Abstract
Recent data suggests that the prevalence of smoking in schizophrenia remains high. While reports suggest that smoking increases the risk of developing schizophrenia, the potential causative role of smoking in this relationship needs further investigation. Smokers with schizophrenia are more likely to have more intense positive symptoms and lower cognitive function, but diminished intensity of extrapyramidal side effects than nonsmoking patients with schizophrenia. They were also more likely to exhibit aggressive behaviour compared to nonsmokers, which could suggest higher levels of baseline aggression. The significant cost associated with regular tobacco expenditure can detract from investment in key domains. Large-scale trials have shown that pharmacotherapy for smoking cessation is effective and does not worsen the risk of developing neuropsychiatric symptoms compared to placebo. Electronic cigarette use among schizophrenia patients is high, and there is emerging evidence supportive of its efficacy. Future improvements include large-scale trials assessing the utility, efficacy, and safety of electronic cigarettes in schizophrenia patients.
Highlights
One is a selfmedicative hypothesis, another is a theory that there is shared genetic propensity in smoking and development of schizophrenia, and the third is smoking itself may play a role in the development of schizophrenia
Evidence suggests pharmacotherapy has a low but measurable effectiveness at attaining smoking cessation schizophrenia patients; current evidence is limited by lack of studies that adjust for active psychiatric symptoms or polysubstance use
While smoking cessation should be encouraged, it is important to note that most the evidence that attests to the safety of smoking cessation and drugs such as varenicline, bupropion, and nicotine replacement therapy (NRT) in schizophrenia patients was in patients in medical and psychiatric remission
Summary
Smokers with schizophrenia inhaled deeper and for longer durations, compared to normal controls, thereby exposing themselves to higher levels of toxic elements of tobacco [5]. They consumed higher quantities of cigarettes and had higher levels of nicotine dependence compared to smokers without schizophrenia [6]. Nicotine action on the nAChRs of neurons that project to the ventral tegmental area (VTA) and the mesolimbic pathway is thought to release dopamine, which occurs partly in relation to the activation of the reward circuitry of the VTA [12]. Nicotine has been shown to modulate the release of most neurotransmitters, including dopamine, glutamate, noradrenaline, serotonin, opioids, acetylcholine, and γ-aminobutyric acid (GABA) [13]
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