Cynthia A. Conklin

Proximal Versus Distal Cues to Smoke: The Effects of Environments on Smokers' Cue-Reactivity

Smokers are highly reactive to smoking-related cues that are directly linked, or most proximal, to actual smoking behavior (e.g., lit cigarettes). However, over the course of smoking, proximal cues may not be the only stimuli to become strongly associated with smoking. Distal cues, such as the environments in which smoking occurs (e.g., bar) might also gain associative properties and come to evoke robust reactivity from smokers. To test this, a pilot study was first conducted to develop standard pictorial stimuli of smoking and nonsmoking environments, all of which were completely devoid of proximal smoking cues. A comparison set of smoking and nonsmoking proximal cues was then created. Using the 12 total pictorial cues developed, 62 adult smokers participated in a cue-reactivity study during which they viewed and rated pictorial smoking and nonsmoking environment and proximal cues. Results demonstrate that, similar to proximal cues, environments associated with smoking can alone function as stimuli capable of evoking strong subjective reactivity from smokers. This work supports a broader conceptualization of drug-related cues in cue-based research and treatment development that includes proximal and distal cues as distinct categories. (PsycINFO Database Record (c) 2008 APA, all rights reserved).

Subjective and Reinforcing Effects of Smoking During Negative Mood Induction.

Two notions strongly held by many smokers are that negative mood increases smoking behavior and that this increase is due to the ability of smoking to alleviate negative affect. This study used a modified mood induction procedure to examine both the impact of smoking on induced mood, as well as the effect of induced mood on actual smoking behavior. Forty-eight smokers were randomly assigned to a smoking or a water-drinking comparison group. Each participant attended 3 sessions during which 1 of 3 mood states (positive, negative, or neutral) was induced. Contrary to expectation, smoking did not attenuate negative affect. However, negative mood induction subsequently quickened latency to smoke and increased number of puffs consumed ad lib.

Dopamine and opioid gene variants are associated with increased smoking reward and reinforcement owing to negative mood.

Negative mood increases smoking reinforcement and risk of relapse. We explored associations of gene variants in the dopamine, opioid, and serotonin pathways with smoking reward (‘liking’) and reinforcement (latency to first puff and total puffs) as a function of negative mood and expected versus actual nicotine content of the cigarette. Smokers of European ancestry (n=72) were randomized to one of four groups in a 2×2 balanced placebo design, corresponding with manipulation of actual (0.6 vs. 0.05 mg) and expected (told nicotine and told denicotinized) nicotine ‘dose’ in cigarettes during each of two sessions (negative vs. positive mood induction). Following mood induction and expectancy instructions, they sampled and rated the assigned cigarette, and then smoked additional cigarettes ad lib during continued mood induction. The increase in smoking amount owing to negative mood was associated with: dopamine D2 receptor (DRD2) C957T (CC>TT or CT), SLC6A3 (presence of 9 repeat>absence of 9), and among those given a nicotine cigarette, DRD4 (presence of 7 repeat>absence of 7) and DRD2/ANKK1 TaqIA (TT or CT>CC). SLC6A3, and DRD2/ANKK1 TaqIA were also associated with smoking reward and smoking latency. OPRM1 (AA>AG or GG) was associated with smoking reward, but SLC6A4 variable number tandem repeat was unrelated to any of these measures. These results warrant replication but provide the first evidence for genetic associations with the acute increase in smoking reward and reinforcement owing to negative mood.

Acute Negative Affect Relief from Smoking Depends on the Affect Situation and Measure but Not on Nicotine

