Department of Psychiatry and Psychology, School for Mental Health and Neuroscience, European Graduate School of Neuroscience, EURON, Maastricht University Medical Centre, Maastricht, the Netherlands.
Can J Psychiatry. 2013 Jan;58(1):44-51. doi: 10.1177/070674371305800109.
Recent studies have provided robust evidence for an association between childhood trauma (CT) and psychosis. Meta-analyses have quantified the association, pointing to odds ratios in the order of around 3, and prospective studies have shown that reverse causation is unlikely to explain the association. However, more work is needed to address the possibility of a gene-environment correlation, that is, whether genetic risk for psychosis predicts exposure to CT. Nevertheless, multiple studies have convincingly shown that the association between CT and psychosis remains strong and significant when controlling for genetic risk, in agreement with a possible causal association. In addition, several studies have shown plausible psychological and neurobiological mechanisms linking adverse experiences to psychosis, including induction of social defeat and reduced self-value, sensitization of the mesolimbic dopamine system, changes in the stress and immune system, and concomitant changes in stress-related brain structures, such as the hippocampus and the amygdala, findings that should be integrated, however, in more complex models of vulnerability. It is currently unclear whether genetic vulnerability plays a role in conferring the mental consequences of adversity, and which genes are likely to be involved. The current, limited evidence points to genes that are not specifically involved in psychosis but more generally in regulating mood (serotonin transporter gene), neuroplasticity (brain-derived neurotrophic factor), and the stress-response system (FKBP5), in line with a general effect of CT on a range of mental disorders, rather than suggesting specificity for psychosis.
最近的研究为儿童创伤（CT）与精神病之间的关联提供了有力的证据。荟萃分析已经量化了这种关联，指出其优势比约为 3，前瞻性研究表明，反向因果关系不太可能解释这种关联。然而，需要做更多的工作来解决基因-环境相关性的可能性，也就是说，精神病的遗传风险是否预测了 CT 的暴露。尽管如此，多项研究令人信服地表明，在控制遗传风险的情况下，CT 与精神病之间的关联仍然强烈且显著，这与可能的因果关联一致。此外，一些研究已经表明，将不良经历与精神病联系起来的合理心理和神经生物学机制，包括诱导社会挫败感和降低自我价值感、中脑边缘多巴胺系统的敏感化、应激和免疫系统的变化，以及伴随而来的与应激相关的大脑结构的变化，如海马体和杏仁核，然而，这些发现应该整合到更复杂的易感性模型中。目前尚不清楚遗传易感性是否在逆境的心理后果中发挥作用，以及哪些基因可能参与其中。目前有限的证据表明，基因易感性不是专门参与精神病，而是更普遍地参与调节情绪（血清素转运体基因）、神经可塑性（脑源性神经营养因子）和应激反应系统（FKBP5），这与 CT 对一系列精神障碍的普遍影响一致，而不是暗示对精神病的特异性。
