Undergraduate University Binge Drinking

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Undergraduate university binge drinking, defined as consuming five or greater drinks in a row for men and four or more drinks for women (Wechsler, Dowdall, Davenport & Castillo, 1995), is a problem negatively affecting the wellbeing of university students (Schall, Kemeny, & Maltzman, 1992). According to the National Survey on Drug Use and Health (2015), full-time undergraduate students, drink more on average (58%) in comparison to their non-student counterparts (48.2%) demonstrating greater alcohol consumption amongst students. Furthermore, adolescent binge drinking patterns (Jefferis, Power & Manor, 2005), and young adulthood (Fillmore, 1975), are predictive of drinking patterns during middle-age life and is significantly associated with increased risks of developing alcohol dependence and abuse problems (Jennison, 2004). These studies collectively highlight the urgency to implement early interventions to help counteract binge drinking amongst the undergraduate student population (Bailer, Stübinger, Dressing, Gass, Rist & Kühner, 2009). However, this task is difficult because alcohol use (AU) is influenced by a multitude of factors (Sher, Grekin, & Williams, 2005), but this essay will focus on the biological factors which influence AU.

Some students may be predisposed to AU due to their genetics. McClearn and Rodgers (1959) demonstrated that mice could be selectively bred to exhibit different preferences for alcohol consumption which corresponded to their inherited genotype. The C57BL strain exhibited the highest alcohol preference in a ‘two-bottle test’, followed by the C3H/2 strain and finally the DBA strain which abstained from alcohol, highlighting a potential genetic predisposition towards AU. Additionally, McClearn’s study was replicated by Wahlsten, Bachmanov, Finn, and Crabbe (2006) who found a 0.85 to 0.98 correlation between both studies for their findings on varying strain preferences, demonstrating the endurance and usefulness of these findings (Crabbe & Phillips, 2014). Therefore, these studies collectively support the biological model of AU by suggesting that various genes are responsible for AU and can be manipulated which will influence an individual’s preference for alcohol. However, once the bottle positions were switched in McClearn and Rodgers’s study (1959), alcohol consumption decreased across the C57BL and C3H/2 breeds implying that the results found may be influenced by habitual learning, rather than biological preference. Additionally, using mice models to study complex biobehavioural phenomena, like alcoholism, may undermine the validity of the findings and restrict their applicability to human individuals (Crabbe, 2008). For instance, behavioral indications of alcoholism, 1) observing the continuation to drink despite the awareness of the potential consequences and, 2) the failure to fulfill social obligations such as work (Becker & Ron, 2014), are not directly inferable from mice in comparison to human participants. Therefore, due to the ambiguity of inferring observations from animal models, the findings should be regarded with caution as it may be inappropriate to extrapolate the findings to human AU. Despite this and no single cluster of genes having yet been identified in humans as responsible for alcoholism (Ioannidis, Ntzani, Trikalinos, & Contopoulos-Ioannidis, 2001), there are various genetic indications of an alcoholic predisposition in both humans and mice which, with further research, could yield the exact genes influencing AU (Edenberg & Foroud, 2013).

