Schizophrenia is as a severe mental illness that is estimated to occur in about 1% of the population (American Psychiatric Association 2000). Schizophrenia is considered a heterogeneous illness because its symptoms, level of impairment and course of illness manifest themselves in different forms.
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Primarily, schizophrenia impairs neurocognitive functioning resulting in problems of perception, interpretation, communication and interaction with others. It is also associated with the impairment of the performance of day to day activities, self-care and other social and occupational activities (Ziedonis et al. 2007). Schizophrenia symptoms are categorized into two groups.
The first group exhibits positive symptoms such as disorganized speech and behavior, hallucinations and delusions. The second group exhibits negative symptoms that include cognitive impairment and restricted effect and motivation. These symptoms have a deleterious impact on the social and occupational functioning of the patients (American Psychiatric Association 2000; Weinberger et al. 2007; Ziedonis et al. 2007).
Individuals with a diagnosis of schizophrenia are reported to be highly susceptible to developing nicotine dependence with an estimated prevalence of up 88% (Kelly & McCreadie 2000 & Lasser et al. 2000; Kumari & Postma, 2005; Steinberg & Williams 2007). This rate is particularly concerning when compared to a prevalence of 23% of smokers who do not have mental illness.
Out of the smokers with schizophrenia, over half are described as being heavy smokers smoking more than 25 cigarettes per day (Kelly & McCreadie 2000, Lasser et al. 2000 & Ferron, et al. 2009; Banham & Gilbody 2010). The estimated rate of smoking cessation amongst those with schizophrenia is approximately 8% compared to 31% of those without a major mental illness.
This high prevalence of heavy smoking amongst individuals with schizophrenia is concerning because it puts them at a significantly higher risk of smoking related illness, such as lung cancer, cardiovascular and respiratory diseases (Ziedonis et al. 2003 & Moss et al. 2010).
It is estimated that the life expectancy of smokers with schizophrenia is reduced by 25 years, with smoking related illness being a significant contributing factor (Ziedonis et al. 2003 & Ferron et al. 2009; Kelly et al. 2000; Moss et al. 2010). Over the years, there have been strong indications that heavy cigarette smoking can be linked to schizophrenia and that smoking may have a connection to the neurobiology of schizophrenic illness.
This paper will critically examine the current body of clinical and neurological research that links nicotine dependence to schizophrenia. We will also examine a self-medication, social and environmental explanations for nicotine dependence. Finally, this paper will offer discussions regarding the implications for assessment and intervention.
Self-Medication of Symptoms
Neurobiological research has established an abundance of nicotinic receptors in the prefrontal cortex of the brain with the nicotinic acetylcholine receptor subtype being the main receptor linked to nicotine dependence. Nicotine has been observed to bond with these receptors resulting in formation of dopamine and serotonin.
Raising dopamine levels has been shown to transiently lead to cognitive dysfunction and negative symptoms associated with schizophrenia. This paper will examine the positive and negative symptoms of schizophrenia that are thought to be targets of self-medication.
These include processes that relate to attention and concentration, the P50 Gating Response and Visuospatial Working Memory (Kelly & McCready 2000; Kumari & Postma 2005).
A common symptom associated with schizophrenia is dysfunctioning of the P50 gating response and it is believed that this is connected to auditory hallucinations. Individuals who do not have a deficit in their P50 gating response can hear more than one sound at the same time, but not all sounds are heard at the same volume. This enables us to focus our attention on what we choose (Kumari & Sharma 2002; Adler et al. 2004).
The neurocognitive deficits associated with a deficit in the P50 gating response can significantly impact on quality of life. It is thought that smoking cigarettes is a method of self-medication to moderate this symptom (Adler et al. 2004; Kumari & Postma 2005; George et al. 2006; Weinberger et al. 2007). Researchers used a controlled study to measure the P50 wave response to auditory stimulation of participants with schizophrenia.
They reported that participants were unable to block the response when a second stimulus was added. However, participants were retested after smoking cigarettes and others chewing 6 mg dose of Nicorette gum. Results from both smoking and chewing Nicorette gum indicated improvement in the P50 wave when an auditory stimulus was added.
