Pharmacological and sensorimotor mechanisms linking obsessive–compulsive symptoms and cigarette smoking: A clinical laboratory study.

Obsessive-compulsive symptoms (OCS)-repeated unwanted, intrusive anxiogenic thoughts and ritualistic distress-suppressing behaviors-are comorbid with persistent cigarette smoking. This clinical laboratory experiment tested a dual-mechanism conceptualization of OCS-smoking comorbidity, which purports that people with OCS persistently smoke because they are hypersensitive to smoking's sensorimotor-ritualistic and nicotine-pharmacologic negative reinforcing properties. Cigarette-smoking adults (n = 129) completed a baseline session to assess clinically significant OCS (yes/no), followed by four overnight tobacco-deprived 8-hr sessions involving exposure to each of four study conditions in a within-subject 2 × 2 factorial randomized design crossing a (a) sensorimotor manipulation that modeled the tobacco self-administration ritual's effects independent of nicotine (smoking very low nicotine cigarettes [VLNC] hourly vs. no smoking) and (b) pharmacologic manipulation that modeled nicotine's effects independent of tobacco self-administration (double-blind 21 mg nicotine vs. placebo transdermal patch). Experimental session outcome measures included self-reported smoking urge (range: 0-5), nicotine withdrawal symptoms (range: 0-5), physical pain (range: 0-10), and negative affect and a behavioral task assessing motivation to reinstate usual brand cigarette smoking. Consistent with hypotheses, participants with versus without clinically significant OCS were more sensitive to the urge-suppressing effects of smoking VLNCs versus no smoking (OCS × VLNC, B = -.14, 95% CI [-.24, -.04]; p = 01) and the pain-suppressing effects of nicotine versus placebo (OCS × Nicotine, B = -.14, 95% CI [-.24, -.03]; p = 02). Counter to hypotheses, participants with clinically significant OCS experienced weaker nicotine-induced withdrawal symptom suppression (OCS × Nicotine, B = .16, 95% CI [.09, .24]; p < .001). Other OCS × VLNC or OCS × Nicotine interactions were nonsignificant. Findings from this study partially support a conceptualization that OCS-smoking comorbidity is explained by a hypersensitivity to some of smoking's nicotine-pharmacologic and sensorimotor-ritualistic negative reinforcing properties (i.e., urge and pain suppression). (PsycInfo Database Record (c) 2026 APA, all rights reserved).