Trait modulation of alcohol-induced laboratory aggression

Psychiatry Research 142 (2006) 129 – 138 www.elsevier.com/locate/psychres

Trait modulation of alcohol-induced laboratory aggression Matthew D. Bailly, Alan R. King * Department of Psychology, University of North Dakota, P.O. Box 8380, Grand Forks, ND 58202-8380, United States Received 29 April 2004; accepted 11 October 2005

Abstract Modest alcohol and aggressive trait effects on laboratory-induced aggression among men have been reported with some consistency in the literature. Relationships between aggressive personality traits and laboratory-induced aggression appear to become less consistent under the influence of alcohol. Several research teams have found suggestions that the effects of alcohol on laboratory aggression may be reduced or even reversed among individuals with aggressive personality traits. This study examined the effects of alcohol on the aggressive responding on the Point Subtraction Aggression Paradigm (PSAP) of eight undergraduate men who generated evidence on the Million Clinical Multiaxial Inventory-II (MCMI-II) of sadistic-aggressive personality disorder features. This sample was compared with a group of 18 undergraduate male peers without MCMI-II elevations described in a previous study. Neither alcohol ingestion (0.8 ml/kg) nor aggressive personality traits predicted laboratory behavior in isolation, but alcohol was found to selectively attenuate (d = 0.75) PSAP responding for the sadistic-aggressive as opposed to the control subjects (i.e., a significant aggressive trait by alcohol interaction). The possible value of this counterintuitive response tendency in identifying men at elevated risk for alcohol-related aggression was discussed. Large, immediate reductions in laboratory-based aggressive responding while under the influence of alcohol might provide a paradoxical high risk indicator that has not been previously identified. D 2006 Elsevier Ireland Ltd. All rights reserved. Keywords: Point Subtraction Aggression Paradigm (PSAP); Laboratory-induced aggression; Aggressive trait; Aggressive personality; Alcohol-induced aggression

1. Introduction Aggression has been defined as a class of behavior intended to harm another person who perceives the action to be undesirable (Baron and Richardson, 1993). Violence is a term usually reserved for physical acts of aggression. Operational definitions of these constructs have varied extensively (Gomberg, 1993), and reliable conclusions regarding the basic factors that mediate human aggressive responding have been elusive. Situational factors such as level of provocation * Corresponding author. Tel.: +1 701 777 3644; fax: +1 701 777 3454. E-mail address: [email protected] (A.R. King).

(Phil et al., 1997), availability of nonaggressive competing responses (Gustafson, 1993), modeling influences (Wolfe and Baron, 1971), and others have proved important and difficult to control even under the best of experimental conditions. Aggressive behavior is further mediated by salient personality dispositions and their state-trait interaction effects (Bailey and Taylor, 1991; Giancola and Zeichner, 1995; Phil et al., 1997; Moeller et al., 1998; Dougherty et al., 1999; Gera et al., 2001; Parrott and Zeichner, 2002). Aggression ultimately emerges as a function of a confluence of contributing factors that has been difficult to deconstruct, quantify, and replicate. Aggression has been measured in many ways in both the laboratory and naturalistic settings. Retrospective

0165-1781/$ - see front matter D 2006 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.psychres.2005.10.015

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counts of violent acts that occur in naturalistic settings are appealing in their social relevance but inadequate for purposes of controlled experimentation. Trait measures such as the Life History of Aggression questionnaire (LHA: Coccaro et al., 1997), Buss–Durkee Hostility Inventory (BDHI: Buss and Durkee, 1957), Buss–Perry Aggression Questionnaire (BPAQ: Buss and Perry, 1992), Conflict Tactics Scale (CTS: Straus, 1979), Overt Aggression Scale (OAS: Yudofsky et al., 1986), Brown History of Violence Scale (BHV: Brown et al., 1979), and Trait Anger Scale (TAS: Spielberger et al., 1983) have provided popular psychometric measures of malicious intent and behavioral proclivity that may not always predict aggression as it occurs in naturalistic settings. Questionnaire and life history data can identify predictors of aggression for subsequent controlled experimentation.