BACKGROUND Smoking acutely relieves negative affect (NA) due to smoking abstinence but may not relieve NA from other sources, such as stressors. METHODS Dependent smokers (n = 104) randomly assigned to one of three smoking conditions (nicotine or denicotinized cigarettes, or no smoking) completed four negative mood induction procedures (one per session): 1) overnight smoking abstinence, 2) challenging computer task, 3) public speech preparation, and 4) watching negative mood slides. A fifth session involved a neutral mood control. The two smoking groups took four puffs on their assigned cigarette and then smoked those same cigarettes ad libitum during continued mood induction. All subjects rated their level of NA and positive affect on several measures (Mood Form, Positive and Negative Affect Scale, Stress-Arousal Checklist, and State-Trait Anxiety Inventory-state). They also rated craving and withdrawal. RESULTS Negative affect relief from smoking depended on the NA source (i.e., mood induction procedure) and the affect measure. Smoking robustly relieved NA due to abstinence on all four measures but only modestly relieved NA due to the other sources and typically on only some measures. Smokings effects on positive affect and withdrawal were similar to effects on NA, but relief of craving depended less on NA source. Smoking reinforcement only partly matched the pattern of NA relief. Few responses differed between the nicotine and denicotinized smoking groups. CONCLUSIONS Acute NA relief from smoking depends on the situation and the affect measure used but may not depend on nicotine intake. These results challenge the common assumption that smoking, and nicotine in particular, broadly alleviates NA.

Differences in negative mood-induced smoking reinforcement due to distress tolerance, anxiety sensitivity, and depression history

RationaleNegative mood increases smoking reinforcement and may do so to a greater degree in smokers vulnerable to negative mood dysregulation.MethodsAdult smokers (N = 71) without current depression were randomly assigned to one of two smoking conditions (nicotine or denic cigarettes, presented blind) maintained across all sessions. Subjects completed one neutral mood session and four negative mood induction sessions. Negative mood inductions included one each of the following: 1) overnight smoking abstinence, 2) challenging computer task, 3) public speech preparation, 4) watching negative mood slides. In each session, subjects took 4 puffs on their assigned cigarette, rated it for “liking” (reward), and then smoked those cigarettes ad libitum (reinforcement) during continued mood induction. Affect was assessed intermittently before and after smoking. Differences in responses were examined as functions of self-reported history of major depression and levels of distress tolerance and anxiety sensitivity.ResultsSmoking reinforcement, but not reward or negative affect relief, was greater in all sessions in those with a history of depression and greater after overnight abstinence in those with lower distress tolerance. Reward and affect relief, but not reinforcement, were greater during speech preparation among those high in anxiety sensitivity.ConclusionsLow distress tolerance may enhance acute smoking reinforcement due to abstinence, while depression history may broadly increase acute smoking reinforcement regardless of mood. Neither smoking reward nor affect help explain these individual differences in smoking reinforcement.

Mood influences on acute smoking responses are independent of nicotine intake and dose expectancy.

Acute responses to smoking are influenced by nicotine and by nonpharmacological factors such as nicotine dose expectancy and sensory effects of smoke inhalation. Because negative mood increases smoking reinforcement, the authors examined whether these effects may be altered by mood context. Smokers (n=200) participated in 2 sessions, negative or positive mood induction, and were randomized to 1 of 5 groups. Four groups comprised the 2x2 balanced placebo design, varying actual (0.6 mg vs. 0.05 mg yield) and expected nicotine dose (expected nicotine vs. denicotinized [denic]) of cigarettes. A fifth group was a no-smoking control. Smoking, versus not smoking, attenuated negative affect, as well as withdrawal and craving. Negative mood increased smoking reinforcement. However, neither actual nor expected nicotine dose had much influence on these responses; even those smokers receiving and expecting a denic cigarette reported attenuated negative affect. A follow-up comparison suggested that the sensory effects of smoke inhalation, but not the simple motor effects of smoking behavior, were responsible. Thus, sensory effects of smoke inhalation had a greater influence on relieving negative affect than actual or expected nicotine intake.

