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For example, a meta-analysis by Miles and Carey (1997) found that both genetics
and common environment (e.g., aspects of the social environment shared by siblings)
account for individual differences in aggressive behavior. They also reported that genetic
factors were slightly more important for males than females and that genetic factors
were less powerful among younger subjects. In a study comparing monozygotic twins
(twins that develop from a single egg and share genetic material) and dizygotic twins
(twins that develop from two separate eggs and share less genetic material), Hines and
Saudino (2004) found that “intimate partner aggression” (physical and psychological)
has a genetic component. Hines and Saudino concluded that “familial resemblance in
psychological aggression arises because members share the genes that in¬‚uence this
behavior” (p. 714). They suggest that children inherit genes from their parents that
Social Psychology
364

predispose the children for aggression. Interestingly, Hines and Saudino suggest that
whether the aggressive behavior is expressed overtly may be more strongly related to
af¬liation with aggressive peer groups than parental use of partner aggression.
In addition to the two studies just discussed, other studies also support the idea
that aggression is at least partially determined by oneʼs genetic makeup (e.g., Vierikko,
Pulkkinen, Kaprio, Viken, & Rose, 2003). However, we need to be cautious when inter-
preting the results from these studies for a number of reasons. First, the number of studies
establishing the genetic-aggression link is relatively small. Clearly, more research is
needed in this area. Second, the degree of contribution of genetics depends on the meth-
odology used. For example, observational studies tend to show stronger links between
heredity and aggression than do laboratory studies (Miles & Carey, 1997). Finally, we
must underscore that it is important to keep results that show a genetic in¬‚uence in their
proper perspective. There is little evidence that genetics has a direct effect on aggression.
Instead, genetics appears to in¬‚uence characteristics (e.g., personality characteristics)
that predispose a person to aggression. Just because someone has a genetic predisposi-
tion toward aggression does not mean that the person will behave aggressively.

The Physiology of Aggression
The brain and endocrine systems of humans and animals play an intricate role in mediat-
ing aggression. Research on the physiology of aggression has focused on two areas: brain
mechanisms and hormonal in¬‚uences. The sections that follow explore each of these.

Brain Mechanisms
Research on brain mechanisms has focused on the brain structures that mediate aggres-
sive behavior. Researchers have found, for example, that aggressive behavior is elicited
hypothalamus A structure in when parts of the hypothalamus are stimulated. The hypothalamus is part of the limbic
the limbic system of the brain system, a group of brain structures especially concerned with motivation and emotion.
associated with aggressive Stimulation of different parts of the hypothalamus (called nuclei) produce different
behavior.
forms of aggressive behavior.
In one study, researchers implanted electrodes in the brains of cats in various parts
of the hypothalamus (Edwards & Flynn, 1972). A small electric current was then passed
through these structures. When one part of the hypothalamus was stimulated, the cats
displayed the characteristic signs of anger and hostile aggression: arched back, hissing
and spitting, ¬‚uffed tail. This reaction was nondiscriminating; the cats attacked any-
thing placed in their cage, whether a sponge or a live mouse. When another part of the
hypothalamus was stimulated, the cats displayed selective predatory aggression. They
went through the motions of hunting; with eyes wide open, they stalked and pounced
on a live animal, but they ignored the sponge.
Research shows that other parts of the brain are also involved in aggression. There
is a neural circuit in the brain, including parts of the limbic system and the cortex, that
organizes aggressive behavior. No single brain structure is the master controller of
aggression.
Furthermore, brain stimulation does not inevitably lead to aggression. In one
study, brain stimulation led to an aggressive response if a monkey was restrained in
a chair (Delgado, 1969). But if the monkey was placed in a cage with another docile
monkey, the same brain stimulation produced a different behavior: The monkey ran
across the cage making repeated high-pitched vocalizations. The expression of aggres-
sive behavior also depended on a monkeyʼs status within a group. If a more dominant
monkey was present, brain stimulation did not lead to aggression. If a less dominant
Chapter 10 Interpersonal Aggression 365

monkey was present, stimulating the same part of the brain did lead to aggression.
Thus, even with brain stimulation, aggressive behavior occurred only under the “right”
social conditions.