of 21 community subjects who each completed six PSAP sessions in a single day. Aggressive responding dropped after the third session by two-thirds from that found at intake. Allen et al. (1997) reported a similar result that was not replicated in several other studies (Bjork et al., 1997; Kouri et al., 1999; Bailly and King, 2004). The construct validity of laboratory-induced aggression procedures has been challenged (Tedeschi and Quigley, 1996), defended (Giancola and Chermack, 1998), and revisited (Tedeschi and Quigley, 2000) in recent years. PSAP scores have been found, however, to discriminate between subjects with and without violent (Cherek et al., 1997, 2000), antisocial (Moeller et al., 1997, 1998), substance abuse (Allen et al., 1997; Kouri et al., 1999;), and even contact-sport athletic (Huang et al., 1999) histories.

1.1. Experimentally induced aggression

1.2. Alcohol effects on experimentally induced aggression

An alternative behavioral measurement methodology has been provided by aggression-elicitation laboratory procedures such as the Taylor Aggression Paradigm (TAP: Taylor, 1967) and the Buss Aggression Paradigm (Buss, 1961). These tasks require subjects to administer shocks of optional intensities to a fictitious and provocative competitor seated in a separate location. Laboratory-based studies have relied on less rigorous operational definitions of aggression that revolve around the delivery of noxious stimulation to another organism (Buss, 1961; Taylor, 1967; Cherek, 1981; Bushman, 1993) without verification of malicious intent. The Point Subtraction Aggression Paradigm (PSAP: Cherek, 1981) has provided an alternative laboratorybased measurement procedure derived from the retaliatory responses of subjects engaged in a competitive, monetary-reinforced computer game. PSAP scores quantify the subjects efforts to reduce the profits of an annoying (i.e., one who interferes with subject’s monetary gain) fictional opponent. PSAP results are typically averaged over 25-min sessions that vary in number from a low of one in a single day (Gerra et al., 1999) to a high of 78 over a 13-day period (Moeller et al., 1996). Most of the three dozen published studies report data collected from 12 to 18 individual sessions scheduled over about 5 days of testing. Subjects such as violent parolees tend to generate around 350 to 475 aggressive (Button B) responses per session or double that expected for control subjects (Cherek et al., 1997). Analyses of the impact of repeated sessions alone on PSAP responding have yielded mixed results. Allen et al. (1996) provided perhaps the most focused analysis

The effects of alcohol on laboratory aggression among women appear to be modest (Rohsenow and Bachorowski, 1984; Bond and Lader, 1986; Dougherty et al., 1996, 1999) and not always observed (Gustafson, 1991; Giancola and Zeichner, 1995). Alcohol-induced aggression has been found more consistently among men (Bushman and Cooper, 1990; Gantner and Taylor, 1992; Giancola and Zeichner, 1995; Moeller et al., 1998; Dougherty et al., 1999;) and is more likely to appear as a dose-dependent function (Taylor and Gammon, 1975; Kelly et al., 1989; Dougherty et al., 1999). These experimental studies of laboratory aggression under the influence of alcohol are supplemented by an extensive literature establishing intoxication as a high-risk predictor of violent behavior in naturalistic settings (Bushman and Cooper, 1990; Murdoch et al., 1990; Leonard and Senchak, 1993; Leonard et al., 1985; Taylor and Chermack, 1993; Miczek et al., 1994; Zhang et al., 1997). 1.3. Aggressive trait predictors of laboratory-induced aggression Personality variables have often been used to predict aggressive behavior in both clinical and experimental settings. Indeed, anger-management deficits are recognized in many of the DSM-IV (American Psychiatric Association, 1994) personality disorder symptoms. Antisocial personalities are described as showing a lack of remorse, disregard for the safety of others, and irritability and aggressiveness as manifested in repeated

