How cigarette smoking may increase the risk of anxiety symptoms and anxiety disorders: A critical review of biological pathways

Deakin University School of Medicine Barwon Health, Geelong, Victoria, Australia.
Brain and Behavior (Impact Factor: 2.24). 05/2013; 3(3):302-26. DOI: 10.1002/brb3.137
Source: PubMed


Multiple studies have demonstrated an association between cigarette smoking and increased anxiety symptoms or disorders, with early life exposures potentially predisposing to enhanced anxiety responses in later life. Explanatory models support a potential role for neurotransmitter systems, inflammation, oxidative and nitrosative stress, mitochondrial dysfunction, neurotrophins and neurogenesis, and epigenetic effects, in anxiety pathogenesis. All of these pathways are affected by exposure to cigarette smoke components, including nicotine and free radicals. This review critically examines and summarizes the literature exploring the role of these systems in increased anxiety and how exposure to cigarette smoke may contribute to this pathology at a biological level. Further, this review explores the effects of cigarette smoke on normal neurodevelopment and anxiety control, suggesting how exposure in early life (prenatal, infancy, and adolescence) may predispose to higher anxiety in later life. A large heterogenous literature was reviewed that detailed the association between cigarette smoking and anxiety symptoms and disorders with structural brain changes, inflammation, and cell-mediated immune markers, markers of oxidative and nitrosative stress, mitochondrial function, neurotransmitter systems, neurotrophins and neurogenesis. Some preliminary data were found for potential epigenetic effects. The literature provides some support for a potential interaction between cigarette smoking, anxiety symptoms and disorders, and the above pathways; however, limitations exist particularly in delineating causative effects. The literature also provides insight into potential effects of cigarette smoke, in particular nicotine, on neurodevelopment. The potential treatment implications of these findings are discussed in regards to future therapeutic targets for anxiety. The aforementioned pathways may help mediate increased anxiety seen in people who smoke. Further research into the specific actions of nicotine and other cigarette components on these pathways, and how these pathways interact, may provide insights that lead to new treatment for anxiety and a greater understanding of anxiety pathogenesis.

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    • "Epidemiological and clinical research has provided substantial evidence of an association of smoking with depression and anxiety disorders (Chaiton et al., 2009; Cosci et al., 2010; Morrell and Cohen, 2006; Moylan et al., 2013; Zvolensky et al., 2005). "
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    • "Smoking may itself lead to increased anxiety, anxiety may increase smoking rates, and both may be influenced by shared vulnerability factors in both adults and adolescents (Moylan et al., 2013). Structural brain changes (e.g., reduced gray matter volumes in the prefrontal cortices, reduced volumes of the frontal lobes, temporal lobes, and the cerebellum) seen in smokers overlap to some degree with neuroimaging changes observed with anxiety disorders (Moylan et al., 2013). "
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    • "There is now extensive evidence that poor diet quality is a risk for adolescent depression (110), and new data suggests that maternal diet influences the mental health of offspring (111). Similarly, smoking increases the risk of mood and anxiety disorders, and appears to influence similar biological pathways (112, 113). Parents and care givers of younger children need to be informed of the potential impact that a healthy lifestyle can have in mitigating mood-related symptoms and problematic behaviors. "
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