Abstract

Tobacco smoking is associated with high morbidity and mortality rates. It harms virtually every organ of the body, causes several health problems (e.g., cancer, abdominal obesity, cardiovascular diseases, and pulmonary diseases), and exposes the body to a high risk of death. Tobacco smoking also has effects on stress and hunger. On the other hand, tobacco smoking cessation has several health benefits, although short-term withdrawal symptoms may accompany the effort to quit. Several factors militate against efforts to quit tobacco smoking. In this review, I examined the evidence on the effects of tobacco smoking and its cessation on stress, hunger, and health and provided insight and motivation to overcome several essential factors interfering with quitting smoking. The study also highlighted evidence of many beneficial effects of tobacco smoking cessation. Additionally, the study underscored numerous treatment programs that have been developed to help tobacco smokers quit smoking and handle cravings and nicotine withdrawal symptoms. The study concludes that the benefits of tobacco smoking cessation outweigh its negative impacts. These benefits cannot be compared to the elusive benefits of tobacco smoking, which eventually become harmful to health.

Keywords: Tobacco; Smoking; Cigarette; Addiction; Cessation; Health; Hunger; Stress

Introduction

Tobacco smoking is a behavior that easily ends in addiction. This is because smoking is embedded in the social context; tobacco smoke contains nicotine, which has addictive properties, and people find it extremely difficult to deal with withdrawal symptoms when trying to break their smoking habit (Butcher et al., 2014). Smoking addiction involves continuously engaging in smoking behavior despite adverse outcomes, unsuccessful attempts at quitting, significant interference with personal work, tolerance, and withdrawal (Lewis, 2014). Unfortunately, studies have shown that, in addition to nicotine, tobacco smoke also contains more than 4000 chemical substances, such as carbon monoxide. Like nicotine, a poisonous alkaloid, most of these chemicals have various harmful effects on the body, including reduction of appetite, higher levels of stress and anxiety, poor health, and a high mortality rate (Papathanasiou et al., 2014).

Statistically, tobacco smoking is the most common cause of preventable deaths and diseases in the developed world. One in seven deaths is associated with tobacco consumption (Naqvi et al., 2007; Papathanasiou et al., 2014). These findings are worrisome because many people are chronic smokers and struggle to quit smoking even when it has caused them serious illnesses, such as lung cancer. Studies have also shown that most smokers who attempt to quit do not use recommended cessation methods, and most of them relapse within the first eight days after quitting (CDC, 2008). Only 4% – 7% of adults who do not use recommended cessation methods are likely to be successful in quitting smoking (CDC, 2008). The purpose of this study is to provide a comprehensive explanation of the potential effects of smoking addiction and cessation on stress, health, and appetite using several literature reviews. This explanation will provide essential insight regarding helping clients quit smoking tobacco. I will also briefly highlight numerous treatment programs that have been developed to help smokers quit smoking and handle nicotine withdrawal symptoms.

Effects of Smoking Addiction and Cessation on Stress

In response to stress, the body activates the sympathetic-adrenomedullary (SAM) system and the hypothalamus-pituitary-adrenal (HPA) system (Butcher et al., 2014). Activating both systems leads to the production of stress hormones (e.g., cortisol, adrenaline, and noradrenaline), the release of the body’s store of energy, and subsequent readiness of the body for fight or flight. Along the SAM axis, the hypothalamus activates the sympathetic nervous system (SNS), which stimulates the core adrenal gland known as the adrenal medulla. Consequently, the adrenal medulla releases the hormones adrenaline (epinephrine) and noradrenaline (norepinephrine), which increase the heart rate, breathing, muscle tension, concentration of attention on the stressors, etc. Along the HPA axis, the hypothalamus stimulates the anterior pituitary gland by secreting corticotropin-releasing hormone (CRH). The anterior pituitary gland, in turn, releases the adrenocorticotrophic hormone (ACTH), which stimulates the outer adrenal gland known as the adrenal cortex. The adrenal cortex secretes hormones, such as glucocorticoid (known as cortisol in humans), which also prepares the body for action by, among other things, increasing the blood sugar level and metabolism (Breedlove & Watson, 2018; Butcher et al., 2014). However, long-term activation of SAM and HPA systems in response to prolonged stress is dangerous to health because it keeps a high level of stress hormones in circulation, causing a reduced body immune system.