Hormonal In¬‚uences
Researchers also have investigated the role of hormones in aggressive behavior. As men-
tioned earlier, high levels of the male hormone testosterone are generally associated with
increased aggression (Christiansen & Knussmann, 1987). However, the in¬‚uence of tes-
tosterone on aggressive behavior”like the effect of brain stimulation”is complex.
Hormones come into play twice during the normal course of development in humans:
¬rst, during prenatal development, and later, at puberty. Prenatally, testosterone in¬‚u-
ences the sex organs and characteristics of the unborn child. Testosterone levels are
higher for a genetic male than for a genetic female. The hormone permeates the entire
body, including the brain, making it possible that the male brain is “wired” for greater
aggression. Early in life, testosterone exposure serves an organization function, in¬‚u-
encing the course of brain development. Later in life, it serves an activation function
(Carlson, 1991), activating behavior patterns, such as aggression, that are related to
testosterone levels.
These two effects were shown clearly in an experiment conducted by Conner
and Levine (1969). Conner and Levine castrated rats either neonatally (immediately
after birth) or as weanlings (about 3 weeks after birth). (In rats, the critical period for
exposure to testosterone is within a day or so after birth. Castrating males immedi-
ately after birth effectively prevents exposure to the necessary levels of testosterone
for normal masculinization. The rats castrated as weanlings were exposed to the early
necessary levels of testosterone and were masculinized normally.) Other rats were not
castrated. Later, as adults, the castrated rats were exposed either to testosterone or to
a placebo.
The experiment showed that for the rats castrated neonatally, the levels of aggression
displayed after exposure to testosterone as adults did not differ signi¬cantly from the
levels displayed after exposure to a placebo. For the weanling rats, exposure to testos-
terone as adults increased the level of aggression compared to that of the rats receiving
the placebo. The levels of aggression after exposure to the testosterone or placebo did
not differ for noncastrated rats.
This study showed that early exposure to male hormones is necessary in order for
later exposure to a male hormone to increase aggression. Those rats castrated at birth
missed the “organizing function” of the male hormone; the normal process of masculin-
ization of the brain did not occur. Later injections of testosterone (activation function)
thus had little effect. Rats castrated as weanlings were subjected to the organization
function of the male hormone. Their brains were normally masculinized and more recep-
tive to the activation function of the testosterone injections received later in life. We
can conclude that high testosterone levels are effective in elevating levels of aggression
only if there is normal exposure to male hormones early in life.
Another experiment demonstrated that hormonal in¬‚uences interact with social
in¬‚uences to affect aggression. In this experiment, male rats were castrated and then
implanted with a capsule (Albert, Petrovic, & Walsh, 1989a). For some rats the capsule
was empty; for others it contained testosterone. These rats were then housed with another
rat under one of two conditions. Half the rats were housed with a single feeding tube,
requiring the animals to compete for food. The other half were housed with two feeding
tubes, so no competition was necessary. The treated rats were then tested for aggression.
Social Psychology
366

