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Research output: Contribution to Journal/Magazine › Journal article › peer-review
Research output: Contribution to Journal/Magazine › Journal article › peer-review
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TY - JOUR
T1 - The Microbiome and the Entropy Paradox
T2 - An Evolutionary Perspective
AU - Morris, James A.
AU - Rigby, Rachael
AU - Wray, Marisa
AU - Taylor, Adam
PY - 2024/3/28
Y1 - 2024/3/28
N2 - The mucosal tissue microbiota, measured in millions, cause inflammation which contributes to the pathogenesis of a wide range of disease including neurodegeneration, atherosclerosis, cancer and psychiatric conditions. A broad range of pathological factors, both psychosocial and physical, interact with, amplify and otherwise modify the inflammatory process and thereby contribute todisease in general. In order to diagnose mucosal tissue dysbiosis and assess its severity in individual cases, it will be necessary to measure markers of inflammation and assess bacterial carriage of specific pathogens in faeces, using quantitative polymerase chain reaction (qPCR). Current methods of analysis of the gut microbiome, using 16S rRNA amplicon sequencing and DNA metagenomics, reveal the composition of the trillions of bacteria in the colonic lumen but not the millions in the wall. The relationship between the mucosal luminal microbiota, the mucosal tissue microbiota and the host; its evolutionary origin andimportance in disease is analysed, in this paper, using concepts from information theory. The analysis explains the entropy paradox (increased entropy is usually a marker of disease but in the case of the faecal microbiome it is an indicator of health) and the affluence paradox (diseases which are a consequence of affluence disproportionately affect the least affluent members of the population). An increasingly sterile diet in affluent countries is leading to a sub-optimal mucosal luminal microbiota and as a consequence increased mucosal tissue microbiota induced inflammation. A rising tide of illness has followed and we need togive urgent attention to our diet. Increased consumption of milk and yoghurt will provide the diverse but safe supply of bacteria that we need.
AB - The mucosal tissue microbiota, measured in millions, cause inflammation which contributes to the pathogenesis of a wide range of disease including neurodegeneration, atherosclerosis, cancer and psychiatric conditions. A broad range of pathological factors, both psychosocial and physical, interact with, amplify and otherwise modify the inflammatory process and thereby contribute todisease in general. In order to diagnose mucosal tissue dysbiosis and assess its severity in individual cases, it will be necessary to measure markers of inflammation and assess bacterial carriage of specific pathogens in faeces, using quantitative polymerase chain reaction (qPCR). Current methods of analysis of the gut microbiome, using 16S rRNA amplicon sequencing and DNA metagenomics, reveal the composition of the trillions of bacteria in the colonic lumen but not the millions in the wall. The relationship between the mucosal luminal microbiota, the mucosal tissue microbiota and the host; its evolutionary origin andimportance in disease is analysed, in this paper, using concepts from information theory. The analysis explains the entropy paradox (increased entropy is usually a marker of disease but in the case of the faecal microbiome it is an indicator of health) and the affluence paradox (diseases which are a consequence of affluence disproportionately affect the least affluent members of the population). An increasingly sterile diet in affluent countries is leading to a sub-optimal mucosal luminal microbiota and as a consequence increased mucosal tissue microbiota induced inflammation. A rising tide of illness has followed and we need togive urgent attention to our diet. Increased consumption of milk and yoghurt will provide the diverse but safe supply of bacteria that we need.
U2 - 10.29011/2575-7091.100194
DO - 10.29011/2575-7091.100194
M3 - Journal article
SP - 1
EP - 9
JO - Food & Nutrition Journal
JF - Food & Nutrition Journal
SN - 2575-7091
ER -