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      Does tobacco use cause psychosis? Systematic review and meta-analysis

      research-article
      , MD a , , , Dr, MRCPsych b , , * , , FRS b , , FRCPsych b
      The Lancet. Psychiatry
      Elsevier

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          Summary

          Background

          Although the association between psychotic illness and cigarette smoking is well known, the reasons are unclear why people with psychosis are more likely to smoke than are the general population. We aimed to test several hypotheses. First, that daily tobacco use is associated with an increased risk of psychotic illness in both case-control and prospective studies. Second, that smoking is associated with an earlier age at onset of psychotic illness. Finally, that an earlier age at initiation of smoking is associated with an increased risk of psychosis. We also aimed to derive an estimate of the prevalence of smoking in patients presenting with their first episode of psychosis.

          Methods

          We searched Embase, Medline, and PsycINFO and selected observational studies in which rates of smoking were reported in people with psychotic disorders, compared with controls. We calculated the weighted mean difference for age at onset of psychosis and age at initiation of smoking. For categorical outcomes, we calculated odds ratios from cross-sectional studies and risk ratios from prospective studies.

          Findings

          Of 3717 citations retrieved, 61 studies comprising 72 samples met inclusion criteria. The overall sample included 14 555 tobacco users and 273 162 non-users. The prevalence of smoking in patients presenting with their first episode of psychosis was 0·57 (95% CI 0·52–0·62; p<0·0001). In case-control studies, the overall odds ratio for the first episode of psychosis in smokers versus non-smokers was 3·22 (95% CI 1·63–6·33), with some evidence of publication bias (Egger's test p=0·018, Begg's test p=0·007). For prospective studies, we calculated an overall relative risk of new psychotic disorders in daily smokers versus non-smokers of 2·18 (95% CI 1·23–3·85). Daily smokers developed psychotic illness at an earlier age than did non-smokers (weighted mean difference −1·04 years, 95% CI −1·82 to −0·26). Those with psychosis started smoking at a non-significantly earlier age than did healthy controls (−0·44 years, 95% CI −1·21 to 0·34).

          Interpretation

          Daily tobacco use is associated with increased risk of psychosis and an earlier age at onset of psychotic illness. The possibility of a causal link between tobacco use and psychosis merits further examination.

          Funding

          NIHR Maudsley Biomedical Research Centre.

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          Most cited references85

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          Analysis of variance—why it is more important than ever

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            Causal association between cannabis and psychosis: examination of the evidence.

            Controversy remains as to whether cannabis acts as a causal risk factor for schizophrenia or other functional psychotic illnesses. To examine critically the evidence that cannabis causes psychosis using established criteria of causality. We identified five studies that included a well-defined sample drawn from population-based registers or cohorts and used prospective measures of cannabis use and adult psychosis. On an individual level, cannabis use confers an overall twofold increase in the relative risk for later schizophrenia. At the population level, elimination of cannabis use would reduce the incidence of schizophrenia by approximately 8%, assuming a causal relationship. Cannabis use appears to be neither a sufficient nor a necessary cause for psychosis. It is a component cause, part of a complex constellation of factors leading to psychosis. Cases of psychotic disorder could be prevented by discouraging cannabis use among vulnerable youths. Research is needed to understand the mechanisms by which cannabis causes psychosis.
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              Smoking-induced ventral striatum dopamine release.

              Substantial evidence from animal models demonstrates that dopamine release in the ventral striatum underlies the reinforcing properties of nicotine. The authors used [(11)C]raclopride bolus-plus-continuous-infusion positron emission tomography (PET) to determine smoking-induced ventral striatum dopamine release in humans. Twenty nicotine-dependent smokers (who smoked > or =15 cigarettes/day) underwent a [(11)C]raclopride bolus-plus-continuous-infusion PET session. During the session, subjects had a 10-minute break outside the PET apparatus during which 10 subjects smoked a cigarette and 10 did not smoke (as a control condition). The group that smoked had greater reductions in [(11)C]raclopride binding potential in ventral striatum regions of interest than the group that did not smoke, particularly in the left ventral caudate/nucleus accumbens and left ventral putamen (range for smoking group=-25.9% to -36.6% reduction). Significant correlations were found between change from before to after the smoking break in craving ratings and change from before to after the break in binding potential for these two regions. Nicotine-dependent subjects who smoked during a break in PET scanning had greater reductions in [(11)C]raclopride binding potential (an indirect measure of dopamine release) than nicotine-dependent subjects who did not smoke. The magnitude of binding potential changes was comparable to that found in studies that used similar methods to examine the effects of other addictive drugs.
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                Author and article information

                Contributors
                Journal
                Lancet Psychiatry
                Lancet Psychiatry
                The Lancet. Psychiatry
                Elsevier
                2215-0366
                2215-0374
                10 July 2015
                August 2015
                10 July 2015
                : 2
                : 8
                : 718-725
                Affiliations
                [a ]Torrevieja's Hospital, Alicante, Spain
                [b ]Department of Psychosis Studies, King's College, London, UK
                Author notes
                [* ]Correspondence to: Dr Sameer Jauhar, Department of Psychosis Studies, King's College, London SE5 8AF, UK sameer.jauhar@ 123456kcl.ac.uk
                [†]

                Joint first authors

                Article
                S2215-0366(15)00152-2
                10.1016/S2215-0366(15)00152-2
                4698800
                26249303
                1944923d-8496-4ebe-88f4-64c038aab324
                © 2015 Gurillo et al. Open Access article distributed under the terms of CC BY-NC-ND

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by-NC-ND/4.0/).

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