Placebo effects of tobacco smoking and other nicotine intake

Nicotine intake is a necessary but insufficient factor in maintaining tobacco smoking behavior, and nonpharmacological factors associated with smoking play a key role. Some of these factors may influence smoking behavior by eliciting placebo effects, or responses related specifically to the belief that one is consuming a drug. Greater knowledge of placebo effects of smoking would improve our understanding of factors that maintain smoking behavior, thereby aiding efforts to develop treatments to counter the influence of these factors. In addition, better understanding of placebo effects from other means of nicotine intake could help determine mechanisms of the therapeutic actions of nicotine replacement therapy, perhaps enhancing its efficacy in smoking cessation. Placebo effects of smoking or other nicotine intake have received little research attention. In this review, we first discuss common terms and methods of placebo research, especially the balanced-placebo design. We then examine the limited research directly assessing placebo effects of smoking and other nicotine intake, namely studies that manipulated instructions to subjects about the drug content of an ingested substance. Finally, we examine other studies relevant to gauging the likely magnitude of placebo smoking effects. In an effort to encourage more research on these placebo effects, we pay substantial attention to future directions. Among recommendations are testing the utility of the balanced-placebo design and other rigorously controlled designs, and including multiple measures of placebo effects in addition to self-report. Future research also should explore the moderating influences of the environmental context and of individual difference factors on placebo effects of smoking and other nicotine intake.

The influence of instructions and nicotine dose on the subjective and reinforcing effects of smoking.

Subjective and reinforcing effects of smoking a cigarette were examined within a 2 x 2 modified balanced-placebo design, which manipulated instructions about nicotine content (i.e., told regular nicotine vs. told low nicotine) and actual nicotine dose (given a regular nicotine brand vs. a denicotinized brand). Most ratings of the nicotine content and reward value of cigarettes were higher for those told regular nicotine versus told low nicotine, and for those given regular nicotine versus given low nicotine. Nicotine and instructions did not affect craving, withdrawal, or smoke-reinforced responding, but instructions affected the number of puffs earned for those given low nicotine (i.e., placebo effect). Thus, verbal information (instructions) can influence some responses to smoking consistent with the presence of placebo and antiplacebo effects.

The impact of imagining completed versus interrupted smoking on cigarette craving.

A brief imagery procedure was used to determine the effects of imagining completed versus interrupted smoking on self-reported craving, mood, autonomic functioning, and reaction time to an auditory probe. Cigarette smokers (N = 60) imagined actively participating in 3 types of scenarios in which they (a) engaged in smoking behavior, (b) attempted to smoke but were interrupted by a lack of cigarettes, and (c) were not confronted with smoking cues. Imagining both completed and interrupted smoking produced equivalent increases in craving compared with imagining neutral scenarios. Imagery of interrupted smoking was associated with higher heart rate and increased negative mood relative to the other scenario types, whereas imagery of completed smoking was associated with slower reaction time on the probe reaction-time task. Theoretical and methodological implications of the results are discussed.

IS SELF-EFFICACY FOR SMOKING ABSTINENCE A CAUSE OF, OR A REFLECTION ON, SMOKING BEHAVIOR CHANGE?

Social learning theory considers self-efficacy as a causal factor in behavior change. However, in line with behavioral theory, recent clinical research suggests self-efficacy ratings may reflect, rather than cause, behavior change. To test these two disparate views, self-efficacy was related to actual smoking abstinence on the next day (i.e., self-efficacy causes change), and abstinence status over 1 day was tested as a predictor of rated self-efficacy for quitting the next day (i.e., reflects change). All data were from two similar crossover studies evaluating the short-term effects of both placebo versus medication, nicotine patch (n = 209) or varenicline (n = 123), on smoking abstinence during week-long practice quit attempts. Placebo and active medication periods were separated by an ad lib smoking washout, and analyses were controlled for prior-days abstinence or self-efficacy values. Results were very consistent between studies in showing essentially bidirectional associations: daily self-efficacy predicted next-days abstinence, and current-days abstinence status predicted self-efficacy for abstinence the next day. However, secondary factors differentially predicted abstinence and, to a lesser extent, self-efficacy, between these two medication studies. These data provide some support for both social learning and behavioral theories of smoking behavior change, although self-efficacy may only briefly predict subsequent short periods of abstinence as assessed in these studies. Nonetheless, because self-efficacy has long been assumed to cause behavior change, including smoking cessation, the notion of self-efficacy as a reflection of recent smoking behavior change in these studies warrants greater attention in clinical research on smoking cessation treatment.