The results were striking. Testosterone increased aggression only if the rats competed
for food. If the rats were not required to compete, the levels of aggression were quite
low, about the same as those for the rats implanted with the empty capsule.
Another example of how situational factors can affect testosterone levels and aggres-
sion is provided by Kleinsmith, Kasser, and McAndrew (2006), who conducted an
experiment to see if handling a gun would increase testosterone levels and aggression.
Kleinsmith et al. informed male participants that they would be taking part in an experi-
ment on how taste sensitivity is affected by attention to detail. Kleinsmith et al. obtained
a saliva sample as soon as participants arrived at the lab. Testosterone levels were mea-
sured with the saliva sample. Then participants were led into another room where they
would perform an attention task. Some participants were given a pellet gun that was a
model of a Desert Eagle automatic pistol. Other participants were given the childʼs game
Mousetrap. Both groups of participants were instructed to write a set of instructions on
how to assemble or disassemble the gun or game. Following this task another saliva
sample was obtained. Next, participants were given a cup of water that had a drop of hot
sauce in it. Participants were told that a previous participant had prepared the sample.
After drinking the water sample, participants rated the sample. Finally, participants were
told to prepare a water sample for the next participant. They were provided with a small
cup of water and a bottle of hot sauce and told to add as much hot sauce to the water as
they wished. The results of the experiment showed that participants who handled the
gun showed a large increase in testosterone level when pre- and post-manipulation saliva
samples were analyzed (average change was 62 pg/ml). Participants who handled the game
showed a negligible increase (average change was .68 pg/ml). Additionally, participants
who handled the gun added far more hot sauce to the water (average was 13.61 grams)
than participants who handled the game (average was 4.23 grams).
Female aggression may also be mediated by hormones. In another study, the ovaries
were removed from some female rats but not from others (Albert, Petrovic, & Walsh,
1989b). The rats were then housed with a sterile yet sexually active male rat. Weekly,
the male rat was removed and an unfamiliar female rat was introduced into the cage.
Female rats whose ovaries had been removed displayed less aggression toward the
unfamiliar female than those whose ovaries had not been removed, suggesting a role
of female hormones in aggression among female rats.

Alcohol and Aggression
Our ¬nal topic relating physiology and aggression is to explore the relationship between
alcohol (a powerful drug affecting the nervous system) and aggression. There is ample
evidence showing a connection between alcohol consumption and aggression (Bushman
& Cooper, 1990; Quigley & Leonard, 1999). What is it about alcohol that increases
violent behavior? Is there something about the drug effects of alcohol, or is it a func-
tion of the social situations in which alcohol is used?
There is no question that alcohol has pharmacological (drug-related) effects on the
body, especially on the brain. Alcohol becomes concentrated in organs with a high water
content, and the brain is one such organ. Alcohol lowers reaction time, impairs judg-
ment, and weakens sensory perception and motor coordination. Under the in¬‚uence of
alcohol, people focus more on external cues, such as people or events in the situation
that seem to encourage them to take action, and less on internal ones, such as thoughts
about risks and consequences.
Although alcohol is a central nervous system depressant, it initially seems to act as
a stimulant. People who are drinking at ¬rst become more sociable and assertive. This
is because alcohol depresses inhibitory brain centers (Insel & Roth, 1994). As more
Chapter 10 Interpersonal Aggression 367

alcohol is consumed, however, the effects change. Drinkers often become irritable and
are easily angered. Levels of hostility and aggressiveness increase. Considering all the
effects of alcohol, it is not surprising that it is a major factor not only in automobile
crashes and fatal accidents of other kinds (such as drownings, falls, and ¬res) but also
in homicides, suicides, assaults, and rapes.
Research con¬rms that levels of aggression increase with the amount of alcohol
consumed (Kreutzer, Schneider, & Myatt, 1984; Pihl & Zacchia, 1986; Shuntich &
Taylor, 1972). In one study, participants who consumed 1.32 g/kg of 95% alcohol were
more aggressive than participants receiving a placebo (nonalcoholic) drink or no drink
at all (Pihl & Zacchia, 1986). The type of beverage consumed affects aggression as
well (Gustafson, 1999; Pihl, Smith, & Farrell, 1984). As shown in Figure 10.1, par-
ticipants who consumed a distilled beverage gave more severe shocks to a target than
those who consumed wine or beer (Gustafson, 1999). Gustafson also found that longer
shocks were given after consuming a distilled beverage compared to wine and beer.
In another study, participants in a bar were approached and asked a series of annoying
questions. In this natural setting, bar patrons drinking distilled beverages displayed
more verbal aggression toward the interviewer than those drinking beer (Murdoch &
Pihl, 1988).
How does alcohol increase aggression? Most likely, alcohol has an indirect effect
on aggression by reducing a personʼs ability to inhibit behaviors that are normally sup-
pressed by fear, such as aggression (Pihl, Peterson, & Lau, 1993). Although the precise
brain mechanisms that are involved in this process are not fully known, there is evi-
dence that alcohol is associated with a signi¬cant drop in the amount of brain serotonin
(a neurotransmitter), which makes individuals more likely to engage in aggression in
response to external stimuli (Badaway, 1998; Pihl & Lemarquand, 1998). Serotonin,
when it is operating normally, inhibits antisocial behaviors such as aggression through
the arousal of anxiety under threatening conditions (Pihl & Peterson, 1993). When
serotonin levels are reduced, anxiety no longer has its inhibitory effects, but intense
emotional arousal remains, resulting in increased aggression under conditions of threat
(Pihl & Peterson, 1993).




