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published_or_final_version / Pharmacology / Doctoral / Doctor of Philosophy

The present thesis and series of studies explores the underlying cognitive and neuropsychological processes that underlies propensity for aggressive response in adult men and women, both sober and intoxicated. Previous research demonstrated that poor executive functioning, either pre-existing (idiopathic) or induced by alcohol-intoxication, was associated with heightened aggressive responses. The first study demonstrates that although cognitively impaired when alcohol intoxicated, men with above average pre-alcohol Executive Cognitive Functioning (ECF) do not act aggressively if they are properly motivated to remain non-aggressive, suggesting some ability to use residual executive function. The second study directly compares the aggression-eliciting effects of alcohol in both men and women, an under-investigated issue. Results indicate that aggression levels in the women are not significantly less than those of men, and that alcohol-intoxication is not as predictive a factor in women as in men. The third study, a post-hoc analysis of the second, indicates that like for men, executive function level in women is highly related to propensity for aggressive response, in fact far more predictive than acute alcohol-intoxication. The fourth study was intended to investigate a possible behavioural explanation for the ECF-aggression relationship. Specifically, this study was designed to assess whether the aggression manifested by individuals with poor ECF was rapid or impulsive, i.e. due to a disinhibition process. Contrary to this popular contention, this study demonstrates that when faced with complex, social interactions, low-ECF individuals act aggressively, but only after a somewhat slow period of apparent contemplation. These findings and others conducted by the author are discussed in a speculative model of the ECF-aggression relationship. Means by which to test this model are proposed, as are other theoretical implications of the work.

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Alcohol abuse is the second most prevalent lifetime psychiatric disorder. However, individuals do not face an equal risk of developing problematic alcoholrelated behaviors. Alcohol use disorders are heterogeneous conditions whose development may be caused by a variety of factors and vulnerabilities. The identification of markers of risk is necessary in order to identify individuals at higher risk for addiction early on as well as to help develop treatment interventions which target an individual's specific risk factors. The goal of the present dissertation is to increase our understanding of the role that one putative risk factor, an exaggerated cardiac response to alcohol, may play in the development of addictive behaviors. Five studies are reported. / The first study revealed that an exaggerated heart rate response to alcohol is associated with subjective reports of increased alcohol-induced stimulation. In a second study, the relationship between the cardiac response to alcohol and personality characteristics was examined. Individuals who demonstrated the elevated cardiac response to alcohol displayed a distinct personality profile characterized by high sensation-seeking and sensitivity to reward. Two separate studies followed investigating the relationship between this physiological response to alcohol and other addictive behaviours. One study found that individuals with an exaggerated cardiac response to alcohol were more likely to obtain superior scores on a measure of pathological gambling, while the next study found that users of psychostimulants (e.g., cocaine) also displayed heightened alcohol-induced cardiac responses. A final study examined the impact of conditioned cues of reward and non-reward on alcohol-induced cardiac responses. Individuals who had previously displayed elevated cardiac responses to ethanol showed reduced cardiac reactivity when alcohol ingestion occurred in a non-rewarding environment. Overall, these findings suggest that the cardiac response to alcohol is a marker of a pathway that may lead to addictive behaviors through increased sensitivity to incentive reward.

Social drinkers (healthy males aged 18--34) participated in three experiments that examined some of the mechanisms that may be responsible for the effects of alcohol on emotionally charged memory. In a study on incidental learning, alcohol enhanced neutral, positive and negative memory, possibly by a nonselective consolidation mechanism. Alcohol's enhancement of memory was found to not be associated (contingently related) with its incentive reward and relief effects. In another study on intentional learning, alcohol enhanced positive memory and/or inhibited negative memory, possibly reflecting a contingent relationship to its incentive effects. When the role of individual differences was examined, relatively little influence was found in mediating the effects of alcohol on incidental memory. However, alcohol's effect on intentional memory was predicted by individual differences in response to some of alcohol's acute incentive effects. The studies demonstrate that alcohol's effects on memory are independent from, and can be combined with, its incentive effects. Further, consumption of alcohol may be influenced by separate effects on memory and incentive, and by their association.

Epidemiological and laboratory research supports a relationship between acute alcohol intoxication and aggression. Recent data suggest that alcohol disrupts cognitive abilities associated with frontal lobe function. Moreover, neuropsychological research provides suggestive evidence that frontal lobe dysfunction may predispose an individual to increased aggression. The research recounted in this thesis was conducted to investigate the role of individual differences of cognitive abilities associated with the dorsolateral frontal cortex in aggressive behaviour and to test the hypothesis that alcohol indirectly potentiates aggression by impairing these cognitive abilities. The three experiments included in this thesis demonstrated that: (1) acute alcohol intoxication interferes with the ability to integrate previously acquired knowledge in the formulation of behavioral strategies; (2) individuals grouped according to performance on two neuropsychological tests of cognitive abilities associated with frontal lobe function differ in degree of aggressive response. Specifically, individuals in the lower versus upper performance quartiles became more aggressive when provoked; and (3) individuals in the upper cognitive performance quartile demonstrate significantly greater reductions of unprovoked aggression in response to monetary reward.

Dietary factors such as the consumption of tryptophan, the precursor of serotonin, or sugar, may play an important role in influencing alcohol-induced impairment. Study I used an amino acid diet to manipulate plasma tryptophan in male social drinkers in a 3 (supplemented, balanced, and depleted tryptophan) x 3 (alcohol, placebo, sober) design with 12 subjects per cell. A variety of mood, memory, and psychomotor performance measures were taken at baseline, five hours after amino acid ingestion, and after alcohol consumption. Strong alcohol effects were produced but no tryptophan, nor alcohol-tryptophan interaction effects were found. / Study II examined the combined effects of sucrose and alcohol in a 3 (100 g sugar, 35 g sugar, 0 g sugar) x 3 (alcohol, placebo, sober) design with 15 subjects per cell. Subjects were tested on tasks similar to those used in Study I at a variety of times following intoxication (i.e., 0.5 hours, 1.5 h, 3.5 h) in order to examine effects when blood glucose peaked as well as at a point when hypoglycemic rebound can occur in some subjects. A strong alcohol x sugar interaction was seen 0.5 h after drinking, with high doses of sugar attenuating intoxication without influencing blood alcohol levels. No hypoglycemia was produced after 3.5 h. / Study III replicated Study II using a simpler design which controlled for the possible effects of aspartame (the placebo sweetener used in Study II). A variety of gastric or central mechanisms, which can account for the finding that sucrose can reduce the intoxicating effects of ethanol, are discussed.

Bibliography: leaves 246-263. / xiii, 263 leaves : col. ill. ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Previous investigations have established that there is a syndrome that occurs with abstinence from alcohol, and that it is characterised by certain signs and symptoms. This thesis aims to redress the paucity of information on symptom intensity and duration, predictors of withdrawal severity, and relationship of withdrawal severity to relapse. / Thesis (Ph.D.)--University of Adelaide, Dept. of Clinical and Experimental Pharmacology, 2000

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