Smoking is the leading preventable cause of poor health outcomes, and although the rate of smoking behavior has decreased in the last decade, a considerable number of individuals begin smoking each year (Godtfredsen & Prescott, 2011). Approximately 23% of men and 19% of women in the United States smoke (Audrain-McGovern & Benowitz, 2011), and more than 400,000 individuals die prematurely from smoking-related diseases. Globally, 6 million people die prematurely from smoking related illnesses (Godtfredsen & Prescott, 2011). Although the risks of this behavior are well-established, and for the most part, understood by most smokers, smoking addiction and the attitudes surrounding this issue remain difficult to change (Ansell, Gu, Tuit, & Sinha, 2012).
The initiation of smoking behavior has several psychological and biological antecedents such as a biological predisposition to addictive behavior, depression, and general lack of psychological well-being. Smoking addiction as well as smoking cessation have powerful effects on biological and psychological systems. The goal of this paper is to identify and explicate the effects of smoking addiction and smoking cessation on appetite, stress, and physical and psychological health.
The Effects of Smoking Addiction
Heishman (1999) described smoking addiction as a "complex process that involves biological, psychological, behavioral, and cultural factors" (p. 143). It has intense biological effects on individuals. When addicted smokers are deprived of nicotine, the effects include cognitive impairments as well as a deficit in attention span (Heishman, 1999). The confluence of complex factors involved in smoking addiction are involved in the maintenance of the compulsive and repetitive use of tobacco, although it remains a challenge to determine exactly how these mechanisms combine in a biologically and psychologically unique individual.
For smokers, nicotine is a way to regulate behavior (Heishman, 1999). Although smokers may not completely understand the mechanisms by which this takes place, research has shown that the reinforcing effects begin within the brain (Heishman, 1999). Research has determined that the dopaminergic system mediates the reinforcing effects of nicotine as well as other drugs, although the confluence of biological, psychological, cultural, and behavioral processes by which reinforcement encourages addictive behavior is a complex process.
The Effects of Smoking Addiction on Appetite
Some smokers claim they smoke for weight control because it decreases their appetite (Mineur et al., 2011). The mechanisms by which this decrease takes place are neurobiological, but not well understood until the last several years. Mineur et al., (2011) discovered the hypothalamic melancortin system played a significant role in nicotine's tendency to decrease body weight and the amount of food consumed. Furthermore, the neurotransmission of nicotinic acetylcholine receptors were involved as well (Mineur et al., 2011).
Rodent studies have shown that nicotine decreases hunger and food intake (Jessen, Buemann, Toubro, Skovgaard, & Astrup, 2004). The decrease is caused by changes in neurotransmitters located in the hypothalamus. Additionally, the dopaminergic and serotonergic systems in the hypothalamus become activated. These studies have been especially pertinent for designing strategies to help smokers prevent weight gain during smoking cessation (Jessen et al., 2004). Many smokers do not quit because they anticipate weight gain, and according to some health care providers, the weight gain that follows smoking cessation counteracts some aspects of the benefit of quitting (Audrain-MCGovern & Benowitz, 2011).
Weight control is a commonly reported reason for smoking, especially for women (Copeland & Carney, 2003). Although women smokers believe their smoking behavior helps curb their appetite and control their weight, most of these women report they want to quit smoking by utilizing a program that would help them quit and not gain weight. Copeland & Carney (2003) found women who generally ate a better diet and had more self-control over their food consumption relied on smoking less than the women who has less self-control over their diet.
The Effects of Smoking Addiction on Stress
When smokers experience stress, they are more likely to want to smoke, and they smoke more. One common belief about smoking is that it relieves stress, although no scientific evidence exists to prove it (Heishman, 1999). Smokers, however, smoke more when they are experiencing stress. Cumulative stress, however, has an effect on the initiation of smoking behavior (Brown, Lewinsohn, Seeley, & Wagner, 1996). Utilizing the stress-vulnerability model of addiction, Ansell et al. (2012) found that environmental circumstances, specifically cumulative stress results in individuals losing self-control as well as increases their ability to regulate impulsivity. Further, research has determined that cumulative stress is a risk factor that increases individuals' susceptibility to a number of addictive behaviors (Sinha, 2008). The mechanism by which stress increases this susceptibility may be through a loss of self-efficacy, social support, and sense of control (Stewart, Greaves, Kushner, Letourneau, Spitzer, & Boscoe, 2011).