Nicotine is a strong activator of both SAM and HPA axes (Richards et al., 2011; Rohleder & Kirschbaum, 2006). Along the HPA axis, it binds to cholinergic receptors on the locus coeruleus and hypothalamus, inducing the release of CRH and subsequent production of cortisol. Along the SAM axis, smoking causes the release of adrenaline and noradrenaline, as well as an increase in systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate, and respiration (Richards et al. 2011). In other words, among smokers, there is a tendency for increased levels of stress hormones (e.g., cortisol and adrenaline) and physiological responses (e.g., increased heart rates and respiratory rates). On this note, researchers observed that similar to behavioral stressors, cigarette smoking stresses the body by eliciting physiological responses, including an increase in cortisol release, heart rate, breathing, arterial blood pressure, and forearm blood flow (Richards et al., 2011; Tsuda et al.,1996). Hence, smoking addiction has been associated with stress responsiveness. For instance, Kirschbaum et al. (1992) reported a constant increase in cortisol levels compared to nonsmokers. In this study, they collected saliva samples of ten female smokers and ten female nonsmokers at 20-minute intervals over a 12-hour period. They observed that smokers showed a significant elevation of cortisol levels compared to nonsmokers. Similarly, Steptoes and Ussher (2006) reported that cigarette smoking is associated with a sharp elevation of cortisol levels. In the first part of their study, they collected saliva samples of 196 middle-aged men and women on working and weekend days and found that cortisol levels were significantly higher in smokers. In the second part of the study, they monitored the cortisol levels of 112 smokers who ceased smoking for about six weeks. Conversely, they found that smoking cessation was associated with abrupt decreases in salivary cortisol.

Further research has also shown that chronic smoking causes a blunted responsiveness in the HPA axis. For instance, Richards et al. (2011) noted that tolerance to the action of the HPA system builds as smoking continues. In this situation, the stress hormones, such as cortisol, adrenaline, and noradrenaline, continue to be high but with an acute tolerance to the physiological effects (e.g., increased heart rates and breathing) due to the activation of these axes. Hence, the result is blunted HPA axis stress reactions, preventing the body from responding appropriately to other stressful stimuli. According to Richards et al. (2011), this physiological tolerance is associated with decreased reinforcing effects of smoking. Such blunted responsiveness to stress has been associated with the disinhibition of inflammatory pathways and consequent stimulation of cardiovascular morbidity and mortality among smokers (Rohleder & Kirschbaum, 2006).

Furthermore, tobacco smoking also causes increased oxidative stress, an imbalance between free radicals (oxygen-containing molecules) and antioxidants in the body. Tobacco smoke contains a large number of free radicals and weakens the antioxidant defensive mechanism that regulates these large number of smoking-mediated free radicals (Papathanasiou et al., 2014). Consequently, chronic smoking leads to increased oxidative stress, which causes damage to cells and changes cellular deoxyribonucleic acid (DNA), impairing the immune response, worsening existing diseases, and increasing inflammation (Hoey & Van, 2019). In addition, smoking addiction leads to chronic high blood sugar accumulation that stresses organ functions. As already seen, nicotine activates both SAM and HPA systems, causing the release of stress hormones, such as cortisol, adrenalin, and noradrenaline. This response strongly hampers insulin production, which reduces glucose catabolism (Papathanasiou et al., 2014). Hence, researchers have observed that smoking addiction leads to chronic accumulation of glucose in the body, which stresses organ functions and results in many health problems (Hoey & Van, 2019; Papathanasiou et al., 2014).

