Alcohol-Related Aggression during the College Years: Theories, Risk Factors
and Policy Implications*
PETER R. GIANCOLA, Ph.D.†
Department of Psychology, University of Kentucky, 115 Kastle Hall, Lexington, Kentucky 40506-0044
ABSTRACT. Objective: The purpose of this article is to present
an overview of the research literature on alcohol-related aggression with a
focus on college students. Method: Data from both survey studies and
experimental laboratory investigations conducted on college students are reviewed.
Various methodological approaches to studying the alcoholaggression relation,
and their associated limitations, are then presented and discussed. Results:
The literature indicates that alcohol consumption facilitates aggressive behavior
and increases the risk of being the victim of a violent act, particularly in
heavy drinkers. Results from these studies are then placed into a context by
reviewing 12 influential theories of aggression and alcohol-related aggression.
On the basis of these theories and empirical data, a preliminary risk profile
is presented to help identify which factors are likely to be important in predicting
who will and who will not become aggressive after drinking alcohol. Conclusions:
Although much research is still needed to elucidate the intricate causes of
alcohol-related aggression, current prevention efforts might focus on modifying
key risk factors such as poor cognitive functioning and inaccurate expectations
about the effects of alcohol. Other prevention efforts directed specifically
at college students might focus on helping them to identify risky situations
that might facilitate the expression of intoxicated aggression. (J. Stud. Alcohol,
Supplement No. 14: 129-139, 2002)
ENTRANCE INTO college marks a time of significant change in the life of a young
adult. For many students, college is a place where drinking alcohol either begins
or increases in frequency. Subsequent to this rise in drinking, a substantial
number of college students develop alcoholrelated problems. Fortunately, for
the majority of students, this rise in "college drinking" diminishes after they
graduate, at which time they go on to live more productive lives (Chen and Kandel,
1995; Gotham et al., 1997). However, what is problematic for these individuals
are the consequences of their drinking during the college years.
Very little research has been conducted to characterize the prevalence and
patterns of alcohol-related aggression in college students. Although not specifically
intended to target college students, a large study on adolescent development
found that of 391 young adults between 18 and 22 years of age (mostly college
students), 30% of males and 25% of females reported having engaged in a fight
while intoxicated (H. White, personal communication, 1999). In another large
study that sampled college students from 140 U.S. colleges in 1993 and then
resampled students from 130 of these schools in 1997, it was found that 19-24%
of students reported being intoxicated while exhibiting verbal aggression, 9-10%
reported being intoxicated while engaging in property damage and 4-6% reported
being intoxicated when apprehended by police (Wechsler et al., 1998). However,
these numbers were found to be substantially higher in heavier drinkers (Wechsler
et al., 1994, 1998). Furthermore, another report on this sample indicated that
a large proportion of college students reported being victimized by intoxicated
individuals. Specifically, 12% reported being pushed, hit or assaulted; 20%
reported being the recipients of unwanted sexual advances; and 22% reported
being involved in verbally aggressive interactions (Wechsler et al., 1995).
Again, these percentages were found to be significantly higher in heavy drinkers.
Interestingly, this suggests that one is more likely to be victimized by an
intoxicated assailant if one is a heavy drinker. Finally, when considering schools
with high levels of student drinking, 61% of college administrators indicated
that physical assaults were a moderate or major problem at their school, 53%
indicated a problem with damage to campus property and 86% indicated a problem
with sexual assault (Wechsler et al., 1995).
Methodological Approaches and Limitations
The studies described above indicate that alcohol-related
aggression is a serious problem both on and off our college
campuses. However, methodological issues surrounding the
correlational nature of these findings preclude the formulation
of statements suggesting a causal relationship between
alcohol use and aggressive behavior. At best, what can be
determined from these investigations is the percentage of
individuals apprehended for, or reporting, an alcohol-related
incident. Another difficulty is one of base rates. That is,
the above results do not indicate whether alcohol is associated
with aggression at a higher rate than would be expected
by chance alone. Furthermore, there is the problem
of directionality. That is, does alcohol cause aggression or
do aggressive individuals tend to drink more? Other limitations
of some of the above studies include insufficient information
regarding whether alcohol was present at the time
of the transgression and a reliance on self-report methods
that are troubled by response biases, problems in recollection
and problems with making inferences about another
person's state of intoxication. Despite these limitations, these
studies portray a compelling relation between alcohol and
aggression, particularly on college campuses. Nevertheless,
it is clear that more survey studies utilizing innovative methodologies
are needed to characterize the alcohol-aggression
relation in college students. The literature pertaining to
sexual assault among college students serves as a good example
of worthy approaches for documenting the alcohol-aggression
link with survey data (Abbey, this supplement).
