Angela K. Stevens, Brittany E. Blanchard, Molin Shi, and Andrew K. Littlefield
Department of Psychological Sciences, Texas Tech University, Lubbock, TX, USA
In addition to the host of short‐term consequences associated with alcohol consumption, chronic use of alcohol, especially chronic misuse, is associated with several detrimental health outcomes. In fact, 25 chronic diseases in the International Classification of Disease (ICD‐10) are completely attributable to long‐term alcohol consumption, and chronic alcohol consumption is a component of more than 200 other diseases in the ICD‐10 (see Shield, Parry, & Rehm, 2014). Notably, alcohol shows a dose–response relation to many chronic diseases, in which the risk of disease onset and death from disease depends on the total volume of alcohol consumed (Shield et al., 2014). Further, between 1990 and 2010, alcohol was the third leading risk factor for global disease burden; however, for individuals between the ages of 15 and 49, it was the top risk factor worldwide (Lim et al., 2013).
Chronic, heavy drinking has been implicated as a risk factor for several deleterious health outcomes, including high blood pressure (Fuchs, Chambless, Whelton, Nieto, & Heiss, 2001), hemorrhagic and ischemic stroke (Rehm et al., 2009), Korsakoff's syndrome (i.e., a chronic memory disorder), and Wernicke's encephalopathy (i.e., alcohol‐related dementia; see Pitel, Segobin, Ritz, Eustache, & Beaunieux, 2015). Indeed, alcohol‐related Korsakoff's syndrome results from chronic, heavy alcohol consumption and thiamine (vitamin B1) deficiency, which is a consequence of a poor diet characteristic of excessive alcohol use (Pitel et al., 2015). Excessive alcohol consumption is also associated with epilepsy, or a predisposition for epileptic seizures (Shield et al., 2014). Research in this area has revealed a dose–response relation between alcohol consumption and the risk for epilepsy, such that repeated withdrawals from alcohol consumptions by heavy drinkers may increase risk for inducing an epileptic episode (see Shield et al., 2014 for more details). Other neuropsychiatric conditions associated with chronic alcohol consumption include unipolar depression, Alzheimer's disease, and vascular dementia (Shield et al., 2014).
Because chronic alcohol misuse is also linked to several types of cancers, alcohol is considered a carcinogen. Some of the cancers associated with problematic use include those of the prostate, upper digestive track (e.g., oral cavity, esophagus, and larynx), lower digestive track (e.g., colon, rectum, and liver), and breast (Rehm et al., 2009). Further, chronic alcohol consumption is associated with liver diseases (e.g., liver cirrhosis, alcoholic hepatitis); in 2010, an estimated 493,300 deaths were attributed to alcohol‐related cirrhosis of the liver (Rehm, Samokhvalov, & Shield, 2013). Further, a recent meta‐analysis found that alcohol consumption increased the risk of developing pancreatitis (though the dose–response relation for acute pancreatitis differed across men and women; see Samokhvalov, Rehm, & Roerecke, 2015). Moreover, chronic alcohol use increases the likelihood of developing diabetes mellitus, a condition commonly caused by pancreatitis (Rehm et al., 2009). Alcohol consumption affects blood pressure, and chronic alcohol misuse is predictive of hypertensive heart disease and ischemic heart disease (Rehm et al., 2009). There is also evidence that chronic alcohol use is associated with infectious diseases such as tuberculosis (World Health Organization [WHO], 2014). Although the biological evidence to support the causal link is lacking, observational research has indicated that alcohol consumption may exacerbate the disease progression of psoriasis, which is a chronic inflammatory autoimmune skin disease (Shield et al., 2014). Thus, chronic, heavy alcohol consumption puts an individual at risk for a myriad of negative physical conditions and diseases.
Detrimental outcomes of alcohol consumption during pregnancy include low birth weight (Rehm et al., 2009) and the development of fetal alcohol spectrum disorders, such as fetal alcohol syndrome (FAS), alcohol‐related birth defects, and alcohol‐related neurodevelopmental disorders (see Riley, Infante, & Warren, 2011). Specifically, infants with FAS exhibit growth deficiencies, craniofacial abnormalities, and heart defects (Riley et al., 2011). Individuals with FAS experience significant problems in adaptive, academic, and behavioral functioning (Streissguth et al., 2004). More specifically, fetal alcohol effects are associated with lower levels of intelligence, disrupted school experiences, criminal behavior and/or incarceration, inappropriate sexual behavior, and alcohol/drug problems (Streissguth et al., 2004). FAS is the leading preventable (i.e., nongenetic) cause of intellectual development disorder (previously known as mental retardation) and birth defects (O'Leary et al., 2013). In sum, alcohol consumption during pregnancy can lead to debilitating long‐term health‐related consequences for the offspring.
