Nicotine addiction in patients with schizophrenia Essay
Nicotine addiction in patients with schizophrenia
More Essay Examples on Nicotine Rubric
A significant portion of the human population suffers from addiction, which is a primary chronic relapsing disease that is characterized by compulsive drug seeking and abuse and by an enduring neurochemical and molecular changes in the brain (NIDA, 2006). The development of addiction is influenced by genetic, psychosocial and environmental factors. Addiction is a different from physical dependence and tolerance, both of which are physical adaptations. Physical dependence is represented by a drug-specific withdrawal symptom that results when the intake of a drug is suddenly ceased, or decreased in dose, or counteracted by an antagonist chemical (Savage et al - Nicotine addiction in patients with schizophrenia Essay introduction. 2001). On the other hand, tolerance ensues when exposure to a drug induces changes that result in the reduction of a drug’s effect over time. Addiction is an unpredictable drug effect that represent a peculiar adverse reaction in individuals who are easily affected by biological and psychosocial changes. It should be known that most exposures to drugs do indeed stimulate the brain’s signaling pathways but do not result in addiction. For example, patients who are experiencing severe pain are treated with opiates and become physically dependent and tolerate the doses of opiates, yet they do not develop an addiction to this drug. Hence, exposure to drugs is only one of a number of etiologic factors in its development.
Characteristics of addiction to a drug include an impaired control, compulsive use and craving, and continued use amidst knowledge that the drug may cause deleterious physical, mental and social effects. The behavior of an individual may possibly reflect a strong need to find immediate sense of pleasure that will relieve an individual from his current condition of extreme discomfort or pain, that his judgment on the use of the drug has changed. It has been also observed that an individual is addicted to a particular drug if he is unable to administer medications according to the prescribed conditions and instead, take more than what has been advised at more frequent intervals. Such behavior usually results in a frantic search for a doctor that will assist him in procuring more drugs for further consumption, prescription theft and detachment and isolation from family and friends. The individual may also try experimenting with cocktails of different drugs in order to find an even stronger concoction that will enhance the pleasurable effects he wants to feel from such intake. The additional drugs may be comprised of the simple analgesic, sedatives and any other over-the-counter pain or non-pain medications. Such illicit drug use results in sedation or intoxication, severe functional impairment, psychological problems such as extreme irritability, anxiety and/or depression and apathy. Diagnosis of an addiction can not be based on a single event but rather from a pattern of behavior that is observed over a course of time.
NICOTINE ADDICTION: MECHANISMS AND TREATMENT
Nicotine has lately been identified as an addictive drug that instills an equivalent sense of craving as heroin or cocaine (Briton et al., 2000). Comprehensive studies on the behavior and inflexibility of smokers to change has deemed this population as addicted to nicotine. Debates have ensued regarding nicotine’s mechanism of control by physiological addiction. According to the guidelines of the World Health Organization (WHO), a drug is an addictive if it generates a psychic and sometimes physical state that includes compulsion to take the drug on a continuous basis in order to experience its psychic effects and its absence results in discomfort (WHO, 1969). Nicotine is a dual-function drug that induces both stimulation and relaxation by triggering the release of dopamine, a neurotransmitter responsible for sensing pleasure. The pharmacokinetics of nicotine is very efficient that its effects can be observed within the first 10 seconds of inhalation. The acute effects of nicotine are dispelled after a few minutes and this causes the smoker to keep on smoking to achieve the pleasurable effects and prevent withdrawal. It has been lately determined that long-term use of nicotine reduces the ability of the brain to achieve the feeling of pleasure (Epping et al., 1998). Hence, smokers tend to smoke more cigarettes in order to reach their own personal level of contentment. Cessation from smoking usually results in the onset of withdrawal symptoms, which are actually very uncomfortable to a chronic smoker, hence the smoker resorts to keep on smoking in order to avoid experiencing withdrawal symptoms.
Smoking significantly decreases the levels of monoamine oxidase (MAO) in the brain, an enzyme that regulates the levels of dopamine. With this setting, dopamine levels are maintained at a constant high level, resulting in a sense of pleasure, which in turn teaches the brain to appreciate smoking because of the good feelings it triggers. Research has shown that acetaldehyde, which is also present in cigarette smoke, enhances the effects of nicotine in the body, resulting to the addiction. It has been reported that the enhancing effect is age-related, wherein adolescents appear to be more sensitive to this effect, suggesting that adolescents are more susceptible to nicotine addiction.