In addition to these studies, a large number of controlled
experimental laboratory investigations have also demonstrated
a strong relation between alcohol use and aggressive
behavior. Experimental studies are advantageous over
correlational studies in that their design structure allows
for the formulation of causal inferences. Furthermore, for
the purposes of this article, another important reason for
paying attention to the results of experimental studies is
that although many of these studies utilize samples of convenience,
these samples tend to consist mainly of college
Most experimental studies that have investigated the alcohol-
aggression relation in college students have measured
aggression using the Taylor Aggression Paradigm (TAP;
Taylor, 1967). Using the TAP, subjects compete against a
fictitious opponent under the guise of a reaction time (RT)
task. Prior to each RT trial, subjects select 1 of 10 shock
intensities that they wish to administer to their opponent.
An RT trial then follows. In the event that the subject wins
the trial, his or her opponent ostensibly receives the selected
shock. In the event that the subject loses the trial,
the subject receives a shock ostensibly from his or her opponent.
To manipulate the level of provocation, subjects
receive both high and low intensity shocks. In actuality, no
opponent exists. The TAP operationalizes aggressive behavior
as the average shock intensity selected over trials.
In some modifications of the TAP, shock duration is also
used as a dependent variable. The TAP is a useful tool for
assessing the effects of alcohol on aggressive behavior. This
is accomplished by comparing shock intensity and duration
selections between sober and intoxicated persons.
The TAP has been criticized for having a number of
limitations, including adhering to demand characteristics,
measuring constructs other than aggression and not incorporating
a nonaggressive response option (Tedeschi and
Quigley, 1996). However, a number of theorists have responded
to these and other concerns (Anderson and Bushman,
1997; Berkowitz and Donnerstein, 1982; Giancola and
Chermack, 1998). Furthermore, they have shown that the
construct validity of the TAP is well established, in part,
by studies demonstrating its convergent and discriminant
validity. Convergent validity has been shown through positive
associations between shock selections and self-report
measures of physical assault, behavioral hostility and outwardly
directed anger (Giancola and Zeichner, 1995a; Hammock
and Richardson, 1992). Discriminant validity has been
demonstrated through the lack of relations between shock
selections and measures of guilt, suspicion, resentment, inwardly
directed anger (Giancola and Zeichner, 1995c), helping
and competition (Bernstein et al., 1987). Additional data
supporting the construct validity of the TAP come from
studies showing that adolescents with high teacher ratings
of aggression are more aggressive on a modified version of
the TAP than adolescents with low ratings (Shemberg et
al., 1968; Williams et al., 1967). Violent offenders also
respond more aggressively on the TAP compared with nonviolent
offenders (Hartmann, 1969; Wolfe and Baron, 1971).
Although the criticisms marshaled against the TAP reveal
some of its limitations, available data indicate that the TAP
is a good index of aggression. Because most tools that assess
complex social constructs such as aggression are less
than perfect, it is recommended that a better manner in
which to measure these variables is to employ multiple and
In most investigations that have used the TAP to study
alcohol-related aggression, subjects have typically been assigned
to one of three beverage groups: alcohol, no alcohol
or placebo. Placebo groups are used to control for the possibility
that aggression is the result of the mere belief that
one has consumed alcohol. Although some studies have
shown full (Lang et al., 1975) or partial (Pihl et al., 1981)
placebo effects on aggression, the majority of investigations
have found that the mere belief that alcohol has been
consumed does not significantly influence aggressive behavior
in college students (e.g., Chermack and Taylor, 1995;
Giancola and Zeichner, 1995b; Zeichner and Pihl, 1979,
1980). Moreover, three large meta-analytic reviews concur
that believing that alcohol has been consumed plays a negligible
role in affecting aggression (Bushman and Cooper,
1990; Hull and Bond, 1986; Steele and Southwick, 1985).
Parenthetically, a methodology termed the balanced placebo
design was created to separate the pharmacological
effects of alcohol from placebo effects. This design involves
the use of the three groups described above as well as a
group of subjects who receive alcohol but are told that they
are consuming a nonalcoholic beverage (i.e., "antiplacebo"
condition). Although this design is theoretically useful, it is
not practically useful because of the near impossibility of
convincing antiplacebo subjects that they have not consumed
alcohol, particularly at the higher doses needed to facilitate
aggression (Martin and Sayette, 1993). To the author's
knowledge, only two studies have used the balanced placebo
design to examine the effects of alcohol on aggression
as measured by the TAP (Lang et al., 1975; Pihl et al.,
1981). Results were mixed in that only one study found an
increase in aggression for the antiplacebo group (Pihl et
A series of more than 20 studies on the alcohol-aggression
relation, conducted by Taylor and colleagues, using
the TAP, documented robust and reliable findings. College
students who received alcohol evidenced higher levels of
aggression than those who received placebo or nonalcoholic
beverages (e.g., Bailey and Taylor, 1991; Chermack
and Taylor, 1995; Leonard, 1989; Taylor and Gammon,
1975; Taylor et al., 1976). Using a modified version of the
TAP, Pihl and colleagues also found (in more than 10 studies)
that college students who received alcohol administered
higher shock intensity levels and longer shock
durations compared with those who received a placebo or a
nonalcoholic control beverage (e.g., Hoaken et al., 1998;
Lau and Pihl, 1994; Pihl et al., 1990; Pihl and Zacchia,
1986; Zeichner and Pihl, 1979). Furthermore, using other
modifications of the TAP, Giancola and colleagues replicated
the above results (Giancola et al., in press; Giancola
and Zeichner, 1995b,c, 1997; Zeichner et al., 1994, 1995).
