Brittany E. Blanchard, Angela K. Stevens, Molin Shi, and Andrew K. Littlefield
Department of Psychological Sciences, Texas Tech University, Lubbock, TX, USA
Initially, alcohol use disorder (AUD), labeled alcoholism, was classified under the personality and other nonpsychotic disorders sections in the first two editions of the Diagnostic and Statistical Manual of Mental Disorders (DSM), and this personality‐based conceptualization of AUDs remained prominent in mental health until 1980 (American Psychiatric Association [APA], 1980). Although the disease concept of alcoholism, which led to the medicalization of this disorder, appeared in 1956 (see Jellinek, 1960), it was not until the third edition of the DSM that “alcoholism” was replaced with alcohol abuse and dependence and was moved to the substance use disorder section (APA, 1980). These changes, in part, reflected the conceptualization of alcohol dependence syndrome (see Edwards & Gross, 1976).
Recently, the fifth edition of the DSM drastically changed the classification of alcohol‐related diagnoses (and other substance use disorders). In addition to abolishing the biaxial system in favor of single AUD, which combines abuse and dependence criteria, critical changes to criteria were made based on research conducted since the publication of DSM‐IV (e.g., removal of legal issues and addition of craving; APA, 2013; see Hasin et al., 2013). Under DSM‐5 criteria, an individual must exhibit at least 2 of the 11 criteria in the past year (i.e., briefly, hazardous use, difficulty quitting, social/occupational problems, tolerance, withdrawal, drinking for larger/longer than intended, great deal of time spent obtaining/using/recovering from alcohol, craving, failure to fulfill role obligations, continued drinking despite interpersonal/social problems, continued drinking despite psychological/physical problems; see APA, 2013), and these symptoms must yield significant distress and/or impairment for diagnosis (APA, 2013, p. 491). A severity specifier allows clinicians to rate severity of the AUD based on a symptom count (APA, 2013).
Because only one symptom was necessary to establish an alcohol abuse diagnosis in DSM‐IV (APA, 2000), the latest criteria change (i.e., 2+ symptoms required) may improve diagnostic reliability and validity by reducing the number of diagnostic imposters (Lane & Sher, 2015). Although the newest edition of the DSM has made great improvements in classification of individuals with AUD for clinical and research purposes, several limitations remain (e.g., varying severity among symptoms, disregard for symptom constellations; see Lane & Sher, 2015). One proposal to rectify this issue is to require both harm (e.g., presence of alcohol‐related problems) and dysfunction (e.g., presence of either compulsive use or withdrawal) to make an AUD diagnosis (Wakefield & Schmitz, 2015).
Based on data from the 2012 to 2013 National Epidemiologic Survey on Alcohol and Related Conditions III, a representative US noninstitutionalized civilian sample of adults 18 years or older, the lifetime and 12‐month prevalence of DSM‐5 AUD were 29.1 and 13.9%, respectively (Grant et al., 2015). Both lifetime and past‐year rates of AUD were highest among males, White and Native American individuals, and younger, never married, or previously married adults (Grant et al., 2015). Normatively, the prevalence of AUD and levels of heavy, problematic alcohol use peak in the early 20s and decline thereafter into later adulthood, although heterogeneity exists in trajectories of alcohol outcomes (see Chassin, Sher, Hussong, & Curran, 2013).
A myriad of theoretical conceptualizations that attempt to explain the mechanisms responsible for the onset, maintenance, and relapse processes of AUD have been proffered (e.g., Cox & Klinger, 1988; Sher, Grekin, & Williams, 2005). Extant literature highlights multiple etiological pathways for problematic alcohol involvement. Importantly, different pathways are not mutually exclusive, and there is potential for both additive and superadditive effects (see Sher, Martinez, & Littlefield, 2011, for a detailed review). Most widely accepted models in research and clinical work utilize the biopsychosocial framework, which posits that biological (e.g., genetics, neuroadaptation, pharmacological vulnerability; see Kendler, Myers, & Prescott, 2007; Sher, Trull, Bartholow, & Vieth, 1999; Volkow, Koob, & McLellan, 2016), psychological (e.g., expectancies, motives, personality; see Jones, Corbin, & Fromme, 2001; Kuntsche, Knibbe, Gmel, & Engels, 2005; Littlefield & Sher, 2014), and social factors (e.g., parental and peer influences; Nash, McQueen, & Bray, 2005) contribute to the onset and maintenance of AUD (Marlatt, Baer, Donovan, & Kivlahan, 1988). For example, the motivational model of alcohol use postulates that historical factors (biochemical reactivity, personality, and sociocultural factors), current factors (current affective state and alcohol availability), and alcohol‐related expectancies interact to affect decision‐making processes regarding alcohol consumption (Cox & Klinger, 1988). Diathesis–stress models (including genetic diathesis; see Dick et al., 2008) propose that individuals have biological and/or psychological vulnerabilities, which trigger the onset of AUD in the face of stressful life events (Goldstein, Abela, Buchanan, & Seligman, 2000). Supporting this model are findings from gene–environment interaction research, which suggests that individuals with specific genetic variants develop AUD only under certain environmental conditions (Caspi & Moffitt, 2006).