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physical fights or assaults. Paranoid personalities are described as suspecting harm from others without sufficient basis, bearing grudges, and quickly and angrily reacting with counterattack in response to provocation. The DSM-III-R (American Psychiatric Association, 1987) concept of sadistic personality disorder was characterized by physical cruelty or violence for purposes of establishing dominance, lying for purposes of harming or inflicting pain on others, and the humiliation and demeaning of others. PSAP scores have differentiated antisocial and control subjects in two studies (Moeller et al., 1997, 1998). Other links between DSM-IV diagnoses and PSAP responding have not been established. A variety of anger trait measures have been successfully used to predict PSAP responding. Gera et al. (2001) found close relationships between PSAP responses and BDHI Direct Aggressiveness, r = 0.78, P b 0.001, and Irritability, r = 0.64, P b 0.01, scores in a sample of 20 healthy male control subjects recruited from a hospital staff. Significant correlations have also been found between PSAP responding and the BHV (Brown et al., 1979), OAS (Yudofsky et al., 1986), BPAQ (Buss and Perry, 1992), and HHA (Coccaro et al., 1997). 1.4. Potential trait by alcohol interaction effects Kelly and Cherek (1993) emphasized the wide individual differences found in participant responses to alcohol and concluded that balcohol does not engender aggressive respondingQ but instead bmodifies the probability of aggressive behavior engendered by other contextual factorsQ such as schedule of provocation, response options, and the social context in which the provocation occurs (p. 51). Their analysis points to the need for researchers to accelerate the search for mediating interaction variables in efforts to understand the role of alcohol in disinhibiting aggression in the laboratory and naturalistic environment. A number of personality traits have been found to predict alcohol-induced aggression observed in the laboratory. College men with moderate or high aggressive dispositions as indicated by scores on the BDHI Assault subscale scores delivered significantly higher TAP shock intensities when provoked under the influence of blood-alcohol levels (BALs) at 84 mg% (Bailey and Taylor, 1991). Giancola and Zeichner (1995) found that the BDHI Assault subscale effectively predicted the shock intensities delivered by intoxicated (BAL of 100 mg%) men recruited from a community sample in both high provocation conditions (r = 0.54, P b 0.01) and low provocation conditions (r = 0.48, P b 0.01). Dougherty et al. (1999) found that subjects generating

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higher PSAP scores in response to placebo tended to show greater increases in aggression while under the influence of alcohol than controls. Phil et al. (1997) offered the first suggestion that aggressive personality effects on laboratory-induced behavior are more complicated than previously suspected. This team found that aggressive proclivities as measured by a median split of the Overt Anger subscale of the McGill Alcohol Research Lab Subject Interview Schedule predicted higher TAP shock intensities among highly provoked sober subjects recruited from the community. A significant interaction was found, however, between trait anger and alcohol intoxication (sober versus 110 mg%) level on TAP aggression. Subjects with aggressive dispositions responded more aggressively to high provocation when sober than intoxicated. It was the control group that showed higher levels of potentiation of laboratory-induced aggression under the influence of alcohol. Parrott and Zeichner (2002) extended this analysis by using the TAS to predict shock intensities as delivered by college men during the absorption phase (80 mg%) of acute intoxication using the Response Choice Aggression Paradigm (RCAP: Zeichner et al., 1999). The RCAP differs from the TAP in allowing an escape or noresponse option. College men exhibiting moderate levels of TAS trait anger were found to be the most aggressive under the influence of alcohol. High TAS scores were associated with the delivery of high shock intensities and other RCAP indices under conditions of sobriety, but these aggressive tendencies were curiously not potentiated by alcohol as found in the moderate TAS group. Low TAS scores predicted unaggressive responding in both sober and intoxicated conditions. Moeller et al. (1998) found curious differences in laboratory-induced aggression under the influence of alcohol between subjects with and without antisocial personality disorder as measured by a structured clinical interview. Four different dosage levels (placebo, 0.25 g/kg, 0.5 g/kg, and 1.0 g/ kg) were administered in a rigorous repeated measures design. Significant group differences in PSAP responding were only found for the lowest dose which produced a mean BAL of only around 20 mg%. The clinical literature is replete with inconsistent, sometimes paradoxical, findings regarding the performance of antisocial subjects in any number of cognitive, behavioral and interpersonal tasks. Sutker et al. (1993) provided an extensive review of this complicated literature regarding antisocial performance in a variety of experimental paradigms. They concluded that the most consistent difference between antisocial and normal functioning lies in the variability of reactions that seems to emerge as a partial function of subtle contextual influences (e.g., type of