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This finding indicates that nicotine has the ability to temporarily improve the ability to filter and suppress the response to auditory stimulation (George et. al. 2006). It should however be noted that the improvement is only temporary.
It would be a medical disaster to encourage people with schizophrenia to use smoking as a remedy because it would mean that they smoke frequently to improve their ability to filter. This would not solve the problem and would instead expose the people to a high risk of smoking related complications like lung cancer.
A second neurocognitive function that is reported to improve with nicotine is visuospatial working memory (VSWM). Dysfunction of dopamine activity in the anterior cortex has in some cases been linked to Schizophrenia. This dysfunction affects the cognitive process that facilitates visualization of the relative positions of items in the environment.
It requires encoding and remembering location of objects and landmarks. These functions are necessary for allowing performance and motivation to start and complete simple and complex tasks and activities (Snyder 2006). This process is referred to as visuospatial working memory (VSWM). Animal testing reports that VSWM functioning is enhanced with nicotine (George et al. 2006).
It is thought that smoking cigarettes enhances VSWM in people with schizophrenia by increasing dopamine activity (Depatie et al. 2002; George et al. 2006). Symptoms of tobacco withdrawal are reported to impair VSWM with the impairment abated when smoking is resumed (George et al. 2002).
A controlled study using nicotine and functional magnetic resonance scanning (fMRI) by Jacobson and colleagues (2004) reports improvement in participants with schizophrenia’s performance of tasks involving attention and memory when nicotine was administered.
However, the researchers acknowledged that they were unable to state with certainty, whether improved function was associated with nicotine or antipsychotic medication that the participants were taking.
Another study to examine whether nicotine improved attention and VSWM in participants with schizophrenia reported only slight improvement in attention and no improvement reported in any other area of cognitive function (Harris et al. 2004). According to these reports, it cannot be concluded without doubt that nicotine indeed aids in reducing VSWM impairment. Further controlled tests need to be carried out to ascertain this.
Attention and Concentration
It has been reported that nicotine improves the ability to focus attention and concentration in tasks that involve working memory as well as selective attention. This is believed to occur as nicotine stimulates activation and functional connectivity in the prefrontal cortex region of the brain (Jacobsen et al. 2004; Weinberger et al. 2007).
However, results of improved attention and concentration varied when nicotine was administered via different delivery systems. The first study, a controlled double-blind study conducted by Depatie and colleagues (2002), determined that attention and concentration was diminished with overnight nicotine abstinence and improved once a nicotine replacement patch was administered.
In a second study, Weinberger and colleagues (2007) report that in a controlled study, only minimal improvement in attention and concentration was reported when nicotine nasal spray was administered and even less effect noted in a third study with administration of nicotine gum.
These varied results in the tests could be an indication that maybe there is some stimulation that affects and possibly improves attention and concentration but is not necessarily nicotine. Schizophrenic Cigarette smokers can be encouraged to try different natural stimulants and more research done to establish the accurate relationships between the two.
There are reports that suggest that smoking reduces other negative symptoms of schizophrenia, such as anergia, amotivation and flattened affect (Smith et al. 2002; Tidey & Williams 2007). However, Barnes and colleagues (2006) report that this was not consistent with their research as they found no association of heavy smoking and decreased negative symptoms.
Tidey and Williams (2007) note that there are limited controlled studies comparing smokers with schizophrenia to non-smokers with schizophrenia to determine whether negative symptoms are impacted by nicotine use and cessation.
It is frequently reported that smoking is associated with regulating mood (Baker et al. 2004; Perkins et al. 2010). In a research conducted by Tidey and Williams (2007) measuring smoking outcome expectancies, it was found that smokers with schizophrenia also shared the perception that smoking alleviated feelings of anxiety and irritability.
However, they suggest that increased irritability and anxiety are symptoms of nicotine withdrawal. If there is an expectation that smoking will reduce anxiety, the smokers will smoke; this will alleviate withdrawal symptoms and might falsely appear to relieve the anxiety and irritability.
Medication Side Effects
In addition to alleviating symptoms of schizophrenia, nicotine is reported as being used as an antidote to unpleasant side effects of neuroleptic medication used to treat schizophrenia (Kelly & McCready 2000; Kumari & Postma 2005). Kumari and Postma (2005) suggest that hydrocarbons in cigarette smoke decrease the efficiency and can shorten the half-life of neuroleptic medication by 50%.
