Influence of Nicotine Metabolism Ratio on [11C]-(+)-PHNO PET Binding in Tobacco Smokers

Ciano, Patricia Di; Tyndale, Rachel F.; Mansouri, Esmaeil; Hendershot, Christian S.; Wilson, Alan A.; Lagzdins, Dina; Houle, Sylvain; Boileau, Isabelle; Foll, Bernard Le

doi:10.1093/ijnp/pyx119

Cited by 9 publications

(5 citation statements)

References 58 publications

(107 reference statements)

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“…Specifically, following cigarette smoking, a 12% to 15% reduction in D2 and D3 receptor binding potential was observed compared to control conditions [ 46 ]. These findings are likely influenced by genetics, where, during abstinence, slow metabolizers of nicotine had lower [ 11 C]PHNO-binding potential compared to fast metabolizers within the D2 regions of the striatum [ 47 ]. Interestingly, there was no change in [ 11 C]PHNO-binding potential in the striatum of nicotine-dependent individuals following the presentation of tobacco-associated cues [ 48 ].…”

Section: Discussionmentioning

confidence: 99%

Food Addiction and Tobacco Use Disorder: Common Liability and Shared Mechanisms

et al. 2020

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As food addiction is being more commonly recognized within the scientific community, parallels can be drawn between it and other addictive substance use disorders, including tobacco use disorder. Given that both unhealthy diets and smoking are leading risk factors for disability and death, a greater understanding of how food addiction and tobacco use disorder overlap with one another is necessary. This narrative review aimed to highlight literature that investigated prevalence, biology, psychology, and treatment options of food addiction and tobacco use disorder. Published studies up to August 2020 and written in English were included. Using a biopsychosocial lens, each disorder was assessed together and separately, as there is emerging evidence that the two disorders can develop concurrently or sequentially within individuals. Commonalities include but are not limited to the dopaminergic neurocircuitry, gut microbiota, childhood adversity, and attachment insecurity. In addition, the authors conducted a feasibility study with the purpose of examining the association between food addiction symptoms and tobacco use disorder among individuals seeking tobacco use disorder treatment. To inform future treatment approaches, more research is necessary to identify and understand the overlap between the two disorders.

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Section: Discussionmentioning

confidence: 99%

Food Addiction and Tobacco Use Disorder: Common Liability and Shared Mechanisms

et al. 2020

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“…These differences, however, were not observed among participants without a history of smoking, underscoring the possible gene (fast vs. slow nicotine metabolism) Â environment (exposure to nicotine) interaction. In addition, PET imaging research by Di Ciano and colleagues (96) showed that slower metabolizers had fewer D2-type dopamine receptors than faster metabolizers, drawing a link between NMR and dopaminergic signaling. While further research is required to fully delineate the relationships between the NMR and brain circuitry, the existing evidence strongly suggests that personalized approaches have implications for smoking cessation treatments that extend beyond acute withdrawal.…”

Section: What Are Potential Mechanisms Through Which the Nmr May Operate To Personalize Smoking Cessation Treatments?mentioning

confidence: 99%

The Use of the Nicotine Metabolite Ratio as a Biomarker to Personalize Smoking Cessation Treatment: Current Evidence and Future Directions

Siegel

Lerman²,

Flitter

et al. 2020

Cancer Prevention Research

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The nicotine metabolite ratio (NMR), a genetically informed biomarker of rate of nicotine metabolism, has been validated as a tool to select the optimal treatment for individual smokers, thereby improving treatment outcomes. This review summarizes the evidence supporting the development of the NMR as a biomarker of individual differences in nicotine metabolism, the relationship between the NMR and smoking behavior, the clinical utility of using the NMR to personalize treatments for smoking cessation, and the potential mechanisms that underlie the relationship between NMR and smoking cessation. We conclude with a call for additional research necessary to determine the ultimate benefits of using the NMR to personalize treatments for smoking cessation. These future directions include measurement and other methodologic considerations, disseminating this approach to at-risk subpopulations, expanding the NMR to evaluate its efficacy in predicting treatment responses to e-cigarettes and other noncigarette forms of nicotine, and implementation science including costeffectiveness analyses.See all articles in this Special Collection Honoring Paul F. Engstrom, MD, Champion of Cancer Prevention

