Stress and smoking
Stress is a complex and natural response that triggers physiological and psychological changes in the body, often preparing it to deal with various challenges. The relationship between stress and smoking is intricate; while nicotine from tobacco products can provide immediate relief from anxiety, it also activates stress responses in the body, increasing levels of hormones like epinephrine and cortisol. This paradox means that while smokers may perceive nicotine as a stress reliever, it can actually exacerbate stress and anxiety over time, creating a cycle of dependence.
Chronic exposure to stress can lead individuals to seek relief through smoking, as the immediate dopamine release from nicotine can temporarily improve mood and concentration. However, this effect is fleeting, and as tolerance builds, smokers often find themselves needing to consume more nicotine to achieve the same relief. Additionally, the adverse health effects of smoking can further contribute to stress, creating a vicious circle of addiction and reliance on nicotine for emotional regulation.
Breaking this cycle often requires developing new coping strategies to manage stress, and nicotine replacement therapies or medications can assist those looking to quit. Understanding the dual role of stress in smoking addiction highlights the importance of addressing both psychological and physical aspects for effective smoking cessation.
Stress and smoking
DEFINITION: Stress is tenuously associated with smoking addiction and relapse, but the complex connections between smoking and stress remain unresolved. Nicotine, the primary addictive substance in cigarettes, nicotine vapes, and other inhaled tobacco products, appears to both ease and instigate stress in a conflicting manner.
Stress Responses
Stress is a natural, reactive response involving physical and psychological changes that helps the body adapt to a variety of events and exposures. Stress responses trigger the hypothalamic-pituitary axis (HPA), which regulates multiple hormones simultaneously and connects their actions to chemicals in the nervous system.
During an acute stress event, hormonal and chemical fluctuations facilitate tension in the body; epinephrine, also known as adrenaline, and cortisol peak and cause increased heart rate and blood pressure, sweating, muscle tension, headache, and rapid respiration. Cortisol guides an inflammatory response and can counteract immune system functions.
Stress is useful when these processes activate the body’s defenses or increase the adrenaline necessary to overcome a challenge. Sometimes, stress can be motivating and encourage positive change. However, acute stress can produce neurochemical responses that result in psychological changes that can lead to short- and long-term emotional instability and anxiety. With chronic stress exposure, deeper problems develop: excessive stimulation of cortisol release causes obesity, heart disease, depression, and other chronic diseases. Chronic stress increases the likelihood that a person will turn to substance abuse in an attempt to counteract the body’s hyper-reactive state; drug and food abuse can relieve immediate psychological anxiety through dopamine release but cannot stop the long-term physical or psychological damages of stress.
Nicotine and Stress
Smoking physically stresses the body immediately and in the long term, worsening other conditions and increasing anxiety. When inhaled nicotine enters the bloodstream, the HPA is triggered to release epinephrine and cortisol—the same physical response to everyday stressors. Thus, heart rate, respiratory rate, and blood pressure all increase after nicotine use.
Tolerance to the nicotine effect on the HPA builds as smoking continues; although the physical effects wane, the levels of cortisol and epinephrine in the body remain high with chronic HPA activation. The result is a blunted natural stress reaction that prevents the body from responding appropriately to other stressors.
Nicotine also increases glucose secretion and prevents insulin release, causing chronically high blood sugar concentrations that stress organ functions. Oxidative stress reactions to nicotine throughout the body cause damage to cells and change cellular deoxyribonucleic acid (DNA), which impairs the immune response, worsens existing diseases, and increases inflammation.
In the central nervous system, nicotine use is rewarded by an apparent and immediate relief of anxiety through neurochemical changes. When tobacco is inhaled, nicotine enters the brain within ten seconds to stimulate dopamine, acetylcholine, and norepinephrine. Through these actions, nicotine quickly induces pleasure, improves mood, and enhances concentration and focus. Each cigarette provides hundreds of rapidly fleeting nicotine hits that, in turn, cause short bursts of euphoria. The subjective psychological boost hides the physical impairment and is short-lived as the body develops tolerance to the fleeting neurologic highs.
Although individuals who smoke generally believe that nicotine reduces their stress, repeated dopamine stimulation provides negative reinforcement of cigarette use. Chronic smoking leads to the compulsion of greater use to try to minimize the anxiety that results from lower dopamine levels when the nicotine effect wears off between cigarettes.
