Aggression/Hostility/Anger/Agreeableness 105noradrenergic and the peripheral autonomic stress system.
Another possibility is that there is a difference between the
psychopathic type of aggression, which is often notaccom-
panied by high arousal, and the impulsive-angry type of
aggression in which emotional disinhibition is typical. Netter,
Hennig, and Rohrmann (1999) believed that they can
distinguish the two types of aggressiveness on the basis of
selective types of challenges to the monoamine systems. The
serotonergic challenge was primarily correlated with
Eysenck’s P scale, assessing the psychopathic type of aggres-
sion, whereas another type of challenge more closely related
to dopamine reactivity was related to the nonpsychopathic
type of aggression.
Increasing levels of brain dopamine in rats increases im-
pulsive aggressive responding, but it takes a great deal of
dopamine depletion to reduce aggressive behavior (Volavka,
1995). Little research has been done on dopamine specifi-
cally although the aggression producing effects of ampheta-
mine may be a function of stimulation of dopaminergic as
well as noradrenergic systems. A study of the neuroendocrine
responses to glucose challenge in a group of substance
abusers showed that those participants characterized by anti-
social hostility had responses suggestive of increased
dopaminergic activity (Fishbein, Dax, Lozovsky, & Jaffe,
1992).
Hormones
The hypothesis of an influence of T on aggressive behavior
has a prescientific origin in that the pacifying effects of cas-
tration in animals were known and used for that purpose.
Sexual competition among males is one form of aggression
influenced by T, but other forms are also affected. Castration
reduces aggression in males in most species, and T replace-
ment reverses this effect.
Studies of the relationships between T and hostility or ag-
gression in humans have produced mixed results, but a meta-
analysis of such studies found a moderate effect size of .40
over all studies (Archer, Birring, & Wu, 1988). An earlier re-
view by Archer (1991) suggested that results were more pos-
itive in studies where behavioral assessments (usually in
prisoners) were used and less powerful in studies of trait
(self-report) hostility or aggression (usually in college stu-
dent samples). The newer meta-analysis failed to support this
hypothesis. Better results were obtained in studies using sali-
vary T as opposed to T derived from blood. A study using
salivary T in 306 students found T positively correlated with
aggression and negatively with prosocial scales in both men
and women (Harris, Rushton, Hampson, & Jackson, 1996),
but in other studies using either blood (Archer et al., 1998) or
salivary T (Campbell, Muncer, & Odber, 1997) in large sam-
ples of male students no relationship was found. In still an-
other study of blood T in students, both T and estradiol were
postively correlated with self-reported aggression in men, but
the correlations were negative in women (Gladue, 1991).
More consistent results have been obtained with behav-
ioral (non-self-report) assessments. A study of nearly 700
male prison inmates found that salivary T was related to a
history of violent crimes, particularly rape, homicide, and
child molestation, as well as violations of prison rules, partic-
ularly those involving assault (Dabbs, Carr, Frady, & Riad,
1995). A study of female inmates showed a relationship of T
with aggressive dominance in prison but not with the history
of criminal violence. A group of alcoholics with a history of
violence had elevated levels of serum T relative to other al-
coholics (Bergman & Brismar, 1994).
Even among nonclinical samples there is correlational ev-
idence of a relationship between T and aggression. T corre-
lated with more aggressive fighting in men during judo
contests (Salvador, Suay, Martinez, Simon, & Brain, 1999)
and in amount of shock given to an opponent in a contrived
laboratory situation (Berman, Gladue, & Taylor, 1993).
Whether self-report or behavioral, correlational studies
cannot establish cause and effect. There is ample evidence in
both animal and human studies that aggressive experience
in competition may raise T levels in victors or lower them in
those who are defeated. Experimental studies in which the ef-
fects of raised T levels on aggression are observed might be
helpful. Clinical studies of steroid users have shown in-
creased aggressiveness in some of them (Pope & Katz, 1994).
Archer (1991) reviewed studies in which T or T-stimulating
hormones were given and effects on aggression assessed by
self-report. Although there is some evidence that T can affect
hostility, there are also some negative findings from other
studies. In all likelihood there is a continuous interaction be-
tween endogenous levels of T and life experiences (affecting
current levels) during life. T makes one more likely to
aggress, and aggression or its anticipation raises T levels.
Longitudinal studies may also elucidate the complex causal
pattern. In one study a group of boys was followed from 6 to 13
years of age (Tremblay et al., 1998). T at age 12 and body mass
predicted social dominance in adolescence but only body mass
independently predicted physical aggression. The authors sug-
gest that the relation between aggression and T in adolescents
may be mediated by the effect of T in the change in physique
in the context of dominance. A similar study followed males
from pre- or early adolescence (12–13 years) and found little
relationship between early or concurrent measure of T and ag-
gression; the few that were found did not persist over time
(Halpern, Udry, Campbell, & Suchindran, 1993).