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Abstract：
Previous studies have indicated that smoking is linked to an increased risk of developing schizophrenia, and that individuals with schizophrenia are more prone to engaging in antisocial behavior. However, the causal effects of smoking behaviors on antisocial behavior and the potential mediating role of schizophrenia remains largely unclear.
In the present study, using the summary data from genome wide association studies of smoking phenotypes (N = 323,386-805,431), schizophrenia (Ncases = 53,386, Ncontrols = 77,258), and antisocial behavior (N = 85,359), we assessed bidirectional causality between smoking phenotypes and schizophrenia by the Mendelian randomization (MR) approach. Using a two-step MR approach, we further examined whether causal effects of smoking phenotypes/schizophrenia on antisocial behavior were mediated by schizophrenia/smoking phenotypes.
The results showed that smoking initiation (SmkInit) and age of smoking initiation (AgeSmk) causally increase the risk of schizophrenia (SmkInit: OR = 2.06, 95% CI = 1.77-2.39, p = 4.36 × 10-21 ; AgeSmk: OR = 0.32, 95% CI = 0.16-0.62, p = 8.11 × 10-4 , Bonferroni corrected). However, there was no causal effect that liability to schizophrenia leads to smoking phenotypes. MR evidence also revealed causal influences of SmkInit and the amount smoked (CigDay) on antisocial behavior (SmkInit: OR = 1.28, 95% CI = 1.17-1.41, p = 2.53 × 10-7 ; CigDay: OR = 1.16, 95% CI = 1.06-1.27, p = 1.60 × 10-3 , Bonferroni corrected). Furthermore, the mediation analysis indicated that the relationship between SmkInit and antisocial behavior was partly mediated by schizophrenia (mediated proportion = 6.92%, 95% CI = 0.004-0.03, p = 9.66 × 10-3 ).
These results provide compelling evidence for taking smoking interventions as a prevention strategy for schizophrenia and its related antisocial behavior.
In the present study, using the summary data from genome wide association studies of smoking phenotypes (N = 323,386-805,431), schizophrenia (Ncases = 53,386, Ncontrols = 77,258), and antisocial behavior (N = 85,359), we assessed bidirectional causality between smoking phenotypes and schizophrenia by the Mendelian randomization (MR) approach. Using a two-step MR approach, we further examined whether causal effects of smoking phenotypes/schizophrenia on antisocial behavior were mediated by schizophrenia/smoking phenotypes.
The results showed that smoking initiation (SmkInit) and age of smoking initiation (AgeSmk) causally increase the risk of schizophrenia (SmkInit: OR = 2.06, 95% CI = 1.77-2.39, p = 4.36 × 10-21 ; AgeSmk: OR = 0.32, 95% CI = 0.16-0.62, p = 8.11 × 10-4 , Bonferroni corrected). However, there was no causal effect that liability to schizophrenia leads to smoking phenotypes. MR evidence also revealed causal influences of SmkInit and the amount smoked (CigDay) on antisocial behavior (SmkInit: OR = 1.28, 95% CI = 1.17-1.41, p = 2.53 × 10-7 ; CigDay: OR = 1.16, 95% CI = 1.06-1.27, p = 1.60 × 10-3 , Bonferroni corrected). Furthermore, the mediation analysis indicated that the relationship between SmkInit and antisocial behavior was partly mediated by schizophrenia (mediated proportion = 6.92%, 95% CI = 0.004-0.03, p = 9.66 × 10-3 ).
These results provide compelling evidence for taking smoking interventions as a prevention strategy for schizophrenia and its related antisocial behavior.
摘要：
目的：以前的研究表明，吸烟与患精神分裂症的风险增加有关，精神分裂症患者更容易从事反社会行为。然而,吸烟行为对反社会行为的因果关系以及精神分裂症的潜在中介作用尚不清楚。
方法：在本研究中，使用来自吸烟表型全基因组关联研究的汇总数据(N=323,386-805,431)，精神分裂症（Ncases=53,386，Ncontrols=77,258），和反社会行为(N=85,359)，我们通过孟德尔随机化(MR)方法评估了吸烟表型与精神分裂症之间的双向因果关系.使用两步MR方法，我们进一步研究了吸烟表型/精神分裂症对反社会行为的因果效应是否由精神分裂症/吸烟表型介导.
结果：结果显示，开始吸烟（SmkInit）和开始吸烟年龄（AgeSmk）会增加精神分裂症的风险（SmkInit：OR=2.06，95％CI=1.77-2.39，p=4.36×10-21；AgeSmk：OR=0.32，95％CI=0.16-0.62，p=8.11×10-4，Bonferroni更正）。然而,精神分裂症责任导致吸烟表型没有因果关系.MR证据还揭示了SmkInit和吸烟量（CigDay）对反社会行为的因果关系（SmkInit：OR=1.28，95％CI=1.17-1.41，p=2.53×10-7；CigDay：OR=1.16，95％CI=1.06-1.27，p=1.60×10-3，Bonferroni更正）。此外，中介分析表明，SmkInit与反社会行为之间的关系部分是由精神分裂症介导的(中介比例=6.92%，95%CI=0.004-0.03，p=9.66×10-3)。
结论：这些结果为将吸烟干预作为精神分裂症及其相关反社会行为的预防策略提供了令人信服的证据。
方法：在本研究中，使用来自吸烟表型全基因组关联研究的汇总数据(N=323,386-805,431)，精神分裂症（Ncases=53,386，Ncontrols=77,258），和反社会行为(N=85,359)，我们通过孟德尔随机化(MR)方法评估了吸烟表型与精神分裂症之间的双向因果关系.使用两步MR方法，我们进一步研究了吸烟表型/精神分裂症对反社会行为的因果效应是否由精神分裂症/吸烟表型介导.
结果：结果显示，开始吸烟（SmkInit）和开始吸烟年龄（AgeSmk）会增加精神分裂症的风险（SmkInit：OR=2.06，95％CI=1.77-2.39，p=4.36×10-21；AgeSmk：OR=0.32，95％CI=0.16-0.62，p=8.11×10-4，Bonferroni更正）。然而,精神分裂症责任导致吸烟表型没有因果关系.MR证据还揭示了SmkInit和吸烟量（CigDay）对反社会行为的因果关系（SmkInit：OR=1.28，95％CI=1.17-1.41，p=2.53×10-7；CigDay：OR=1.16，95％CI=1.06-1.27，p=1.60×10-3，Bonferroni更正）。此外，中介分析表明，SmkInit与反社会行为之间的关系部分是由精神分裂症介导的(中介比例=6.92%，95%CI=0.004-0.03，p=9.66×10-3)。
结论：这些结果为将吸烟干预作为精神分裂症及其相关反社会行为的预防策略提供了令人信服的证据。
