Serotonin and Impulse Aggression: Not So Fast
Joel Wallman, HFG Program Officer
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The quest to root violent criminality in organic shortcomings has a long and, viewed with the wisdom of hindsight, sometimes silly history. Lombroso's diagnostic taxonomy of criminal physical features, the phrenology of Gall, Kretschmer's body typing and, more recently, the attempt to link the XYY or "supermale" genetic constitution to criminality are textbook cases of fruitless efforts to explain bad behavior as the outcome of bad biology.

Contemporary endeavors are, on the whole, far more sound in their scientific methods, if thus far not much more compelling. Studies linking persistent impulsive aggression to deficits or excesses of various juices of the brain (dopamine, GABA, MAOA), the nether regions (testosterone, estrogen), or parts in between (adrenal steroids) have yielded occasionally suggestive but generally equivocal findings. The same applies to research on areas of the brain, the most traveled in this search being the frontal and temporal lobes, amygdala, and hypothalamus.

One promising exception is the neurotransmitter serotonin. Dozens of studies have found that people with documented histories of impulsive violence have, on the average, a reduction in function of the serotonin system relative to people without such a profile. This has been found whether serotonin function is assessed by lumbar spinal tap of cerebrospinal fluid to determine the quantity of serotonin's metabolic byproduct or by less direct measures, such as the magnitude of biochemical response to ingestion of a substance that increases serotonin production.

These and other methods are quite removed from direct assay of serotonin function in the brain, but the correlation between serotonin deficit and impulsive violence, both self- and other-directed, is a recurrent finding nonetheless. Moreover, studies in non-human animals in which serotonin levels were experimentally reduced through chemical intervention found an increase in aggressive behavior (compared to control animals subjected to identical delivery of an inert substance), suggesting that the correlation found in human research reflects a true causal relationship.

In the serotonin deficit, then, we seem to have a constitutional flaw underlying the syndrome of impulsive violent behavior. If serotonin abnormalities are truly linked in a specific way to aggression as opposed to behavior problems more generally, then we have a window into not just pathologies of aggression but the normal neurobiology of aggression as well. This discovery also provides a basis for intelligent conjecture about the selective forces governing the evolution of both serotonin and aggression in animals in general, primates more specifically, and humans in particular.

Yet one needn't be a student of neurotransmitters to wonder about the specificity of the connection between serotonin and aggression. A regular reader of New York Times articles on human behavior and health, for example, might well be troubled in attempting to collate the implicit claim that serotonin is the "aggression chemical" with reports that underactive serotonin circuits are also the cause of migraines (July 24, 1996, section C, p. 8), extreme shyness (May 18, 1999, section C, p. 1), obsessive-compulsive disorder (February 16, 1997, section 13CN, p. 3), anxiety and pessimism (November 29, 1996, section A, p. 1), and "restless leg" syndrome (night cramps) (April 10, 1996, section C, p. 10). A survey of popular books on the virtues of keeping one's serotonin up will reveal that a deficit of this substance is responsible for craving and hence addiction to gambling, drugs, sex, and food (The Craving Brain, Ronald Ruden and Marcia Byalick); that, in addition to controlling emotion, serotonin is in charge of "intellect" (Naturally Slim & Powerful, Philip Lipetz and Jean Zevnik); and that serotonin is the culprit in insomnia (5-HTP: The Natural Way to Boost Serotonin and Overcome Depression, Obesity and Insomnia, Michael T. Murray). Combine this litany of affliction with the knowledge that tens of millions of people are being prescribed Prozac, a serotonin enhancer, on the apparently well-established medical belief that depression derives from—yes—a serotonin deficit, and, unless all of these reports and claims are dismissed as baseless, one is justified in concluding that a serotonin shortage manifests itself in a congeries of emotional and behavioral problems, including but by no means limited to aggression.

That conclusion is certainly consonant with the fact that serotonergic neurons, which reside in the brainstem, project their axons into many and functionally diverse regions of the brain, including the amygdala, hypothalamus, hippocampus, cerebellum, and temporal and prefrontal regions of the cerebral cortex. It would be surprising, given this wide ramification, if abnormalities of the serotonin system affected aggression in a specific way.

Just how sound are the numerous studies reporting a specific association between diminished serotonin function and violent behavior? A meta-analysis of this literature by Balaban and colleagues (1996) is illuminating. From 70 studies, Balaban chose 39 that provided sufficient information for an analysis employing the variables Balaban thought pertinent to answering the question. The subjects in these studies fall into three categories: violent psychiatric patients, nonviolent psychiatric or neurological patients, and normal, healthy control subjects. Not all studies employed all three groups, but a typical finding of those that did was reduced serotonin in the violent psychiatric group compared to both the nonviolent patients and normal controls, with no difference between the latter two, indicating that serotonin deficiency is associated specifically with violent psychiatric conditions rather than with serious psychiatric problems in general.

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