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Historical Overview of Theory
The study of the relationship between stress and nicotine required broad investigation to reveal the effects of smoking on mental health. Scholars have been observing and discovering facts that aimed to prove that nicotine intake can increase stress levels and lead to various neurological issues. History overview of literature gives an idea of how researchers investigated an arising issue at that time.
Researchers were concerned regarding the relationship between stress and nicotine as they could indicate the connection which required further explanation. Pomerleau (1987) emphasized the need for integration behavioral, physiological, and biochemical research (para. 1) to understand stress and nicotine intake better. He analyzed recent findings that involved nicotines effect on the hypophysealadrenal axis, which allowed to suggest that behavioral compensation for inhibited sensitivity due to increased nicotine use during stress exposure can occur, initiated by nicotine-stimulated corticosteroid release.
Pomerleau (1987) indicated that corticosteroids could decrease central nervous system sensibility, which could help with an anxiety reduction. However, he also considers that anxiety can be an epiphenomenon in such a case. Therefore, the lack of research at that time made the scholars understand the importance of further investigation of an issue to see the complexity of an arising problem.
The scholars observed patterns in behavior to reveal how stress and nicotine are connected. An article written by Parrott (1999) showed the possible connection between stress and nicotine, suggesting that nicotine can increase the stress level as worsening of the mood between smoking periods has been detected. This gave a basis to consider how stress relates to nicotine and whether it can exacerbate the stress. He also points out that nicotine depletion causes increased irritability and tension, which allows concluding that subject has been observed by scholars back at that time. However, it required far more investigation to reveal the connection and to understand the underlying mechanism.
As the research moved forward, scholars discovered the negative effects of smoking on human health, finding not only the relationship between stress and nicotine but also a relation to depressive episodes and neurological issues. Moreover, researchers investigated how secondhand smoke can influence mental health and conducted a relative study. Hamer, Stamatakis, and Batty (2010) considered smoking and non-smoking adults without a history of mental illness that was drawn from the Scottish Health Survey.
They concluded that high secondhand smoke exposure among people who do not smoke was linked to higher odds of psychological distress. Therefore, future risk of psychiatric issues development became possible to assume. The study that has proven the influence of nicotine on mental health showed a necessity to reduce the percentage of smokers. It also showed unfavorable consequences on the health of secondary smokers, which also emphasized the importance of the further investigation.
Contemporary Review of Theory
It is important to prove the presence of a connection between stress and nicotine to understand how such connection can impair certain functions in the brain. Kennedy et al. (2019) conducted a study to find and an association between stress resilience and the development of addictive health behaviors in the middle-aged group. He concluded that individuals with low-stress resistance in adolescence could result in addiction, such as nicotine or alcohol use, as higher nicotine dependence has been detected.
Even though the connection between stress and nicotine has been established, the influence of smoking may vary depending on the period of nicotine consumption and other factors. The study conducted by Elbejjani, Auer, and Dolui (2019) investigated how smoking relates to cerebral blood flow (CBF) as it has not been discovered thoughtfully. Cerebral blood flow is a blood supply to the brain for a particular period of time. Scholars aimed to find a connection between smoking behavior and arterial spin labeling in regions of the brain linked to dementia.
Researchers considered various characteristics such as status, age of a smoker, time of consumption, time after quitting, and tested the presence of an association between current and former smokers. Elbejjani et al. (2019) discovered that former-smokers had lower CBF in the parietal and occipital lobes, cuneus, precuneus, putamen, and insula (para. 3), where current smokers did not show low CBF. The findings allow concluding that the connection between smoking and CBF exists in regions that are associated with the addictive and cognitive processes, and such influence may vary depending on time and history of smoking exposure.
Understanding how short and long periods of smoking exposure influence the body and evaluating individuals with a short history of nicotine addiction can contribute to minimizing unfavorable effects of chronic nicotine use, which can help to discover neurobiological substances associated with nicotine dependence. For this purpose, Morris, Mielock, and Rao (2016) examined the sympathetic nervous system and hypothalamic-pituitary-adrenal axis responses to the Trier Social Stress Test among individuals with a short history of nicotine dependence. Scholars investigated salivary biomarkers in response to the test, behavioral measures of nicotine dependence and withdrawal, and indicators of recent smoking such as salivary cotinine and carbon monoxide in the breath. (Morris, Mielock & Rao, 2016).
The study found that people with a lower level of nicotine addiction had elevated cortisol responses to the stressors. Contrastingly, individuals with higher nicotine dependence levels did not show cortisol changes in response to the stressor. Therefore, different levels of nicotine dependence severity may involve various factors. Consequently, the stress response system can be impaired among individuals with a more severe level of dependency, which proves the need to find ways to prevent smoking behavior among individuals with a short period of smoking consumption.
