Tuesday, June 26, 2012

What is the relationship between stress and smoking?


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.


Acute stress is useful when these processes activate the body’s defenses or increase the adrenaline necessary to overcome a challenge. However, neurochemical responses can 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 DNA (deoxyribonucleic acid), 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 smokers generally believe that nicotine reduces their stress, the 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 smokers report higher cigarette use during times of known external stressors. In addition, the body of a smoker develops chronic physical health problems from nicotine damage that facilitate stress responses.


Smokers 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 empiric evidence supports a consistent difference in stress between smokers and nonsmokers until after smoking begins. Nicotine heightens baseline stress between cigarette use, and smokers only attain normal, lower stress signals when cigarettes are used.


Stress is a vital body mechanism for protection, but it contributes to smoking addiction and the frequency of relapse, as smokers 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. Relief of stress 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 a sign 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.




Bibliography


Cougle, J. R., et al. “The Role of Comorbidity in Explaining the Associations between Anxiety Disorders and Smoking.” Nicotine and Tobacco Research 12 (2010): 355–64. Print.



Mendelsohn, C. “Women Who Smoke: A Review of the Evidence.” Australian Family Physician 40 (2011): 403–7. Print.



“Psychological Stress and Cancer: Questions and Answers.” Cancer.gov. Natl. Cancer Inst., 29 Apr. 2008. Web. 8 Apr. 2012.



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 88.1 (2011): 1–12. Print.



Wang, Wendy, and Paul Taylor. “Smokers Can’t Blow Off Stress.” Pew Research Center Social & Demographic Trends. Pew Research Center, 8 Apr. 2009. Web. 9 Nov. 2015.

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