Abstract
An extensive body of evidence documents the importance of the gut microbiome both in health and in a variety of human diseases. Cell and animal studies describing this relationship abound, whilst clinical studies exploring the associations between changes in gut microbiota and the corresponding metabolites with neurodegeneration in the human brain have only begun to emerge more recently. Further, the findings of such studies are often difficult to translate into simple clinical applications that result in measurable health outcomes. The purpose of this paper is to appraise the literature on a select set of faecal biomarkers from a clinician’s perspective. This practical review aims to examine key physiological processes that influence both gastrointestinal, as well as brain health, and to discuss how tools such as the characterisation of commensal bacteria, the identification of potential opportunistic, pathogenic and parasitic organisms and the quantification of gut microbiome biomarkers and metabolites can help inform clinical decisions of nutrition and lifestyle medicine practitioners.
Highlights
A growing body of preclinical and clinical evidence supports the concept of bidirectional microbiota-gut-brain interactions
As examples of how dietary patterns have the ability to contribute to dysbiosis, the reader may find that the following papers highlight the effects of a “Western diet” on the gut microbiota and how changes mediated by a diet that is typically low in fibre from fresh foods, but high in refined carbohydrates, and damaged dietary fats from ultra-processed foods are seen as instrumental in the emergence of symptoms relating to metabolic disease, including cardiovascular [13,14], obesity [15], as well as other related conditions like asthma [16,17,18,19] and oestrogen dysregulation [20,21], to name but a few
Aside of poor dietary fibre intake, other factors known to contribute to increased intestinal permeability include nutritional deficiencies, e.g., vitamin A [36], vitamin D [37], zinc [38], magnesium [39] and, based on animal models, a high-fat/high-carbohydrate diet [40] and a high-fructose diet, both of which have the potential to induce changes in gut microbiota leading to microbial dysbiosis, metabolic endotoxemia and inflammation that could contribute to increased intestinal permeability, traditionally referred to as “leaky gut”, seen alongside increased blood-brain barrier permeability mediating the pathogenesis of neurodevelopmental disorders such as autism [41], neuroimmune dysregulation disorders such as multiple sclerosis [42,43,44] and neurodegenerative conditions such as Alzheimer’s disease (AD) [45,46]
Summary
A growing body of preclinical and clinical evidence supports the concept of bidirectional microbiota-gut-brain interactions. Aside of poor dietary fibre intake, other factors known to contribute to increased intestinal permeability include nutritional deficiencies, e.g., vitamin A [36], vitamin D [37], zinc [38], magnesium [39] and, based on animal models, a high-fat/high-carbohydrate diet [40] and a high-fructose diet, both of which have the potential to induce changes in gut microbiota leading to microbial dysbiosis, metabolic endotoxemia and inflammation that could contribute to increased intestinal permeability, traditionally referred to as “leaky gut”, seen alongside increased blood-brain barrier permeability mediating the pathogenesis of neurodevelopmental disorders such as autism [41], neuroimmune dysregulation disorders such as multiple sclerosis [42,43,44] and neurodegenerative conditions such as Alzheimer’s disease (AD) [45,46]. Alpha-synuclein deposition and the associated neurodegeneration that takes place in the enteric nervous system contribute to gastrointestinal dysfunction [53], increased intestinal permeability [54], increased oxidative stress [55] and local inflammation [56] that feature alongside constipation in Parkinson’s disease (PD) patients
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