修回日期: 2025-05-26
接受日期: 2025-07-01
在线出版日期: 2025-07-28
饮食-肠道微生物-脑肠轴的交互作用在情绪调节领域受到广泛关注. 这一轴系构成了大脑与肠道间的复杂双向通信网络, 涉及神经信号的传递、免疫反应的调节和内分泌系统的互动等多个方面. 肠道微生物群通过产生短链脂肪酸和神经递质前体等代谢产物, 对情绪产生影响. 同时, 饮食成分直接影响肠道微生物的组成与功能, 可能进一步影响大脑健康. 这一机制为通过调节饮食和微生物群管理与情绪疾病提供了新视角. 未来研究需深入探索饮食-肠道微生物-脑肠轴的详细作用机制, 建立标准化研究方法, 并识别关键生物标志物, 以促进新的预防和治疗策略的发展, 改善人类情绪健康.
核心提要: 饮食-肠道微生物-脑肠轴通过整合神经、内分泌及免疫系统的多通路网络, 动态调控饮食摄入、肠道菌群与中枢神经系统功能间的相互作用, 能够对心理及大脑健康产生影响. 因此, 调节饮食和微生物群管理可能为治疗情绪疾病提供新策略.
引文著录: 成杰, 马宇, 蔡丽颖, 唐启群. 饮食-肠道微生物-脑肠轴的交互作用对情绪影响的研究进展. 世界华人消化杂志 2025; 33(7): 522-526
Revised: May 26, 2025
Accepted: July 1, 2025
Published online: July 28, 2025
The interaction between diet, the gut microbiota, and the gut-brain axis has received widespread attention in the field of emotion regulation. This axis constitutes a complex bidirectional communication network between the brain and the intestine, involving multiple aspects such as the transmission of neural signals, regulation of immune responses, and interaction of the endocrine system. The gut microbiota affects emotions by producing metabolites such as short chain fatty acids and neurotransmitter precursors. Meanwhile, dietary components directly affect the composition and function of the gut microbiota, which may further impact brain health. This mechanism provides a new perspective for managing emotional disorders by regulating diet and the microbiota. Future research needs to delve into the detailed mechanisms of the diet-microbiota-brain-gut axis, establish standardized research methods, and identify key biomarkers to promote the development of new prevention and treatment strategies and improve human emotional health.
- Citation: Cheng J, Ma Y, Cai LY, Tang QQ. Progress in research of impact of interaction between diet, gut microbiota, and brain-gut axis on emotions. Shijie Huaren Xiaohua Zazhi 2025; 33(7): 522-526
- URL: https://www.wjgnet.com/1009-3079/full/v33/i7/522.htm
- DOI: https://dx.doi.org/10.11569/wcjd.v33.i7.522
近年来, 肠道微生物组与情绪调节的相互作用逐渐成为医学研究的前沿热点. 其中脑肠轴通过神经-内分泌-免疫网络介导肠脑双向通讯系统, 是解析饮食-肠道微生物-大脑交互机制的核心框架. 肠道菌群通过代谢产物(如SCFAs、γ-氨基丁酸、5-羟色胺前体)、免疫因子和迷走神经通路等途径, 影响神经递质平衡、下丘脑-垂体-肾上腺轴活性及神经炎症反应, 从而参与精神疾病的发生发展[1-3]. 饮食作为塑造肠道菌群结构和功能的关键环境因素, 在脑肠轴调控网络中占据重要地位. 研究显示, 高脂饮食可显著降低拟杆菌门丰度, 促进促炎性微生物增殖, 导致海马体神经营养因子表达下调, 诱发焦虑样行为[4]; 而富含膳食纤维的地中海饮食模式能促进产丁酸菌增殖, 通过组蛋白去乙酰化酶抑制机制增强前额叶皮层突触可塑性, 改善抑郁症状[5]. 此外, 益生元/益生菌膳食补充可调节色氨酸代谢通路, 降低抑郁症患者血清犬尿氨酸/色氨酸比值, 显著缓解负性情绪[6]. 因此, 本文通过综述饮食-肠道微生物-脑肠轴的多维度作用机制, 分析其对情绪影响的通路, 旨在基于个体化菌群特征的膳食干预策略, 为情绪障碍的防治开辟全新的转化医学路径[7].
