| Nicotine dependence | |
|---|---|
| Other names | tobacco dependence; tobacco use disorder, cigarette dependence |
| Video of medical explanation of nicotine dependence and its health effects | |
| Complications | Health effects of tobacco |
| Prognosis | 10-year shorter lifespan[notes 1] |
| Prevalence | 1.2 billion tobacco users globally (2022)[2] |
| Deaths | 8 million per year (2023)[3] |
Nicotine dependence[notes 2] is a state of substance dependence on nicotine.[4] It is a chronic, relapsing disease characterized by a compulsive craving to use the drug despite social consequences, loss of control over drug intake, and the emergence of withdrawal symptoms.[8] Tolerance is another component of drug dependence.[9] Nicotine dependence develops over time as an individual continues to use nicotine.[9] While cigarettes are the most commonly used tobacco product, all forms of tobacco use—including smokeless tobacco and e-cigarette use—can cause dependence.[3][10] Nicotine dependence is a serious public health problem because it leads to continued tobacco use and the associated negative health effects. Tobacco use is one of the leading preventable causes of death worldwide, causing more than 8 million deaths per year and killing half of its users who do not quit.[3][11] Current smokers are estimated to die an average of 10 years earlier than non-smokers.[1]
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."[12] The WHO estimates that there were 1.24 billion tobacco users globally in 2022[update], with the number projected to decline to 1.20 billion in 2025.[2] Of the 34 million smokers in the United States in 2018, 74.6% smoked every day, indicating the potential for some level of nicotine dependence.[13] There is an increased incidence of nicotine dependence in individuals with psychiatric disorders, such as anxiety disorders and substance use disorders.[14][15]
Various methods exist for measuring nicotine dependence.[6] Common assessment scales for cigarette smokers include the Fagerström Test for Nicotine Dependence, the Diagnostic and Statistical Manual of Mental Disorders criteria, the Cigarette Dependence Scale, the Nicotine Dependence Syndrome Scale, and the Wisconsin Inventory of Smoking Dependence Motives.[6]
Nicotine is a parasympathomimetic stimulant[16] that binds to nicotinic acetylcholine receptors in the brain.[17] 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.[4] In contrast, the effect of nicotine on human brain structure (e.g., gray matter and white matter) is less clear.[18] Genetic risk factors contribute to the development of dependence.[19] For instance, genetic markers for specific types of nicotinic receptors (the α5–α3–β4 nicotinic receptors) have been linked to an increased risk of dependence.[19] Evidence-based treatments—including medications such as nicotine replacement therapy, bupropion, varenicline, or cytisine, and behavioral counseling—can double or triple a smoker’s chances of successfully quitting.[20]
D'Souza2011 was invoked but never defined (see the help page).PiperMcCarthy2006 was invoked but never defined (see the help page).AkermanBrunette2015 was invoked but never defined (see the help page).SG1988 was invoked but never defined (see the help page).MoylanJacka2012 was invoked but never defined (see the help page).BeebeMyers2012 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.
Saccone2010 was invoked but never defined (see the help page).Fiore2008 was invoked but never defined (see the help page).
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