Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
International Max Planck Research School for Translational Psychiatry (IMPRS-TP), Munich, Germany.
Transl Psychiatry. 2022 Jun 22;12(1):259. doi: 10.1038/s41398-022-02022-9.
Depression and psychosis are often comorbid; they also have overlapping genetic and environmental risk factors, including trauma and area-level exposures. The present study aimed to advance understanding of this comorbidity via a network approach, by (1) identifying bridge nodes that connect clusters of lifetime depression and psychosis symptoms and (2) evaluating the influence of polygenic and environmental risk factors in these symptoms. This study included data from European ancestry participants in UK Biobank, a large population-based sample (N = 77,650). In Step 1, a network model identified bridge nodes between lifetime symptoms of depression and psychosis and functional impairment. In Step 2, genetic and environmental risk factors were incorporated to examine the degree to which symptoms associated with polygenic risk scores for depression and schizophrenia, lifetime exposure to trauma and area-level factors (including deprivation, air pollution and greenspace). Feelings of worthlessness, beliefs in unreal conspiracy against oneself, depression impairment and psychosis impairment emerged as bridges between depression and psychosis symptoms. Polygenic risk scores for depression and schizophrenia were predominantly linked with depression and psychosis impairment, respectively, rather than with specific symptoms. Cumulative trauma emerged as a bridge node associating deprivation with feelings of worthlessness and beliefs in unreal conspiracy, indicating that the experience of trauma is prominently linked with the co-occurrence of depression and psychosis symptoms related to negative views of oneself and others. These key symptoms and risk factors provide insights into the lifetime co-occurrence of depression and psychosis.
抑郁和精神病经常共病；它们也有重叠的遗传和环境风险因素，包括创伤和区域水平暴露。本研究旨在通过网络方法来增进对这种共病的理解，方法是：(1)确定连接一生的抑郁和精神病症状集群的桥梁节点；(2)评估这些症状中的多基因和环境风险因素的影响。本研究包括来自 UK Biobank 的欧洲血统参与者的数据，UK Biobank 是一个大型基于人群的样本（N = 77650）。在步骤 1 中，网络模型确定了抑郁和精神病一生症状与功能障碍之间的桥梁节点。在步骤 2 中，纳入了遗传和环境风险因素，以检查与抑郁和精神分裂症多基因风险评分、一生创伤暴露以及区域水平因素（包括贫困、空气污染和绿地）相关的症状在多大程度上与多基因风险评分相关。无价值感、对不真实阴谋的信念、抑郁障碍和精神病障碍是抑郁和精神病症状之间的桥梁。抑郁和精神分裂症的多基因风险评分主要与抑郁和精神病障碍相关，而不是与特定症状相关。累积创伤是将贫困与无价值感和对不真实阴谋的信念联系起来的桥梁节点，表明创伤经历与与对自己和他人的负面看法相关的抑郁和精神病症状的同时发生密切相关。这些关键症状和风险因素提供了对抑郁和精神病一生共病的深入了解。