脑肠轴作为中枢神经系统与肠道的双向信息交互系统, 通过神经、内分泌和免疫途径实现动态调控. 肠道微生物群在其中发挥核心作用: 一方面, 其代谢膳食纤维生成的SCFAs可激活GPR41/43受体调节神经元活性, 同时合成血清素、多巴胺等神经递质直接参与神经信号传导; 另一方面, 通过调控肠屏障功能及免疫细胞的细胞因子分泌, 影响中枢神经炎症水平[2,8]. 肠神经系统作为独立于中枢的"第二大脑", 不仅自主调控胃肠功能, 还可通过迷走神经与中枢形成神经-内分泌-免疫网络, 在应激反应和情绪调节中起枢纽作用[5,9].
肠道微生物通过代谢食物成分产生多种代谢产物, 这些代谢产物对神经传导有重要影响. 例如, SCFAs是肠道微生物发酵膳食纤维的产物, 能够通过激活G蛋白偶联受体(如GPR41和GPR43)影响神经元的活动, 进而调节情绪和行为[3,6]. 此外, 肠道微生物还可以通过合成神经递质直接影响神经传导, 这些神经递质在调节情绪和认知功能中起着关键作用[10,11].
研究发现, 肠道微生物的组成和功能变化与多种神经精神疾病密切相关, 表明微生物代谢产物在脑肠轴的信号传递中发挥着重要作用[5,12]. 胆汁酸通过激活法尼醇X受体(farnesoid X receptor, FXR)与TGR5受体双向调节下丘脑-垂体-肾上腺轴活性, 下丘脑FXR抑制促肾上腺皮质激素释放激素分泌, 而TGR5则呈现促分泌效应[13]. 支链氨基酸作为哺乳动物雷帕霉素靶蛋白通路激活剂, 参与突触蛋白合成与胰岛素信号转导; 支链氨基酸缺乏可导致海马长时程增强受损, 而补充亮氨酸可通过ERK/CREB通路逆转认知障碍[14,15].
饮食通过多维度机制调控肠道菌群-脑肠轴交互作用进而影响情绪功能. 在宏观模式层面, 西方高脂高糖饮食导致厚壁菌门/拟杆菌门比值失调及菌群多样性降低, 诱发代谢性内毒素血症; 而地中海饮食通过富集双歧杆菌和乳酸菌、促进膳食纤维发酵生成SCFAs, 增强肠道屏障功能并抑制TLR4/NF-κB炎症通路[2,8]. 微观成分层面, 益生元(如β-葡聚糖)可特异性促进罗斯氏菌属/普拉梭菌增殖激活SCFAs-IL-10抗炎通路, 其作用特征在于提升短链脂肪酸总量而非特定类型(如菊粉可同时促进双歧杆菌、乳酸菌等多种菌属产酸), 同时通过调控胆汁酸代谢(如低聚果糖激活FXR通路)间接影响脂质代谢与炎症反应; 而益生菌(如乳杆菌属)通过直接分泌神经活性物质调节色氨酸代谢平衡5-羟色胺合成, 并降解脂多糖缓解神经炎症, 其代谢产生的SCFAs以丁酸为主, 可为肠上皮细胞提供能量来源, 并通过肠脑轴间接影响神经可塑性和突触功能, 同时能特异性降解膳食成分(如将色氨酸转化为吲哚衍生物等神经活性代谢物), 是改善情绪与认知的关键治疗靶点[3,19,20]. 关键代谢产物SCFAs和吲哚衍生物既能经迷走神经调控杏仁核-前额叶情绪环路, 又可穿透血脑屏障调节下丘脑-垂体-肾上腺轴活性, 构成饮食干预改善焦虑/抑郁的分子基础[5,21]. 研究显示[3,7], 地中海饮食提供的Omega-3脂肪酸不仅作为神经递质前体直接改善情绪[5,7], 其膳食纤维与益生元还可增强肠屏障功能并调节血清素水平. 此外, 肠道菌群对色氨酸代谢的调控[如5-羟色胺(5-hydroxytryptamine, 5-HT)前体供应及犬尿氨酸通路平衡]直接关联中枢5-HT水平, 为抑郁症的个性化营养干预提供切入点; 迷走神经作为肠脑直接通讯通路, 其电刺激或营养调控可能增强肠源性信号对边缘系统的调节作用[7].