Clearly, the results of these studies support a strong relation
between acute alcohol consumption and aggressive behavior
in college students.
Many of the investigations reviewed above, and others,
have been included in meta-analytic studies. As would be
expected, the results of these studies support the contention
that acute alcohol intoxication facilitates aggressive behavior.
For example, Bushman and Cooper (1990) determined
that the average effect sizes for alcohol versus placebo conditions
and placebo versus nonalcohol conditions were 0.61
and 0.10, respectively. In a later study, Bushman (1993)
reported similar mean effect sizes for these comparisons
(i.e., 0.49 and 0.0028). In summary, these statistics clearly
indicate that acute alcohol consumption significantly increases
the expression of aggressive behavior in college
General theories of aggression
Clearly, there is a need for effective prevention interventions
aimed at attenuating alcohol-related aggression in
college students. However, it has been argued that for prevention
interventions to make a significant and lasting impact,
they must spawn from theoretically based empirical
research that elucidates the causal structure of the alcoholaggression
relation (Chermack and Giancola, 1997). Given
the important need for theory in guiding research, some
important models of alcohol-related aggression are presented
below. However, insofar that such specialized models are a
subset of more general theories, it would be useful first to
review some broad theories of aggression. Geen (1990) and
Berkowitz (1993) provided two such prominent contemporary
Geen's (1990) major premise is that the elicitation of
aggression is dependent on the interaction of two general
factors. The first involves "background variables" such as
genetics, physiology, temperament, personality, social-cultural
expectations and exposure to violence. According to
Geen, deviations on these variables serve to predispose toward
aggression. The second factor involves frustrating or
provocative environmental stimuli that produce stress,
arousal and anger. These stimuli can take many forms such
as a verbal or physical attack, family conflict, hot temperatures
and physical pain. Geen explained that the manner in
which these provocative or frustrating stimuli are interpreted
will moderate the amount of stress, arousal and anger that
is experienced, which will then affect whether aggression
is or is not expressed. Specifically, if an aversive situation
is interpreted as justifiable or nonintentional, the result will
be little arousal and anger, which will lead to little or no
aggression. Conversely, if a situation is interpreted to be
malicious or arbitrary, the result will be high levels of
arousal and anger and thus a higher probability of an aggressive
response. Finally, Geen added that even in a highly
aroused or angered state, the expression of aggression can
still be moderated by paying attention to alternative
nonaggressive means of coping with the situation. However,
if such attentional resources are lacking, the probability
of an aggressive response will be heightened.
Berkowitz (1993) put forth a theory postulating that the
desire to behave in an aggressive manner is the result of
experiencing negative affect. Negative affect is defined as
any unpleasant feeling that can be brought on by a number
of factors such as frustration, insults, attacks, hot temperatures
and noise. Berkowitz made the point that it is not the
direct effect of such instigating factors that produces aggression
(i.e., damaged self-image, being punched in the
face), but instead the psychological damage (i.e., negative
affect) that they produce. According to the theory, the experience
of negative affect results in the activation of
aggression- or fear-related cognitions, feelings and expressive-
motor and physiological reactions that are associated
with both basic fight and flight tendencies. Once the primary
reactions to an aversive event have occurred, more
differentiated feelings later arise as the result of higher order
cognitive processing (e.g., making causal attributions,
thinking about possible consequences of aggression, paying
attention to social rules). According to Berkowitz, this
higher order reasoning differentiates the original more ba-
sic experience, thus intensifying some of its aspects and
suppressing others. Therefore, an initial basic response to
aggress can be modified by "thinking" about alternative
nonaggressive solutions to the situation.
Although these theories have not been covered in great
detail, both attempt to explain aggressive behavior by implicating
fairly broad constructs and processes (i.e., arousal,
anger, negative affect, social cognition). Furthermore, both
theories also suggest that variations in a number of key
individual difference variables (e.g., biology, personality)
and situational variables (e.g., provocation, temperature) are
crucial for the expression of aggression. These models are
important because they provide good overarching explanations
of aggressive behavior and offer excellent conceptual
frameworks from which to test more specific hypotheses
about the causes of aggression.
Alcohol and aggression: Disinhibition and expectancy
The disinhibition model is considered to be a very general
explanation of the alcohol-aggression relation. It contends
that alcohol has a direct effect on aggression by
pharmacologically disinhibiting brain centers important in
maintaining inhibitory control over behavior (Graham,
1980). This model has limited empirical support because
not all persons become aggressive when they drink alcohol.