There are a number of treatments for nicotine addiction. The immediate results of smoking cessation can be observed within the first 24 hours of quitting, wherein the individual’s blood pressure decreases. Other health benefits of stopping smoking include a significant decrease in probability of suffering from heart attack, stroke, lung cancer and other types of cancers and coronary heart disease. Smoking cessation may increase an individual’s life expectancy by at least 5 years.
The primary treatment for nicotine addiction is nicotine replacement therapy, which employs either the nicotine gum or the transdermal nicotine patch as a pharmacological substitute for cigarette smoking. Since this type of treatment involves usage of materials that contain low doses of nicotine, they result in upsetting physiological effects in an individual, as well as present a negligible chance to be misused and abused. More importantly, the nicotine substitutes do not expose an individual to carcinogenic substances that are naturally found in cigarette smoke. The effects of nicotine replacements are enhanced when couple with behavioral treatment, which involves modifying routine tasks that an individual may strongly associate with cigarette smoking. Nicotine substitutes have been available in the market since 1984 for over-the-counter sales and its appreciation has been selective, depending on individual’s taste and lifestyle. The transdermal nicotine patch was introduced as a prescription drug in 1991, and in 1998, a nicotine inhaler was developed. Such development provided more choice for the consumer, each of which was equally effective.
In 1997, another pharmacological treatment for nicotine addiction was introduced. It involves the use of bupropion, an antidepressant known by the brand name Zyban. This was followed by Varenicline tartrate (Chantix), which acts on the brain for ease during withdrawal and for blocking the effects should there be any case of smoking relapse. Several other antidepressants and anti-hypertensives are currently being developed for tobacco treatment, as well as the prospects of designing a vaccine that targets nicotine during relapse, to stimulate antibody production that would inhibit nicotine from affecting the brain.
Behavioral treatment may also facilitate smoking cessation by teaching participants to identify situations that may induce them to resume smoking, to learn new strategies on coping, to manage stressful situations, to develop skills in problem-solving and to provide social support. It has also been determined that custom-designed therapies tend to be more effective in supporting smoking cessation programs. Initial behavioral therapies for smoking cessation were constructed using formal settings, such as clinics specifically designed for smoking cessation, as well as community and public health locales. Today, behavioral therapy may be delivered by mail, telephone and the internet, all of which have been appreciated because of their accessibility and availability. Nationwide networks utilizing smoking cessation hotlines have been maintained through the help of the National Cancer Institute (NCI) of the National Institutes of Health (NIH). There are also numerous internet-based information websites that provide advice and other supporting information on how to quit smoking.
Since nicotine is known to be addictive, quitting smoking can be very difficult. Most support program for smoking cessation last between one to three months, and within six months, approximately 80% of the program participants have gone back to smoking again. It has been shown that prolonged treatment or therapy that continues beyond the usual 3 months treatment program can facilitate higher success rates in smoking cessation.
SCHIZOPHRENIA AND NICOTINE ADDICTION
Schizophrenia is a neurodevelopmental disorder of unknown etiology, pathogenesis and mechanism. Both genetic and environmental factors have been suggested to play a key role in its etiology. The disorder occurs in approximately 1% of the population and is fully symptomatic in the late teens to early adult life (Buckley et al., 2001). Schizophrenia is diagnosed through behavioral observation and voluntary reporting of mental difficulties. The diagnosis is difficult because of its unknown etiology, hence confirmation of the disorder is achieved by deduction from a list of other mental health diseases. Onset of schizophrenia is between the age of 15 and 25 in the males, while that in females is 3 to 5 years later. Approximately half of individuals with schizophrenia are prone to suicidal tendencies. Patients with schizophrenia generally present with co-morbid drug abuse. Schizophrenia is identified using positive symptoms such as delusions, hallucination, incoherent speech and depression (Kington and Murray, 2003). Negative symptoms of schizophrenia consist of dissociation from society, lack of motivation, impaired reasoning abilities and poor personal hygiene. A history of social functions in the home and workplace is also helpful in the diagnosis.
The brain of patients diagnosed with schizophrenia is markedly different from that of a normal brain. There is thinning of the cortex and an increase in size of the ventricles. In addition, glial cells were abnormally distributed in patients with schizophrenia, accumulating in the white matter instead of localizing in the cortex (Akbarian et al. 1993). This change in location disrupts the proper migration of neurons to the fetal cortex. It has also been observed that the prefrontal gamma-aminobutyric acid (GABA) axon terminals in schizophrenia patients are distorted, thereby affecting the secretion of GABA which is responsible for the excitation of neurons (Lewis, 1998). The sizes of the neurons were also observed to be smaller in size and lower in numbers, affecting the transmission of nerve impulses across the rest of the body.