肠道微生物是由定植于人体消化道的细菌、真菌、病毒及古菌等构成的复杂生态系统, 其组成受年龄、饮食、环境和遗传等多因素动态调控[22]. 健康成人肠道菌群以拟杆菌门(Bacteroidetes)、厚壁菌门(Firmicutes)、变形菌门(Proteobacteria)和放线菌门(Actinobacteria)为主导, 通过参与营养代谢、免疫调节及肠黏膜屏障维护等机制影响宿主健康[23]. 研究显示, 肠道微生物失衡与肥胖、糖尿病、抑郁症等代谢-精神共病的病理进程密切相关[24,25], 特别是高脂肪、高糖饮食能够显著改变肠道微生物的组成,导致微生物多样性降低[26,27].
肠道微生物通过多维度功能参与宿主生理稳态调控: 在代谢层面, 其通过发酵不可消化碳水化合物生成SCFAs, 既为肠上皮细胞供能, 又发挥抗炎及免疫调节作用[28]; 在肠道屏障维护方面, 通过竞争性抑制病原体定植、分泌抗菌肽及增强上皮细胞紧密连接实现生物防御[26]; 免疫调节方面则通过代谢产物-免疫细胞互作平衡Th17/Treg等免疫亚群, 降低慢性炎症风险[29]. 尤为重要的是, 肠道菌群通过合成5-羟色胺前体、调节色氨酸代谢等途径影响神经递质水平, 并借助迷走神经、神经内分泌及免疫通路构成肠-脑双向通讯网络, 这为阐释饮食-菌群互作影响情绪障碍提供了关键分子基础[26,28-30].
肠道微生物组与心理健康存在双向调控关系, 研究显示, 抑郁症患者肠道菌群多样性降低、特征性菌属(如厚壁菌门/拟杆菌门比值异常)改变等生物标志物特征[31-33], 其病理机制涉及微生物代谢产物通过神经内分泌-免疫网络调控中枢神经系统: 菌群衍生的色氨酸代谢产物可调节5-羟色胺生物合成, 而SCFAs通过抑制组蛋白去乙酰化酶影响神经可塑性; 同时, 菌群失调引发的肠屏障损伤导致脂多糖入血, 通过Toll样受体4激活全身低度炎症, 该过程与下丘脑-垂体-肾上腺轴过度激活存在显著相关性[34]. 此外, 靶向菌群的膳食调节及益生菌干预已被证实能改善焦虑/抑郁量表评分, 其效应与恢复γ-氨基丁酸合成、降低促炎细胞因子水平等机制密切相关, 这为基于微生物-肠-脑轴的情绪障碍精准干预提供了转化医学依据[35], 但菌群移植的长期安全性及个体化治疗策略仍需前瞻性研究验证.
肠道微生物组的组成特征与情绪障碍存在显著关联. 抑郁患者普遍表现出菌群多样性降低的特征性改变: 具有神经保护作用的乳酸菌、双歧杆菌等有益菌丰度下降, 而促炎性的克雷伯氏菌、肠杆菌等条件致病菌异常增殖[30]. 这种菌群失调可能通过影响血清素等关键神经递质的生物合成, 以及激活脑肠轴免疫炎症通路, 共同导致情绪调节功能障碍[36].