The underlying neural mechanism can explain how nicotine intake relates to stress and other addictions such as alcohol. Ostroumov and Dani (2018) aimed to discover how stress and tobacco smoking can become a risk factor for alcoholism, stating that some of the actions in the brain converge onto the same mechanism for tobacco, stress, and alcohol even though they all have an individual effect on the brain.
Scholars explain that stress modulates alcohol-evoked plasticity via the release of signaling molecules that influence synaptic transmission (Ostroumov & Dani, 2018, para. 1). Nicotine can also activate such signaling molecules and cells, which leads to merging stress and nicotine into one plasticity mechanism that can influence alcohol self-administration. Therefore, a combination of stress and nicotine can lead to unfavorable consequences such as vulnerability to alcohol addiction as they initiate neural change that modifies alcohol-induced synaptic plasticity, which increases the risk of alcohol addiction.
To find the connection between nicotine and stress and to reveal how it can be connected to the development of mental issues, one should understand the primary mechanism of stress and depression development. Researchers found that stress alters neurotransmitters systems, such as monoamine (dopamine, serotonin, and noradrenalin), gamma-aminobutyric acid (GABA), and glutamatergic (Biala et al., 2018, para. 5).
Moreover, stress has been found to initiate changes in neural pathways that causes worsening of rewarded-related behaviours. A deficiency of particular neurotransmitters has been linked to depression and anxiety, and one of the most common hypotheses that aimed to explain its relation is monoamine neurotransmitter hypothesis. This hypothesis states that depletion in the levels of serotonin, norepinephrine, and/or dopamine may explain the onset of depression.
This hypothesis was presented based on antidepressant studies as agents that increase the level of the listed neurotransmitters in the brain, contribute to the eradication of depressive symptoms. However, the hypothesis does not explain the latency of response to antidepressants. (Boku et al., 2018). Even though antidepressant treatment has proven to be effective in some instances, convenient evidence on the connection between monoamine depletion and depression has not been found.
Stress sensitivity is considered to be a primary factor that contributes to the development of mood disorders. The study conducted by Morel et al. (2018) aims to prove that nicotine exposure increases stress sensitivity as nicotine and stress can induce long-lasting cellular adaptations within the dopamine system. Also, researchers are interested in discovering the physical effects of drug withdrawal, as most individuals report mood irritability, anxiety, and depressed mood. (Morel et al., 2018).
The interest allows concluding that nicotine can be associated with depressive symptoms that can lead to mental issues; however, the relationship between the substance and symptoms is complex. Even though nicotine can increase the possibility of depression development, adverse effects are observed as depression can also lead to the initiation of smoking. Moreover, drug withdrawal episodes are associated with people who had depression already, which can complicate the process of quitting for an individual.
Context for Study
Understanding the relationship between stress and nicotine helps to see a broader image of the global issue that society faces as nicotine creates global economic and health problems. Addiction is a chronic psychiatric disease, and stress is one of the leading factors of the addiction. Understanding the relationship between stress and nicotine is also critical due to the necessity to implement adequate management and prevent unfavorable consequences.
Health problems associated with smoking create not only physical but also mental issues, which impact the quality and duration of a persons life. A report by Action on Smoking and Health explains that smoking is the primary reason why people with mental illness have a life expectancy 10-20 years lower than the general population (Burki, 2016). Due to the relationship between stress, nicotine, and mental issues and the complexity of the subject, the research revealing the relationship between the components is critical. The connection between nicotine intake and mental illness proves the need to investigate an issue among all age groups to prevent unfavorable consequences among smokers.
Comparing historical and contemporary findings, one can conclude that the issue is being investigated. Even though underlying mechanisms remain unknown, many types of research that were conducted over the years revealed new information on how stress and nicotine are related. Such information helps to investigate an issue further to develop a plan for problem management, find new ways of dealing with the consequences of nicotine consumption.
As middle-aged groups experience undesirable effects, scholars focus on developing strategies to prevent use in adolescents and young adults to end the tobacco epidemic in the United States. Zhou et al. (2019) suggest addressing behavioral health challenges and increase access to mental health services. As psychological issues such as depression can lead to an increase in nicotine addiction, access to mental health institutions can be a valid solution.
Also, researchers should focus on the study of various groups to understand the group and population that is the most vulnerable to substances. For instance, Torres and ODell (2016) discovered that women are consuming more tobacco products, which is associated with various factors. Firstly, women are more susceptible to anxiety disorders than men, which initiates smoking behavior as they use nicotine to cope with stress. Secondly, women associate continuous tobacco use with anxiety-reducing effects, which prevents them from quitting. Finally, women experience more stress during withdrawal than men. Listed factors give a basis to conclude that stress contributes not only to the initiation of tobacco use but also to the relapse during abstinence, which means that the process of quitting can be more challenging for women, which requires further investigation.