In direct opposition is the expectancy model, which stipulates
that it is not the pharmacological properties of alcohol
that facilitate aggression, but rather the mere belief that
one has consumed alcohol (MacAndrew and Edgerton,
1969). This model rests on the assumption that people have
a priori beliefs that alcohol will lead to aggression. As noted
above, previous studies have demonstrated negligible differences
in aggression between subjects receiving a placebo
beverage versus those who knowingly drank a
nonalcoholic beverage. These data are typically used to argue
against the position that alcohol expectancies affect
aggressive behavior. However, this is an erroneous argument
because placebo manipulations do not take into account
individual differences in beliefs that alcohol will
increase aggression. That is, it may be that placebo manipulations
are indeed effective in increasing aggression but
only in persons who believe that alcohol will increase aggression.
The few published studies that take into account
individual differences in alcohol expectancies for aggression
have shown modest to good support that expectancies
interact with alcohol to increase aggression (Chermack and
Taylor, 1995; Dermen and George, 1989; Leonard and
Another model, a more refined version of the disinhibition
explanation, is the indirect cause model (Graham, 1980).
This model suggests that alcohol detrimentally affects certain
psychological and/or physiological processes that then
lead to the expression of aggressive behavior. Some of the
most prominent contemporary theories of alcohol-related
aggression are variants of the indirect cause model. Specifically,
most of them are cognitive models that suggest
that alcohol disrupts a specific type of cognitive function
that then increases the probability of aggression. Due to
their influential nature in the current research literature on
alcohol-related aggression, seven of these models are reviewed
Pernanen (1976) hypothesized that alcohol consumption
increases the probability of an aggressive reaction by reducing
the number of available psychological coping mechanisms
that rely on conceptual/abstract reasoning. According
to this model, alcohol creates a "narrowing of the perceptual
field" (p. 415), which reduces the ability to detect both
internal and external cues that may provide crucial information
about another person's intentions in a precarious
situation. Consequently, a reduction in these cues will result
in a random or an arbitrary interpretation of the other
person's intentions. Accordingly, when intoxicated, it is this
tendency to interpret incoming information as random or
arbitrary (especially if the incoming information is aggressive
in nature) that will increase the probability of a violent
Taylor and Leonard (1983) postulated that aggressive
behavior is determined by the relative balance of a combination
of both instigative (e.g., threats, insults) and inhibitory
(e.g., anxiety, norms of reciprocity) cues present in
hostile interpersonal situations. Instigative cues increase the
probability of an aggressive encounter, whereas inhibitory
cues decrease that probability. These theorists reasoned that
the cognitive disruption produced by alcohol reduces the
number of information sources (i.e., cues) that one can attend
to in any given situation. Therefore, aggressive behavior
is most likely to occur in a context where instigatory
cues are paramount as opposed to a situation dominated by
Steele and Josephs (1990) proposed an attention allocation
model in which alcohol interferes with information processing
in such a manner as to disrupt the ability to allocate
attention to multiple aspects of a situation effectively. Accordingly,
alcohol creates a "myopic" or narrowing effect
on attention, which results in attention being allocated only
to the most salient aspects of a particular situation and not
to other less salient cues. Alcohol will therefore decrease
the ability to extricate important meaning from less salient,
possibly inhibitory, cues. It is thus maintained that in a
conflict or a provocative situation, alcohol's myopic effect
on attention may facilitate aggression by forcing attention
to the most salient (i.e., provocative) aspects of that situation
and not to other less salient (i.e., inhibitory) cues.
As can be seen quite clearly, Taylor and Leonard's (1983)
and Steele and Josephs' (1990) models are very similar
(i.e., both maintain that alcohol impairs the ability to attend
to inhibitory cues). The main difference between the two
models is that Steele and Josephs explicitly posited the hypothetical
mechanism of inhibition conflict as a determinant
of when alcohol will, and will not, facilitate aggression.
Inhibition conflict refers to the magnitude of conflict between
two opposing response tendencies (Steele and
Southwick, 1985). According to Steele and colleagues
(Steele and Josephs, 1990; Steele and Southwick, 1985), a
considerable degree of inhibition conflict must be present
if alcohol is to facilitate aggression. Steele and Josephs'
model predicts that an intoxicated person is likely to attack
another individual in the presence of both inhibitory and
instigatory cues (high conflict) because attention will be
focused on the most salient cues (i.e., provocative/
instigatory). However, in the absence of any inhibitory cues
(low conflict), the model predicts that the effects of alcohol
will be irrelevant. That is, without inhibitory cues, an attacker
will be just as likely to emit an aggressive response
in either an intoxicated or a sober state due to the lack of
any internal or external proscriptions against aggression.
Similarly, if no provocative cues are present, a person should
not react aggressively whether intoxicated or sober. Parenthetically,
the mechanism of inhibition conflict is nonetheless
implicit in Taylor and Leonard's model.