Stress Fuels Nicotine Addiction
Smoking and nicotine addiction are aggravated by additional outside sources of stress, as individuals report higher cigarette use during times of known external stressors. In addition, the human body develops chronic physical health problems from nicotine damage that facilitates stress responses.
Individuals who smoke claim to have more psychological stress than nonsmokers, and stress is provided as a reason for smoking because of its apparent relaxing effects. However, no empirical evidence supports a consistent difference in stress between those who do and those who do not use cigarettes until after smoking begins. Nicotine heightens baseline stress between cigarette use, and normal, lower stress signals are only attained when cigarette use is resumed.
Stress is a vital body mechanism for protection, but it contributes to smoking addiction and the frequency of relapse, as people use nicotine to relieve immediate sensations of anxiety. When nicotine is chronically present, the nervous system and HPA adapt to it as a stressor, even more nicotine is needed to respond to daily stress.
Stress itself increases the craving for nicotine as tolerance builds, and anxiety encourages drug-seeking behavior. As the central nervous system adapts to frequent and repeated norepinephrine and dopamine stimulation, more nicotine is necessary to obtain the same pleasure, focus, and stress-relief responses. Stress relief is harder to achieve as smoking continues. Thus, stress increases the amount, frequency, duration, and intensity of cravings for nicotine.
Withdrawal from nicotine is probably the best example of the connection between stress and smoking habits. Although physical withdrawal from nicotine can cause increased appetite and headaches, the psychological reactions of withdrawal are the key causes of stress and ultimate nicotine dependence. Irritability, attention problems, sleep disturbances, and tobacco cravings are common and are signs of the damaging changes from smoking, not proof of nicotine’s stress-relieving effects.
Without the rapid and repeated bursts of nicotine, anxiety and physical stress become evident. Nicotine abstinence breaks the cycle of stress-induced smoking and smoking-induced stress, but it ultimately requires learning new coping skills to manage stress without smoking. Nicotine replacement therapy (NRT) can help individuals break this cycle. NRT products are available over the counter, like nicotine patches, gum, and lozenges, and by prescription, like nicotine inhalers. Non-nicotine prescription options include bupropion (Wellbutrin) and varenicline (Chantix), which are often combined with a nicotine option to decrease cravings and withdrawal symptoms and increase the success of individuals who want to stop smoking.
Bibliography
Cougle, J. R., et al. “The Role of Comorbidity in Explaining the Associations between Anxiety Disorders and Smoking.” Nicotine and Tobacco Research, vol. 12, 2010, pp. 355–64.
Guarnotta, Emily. "The Connection between Stress and Substance Abuse." Oxford Treatment Center, 7 Mar. 2023, oxfordtreatment.com/substance-abuse/co-occurring-disorders/stress. Accessed 20 Sept. 2024.
Kim, S. J., et al. "The Impact of Smoking Cessation Attempts on Stress Levels." BMC Public Health, vol. 19, no. 267, 2019. doi.org/10.1186/s12889-019-6592-9.
Lawless, Michael H., et al. "Perceived Stress and Smoking-Related Behaviors and Symptomatology in Male and Female Smokers." Addictive Behaviors, vol. 51, 26 July 2015, pp. 80–83, doi:10.1016/j.addbeh.2015.07.011. Accessed 1 Dec. 2022.
"Nicotine Use and Stress." Truth Initiative, 2022, truthinitiative.org/research-resources/emerging-tobacco-products/nicotine-use-and-stress. Accessed 20 Sept. 2024.
Perski, Olga, et al. "Associations between Smoking to Relieve Stress, Motivation to Stop and Quit Attempts Across the Social Spectrum: A Population Survey in England." PLoS ONE, vol. 17, no. 5, 2022. doi.org/10.1371/journal.pone.0268447.
Richards, J. M., et al. “Biological Mechanisms Underlying the Relationship between Stress and Smoking: State of the Science and Directions for Future Work.” Biological Psychology, vol. 88, no. 1, 2011, pp. 1–12.
Wang, Wendy, and Paul Taylor. “Smokers Can’t Blow Off Stress.” Pew Research Center Social & Demographic Trends, 8 Apr. 2009, www.pewresearch.org/social-trends/2009/04/08/smokers-cant-blow-off-stress. Accessed 20 Sept. 2024.