Genomes for Life-GCAT Lab, Germans Trias i Pujol Research Institute (IGTP), Badalona, Spain.
Research Group on the Impact of Chronic Diseases and Their Trajectories (GRIMTra), Germans Trias i Pujol Research Institute (IGTP), Badalona, Spain.
Sci Rep. 2024 Jun 12;14(1):13562. doi: 10.1038/s41598-024-64200-7.
Risk of depression increased in the general population after the COVID-19 pandemic outbreak. By examining the interplay between genetics and individual environmental exposures during the COVID-19 lockdown, we have been able to gain an insight as to why some individuals are more vulnerable to depression, while others are more resilient. This study, conducted on a Spanish cohort of 9218 individuals (COVICAT), includes a comprehensive non-genetic risk analysis, the exposome, complemented by a genomics analysis in a subset of 2442 participants. Depression levels were evaluated using the Hospital Anxiety and Depression Scale. Together with Polygenic Risk Scores (PRS), we introduced a novel score; Poly-Environmental Risk Scores (PERS) for non-genetic risks to estimate the effect of each cumulative score and gene-environment interaction. We found significant positive associations for PERS (Social and Household), PERS (Lifestyle and Behaviour), and PERS (Wider Environment and Health) scores across all levels of depression severity, and for PRS (Broad depression) only for moderate depression (OR 1.2, 95% CI 1.03-1.40). On average OR increased 1.2-fold for PERS and 1.6-fold for PER and PER from mild to severe depression level. The complete adjusted model explained 16.9% of the variance. We further observed an interaction between PERS and PRS showing a potential mitigating effect. In summary, stressors within the social and behavioral domains emerged as the primary drivers of depression risk in this population, unveiling a mitigating interaction effect that should be interpreted with caution.
COVID-19 大流行爆发后，普通人群患抑郁症的风险增加。通过研究 COVID-19 封锁期间遗传与个体环境暴露之间的相互作用，我们深入了解了为什么有些人更容易患抑郁症，而有些人则更具韧性。这项在西班牙队列 9218 人（COVICAT）中进行的研究包括全面的非遗传风险分析、外显子组，以及在 2442 名参与者的亚组中进行的基因组学分析。使用医院焦虑和抑郁量表评估抑郁水平。除了多基因风险评分 (PRS) 之外，我们还引入了一个新的评分——多环境风险评分 (PERS) 来评估每个累积评分和基因-环境相互作用的非遗传风险。我们发现，在所有严重程度的抑郁水平下，PERS（社会和家庭）、PERS（生活方式和行为）和 PERS（更广泛的环境和健康）评分均呈显著正相关，而 PRS（广泛抑郁）仅在中度抑郁时呈显著正相关（OR 1.2，95%CI 1.03-1.40）。平均而言，PERS 和 PER 从轻度到重度抑郁水平的 OR 分别增加了 1.2 倍和 1.6 倍。完全调整后的模型解释了 16.9%的方差。我们进一步观察到 PERS 和 PRS 之间存在交互作用，表明存在潜在的缓解作用。总之，社会和行为领域的压力源是该人群中抑郁风险的主要驱动因素，揭示了一种需要谨慎解释的缓解交互作用。