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Genes influence the enzymes which metabolize alcohol, therefore influencing student AU. Alcohol is metabolized by alcohol dehydrogenase (ADH1B) producing acetaldehyde, the compound associated with nausea, flushing, and headaches upon alcohol consumption (Wolff, 1972). Acetaldehyde is metabolized further by acetaldehyde dehydrogenase (ALDH2), removing negative physiological effects of alcohol, highlighting the importance of possessing the functional enzymes, ADH1B and ALDH2, for an individual’s AU. Yoshida, Huang, and Ikawa (1984) found approximately 50% of southeast Asians possess the inert form of the ALDH2 enzyme (ALDH2*2), inhibiting their ability to metabolize acetaldehyde resulting in negative symptoms. Additionally, individuals possessing the ALDH2*2 enzyme are less likely to develop alcohol problems (Luczak, Glatt & Wall, 2006) or be diagnosed with alcoholism (Enoch & Goldman, 2001). In supporting the previous studies, another study reported that the ALDH2*2 enzyme was more prevalent amongst the Japanese general population than the Japanese alcoholic population (Harada, Agarwal, Goedde, Tagaki & Ishikawa, 1982), suggesting that the ALDH2 enzyme may function as a protective factor against AU (Irons, Iacono, Oetting & Mcgue, 2012). These studies collectively emphasize the importance of an individual’s biological predisposition towards AU, by demonstrating the influence of an antagonistic internal environment in reducing the likelihood that an individual will drink; which is subject to their inherited genes. Nonetheless, some south-east Asian individuals, despite possessing an antagonistic biological predisposition toward AU, still choose to drink alcohol during young adulthood (Takeshita & Morimoto, 1999) which contradicts the previous literature by implying that biological factors alone may not be the crucial determining factor in AU. To emphasize this point, during early adulthood the enzymes which typically discourage AU do not function as protective factors unlike they appear to do in middle age, perhaps due to early environmental encouragements to use alcohol (Irons et al, 2012), whereas as we age the effect of the environment diminishes and the influence of genetics increases (Bergen, Gardner & Kendler, 2007), providing an explanation for why these individuals may reduce their drinking during middle-age. Importantly, these studies imply that biological factors alone are insufficient in determining AU, highlighting the limitations of a purely reductionist biological model of AU and suggesting that other factors may co-influence AU.

Twin/adoption studies are important contributors to the biological explanation of alcoholism. Monozygotic twins (MZ) share identical DNA whereas dizygotic twins (DZ) share half. Therefore, if alcoholism has a strong hereditary component, MZ twins will likely exhibit higher concordance rates for alcoholism in comparison to the DZ or ordinary siblings due to their greater genetic similarity. This proposition is partially supported, as higher rates of concordance of have been observed between MZ rather than DZ twins in both male (Kaprio, Koskenvuo, Langinvainio, Romanov, Sarna, & Rose, 1987) and female twins (Heath, Jardine, & Martin, 1989), providing support for the hereditary model of AU. Adoption studies provide additional support. Goodwin (1973) found that adopted individuals removed from their alcoholic biological parents were four times more likely than individuals with non-alcoholic biological parents to develop alcoholism, with a later study demonstrating that alcoholism rates did not differ amongst adopted/non-adopted children who shared the same alcoholic biological parent (Goodwin, 1974), emphasizing the importance of genetic contribution towards AU. Notably, however, there are important contradictions and misrepresented findings that challenge the relationship between twin studies and AU. Despite finding greater MZ concordance amongst male twins (Kaprio et al, 1987), other studies reported finding a lower MZ concordance rate amongst men, and no concordance amongst women (Gurling, 1984), conflicting with previous findings. Additionally, Kaprio (1987) also reported that the MZ twins in the study also shared greater social contact during it, implying that social contact was a confounding variable within the study which may have influenced the results. Furthermore, Svikis and Pickens (1988) highlighted that twin and adoption studies of alcoholism often contain various methodological flaws, such as lack of consensus regarding the definition of alcoholism; ranging from alcoholics’ anonymous membership to being arrested for public drunkenness. Later, Svikis and Pickens (1991) also found a lack of distinctive criteria between alcoholic twins, non-alcoholic twins and alcoholics in general within the twin and adoption studies literature, highlighting the potential for the findings to be misleading. Collectively, these studies identify the lack of consensus surrounding the twin and adoption literature into alcoholism and importantly, highlights the insufficiency of relying solely on the biological explanation for AU, as AU is more likely the result of a combination of risky biological predispositions and various other environmental factors (Zucker, Fitzgerald & Moses, 1995).