Social cognitive theories of alcohol use integrate psychological factors (e.g., cognitive expectancies, drinking refusal self‐efficacy, drinking motives) and social environmental influences (e.g., parental and peer alcohol use) to predict alcohol consumption and AUD development (Cooper, Russell, & George, 1988; Giovazolias & Themeli, 2014). The deviance proneness model (Sher et al., 1999) suggests that substance use behavior is a facet of a general pattern of deviant behaviors (i.e., heterotypic continuity; Moffitt, 1993). In addition to the genetic vulnerability of externalizing behaviors in childhood, these behaviors are also thought to be a result of environmental factors such as inadequate socialization and/or associating with a deviant peer group. In sum, multiple integrative models exist within the literature, the most comprehensive of which include examination biological, psychological, and sociocultural/environmental factors in considering etiological pathways to AUD, as well as alcohol consumption, more broadly.
Alcohol consumption is necessary to experience alcohol‐related problems and receives a diagnosis of AUD, yet this is not assessed in the DSM‐5 or the International Classification of Diseases (ICD‐10; World Health Organization, 1992). Despite exclusion from formal criteria for AUDs, alcohol quantity, frequency, and “binge drinking” are typically assessed. Although there are discrepancies in definitions of binge drinking (also called heavy episodic drinking), the current standard is the National Institute on Alcohol Abuse and Alcoholism (NIAAA) definition, which is five or more standard drinks for males and four or more standard drinks for females, over approximately 2 hr. This pattern of consumption increases blood alcohol concentration (BAC) to roughly 0.08 g/dL, the legal limit in the United States (NIAAA, 2004). Other definitions include that of the Substance Abuse and Mental Health Services Administration (SAMHSA), which defines binge drinking as more than five drinks per occasion, with heavy drinking defined as binge drinking on 5 or more days within the past month (Center for Behavioral Health Statistics and Quality, 2015).
Effects of acute alcohol consumption can range from increased talkativeness and relaxation to clumsiness, to, at higher levels of intoxication, respiratory depression, and even death (see Vonghia et al., 2008). Broadly, effects tend to vary as a function of BAC with more severe effects occurring at higher levels of BAC. For example, relaxation is typically experienced by individuals with a BAC of less than 0.05 g/dL, whereas symptoms like respiratory depression and coma occur at BACs of 0.40 g/dL and higher (Vonghia et al., 2008). Although BAC typically increases with consumption, an individual's BAC depends on a number of factors affecting bioavailability, such as genetics, biological sex, eating prior to the drinking episode, and alcohol tolerance (e.g., Ramchandani, Bosron, & Li, 2001). Regardless, within a given drinking episode, an individual will typically experience both stimulant‐like and depressant‐like effects, due to alcohol's biphasic effects (i.e., stimulant‐like effects on the ascending limb of the blood alcohol curve and depressant‐like effects on the descending limb). However, the experience of these effects also varies as a function of individual differences (e.g., alcohol use status; King, De Wit, McNamara, & Cao, 2011).
Acute alcohol consumption can impact a number of physiological functions, which can influence health outcomes. For example, evidence suggests that alcohol consumption often yields increases in appetite and food consumption (Yeomans, 2010). Although evidence is mixed regarding the effects of alcohol intake on sexual arousal, research indicates a decrease in genital arousal, including decreased penile tumescence (see George & Stoner, 2000). Contrary to popular belief, consuming alcohol before bed may negatively impact sleep; more specifically, alcohol appears to delay the onset of rapid eye movement (REM) sleep and increase disruption in the second half of sleep (see Ebrahim, Shapiro, Williams, & Fenwick, 2013). Many individuals also experience hangovers after consuming alcohol, which may include symptoms such as headache, nausea, vomiting, diarrhea, fatigue, and decreased motor and cognitive functioning (Wiese, Shlipak, & Browner, 2000). In some cases hangover may negatively impact or prevent performance of work‐related responsibilities.
Higher doses of alcohol (i.e., BAC of approximately 0.10 g/dL or higher) can impair reaction times and decision making (Vonghia et al., 2008), resulting in an increased chance of risky sexual behaviors, sexual assault, physical injury, homicidal and suicidal behaviors, and motor vehicle accidents (Cooper, 2002; see George & Stoner, 2000). Indeed, the National Highway Traffic Safety Administration (U.S. Department of Transportation, National Highway Traffic Safety Administration, 2015) estimates that approximately 28 people die each day in the United States in alcohol‐related motor vehicle accidents. In sum, at lower doses, alcohol typically produces rewarding effects, such as relaxation and reductions in anxiety, whereas higher doses yield depressant‐like effects and increase the risk of alcohol‐related consequences. In light of this evidence, to maximize the short‐term effects of alcohol and minimize consequences, it is recommended that individuals consume alcohol in a manner consistent with the 2015–2020 Dietary Guidelines for Americans, which defines moderate consumption as no more than two drinks per day for men and one drink a day for women of the legal drinking age, with some exceptions (e.g., those taking certain medications or with certain conditions, pregnant or breastfeeding women; US Department of Health and Human Services and US Department of Agriculture, 2015).
Brittany E. Blanchard is currently a PhD student in clinical psychology at Texas Tech University in the Department of Psychological Sciences. Her research examines individual differences in alcohol and substance use, including use of protective behavioral strategies.
Angela K. Stevens is currently a PhD student in clinical psychology at Texas Tech University in the Department of Psychological Sciences. Broadly, her research interests include individual differences in adult problematic substance use.
Molin Shi is currently a PhD student in clinical psychology at Texas Tech University in the Department of Psychological Sciences. Her research focuses on the influences and consequences of substance‐related behaviors, with an emphasis on the familial, social, and acculturative impact of substance use in minority subgroups.
Andrew K. Littlefield is currently an assistant professor at Texas Tech University in the Department of Psychological Sciences. He obtained his predoctoral training in clinical psychology at the University of Missouri and completed his clinical internship at the University of Mississippi Medical Center. Dr. Littlefield's research focuses on addictive behaviors.