Medication is metabolized quickly and cleared from the system and this is thought to reduce associated side effects. The implication of this is that schizophrenic smokers would need a higher dose of the medicine for the same remedial effect. Some researchers suggest that this under-medication may be an explanation as to why schizophrenia patients who smoke account for more frequent hospitalizations compared to non-smokers.
Also they are reported to experience increased psychiatric symptoms such as hallucinations and delusions during an acute episode compared to non-smokers (Kelly & McCready 2000; Kumari & Postma 2005). A study conducted by Yang and colleagues (2002) at an inpatient psychiatric unit in China administered transdermal nicotine and placebo patches to 30 patients with schizophrenia who were prescribed Haldol.
Their findings reported decreased Haldol related Parkinsonism with the nicotine transdermal patch compared to the placebo patch. In a more recent study of 146 adults with schizophrenia, Barnes and colleagues (2006) found that smoking was associated with decreased tardive dyskinesia as well as akathisia.
However, Smith and colleagues (2002) recommend that research findings be interpreted with caution since there lacks a published research of placebo-controlled studies showing consistent improvement of psychiatric symptoms associated with nicotine use.
Also, in the study conducted by Barnes and colleagues (2006), they reported that the association of nicotine dependence and neuroleptic medication was dependent upon the type of medication used.
Older neuroleptics such as Haldol were associated with high prevalence of smoking, whereas, newer medications such as clozapine saw a reduction in smoking behavior. This is thought to occur because the newer medication increases dopamine and decreases negative symptoms of schizophrenia (Barnes et al. 2006).
There is research that suggests the pathophysiology of the illness itself may increase vulnerability to the initiation and maintenance of nicotine dependence since many begin smoking during the prodromal phase of their illness (deLeon & Diaz 2005). Kelly and McCreadie (2000) suggest that smoking may be a marker for schizophrenia.
Psychosocial factors for high tobacco use and low cessation
Ziedonis and colleagues (2007) suggest that focusing solely on the self-medication explanation may detract researchers from exploring other hypotheses for nicotine dependence.
Socioeconomic factors that increase smoking risks for this population include limited education, poverty, unemployment and peer influence (American Psychiatric Association 2004; Riala et al. 2005). The attitudes towards smoking within the mental health treatment system are also responsible for perpetuating a smoking culture (Williams & Ziedonis 2003).
Unlike the general population, individuals with schizophrenia are often unemployed which increases their idle time and their inability to engage in social activities in which smoking is not acceptable.
Other potential etiologic factors include living with other smokers in group homes, having a fixed low income, having low education, lacking support and being unmarried (American Psychiatric Association 2004). Schizophrenic people could therefore be leaning towards smoking because of psychosocial factors more than any other medical reasons.
In a meta-analysis of smoking and severe mental illness, de Leon and colleagues (2005) propose that a high rate of smoking exceeds the severe mental illness effect. They suggest that decreased smoking in people with schizophrenia is related to high nicotine dependence and cultural factors. Riala and colleagues (2005) suggest that both social and cultural factors can influence the initiation and maintenance of smoking behavior.
Smoking is perceived to be less socially acceptable in India where they report that only 38% of male patients with schizophrenia smoke This rate is even lower for women.
This is significantly lower than the 88% of smokers with schizophrenia in western society. In a meta-analysis of smoking, Riala and colleagues (2005) propose that smoking is more strongly associated with cultural attitudes and availability of cigarettes, rather than being associated with a diagnosis of schizophrenia.
Ferron and colleagues (2009) report that in the United States, smokers with mental illness account for 46% of cigarette sales. The 46% translates into sales revenue amounting to 37 billion dollars and 180 billion cigarettes.
However, there is evidence that the tobacco industry has invested heavily to promote research that supports this and suppress evidence that counters the association Ferron and colleagues (2009) conducted a review of the tobacco industry documents dating 1955 up to 2004. Their analysis revealed the tobacco industry provided financial backing for research that promulgated three messages:
- Support for the self- medication hypothesis;
- Quitting smoking would lead to deterioration in mental health and
- People with schizophrenia are less susceptible to smoking related disease.