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reward, reinforcement delay, relative probabilities of reward and punishment, timing of discriminative stimuli, perceptions of task, and characteristics of experimenter). They cited Lykken’s (1978) historic call for attention to subtle situational cues in psychopathy research that serve to enhance or detract from subject motivation for a particular experimental task. 1.5. Evidence of trait by alcohol interactions

Shock Intensity

7 6.5 6

High Moderate

5.5

Low

5 4.5 4 0 mg%

80 mg%

Blood Alcohol Level

B Shock Intensity

5.5 5 4.5 4 3.5

300 250 200

High 6B Low 6B

150 100 50 0

Dougherty et al. (1999) provided the only evidence that alcohol-induced aggressive responding in the laboratory was magnified among subjects who showed higher baseline tendencies to aggression when provoked. This data supports an intuitive interaction hypothesis that aggressive responding in the laboratory should be magnified among individuals predisposed, by trait or behavioral history, to aggression against perceived provocateurs. This intuitive notion has gone unchallenged, with alcohol typically described as a classic disinhibiting agent that can trigger aggressive acts among individuals predisposed to aggression. The present study draws attention to the limited laboratory support for this intuitive notion, and conversely posits that available evidence points instead toward alternative ceiling or even paradoxical effects posed by high levels of trait aggression or baseline responding. Phil et al. (1997) and Parrott and Zeichner (2002) speculated that the trait by alcohol interactions

A

350

Unadjusted PSAP Scores

132

High Low

Baseline

Ascent

Peak

Descent

Session Fig. 2. MCMI-II trait predictors of aggression after alcohol intake.

observed in their studies (i.e., increases in aggressive responding only among control subjects) may have occurred as a function of a ceiling effect mediated by the high shock intensities delivered by aggressive subjects under sober conditions. Different measures were used to identify aggressive proclivities in these two studies, but shock intensities were measured on a similar TAP metric with a 5- to 7-point range. The latter study used a three-group classification scheme (low, moderate, and high), while the former study relied on a median split that generated only two conditions for the aggressive disposition. Fig. 1A uses the Parrott and Zeichner (2002) results to illustrate support for a bceilingQ interaction hypothesis. The data of Phil et al. (1997) graphed in Fig. 1B even points to a bparadoxicalQ interaction effect manifested in lower alcohol-induced aggressive responding among subjects identified with trait aggression. It appears at this juncture that researchers need to examine more closely the interaction of trait dispositions and alcohol intoxication on laboratory aggression. A group of eight aggressive subjects, as defined by profile on the Million Clinical Multiaxial Inventory-II (MCMI-II; Millon, 1987), were tested in this study under the influence of alcohol to determine whether their trait disposition was associated with higher or lower reactivity to the experimental provocation. These subjects were compared with 18 others (Bailly and King, 2004) who were screened to assure the absence of MCMI-II personality disorder features (Fig. 2).

3 2.5 2

2. Method 0 mg%

110 mg%

Blood Alcohol Level Fig. 1. bCeilingQ and bParadoxicalQ theoretical trait by alcohol interaction hypotheses. A) Ceiling interaction model. B) Paradoxical interaction model.