Pihl et al. (1993) posited a biosocial model of intoxicated
aggression in which cognitive functioning is but a
single aspect of a multidimensional mechanism. According
to these theorists, acute alcohol consumption disrupts the
functioning of the prefrontal cortex and its subcortical connections,
especially the hippocampus, which, according to
Pihl et al., "is involved in the recognition of threat" (p.
134). Thus, by disrupting these neural regions and circuits,
alcohol eliminates signals of punishment through its
anxiolytic effects (i.e., reduces fear reactions), resulting in
decreased inhibitory control over behavior. Pihl et al. also
posited that aggressive responses are enhanced through
alcohol's psychomotor stimulant properties and an increased
sensitivity to cues of physical pain.
Hull (1981) proposed a general model of the effects of alcohol on self-awareness
in which it is suggested that alcohol intoxication engenders aggressive behavior
through a reduction in self-awareness. According to his model, alcohol disrupts
self-awareness by interfering with the higher order cognitive encoding of self-relevant
information necessary to attain a self-aware state. Such interference then purportedly
disrupts the ability to evaluate self-relevant social and environmental information
that putatively provides feedback concerning appropriate forms of behavior.
Without access to this information, Hull posited the heightened probability
of aggressive behavior.
Sayette (1993) advanced an appraisal disruption model
of alcohol's effects on stress. Ito et al. (1996) invoked this
model to account for the alcohol-aggression relation. According
to Sayette, if alcohol is consumed before the onset
of anxiety-eliciting cues, it will disrupt the cognitive appraisal
of those cues, thus resulting in anxiolysis. In such a
case, as noted by Ito et al., alcohol may facilitate aggression
indirectly by reducing fear and inhibition. This model
shares a commonality with that of Pihl et al. (1993) in that
both make the point that alcohol disrupts, in essence, the
same cognitive ability (i.e., recognition of threat [Pihl et
al.] and information appraisal [Sayette]), which then facilitates
aggression through an attenuation of fear and inhibition.
Giancola (2000a) advanced the idea that all of the cognitive
abilities implicated in the above models are components
of a more general construct termed executive
functioning. Executive functioning is defined as a higher
order cognitive construct involved in the planning, initiation
and regulation of goal-directed behavior (Luria, 1973,
1980; Milner, 1995). The cognitive abilities subsumed
within this construct include attentional control, previewing,
information appraisal, strategic goal planning, abstract
reasoning, temporal response sequencing, self- and social
monitoring, abstract reasoning, cognitive flexibility, hypothesis
generation and the ability to organize and adaptively
utilize information contained in working memory (Kimberg
and Farah, 1993; Stuss and Benson, 1984). Giancola argued
that, compared with models that invoke only one cognitive
ability, a more general model that incorporates a
cluster of conceptually and empirically related abilities
would more accurately reflect the richness and complexity
of the cognitive mechanisms influencing the alcohol-aggression
relation. Based on data showing that low executive
functioning is related to increased aggression and that
acute alcohol consumption disrupts executive functioning,
Giancola put forth a new model. This model postulates that
(1) executive functioning mediates the alcohol-aggression
relation in that acute alcohol intoxication disrupts executive
functioning, which then heightens the probability of
aggression and (2) executive functioning moderates the alcohol-
aggression relation in that acute alcohol consumption
is more likely to facilitate aggressive behavior in
persons with medium to low, rather than high, executive
Beginning to Sketch a "Risk Profile" for the Alcohol-
Although research shows that acute alcohol consumption
is related to the expression of aggressive behavior,
there is a wide range of individual differences among these
data. In other words, not all people become aggressive when
they drink. Therefore, it can be argued that alcohol does
not directly cause aggression solely through its pharmacological
actions (Bushman and Cooper, 1990). Rather, accumulating
evidence indicates that intoxicated aggression is
the product of individual difference and contextual variables
interacting with alcohol pharmacodynamics (Chermack
and Giancola, 1997). Currently, very little is known about
the manner in which these latter variables, and their interactions,
serve as underlying mechanisms of intoxicated aggression.
Therefore, a useful task for investigators would
be to identify which traits characterize individuals who typically
exhibit intoxicated aggression and which situational
conditions are most likely to facilitate such behavior. Below
is a brief examination of some individual difference
and contextual variables that may serve as "risk factors"
for alcohol-related aggression.
Individual difference variables
Dispositional aggressivity. Dispositional aggressivity,
typified by the tendency to be aggressive across a range of
situations, has been shown to be strongly related to selfreported
husband-to-wife violence (Leonard and Senchak,
1993) and violent behavior in male college students (Dermen
and George, 1989). Interestingly, dispositionally aggressive
individuals, such as those with antisocial personality disorder
or conduct disorder, are also characterized by low executive
functioning (Malloy et al., 1990; Moffitt and Henry,
1989). Only one study has assessed the combined effects
of acute alcohol consumption and dispositional aggressivity
on aggression as measured by the TAP in college students
(Bailey and Taylor, 1991). Acute alcohol consumption increased
aggression in men with high levels of dispositional
aggressivity but not in those with low or moderate levels.