When studying smoking behavior and post traumatic stress disorder (PTSD), the severity of the PTSD did not affect smoking intensity, although smoking seemed to effect the individual by the mechanism of emotional numbing (Joseph et al., 2012). The numbing is thought to be somewhat of a self-medication utilized to separate oneself from the stress of recalling traumatic experience (Joseph et al., 2012). In some individuals, especially those with PTSD and other psychiatric disorders, nicotine can be important for the individual's ability to manage their stress with emotional numbing. Because of the personal antecedents of smoking and the various reactions to stress as it relates to smoking behavior, the effects of smoking on stress can be varied and indeterminable without individualized scrutiny (Joseph et al., 2012).
An abundance of research established the association between stress and smoking initiation and continued smoking. In adolescents, an increase in initiating smoking behavior is associated with risk factors that include depression, anxiety, suicidal ideation, and attention deficit disorder (Anda et al., 1990; Brown et al., 1996; Hockenberry et al., 2011). When studying the association between stress and smoking, research found that life stress was indeed provocative for smoking behavior, and work stress was complicit in creating stress as well, but not to the extent that life situations created stress (Cui, Rockett, Yang, & Cao, 2012; Nelson, Yi, Sorensen, & Berkman, 2012). Addicted smokers perceive stress as the single most influential reason that they smoke. Because they believe their smoking behavior ameliorates their stress, one of the primary reasons for avoiding smoking cessation is the concern that they will experience higher levels of stress (Hajek, Taylor, & McRobbie, 2010).
The Effects of Smoking Addiction on Health
Smoking addiction is the cause of death in more than 5.4 million individuals every year (Cui et al., 2012). Eighty percent of these deaths occur in undeveloped countries, such as China, which leads the world in tobacco consumption. Hajek, Taylor, and McRobbie (2010) suggested that smoking not only causes ill physical health, but may also cause psychological health deficits. Nicotine is known to cause powerful effects in the brain within 10 seconds of smoke inhalation (Duaso & Duncan, 2012). It causes the release of dopamine in the brain, which later, during abstinance, provokes a range of withdrawal symptoms such as irritability, inability to focus, headache, and nausea (Duaso & Duncan, 2012).
Smoking is known to increase the risk of respiratory disease. Further, it is the primary cause of almost 90% of all chronic obstructive pulmonary disease (Shahab, Jarvis, Britton, & West, 2006). Smoking is the primary cause of cardiovascular disease and it increases the risk of coronary heart disease, abdominal aortic aneurysm, atherosclerosis, and stroke (Duaso & Duncan, 2012). Smoking is the primary preventable cause of death in industrialized countries (Hooten et al., 2011). Although it has been shown to cause approximately 90% of all lung cancers, it causes a variety of other cancers as well, including oral cancer, cancer of the sinuses, esophagus, stomach, pancreas, liver, kidney, bladder, cervix, ureter, uterus, cervix, colon, and rectum, one type of ovarian cancer, and leukemia (Duaso & Duncan, 2012). It causes complications in pregnancy and long-term effects on the newborn, such as respiratory problems (Duaso & Duncan, 2012). Second hand-smoke is a danger to children and adults as well, and has been proven to cause long-term respiratory illness and increases the risk of heart disease (Duaso & Duncan, 2012). For women, smoking is associated with lower bone density and increases the risk of hip fractures.