Additionally, tobacco smoking cessation leads to withdrawal symptoms, including anxiety, increased appetite, restlessness, anger, depressed mood, irritability, frustration, attention problems, and insomnia (APA, 2013). These symptoms are very stressful and can even cause clinically significant impairment in social, occupational, or other important areas of functioning (APA, 2013). In their study on the effects of recent smoking and temporary cessation, Tsuda et al. (1996) found that compared to recent smokers, the abstinent group had mood deterioration, a heightened perception of stress during the task, high ratings of restlessness, the urge to smoke, and impairment of behavioral performance. According to Hoey and Van (2019), physiological reactions to tobacco withdrawal are the major causes of stress and nicotine dependence. Because withdrawal symptoms due to smoking cessation (e.g., anxiety, increased appetite, restlessness, anger, depressed mood, irritability, frustration, attention problem, insomnia) are very stressful and can cause clinically significant impairment in social, occupational, or other important areas of functioning, smokers are discouraged from quitting smoking. This is because negative reinforcement occurs when resuming tobacco smoking eliminates or reduces unpleasant feelings. Such negative reinforcing effects often contribute to physical dependence (Carlson & Birkett, 2017). Although withdrawal symptoms and negative reinforcement cannot completely explain tobacco addiction and physical dependence, how knowledge of such phenomena is a source of power to quitting smoking

Effect of Smoking Addiction and Cessation on Health

As indicated earlier, tobacco smoking is a leading cause of preventable deaths and diseases worldwide. The World Health Organization listed tobacco as one of the greatest public health threats the world has ever faced (WHO, 2021). Although nicotine and CO are the leading culprits of the harmful effects of smoking, other chemical substances in tobacco smoke are also dangerous to health. For instance, empirical evidence has shown that 60 out of 4000 or more chemical substances in tobacco smoke are carcinogenic, leading to cancer of the lungs, mouth, throat (pharynx), voice-box (larynx), esophagus, pancreas, stomach, and bladder, kidney, cervix, and ureter (Papathanasiou et al., 2014). These chemical substances can also cause cellular genetic mutations that make the body very vulnerable to cancer.

Both nicotine and CO in tobacco smoke are implicated in diseases of the heart and the blood vessels or cardiovascular diseases), which include constriction of the coronary artery, heart attack, cerebrovascular disease or stroke, peripheral vascular disease, and aortic aneurysm (DʼAlessandro et al., 2012; Papathanasiou et al., 2014). For instance, tobacco smoking leads to cardiovascular diseases by causing atherosclerosis. Smoking lowers high-density lipoproteins (HDL or good cholesterol), increases low-density lipoproteins (LDL or bad cholesterol), and causes a build-up of bad cholesterol, fats, and other substances (or plaque) in the aorta and coronary arteries (DʼAlessandro et al., 2012; Papathanasiou et al., 2014). This plague build-up leads to atherosclerosis, the thickening of artery walls, leading the arteries to become narrower and slowing down the blood flow. Ultimately, several cardiovascular diseases ensue, including arteriosclerosis (also known as coronary artery disease or coronary heart disease), a condition affecting the arteries that supply the heart with blood; cerebrovascular diseases (stroke); and loss of brain function when blood flow to the brain is interrupted. Atherosclerosis due to smoking is also associated with myocardial infarction, hypercoagulable state, stable angina, peripheral arterial disease, and peripheral vascular disease (Tonstad & Johnston, 2006). Peripheral arterial disease and peripheral vascular disease occur when the thickened and narrowed arteries reduce blood flow to the pelvis, arms, hands, legs, hands, and feet. Similarly, smoking prevents insulin production, which leads to glucose accumulation in the body. In turn, excess fatty tissue glucose is converted to triglycerides, whose high concentration contributes to arteriosclerosis. Therefore, smoke-induced insulin resistance is a significant risk factor for the development of arteriosclerosis, which increases the risk of stroke, heart attack, cardiac arrest, and other cardiovascular diseases (Papathanasiou et al., 2014).