Neurochemical abnormalities are also present in patients with schizophrenia. It has been observed that schizophrenia patients have a significantly higher number of basal ganglia dopamine receptors, resulting in a increase in dopaminergic transmission in response to stimulant administration. This dysregulation may be responsible for the variability in drug responses in the treatment of schizophrenia patients (Pearlson, 2005). Based on this observation, the usual treatment for schizophrenia then includes dopamine antagonists to control the overexpression of dopamine in the patient’s system. There are also changes in the function of N-methyl-D-aspartate (NMDA)/glutamate in patients with schizophrenia. The inhibitory neurotransmitter, GABA, also plays a role in the pathology of schizophrenia. Abnormal GABA expression levels have been observed in the anterior cingulated and hippocampus in schizophrenia brains.
It has been observed that psychiatrically normal individuals who suffered from physical health problems had a stronger attitude towards quitting smoking. On the other hand, individuals with psychological problems, including suspiciousness and disorganization had lower chances to quit smoking (Greene and Clarke
Studies have shown that 74% to 90% of schizophrenia patients smoke and this frequency is much higher than the number of smokers in the general public, as well as the number of smokers in other psychiatric diseases. Several investigators have suggested that smoking in schizophrenia patients must be due to an extreme motivation for smoking (Forchuk et al., 2002). Such motivation is influenced by the psychological effects of smoking in schizophrenia, which in turn triggers the patient to even smoke more. Other investigators have suggested that nicotine in cigarettes helps schizophrenia patients cope with stress, and induces them to relax and aids them in focusing and mental thinking (Gurpegui et al., 2007). Another hypothesis suggests that schizophrenia patients smoke because nicotine reduces the effect of antipsychotic drugs. It has been determined that nicotine affects the pharmacokinetic and pharmacodynamic properties of antipsychotic drugs, probably by influencing drug metabolism and decreasing the uncomfortable side effects of the medication. It may also be possible that nicotine, through its effective and specific chemical reactions in the body, may also decrease the bioavailability of antipsychotic medications in the body and therefore inhibits the effects of the drug on the patient. Nicotine has also been determined to aid in the reduction of side effects induced by the antipsychotic drugs through the regulation of dopamine expression.
Schizophrenia smokers follow a different style of smoking, separate from non-psychiatric smokers (Tidey et al. 2005). Major differences in smoking include the ratio between the number of measures to the number of puffs taken during a smoking session, the number of puffs smoked per cigarette, the total volume of each cigarette puff and the time between two puffs. Such differences in smoking style are essential in determining the blood nicotine levels in schizophrenia patients. The nicotine levels in the blood are usually higher when cigarette smoke in kept within the body for a longer period of time. It has also been determined that the puff volume and dration were not related.
The good test–retest reliabilities of the smoking topography measures indicate that the participants’ smoking behaviors were stable from day-to-day, as would be expected
from long-term smokers. It remains to be determined whether the topography measures reported are valid measures of normal smoking behavior in people with schizophrenia. It is possible that these measures are more characteristic of smoking behavior under unusual or somewhat stressful conditions. The differences in smoking behavior observed between participants who took atypical versus typical antipsychotics are consistent with, and may help to explain, results
from prior studies indicating that atypical antipsychotics are associated with lower risk of continued heavy smoking (Tsuang et al., 2005). For example, smokers with schizophrenia who take atypical antipsychotics have more success in smoking cessation treatments and experience lower levels of nicotine withdrawal symptoms following brief abstinence than those who take typical antipsychotics. Several explanations could account for atypical antipsychotics were associated with less intense smoking behavior: characteristics of patients who tend to be prescribed atypical antipsychotics could be associated with protection against ongoing heavy smoking, atypical antipsychotics could indirectly reduce smoking by improving symptoms of schizophrenia, or atypical antipsychotics could directly reduce smoking urges or the reinforcing effects of smoking (Horacek et al., 2006). Both of the latter explanations are supported by prior studies showing that patients with schizophrenia who were switched to clozapine spontaneously reduced their smoking. In addition, results from two recent studies indicate that olanzapine reduces smoking urges and nicotine withdrawal symptoms in non-psychiatric heavy smokers. It is noteworthy that smoking topography, nicotine withdrawal symptoms and smoking urges of patients with schizophrenia can be readily examined in the laboratory. Such laboratory procedures can therefore be used to investigate pharmacological and other methods of reducing smoking in this population.
