Trajectories of change in subclinical anxiety and alcohol use during alcohol treatment: A parallel process growth model

Alcohol use disorders (AUD) are prevalent, debilitating and costly, with approximately 14 % of adults meeting criteria for past-year AUD (Grant et al., 2015) and costs associated with alcohol-related mortality and morbidity nearing $250 billion in 2010 (Sacks et al., 2015). Federal and state initiatives have facilitated the development of empirically supported behavioral and pharmacological treatments for AUD. The breadth of treatments for AUD is important given the heterogenous presentation of individuals with AUD. However, extant treatment outcome studies have demonstrated small-to-moderate effects and high rates of symptom recurrence. Whereas past work has examined how depression symptoms influence drinking behavior during the course of treatment (Pettinati et al., 2010), less is known about the trajectories of anxiety symptoms and alcohol use during and following AUD treatment.

Although anxiety disorders are prevalent, and often co-occur with AUD and heighten risk for return to use following AUD treatment (Bradizza et al., 2006, Kushner et al., 2005, Schellekens et al., 2015), subclinical anxiety is more prevalent (Das-Munshi et al., 2008, Haller et al., 2014), and the reciprocal causal relationship between anxiety symptoms and drinking have been implicated in the course and prognosis of AUD (Charney et al., 2005). Theoretical models have identified common neurobiological and psychosocial processes underlying anxiety and alcohol use and have provided insight on the unique role of anxiety on the initiation and maintenance of risky drinking. For example, the revised reinforcement sensitivity theory identifies two neurophysiological systems that explain a positive reinforcement pathway from anxiety to drinking initiation (via the behavioral activation system) and a negative reinforcement pathway from anxiety to drinking maintenance (via the behavioral inhibition system) (Keough and O’Connor, 2014). Relatedly, the neurobiological model of addiction identifies negative emotionality as the broader psychological process underlying anxiety and AUD, such that the pleasurable effects of drinking during the binge/intoxication stage (i.e., drinking initiation) leads to anxiety and other negative emotion states, and contributes to an individual’s transition into the withdrawal/negative affect stage (i.e., drinking maintenance) (Koob, 2011, Koob and Volkow, 2016).

Although clinical researchers have developed and evaluated treatments to address comorbid AUD and anxiety disorders (Smith and Randall, 2012, Stewart and Conrod, 2008), investigations of anxiety symptoms among samples with only AUD have primarily focused on mitigating symptoms in the context of alcohol detoxification (Liappas et al., 2002, Oliva et al., 2018). Specifically, individuals in the acute stage of alcohol withdrawal are commonly prescribed benzodiazepines to manage their anxiety and other withdrawal symptoms. While helpful in the short-term, benzodiazepines are not an effective AUD treatment (Liang and Olsen, 2014) and detoxification services for individuals with AUD are not a sufficient treatment to maintain abstinence (National Institute on Drug Abuse, 2018). Given the influence of anxiety on the course and prognosis of AUD, it is logical to assume that anxiety may continue to fluctuate and influence drinking behaviors in individuals receiving post-detoxification treatment.

The Combined Pharmacotherapies and Behavioral Interventions for Alcohol Dependence (COMBINE) study was a large multi-site, randomized clinical trial of AUD treatment efficacy for individuals seeking outpatient treatment. Investigators aimed to evaluate the efficacy of two medications (naltrexone and acamprosate plus medication management) and a psychosocial intervention (high intensity combined behavioral intervention [CBI]), delivered either alone or in combination, on heavy drinking behaviors up to one-year post-treatment. Although the authors found a small effect of naltrexone and CBI as compared to placebo, their hypotheses that combined treatments would produce better outcomes than any individual treatment were largely unsupported. Commentaries of the COMBINE findings largely critiqued the lack of attention to individual differences and mechanisms of change (Bergmark, 2008, Buhringer and Pfeiffer-Gerschel, 2008), resulting in several investigations to determine which treatment components and/or treatment mechanisms may explain the drinking outcomes (LoCastro et al., 2009, Longabaugh et al., 2010, Subbaraman et al., 2013). Whereas several secondary investigations have examined how changes in mood predict drinking outcomes (Witkiewitz et al., 2012, Witkiewitz et al., 2013), no prior work, to our knowledge, has used the COMBINE data to investigate how changes in anxiety symptoms relate to changes in weekly drinking rates during and following AUD treatment.

The current study is a secondary analysis of COMBINE data to investigate the trajectories of anxiety symptoms and alcohol use during and following a course of AUD treatment in a sample of treatment-seeking individuals with a diagnosis of AUD and without a comorbid anxiety disorder diagnosis. The goals of the current study were threefold. First, we used latent growth curve models to examine trajectories of drinking and anxiety symptoms during treatment and up to one year following treatment. Second, we used parallel process models to evaluate the reciprocal relationship between trajectories of weekly drinking and anxiety symptoms. Finally, we evaluated differences on the above trajectories across treatment groups, particularly those who received only medication versus those who received medication plus behavior therapy given that behavioral therapy included strategies to manage mood.

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