Rationale

AmED is a relatively new consumption trend; the body of research investigating this phenomenon is small despite a recent increase in interest. To date, there have been no major public health campaigns or legislative changes in Australia in relation to AmED use despite calls for reform (Australian Medical Association, December, 2010). Pennay and Lubman (2012b) argue that the impediment is the paucity of research at the community level investigating how people consume AmED;

specifically, the amount, frequency, and context of use, and the motivations behind beverage choice. Those studies which have focused on the consumption patterns and motivations for AmED use have primarily sampled high-risk consumer subgroups (generally university students) in the United States, Canada, and Europe (e.g., L. Berger et al., 2011; de Haan, de Haan, van der Palen, Olivier, & Verster, 2012; Thombs et al., 2010; Woolsey, Waigandt, & Beck, 2010). To date, there has been no

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systematic investigation of the consumption patterns and motivations for AmED use in the Australian community.

Pennay and Lubman (2012b) also claim that efforts towards regulating AmED sales and marketing are further undermined by a dearth of research investigating the causal link between AmED consumption and negative outcomes. The majority of studies in this field of research compare alcohol-related consequences for two consumer groups: AmED versus non-AmED consumers (L. Berger, Fendrich, & Fuhrmann, 2013; Miller, 2012; O'Brien et al., 2008; Penning, de Haan, & Verster, 2011; Snipes & Benotsch, 2013). These studies consistently indicate that AmED consumers experience more negative consequences of alcohol consumption than non-AmED consumers. However, a causal link between AmED consumption and negative physiological, psychological, and behavioural outcomes cannot be inferred from these studies. AmED consumers typically have a unique demographic and personality profile relative to non-AmED consumers, highlighted by their elevated innate tendency towards impulsive and risky behaviour (Brache & Stockwell, 2011). Comparing retrospective self-reported alcohol-related consequences of AmED versus alcohol consumption for the same individuals (within-subject comparison) circumvents this issue. However, there has only been one such study conducted to date (de Haan et al., 2012). In contrast with predictions outlined in Section 1.1., this study by de Haan et al. (2012) indicated that consumers retrospectively self-reported lower rates of alcohol-related consequences after AmED relative to alcohol

consumption. This study focused only on the drinking experiences of European university students; to date, there have been no published attempts to replicate these

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outcomes, nor has there been any research assessing whether these findings are reflected at the community-level or in other drinking cultures.

Self-report of drinking consequences can provide a comprehensive overview of alcohol-related outcomes over multiple drinking sessions. However, these reports can be influenced by biased reporting, particularly when consumers are asked to retrospectively recall events occurring within a lengthy time period (e.g., in the last year). Furthermore, alcohol-related consequences may not be exclusively attributed to the pharmacological effects of the beverage, as internal (e.g., drinking

expectancies) and external (e.g., drinking environment) factors may play a role in the drinking experience. Laboratory-based testing of the acute effects of a blinded dose provides a more direct method of assessing the pharmacological effects of AmED, as the experimenter can control for these confounding variables. Outcomes can be objectively assessed using computer-based tasks, circumventing recall and self- presentation biases inherent in self-report. Despite the advantages of this research design, there has been no targeted controlled laboratory-based research conducted to date assessing whether physiological, psychological, and behavioural harms increase appreciably when AmED is consumed relative to alcohol. This dearth of research precludes any conclusions regarding the direct pharmacological effects of co- ingesting ED, leaving policy-makers with no solid empirical evidence base upon to support regulation of ED sold in conjunction with alcohol.

Focusing specifically on the potential behavioural outcomes of use, it has been well- established in past experimental research that alcohol causes state-dependent

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impulsive behaviour. In regards to the latter behavioural outcome, alcohol appears to exert a differential effect dependent upon the aspect of impulsive behaviour being assessed: impulsive response inhibition, response disinhibition, or impulsive decision-making (de Wit, 2009; Dougherty, Marsh, Hatzis, Nouvion, & Mathias, 2008). Despite previous research showing that stimulant co-ingestion can attenuate alcohol-induced increases in impulsive behaviour (e.g., Fillmore & Vogel-Sprott, 1999), there has been little research assessing the interactive effect of ED in combination with alcohol on the varying aspects of impulsive behaviour. To date, only one study has investigated the effect of AmED on response disinhibition, finding equivalent outcomes regardless of whether ED was co-ingested with alcohol or not (Marczinski et al., 2011); the relative effect of AmED versus alcohol on each of these aspects of impulsive behaviour has not been examined concurrently.

However, the aforementioned shortcomings within this body of literature are overshadowed by one major oversight, the outcomes of which could alter the

methodological and analytical approach adopted when comparing the relative effects of AmED versus alcohol ingestion. The theorised changes in consumption patterns, motivations for, and consequences of, AmED use are generally attributed to AmED- induced reduced perception of intoxication. For this premise to hold true, subjective ratings of intoxication should be lower after AmED versus alcohol consumption, whilst objective intoxication outcomes (e.g., BrAC) remain comparable. In contrast with predictions, the few experimental studies directly assessing objective and subjective intoxication in experimental settings have yielded equivalent outcomes following AmED and alcohol administration (Marczinski et al., 2011; Marczinski, Fillmore, Henges, Ramsey, & Young, 2012, 2013). These studies have generally

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involved administration of a dose equivalent to a single standard 250mL ED (per 70kg person), a lower amount relative to that typically ingested in real-life AmED drinking sessions (Woolsey et al., 2010). This focus on low and simple dosing protocols contributes to the initial development of an evidence-base regarding the relative effects of AmED versus alcohol consumption. However, the paucity of research involving administration of higher doses and adopting more complex dosing protocols limits generalizability to real-life AmED consumption, and precludes conclusions regarding the dose-dependent effects of co-ingestion when consumers engage in excess intake of the two constituents.