Warwickshire Institute for the Study of Diabetes, Endocrinology and Metabolism, University Hospitals Coventry and Warwickshire NHS Trust, Clifford Bridge Road, Coventry CV2 2DX, UK.
Division of Biomedical Sciences, Warwick Medical School, University of Warwick, Coventry CV2 2DX, UK.
Int J Mol Sci. 2021 Mar 28;22(7):3502. doi: 10.3390/ijms22073502.
Over unimaginable expanses of evolutionary time, our gut microbiota have co-evolved with us, creating a symbiotic relationship in which each is utterly dependent upon the other. Far from confined to the recesses of the alimentary tract, our gut microbiota engage in complex and bi-directional communication with their host, which have far-reaching implications for overall health, wellbeing and normal physiological functioning. Amongst such communication streams, the microbiota-gut-brain axis predominates. Numerous complex mechanisms involve direct effects of the microbiota, or indirect effects through the release and absorption of the metabolic by-products of the gut microbiota. Proposed mechanisms implicate mitochondrial function, the hypothalamus-pituitary-adrenal axis, and autonomic, neuro-humeral, entero-endocrine and immunomodulatory pathways. Furthermore, dietary composition influences the relative abundance of gut microbiota species. Recent human-based data reveal that dietary effects on the gut microbiota can occur rapidly, and that our gut microbiota reflect our diet at any given time, although much inter-individual variation pertains. Although most studies on the effects of dietary macronutrients on the gut microbiota report on associations with relative changes in the abundance of particular species of bacteria, in broad terms, our modern-day animal-based Westernized diets are relatively high in fats and proteins and impoverished in fibres. This creates a perfect storm within the gut in which dysbiosis promotes localized inflammation, enhanced gut wall permeability, increased production of lipopolysaccharides, chronic endotoxemia and a resultant low-grade systemic inflammatory milieu, a harbinger of metabolic dysfunction and many modern-day chronic illnesses. Research should further focus on the colony effects of the gut microbiota on health and wellbeing, and dysbiotic effects on pathogenic pathways. Finally, we should revise our view of the gut microbiota from that of a seething mass of microbes to one of organ-status, on which our health and wellbeing utterly depends. Future guidelines on lifestyle strategies for wellbeing should integrate advice on the optimal establishment and maintenance of a healthy gut microbiota through dietary and other means. Although we are what we eat, perhaps more importantly, we are what our gut microbiota thrive on and they thrive on what we eat.
在难以想象的漫长进化时间里,我们的肠道微生物与我们共同进化,形成了一种共生关系,彼此相互依存。我们的肠道微生物远不止局限于消化道的深处,它们与宿主进行着复杂而双向的交流,对整体健康、幸福和正常的生理功能有着深远的影响。在这些交流流中,微生物-肠道-大脑轴占主导地位。许多复杂的机制涉及微生物的直接影响,或通过肠道微生物代谢产物的释放和吸收的间接影响。提出的机制涉及线粒体功能、下丘脑-垂体-肾上腺轴以及自主、神经-体液、肠内分泌和免疫调节途径。此外,饮食成分也会影响肠道微生物的相对丰度。最近的人类研究数据表明,饮食对肠道微生物的影响可以迅速发生,而且我们的肠道微生物在任何给定时间都反映了我们的饮食,尽管存在很大的个体差异。虽然大多数关于饮食宏量营养素对肠道微生物影响的研究都报告了与特定细菌种类丰度相对变化的关联,但总的来说,我们现代的动物源性西方化饮食相对较高的脂肪和蛋白质,而膳食纤维则较少。这在肠道内造成了一场完美风暴,其中菌群失调会促进局部炎症、增加肠道壁通透性、增加内毒素的产生、慢性内毒素血症以及由此产生的低度全身炎症环境,这是代谢功能障碍和许多现代慢性疾病的先兆。研究应进一步关注肠道微生物对健康和幸福的群落效应,以及对致病途径的菌群失调效应。最后,我们应该从把肠道微生物看作是一个沸腾的微生物群体,转变为一个器官状态,我们的健康和幸福完全依赖于这个器官状态。关于促进健康和幸福的生活方式策略的未来指南应该整合通过饮食和其他方式建立和维持健康肠道微生物群的最佳建议。虽然我们吃什么就是什么,但更重要的是,我们的肠道微生物群依赖我们所吃的东西而生存,而它们又依赖我们所吃的东西而茁壮成长。