A number of theories have been proposed to explain increased rates of<unk>  among people with<unk> . 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<unk>  results because many people with<unk>  are unemployed and inactive, so<unk>  relieves boredom. Research has found that this explanation alone cannot account for the extreme amount of<unk>  among people with<unk> . The personality hypothesis focused on the association between<unk>  and higher level of neuroticism and anxiety. This hypothesis proposed that anxiety as a symptom of<unk>  may contribute to<unk> . 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<unk>  often cannot cope with problems in constructive ways, so use of<unk>  as a psychological tool may result in a vicious cycle of more and more<unk> . The self-medication hypothesis argues that people with<unk>  use nicotine to compensate for the cognitive deficits that result from<unk> , the antipsychotic medication used to treat<unk> , or both. The cognitive effects hypothesis suggests that nicotine has positive effects on cognition, so<unk>  is used to improve neurocognitive dysfunction. In these hypotheses, one factor often implicated is the effects of institutionalization and boredom. However, people with<unk>  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<unk>  cessation, as symptoms of<unk>  cessation such as irritable mood, mental dulling, and increased appetite overlap with side effects of atypical antipsychotics. Some also argue that<unk>  works to reduce the side effects of antipsychotics. However, research shows no association between<unk>  and antipsychotic use after controlling for<unk> . Another frequently implicated factor is increased mental acuity associated with<unk> , important because of the mental dulling found over time in<unk> . However, both people with<unk>  and the general population experience this effect, so it cannot fully explain increased<unk>  in people with<unk> . A 2003 study of over 50,000 Swedish conscripts found that there was a small but significant protective effect of<unk>  cigarettes on the risk of developing<unk>  later in life. Many people with<unk>  have smoked<unk>  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<unk>  in the future than their nonsmoking peers. Criticisms One major criticism of social and psychological explanations of<unk>  in<unk>  is that most studies have failed to include personal perspectives of patients with<unk> . Studies including personal perspectives find that people with<unk>  generally start<unk>  for the same reasons as the general population, including social pressures and cultural and socioeconomic factors. People with<unk>  who are current smokers also cite similar reasons for<unk>  as people without<unk> , 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<unk>  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<unk>  and<unk>  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<unk>  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<unk>  have the most positive symptoms and a reduction in negative symptoms. Another area of research is the role of nicotinic receptors in<unk>  and<unk> . Studies show increased numbers of exposed nicotinic receptors, which could explain the pathology of both<unk>  and<unk> . However, others argue that the increase in nicotinic receptors is a result of persistent heavy<unk> , rather than<unk> . Another source of controversy is the relationship between<unk>  and sensory gating in<unk> . 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<unk>  to perceive the environment more effectively and engage in smoother motor functions. However, research shows this effect alone cannot account for increased<unk>  rates.
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