Aside from biological factors that influence the initiation of smoking, certain social factors can contribute to the development of smoking behavior. Jahnel, Ferguson, Shiffman, and Schüz (2019) discovered how socioeconomic disadvantage induce indirect effects on smoking caused by daily stress. The social disadvantage has been measured by educational achievement, income, and race; cigarettes per day have indicated effects on smoking. Researchers used Ecological Momentary Assessment methods for stress measurement. The experiment showed a significant increase in stress exposure among lower educated African American smokers, which led to a rise in tobacco use.
Similarly, Advances in Life Course Research examined students to discover various reasons for individuals to initiate, continue, or quit smoking and discover how social connections influence such behavior and revealed the importance of social connection to the initiation of smoking. (Thomeer, Hernandez, Umberson, & Thomas, 2019). Therefore, the behavioral mechanism of nicotine addiction is also essential, and one should be able to see factors related not only to the initiation of smoking and stress but also to other related factors.
Nicotine intake and issues associated with it creates an economic burden and significant concern for health institutions. Research that reveals the connection between the components such as stress and nicotine is crucial to get a full image of the issue to develop effective strategies toward its eradication. Healthcare providers and researchers should take a closer look at revealing the connection between nicotine addiction and mental illness as it remains unclear whether addiction causes psychological issues or vice versa. Understanding underlying mechanisms, examining groups of people that are exposed the most, and investigating an issue further can contribute to the development of a healthier and safer environment.
References
Biala, G., Pekala, K., Boguszewska-Czubara, A., Michalak, A., Kruk-Slomka, M., Grot, K., & Budzynska, B. (2018). Behavioral and biochemical impact of chronic unpredictable mild stress on the acquisition of nicotine conditioned place preference in rats. Molecular neurobiology, 55(4), 3270-3289.
Boku, S., Nakagawa, S., Toda, H., & Hishimoto, A. (2018). Neural basis of major depressive disorder: beyond monoamine hypothesis. Psychiatry and clinical neurosciences, 72(1), 3-12.
Burki, T. K. (2016). Smoking and mental health. The Lancet Respiratory Medicine, 4(6), 437.
Elbejjani, M., Auer, R., Dolui, S., Jacobs Jr, D. R., Haight, T., Goff Jr, D. C.,& & Launer, L. J. (2019). Cigarette smoking and cerebral blood flow in a cohort of middle-aged adults. Journal of Cerebral Blood Flow & Metabolism, 39(7), 1247-1257.
Hamer, M., Stamatakis, E., & Batty, G. D. (2010). Objectively assessed secondhand smoke exposure and mental health in adults: cross-sectional and prospective evidence from the Scottish Health Survey. Archives of general psychiatry, 67(8), 850-855.
Jahnel, T., Ferguson, S. G., Shiffman, S., & Schüz, B. (2019). Daily stress as link between disadvantage and smoking: an ecological momentary assessment study. BMC public health, 19(1), 1284.
Kennedy, B., Chen, R., Fang, F., Valdimarsdottir, U., Montgomery, S., Larsson, H., & Fall, K. (2019). Low stress resilience in late adolescence and risk of smoking, high alcohol consumption and drug use later in life. J Epidemiol Community Health, 73(6), 496-501.
Morel, C., Fernandez, S. P., Pantouli, F., Meye, F. J., Marti, F., Tolu, S.,& & Moretti, M. (2018). Nicotinic receptors mediate stress-nicotine detrimental interplay via dopamine cells activity. Molecular psychiatry, 23(7), 1597-1605.
Morris, M. C., Mielock, A. S., & Rao, U. (2016). Salivary stress biomarkers of recent nicotine use and dependence. The American journal of drug and alcohol abuse, 42(6), 640-648.
Ostroumov, A., & Dani, J. A. (2018). Convergent neuronal plasticity and metaplasticity mechanisms of stress, nicotine, and alcohol. Annual review of pharmacology and toxicology, 58, 547-566.
Parrott, A. C. (1999). Does cigarette smoking cause stress?. American Psychologist, 54(10), 817.
Pomerleau, C. S., & Pomerleau, O. F. (1987). The effects of a psychological stressor on cigarette smoking and subsequent behavioral and physiological responses. Psychophysiology, 24(3), 278-285.
Thomeer, M. B., Hernandez, E., Umberson, D., & Thomas, P. A. (2019). Influence of social connections on smoking behavior across the life course. Advances in Life Course Research, 42, 100294.
Torres, O. V., & ODell, L. E. (2016). Stress is a principal factor that promotes tobacco use in females. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 65, 260-268.
Zhou, S., Willison, C., & Jarman, H. (2019). Smoking and mental health among college students: Reconceptualizing tobacco control policies. In APHAs 2019 Annual Meeting and Expo (Nov. 2-Nov. 6). American Public Health Association.
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