In patients with chronic pain, smokers have greater levels of pain, more severe depression, anxiety, and take higher doses of prescription medications. Health outcomes for these patients are worse than for non-smokers (Hooten et al., 2011). Smoking plays a significant role in the pathophysiology of pain. Specifically, it provides a distraction for chronic pain patients, although overall, these patients were not as healthy as non-smokers, and did not respond to pain management as well as did non-smokers (Hooten et al., 2011).
The Effects of Smoking Cessation
The Effects of Smoking Cessation on Appetite
When smokers quit, they usually gain weight (Jessen et al., 2004). Within 6-12 months after smoking cessation, abstaining smokers gain an average of 12 pounds, but some gain more. African Americans older than 55 years and individuals in lower socio economic status tend to gain more weight than the average. Heavy smokers also gain more weight than the average smoker after smoking cessation (Audrain-MCGovern & Benowitz, 2011). Women concerned about gaining weight tend to gain approximately 17 pounds, which is more than the average (Levine, Cheng, Kalarchian, Perkins, & Marcus, 2012). Genetic factors too, may be partly culpable in causing more than average weight gain.
Weight gain during smoking cessation takes place because of several factors, but the primary reason was that abstaining smokers eat more than non-abstaining smokers (Cabanac & Frankham, 2002; Levine et al., 2012). Further, female smokers who remain abstinent were previously thought to intake excessive amounts of high carbohydrate snacks and fats (Hughes
& Hatsukami, 1997) or sweet foods (Rodin, 1987), although Levine et al. (2012) found no empirical evidence to support these findings. The appetite-suppressant characteristic of nicotine is well-known (Jessen et al., 2004). After smoking cessation, nicotine's effects on the brain are no longer in effect, so the individual experiences an increase in hunger. Further, food seems to be a replacement for the satisfaction derived from smoking, and when individuals struggled to maintain cigarette abstinence, they utilized food to obtain the same reward satisfaction previously provided by smoking (Spring, Pagoto, McCharque, Hedeker, & Werth, 2003). Further, they began to place higher value on carbohydrate-rich or more appealing snacks (Spring et al., 2003).
The Effects of Smoking Cessation on Stress
As previously discussed, no empirical evidence exists to support the idea that smoking relieves stress. If smoking relieved stress, smokers would likely experience added stress when they quit smoking, however Heishman (1999) found smokers reported less stress after quitting. Nicotine deprivation in addicted individuals typically causes an increase in stress, anxiety, and irritability (Hughes, Higgins, & Hatsukami, 1990). These negative experiences can cause mood swings between each cigarette smoked.
When measuring stress differences between smokers, and smokers who quit smoking, the individuals who had recently stopped smoking experienced less stress than the individuals who continued to be active smokers (Hajek, Taylor, & McRobbie, 2010). These findings suggested that although dependent smokers fear they will experience an inordinate amount of stress if they quit smoking, and they fear they they may lose the ability to cope with stress. Although smokers perceive smoking as a valuable tool for coping, smokers who recently quit experienced no such loss (Croghan, Schroeder, Hays, Eberman, Patten, & Berg, 2005; Hajek et al., 2010).
On the contrary, however, the process of smoking withdrawal produces a stressful state during the initial phase of smoking cessation. This stress can cause a failure to abstain during this vulnerable phase when quitting is first attempted. Wardle, Munafò, & de Wit (2011) found some evidence that suggests the withdrawal effects of smoking cessation affects individuals’ ability to respond to acute stress. Further, the effects of long-term use of nicotine causes neuroadaptations in the biological systems that respond to stress (Wardle, Munafò, & de Wit, 2011). This can leave a quitter vulnerable to stress without the normal ability to cope during smoking cessation attempts. This may be especially true when the withdrawal symptoms are strongest (Wardle, Munafò, & de Wit, 2011).
