Aetiology of excessive alcohol consumption and Alcohol Use Disorder in young adults: Identifying change mechanisms to inform intervention strategies.

Abstract

Alcohol use is a leading cause of death and disability-adjusted life-years lost among young adults, and the social costs of alcohol consumption extend the burden beyond the individual. At least two kinds of alcohol-related harms can be conceptualised. One being those harms directly caused by the effect ethanol molecules have on cells in the body, and the other arises when alcohol use interacts with features of a person to interfere with their day-to-day functioning. Consistent with this framing, alcohol use is commonly considered to be a problem when consumption is more frequent or in greater volume than is consistent with an acceptable risk of physiological harm (excessive alcohol consumption; EAC); or when consuming alcohol causes clinically significant impairment or distress (alcohol use disorder; AUD). The onset and prevalence of each of these kinds of harm peaks in young adults and each is associated with both proximal and lifetime consequences. The literature is undecided, however, on whether EAC and AUD are products of the same causal processes, leaving it unclear if change strategies designed to reduce the incidence of one will influence the other. This thesis considers if these two kinds of harm appear to be products of the same aetiological processes. The thesis also proposes a conceptual framework to explain the development of EAC. Within this framework, the disposition to employ different classes of experiential avoidance strategy are examined for insight into the operation of mechanisms contributing to the development of EAC. Analyses were conducted in a sample of young adults (n=450; 52% male; mean age 19.8 years) from a prospective cohort study and found support for the proposition that differences exist in the pathways leading to EAC and AUD. It was also found that specific avoidance strategies moderated the operation of those pathways, and the pathways appeared to differ between males and females. The implications of these findings are discussed.