van Os J, Marcelis M
Department of Psychiatry and Neuropsychology, European Graduate School of Neuroscience, Maastricht University, The Netherlands.
Schizophr Res. 1998 Jul 27;32(2):127-35. doi: 10.1016/s0920-9964(98)00049-8.
Schizophrenia is generally 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 schizophrenia 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 schizophrenia is mediated through (sensitivity for) environmental risk factors such as a dysfunctional early family rearing environment, cannabis, viral infections, complications of birth and pregnancy, stressful life events and unknown environmental risk factors associated with urban birth or residence 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 schizophrenia.
精神分裂症通常被认为是遗传易感性和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(基因型-环境相互作用),或使个体更有可能选择高风险环境(基因型-环境关联),从而增加患精神分裂症的风险。基因对精神分裂症发生的影响很可能至少部分是通过对环境风险因素(如功能失调的早期家庭养育环境、大麻、病毒感染、出生和妊娠并发症、生活应激事件以及与城市出生或居住和特定种族群体成员身份相关的未知环境风险因素)的(敏感性)介导的。随着分子遗传学的出现,迫切需要进一步了解可能的基因型-环境相互作用,以便制定和改进精神分裂症的预防和早期治疗策略。