Despite the many potential adverse consequences associated with alcohol consumption, empirical evidence suggests that light‐to‐moderate drinking may provide some health benefits. For example, some data indicated that light‐to‐moderate drinking yields a reduction in risk for coronary heart disease and stroke (Shield et al., 2014). Further, alcohol use may reduce the risk of type 2 diabetes (Shield et al., 2014) and dementia (Peters, Peters, Warner, Beckett, & Bulpitt, 2008). There is also some evidence that alcohol consumption might lower the risk of certain types of cancers, including renal cell carcinoma, Hodgkin's lymphoma, andnon‐Hodgkin's lymphoma (see Shield et al., 2014). Despite these findings, the health benefits of moderate alcohol use have recently been called into question (see Chikritzhs et al., 2015), and the benefits may not outweigh the consequences.
Numerous treatment approaches to AUDs are available. Though non‐exhaustive, provided below are brief summaries of several relevant, empirically supported treatments for AUDs and related problems.
Brief interventions are evidence‐based practices designed to motivate individuals to understand, reduce, and/or eliminate alcohol use, usually delivered in a 5‐ to 20‐min session (Center for Substance Abuse Treatment, Substance Abuse and Mental Health Services Administration, 1999). Findings from a meta‐analytic review suggest that brief interventions are as efficacious as extended alcohol treatments (Moyer, Finney, Swearingen, & Vergun, 2002). Common brief interventions typically used on college campuses are variants of brief motivational interventions (Murphy et al., 2001), such as the Brief Alcohol Screening and Intervention for College Students (BASICS) (Dimeff, Baer, Kivlahan, & Marlatt, 1999). Brief interventions have also demonstrated effectiveness in community mental health and primary care settings (O'Donnell et al., 2014).
Motivational interviewing (MI) is a brief, client‐centered method used in conjunction with individual therapy that has strong research support for its efficacy in treating individuals with alcohol‐related problems (Rollnick, Miller, & Butler, 2008). MI seeks to evoke self‐efficacy and motivation while encouraging individuals to use their own reasons for change to resolve ambivalence, reduce resistance, and progress in their readiness to change (Rollnick et al., 2008). Similarly, motivational enhancement therapy, which combines MI techniques and personal feedback, has also been used to promote motivation for positive change in individuals who engage in problematic drinking (Miller, Zweben, DiClemente, & Rychtarik, 1992). Research has demonstrated strong support for the integration and use of MI as part of treatment for substance use disorders, including AUDs (see Lundahl & Burke, 2009).
Numerous cognitive behavioral (CB) interventions to treat alcohol dependence have been developed and empirically tested (see Witkiewitz, Marlatt, & Walker, 2005). The CB approach targets cognitive, affective, and behavioral factors related to problematic drinking. It is hypothesized that deficits in abilities to cope effectively with stress serve to maintain excessive and subsequent drinking (Morgenstern & Longabaugh, 2000). As such, CB interventions typically include standardized, performance‐based techniques, such as behavioral rehearsal and modeling, which teach individuals to have a sense of mastery in stressful situations without resorting to alcohol consumption.
Behavioral couples therapy for AUD (ABCT) is the most extensively studied approach of treatment at the couple level and has strong research support. ABCT is an outpatient, conjoint treatment that may be used as an additional component of, or subsequent to, individual therapy for those with AUDs and their partners (Epstein & McCrady, 1998). The underlying assumption posits that alcohol‐related problems and intimate relationships are reciprocal and reinforcing of the alcohol use (Powers, Vedel, & Emmelkamp, 2008). A meta‐analysis of 12 randomized controlled trials found that ABCT demonstrated a significantly greater effect compared with individual treatment alone for individuals with alcohol use problems in relationships (Powers et al., 2008).
Although support groups such as Alcoholics Anonymous (AA) are commonly utilized in the treatment of AUDs, findings are mixed with regard to effectiveness of AA (Tonigan, Toscova, & Miller, 1996). However, some components of AA are supported by research (e.g. recovering individuals as therapists, peer‐led self‐help groups; Kownacki & Shadish, 1999). Although AA and 12‐step programs may not be effective for individuals with certain traits (e.g., severe mental illness), self‐help groups such as these represent a viable option for many individuals who are motivated to maintain abstinence (Montalto, 2016).