2.1. Subjects Course extra credit and an average of $30 were awarded to each of the 26 men recruited to complete a

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single data collection session about 6 h in duration involving an evaluation of the effects of alcohol on performance in a bcompetitive computer taskQ. Subjects were required to be at least 21 years of age and those with Michigan Alcoholism Screening Test (MAST; Selzer, 1971) scores in excess of 11 or Khavari Alcohol Test (KAT; Khavari and Farber, 1978) reports of more than 2 oz/day over the past year were excluded. A brief medical history questionnaire was used to exclude individuals describing earlier chemical abuse or present physical illness (e.g., ulcers, hypertension, cardiovascular disease, epilepsy, diabetes, and allergies) that might affect metabolic or behavioral responses to alcohol. 2.2. Research design PSAP responding was recorded at four phases of alcohol intoxication among subjects assigned to either the Aggressive or Comparison group (4  2 mixed group ANOVA design). All subjects completed 25min PSAP sessions during the Baseline, Ascent, Peak (70 mg%), and Descent (40 mg%) phases of the alcohol absorption and elimination process. All subjects were required to complete the MCMI-II on a day prior to their experimental session. Eligible subjects then were sorted into groups with and without a Sadistic-Aggressive scale elevation (BR N 74). The group of 18 subjects described by Bailly and King (2004) were all similar in their absence of elevations (BR N 74) on any of the 13 personality disorder scales. The eight men added to the present analysis were selected because of their elevation on the Sadistic-Aggressive scale. 2.3. Procedure A total of 41 men met the screening requirements described for this study. Thirty-three of these men generated unremarkable (no elevations) MCMI-II profiles that qualified them for participation in the previous study of Bailly and King (2004), which involved the administration of alcohol to a random sample of 18 subjects from this initial group. The remainder of the original pool all showed an MCMI-II Sadistic-Aggressive elevation that afforded an opportunity to examine PSAP responding under the influence of alcohol among men with (n = 8) and without (n = 18) aggressive traits. The two cells were referred to as the bAggressiveQ and bComparisonQ groups for purposes of this analysis. All 26 men included in this analysis completed a 4to 6-h experimental session with an unidentified (and fictitious) partner that involved competition in a computer task while under the influence of alcohol (ban

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amount not sufficient to raise your blood-alcohol level above the legal limitQ). Subjects were asked to abstain from food and drink after noon on the day of their session and to commit to remain in the laboratory until completion of four 25-min competitive tasks and full sobriety (breath alcohol readings below 20 mg%). They were required not to drink alcohol for at least 24 h prior to the session. Subjects arrived for their session at 1600 h and were questioned to determine if they complied with the food, drink, and alcohol restrictions. Subjects were then weighed, and a baseline BAL was taken to assure their complete sobriety (0 mg%). Bloodalcohol levels were determined from breath samples using an Alcomonitor (Model CC; Intoximeters Inc., St. Louis, MO). Breath and alcohol samples have been found to be highly (r N 0.98) correlated using this device (Inns et al., 1979). All subjects were aware that they would be administered alcohol after completion of an initial 25-min PSAP session. PSAP sessions took place in a room having minimal noise or interruption. Subjects held on their lap a customized three-button console. They were seated at a monitor linked to a PC-compatible computer using an interface card (Med Associates, Inc., Georgia, VT). The monitor displayed a counter that kept track of the points earned and those earned by their (fictitious) opponent. The computer and interface controlled and recorded all events during the session. Subjects were read the following standardized instructions (Moeller et al., 1998, p. 1899): bYou will be seated in a room in front of a computer monitor and a panel containing response buttons A and B. A counter will be displayed in the middle of the computer screen. Pressing button A will accumulate money. You will be paid according to the number of points you accumulate on this counter. At the end of each day, you will be paid the amount of money earned during each session. During sessions, you will be paired with another subject at another location. During any session, you may have money subtracted from you by another research subject. Money subtracted from you will be added to the other person’s earnings. Pressing button B will result in the subtraction of money from the subject you are paired with whom is also responding to accumulate money. You will not receive the money you choose to subtract from the other subject. During each session, you can press button A or button B frequently (often), infrequently (seldom), or not at all.Q It has been customary to analyze total aggressive (bBQ button) responses as the primary PSAP dependent measure. After completion of baseline PSAP testing, all subjects were administered a 0.80 ml/kg dose of 95% ethanol mixed with soda in a 1:5 ethanol/soda ratio.