Alcohol expectancies. Alcohol expectancies are defined as beliefs about
the effects of alcohol on behavior (Leigh, 1987). As noted above, some research
suggests that intoxicated aggression results, in part, from the belief that
alcohol increases aggression. It is well known that people vary in their belief
that alcohol increases arousal, power, assertiveness, verbal aggression and
physical aggression (Brown et al., 1980; Rohsenow and Bachorowski, 1984). Significantly,
self-report studies indicate that the association between alcohol consumption
and aggression is stronger among individuals who expect alcohol to increase
aggression (Dermen and George, 1989; Leonard and Senchak, 1993). One published
study, using the TAP, attempted to determine whether individual differences
in alcohol- aggression expectancies would affect aggression under the influence
of alcohol in male college students (Chermack and Taylor, 1995). Results indicated
that under conditions of high provocation, intoxicated subjects with high expectancies
about the effects of alcohol on aggression were more aggressive than were those
with low expectancies.
Drinking history. Quantity of past alcohol consumption is positively
related to self-reported aggression in male (Dermen and George, 1989) and female
(West et al., 1990) social drinkers. Theory suggests that increased alcohol
consumption and aggressive behavior are both components of an overarching construct
of "deviant behavior" (Jessor and Jessor, 1977; Pernanen, 1991). However, the
underlying mechanisms, or causal dynamics, of that construct are not known.
One laboratory study found that acute alcohol consumption increased aggression
on the TAP in male college students, but only in those with low, rather
than moderate or high, levels of past-year drinking (LaPlace et al., 1994).
The authors hypothesized that alcohol's detrimental effects on cognition were
greater in those with a low tolerance for alcohol compared with those with a
Executive functioning. Low executive functioning capacity
has been found to be related to increased aggression in
young boys and young adult males; fighting in normal preadolescent
boys; and increased disruptive, delinquent and
physically aggressive behavior in adolescent females
(Giancola and Zeichner, 1994; Giancola et al., 1996, 1998;
Seguin et al., 1995). It has been hypothesized that low executive
functioning facilitates the expression of aggression
by impeding the cognitive regulation of behavior and interfering
with the ability to generate alternative, nonaggressive
responses in provocative situations (Giancola, 1995, 2000a).
Only one study has assessed the relation between executive functioning, acute
alcohol consumption and aggression (Lau et al., 1995). Normal male college students
were administered two neuropsychological tests of executive functioning and
were then separated into "high" and "low" functioning groups. They were administered
either an alcohol or a nonalcohol beverage and then tested on the TAP. Alcohol
and low executive functioning had independent effects on aggression; however,
an interaction between executive functioning and alcohol consumption was not
observed. An interaction was predicted because theory suggests that alcohol
increases aggression to a greater extent in individuals with medium to low,
compared with high, executive functioning (Giancola, 2000a). Conclusions from
this study are limited because only two executive functioning tests were used,
and statistical power was too low to detect a significant Executive Functioning
x Alcohol interaction.
Hostile attributional biases. Research has shown that
aggressive children are more likely than their nonaggressive
counterparts to erroneously attribute hostile intent to another
child's provocative actions, even if those actions are,
from an objective standpoint, ambiguous in intent (Dodge,
1980; Dodge and Frame, 1982). Furthermore, hostile
attributional biases have been shown to be positively related
to undersocialized aggressive conduct disorder, reactive
aggression and number of violent crimes committed in
a sample of highly aggressive juvenile offenders (Dodge et
al., 1990). These data suggest that erroneous hostile
attributional biases may be, in part, responsible for increased
aggression in children. Others have found that adults are
also vulnerable to making erroneous hostile attributions in
ambiguous interactions (Epps and Kendall, 1995). Therefore,
with respect to intoxicated aggression, it is possible
that alcohol may disrupt information processing to the extent
that an individual may distort and/or misinterpret ambiguous
interpersonal information or cues, thus resulting in
the attribution of a hostile bias, which may then lead to an
increased probability of emitting an aggressive response.
Biochemistry. Both animal and human research have
demonstrated a positive relation between testosterone levels
and physical aggression (Volavka, 1995). Berman et al.
(1993) found that healthy male college students with high
levels of testosterone, measured in saliva, were more aggressive
on the TAP than those with low levels. Moreover,
heightened aggression has also been related to low levels
of the brain neurotransmitter serotonin (Berman et al., 1997).
Interestingly, a study using the TAP demonstrated increased
aggression in healthy college males who received a tryptophan-
depleted dietary mixture (Pihl et al., 1995). Tryptophan
is the biochemical precursor for serotonin; its dietary
depletion leads to lowered brain serotonin levels. Theorists
have argued that serotonin is involved, in part, in the inhibition
of behavior (Spoont, 1992; Volavka, 1995). As such,
it may be that the aggression enhancing effects of alcohol
are more likely to occur in individuals with higher baseline
levels of testosterone and lower levels of serotonin.
