Veling W, Mackenbach J P, van Os J, Hoek H W
Parnassia Psychiatric Institute, The Hague, The Netherlands.
Psychol Med. 2008 Sep;38(9):1251-6. doi: 10.1017/S0033291708003474. Epub 2008 May 19.
Cannabis use may be a risk factor for schizophrenia. Part of this association may be explained by genotype-environment interaction, and part of it by genotype-environment correlation. The latter issue has not been explored. We investigated whether cannabis use is associated with schizophrenia, and whether gene-environment correlation contributes to this association, by examining the prevalence of cannabis use in groups with different levels of genetic predisposition for schizophrenia.
Case-control study of first-episode schizophrenia. Cases included all non-Western immigrants who made first contact with a physician for schizophrenia in The Hague, The Netherlands, between October 2000 and July 2005 (n=100; highest genetic predisposition). Two matched control groups were recruited, one among siblings of the cases (n=63; intermediate genetic predisposition) and one among immigrants who made contact with non-psychiatric secondary health-care services (n=100; lowest genetic predisposition). Conditional logistic regression analyses were used to predict schizophrenia as a function of cannabis use, and cannabis use as a function of genetic predisposition for schizophrenia.
Cases had used cannabis significantly more often than their siblings and general hospital controls (59, 21 and 21% respectively). Cannabis use predicted schizophrenia [adjusted odds ratio (OR) cases compared to general hospital controls 7.8, 95% confidence interval (CI) 2.7-22.6; adjusted OR cases compared to siblings 15.9 (95% CI 1.5-167.1)], but genetic predisposition for schizophrenia did not predict cannabis use [adjusted OR intermediate predisposition compared to lowest predisposition 1.2 (95% CI 0.4-3.8)].
Cannabis use was associated with schizophrenia but there was no evidence for genotype-environment correlation.
使用大麻可能是精神分裂症的一个风险因素。这种关联的部分原因可能是基因 - 环境相互作用，部分原因可能是基因 - 环境相关性。后一个问题尚未得到探讨。我们通过检查不同精神分裂症遗传易感性水平组中大麻使用的患病率，来研究使用大麻是否与精神分裂症相关，以及基因 - 环境相关性是否促成了这种关联。
对首发精神分裂症进行病例对照研究。病例包括2000年10月至2005年7月期间在荷兰海牙首次因精神分裂症与医生接触的所有非西方移民（n = 100；遗传易感性最高）。招募了两个匹配的对照组，一组来自病例的兄弟姐妹（n = 63；遗传易感性中等），另一组来自与非精神科二级医疗服务接触的移民（n = 100；遗传易感性最低）。使用条件逻辑回归分析来预测精神分裂症与大麻使用的函数关系，以及大麻使用与精神分裂症遗传易感性的函数关系。
病例使用大麻的频率显著高于其兄弟姐妹和综合医院对照组（分别为59%、21%和21%）。大麻使用可预测精神分裂症[与综合医院对照组相比，病例的调整优势比（OR）为7.8，95%置信区间（CI）为2.7 - 22.6；与兄弟姐妹相比，病例的调整OR为15.9（95%CI为1.5 - 167.1）]，但精神分裂症的遗传易感性不能预测大麻使用[与最低易感性相比，中等易感性的调整OR为1.2（95%CI为0.4 - 3.8）]。
大麻使用与精神分裂症相关，但没有证据表明存在基因 - 环境相关性。