个体差异在饮食、肠道微生物和情绪之间的交互作用中起着重要作用. 研究表明[2], 不同个体对相同饮食干预的反应存在显著异质性, 这可能与基线菌群中特定功能基因的丰度差异相关. 研究显示[6], 标准化饮食干预后, 个体可能由于微生物组的差异, 情绪改善效果并不显著. 提示精准营养策略需结合个体菌群特征进行优化.
肠道菌群移植(fecal microbiota transplantation, FMT)作为一种新兴的治疗方法, 对改善抑郁症状表现出临床应用潜力.研究表明, 健康供体菌群可有效改善抑郁症状, 其机制涉及菌群-肠-脑轴的多重调控: 既恢复神经递质代谢平衡, 又通过调节SCFAs等菌群代谢产物修复血脑屏障功能[36,37]. 此外, FMT还被发现能够调节与情绪相关的神经递质的水平, 从而进一步影响患者的情绪状态[7]. 来自精神分裂症个体的FMT除了诱导精神分裂症样行为外, 还改变了无菌受体小鼠血清和海马中的脂质代谢[38]. 从饮食诱导的肥胖小鼠到幼稚小鼠的FMT反映肥胖供体小鼠的享乐行为反应和改变的多巴胺能活性[39]. 但FMT可能引起受体多重耐药菌感染及对供体菌群产生过度免疫应答, 诱发自身免疫性疾病.
饮食模式通过调控肠道微生物组与脑肠轴交互影响情绪健康. 地中海饮食等富含膳食纤维的饮食结构可促进有益菌群增殖, 其代谢产物通过神经内分泌、免疫调节和迷走神经通路作用于中枢神经系统, 与较低的抑郁焦虑水平相关[40]; 而高脂高糖的西方饮食则易引发菌群失调, 加剧神经炎症和情绪障碍. 尽管研究证实了饮食-肠道微生物-脑肠轴的生物学基础, 但个体遗传背景、生活方式及微生物组异质性导致的干预效果差异仍需深入解析[41-45]. 虽然SCFAs等特异性的生物标志物可以作为评估指标, 但一些食物如发酵食品缺乏可靠的特异性生物标志物, 需要进一步找到合适的评价指标. 并且现有证据主要来源于短期动物实验, 难以反映人类饮食-肠道微生物-脑肠轴的作用机制及对认知与情绪的影响. 此外, 饮食干预的长期效应及安全性证据有限, 尤其是高脂肪、高糖饮食对迷走神经重塑和神经炎症的慢性影响仍需纵向研究验证.
未来研究需聚焦三大方向: (1)开发结合数字技术的个性化饮食干预方案, 针对青少年、孕产妇等特殊群体设计情绪导向的精准营养策略; (2)通过多组学技术阐明特定菌株及其代谢物调控神经递质(如5-HT、γ-氨基丁酸)的分子机制, 探索益生菌/益生元、后生元等微生物靶向疗法的临床转化; (3)建立跨学科研究范式, 整合微生物基因组学、代谢动力学与神经影像学, 构建"饮食-微生物-脑功能"动态模型, 为情绪障碍防治提供从微生物重塑到脑网络调控的系统性解决方案, 实现从症状管理向病因治疗的范式转变.
综上所述, 饮食、肠道微生物与脑肠轴的交互作用提供了一个全新的视角来理解情绪的形成机制. 通过进一步的研究, 有望揭示微生物组与情绪健康之间的潜在联系, 并为情绪障碍的预防和治疗提供新的策略.
学科分类: 胃肠病学和肝病学
手稿来源地: 河北省
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科学编辑: 刘继红 制作编辑:郑晓梅
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