Submitted to: Frontiers in Endocrinology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/19/2018
Publication Date: 1/29/2019
Citation: Lyte, J.M. 2019. Eating for 3.8x10^13: Examining the impact of diet and nutrition on the microbiota-gut-brain axis through the lens of microbial endocrinology. Frontiers in Endocrinology. 9:796. https://doi.org/10.3389/fendo.2018.00796.
Interpretive Summary: Microorganisms are found along the gastrointestinal tracts, including the intestines, of birds, people, and animals. When, for example, a bird, person, or pig eats food, some of the food passes through the gastrointestinal tract and can be used by, or cause changes in, the microbiota. However, much remains to be understood about what food-induced changes in the microbiota mean for the health of the bird, person, or pig. It is important to understand what these changes can mean because this will allow for the strategic formulation of diets which specially target the microbiota of birds, people, and animals in order to improve health and other positive characteristics. In order to design strong scientific studies which identify such health-beneficial diets, new and creative hypotheses must first be proposed. This peer-reviewed scientific publication proposes several new and creative hypotheses for the design and testing of diets which impact the microbiota to benefit people, birds, and animals.
Technical Abstract: The study of host-microbe neuroendocrine crosstalk, termed microbial endocrinology, suggests that the impact of diet on host health and microbial viability is, in part, reliant upon nutritional modulation of the shared host-microbe neuroendocrine axes. In the 1990’s it was first recognized that neuroendocrine pathways are major components of the microbiota-gut-brain axis, and that diet-induced changes in the gut microbiota were correlated with changes in host behavior and cognition. A causative link, however, between nutritional-induced shifts in microbiota composition and change in host behavior has yet to be fully elucidated. Substrates found in food which are utilized by bacteria in the production of microbial-derived neurochemicals, which are structurally-identical to those made by the host, likely represent a microbial endocrinology-based route by which the microbiota causally influence the host and microbial community dynamics via diet. For example, it has been known for decades that food safety is strongly impacted by the microbial production of biogenic amines. While microbial-produced tyramine found in cheese can elicit hypertensive crises, microorganisms which are common inhabitants of the human intestinal tract can convert L-histidine found in common foodstuffs to histamine and thereby precipitate allergic reactions. Hence, there is substantial evidence suggesting a microbial endocrinology-based role by which the gastrointestinal microbiota can utilize host dietary components to produce neuroactive molecules that causally impact the host. Conversely, little is known regarding the reverse scenario whereby nutrition-mediated changes in host neuroendocrine production affect microbial viability, composition, and/or function. Mechanisms in the direction of brain-to-gut, such as how host production of catecholamines drives diverse changes in microbial growth and functionality within the gut requires greater examination considering well-known nutritional effects on host stress physiology. As dietary intake mediates changes in host stress, such as the effects of caffeine on the hypothalamic-pituitary-adrenal axis, it is likely that nutrition can impact host neuroendocrine production to affect the microbiota. Likewise, the plasticity of the microbiota to changes in host diet has been hypothesized to drive microbial regulation of host food preference via a host-microbe feedback loop. This review will focus on food as concerns microbial endocrinology with emphasis given to nutrition as a mediator of host-microbe bi-directional neuroendocrine crosstalk and its impact on microbial viability and host health.