MRC Centre for Environment and Health, Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, UK; National Institute for Health Research Health Protection Research Unit in Chemical and Radiation Threats and Hazards, Imperial College London, UK.
Department of Orthopaedics, The Eighth Affiliated Hospital, Sun Yat-Sen University, China.
Schizophr Res. 2024 Aug;270:85-93. doi: 10.1016/j.schres.2024.06.008. Epub 2024 Jun 16.
Environment and genes both contribute to schizophrenia. However, the impact of different natural environments surrounding residential addresses on schizophrenia in urban settings remains unknown. This study aimed to investigate the association of urbanisation, measured by residential environments, with late-onset schizophrenia and explore whether genetic risk for schizophrenia modified the associations.
We examined the associations between residential environments and late-onset schizophrenia and its interaction with genetic risk factors in UK Biobank, followed from 2006 to 2010 (baseline) to Dec 2021. Residential environments, including greenspace, domestic garden, blue space, and total natural environment, were evaluated using land use coverage percentage. The polygenic risk score (PRS) of schizophrenia was derived using a Bayesian approach and adjusted it against ancestry. Cox proportional hazard regression model was used to assess the associations between per interquartile (IQR) increase of each type of residential environments and late-onset schizophrenia. Interactive effects of PRS and residential environments on late-onset schizophrenia were assessed on both additive and multiplicative scales.
A total of 393,680 participants were included in the analysis, with 844 cases of late-onset schizophrenia being observed after 12.8 years of follow-up. Within 300 m buffer surrounding the residential addresses, per interquartile increase in greenspace (31.5 %) and total natural environment (34.4 %) were both associated with an 11 % (HR = 0.89, 95 % CI 0.80, 0.99) lower risk of late-onset schizophrenia. Domestic garden and blue space did not show significant protective effects on late-onset schizophrenia. A strong dose-response relationship between schizophrenia PRS and schizophrenia was found, while no additive or multiplicative interaction effects were present between residential environments and PRS on late-onset schizophrenia.
Residential greenspace and total natural environment may protect against late-onset schizophrenia in older people regardless of genetic risk. These findings shed light on the prevention of schizophrenia and urban planning to optimise ecosystem benefits linked to schizophrenia.
环境和基因都与精神分裂症有关。然而，居住地址周围不同自然环境对城市环境中迟发性精神分裂症的影响尚不清楚。本研究旨在调查城市环境（通过居住环境来衡量）与迟发性精神分裂症之间的关联，并探讨精神分裂症的遗传风险是否改变了这些关联。
我们在英国生物库中研究了居住环境与迟发性精神分裂症之间的关联及其与遗传风险因素的相互作用，该研究从 2006 年至 2010 年（基线）持续到 2021 年 12 月。居住环境包括绿地、私人花园、蓝色空间和自然环境总量，使用土地利用覆盖率来评估。使用贝叶斯方法计算精神分裂症的多基因风险评分（PRS），并针对祖先进行调整。使用 Cox 比例风险回归模型评估每种居住环境每增加一个四分位距（IQR）与迟发性精神分裂症之间的关联。在加性和乘法尺度上评估 PRS 和居住环境对迟发性精神分裂症的交互作用。
共纳入 393680 名参与者，随访 12.8 年后观察到 844 例迟发性精神分裂症病例。在距居住地址 300 米缓冲区范围内，绿地（31.5%）和自然环境总量（34.4%）每增加一个 IQR，迟发性精神分裂症的风险降低 11%（HR=0.89，95%CI 0.80，0.99）。私人花园和蓝色空间对迟发性精神分裂症没有明显的保护作用。精神分裂症 PRS 与精神分裂症之间存在很强的剂量-反应关系，而居住环境与 PRS 之间不存在迟发性精神分裂症的加性或乘法交互作用。
居住绿地和自然环境总量可能会保护老年人免受迟发性精神分裂症的影响，而与遗传风险无关。这些发现为精神分裂症的预防和优化与精神分裂症相关的生态系统效益的城市规划提供了依据。
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