An Addictions Neuroclinical Assessment Based Treatment for Smokers with an Alcohol Use Disorder

PROJECT SUMMARY/ABSTRACT Together, tobacco and alcohol kill more than half a million people in the United States every year, making co- addiction to these substances the leading cause of preventable death. We propose a contingency management (CM) paradigm based on point-of-care urine tests that measure ethyl glucuronide. Theoretically framed within

the Addiction Neuroclinical Assessment (ANA) with hypothesized mechanisms in core domains (i.e., incentive salience, negative emotionality and cognitive function), and proceeding from a sound and innovative scientific premise, we will, for the first time, target smoking and alcohol use by implementing an evidence-based behavioral

treatment (CM) for alcohol among participants who have initiated frontline pharmacotherapy (varenicline; VC) for smoking cessation. This project seeks to replicate, harness and extend our previous findings from secondary analyses and pilot studies, which demonstrate that applying CM to target the use of alcohol can produce non-

targeted reductions in smoking. We will do so by offering CM for alcohol use to smokers who are simultaneously initiating smoking cessation pharmacotherapy. We also seek to identify the most potent ANA-based mediators (e.g., incentive salience given that CM’s focus is on alternative reinforcement) of behavior change in response

to treatment. Lastly, we will examine the extent to which biologic sex and baseline alcohol use and cigarette smoking interacts with CM to produce different levels of reduced alcohol use and cigarette smoking. Patients will take part in a 2-arm randomized controlled trial to evaluate the ability of a CM intervention to reduce alcohol use

and cigarette smoking. After completing a 2-week induction period, patients will be randomized into 2 trial arms for a 12-week treatment period: 1) a CM intervention group that receives smoking cessation treatment as usual (TAU), which includes varenicline and counseling, and 2) a non-contingent (NC) control group that also receives

TAU. Our Specific Aims are to: 1) Determine if CM+TAU is more effective than NC+TAU for reducing alcohol use and cigarette smoking. We hypothesize that CM will yield lower rates of biochemically-verified alcohol use and cigarette smoking, concurrent biochemically-verified alcohol use and smoking, and self-reported drinks per

day, cigarettes per day, and heavy drinking days during the 12-week treatment and 6-month follow-up periods. 3) Identify the most potent ANA-based mediators of treatment response across the treatment groups. We hypothesize that higher executive dysfunction, negative emotionality, and alcohol- and smoking-related incentive

salience will be associated with higher levels of alcohol use and cigarette smoking across treatments and over time; 3) Determine if biological sex or baseline severity of alcohol use and smoking interacts with treatment assignment to produce differential changes in our primary and secondary outcomes. We hypothesize that

biological sex will significantly interact with treatment to produce differential outcomes, and that those with less severity of alcohol use and smoking at baseline will experience better outcomes. This investigation will support future studies that can identify personalized treatment for different sub-groups of smokers with an AUD.