frustration or punishment cues. The application of this behavioral system towards violent antisocial behavior was conceived by Fowles (1988). Fowles suggested that dysfunction in the BIS may be the causal factor behind aggressive violence in antisocials. HE believed that the disinhibitory, impulsive behaviors displayed by violent antisocials was the result of their inability to learn from punishment cues, and thereby do not inhibit behaviors related to such cues. Gray (1987) states that the BIS has a neural basis and is primarily related serotonergic pathways. Dysfunction in such a system would be consistent with the numerous, and highly significant, serotonin studies, and would thus support Scerbo's causal framework.

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