Schizophrenia and tobacco smoking

Studies across 20 countries showed that people with schizophrenia were much more likely to smoke than those without this diagnosis. For example, in the United States, 90% or more of people with schizophrenia smoked, compared to 20% of the general population in 2006.

It is well established that smoking is more prevalent among people with schizophrenia than the general population as well as those with other psychiatric diagnoses. There is currently no definitive explanation for this difference. Many social, psychological, and biological explanations have been proposed, but today research focuses on neurobiology.

One important reason people smoke cigarettes is due to finding it enjoyable. However, increased rates of smoking among people with schizophrenia have a number of serious impacts, including increased rates of mortality, increased risks of suicidal behavior and cardiovascular disease, reduced treatment effectiveness, and greater financial hardship. Studies have also shown that in a male population, having a schizophrenia spectrum disorder makes it likely for people to use more tobacco. As a result, researchers believe it is important for mental health professionals to combat smoking among people with schizophrenia.

Causes

A number of theories have been proposed to explain increased rates of smoking among people with schizophrenia.

Psychological and social theories

Several psychological and social explanations have been proposed. The earliest explanations were based on psychoanalytic theory.

The socioeconomic/environmental hypothesis proposed that smoking results because many people with schizophrenia are unemployed and inactive, so smoking relieves boredom. Research has found that this explanation alone cannot account for the extreme amount of smoking among people with schizophrenia.

The personality hypothesis focused on the association between smoking and higher level of neuroticism and anxiety. This hypothesis proposed that anxiety as a symptom of schizophrenia may contribute to smoking.

The psychological tool hypothesis argues that smokers use nicotine to manipulate their mental state in response to various environmental conditions, such as reducing stress and managing negative emotions. Research on this hypothesis notes that people with schizophrenia often cannot cope with problems in constructive ways, so use of smoking as a psychological tool may result in a vicious cycle of more and more smoking.

The self-medication hypothesis argues that people with schizophrenia use nicotine to compensate for the cognitive deficits that result from schizophrenia, the antipsychotic medication used to treat schizophrenia, or both.

The cognitive effects hypothesis suggests that nicotine has positive effects on cognition, so smoking is used to improve neurocognitive dysfunction.

In these hypotheses, one factor often implicated is the effects of institutionalization and boredom. However, people with schizophrenia smoke at higher rates and for longer periods than other groups that experience both institutionalization and boredom.

Another factor often implicated is to the side effects of antipsychotics. Atypical antipsychotics may work against smoking cessation, as symptoms of smoking cessation such as irritable mood, mental dulling, and increased appetite overlap with side effects of atypical antipsychotics. Some also argue that smoking works to reduce the side effects of antipsychotics. However, research shows no association between smoking and antipsychotic use after controlling for schizophrenia.

Another frequently implicated factor is increased mental acuity associated with smoking, important because of the mental dulling found over time in schizophrenia. However, both people with schizophrenia and the general population experience this effect, so it cannot fully explain increased smoking in people with schizophrenia.

A 2003 study of over 50,000 Swedish conscripts found that there was a small but significant protective effect of smoking cigarettes on the risk of developing schizophrenia later in life. Many people with schizophrenia have smoked tobacco products long before they are diagnosed with the illness, and a cohort study of Israeli conscripts found that healthy adolescent smokers were more likely to develop schizophrenia in the future than their nonsmoking peers.

Criticisms

One major criticism of social and psychological explanations of smoking in schizophrenia is that most studies have failed to include personal perspectives of patients with schizophrenia. Studies including personal perspectives find that people with schizophrenia generally start smoking for the same reasons as the general population, including social pressures and cultural and socioeconomic factors. People with schizophrenia who are current smokers also cite similar reasons for smoking as people without schizophrenia, primarily relaxation, force of habit, and settling nerves. However, 28% cite psychiatric issues, including response to auditory hallucinations and reducing the side effects of medication. The major themes found in studies of personal perspectives are habit and routine, socialization, relaxation, and addiction to nicotine. It is argued that smoking provides structure and activity, both of which may be lacking in the lives of those with serious mental illness.

Another major criticism is based on the finding that the association between smoking and schizophrenia is about as strong across all cultures. This finding implies that the association is not solely social or cultural, but rather has a strong biological component.

Biological theories

Biological theories focus on the role of dopamine, particularly how negative symptoms such as social withdrawal and apathy may be caused by a deficiency of dopamine in the prefrontal cortex while positive symptoms such as delusions and hallucinations may be caused by excess dopamine in the mesolimbic pathway. Nicotine increases the release of dopamine, so it is hypothesized that smoking helps to correct dopamine deficiency in the prefrontal cortex and thus relieve negative symptoms.

It is unclear, however, how nicotine interacts with positive symptoms, as it would follow from this theory that nicotine would exacerbate excess dopamine in the mesolimbic pathway and thus positive symptoms as well. One theory argues that the beneficial effects of nicotine on negative symptoms outweigh possible exacerbation of positive symptoms. Another theory is based on animal models showing that chronic nicotine use eventually results in a reduction in dopamine, thus alleviating positive symptoms. However, human studies show conflicting results, including some studies that show that smokers with schizophrenia have the most positive symptoms and a reduction in negative symptoms.

Another area of research is the role of nicotinic receptors in schizophrenia and smoking. Studies show increased numbers of exposed nicotinic receptors, which could explain the pathology of both smoking and schizophrenia. However, others argue that the increase in nicotinic receptors is a result of persistent heavy smoking, rather than schizophrenia.

Another source of controversy is the relationship between smoking and sensory gating in schizophrenia. Nicotine may help improve auditory gating, the ability to screen out intrusive environmental sounds. This may help improve attention spans and reduce auditory hallucinations, allowing people with schizophrenia to perceive the environment more effectively and engage in smoother motor functions. However, research shows this effect alone cannot account for increased smoking rates.