Currently, very little is known about the acute effects of
alcohol on testosterone and serotonin in the human brain.
Animal research suggests that low doses of alcohol tend to
enhance blood testosterone levels whereas high doses tend
to have a suppressing effect (K. Miczek, personal communication,
2000). Animal research also suggests that acute
alcohol consumption initially increases, but then decreases,
brain serotonin levels (reviewed in LeMarquand et al.,
1994). Although far less work has been conducted on humans
than on animals, current research suggests that acute
alcohol consumption depletes blood tryptophan levels, thus
suggesting depletions in brain serotonin (reviewed in
Gender. There exist only a small number of published studies on alcohol-related
aggression in women. In a survey investigation, White et al. (1993) reported
that adolescent males engaged in more alcohol-related aggression (e.g., fights,
hurting someone, forced sex, vandalism, setting fires) than their female counterparts.
In contrast, a laboratory study found that low doses of alcohol increased verbal
aggression on an adjective checklist in females but not in males (Rohsenow and
Bachorowski, 1984). In a study using a modified version of the TAP, Bond and
Lader (1986) found that alcohol equally increased aggression (i.e., tone blasts)
for men and women when they were exposed to low levels of provocation (i.e.,
low intensity tone blasts). However, when highly provoked, only men showed increased
aggression with alcohol (Bond and Lader, 1986). In a study using a point subtraction
task, Dougherty et al. (1996) showed that alcohol increased aggression for women.
In another study using men and women, Dougherty et al. (1999) reported that
alcohol equally increased aggression for both genders. In contrast, however,
Gustafson (1991) found that alcohol and provocation had no effects on aggressive
responding (i.e., shock administration) in women.
Giancola and Zeichner (1995b) reported that alcohol increased aggression in
the form of shock intensity and shock duration for men; however, it only slightly
increased shock duration for women. Furthermore, high provocation (i.e., receiving
high intensity shocks) increased aggression for men and women, regardless of
whether they received alcohol. Hoaken and Pihl (2000) found that alcohol increased
shock intensity and duration for men but not for women. Although alcohol did
not affect aggression for women, higher levels of provocation increased their
aggressive responding to the same degree as intoxicated men.
Blood alcohol concentration limb effects. Studies have
generally shown that a blood alcohol concentration (BAC)
of .08% is typically sufficient to facilitate aggression
(Gustafson, 1985; Pihl and Zacchia, 1986). Given this, the
assumption has generally been that as long as one is at a
BAC of .08% or higher, there is a greater likelihood for
aggression. However, Giancola and Zeichner (1997) showed
that this assumption is indeed correct, but only for the ascending
limb of the BAC curve (when alcohol levels in the
bloodstream are rising). That is, in a study measuring two
different groups of male college students on the TAP, those
tested on the ascending limb of the BAC curve (.08% BAC)
were significantly more aggressive that those tested on the
descending limb of the curve (.08% BAC). Those tested on
the descending limb were no more aggressive than were
sober control subjects. The authors explained this finding
by noting that greater executive functioning deficits are
found on the ascending limb compared with the descending
limb of the BAC curve.
Alcohol type and dose. Intoxicated aggression varies depending
on the type of alcoholic beverage that is consumed.
Specifically, distilled beverages such as vodka and bourbon
elicit significantly more aggression on the TAP compared
with brewed beverages such as beer (Pihl et al., 1984).
Further, the dose of alcohol administered also affects aggression.
Research has shown that the relation between alcohol
dose and aggressive behavior follows an inverted
U-shaped curve. That is, at low doses that produce BACs
around .03-.04%, alcohol produces rather small increases,
if any, in physical aggression (reviewed in Pihl, 1983).
Greater levels of aggression are typically seen at BAC levels
of .08% or higher (Giancola and Zeichner, 1995b, 1997;
Pihl, 1983). Of course, studies that produce excessively high
BACs cannot be ethically conducted. However, based on
animal data and anecdotal reports, it is roughly estimated
that, for most persons, BACs above .20-.30% will induce a
biological and psychological state where aggression, and
most other organized and complex behaviors, will not be
Social pressure. It has been demonstrated that social pressure
also helps to moderate the alcohol-aggression relation.
In a study by Taylor and Sears (1988), confederates were
asked to encourage sober and intoxicated male college students
to behave more aggressively toward their opponent
on the TAP. Results demonstrated that only intoxicated subjects
were influenced by the confederates' suggestions to
Provocation. Provocation is a necessary ingredient in an
interpersonal interaction if aggressive behavior is to occur.
In their review of the literature on alcohol and violent crime,
Murdoch et al. (1990) reported that verbal altercations tend
to precede violent interactions. In her study of 307 assaultive
criminals, Mayfield (1976) reported that "in 50% of
the cases the victim attacked or made a move which was
interpreted by the subject as an impending attack immediately
prior to the assault" (p. 289). In the context of a provocative
situation, research has shown greater aggression
on the TAP in intoxicated, compared with sober, male college
students (Taylor et al., 1979).
