Vodovotz Yoram, Arciero Julia, Verschure Paul Fmj, Katz David L
Department of Surgery, University of Pittsburgh, Pittsburgh, PA, United States.
Department of Immunology, Center for Systems Immunology, University of Pittsburgh, Pittsburgh, PA, United States.
Front Sci. 2024;1. doi: 10.3389/fsci.2023.1239462. Epub 2024 Mar 11.
As populations worldwide show increasing levels of stress, understanding emerging links among stress, inflammation, cognition, and behavior is vital to human and planetary health. We hypothesize that inflammation is a multiscale driver connecting stressors that affect individuals to large-scale societal dysfunction and, ultimately, to planetary-scale environmental impacts. We propose a 'central inflammation map' hypothesis to explain how the brain regulates inflammation and how inflammation impairs cognition, emotion, and action. According to our hypothesis, these interdependent inflammatory and neural processes, and the inter-individual transmission of environmental, infectious, and behavioral stressors - amplified via high-throughput digital global communications - can culminate in a multiscale, runaway, feed-forward process that could detrimentally affect human decision-making and behavior at scale, ultimately impairing the ability to address these same stressors. This perspective could provide non-intuitive explanations for behaviors and relationships among cells, organisms, and communities of organisms, potentially including population-level responses to stressors as diverse as global climate change, conflicts, and the COVID-19 pandemic. To illustrate our hypothesis and elucidate its mechanistic underpinnings, we present a mathematical model applicable to the individual and societal levels to test the links among stress, inflammation, control, and healing, including the implications of transmission, intervention (e.g., via lifestyle modification or medication), and resilience. Future research is needed to validate the model's assumptions, expand the factors/variables employed, and validate it against empirical benchmarks. Our model illustrates the need for multilayered, multiscale stress mitigation interventions, including lifestyle measures, precision therapeutics, and human ecosystem design. Our analysis shows the need for a coordinated, interdisciplinary, international research effort to understand the multiscale nature of stress. Doing so would inform the creation of interventions that improve individuals' lives and communities' resilience to stress and mitigate its adverse effects on the world.
随着全球人口的压力水平不断上升,了解压力、炎症、认知和行为之间新出现的联系对人类健康和地球健康至关重要。我们假设炎症是一个多尺度驱动因素,它将影响个体的压力源与大规模社会功能障碍联系起来,并最终与行星尺度的环境影响联系起来。我们提出了一个“中枢炎症图谱”假说,以解释大脑如何调节炎症以及炎症如何损害认知、情绪和行动。根据我们的假说,这些相互依存的炎症和神经过程,以及环境、感染和行为压力源在个体间的传播——通过高通量数字全球通信得到放大——可能会 culminate 在一个多尺度、失控的前馈过程中,这可能会对大规模的人类决策和行为产生不利影响,最终损害应对这些相同压力源的能力。这一观点可以为细胞、生物体和生物群落之间的行为和关系提供非直观的解释,可能包括对全球气候变化、冲突和 COVID-19 大流行等各种压力源的群体层面反应。为了说明我们的假说并阐明其机制基础,我们提出了一个适用于个体和社会层面的数学模型,以测试压力、炎症、控制和愈合之间的联系,包括传播、干预(例如通过生活方式改变或药物治疗)和恢复力的影响。未来需要进行研究以验证模型的假设,扩展所采用的因素/变量,并根据实证基准对其进行验证。我们的模型说明了需要采取多层次、多尺度的压力缓解干预措施,包括生活方式措施、精准治疗和人类生态系统设计。我们的分析表明,需要开展协调一致、跨学科的国际研究工作,以了解压力的多尺度性质。这样做将为制定改善个人生活和社区对压力的恢复力并减轻其对世界的不利影响的干预措施提供信息。