Furthermore, smoking causes respiratory diseases. On this note, Cummings (1982) emphasized that smokers frequently develop severe and prolonged upper respiratory tract infections, bronchitis, and emphysema. Buttressing this fact, Roleder and Kirschbaum (2006) remarked that smokers show signs of low-grade systematic inflammation and are vulnerable to chronic airway inflammation. Although this issue seems to contradict the anti-inflammatory effect of nicotine, they explained that the blunted HPA system responsiveness to acute psychological stress is associated with airway inflammation in smokers. Similarly, Papathanasiou et al. (2014) reported that tobacco smoking results in intravascular inflammation, promoting atherosclerosis and cardiovascular diseases. Other ways tobacco smoking is harmful to health include: CO-induced reduction of oxygen-carrying capacity of the blood, which leads to increased red cell mass; impotence (as a result of atherosclerotic changes in the hypogastric-cavernous arterial bed); endangering the health and life of fetuses among pregnant women who smoke endanger the health and life of their fetuses (e. g., low birth weight, placental abruption, spontaneous abortion, premature births, and low neonatal Apgar score); and peptic ulcer (Cummings, 1982; Mosharraf et al., 2019; Tonstad & Johnston, 2006). It is also worth noting that smoking is associated with health risk behaviors. In their study with 93 adolescents, Busen et al. (2001) found that it was easier for current smokers to use alcohol and marijuana than nonsmokers.

Effects of Smoking Addiction and Cessation on Appetite

According to Chao et al. (2017), tobacco smoking is highly associated with obesity-related behavior, including an unhealthy diet. It is a common belief that smoking suppresses appetite and increases satiety. This view is not far from the truth. According to Jo et al. (2005), nicotine inhibits melanin-concentrating hormone (MCH) neurons of the lateral hypothalamus (LH), thus suppressing appetite. MCH and orexin (or hypocretin) are two major peptides produced by neurons in the LH that have been implicated in stimulating hunger and reducing metabolic rate. Thus, they increase appetite and preserve the body’s energy storage (Carlson & Birkett, 2017; Jo et al., 2005). Both peptides are known as orexigens. Additionally, Miyata et al. (1999) found that nicotine administration into lateral hypothalamic (LH) circuits significantly decreases food intake by modulating the neurotransmitters serotonin and dopamine. 

However, several studies have shown that smokers have more frequent cravings for food high in fat than nonsmokers and so have a significant risk of abdominal obesity. For instance, Pepino et al. (2009) reported that current smokers have more high-fat food cravings and intakes than former smokers among women. In this study, 229 women completed the Food Craving Inventory designed to measure the frequency of overall food cravings and cravings for specific types of food, including high-fat foods, starches, sweets, and fast-food fats. Also, the height and weight of participants were measured, and their body mass index (BMI) was computed. The result of the study indicated that current smokers craved foods higher in fat and carbohydrates than never-smokers. Surprisingly, never-smokers craved high-fat and starchy foods more than former smokers. Thus, this means that craving for high-fat foods among smokers is related to the effects of smoking as such (Pepino et al., 2009). Using more diverse and larger participants (n = 712) who completed questionnaires on food cravings, dietary intake, smoking history, and weight and height, Chao et al. (2017) reported the same effect of smoking on appetite. After controlling for depression, stress, BMI, and demographic factors, they observed that compared to never and former smokers, current smokers more frequently crave and consume foods that are sweet, starchy, and high in fat. Hence, the authors concluded that smokers have a greater risk of abdominal fat accumulation than nonsmokers. In addition, Dare et al. (2015) reported that heavier smokers had the risk of abdominal obesity than light smokers.