In an isolated report, it has been observed that individuals who smoked cigarettes at the peak onset age for schizophrenia were less susceptible to suffer from schizophrenia at any time during the next 27 years. In addition, the research has determined that longer durations of smoking may decrease the probability of developing schizophrenia. It has been estimated that an increase of 10 cigarettes per day will decrease the risk of developing schizophrenia by 10% (Zammit et al., 2003).
Schizophrenia patients who smoke heavily usually have higher rates of health-related admissions to hospitals. Smoking causes an increase in dopamine production, which in turn enhances the positive symptoms of schizophrenia. The negative symptoms of schizophrenia are, on the other hand, reduced by smoking. Reports have observed that smoking decreases blood plasma levels of antipsychotics, most likely due to the chemical reactions that take place between nicotine and the antipsychotic medication (McCloughen, 2003). Therefore, it is a routine response that physicians would prescribe higher doses of the antipsychotic drug to smoking schizophrenia patients in order to achieve the desired blood plasma levels of the antipsychotic drug. The substantial increase in the dosage of antipsychotic drugs can be dangerous to the schizophrenia patient because this will mean that the side-effects of the antipsychotic drug will be stronger. Ina addition, it will be more expensive on the side of the patient to buy more antipsychotic drugs just to be able to reach the desired blood plasma levels. If only the patient were not smoking, the risk of drug side-effects and increased expenses could have been avoided. Once a schizophrenia patients stops smoking, the metabolism and clearance of the psychiatric medication is subdued and the blood plasma levels may increase. This reaction should be dealt with by lowering the dosage of the antipsychotic drug. Cytochrome P450 also processes psychiatric medications, including antipsychotic, antidepressant and anti-anxiety medications. In addition, cytochrome P450 also metabolises tobacco, wherein it destroys hydrocarbon agents but not nicotine.
There are external factors that affect smoking cessation attempts among patients with schizophrenia (Esterberg and Compton, 2005). It is interesting to note that schizophrenia patients do not correlate external social reinforcement to their smoking behavior, while most of the patients live with family members or group homes that had members who also smoke. Such setting usually induces a schizophrenia patient to start or continue, or even increase smoking, and also lose the probability to quit smoking. The scarcity of cessation programs in the immediate area of the schizophrenia patients also decreases the chances for a patient to stop smoking. The lack of programs for a specific population may be due to the knowledge that more effort is needed in order for such cessation program to be successful. It may be possible to provide smoking cessation programs to schizophrenia patients during their stay in the hospital. Since hospitals prohibit smoking at all times, such external setting may facilitate schizophrenia patients to successfully stop smoking. In addition, patients will be taught skills that will help them control their reactions to stressful situations, as well as learn techniques to induce relaxation.
The duration of schizophrenia may also affect the chances of smoking cessation in schizophrenia patients. Patients with early stages of schizophrenia were not fully aware of their addiction to smoking, especially their dependence to nicotine, and feel that it will be an easy task for them to stop smoking. On the other hand, patients with chronic schizophrenia were aware that of their nicotine addiction, as well as their low chances of being able to quit smoking. It should be noted that the degree of schizophrenia is positively correlated with the age of the patient, hence the issue of younger mindsets should also be considered in this scenario. Younger patients are usually more optimistic of achieving their goals, while older schizophrenia patients have a decreased sense of hope that they will be successful in their plan to quit smoking. Hence, the personal attitude of a patient is also a strong influence in smoking cessation success rates.
Interventions for smoking cessation in schizophrenia patients through the use of nicotine replacement therapy have not been successful because of the negative beliefs of the patients on the safety and effectiveness of the therapy. The administration of the antidepressant bupropion in smoking cessation programs was observed to well-tolerated by schizophrenia patients (Jorenby, 2002; Evins et al., 2005). In addition, the antidepressant did not make the symptoms of schizophrenia worse. Bupropion SR was introduced for smoking cessation in 1997 and is the first non-nicotine pharmacological treatment approved for this indication. It is a norepinephrine and dopamine reuptake inhibitor, and is thought to work by enhancing dopaminergic activity in the mesolimbic system and the nucleus accumbens. Bupropion SR is an effective therapy for smoking cessation in the general population and is associated with significantly higher smoking cessation rates than placebo. Treatment with bupropion SR is effective in the prevention of relapse to smoking in patients who have successfully quit and re-treatment with bupropion SR is also effective.
