Brain Nicotinic Acetylcholine Receptor Availability and Response to Smoking Cessation Treatment

Brody, Arthur L.; Mukhin, Alexey G.; Mamoun, Michael; Luu, Trinh; Neary, Meaghan K.; Liang, Lidia; Shieh, Jennifer; Sugar, Catherine A.; Rose, Jed E.; Mandelkern, M.

doi:10.1001/jamapsychiatry.2014.138

Cited by 40 publications

(32 citation statements)

References 93 publications

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“…For demographic and smoking-related information, the Smokers' Profile Form was administered, as in past studies of smoking cessation treatment. [41][42][43] Smoking behavior was assessed with an exhaled carbon monoxide (CO) level (MicroSmokerlyzer, Bedfont Scientific Ltd, Kent, United Kingdom) and the Fagerström Test for Nicotine Dependence (FTND). 44,45 While some investigators have questioned the use of the standard FTND in smokers with schizophrenia, 46,47 there is considerable support in the literature for its use.…”

Section: Baseline and Treatment-related Assessmentsmentioning

confidence: 99%

Combination Extended Smoking Cessation Treatment Plus Home Visits for Smokers With Schizophrenia: A Randomized Controlled Trial

Brody

Zorick

Hubert

et al. 2016

NICTOB

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Introduction: The majority of people with schizophrenia have a diagnosis of tobacco dependence during their lifetime. A major obstacle to reducing the burden of cigarette smoking in this population is that these smokers have lower quit rates when undergoing standard treatment compared to smokers with no mental illness. We sought to determine if combination extended treatment (COMB-EXT) and home visits (HV) would lead to improved outcomes in smokers with schizophrenia. Methods: Thirty-four cigarette smokers with schizophrenia completed either COMB-EXT with HV, COMB-EXT without HV, or treatment as usual (TAU) (random assignment). COMB-EXT consisted of group cognitive-behavioral therapy (CBT), bupropion, nicotine patch, and nicotine lozenge, which were initiated within 2 weeks and continued for 26 weekly visits. HV consisted of biweekly visits to the home with assessment of secondhand smoke (SHS) exposure and brief behavioral therapy with participants and others in the home environment. TAU consisted of group CBT plus serial single or combination medication trials as per standard care. Results: Smokers with schizophrenia who received COMB-EXT (with or without HV) had greater reductions in cigarettes per day than those treated with TAU (both ps < .01). In addition, 7-day point prevalence abstinence rates for the three groups were 45%, 20%, and 8%, respectively, which was significantly higher for COMB-EXT plus HV than TAU (χ 2 (1) = 4.8, p = .03). Groups did not differ significantly in the number of adverse events, and HV were easily scheduled. Conclusion: COMB-EXT improves outcomes for smokers with schizophrenia. HV appeared to provide additional benefit for smoking cessation in this treatment-resistant population. Implications: The clear benefit found here of rapidly initiated, combination, extended treatment over TAU suggests that aggressive and extended treatment should be considered in clinical practice for smokers with schizophrenia. Furthermore, HV to address SHS exposure showed initial promise for assisting smokers with schizophrenia in maintaining abstinence, indicating that this intervention may be worthy of future research.

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Section: Baseline and Treatment-related Assessmentsmentioning

confidence: 99%

Combination Extended Smoking Cessation Treatment Plus Home Visits for Smokers With Schizophrenia: A Randomized Controlled Trial

Brody

Zorick

Hubert

et al. 2016

NICTOB

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“…In an exploratory analysis, pre-treatment markers for nAChR density had trend-level indications that lower nAChR density in three brain regions studied was associated with a greater likelihood of quitting. In the second study [147], using the same PET method, a relatively large sample of smokers underwent double-blind, placebo-controlled treatment with nicotine patch. Smokers with lower pretreatment nAChR density (a possible marker of less severe nAChR upregulation) across all brain regions studied were more likely to quit smoking, regardless of treatment group.…”

Section: Brain Imaging Biomarkersmentioning

confidence: 99%

Biomarkers of Response to Smoking Cessation Pharmacotherapies: Progress to Date

et al. 2015

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For the past thirty years, research examining predictors of successful smoking cessation treatment response has focused primarily on clinical variables, such as levels of tobacco dependence, craving, and self-efficacy. Recent research, however, has begun to determine biomarkers (such as genotype, nicotine and metabolite levels, and brain imaging findings) that may have utility in predicting smoking cessation. For genotype, genes associated with nicotinic acetylcholine receptors (nAChRs) and related proteins have been found to predict response to first line medications (e.g., nicotine replacement therapy [NRT], bupropion, or varenicline) or quitting over time without a controlled treatment trial. For nicotine and metabolite levels, function of the CYP 2A6 liver enzyme, which can be assessed with the nicotine metabolite ratio or via genotype, has been found to predict response, with slow nicotine metabolizers having less severe nicotine dependence and a greater likelihood of quitting with NRT than normal metabolizers. And for brain imaging, decreased activation of brain regions associated with emotion regulation and increased connectivity in emotion regulation networks, increased responsiveness to pleasant cues, and altered activation with the Stroop effect have been found in smokers who quit with the first-line medications listed above or counseling. In addition, our group recently demonstrated that lower pre-treatment brain nAChR density is associated with a greater chance of quitting smoking with NRT or placebo. Several of these studies found that specific biomarkers may provide additional information for predicting response beyond subjective symptom or rating scale measures, thereby giving an initial indication that biomarkers may, in the future, be useful for guiding smoking cessation treatment intensity, duration, and type.

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“…[13] The endogenous opioid system also plays some role in nicotine dependence. [14] Other than this, nicotine acts through glutamine, gamma-aminobutyric acid (GABA), dopamine, cannabinoid, and adenosine receptor modulation.…”

Section: Discussionmentioning

confidence: 99%

Nicotine dependence in resistant schizophrenia: A compensation for trihexyphenidyl dependence or just comorbidity

Kar

2015

Int J Nutr Pharmacol Neurol Dis

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A 42-year-old male, suffering from schizophrenia with nicotine dependence and on regular treatment, had reported the overuse of trihexyphenidyl (40-50 mg/day) for the last 2 years in a dependence pattern, which was temporally correlated with increased consumption of nicotine over the same time frame. The patient used to report withdrawal symptoms and craving for trihexyphenidyl, when it was not available. This case report attempts to discover the possible links between nicotine dependence and trihexyphenidyl dependence in schizophrenia with emphasis on the compensatory measure to counter the imbalance in cholinergic system.

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Brain Nicotinic Acetylcholine Receptor Availability and Response to Smoking Cessation Treatment

Cited by 40 publications

References 93 publications

Combination Extended Smoking Cessation Treatment Plus Home Visits for Smokers With Schizophrenia: A Randomized Controlled Trial

Combination Extended Smoking Cessation Treatment Plus Home Visits for Smokers With Schizophrenia: A Randomized Controlled Trial

Biomarkers of Response to Smoking Cessation Pharmacotherapies: Progress to Date

Nicotine dependence in resistant schizophrenia: A compensation for trihexyphenidyl dependence or just comorbidity

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