Most smokers blame stress and negative affect experiences for aborting smoking cessation attempts (Shiffman & Waters, 2004). However, they report feeling happier after quitting, and only 3% said they were not as happy since quitting (Shahab & West, 2013). This should counter any hesitations held by smokers, since the typical belief for the smoking population is that they are better able to control stress with smoking. As previously mentioned, no empirical evidence exists to suggest smoking relieves or diminishes stress (Heishman, 1999). Although a number of reasons may underpin why quitters report being happier after smoking cessation, although they may be less prone to the negative psychological behaviors and experiences of smokers (Shahab & West, 2013). In support of this hypothesis, research found smoking reduces anxiety and stress, and has not been shown to increase adverse psychological behaviors (West & Hajek, 1997).
The Effects of Smoking Cessation on Health
Smokers who quit had a significantly better quality of life after a year of being smoke free (Sales, Oliveira, Mattos, Viana, & Pereira, 2009; Tillmann & Silcock, 1997). Chronic pain patients believed nicotine was a valuable coping strategy, although these patients fared equally well with a form of distraction other than cigarette smoking (Hooten et al., 2011). When their perceptions were altered, they became more aware of the role of their smoking behavior and were able to consider smoking cessation (Hooten et al., 2011).
If smokers quit before the age of 35, they have little to no risk for tobacco-related illnesses or premature death, compared to individuals who have never smoked (Godtfredsen & Prescott, 2011). It has been well-established that nicotine addiction more than doubles the health risks for stroke, cardiovascular disease, coronary heart disease, abdominal aortic aneurism, and peripheral arterial disease (PAD) (Godtfredsen & Prescott, 2011). After the cessation of smoking, the risk of continued cardiovascular disease is reduced significantly and quickly (Chow, Jolly, Rao-Melacini, Fox, Anand, & Yusuf, 2011). Within two to five years after smoking cessation, the risk of stroke decreases considerably, but not to the level of individuals who never smoked. Even after 15 years, smokers who have quit continue to have a somewhat higher risk factor for stroke (Godtfredsen & Prescott, 2011).
The risk for PAD at least doubles for smokers, but the risk decreases considerably after smoking cessation. The decrease, however, is much slower than that of coronary heart disease. Further, quitting smoking does not increase the distance an individual is able to walk with PAD (Godtfredsen & Prescott, 2011). The risk for abdominal aortic aneurism decreases to that of individuals who never smoked. The risk in smokers doubles (Godtfredsen & Prescott, 2011). With chronic lung diseases such as chronic obstructive lung disease, after smoking cessation individuals regained improvement in lung function and symptoms of respiratory illness. After 14 years, mortality risk was significantly reduced. This is not true for individuals with severe COPD, although the effects of quitting smoking have not been investigated in this population (Godtfredsen & Prescott, 2011).
It is well-recognized that smoking exacerbates symptoms of asthma. In addition, smoking reduces decreases the effects of inhaled corticosteroids. Although there is a paucity of research on the effects of smoking cessation on asthmatics, the few studies which have been done show improvements in lung function and asthmatic symptoms. Another study showed better quality of life, and a decrease in the use of rescue inhalants. One study showed that the damage done by smoking was reversed after smoking cessation (Godtfredsen & Prescott, 2011).
Although the benefits of smoking are limited to being little more than a perception of a distraction from pain, a catalyst for psychological numbing used to escape the experience of traumatic experience, and as a remedy for anxiety, the negative health outcomes of smoking addiction are well-established (Ansell, Gu, Tuit, & Sinha, 2012; Hajek, Taylor, & McRobbie, 2010). The effects of smoking addiction are far-reaching. According to health practitioners, as well as the opinion of the secular populace, perpetuate smoking is considered pandemic across the globe. Although most individuals understand the myriad of the health risks associated with smoking behavior, there remains a range of personal, social, and environmental factors that help perpetuate the behavior. The implications of smoking addiction charge a tremendous cost to the healthcare system, and some of the damage done is irreparable (Godtfredsen & Prescott, 2011). Smoking cessation is not without its challenge, although it can, and usually does, reduce the final toll of smoking on psychological and physical health (Sales, Oliveira, Mattos, Viana, & Pereira, 2009; Tillmann & Silcock, 1997).
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