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“…No differences were found in post-cigarette [ 11 C]-(+)-PHNO BP ND between fast and slow metabolizers. 21 However, this could be explained by a number of methodological differences between this study and our study including a less sensitive analysis method and a lengthy delay between cigarette smoking and PET scanning in the work by Di Ciano and colleagues. Fast metabolizers experience greater daily fluctuations in nicotine concentrations which may explain why they experience greater reward from smoking.…”

Section: Discussionmentioning

confidence: 79%

“… 52 , or no group differences in smoking-induced dopamine release, for example, Ref. 21 . The parameter presented herein,

is analogous to BP ND in the literature because it evaluates the change in the level of dopamine binding.…”

Section: Discussionmentioning

confidence: 99%

Nicotine Patch Alters Patterns of Cigarette Smoking-Induced Dopamine Release: Patterns Relate to Biomarkers Associated With Treatment Response

Zakiniaeiz

Liu

Gao

et al. 2022

Nicotine &Amp; Tobacco Research

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Introduction Tobacco smoking is a major public health burden. The first line pharmacological treatment for tobacco smoking is nicotine replacement therapy (e.g., the nicotine patch (NIC)). Nicotine acts on nicotinic-acetylcholine receptors on dopamine terminals to release dopamine in the ventral and dorsal striatum encoding reward and habit formation, respectively. To better understand treatment efficacy, a naturalistic experimental design combined with a kinetic model designed to characterize smoking-induced dopamine release in vivo, was used. Methods Thirty-five tobacco smokers (16 female) wore a nicotine patch (21mg, daily) for 1-week and a placebo patch (PBO) for 1-week in a randomized, counter-balanced order. Following 1-week under NIC and then overnight abstinence, smokers participated in a 90-minute [ 11C]raclopride positron emission tomography scan and smoked a cigarette while in the scanner. Identical procedures were followed for the PBO scan. A time-varying kinetic model was used at the voxel level to model transient dopamine release peaking instantaneously at the start of the stimulus and decaying exponentially. Magnitude and spatial extent of dopamine release were estimated. Smokers were subcategorized by nicotine dependence level and nicotine metabolism rate. Results Dopamine release magnitude was enhanced by NIC in ventral striatum and diminished by NIC in dorsal striatum. More-dependent smokers activated more voxels than the less-dependent smokers under both conditions. Under PBO, fast metabolizers activated more voxels in ventral striatum and fewer voxels in dorsal striatum compared to slow metabolizers. Conclusions These findings demonstrate that the model captured a pattern of transient dopamine responses to cigarette smoking which may be different across smoker subgroup categorizations. Implications This is the first study to show that nicotine patch alters highly localized patterns of cigarette smoking-induced dopamine release and that levels of nicotine dependence and nicotine clearance rate contribute to these alterations. This current work included a homogeneous subject sample with regards to demographic and smoking variables, as well as a highly sensitive model capable of detecting significant acute dopamine transients. The findings of this study add support to recent identification of biomarkers for predicting the effect of nicotine replacement therapies on dopamine function which could help refine clinical practice for smoking cessation.

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Influence of Nicotine Metabolism Ratio on [11C]-(+)-PHNO PET Binding in Tobacco Smokers

Cited by 9 publications

References 58 publications

Food Addiction and Tobacco Use Disorder: Common Liability and Shared Mechanisms

Food Addiction and Tobacco Use Disorder: Common Liability and Shared Mechanisms

The Use of the Nicotine Metabolite Ratio as a Biomarker to Personalize Smoking Cessation Treatment: Current Evidence and Future Directions

Nicotine Patch Alters Patterns of Cigarette Smoking-Induced Dopamine Release: Patterns Relate to Biomarkers Associated With Treatment Response

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