7

6
Mean Shock Severity




5

4

3

2

1 Figure 10.1 Mean
shock severity as a function
0
of type of alcoholic
Distilled Wine Beer beverage consumed.
Type of Beverage Based on data from Gustafson (1999).
Social Psychology
368

Alcohol has also been found to in¬‚uence the functioning of the prefrontal cortex
of the brain, disrupting executive cognitive functioning (ECF), or functions that help
one use higher cognitive processes such as attention, planning, and self-monitoring
(Hoaken, Giancola, & Pihl, 1998; Pihl, Assad, & Hoaken, 2003). These executive func-
tions play a major role in oneʼs ability to effectively regulate goal-directed behavior
(Hoaken et al., 1998). In individuals with low-functioning ECF, aggression is more
likely than among individuals with high-functioning ECF, regardless of alcohol con-
sumption (Hoaken et al., 1998). If the ECF remains active after alcohol consumption,
alcohol-related aggression is lower than if the ECF is inhibited (Giancola, 2004). It is
apparent, then, that the inhibitory effect of alcohol on ECF is one factor contributing
to increased aggression after alcohol consumption.
When in an intoxicated state, one can override the effects of alcohol if properly
motivated (Hoaken, Assaad, & Pihl, 1998). Hoaken and his associates (1998) placed
intoxicated and sober individuals into a situation where they could deliver electric shocks
to another person. Half the participants in each group received an incentive to deliver
low levels of shocks (the promise of money). The results showed that intoxicated par-
ticipants were just as able as their sober counterparts to reduce the severity of shocks
delivered when the incentive was provided. However, when no incentive was provided,
intoxicated participants delivered higher shock levels than the sober participants.
Although the amount and type of alcohol consumed affect aggression, research
shows that oneʼs expectations about the effects of alcohol also have an impact on aggres-
sion (Lang, Goeckner, Adesso, & Marlatt, 1975; Leonard, Collins, & Quigley, 2003;
Kreutzer, Schneider, & Myatt, 1984; Rohsenow & Bachorowski, 1984). Generally,
participants in experiments who believe they are drinking alcohol display elevated
levels of aggression, even if in reality they are drinking a nonalcoholic placebo. The
mere belief that one has consumed alcohol is enough to enhance aggression. In fact,
even the experimenterʼs knowledge of who has consumed alcohol can affect the level
of aggression observed in experiments like this. An analysis of the literature shows that
the effects of alcohol on aggression are smaller when the experimenter is blind to the
conditions of the experiment (Bushman & Cooper, 1990).This relationship also holds
outside the laboratory. Leonard, Collins, and Quigley (2003) conducted a study in which
male participants were asked about aggressive events that happened to them in bars.
Leonard et al. measured several personality and situational variables. They found that
a belief that alcohol was the cause for aggression was related to the occurrence (but not
severity) of an aggressive encounter in a bar.
Expectations cannot account for the entire effect of alcohol, however. In some cases
even when there is an expectation that alcohol may lead to aggression, such an expecta-
tion does not increase aggression, whereas actual alcohol consumption does (Quigley
& Leonard, 1999). Social cues, expectations, and attitudes play some part in mediating
alcohol-induced aggression. However, the pharmacological effects of alcohol on the
body and brain are real. Probably through a combination of reducing inhibitions and

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