Neuropsychiatric Epidemiology Research Unit, School of Population and Global Health, The University of Western Australia, Perth, WA, Australia.
Centre for Clinical Research in Neuropsychiatry, Division of Psychiatry, Medical School, The University of Western Australia, Perth, WA, Australia.
Aust N Z J Psychiatry. 2019 Nov;53(11):1105-1115. doi: 10.1177/0004867419864427. Epub 2019 Jul 24.
The interplay between genetic and environmental factors on risk for psychotic illness remains poorly understood. The aim of this study was to estimate independent and combined effects of familial liability for schizophrenia and exposure to obstetric complications on risk for developing psychotic illness, covarying with exposure to other environmental stressors.
This whole-population birth cohort study used record linkage across Western Australian statewide data collections (midwives, psychiatric, hospital admissions, child protection, mortality) to identify liveborn offspring ( = 1046) born 1980-1995 to mothers with schizophrenia, comparing them to offspring of mothers with no recorded psychiatric history ( = 298,370).
Both maternal schizophrenia and pregnancy complications were each significantly associated with psychotic illness in offspring, with no interaction. Non-obstetric environmental stressors significantly associated with psychotic illness in offspring included the following: being Indigenous; having a mother who was not in a partnered relationship; episodes of disrupted parenting due to hospitalisation of mother, father or child; abuse in childhood; and living in areas of greatest socioeconomic disadvantage and with elevated rates of violent crime. Adjustment for these other environmental stressors reduced the hazard ratio for maternal schizophrenia substantially (from hazard ratio: 5.7, confidence interval: 4.5-7.2 to hazard ratio: 3.5, confidence interval: 2.8-4.4), but not the estimate for pregnancy complications (hazard ratio: 1.1, confidence interval: 1.0-1.2). The population attributable fraction for maternal schizophrenia was 1.4 and for pregnancy complications was 2.1.
Our finding of a substantial decrease in risk of psychotic illness associated with familial liability for psychosis following adjustment for other environmental stressors highlights potentially modifiable risk factors on the trajectory to psychotic illness and suggests that interventions that reduce or manage exposure to these risks may be protective, despite a genetic liability.
遗传和环境因素对精神病风险的相互作用仍知之甚少。本研究旨在估计精神分裂症家族易感性和产科并发症暴露对发展精神病风险的独立和综合影响，同时考虑到其他环境应激源的暴露。
这项全人群出生队列研究使用西澳大利亚全州范围的数据收集（助产士、精神病、住院、儿童保护、死亡率）进行记录链接，以确定 1980 年至 1995 年期间患有精神分裂症的母亲所生的活产后代（ = 1046），并将其与没有记录的精神病史的母亲的后代（ = 298370）进行比较。
母体精神分裂症和妊娠并发症都与后代的精神病显著相关，没有相互作用。与后代精神病显著相关的非产科环境应激源包括以下内容：原住民；母亲未处于伴侣关系中；母亲、父亲或孩子住院导致的育儿中断；儿童时期受虐待；以及生活在社会经济最不利和暴力犯罪率较高的地区。调整这些其他环境应激源后，母体精神分裂症的危险比大大降低（从危险比：4.5-7.2 到危险比：2.8-4.4），但妊娠并发症的估计值没有降低（危险比：1.1，置信区间：1.0-1.2）。母体精神分裂症的人群归因分数为 1.4，妊娠并发症的人群归因分数为 2.1。
我们发现，在调整其他环境应激源后，与精神病家族易感性相关的精神病风险显著降低，这突出了精神病轨迹上潜在的可改变风险因素，并表明尽管存在遗传易感性，但减少或管理这些风险的干预措施可能具有保护作用。
