Nicotine dependence | |
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Other names | tobacco dependence; tobacco use disorder |
Video explanation |
Nicotine dependence[notes 1] is a state of dependence upon nicotine.[1] Nicotine dependence is a chronic, relapsing disease defined as a compulsive craving to use the drug, despite social consequences, loss of control over drug intake, and emergence of withdrawal symptoms.[5] Tolerance is another component of drug dependence.[6] Nicotine dependence develops over time as a person continues to use nicotine.[6] The most commonly used tobacco product is cigarettes, but all forms of tobacco use and e-cigarette use can cause dependence.[7][8] Nicotine dependence is a serious public health problem because it leads to continued tobacco use, which is one of the leading preventable causes of death worldwide, causing more than 8 million deaths per year.[7]
According to the World Health Organization, "Greater nicotine dependence has been shown to be associated with lower motivation to quit, difficulty in trying to quit, and failure to quit, as well as with smoking the first cigarette earlier in the day and smoking more cigarettes per day."[9] The WHO estimates that there are 1.1 billion smokers globally.[10] Of the 34 million smokers in the US in 2018, 74.6% smoked every day, indicating the potential for some level of nicotine dependence.[11] There is an increased frequency of nicotine dependence in people with anxiety disorders.[12]
There are different ways of measuring nicotine dependence.[3] Common dependence assessment scales for cigarette smokers are the Fagerström Test for Nicotine Dependence, the Diagnostic and Statistical Manual of Mental Disorders, the Cigarette Dependence Scale, the Nicotine Dependence Syndrome Scale, and the Wisconsin Inventory of Smoking Dependence Motives (WISDM).[3]
Nicotine is a parasympathomimetic stimulant[13] that attaches to nicotinic acetylcholine receptors in the brain.[14] Neuroplasticity within the brain's reward system, including an increase in the number of nicotine receptors, occurs as a result of long-term nicotine use and leads to nicotine dependence.[1] In contrast, the effect of nicotine on human brain structure (e.g. grey matter and white matter) is less clear.[15] There are genetic risk factors for developing dependence.[16] For instance, genetic markers for a specific type of nicotinic receptor (the α5-α3-β4 nicotine receptors) have been linked to increased risk for dependence.[16] Evidence-based treatments, including medications (nicotine replacement therapy, bupropion, varenicline, or cytisine) and behavioral counseling, can double or triple a smoker's chances of quitting successfully.[17]
D'Souza2011
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was invoked but never defined (see the help page).Bullen2014
was invoked but never defined (see the help page).Heavy nicotine use in the form of smoking tobacco has been linked to neuropathy (Brody, 2006), often manifesting as prefrontal gray matter atrophy (Gallinat et al., 2006; Zhang et al., 2011). Conversely, consumption of nicotine via smoking has been associated with higher white matter volume (Gazdzinski et al., 2005; Yu et al., 2011). Studies examining nicotine use via DTI have found similarly conflicting results. In chronic nicotine users, heavy consumption has been associated with lower FA (Lin et al., 2013) and higher FA (Paul et al., 2008), as well has both lower RD (Wang et al., 2017) and higher RD (Lin et al., 2013). The results of studies examining non-chronic, regular nicotine use are similarly split. Regular nicotine use has been associated with lower FA (Huang et al., 2013; Liao et al., 2011; Zhang et al., 2011) and higher FA (Hudkins et al., 2012; Wang et al., 2017). These seemingly conflicting nicotine results may be partly accounted for by the developmental stage in which it is consumed, with higher FA more commonly observed in younger nicotine users (Hudkins et al., 2012; Jacobsen et al., 2007). Alternatively, it maybe that the association between nicotine use and higher FA in adolescents is temporary, eventually leading to microstructural declines with chronic use. Future longitudinal studies could formally address this theory.
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