A fundamental question in alcohol research, the answer to which has remained elusive, is what is the relative contribution of genetic, psychological and social factors in alcohol dependence? This thesis examines the role of alcohol expectancies and drinking restraint, two key psychological constructs in influencing the severity of drinking and dependence. The role of the D2 dopamine receptor gene as it impacts across a range of common problem drinking parameters is then examined. The final study reported integrates both genetic and cognitive models of problem drinking and explores their relative contribution and interrelationship across a range of problem drinking indices.
Two contemporary cognitive drinking constructs, alcohol expectancies and drinking restraint, have made important contributions to our understanding of problem drinking. Balanced-placebo studies have shown that we hold a number of common expectancies, both behavioural and emotional, about the effects of alcohol. Several measurement instruments have been developed to measure these expectancies. In Study 1 the theoretical and predictive utility of the most widely used alcohol expectancy measure, the Alcohol Expectancy Questionnaire (AEQ) (Brown, et al., 1980, 1987), was compared with the Drinking Expectancy Profile (DEP) (Young & Oei, 1996). Within a student sample it was found that the more theoretically robust DEP was a superior measure of alcohol expectancies, accounting for approximately twice as much variance as the AEQ across problem drinking indices.
Typically, those who are termed "restrained drinkers" are preoccupied with their levels of alcohol consumption, but have poor control strategies to restrain drinking. Collins and Lapp (1992) developed The Temptation and Restraint Inventory (TRI) to measure these restraint cognitions. The TRI contains two components- Cognitive-Emotional Preoccupation and Cognitive-Behavioural Control, and interaction of these constructs was seen by Collins and Lapp (1992) to regulate problem drinking behaviour. Within a student sample, Studv 2 found limited support for Collins and Lapp's (1992) interactional model and recommended that drinking restraint be measured as a unitary construct. The unitary measure demonstrated good predictive power to a range of problem drinking indices.
While developed from similar social learning platforms, alcohol expectancies and drinking restraint have not been examined together with regard to their relative predictive power towards problem drinking. Studv 3 examined this relationship within a student population. Drinking restraint and alcohol expectancies measured kindred but unique cognitive sub-sets and provide possible insight into the progression of alcohol problems. It was proposed that alcohol expectancy and the related construct, drinking refusal self-efficacy, might be acquired early in the development of drinking behaviour, as evidenced by stronger associations with hazardous drinking. Drinking restraint and its associated loss of control factors appear to be more specifically related to problem drinking. It was concluded that expectancies and drinking refusal self-efficacy may have greater use in the broad assessment of drinking behaviour.
It is generally accepted that approximately one half of the risk of alcohol dependence can be attributed to heritability factors. Family, twin and adoption studies have provided robust evidence of a genetic predisposition to alcohol use disorders. Even with the increasingly sophisticated research designs that attempt to disentangle the genetic/environment relationship, these studies are restricted to statistically estimating potential genetic influences, as opposed to examining specific genetic loci. With the advent of new molecular biological techniques, the identification of genetic influences on alcohol dependence has advanced into the exploration of candidate genes. A number of potential genetic markers have been proposed. In Study 4 the A1 allele of the D2 dopamine receptor gene (DRD2) is examined. The DRD2 A1 allele has been implicated in alcohol abuse and dependence though association studies comparing the frequency of allele types in alcoholic and control (non-alcoholic) populations. Studv 4 extended beyond the association study methodology and demonstrated that, within an alcohol dependent sample, those who are A1+ (A1/A1 and A1/A2 genotypes) have more extreme drinking behaviour, on average, than their Aiallelic (A2/A2 genotype) counterparts. In particular, those with A1+ allelic status showed significantly higher levels of consumption, higher ADS scores, earlier age of onset of problem drinking, a shorter period between the age of first introduction to alcohol to the onset of alcohol problems, and had more hospital based detoxification attempts.
Integration of Models
Exponential advances in substance abuse research often occur when fields of science consolidate knowledge to collectively address common research challenges. Studies 1 to 3 showed that the cognitive drinking models of alcohol expectancies and drinking restraint are sound predictors of problem drinking. Studv 4 reported for the first time how a genetic marker is associated with problem drinking behaviour within an alcohol dependent population. In the final study (Studv 5), these factors are combined in one analysis, along with other indicators of problem drinking such as onset of dependence and family history, also within an alcohol dependent population.
Path analyses identified that across genetic, psychosocial and psychological parameters, drinking refusal self-efficacy beliefs, a integral component of the alcohol expectancy model examined in this thesis, were the most consistent and powerful predictors of severity of dependence and quantity and frequency of drinking. The remaining measured psychological constructs of drinking restraint and alcohol expectancies also provided strong significant predictive power across all three dependent drinking measures. While drinking restraint was a direct predictor of severity of dependence, quantity and frequency of drinking, alcohol expectancies were mediated through the drinking refusal selfefficacy beliefs, consistent with the generic outcome expectancy models derived from Social Learning Theory. The results of the path analyses demonstrate that the psychological constructs investigated were consistently superior predictors of problem drinking across a broad range of drinking parameters, than the genetic or psychosocial factors examined.
DRD2 type directly influenced quantity of drinking. The presence of A1+ allelic status indirectly influenced severity of dependence in that A1+ allelic status was significantly associated with a lower age of onset, and lower age of onset significantly associated with more severe levels of dependence. Contrary to predictions, allele status was not associated with family history or any of the cognitive drinking models examined. For this reason it is proposed that the development of both alcohol expectancies and restrained drinking cognitions are based on environmental influences (or other genetic marker not examined in this thesis), with A1+ status playing a negligible role in the construction and modification of these drinking-related cognitions in the population studies. It is proposed that the examination of non-alcohol specific constructs such as personality characteristics, not identified in the models tested, be incorporated in subsequent estimations of problem drinking risk.
The findings across the series of studies provide us with a richer understanding of the factors that contribute to the severity of problem drinking. Recent advances in the treatment of alcohol use disorders, such as the use of pharmacogenetic and cognitive-behavioural therapies, have paralleled the development of genetic and cognitive models of problem drinking. The opportunity now exists for researchers and clinicians to profile individuals on the basis of their genetic and psychological risk to tailor psychological and pharmacological interventions, potentially increasing the efficacy of treatment within this population.