Schizophrenia is a neurodevelopmental disorder that is phenotypically expressed as a non-psychotic abnormal personality trait with cognitive, anatomical and psychophysiological symptoms. It has been categorized as a neurodevelopmental disorder because it is characterized by a decrease in number of neuropil and the absence of brain cell apoptosis. It has been suggested that schizophrenia is caused by abnormalities in cell migration in the fetal brain. Biochemical markers that identify schizophrenia include dopamine, GABA and glutamate systems, and NMDA and nicotinic receptors. Structural and functional brain imaging studies suggest both global and regional abnormalities as well as “disconnections” of specific
cerebral circuits. Despite the lack of knowledge regarding pathophysiology, there are reasonably effective treatments for schizophrenia. As the neurobiology of the disorder is unraveled, more effective, targeted treatments will become available.
Akbarian S, Vinuela A, Kim JJ, et al. (1993): Distorted distribution of nicotinamide-adeine dinucleotide phosphate-diaphorase neurons in temporal lobe of schizophrenics implies anomalous cortical development. Arch. Gen. Psych. 50:178–187.
Britton J, Bates C, Channer K, Cuthbertson L, Godfrey C, Jarvis M and McNeill A (2000): Nicotine Addiction in Britain. London: Royal College of Physician of London.
Buckley PF, Dayem M, Parker G and Weisser L (2001): Schizophrenia today: What do we know— and how sure are we? J. Psych. Prac. 7:244–246.
Epping-Jordan, MP, Watkins SS, Koob GF and Markou A (1998): Dramatic decreases in brain reward function during nicotine withdrawal. Nature 393(6680):76-79.
Esterberg ML and Compton MT (2005): Smoking behavior in persons with a schizophrenia-spectrum disorder: a qualitative investigation of the transtheoretical model. Soc. Sci. Med. 61:293–303.
Evins AE (2005): A double-blind placebo controlled trial of bupropion sustained release from smoking cessation in schizophrenia. J. Clin. Psychopharmacol. 25(3):218-225.
Forchuk C, Norman R, Malla A, Martin M-L, McLean T, Cheng S, Diaz K, McIntosh E, Rickwood A, Vos S and Gibney C (2002): Schizophrenia and the motivation for smoking. Pers. Psychiat. Care 38(2):41-49.
Gurpeguia M, Martı´nez-Ortegaa JM, Juradob D, Aguilara MC, Diazc FJ and de Leona J (2007): Subjective effects and the main reason for smoking in outpatients with schizophrenia: a case-control study. Comprehen. Psych. 48:186– 191.
Horacek J, Bubenikova-Valesova V, Kopecek M, Palenicek T, Dockery C, Mohr P and H¨oschl C (2006): Mechanism of action of atypical antipsychotic drugs and the neurobiology of schizophrenia. CNS Drugs 20(5):389-409.
Jorenby D (2002): Clinical efficacy of bupropion in the management of smoking cessation. Drugs 62 S2:25-35.
Kington J and Murray RM (2003): Schizophrenia: The new evidence. Ment. Health Rev. 8(3):31-34.
Lewis DA (1998): Chandelier cells: shedding light on altered cortical circuitry in schizophrenia. Mol. Psych. 3:466–471.
McCloughen A (2003): The association between schizophrenia and cigarette smoking: A review of the literature and implications for mental health nursing practice. Int. J. Ment. Health Nurs. 12:119–129.
National Institute on Drug Abuse (NIDA) (2006): Tobacco Addiction. NIH Publication Number 06-4342.
Pearlson GD (2005): Neurobiology of schizophrenia. Ann. Neurol. 48:556–566
Savage S, Covington EC, Heit HA, Hunt J, Joranson D and Schnoll SH (2001): Definitions Related to the Use of Opioids for the Treatment of Pain. American Academy of Pain Medicine, American Pain Society and the American Society of Addiction Medicine newsletter.
Tidey JW, Rohsenow DJ, Kaplan Gb and Swift RM (2005): Cigarette smoking topography in smokers with schizophrenia and matched non-psychiatric controls. Drug Alcoh. Dep. 80:259–265
Tsuang J, Fong TW and Pi E (2005): Pharmacological treatment of patients with schizophrenia and substance abuse disorders. Addict. Dis. Treat. 4(4):127-137.
World Health Organization (WHO) (1969): Technical Report. Series No. 407, Geneva.
Zammit S, et al. (2003): Investigating the association between cigarette smoking and schizophrenia in a cohort study. Am. J. Psych. 160(12):2216–2221.