Ben Amar Mohamed, Potvin Stéphane
Faculties of Continuing Education and Graduate Studies, University of Montreal, Quebec, Canada.
J Psychoactive Drugs. 2007 Jun;39(2):131-42. doi: 10.1080/02791072.2007.10399871.
Growing evidence supports the hypothesis that cannabis consumption is a risk factor for the development of psychotic symptoms. Nonetheless, controversy remains about the causal nature of the association. This review takes the debate further through a critical appraisal of the evidence. An electronic search was performed, allowing to identify 622 studies published until June 1st 2005. Longitudinal studies and literature reviews were selected if they addressed specifically the issues of the cannabis/psychosis relationship or possible mechanisms involved. Ten epidemiological studies were relevant: three supported a causal relationship between cannabis use and diagnosed psychosis; five suggested that chronic cannabis intake increases the frequency of psychotic symptoms, but not of diagnosed psychosis; and two showed no causal relationship. Potential neurobiological mechanisms were also identified, involving dopamine, endocannabinoids, and brain growth factors. Although there is evidence that cannabis use increases the risk of developing psychotic symptoms, the causal nature of this association remains unclear. Contributing factors include heavy consumption, length and early age of exposure, and psychotic vulnerability. This conclusion should be mitigated by uncertainty arising from cannabis use assessment, psychosis measurement, reverse causality and control of residual confounding.
越来越多的证据支持这样一种假说,即吸食大麻是出现精神病症状的一个风险因素。尽管如此,关于这种关联的因果性质仍存在争议。本综述通过对证据的批判性评估进一步展开了这场辩论。进行了一次电子检索,共识别出截至2005年6月1日发表的622项研究。如果纵向研究和文献综述专门探讨了大麻与精神病的关系或所涉及的可能机制问题,则将其纳入。有10项流行病学研究与之相关:3项支持大麻使用与已诊断精神病之间存在因果关系;5项表明长期吸食大麻会增加精神病症状的发生频率,但不会增加已诊断精神病的发生频率;2项显示不存在因果关系。还确定了潜在的神经生物学机制,涉及多巴胺、内源性大麻素和脑生长因子。虽然有证据表明使用大麻会增加出现精神病症状的风险,但这种关联的因果性质仍不清楚。促成因素包括大量吸食、接触的时长和年龄以及精神病易感性。大麻使用评估、精神病测量、反向因果关系和残余混杂因素控制所产生的不确定性会削弱这一结论。