However, there are non-psychiatric sources of variability
in serotonin level, and few of the serotonin studies take
them into account (i.e., statistically control for them) in
all subject categories used. In particular, serotonin (actually
5-HIAAA, its main break-down product) measured at the lumbar
level through spinal tap is lower in males, goes up with age,
and declines with stature. (Serotonin diffuses out of the
brain into the cerebrospinal fluid. From there, most of it
is transported to the bloodstream; the fraction making it
down as far as the lumbar region decreases with increasing
Using those studies in the set of 39 that provided information
on height, age, and sex of normal controls, Balaban computed
the effects of those variables alone on serotonin level. These
values were then used to adjust the measured serotonin levels
in all studies for all subject categories for which mean height
and age and male-female ratio were published. Because the
three subject categories happened to consistently differ in
these traits, correcting for these non-psychiatric determinants
of serotonin level yields results that are quite different
from what is typically reported: violent psychiatric patients
do indeed have somewhat lower levels than normal controls,
but so do the non-violent psychiatric and neurological patients,
and the psychiatric groups do not differ from each other.
In short, people with a history of being in an institution
or under psychiatric or neurological treatment have lower
levels of serotonin than normal nonpatients.
In addition to the reasons adduced above for questioning
the usefulness of low serotonin as a marker for impulsive
aggression, there are reports in the scientific literature
that, while far from refuting the claim that low serotonin
increases impulsive aggression, contradict it and thus warrant
weighing in the balance. These are not simply studies that
fail to find a relationship between low serotonin and aggressionunless
the relationship were extremely strong in a statistical sense,
one would expect a certain number of studies to come up empty
by chance even if the relationship were generally valid. One
kind of contradictory finding is the observation in at least
two studies that highly aggressive children evince not a reduction
but an increase in serotonin function (Castellanos et al.
1994; Halperin et al. 1994). And there is the much-cited discovery
in a large Dutch family of an association between a genetic
deficiency of the enzyme MAOA and impulsive violent behavior
(Brunner et al. 1993). What has gone unremarked on in the
discussion of this finding (which, predictably, was heralded
in the non-technical media as the revelation of a "gene
for aggression") is the problem it poses for the other
major putative organic cause of abnormal aggression, serotonin.
For MAOA is the enzyme that, among other functions, breaks
down serotonin, which means that the affected men in this
group would, arguably, have an excessively high level of serotonin.
And, finally, the same primate experiments mentioned earlier,
which showed that altering serotonin level affects behavior,
also provide evidence that serotonin is equally a result of
behavior. If the dominant male is removed from a group of
vervet monkeys, an aggressive contest for dominance results.
The male that ascends to top rank will experience an increase
in serotonin level, and the exiled alpha male, if not returned
to its group, will undergo a serotonin drop (McGuire and Troisi
1998). To the extent that it is legitimate to extrapolate
to humans, this observation calls into question the assumption
that serotonin abnormality precedes the behavioral problems
with which it has been linked.
The correct inference from all of the foregoing is not that
anyone low on the serotonin scale should be a dangerous, depressed,
and overweight compulsive gambler, torn between shyness and
nymphomania, who would be kept awake at night by their headaches
and restless legs even if they didn't suffer from insomnia.
It is rather that serotonin is not a very discriminating marker
for violence and that the neurophysiological and neurochemical
characteristics that accompany low serotoninwhether
as causes, consequences, or bothare not limited to brain
regions that govern aggression.
But what if there were no ambiguity about the serotonin-aggression
relationship? If it were clearly established that underactive
serotonin circuits increased the risk for serious aggressive
behavior, and only that risk, what insight would be gained
into human violence? Would it help us understand the shocking
increase in youth homicide in the United States beginning
in the middle 1980s or the decrease of recent years? Would
it clarify why the rate of violent crime has declined in New
York, Los Angeles, and Tampa but increased in New Orleans
and Richmond, why Nevada's murder rate is 10 times higher
than South Dakota's, or why the U.S. rate is 15 times higher
The explanation of these facts will come not from research
in neurobiology but from understanding economic forces, variation
in cultural mores regarding the acceptability of violence,
diversity in the kinds and efficacy of means of informal and
formal social control, and availability of firearms. A reasonable
response to this assertion would be to suggest that individual
differences in serotonin could explain why this person rather
than the next succumbs to the distinctive mix of violence-promoting
influences impinging on a given neighborhood, ethnic group,
class, or nation. I am rather pessimistic about the potential
of this approach, however. But that may just be the serotonin
Balaban, E., J. S. Alper, and Y. L. Kasamon. 1996. Mean genes
and the biology of aggression: A critical review of recent
animal and human research. J. Neurogenetics 11: 1-43.
Brunner, H. G., M. Nelen, X. O. Breakefield, H. H. Ropers,
and B. A. van Oost. 1993. Abnormal behavior associated with
a point mutation in the structural gene for monoamine oxidase
A. Science 262: 578-80.
Castellanos, F. X., J. Elia, M. J. Kruesi, C. S. Gulotta,
I. N. Mefford, W. Z. Potter, G. F. Ritchie, and J. L. Rapopor.
1994. Cerebrospinal fluid monoamine metabolites in boys with
attention-deficit hyperactivity disorder. Psychiatry Research
Halperin, J. M., V. Sharma, L. J. Siever, S. T. Schwartz,
K. Matier, G. Wornell, and J. H. Newcorn. 1994. Serotonergic
function in aggressive and nonaggressive boys with attention
deficit hyperactivity disorder. Am J Psychiatry 151: 243-8.
McGuire, M. and A. Troisi. 1998. Darwinian Psychiatry. New
York: Oxford University.
1 | 2 | back to TOC