The US Food and Drug Administration (FDA) has approved three pharmacological treatments for AUDs: disulfiram (e.g., Antabuse), oral and extended‐release naltrexone (e.g., ReVia, Vivitrol), and acamprosate (e.g., Campral; Mark, Kassed, Vandivort‐Warren, Levit, & Kranzler, 2009). Although disulfiram (an aldehyde dehydrogenase inhibitor) is meant to condition an individual to avoid alcohol intake by inducing nausea when individuals consume alcohol, it appears to reduce consumption but often fails to yield abstinence (Garbutt, West, Carey, Lohr, & Crews, 1999). Naltrexone (ReVia, Vivitrol) is an opioid antagonist, which lessens the positively reinforcing effects of alcohol (Petrakis et al., 2005). Studies have demonstrated its relative effectiveness in reducing overall alcohol consumption (Petrakis et al., 2005), as well as rate of relapse (Carmen, Angeles, Ana, & María, 2004). Naltrexone has also been shown to enhance treatment effectiveness when used in conjunction with other treatment modalities, such as psychosocial therapies or coping skills therapy (Jarosz, Miernik, Wachal, Walczak, & Krumpl, 2013). Acamprosate (Campral) is thought to enhance the inhibitory effects of the neurotransmitter gamma‐aminobutyric acid (GABA) (Hunt, 1993) and acts primarily as a functional glutamate antagonist. Meta‐analytic reviews suggest that acamprosate is also effective as a complementary treatment with different psychosocial interventions in treating alcohol dependence and appears to be as effective as naltrexone (Carmen et al., 2004; Garbutt et al., 1999).
Detoxification from chronic alcohol consumption is an important first step in treatment and often requires medical supervision, given the potential fatality of alcohol withdrawal symptoms (i.e., delirium tremens; see Kosten & O'Connor, 2003). Benzodiazepines have demonstrated effectiveness for managing seizures and delirium related to detoxification (Kosten & O'Connor, 2003). Further, anticonvulsants (e.g., carbamazepine) and alpha‐agonists (e.g., clonidine) appear to decrease severity of withdrawal symptoms, and beta‐blockers reduce cravings for alcohol (Kosten & O'Connor, 2003). Indeed, medication to manage withdrawal symptoms can be delivered on a fixed schedule or as needed, though the latter requires more frequent monitoring yet leads to a more rapid detoxification. Without pharmacological intervention withdrawal symptoms are expected to peak within 72 hr after last use, but medications reduce these symptoms within hours of delivery (see Kosten & O'Connor, 2003 for more details).
The cornerstone of treatment for alcoholic liver disease is abstinence, as significant improvement in disease progression can be observed in as little as 3 months. However, nutrition therapy also appears to be effective, given that the severity of malnutrition related to chronic alcohol consumption is correlated with disease severity and negative outcomes (see O'Shea, Dasarathy, & McCullough, 2010). Steroid treatment for alcoholic hepatitis has received the most attention in the extant literature, and there is evidence to suggest that a tapered dose of prednisolone over 2 weeks is most effective; however, studies often exclude individuals at an advanced stage of liver disease, which limits the generalizability of these findings (O'Shea et al., 2010). Notably, alcoholic liver disease is the second most common indicator for a liver transplant; however, given the stigma related to alcoholic liver disease (i.e., a “self‐induced” disease), less than 5% of patients with advanced liver disease resulting from chronic alcohol consumption are formally evaluated for candidacy for liver transplantation (O'Shea et al., 2010).
AUDs are among the most commonly experienced psychiatric disorders in the United States, with especially high rates among young adults. Although many individuals who experience AUDs during adolescence and young adulthood will subsequently recover, underage alcohol use is more likely to be fatal among young people than all other illegal drugs combined (Grunbaum et al., 2002). In addition to alcohol‐related injuries, alcohol consumption has been linked to over 200 health conditions (WHO, 2014). Given that alcohol use is normative and problematic use is common, treatment options to increase treatment involvement and retention rates, such as MI and stepped care approaches, may be especially beneficial (see Littlefield & Sher, 2009). Further, in light of data supporting the so‐called prevention paradox (i.e., most alcohol‐related harm in a given population arises within drinkers that are “low risk”; see Rossow & Romelsjo, 2006) and the health perils of acute intoxication regardless of disorder status, preventing alcohol‐related health problems through prevention policy efforts, should also be considered in addition to treatments aimed at individuals with AUDs (see Gruenewald, 2011).
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.
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.
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.