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Equal amounts of alcohol and placebo beverage were poured into cups of three equal amounts and consumed at a rate of 5 min each. Immediately after ingestion of the beverage, subjects completed the second PSAP session, which coincided with absorption of the beverage into the bloodstream (ascent). BALs were taken every 5 min after completion of the second PSAP session to establish the 70 mg% point (roughly peak) when the third PSAP session was initiated. BALs were taken every 10 min until the 40 mg% point was reached and the final PSAP session was initiated. Subjects were dismissed when their BAL dropped below 20 mg%. 3. Results Table 1 illustrated that the two groups in the present analysis ultimately differed significantly on the following MCMI-II scales: Sadistic-Aggressive, F(1,24) =57.67, P b 0.001; Narcissistic, F(1,24) = 43.33, P b0.001; Antisocial, F(1,24)=35.11, P b 0.001; Histrionic, F(1,24) = 14.91, P b 0.001; Paranoid, F(1,24) = 12.17, P b 0.01; Passive-Aggressive, F(1,24) = 7.77, P b 0.01; Borderline, F(1,24) = 7.18, P b 0.01; and Schizoid, F(1,24) = 5.59, P b 0.05. The eight men in the present sample exhibited a particularly diverse cluster of personality disorder attributes reflected in an average of 4.5 scale elevations per subject. Significant group differences were not found for the MCMI-II Dysthymia, Anxiety, or Psychotic Depression scales. None of the MCMI-II base rate scores (nor their average or total Table 1 MCMI-II personality base rate means and standard deviations for subjects assigned to the Aggressive (n = 8) and Comparison (n = 18) groups Scale/variable

(1) Schizoid (2) Avoidant (3) Dependent (4) Histrionic (5) Narcissistic (6A) Antisocial (6B) Aggressive (7) Compulsive (8A) Passive-aggressive (8B) Self-defeating (S) Schizotypal (B) Borderline (P) Paranoid a

Comparisona

Aggressive

M

S.D.

M

S.D.

52 41 56 61 55 55 56 60 40 42 48 36 54

24 32 25 17 16 12 9 19 23 26 24 23 14

28 26 50 88 98 88 90 63 68 38 49 56 74

21* 29 23 15*** 14*** 16*** 13*** 18 26** 27 10 29** 12**

Data from this group are also reported by Bailly and King (2004). * P b 0.05. ** P b 0.01. *** P b 0.001.

Table 2 PSAP means and standard deviations for subjects assigned to the Aggressive (n = 8) and Comparison (n = 18) groups Phase

Comparisona M

S.D.

M

S.D.

(1) (2) (3) (4)

141 148 157 115

231 260 267 144

305 163 175 119

311 101 141 71

Baseline Ascent Peak Descent

Aggressive

Significant group differences were not observed during any of these four phases of testing. a Data from this group are also reported by Bailly and King (2004).

