Cigarette smoking, nicotine dependence and anxiety disorders: A systematic review of population-based, epidemiological studies

BMC Medicine (Impact Factor: 7.25). 10/2012; 10(1):123. DOI: 10.1186/1741-7015-10-123
Source: PubMed


Multiple studies have demonstrated that rates of smoking and nicotine dependence are increased in individuals with anxiety disorders. However, significant variability exists in the epidemiological literature exploring this relationship, including study design (cross-sectional versus prospective), the population assessed (random sample versus clinical population) and diagnostic instrument utilized.

We undertook a systematic review of population-based observational studies that utilized recognized structured clinical diagnostic criteria (Diagnostic and Statistical Manual of Mental Disorders (DSM) or International Classification of Diseases (ICD)) for anxiety disorder diagnosis to investigate the relationship between cigarette smoking, nicotine dependence and anxiety disorders.

In total, 47 studies met the predefined inclusion criteria, with 12 studies providing prospective information and 5 studies providing quasiprospective information. The available evidence suggests that some baseline anxiety disorders are a risk factor for initiation of smoking and nicotine dependence, although the evidence is heterogeneous and many studies did not control for the effect of comorbid substance use disorders. The identified evidence however appeared to more consistently support cigarette smoking and nicotine dependence as being a risk factor for development of some anxiety disorders (for example, panic disorder, generalized anxiety disorder), although these findings were not replicated in all studies. A number of inconsistencies in the literature were identified.

Although many studies have demonstrated increased rates of smoking and nicotine dependence in individuals with anxiety disorders, there is a limited and heterogeneous literature that has prospectively examined this relationship in population studies using validated diagnostic criteria. The most consistent evidence supports smoking and nicotine dependence as increasing the risk of panic disorder and generalized anxiety disorder. The literature assessing anxiety disorders increasing smoking and nicotine dependence is inconsistent. Potential issues with the current literature are discussed and directions for future research are suggested.

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    • "Recent studies have suggested that individuals with uni-or bipolar illness have increased ACh levels throughout the brain when they are acutely depressed (Saricicek et al, 2012). A number of studies have also addressed the possibility that nAChRs could be involved in depression, because depressed individuals are twice as likely to smoke, have a harder time quitting, and can develop symptoms of depression during withdrawal (for reviews see Moylan et al, 2012; Picciotto et al, 2012). Despite controversy about the connection that may exist between nAChRs and mood regulation, many studies have shown that decrease ACh signaling through nAChRs can have antidepressant-like properties in mice (Mineur et al, 2009; Mineur et al, 2007) and can improve symptoms of depression in some clinical studies (George et al, 2008). "
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    ABSTRACT: Electrophysiological and neurochemical studies implicate cholinergic signaling in the basolateral amygdala in behaviors related to stress. Both animal studies and human clinical trials suggest that drugs that alter nicotinic acetylcholine receptor (nAChR) activity can affect behaviors related to mood and anxiety. Clinical studies also suggest that abnormalities in cholinergic signaling are associated with major depressive disorder, whereas pre-clinical studies have implicated both β2 subunit-containing (β2*) and α7 nAChRs in the effects of nicotine in models of anxiety- and depression-like behaviors. We therefore investigated whether nAChR signaling in the amygdala contributes to stress-mediated behaviors in mice. Local infusion of the non-competitive non-selective nAChR antagonist mecamylamine or viral-mediated down-regulation of the β2 or α7 nAChR subunit into the amygdala all induced robust anxiolytic- and antidepressant-like effects in several mouse behavioral models. Further, whereas α7 nAChR subunit knockdown was somewhat more effective at decreasing anxiety-like behavior, only β2 subunit knockdown decreased resilience to social defeat stress and c-fos immunoreactivity in the basolateral amygdala. In contrast, α7, but not β2, subunit knockdown effectively reversed the effect of increased ACh signaling in a mouse model of depression. These results suggest that signaling through β2* nAChRs is essential for baseline excitability of the basolateral amygdala, and a decrease in signaling through β2 nAChRs alters anxiety- and depression-like behaviors even in unstressed animals. In contrast, stimulation of α7 nAChRs by acetylcholine may mediate the increased depression-like behaviors observed during the hypercholinergic state observed in depressed individuals.Neuropsychopharmacology accepted article preview online, 16 October 2015. doi:10.1038/npp.2015.316.
    Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology 10/2015; DOI:10.1038/npp.2015.316 · 7.05 Impact Factor
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    • "For example, smoking cessation needs to be routinely communicated as part of clinical care, with individuals being offered evidence-based smoking cessation interventions when appropriate (Berk, 2007). Smoking cigarettes not only has harmful physical affects, but may also increase the risk for mental health disorders (Choi et al., 1997; Wu and Anthony, 1999; Johnson and Breslau, 2006; Klungsoyr et al., 2006; Moylan et al., 2012). In both unipolar depression and bipolar disorder, smoking has a negative effect on symptom severity (Jamal et al., 2012) and may also interfere with treatment response (Berk et al., 2008; Dodd et al., 2010). "
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    Asia-Pacific Psychiatry 09/2015; 7(4). DOI:10.1111/appy.12212 · 0.63 Impact Factor
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    • "Nicotine consumption through tobacco products is highly comorbid with mood disorders, including depression, anxiety and irritability; however the connection between nicotine use and behavioral regulation remains unclear and is still debated (Moylan et al., 2012). For instance, the overall incidence of smoking in depressed patients is twice as high as in the general population (Glassman et al., 1990) and the rate of smoking relapse is greater in patients with depression (Covey et al., 1998). "
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    Neuropharmacology 01/2015; 96(Pt B). DOI:10.1016/j.neuropharm.2014.12.028 · 5.11 Impact Factor
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