Stressor-elicited smoking and craving during a smoking cessation attempt.

Stressors can undermine smokers' attempts to quit smoking. Although contemporary theories and animal models support this idea, human research has struggled to demonstrate definitively the relationship between stressors and smoking. Researchers have employed more ecologically valid methods like ecological momentary assessment to address this question, but studies focusing explicitly on stressors remain sparse and findings inconsistent. The purpose of this study was to examine the effect of stressful event intensity on smoking and craving among cigarette smokers during a quit attempt. We conducted preregistered, complementary concurrent and prospective (i.e., 8-hour lag window between stressful event and outcomes) analyses to maximize statistical power and provide temporal ordering, respectively. We also conducted follow-up moderation (Lag × Stressful Event Intensity) analyses. We hypothesized that smokers would be more likely to report both smoking and craving as the intensity of stressful events increased. Cigarette smokers (N = 125; 77 male) were randomly assigned to take nicotine replacement therapy (NRT) or placebo and provided 4x daily self-reports during the first 2 weeks of a quit attempt. Stressful events increased craving and the probability of smoking in concurrent analyses, and lag moderated the effect of stressful event intensity in follow-up prospective lagged analyses. NRT reduced the probability of smoking but not craving and did not moderate the effect of stressful events on smoking or craving. This study supports a prospective relationship between stressful events and smoking/craving in situ and demonstrates that NRT does not reduce the impact of stressors on smoking or craving. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Controlling for caffeine in cardiovascular research: A critical review.

Caffeine, the most widely consumed drug in the world, exerts numerous effects on cardiovascular activity. Thus, it is important and advisable to control for caffeine consumption in studies examining caffeine and/or cardiovascular activity and reactivity. This paper 1) reviews the literature concerning caffeine's effects on cardiovascular parameters; 2) summarizes the widely varying protocols used to control for the drug in extant cardiovascular literature, and 3) provide guidelines for caffeine control procedures to minimize potentially confounding acute and withdrawal effects of the drug. An abstention period equal to the average half-life of the drug is recommended for creation of methodological controls for caffeine. Additional methodological recommendations are described concerning factors that moderate the half-life of caffeine. When feasible, researchers should consider and aim to control for caffeine's acute and extended psychophysiological effects. This understudied issue has fundamental implications for caffeine-related investigations and research in psychophysiology and behavioral medicine.

Probing for Neuroadaptations to Unpredictable Stressors in Addiction: Translational Methods and Emerging Evidence.

Stressors clearly contribute to addiction etiology and relapse in humans, but our understanding of specific mechanisms remains limited. Rodent models of addiction offer the power, flexibility, and precision necessary to delineate the causal role and specific mechanisms through which stressors influence alcohol and other drug use. This review describes a program of research using startle potentiation to unpredictable stressors that is well positioned to translate between animal models and clinical research with humans on stress neuroadaptations in addiction. This research rests on a solid foundation provided by three separate pillars of evidence from (a) rodent behavioral neuroscience on stress neuroadaptations in addiction, (b) rodent affective neuroscience on startle potentiation, and (c) human addiction and affective science with startle potentiation. Rodent stress neuroadaptation models implicate adaptations in corticotropin-releasing factor and norepinephrine circuits within the central extended amygdala following chronic alcohol and other drug use that mediate anxious behaviors and stress-induced reinstatement among drug-dependent rodents. Basic affective neuroscience indicates that these same neural mechanisms are involved in startle potentiation to unpredictable stressors in particular (vs. predictable stressors). We believe that synthesis of these evidence bases should focus us on the role of unpredictable stressors in addiction etiology and relapse. Startle potentiation in unpredictable stressor tasks is proposed to provide an attractive and flexible test bed to encourage tight translation and reverse translation between animal models and human clinical research on stress neuroadaptations. Experimental therapeutics approaches focused on unpredictable stressors hold high promise to identify, repurpose, or refine pharmacological and psychosocial interventions for addiction.

Using the threat probability task to assess anxiety and fear during uncertain and certain threat.

Fear of certain threat and anxiety about uncertain threat are distinct emotions with unique behavioral, cognitive-attentional, and neuroanatomical components. Both anxiety and fear can be studied in the laboratory by measuring the potentiation of the startle reflex. The startle reflex is a defensive reflex that is potentiated when an organism is threatened and the need for defense is high. The startle reflex is assessed via electromyography (EMG) in the orbicularis oculi muscle elicited by brief, intense, bursts of acoustic white noise (i.e., "startle probes"). Startle potentiation is calculated as the increase in startle response magnitude during presentation of sets of visual threat cues that signal delivery of mild electric shock relative to sets of matched cues that signal the absence of shock (no-threat cues). In the Threat Probability Task, fear is measured via startle potentiation to high probability (100% cue-contingent shock; certain) threat cues whereas anxiety is measured via startle potentiation to low probability (20% cue-contingent shock; uncertain) threat cues. Measurement of startle potentiation during the Threat Probability Task provides an objective and easily implemented alternative to assessment of negative affect via self-report or other methods (e.g., neuroimaging) that may be inappropriate or impractical for some researchers. Startle potentiation has been studied rigorously in both animals (e.g., rodents, non-human primates) and humans which facilitates animal-to-human translational research. Startle potentiation during certain and uncertain threat provides an objective measure of negative affective and distinct emotional states (fear, anxiety) to use in research on psychopathology, substance use/abuse and broadly in affective science. As such, it has been used extensively by clinical scientists interested in psychopathology etiology and by affective scientists interested in individual differences in emotion.