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Nicotine deprivation increases pain intensity, neurogenic inflammation, and mechanical hyperalgesia among daily tobacco smokers.

ABSTRACT: An evolving reciprocal model posits that pain and tobacco smoking behavior interact in the manner of a positive feedback loop, resulting in greater pain and the maintenance of nicotine dependence. There is also reason to believe that abstaining from smoking may increase pain during the early stages of smoking cessation. The goal of this study was to test the effects of nicotine deprivation on experimental pain reactivity. Daily tobacco cigarette smokers (N = 165; 43% female) were randomized to either extended nicotine deprivation (12-24 hr smoking abstinence), minimal deprivation (2 hr smoking abstinence), or continued smoking conditions, prior to undergoing pain induction via topical capsaicin. As hypothesized, results indicated that extended deprivation (relative to continued smoking) increased capsaicin-induced pain intensity ratings, neurogenic inflammation, and mechanical hyperalgesia, thus implicating both central and peripheral mechanisms of action in the effects of smoking abstinence on pain reactivity. Pain intensity ratings were also positively correlated with nicotine withdrawal symptoms, and exploratory analyses suggest that pain sensitivity may increase with duration of smoking abstinence. Collectively, these findings indicate that smokers may experience a variety of negative pain-related sequelae during the early stages of a quit attempt. Future research should examine pain as a consequence or correlate of the nicotine withdrawal syndrome, and determine whether smokers may benefit from tailored cessation interventions that account for nicotine deprivation-induced amplification of pain. (PsycINFO Database Record

SUBMITTER: Ditre JW

PROVIDER: S-EPMC6089646 | biostudies-literature | 2018 Aug

REPOSITORIES: biostudies-literature

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Nicotine deprivation increases pain intensity, neurogenic inflammation, and mechanical hyperalgesia among daily tobacco smokers.

Ditre Joseph W JW Zale Emily L EL LaRowe Lisa R LR Kosiba Jesse D JD De Vita Martin J MJ

Journal of abnormal psychology 20180521 6

An evolving reciprocal model posits that pain and tobacco smoking behavior interact in the manner of a positive feedback loop, resulting in greater pain and the maintenance of nicotine dependence. There is also reason to believe that abstaining from smoking may increase pain during the early stages of smoking cessation. The goal of this study was to test the effects of nicotine deprivation on experimental pain reactivity. Daily tobacco cigarette smokers (N = 165; 43% female) were randomized to e ...[more]

PMID: 29781659

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Project description:IntroductionThe high smoking prevalence amongst individuals with psychiatric disorders constitutes a major public health disparity. Negative reinforcement models of addiction posit that severe tobacco withdrawal symptoms, related to the affective vulnerabilities of these smokers, may thwart their quitting smoking successfully. However, relatively few studies have prospectively examined the effects of nicotine deprivation on withdrawal symptoms in these groups.MethodsThis study compared the level of withdrawal symptoms both before and after nicotine deprivation in those diagnosed with posttraumatic stress disorder (PTSD) or major depressive disorder (MDD) and in those without psychiatric diagnoses. Participants were US veterans who smoked (≥10 cigarettes/day) and met diagnostic criteria for PTSD (n = 38), MDD (n = 43), or no psychiatric diagnosis ("controls" n = 44). Participants attended study visits before and during 48-hour nicotine deprivation to report tobacco withdrawal symptoms. Analyses evaluated withdrawal symptom levels (baseline and during nicotine deprivation) and the change in symptoms related to nicotine deprivation and compared (1) participants with a psychiatric diagnosis versus controls, and (2) participants with PTSD versus MDD.ResultsContrary to hypotheses, nicotine deprivation produced greater increases in most withdrawal symptoms amongst controls than in those with psychiatric diagnoses. Compared with controls, those with PTSD or MDD reported elevated symptom levels both before and after tobacco deprivation for most withdrawal symptoms.ConclusionsThese findings suggest that chronically high levels of distress and craving, rather than acute increases in withdrawal symptoms because of nicotine deprivation, may account for the quitting difficulties of those with comorbid conditions such as PTSD and MDD.ImplicationsSevere tobacco withdrawal may account for the higher quitting difficulties of smokers with either posttraumatic stress disorder (PTSD) or major depressive disorder (MDD). Paradoxically, this study showed that individuals with no psychiatric diagnosis had greater increases in tobacco withdrawal severity because of nicotine deprivation than did those with either PTSD or MDD. Those with either PTSD or MDD showed high stable levels of withdrawal symptom severity both before and during two days of abstinence, suggesting that their quitting difficulties may be related to their chronically high levels of distress rather than nicotine deprivation per se.

Project description:IntroductionVariation in CYP2A6, the primary enzyme responsible for nicotine metabolism, is associated with nicotine dependence, cigarette consumption, and abstinence outcomes in smokers. The impact of CYP2A6 activity on nicotine reinforcement and tobacco cue-reactivity, mechanisms that may contribute to these previous associations, has not been fully evaluated.Aims and methodsCYP2A6 activity was indexed using 3 genetic approaches in 104 daily smokers completing forced-choice and cue-induced craving tasks assessing nicotine reinforcement and tobacco cue-reactivity, respectively. First, smokers were stratified by the presence or absence of reduced/loss-of-function CYP2A6 gene variants (normal vs. reduced metabolizers). As nicotine metabolite ratio (NMR) is a reliable biomarker of CYP2A6 activity, our second and third approaches used additional genetic variants identified in genome-wide association studies of NMR to create a weighted genetic risk score (wGRS) to stratify smokers (fast vs. slow metabolizers) and calculate a wGRS-derived NMR.ResultsControlling for race and sex, normal metabolizers (vs. reduced) selected a greater proportion of puffs from nicotine-containing cigarettes (vs. denicotinized) on the forced-choice task (p = .031). In confirmatory analyses, wGRS-based stratification (fast vs. slow metabolizers) produced similar findings. Additionally, wGRS-derived NMR, which correlated with actual NMR assessed in a subset of participants (n = 55), was positively associated with the proportion of puffs from nicotine-containing cigarettes controlling for race and sex (p = .015). None of the CYP2A6 indices were associated with tobacco cue-reactivity in minimally deprived smokers.ConclusionsFindings suggest increased nicotine reinforcement is exhibited by smokers with high CYP2A6 activity, which may contribute to heavier smoking and poorer cessation outcomes previously reported in faster metabolizers.ImplicationsCYP2A6 activity is a key determinant of smoking behavior and outcomes. Therefore, these findings support the targeting of CYP2A6 activity, either therapeutically or as a clinically relevant biomarker in a precision medicine approach, for tobacco use disorder treatment.

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Nicotine deprivation increases pain intensity, neurogenic inflammation, and mechanical hyperalgesia among daily tobacco smokers.

Publications

Nicotine deprivation increases pain intensity, neurogenic inflammation, and mechanical hyperalgesia among daily tobacco smokers.

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