On the other hand, smoking cessation causes increased appetite. One explanation of this phenomenon is that the body has reversed its ability to suppress appetite. On this note, Carlson and Birkett (2017) maintained that the absence of nicotine in the brain resumes the stimulation of MCH, increasing appetite and decreasing metabolic rate. Another explanation is the possibility of reinforcement substitution in which rewards of food replace rewards of smoking (Harris et al., 2016). Additionally, the view that taste buds and smell are reactivated after quitting smoking, causing increased food intake, is an impelling explanation for this phenomenon. Consequently, when people try to quit smoking, they are often discouraged by the high level of hunger, overeating, and weight gain that accompanies it (Harris et al., 2016; Jo et al., 2005). Therefore, awareness of this phenomenon will help both therapists and clients gain insight into clients’ struggles to quit tobacco smoking.

Beneficial Effects of Smoking Cessation

All hope is not lost regarding the harmful effects of tobacco smoking. Fortunately, scientific evidence has revealed many beneficial effects of smoking cessation at any age, but indicating that quitting at younger ages is associated with greater decreases in premature mortality (CDC, 2008). According to Tonstad and Johnston (2006), some of the mechanisms by which smoking causes its deleterious effects on the body are reversible. For instance, smoking cessation decreases inflammatory responses, rapid restoration of circulating endothelial progenitor cells, and prevents the progression of irreversible smoking-induced cardiovascular diseases, such as atherosclerosis and lipid deposits in the intima artery (Tonstad & Johnston, 2006). On this note, a large number of studies have shown that, compared to current smokers, former smokers have a reduced risk of death from coronary heart disease after about two years of quitting smoking (Fichtenberg & Glantz, 2000). This risk declines to the level of never smokers after about ten years (Tonstad & Johnston, 2006). Similarly, the risk of myocardial infarction decreases to the level of never smokers after about three years (Rosenberg et al., 1985; Rosenberg et al.,1990).

Furthermore, Tonstad and Johnston (2006) also remarked that smokers with peripheral vascular diseases who stopped smoking had a decreased risk of amputation following surgery and an increased chance of overall survival. Besides, they have increased exercise tolerance. Compared to current smokers, former smokers also have a lower risk of abdominal aortic aneurysms (Tonstad & Johnston, 2006). Moreover, Cummings (1982) reported that smoking cessation reduces cough and sputum production, improves forced respiratory volume, and serves as essential ulcer treatment as medication. In general, smoking cessation is associated with many health benefits, including reducing mortality from cardiovascular diseases, pulmonary diseases, and cancer. West (2017) reported that coronary heart disease, stroke, chronic obstructive pulmonary disease, and cancers of the lungs and upper airways are preventable if smoking cessation occurs in early adulthood. Existing coronary heart disease and stroke due to tobacco smoking are reversible if smoking cessation occurs in early adulthood. West (2017) also underscored that miscarriages and underdevelopment of the fetus are preventable if smoking cessation occurs early in pregnancy. Similarly, this risk is mitigated by quitting smoking at any time in pregnancy. Therefore, the benefits of tobacco smoking cessation outweigh its negative impacts. These benefits cannot be compared to the elusive benefits of tobacco addiction.

Treatment Programs for Quitting Smoking

As highlighted earlier, people find it very discouraging to quit smoking because of cravings for smoking and withdrawal symptoms, such as anxiety, increased appetite, restlessness, anger, depressed mood, irritability, frustration, and insomnia. Methods adopted to help smokers handle cravings and nicotine withdrawal effects while quitting smoking include physicians’ advice, contingency contracting, enhancing self-efficacy, relaxation training, deep breathing, aversive conditioning, remembering the reason for quitting, and stimulus control techniques (Cummings, 1982). For instance, physicians’ advice to quit is very beneficial, especially for those who have developed withdrawal symptoms. Cummings (1982) reported that 63% of smokers with myocardial infarctions who received antismoking advice from physicians ceased smoking and remained abstinent for at least one year. In contingency contracting, the smoker goes into a contract with nonsmokers to quit and remain abstinent by depositing something (e.g., money) that will be lost if the quitting fails.