elevation number) provided significant predictors of Baseline PSAP responding or changes across sessions. The two groups were close to identical in their KAT scores, F(1,24) = 0.01, P = 0.95, which indicated an average level of daily alcohol consumption of 0.77 ml or 1–2 drinks per day over the past year. Peak BALs did not differ significantly between the Aggressive (M = 71 mg%, S.D. = 8 mg%) and Comparison (M = 67 mg%, S.D. = 8 mg%) groups, F(1,24) = 1.12, P = 0.30. Elimination times (minutes from peak to completion) also were similar for Aggressive (M = 217, S.D. = 42) and Comparison (M = 255, S.D. = 51) subjects, F(1,22) = 2.46, P = 0.13. Table 2 presents a summary of the PSAP data. Baseline aggressive responding did not differ between subjects in the Aggressive (M = 305, S.D. = 206) versus Comparison (M = 141, S.D. = 348) condition, F(1,24) = 2.25, P = 0.15. These mean response rates and variabilities appeared consistent with other published findings. Mean PSAP scores collapsed over the four sessions were 128 (S.D. = 203) and 186 (S.D. = 122) for the Comparison and Aggressive groups, respectively. Mean PSAP scores collapsed over the two groups were as follows: Baseline (M = 191, S.D. = 219); Ascent (M = 152, S.D. = 219); Peak (M = 162, S.D. = 240); and Descent (M = 113, S.D. = 133). PSAP responding in the Baseline condition was closely associated with aggression scores in the Ascent, r = 0.75, P b 0.001, Peak, r = 0.72, P b 0.001, and Descent, r = 0.70, P b 0.001, phases of data collection (trend toward weaker correlations for the Aggressive group). A 2 (group)  4 (phase) ANOVA of PSAP scores found no effects for Group (at any of the four phases of data, significant reductions across phase F(3,66) = 5.53, P = 0.002, which were larger among Aggressive subjects, F(3,66) = 4.95, P = 0.004). While significant group differences were not observed at Baseline (P = 0.15), changes (reductions) in PSAP responding under the influence of alcohol were substantially larger for the Aggressive group at the Ascent, t (24) = 2.11,

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P = 0.04, Peak, t (23) = 2.48, P = 0.02, and Descent, t (22) = 2.5, P = 0.02, phases of data collection (see Fig. 1). The larger reductions in PSAP responding for the Aggressive group at Ascent, Peak and Descent can be shown as well through an ANCOVA that used Baseline scores as the covariate, F(1,21) = 4.80, P = 0.04. The Baseline to Ascent difference of the Aggressive group translated into an effect size of 0.75 standard deviations (S.D. pooled over the four sessions). 4. Discussion The success of the PSAP and other laboratory-based procedures in discriminating between subjects with high (e.g., felons, substance abusers, and antisocial individuals) versus low risk for aggression has been wellestablished. The effects of alcohol on experimentally induced aggression have been examined in at about eight studies with mixed results. The three alcohol studies conducted to date on PSAP responding (Dougherty et al., 1996, 1999; Moeller et al., 1998) have suggested that alcohol had only modest and inconsistent effects. The present study examined the effects of 0.8 ml/kg of alcohol on the PSAP responding of eight healthy college men with MCMI-II sadistic-aggressive (Scale 6B) elevations during the Baseline, Ascent (immediately after ingestion), Peak (about 70 mg%), and Descent (40 mg%) phases of alcohol absorption and elimination. PSAP responding was found to decrease substantially from Baseline to Ascent, Peak and Descent for the Aggressive subjects. Fig. 1 illustrated that this effect was driven by somewhat higher Baseline PSAP responding among the Aggressive subjects. This Baseline trend (P = 0.15) for elevated aggressive responding among individuals identified with irascible trait dispositions appeared generally consistent with prior TAP and PSAP research. A number of paper-and-pencil measures (e.g., BHV, OAS, HHA, Aggressiveness and Irritability subscales of the BDHI) have been linked to higher aggressive responding in the laboratory. Moeller et al. (1998) showed elevated PSAP responding at baseline and under a low-dose alcohol condition for men identified with antisocial personality disorder. Within this context, however, the most notable Baseline finding in the present study was the absence, rather than presence, of significant differences between the Aggressive and Comparison subjects. Our focus has been on evidence of an attenuation in PSAP responding among aggressive men while under the influence of alcohol. This basic finding was consistent with the bparadoxicalQ interaction hypothesis advanced from the data of Phil et al. (1997) that was

