超加工食品、MASLD和认知衰老：以加工为中心的肠肝脑轴视角
Ultra-Processed Foods, MASLD, and Cognitive Aging: A Processing-Centered Gut-Liver-Brain Axis Perspective.
摘要(中文译文)
超加工食品（UPFs）日益被视为与心脏代谢、肝脏和神经认知结局相关的膳食暴露因素。然而，超加工食品往往主要被当作营养贫乏的食品对待，而其与加工相关的特征可能扰乱肠-肝-脑交流。本综述探讨代谢功能障碍相关脂肪性肝病（MASLD）能否被概念化为一个肝脏代谢放大器，将超加工食品暴露与认知老化联系起来。我们于2010年1月至2026年5月11日对PubMed/MEDLINE、Web of Science核心合集和Scopus进行了结构化叙述性检索，涵盖四个证据模块：超加工食品与MASLD/NAFLD；超加工食品与认知老化或痴呆；超加工食品与肠-肝-脑机制；以及MASLD/NAFLD与认知老化。代表性研究依据与所提出轴线的直接相关性、研究设计、暴露与结局的效度、机制特异性以及对重大证据缺口的贡献进行优先排序。观察性和机制性证据将较高的超加工食品消费与肝脏脂肪变性、MASLD/NAFLD相关结局、认知下降、认知障碍、卒中及痴呆相关结局联系起来，尽管因果关系尚未完全确立，且残余混杂因素具有重要意义。候选通路包括食物基质破坏、进食过快、微生物底物被替代、特定添加剂和加工衍生化合物、肠道屏障功能障碍、代谢性内毒素血症、胆汁酸信号传导、肝脏脂毒性、全身性炎症、血管功能障碍和神经免疫激活。许多通路与一般心脏代谢功能障碍重叠；以加工为中心的贡献在于将工业配方定位为上游暴露，并将MASLD定位为一个肝脏节点，该节点可能放大与脑老化相关的肠源性和代谢性信号。以加工为中心的肠-肝-脑框架将超加工食品、MASLD和认知老化整合为相互关联的代谢-老化现象。未来研究应使用肝脏影像学、微生物组分析、代谢组学、胆汁酸和炎症生物标志物、神经影像学及认知评估来检验超加工食品替代的影响。
Abstract
Ultra-processed foods (UPFs) are increasingly recognized as dietary exposures associated with cardiometabolic, hepatic, and neurocognitive outcomes. However, UPFs are often treated mainly as nutrient-poor foods, whereas their processing-related features may perturb gut-liver-brain communication. This review examines whether metabolic dysfunction-associated steatotic liver disease (MASLD) can be conceptualized as a hepatic metabolic amplifier linking UPF exposure to cognitive aging. We conducted a structured narrative search of PubMed/MEDLINE, Web of Science Core Collection, and Scopus from January 2010 to 11 May 2026 across four evidence modules: UPFs and MASLD/NAFLD; UPFs and cognitive aging or dementia; UPFs and gut-liver-brain mechanisms; and MASLD/NAFLD and cognitive aging. Representative studies were prioritized according to direct relevance to the proposed axis, study design, exposure and outcome validity, mechanistic specificity, and contribution to major evidence gaps. Observational and mechanistic evidence links higher UPF consumption with liver steatosis, MASLD/NAFLD-related outcomes, cognitive decline, cognitive impairment, stroke, and dementia-related outcomes, although causality remains incompletely established and residual confounding is important. Candidate pathways include food-matrix disruption, rapid eating, displacement of microbial substrates, selected additives and processing-derived compounds, intestinal barrier dysfunction, metabolic endotoxemia, bile acid signaling, hepatic lipotoxicity, systemic inflammation, vascular dysfunction, and neuroimmune activation. Many pathways overlap with general cardiometabolic dysfunction; the processing-centered contribution lies in positioning industrial formulation as an upstream exposure and MASLD as a hepatic node that may amplify gut-derived and metabolic signals relevant to brain aging. A processing-centered gut-liver-brain framework integrates UPFs, MASLD, and cognitive aging as linked metabolic-aging phenomena. Future studies should test UPF substitution using liver imaging, microbiome profiling, metabolomics, bile acid and inflammatory biomarkers, neuroimaging, and cognitive assessment.
如何引用
AMA
Yirui Chen, Hongxin Gui, Tieniu Zhao, Chang Liu, Ye Zhang, Mengyang Wang, et al. Ultra-Processed Foods, MASLD, and Cognitive Aging: A Processing-Centered Gut-Liver-Brain Axis Perspective.. Nutrients. 2026; doi:10.3390/nu18132041.
APA
Yirui Chen, Hongxin Gui, Tieniu Zhao, Chang Liu, Ye Zhang, Mengyang Wang, et al (2026). Ultra-Processed Foods, MASLD, and Cognitive Aging: A Processing-Centered Gut-Liver-Brain Axis Perspective.. Nutrients. https://doi.org/10.3390/nu18132041
GB/T 7714
Yirui Chen, Hongxin Gui, Tieniu Zhao, Chang Liu, Ye Zhang, Mengyang Wang, et al. Ultra-Processed Foods, MASLD, and Cognitive Aging: A Processing-Centered Gut-Liver-Brain Axis Perspective.[J]. Nutrients, 2026 doi:10.3390/nu18132041.
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