Van Os J, Verdoux H
Department of Psychiatry and Neuropsychology, European Graduate School of Neuroscience, Maastricht University, The Netherlands.
Encephale. 1998 Mar-Apr;24(2):125-31.
Psychiatric disorders are thought to arise as a result of interactions between genetic vulnerability and environmental risk factors. However, research methods to actually investigate the pattern of hypothesized interactions have only recently been developed. In this article, we review the evidence that genes increase the risk for psychosis by making individuals more sensitive to environmental risk factors (genotype-environment interaction), or by making individuals more likely to select high-risk environments (genotype-environment correlation). It is likely that at least some of the impact of genes on the occurrence of psychosis is mediated through (sensitivity for ) environmental risk factors such as a dysfunctional early family rearing environment, paternal absence, use of cannabis, complications of birth and pregnancy, stressful life events and unknown environmental risk factors associated with urban life and membership of certain ethnic groups. With the advent of molecular genetics, further knowledge about possible genotype-environment interactions is urgently required in order to develop and improve strategies for the prevention and early treatment of psychosis.
精神障碍被认为是遗传易感性与环境风险因素相互作用的结果。然而,实际研究假设相互作用模式的研究方法直到最近才得以发展。在本文中,我们回顾了相关证据,即基因通过使个体对环境风险因素更敏感(基因-环境相互作用),或使个体更有可能选择高风险环境(基因-环境相关性),从而增加患精神病的风险。基因对精神病发生的影响很可能至少部分是通过对环境风险因素的(敏感性)介导的,这些环境风险因素包括功能失调的早期家庭养育环境、父亲缺席、使用大麻、出生和怀孕并发症、压力性生活事件以及与城市生活和某些种族群体成员身份相关的未知环境风险因素。随着分子遗传学的出现,迫切需要进一步了解可能的基因-环境相互作用,以便制定和改进预防和早期治疗精神病的策略。