104 Biological Bases of Personality
responses than did low hostile subjects who were harassed
(Suarez, Kuhn, Schanberg, Williams, & Zimmermann,
1998). This kind of cardiovascular reactivity may occur in
frequent situations like stressful marital interactions (Smith
& Gallo, 1999), and general day-to-day living (Räikkönen,
Matthews, Flory, & Owens, 1999), and thus put a strain on
the cardiovascular system that can result in cardiovascular
disease, including hypertension (Lawler et al., 1998; Miller,
Dolgoy, Friese, & Sita, 1998) and isochemic heart disease
(IHD; Gallagher, Yarnell, Sweetnam, Elwood, & Stansfied,
1999). Persons with a family history of hypertension exhibit
the same pattern of hostility and anger arousal with elevated
blood pressure as do those who have developed the disorder
suggesting that there may be a genetically influenced source
to the cardiovascular overreactivity associated with anger
arousability. However, how the anger is dealt with is a factor
in vulnerability to heart disease. In a prospective study of
nearly 3,000 men in their 50s and 60s Gallager et al. (1999)
found that suppressed anger was most predictive of the inci-
dence of IHD even when other risk factors were statistically
controlled.
Monoamines
Åsberg’s (1994) review of the role of the monoamine neuro-
transmitters in human aggressiveness and violence attributes
a primary importance to the role of serotonin. In animals
serotonin is associated with inhibition of aggressive behavior
and lowered serotonin with disinhibition of such behavior
(Soubrié, 1986). In humans low levels of the serotonin
metabolite, 5-HIAA, have been consistently found in those
who attempt or complete suicide using violent means and in
violent criminal offenders, particularly those characterized
by impulsive violence or murder (Åsberg, 1994). Personality
disorders like antisocial and borderline disorder have a high
incidence of aggressive behaviors and suicide attempts.
Homicide and suicide are not antithetical; homicide offend-
ers have increased suicide rates. Within a group with person-
ality disorders a negative correlation was found between CSF
5-HIAA and lifetime aggressive behavior (Brown et al.,
1982).
Hormonal responses to serotonergic agonists and antago-
nists have also been used to assess the reactivity of the sys-
tem in relation to aggression. They generally support the
hypothesis of an inverse relationship between serotonin func-
tion and aggression/hostility (Cleare & Bond, 1997; Coccaro,
Kavoussi, Sheline, Berman, & Csernansky, 1997; Moss, Yao,
& Panzak, 1990).
Tryptophan is a precursor of serotonin in the brain (see
Figure 4.2). Tryptophan depletion provides an experimental
approach to the serotonin-aggression hypothesis, and unlike
correlational studies it can provide evidence of a causal link
with aggression. Studies have found that tryptophan deple-
tion increases aggressive responses in laboratory behavioral
tests (Cleare & Bond, 1995; Dougherty, Bjork, Marsh, &
Moeller, 1999) as well as subjective feelings of anger, ag-
gression, and hostile mood (Cleare & Bond, 1995; Finn,
Young, Pihl, & Ervin, 1998), but the effect is limited to per-
sons who are high in trait measures of hostility. The inference
is that hostile persons, who are already low in serotonergic
activity, tend to react aggressively with even more lowering
of serotonin stores. There is the further suggestion that sero-
tonin agonists or selective serotonin reuptake inhibitors
(SSRIs) may reduce aggression in aggression-prone persons.
A study by Knutson et al. (1998) showed that an SSRI re-
duced focal indices of hostility through a general decrease in
negative affect without altering positive affect. In addition,
the SSRI increased agreeableness on a behavioral index and
cooperativeness in a puzzle-solving task.
SSRI’s are used to treat depression, but can they change
other emotions like anger-hostility? A study of SSRI therapy
for depressed outpatients showed a significant decrease in
anger-hostility as well as neuroticism (Bagby et al., 1999).
The decrease in neuroticism, however, was correlated with
the decrease in clinical depression severity, whereas the de-
crease in anger-hostility was independent of the reduction of
depression.
NE mediates a primary arousal system in the brain begin-
ning in the locus-coeruleus and extending through limbic
structures to innervate all areas of cerebral cortex. As such it
has been implicated in the arousal of anxiety as previously
discussed. But anger is also associated with an arousal effect
as shown by the cardiovascular reactivity in highly hostile
and angry persons as previously discussed. A study of ag-
gression in free-ranging monkeys found a negative correla-
tion between aggressivity and CSF 5-HIAA, congruent with
the serotonin-aggression hypothesis, but it also found an
equally strong positive correlation between aggressivity and
CSF MHPG, the NE metabolite. The Ballenger et al. (1983)
study of humans (normals) found a very high positive corre-
lation (.64) between plasma MHPG and the Assault scale
from the BDHS. Use of a noradrenergic challenge revealed a
correlation of noradrenergic reactivity and irritability and
assault scales (Coccaro et al., 1991).
On the other hand, low levels of the catecholamines epi-
nephrine and NE, obtained from urine, are inversely related
to aggressiveness (Magnusson, 1987). Psychopathic youths
have low reactivity in these peripheral catecholamine sys-
tems in stressful situations (Lidberg, Levander, Schalling, &
Lidberg, 1978). The difference may lie between the central