Additionally, stimulus control techniques help smokers identify and record smoking-associated stimuli (e. g., social-environmental cues) that have acquired the ability to produce craving, drug effects, and withdrawal symptoms; avoid these situations or modify responses to them; and reduce cravings for smoking. One way to modify responses to social-environmental cues associated with smoking is by learning combine cue exposures to extinguish conditioned responses to these cues. According to Brandon et al. (2007), repeated exposures to drug-associated stimuli without reinforcement enhances the extinction of conditioned responses to these stimuli. Similarly, providing clients with a portable stimulus associated with extinction (e.g., token, cognitive cue) improves the efficacy of cue exposure and improves smoking addiction treatment. Empirical evidence has also shown that extinction cues significantly aid clients’ retrieval of the extinction memory and significantly reduce craving and salivation to substance-associated cues in a novel context following extinction (Brook, 2000; Collins & Brandon, 2002).

Furthermore, enhancing self-efficacy among clients struggling to quit smoking can also be effective. Several strategies exist to facilitate self-efficacy among clients. According to Kaddena and Litta (2011), an essential way to improve self-efficacy for positive treatment outcomes is by using motivational interviewing (MI). In this procedure, therapists will be supportive of clients and express their confidence in clients’ ability to change, elicit change talks in the client (e.g., How is tobacco smoking affecting your health?) and commitment language (e.g., How strong is your commitment to stop tobacco smoking? What steps have you already taken to smoking?). Therapists also enhance clients’ self-efficacy by using use the confidence ruler exercise (e.g., what would help your confidence to rise from a 2 to a 3), setting a small behavioral task for clients to accomplish (e.g., reducing smoking from one a day to one in four days), celebrating clients or use reinforcement means when they accomplish the task and reviewing clients’ past success and current strength. Other ways to enhance self-efficacy include assisting clients in clearing out negative thoughts, learning from others’ success, and using coping skills (e.g., problem-solving, communication skills, and social skills).

Conclusion

Addiction to smoking has dangerous effects on health, including oxidative stress, abdominal obesity, cardiovascular diseases, pulmonary diseases, and cancer. Smoking harms virtually every organ of the body, exposing the body to a high risk of death. On the other hand, smoking cessation has several health benefits, especially reducing the risk of death from these diseases, although short-term withdrawal symptoms may accompany the effort to quit. However, the benefits of tobacco smoking cessation outweigh its negative impacts. These benefits cannot be compared to the elusive benefits of tobacco smoking, which eventually become harmful to health. Therefore, it is advisable for smokers who are trying to quit to seek advice from physicians or other medical experts and employ several other techniques to handle their nicotine withdrawal effects. In addition to the physician’s advice, empirical evidence supports that other methods, including contingency contracting, enhancing clients’ self-efficacy, relaxation training, remembering the reason for quitting, and stimulus control techniques, are effective in helping clients quit smoking. However, more research is needed to understand specific situations and conditions in which each technique works best.

Acknowledgments

I thank God almighty for the health and wisdom to produce this work. Many thanks also go to all those who provided me with a conducive environment while producing this work

Data Availability Statement

Data sharing was not applicable to this study as no datasets were generated or analyzed during the current study. The data collection method was solely previous studies on the effects of tobacco smoking on stress, hunger, and health.

Statement Regarding Informed Consent

Informed consent from individual participants was not applicable for the current study as data sharing was not applicable, and no datasets were generated or analyzed in the current study.

Statement Regarding Ethical Approval

All the previous studies used for the current study were duly acknowledged. Additionally, the current study does not involve human participants or data sharing. Therefore, ethical approval regarding participants and data sharing was not applicable for the current study.

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