Nortriptyline for smoking cessation: a review.

Departments of Psychiatry, Psychology, and Family Practice, University of Vermont, Burlington, VT 05401, USA.
Nicotine & Tobacco Research (Impact Factor: 2.81). 09/2005; 7(4):491-9. DOI: 10.1080/14622200500185298
Source: PubMed

ABSTRACT This article reviews the efficacy of nortriptyline for smoking cessation based on a meta-analysis of the Cochrane Library. Six placebo-controlled trials have shown nortriptyline (75-100 mg) doubles quit rates (OR = 2.1). Between 4% and 12% of smokers dropped out because of adverse events, but no serious adverse events occurred. The efficacy of nortriptyline did not appear to be related to its antidepressant actions. Nortriptyline is an efficacious aid to smoking cessation with a magnitude of effect similar to that for bupropion and nicotine replacement therapies. Whether nortriptyline produces serious side effects at these doses in healthy, nondepressed smokers remains unclear because it has been tested in only 500 smokers. The finding that nortriptyline and bupropion are effective for smoking cessation but that selective serotonin-reuptake inhibitors are not suggests that dopaminergic or adrenergic, but not serotonergic, activity is important for cessation efficacy. Until further studies can verify a low incidence of significant adverse events, nortriptyline should be a second-line treatment for smoking cessation.

  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Smoking is a significant health concern and strongly correlated with clinical depression. Depression is associated with decreased extracellular NE concentrations in brain. Smokers may be self-medicating and alleviating their depression through nicotine stimulated norepinephrine (NE) release. Several antidepressants inhibit NE transporter (NET) function, thereby augmenting extracellular NE concentrations. Antidepressants, such as bupropion, also inhibit nicotinic receptor (nAChR) function. The current study determined if a recently discovered novel nAChR antagonist, N,N'-dodecane-1,12-diyl-bis-3-picolinium dibromide (bPiDDB), inhibits nicotine-evoked NE release from superfused rat hippocampal slices. Previous studies determined that bPiDDB potently (IC(50)=2 nM) inhibits nicotine-evoked striatal [(3)H]dopamine (DA) release in vitro, nicotine-evoked DA release in nucleus accumbens in vivo, and nicotine self-administration in rats. In the current study, nicotine stimulated [(3)H]NE release from rat hippocampal slices (EC(50)=50 microM). bPiDDB inhibited (IC(50)=430 nM; I(max)=90%) [(3)H]NE release evoked by 30 microM nicotine. For comparison, the nonselective nAChR antagonist, mecamylamine, and the alpha7 antagonist, methyllycaconitine, also inhibited nicotine-evoked [(3)H]NE release (IC(50)=31 and 275 nM, respectively; I(max)=91% and 72%, respectively). Inhibition by bPiDDB and mecamylamine was not overcome by increasing nicotine concentrations; Schild regression slope was different from unity, consistent with allosteric inhibition. Thus, bPiDDB was 200-fold more potent inhibiting nAChRs mediating nicotine-evoked [(3)H]DA release from striatum than those mediating nicotine-evoked [(3)H]NE release from hippocampus.
    Biochemical pharmacology 08/2009; 78(7):889-97. DOI:10.1016/j.bcp.2009.07.010 · 4.65 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The study was a randomized placebo-controlled trial testing whether fluoxetine selectively enhances cessation for smokers with a history of depression. Euthymic smokers with (H+, n = 109) or without (H-, n = 138) a history of major depression received 60 mg fluoxetine or placebo plus group behavioral quit-smoking treatment for 12 weeks. Fluoxetine initially enhanced cessation for H+ smokers (p = .02) but subsequently impaired cessation regardless of depressive history. Six months after quit date, fluoxetine-treated participants were 3.3 times more likely to be smoking (p = .02). Further research is warranted to determine why high-dose fluoxetine produces continuing effects that oppose tobacco abstinence.
    Journal of Consulting and Clinical Psychology 03/2007; 75(1):85-94. DOI:10.1037/0022-006X.75.1.85 · 4.85 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Why and how to help smoking patients in cessation of tobacco use The lecture is devoted to physicians’ possibilities in providing smoking cessation help (PSCH). Because of insufficient SCH in the former USSR countries, a large proportion of smokers stop being smokers due to deaths and not quitting smoking. Physicians are more likely to ask about smoking those patients who are older and have chronic diseases while younger smokers would more likely benefit. Stop smoking advice from health worker is an evidence-based intervention. Physicians should keep up-to-date records of patients’ smoking status, advise smokers to stop, and offer them assistance with doing so. Recent evidence-based data regarding smoking cessation is reviewed. Physician’s activities, content of brief interventions, diagnostics of nicotine dependence and readiness to quit, and pharmacotherapy for smoking cessation are described. Андреева Т.И. Зачем и как следует помогать пациентам-курильщикам в отказе от курения / Т.И.Андреева // Вестник современной клинической медицины. – 2010. – Т.3. – Приложение 2. – С. 134-146.