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depicted in Fig. 1B. Four (Phil et al., 1997; Dougherty et al., 1999; Parrott and Zeichner, 2002; present data) of five (not Bailey and Taylor, 1991) studies have now shown a significant trait by alcohol laboratory-induced aggression interaction (three supporting ceiling or paradoxical hypotheses with one in the intuitive direction). In addition, Moeller et al. (1998) found that the alcohol effect on antisocial subjects was restricted to the low doses. Evidence is emerging that a subset of aggressive men respond counterintuitively to provocation while in the laboratory and under the influence of alcohol. 4.1. Possible interaction mediators High rates of baseline PSAP responding may limit the extent to which aggression scores can be increased over the course of an acute alcohol intoxication study. Reductions in subsequent response rates referred to here as evidence of support for a bparadoxicalQ interaction hypothesis may reflect simple regression to the mean. Data collection in this and prior studies (Phil et al., 1997; Parrott and Zeichner, 2002) occurred on a single day, a factor that might diminish the replicability of the finding. Conversely, the present design may generalize more effectively to the common experience of the social drinker who responds to mild provocation from a competitor while under the influence of moderate levels of intoxication (70 mg%). Proposed explanations that extend beyond ceiling effects or regression to the mean may prove to be conceptually complex and difficult to frame into testable hypotheses. Dougherty et al. (1996) anticipated the individual differences that were likely to be found in subject PSAP testing under conditions of alcohol intoxication. They cautioned researchers that alcohol effects were anything but uniform and that a substantial subset of subjects, particularly women, would not show increased aggressiveness while in the laboratory and intoxicated. They challenged future researchers to btry to determine what variables may contribute to these individual differencesQ so that befforts in this area may lead to a better understanding of the relevant controlling variables involved in alcohol-induced aggressionQ (p. 185). Kelly and Cherek (1993) pointed out that only an unclearly specified subset (perhaps sometimes as low as 25%) of subjects increased their aggressiveness in the laboratory while under the influence of alcohol. Indeed, an important contributor to the interaction reported in this study is the unresponsiveness of the Comparison group to the alcohol. Only about 5% of the Comparison subjects showed noteworthy (N 100 point) increases in PSAP responding from Baseline to Ascent. This interaction

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effect would have been much larger if our Comparison group more closely approximated the alcohol-related aggression increases found in other studies. This Comparison group can be distinguished from others in the PSAP literature by the extra efforts taken to assure an absence of prominent personality disorder traits of any kind. These results and the general unresponsiveness of this particular Comparison group raised questions about the possible necessity of heterogeneous (in terms of personality features) samples to produce the expected disinhibiting effects of alcohol on aggressive responding. The motivation level of subjects in experimental studies of aggression warrants closer future attention. Lykken (1978) speculated that antisocial subjects may alter their behavior as a function of the extent to which the experimental task catches their fancy. A relatively high subset of subjects identified with personality disorder traits may find alcohol administration under laboratory conditions to be stimulating and enticing. The experience may grow more captivating with higher doses. Conversely, such individuals could also become quickly bored, leading to the sharp reductions in aggressive responding after an initial session, such as the pattern possibly observed in this study. Issues of personality, motivation and situational determinants require systematic attention in future studies.

PSAP scores would prove less meaningful if found at similar levels for other aggressive subjects across retesting under sober or placebo conditions.

4.2. Design limitations

References

Discussion of the trait by alcohol interaction reported in this study should be qualified by at least two important design limitations. The two comparison groups differed significantly on no fewer than 8 (of 13) MCMI-II personality disorder scales (Sadistic-Aggressive, Narcissistic, Antisocial, Histrionic, Paranoid, Passive-Aggressive, Borderline and Schizoid in order of statistical significance). Personality differences between the two groups obviously extend beyond baggressiveQ trait dispositions. The two groups did not, however, differ significantly in their MCMI-II Dysthymia, Anxiety or Psychotic Depression features. The most substantive design limitation in the present study was the absence of placebo and time control groups. Aggressive subjects could have reduced their PSAP responding from Baseline to Ascent, Peak and Descent as a partial function of alcohol expectancy effects. The aggressive subjects could also have become bored or fatigued more or less quickly with the PSAP task. While evidence of reduced PSAP responding over time was reviewed previously, no study to date has shown substantive changes as quickly as the second session. Nevertheless, Baseline to Ascent changes in

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