A student’s biological predisposition will affect their cognitive motivation also. For example, there are individual differences amongst people’s sensitivity to alcohol (Vesell, Page & Passananti, 1971), and young men who have a family history (FH) of alcoholism typically report experiencing diminished subjective response to low or moderate doses of alcohol in comparison to the control group (Schuckit, 1980). Furthermore, the diminished response findings were replicated (Schuckit, 1984) and within different laboratories (Heath, & Martin, 1992), highlighting the strength of this relationship. These studies are important for demonstrating the relationship between biological predispositions and a person’s cognitive response to alcohol. More importantly, Sher, Grekin, and Williams (2005) found that individuals with an FH of alcoholism were more likely to experience enhanced reinforcing effects from alcohol, potentially influencing and encouraging their future AU patterns. Therefore, due to different individuals experiencing different amounts of subjective reinforcement from drinking, individuals that possess an FH of alcoholism are more likely to drink alcohol (Lopez-Vergara, Colder, Hawk, Wieczorek, Eiden, Lengua & Read, 2012) and, logically, are therefore directly more motivated to seek alcohol (Cox & Klinger, 1988) due to obtaining greater reinforcement from drinking. Hence, targeting motivational change is also a viable alternative to targeting biological factors within the student population as both factors are interlinked.

Notably, some of the previous literature reviewed has been derived from US undergraduates, rather than UK ones, potentially limiting the generalizability of the findings. However, despite the potential differences between the countries, the same factors which were predictive of US undergraduate student drinking, such as sensation seeking, positive expectancies and self-efficacy were also predictive of UK undergraduate drinking (Atwell, Abraham, & Duka, 2011), with another study highlighting the same finding between US and Swedish undergraduate drinking (Ståhlbrandt, Andersson, Johnsson, Tollison, Berglund & Larimer, 2008) demonstrating the applicability of the AU findings inter-continentally. Therefore, the literature evidenced from the US would apply to UK undergraduate university drinking within Bangor University.

Disulfiram, Antabuse, is a pharmacological drug that induces negative physiological effects if alcohol is ingested (Chick, Gough, Falkowski, Kershaw, Hore, Mehta, … & Torley, 1992). Antabuse facilitates the activity of ADHB1 and inhibits the activity of ALDH2, therefore metabolizing alcohol at a slower rate and therefore inducing symptoms of sickness and nausea (Wolff, 1972). The pharmacodynamics of Antabuse is supported within mice models (Rivera-Meza, Quintanilla, & Tampier, 2012) and has been demonstrated to be effective in reducing the volume and frequency of alcohol consumption (Hughes & Cook, 1997), highlighting its potential for undergraduate use. However, only a minority of students would qualify for Antabuse; with only 4.6% of students experiencing severe alcoholism problems (Mekonen, Fekadu, Chane, & Bitew, 2017) which qualify for medication. Therefore, the other students who also struggle with AU issues may not be provided with medication, thereby limiting the practicality of medicinal treatment for reducing undergraduate drinking.

However, due to the relationship between biological predisposition and motivation, it may be both more practical and beneficial to target motivational factors. Brief Interventions (BI) are a time-limited intervention that helps to reduce client drinking, by providing an assessment and feedback for change. Brief motivational interventions (BMI), which highlights the discrepancy between the client’s current situation and their idealized goal (Rollnick & Miller, 1995) (Miller, & Rollnick, 2003), would be most helpful for undergraduate students (Larimer & Cronce, 2002) as BMI is most effective with nondependent heavy drinkers (Hester & Miller, 2003). BMI outperforms other treatments, by demonstrating the strongest efficacy in comparison to other non-biological treatment approaches (Miller & Wilbourne, 2002), therefore highlighting the BMI’s effectiveness (Bertholet, 2005). Furthermore, individuals engaging in BMI show significant reductions in their volume of weekly alcohol consumption, their monthly AU frequency and display higher rates of abstinence after a two-year follow-up (Borsari & Carey, 2000). This finding has also been replicated (Marlatt, Baer, Kivlahan, Dimeff, Larimer, Quigley,… & Williams, 1998) and BMI has been used in the Bangor University undergraduate population and has shown to reduce student drinking (Vasilaki, Hosier & Cox, 2006). These studies demonstrate the effectiveness of using BMI and its use in the undergraduate population, providing an alternative approach to altering biology by altering motivational factors instead.

Student binge drinking is higher than in previous decades (Gill, 2002), with influential biological influences such as genetics, enzymes and hereditary factors contributing to AU. However, enhancing motivation using BMI may mediate AU due to the interrelationship between biology and motivation. Therefore, to counteract undergraduate binge drinking, implementing BMI may help to decrease rates of drinking amongst undergraduates within Bangor University.


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