The tobacco industry monitored and suppressed research that did not support the industry’s agenda. The tobacco industry has also used the self-medication hypothesis to encourage cigarette use in mental institutions and frustrated efforts to ban cigarette use in hospitals.
These targeted strategies by the tobacco industry increased the barriers to smoking cessation by discounting the effectiveness of smoking cessation treatment for this population and discouraging the implementation of no smoking policies in mental health treatment facilities.
The tobacco industry’s close relationship with mental health research influenced the mental health clinician’s knowledge and attitudes about nicotine use. Although schizophrenia represents 1% in the general population, schizophrenia is primarily treated in mental health settings (Ziedonis et al. 2007).
Supported by research funded by the tobacco industry, smoking was not only perceived as being an acceptable practice on inpatient psychiatric units but also patient smoking was condoned in these settings. Positive patient behaviors were rewarded and reinforced with cigarettes as part of a token economy.
This practice in mental health treatment settings has likely contributed to the high rates of tobacco use and low rates of successful smoking cessation attempts among individuals with schizophrenia (Ziedonis et al. 2003). Patients with serious mental illness have described smoking cigarettes as a fundamental need that was more important than food and even helped them to prevent relapse of schizophrenia (Forchuk et al. 2002).
The self-medication explanation was widely accepted and efforts to change the culture within psychiatric community were met with resistance. In addition to the self-medication rationale, there was a common perception that smoking was one of the few pleasures they could have in their lives (Ziedonis et al. 2007).
Other concerns expressed by health care providers, families and the patients include the potential for exacerbation of mental health symptoms, relapse, anger, aggression and detrimental effect on neuroleptic medications.
Mental health clinicians have been reluctant to accept smoking bans on psychiatric units (Willemsen et al. 2004) despite growing evidence that such bans do not have a negative impact on the management of psychiatric patients in these settings. Furthermore, there was concern regarding the health risk if patient’s continued to smoke while using nicotine replacement therapy.
Another concern expressed was that staff and patients would lose the opportunity to connect and bond while having a cigarette together. Health care providers expressed concern that their patients who are primarily on fixed limited income, would not be able to afford the price of over the counter smoking cessation treatments and that promoting smoking cessation treatment would further marginalize this population.
This argument is easily countered by Steinberg and colleagues’ (2004) findings that in the high tobacco taxation states in the U.S., smoking consumes 27% of people with severe mental illness’s fixed monthly income.
Implications for Assessment
The low motivation for smoking cessation amongst people with schizophrenia may be attributable to three primary factors. The first pertains to the high rate of nicotine dependence amongst this group. The second factor pertains to perceived benefits of smoking which are associated with the self-medication explanation.
Smoking cessation is reported to be a challenge as it is reported that nicotine withdrawal can result in their psychiatric symptoms temporarily worsening. The third factor pertains to an overall lack of support for smoking cessation and unavailability of targeted smoking cessation treatment (Ziedonis et al 2003; Barnes et al. 2006).
Formal institutional and system barriers that further contribute to this problem include restricted formularies and insurance reimbursement for smoking cessation treatments, exceptions to smoking bans in psychiatric facilities and inadequate staff training on smoking cessation (Ziedonis et al. 2003).
Among mental health professionals, training on tobacco dependence treatment is lacking and primary care providers and tobacco control specialists do not focus on this issue, perhaps due to stigma, lack of information or perceived hopelessness regarding abstinence (Ziedonis et al. 2007).
Because patients with schizophrenia often receive treatment in a variety of intensive settings (e.g. psychiatric hospitals, residential facilities, day treatment programs) these settings allow for the delivery of an intensive smoking cessation treatment integrated with mental health care. However, only recently have some psychiatric treatment settings begun to address tobacco use (Ziedonis et al. 2007).
Implications for Intervention
Kelly & McCreadie (2000) suggest that targeted smoking intervention during the first episode of schizophrenia could be beneficial. Although the percentage of smokers in the first episode is equivalent to those with chronic schizophrenia, they found that the number of cigarettes smoked per day was lower.
