More than half patients with schizophrenia are smokers. Heavy smoking has been correlated to more severe positive symptoms, a higher number of hospitalizations and a less efficiency of antipsychotics. Unfortunately, abstinence is difficult to achieve in these patients, therefore it is importance of understanding the link between smoking and psychosis.

Analyzing the complex relationship between schizophrenia and nicotine’s effects on the human brain.

The study was a review of literature over the past 10 years based on the pubmed database.

Smoking might be a precipitating factor in the development of schizophrenia since it preceded the onset of this illness for several years.Shared genetic background was also emphasized establishing a complex biological link between nicotine and schizophrenia.

In another approach, the “self-medication hypothesis” has been proposed suggesting a beneficial effect of nicotine on both cognitive impairment and negative symptoms in schizophrenia, related to the regulation of the dopamine and nicotinic receptor systems. But this conclusion is controversial since other studies concluded to a more neurocognitive impairment in smokers compared to controlled population.

Smoking in schizophrenia is a complex “phenomenon” that remains, so far, misunderstood. Greater differences might exist between heavy and light smokers making it more difficult to point out the exact effect of nicotine on the brain. Smoking cessation therapies taking into account the specificity of patients with schizophrenia should be more developed.

No significant relationships.

Limited evidence has suggested that quitting smoking increases the incidence of major depressive episodes (MDEs), particularly for smokers with a history of depression. Further evidence for this increase would have important implications for guiding smoking cessation.

Spanish- and English-speaking smokers without a current MDE (n=3056) from an international, online smoking cessation trial were assessed for abstinence 1 month after their initial quit date and followed for a total of 12 months. Incidence of screened MDE was examined as a function of abstinence and depression history.

Continued smoking, not abstinence, predicted MDE screened at 1 month [smoking 11.5% v. abstinence 7.8%, odds ratio (OR) 1.36, 95% confidence interval (CI) 1.04–1.78, p=0.02] but not afterwards (smoking 11.1% v. abstinence 9.8%, OR 1.05, 95% CI 0.77–1.45, p=0.74). Depression history predicted MDE screened at 1 month (history 17.1% v. no history 8.6%, OR 1.71, 95% CI 1.29–2.27, p<0.001) and afterwards (history 21.7% v. no history 8.3%, OR 3.87, 95% CI 2.25–6.65, p<0.001), although the interaction between history and abstinence did not.

Quitting smoking was not associated with increased MDE, even for smokers with a history of depression, although a history of depression was. Instead, not quitting was associated with increased MDE shortly following a quit attempt. Results from this online, large, international sample of smokers converge with similar findings from smaller, clinic-based samples, suggesting that in general, quitting smoking does not increase the incidence of MDEs.