Clearly, multiple factors contribute to the expression of
alcohol-related aggression. It should be made clear, however,
that the risk factors described here are not an exhaustive
list. Other traits that are potentially important in
moderating the alcohol-aggression relation include age, perspective-
taking, self-awareness, negative affect, temperament,
affect regulation, emotionality, sensation seeking,
anxiety, irritability, hostility, frustration tolerance, impulsivity,
psychopathology, early physical abuse, perceived
self-esteem and tolerance and sensitivity to alcohol. Unfortunately,
there is no single profile that will predict intoxicated
aggression in all persons. However, studying these
and other variables is important because it will provide researchers
with a better understanding of the mechanisms
that underlie the alcohol-aggression relation.
This article makes the point that acute alcohol consumption
per se does not directly cause aggression. Instead, it
argues that alcohol interacts with a host of individual difference
and contextual variables to facilitate aggression. In
other words, although alcohol does have some involuntary
biological effects that predispose toward aggression (impairing
brain functioning), there are also a number of psychological
factors that contribute to alcohol-related
aggression. Other than attempting to institute radical and
clearly untenable preventative initiatives (e.g., alcohol prohibition,
lacing alcoholic beverages with serotonin-enhancing
and testosterone-reducing additives), changes in social
policy will probably have little effect on the biological
causes of alcohol-related aggression. However, one area in
which both scientists and policy-makers can direct their
attention is the development of psychological harm reduction
strategies, strategies aimed at reducing the possibility
of alcohol-related aggressive behavior.
This article identifies a number of psychological risk
factors for intoxicated aggression. What appears to be
needed are intervention programs aimed at modifying key
risk factors so that alcohol consumption will be less likely
to engender aggression. However, to be most effective, these
interventions must be implemented in the proper context.
For example, such programs could begin by educating
people about the effects of alcohol on behavior. Specifically,
it can be clarified that alcohol, in and of itself, does
not cause aggression; it merely "drowns" the inhibitions
that typically keep us from behaving aggressively or inappropriately.
The message must be clearly sent that alcohol
will not facilitate any behaviors for which there is no psychological
predisposition. Given the early ages at which
adolescents begin to consume alcohol in the United States,
it would be prudent to begin such interventions at the junior
high-school level and continue throughout the college
years. This message could be conveyed through classroom
teachings. Furthermore, fraternities, sororities, dormitories,
athletic programs and other establishments and institutions
could also be required to convey these messages to their
members and residents. In addition, cognitive restructuring
techniques could be similarly implemented to alter preexisting
expectations that alcohol causes aggressive behavior
(Darkes and Goldman, 1993).
With regard to executive functioning, interventions could
be modeled after neuropsychological rehabilitation efforts
aimed at strengthening cognitive functioning (Giancola,
2000b). Moreover, interventions could also be aimed at
teaching social interaction and interpretation skills so that
persons with aggressive or hostile dispositions and
attributional biases can remain nonargumentative and nonviolent
when drinking. Such interventions would probably
be implemented most successfully in specialized mental
health clinics for disruptive, delinquent and violent children,
adolescents and adults. Finally, interventions can also
be used to educate about contextual influences on intoxicated
aggression, particularly those that can be prevented
or avoided (e.g., alcohol type, social pressure, provocation).
Again, these messages can be conveyed in classrooms from
junior high on to college as well as other college settings
such as dormitories, fraternities and athletic programs.
The risk factors for intoxicated aggression that are listed in this article
are clearly not specific to college students. However, when it comes to focusing
on this special population, other well-known variables come into play that are
as important, if not more important, than those listed above. These would include
contextual factors such as "keg" parties, sporting events, fraternity life and
coed dormitories. It would also be important to consider other dispositional
traits that could increase the probability of exposure to such "high-risk" contexts
such as problem behaviors prior to college and preexisting attitudes that promote
disinhibited behavior, violence and excessive drinking. Although many universities
and colleges already have educational programs in operation, at various levels,
to inform students about the dangers of alcohol, negative, and sometimes disastrous,
outcomes are nonetheless still too high. Clearly, a problem cannot be effectively
prevented or treated if the cause is not known. If effective policy aimed at
reducing intoxicated aggression in college students is to be implemented, more
research will be needed to understand how alcohol interacts with basic dispositional
traits, environmental variables, problem behaviors and attitudes that are present
before one arrives at college and contextual variables that are typically specific
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*Preparation of this article was supported, in part,
by National Institute on Alcohol Abuse and Alcoholism grant ROI-AA-11691 and
the University of Kentucky Research Challenge Trust Fund.
†Peter R. Giancola may be reached at the above address
or via e-mail at: firstname.lastname@example.org.
Last reviewed: 9/23/2005