It was also established that although many patients experience difficulties and may relapse, they are interested in reducing smoking (Forchuk et al. 2002). Individuals with schizophrenia appear to be able to quit tobacco with the support of psychosocial treatment, nicotine dependence treatment medications and social support.
These patients must therefore be supported in these areas and be encouraged to quit smoking. Tobacco companies cannot be expected to spread this message, but they must desist from suppressing this message.
Clinical studies report that different intensity psychosocial treatment interventions have been effective, including one-to-one and group based counseling using modified American Lung Association interventions, cognitive-behavioral therapy approaches, social skills training and contingency monetary reinforcement.
Most of the studies using nicotine replacement or buproprion in this population have included a psychosocial treatment component.
Motivational interviewing for less motivated smokers
Engaging less motivated patients with psychosocial interventions is important given the high rates of tobacco dependence and the smaller number of individuals with schizophrenia who are prepared to quit smoking.
Motivational interviews with personalized feedback (e.g. Carbon monoxide level, personal annual cost of cigarettes, personal medical conditions caused or exacerbated by smoking) was found effective in motivating 32% of smokers with schizophrenia to seek smoking cessation treatment within one month of the single session intervention compared to 11% among those receiving an educational intervention and 0% among those provided with information only (Steinberg, et al. 2004).
From these statistics, it is clear that motivational interviewing is a powerful tool that can be used to motivate schizophrenic patients and convince them to quit smoking.
Interventions for smokers ready to quit
Medication treatment studies on smoking cessation have been primarily small, uncontrolled and usually combined with psychosocial treatments for smoking cessation. Bupropion appears to be tolerated and to help reduce smoking and expired air carbon monoxide (George et al 2002).
Nicotine patch on the other hand appears safe and well-tolerated but has achieved lower than expected long-term abstinence rates (Williams & Hughes 2003) while Nicotine nasal spray appears helpful among schizophrenic individuals (Williams et al. 2004) and may produce short term reduction in schizophrenia symptoms and cognition.
Tobacco dependence outcomes may also be affected by the pharmacological treatment for the mental disorder itself. Treatment with typical antipsychotics, particularly clozapine, has been associated with more successful quit attempts among schizophrenia patients motivated to stop smoking than among those treated with typical antipsychotics (George et al. 2000).
What role does exercise play in the treatment process
Exercise may exert beneficial effects by addressing psychosocial and physiological needs that nicotine replacement alone does not (Williams & Hughes 2003). Exercise has been shown to help in health behavioral change such as aiding women in stopping habits such as smoking and can also reduce aging that is induced by stress. Physical exercise is also important in managing weight after cessation.
The newest FDA-approved remedy for smoking surcease is Varenicline. It preys upon α-4 and β-2 receptors and behaves like a partial resister.
This means that it mildly stimulates the nicotine receptor, but not sufficiently to allow the release of dopamine which is important for the rewarding effects of nicotine (Williams & Hughes 2003). As a resister, Varenicline prevents nicotine from triggering dopamine thereby reducing the urge to smoke.
Behavior based Treatment
Behavioral training is important because it trains patients on what changes to make in their lifestyles to avoid relapse. A synergic effect is achieved with the combined approach of using behavioral and pharmacological treatments.
Harris and colleagues (2004) reported that the impact was bidirectional with decreased functioning in the participants who were smokers and improved functioning in the group that were non-smokers. There is a scarcity of longitudinal research to investigate whether cognitive functioning worsens after confirmed abstinence.
George et al. (2000) reports that one study conducted in 1996 noted an increase in psychotic symptoms after smoking cessation. However, in a controlled study of smoking cessation interventions using bupropion, there was no evidence of worsening psychiatric symptoms (George et al. 2000).
Researchers in these studies admit to have had methodological challenges. Data collection was difficult because the sample sizes were small and the methodologies were cross-sectional.
The high prevalence of tobacco dependence in patients with schizophrenia may be associated with dysfunction in the neurobiology associated with dopamine systems, while there is a focus on the research to suggest that people with schizophrenia smoke to self-medicate the cognitive and clinical symptoms associated with the illness and side-effect profiles of neuroleptic medication (Kelly & McCreadie 2000; deLeon & Diaz 2005; Barnes et al. 2006)
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