Re: Caution urged in interpreting a negative study of cannabis use and schizophrenia: a response to Dr. Christine Miller.
Re: Caution urged in interpreting a negative study of cannabis use and schizophrenia: a response to Dr. Christine Miller.
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回复：在解释大麻使用和精神分裂症的负面研究时应谨慎：对克里斯汀·米勒博士的回应。
DOI：
10.1016/j.schres.2014.02.012
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发表时间：
2014
影响因子：
4.5
通讯作者：
Delisi,LynnE
中科院分区：
文献类型：
--
作者：
Delisi,LynnE
代表我的合著者，我感谢米勒博士对我们研究的深思熟虑的评论(Proal等人，2014年)。然而，她的标题具有相当的误导性，因为它暗示我们的研究是“负面的”，我们只是报告大麻不会“导致”精神分裂症。事实并非如此；不幸的是，结论中的一句话被断章取义，因此具有误导性。我们的研究是对青少年时期有和没有滥用大麻的人进行的家庭研究。有4组人：有和没有滥用大麻的非精神病患者和患病前有和没有滥用大麻的精神分裂症患者。主要的研究分析表明，那些在青少年使用大麻后患上精神分裂症的人比那些使用大麻但没有患精神分裂症的人有更多的精神分裂症家族史，而且家庭病史升高与那些从不使用大麻的精神分裂症患者没有什么不同。这些结果表明，确定一个人在使用大麻后是否患上精神分裂症的关键因素是遗传风险增加。在这项研究设计中，我们没有测试没有精神病家族史的大麻使用是否会导致精神分裂症。为了验证这一假设，人们需要进行一项纵向研究，检查没有精神分裂症家族史的吸食大麻和不吸食大麻的人，并确定随着时间的推移，与不吸食大麻的人相比，吸食大麻的人是否会出现明显的精神分裂症过剩。我们建议将这一纵向设计作为我们研究的下一步，相反的是，我们将检查精神分裂症的高遗传风险人群，并比较那些滥用大麻和不滥用大麻的人在精神分裂症未来发展中的显著差异。后者将显示导致疾病的基因与环境的相互作用。前者可能表明，单靠大麻就可能“导致”精神分裂症。我们认为，与其说问题在于样本量不足以发现相关差异，不如说是
On behalf of my co-authors, I thank Dr. Miller for her thoughtful comments about our study (Proal et al., 2014). However, her title is quite misleading in that it implies that our study was “negative” and that we were simply reporting that cannabis does not “cause” schizophrenia. This is not so; unfortunately one sentence in the conclusion was taken out of context and as such was misleading. Our study was a family study of people who did and did not abuse cannabis as adolescents. There were 4 groups: non-psychotic individuals who did and did not abuse cannabis and people with schizophrenia who did and did not abuse cannabis prior to their illness. What the main study analysis showed was that those individuals who developed schizophrenia after cannabis use in adolescents had a significantly greater family history of schizophrenia than those who used cannabis and did not develop schizophrenia and an elevated family history no different than those with schizophrenia who never used cannabis. These results suggest that the key element for determining whether someone develops schizophrenia after cannabis use is an elevated genetic risk.We did not test in this study design whether cannabis use without a family history of psychosis could cause schizophrenia. In order to test that hypothesis one would need to perform a longitudinal study examining people with and without cannabis abuse who have no family history of schizophrenia and determine whether over time there would be a significant excess of schizophrenia in those that used cannabis compared with those who did not. The converse of this longitudinal design, which we proposed as the next step to our study, would be to examine people at high genetic risk for schizophrenia and compare those who did and did not abuse cannabis for significant differences in later development of schizophrenia. The latter would show an interaction of genes with environment to cause illness. The former might show that cannabis alone could “cause” schizophrenia. We believe the issue is not so much that the sample size was underpowered to detect differences related
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