@article{Turner:2024:10.1111/acer.15396,
author = {Turner, BRH and Jenkinson, PI and Huttman, M and Mullish, BH},
doi = {10.1111/acer.15396},
journal = {Alcohol, Clinical and Experimental Research},
pages = {1451--1465},
title = {Inflammation, oxidative stress and gut microbiome perturbation: A narrative review of mechanisms and treatment of the alcohol hangover},
url = {http://dx.doi.org/10.1111/acer.15396},
volume = {48},
year = {2024}
}

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TY  - JOUR
AB  - <jats:title>Abstract</jats:title><jats:p>Alcohol is the most widely abused substance in the world, the leading source of mortality in 15–49yearolds, and a major risk factor for heart disease, liver disease, diabetes, and cancer. Despite this, alcohol is regularly misused in wider society. Consumers of excess alcohol often note a constellation of negative symptoms, known as the alcohol hangover. However, the alcohol hangover is not considered to have longterm clinical significance by clinicians or consumers. We undertook a critical review of the literature to demonstrate the pathophysiological mechanisms of the alcohol hangover. Hereafter, the alcohol hangover is redefined as a manifestation of sickness behavior secondary to alcoholinduced inflammation, using the BradfordHill criteria to demonstrate causation above correlation. Alcohol causes inflammation through oxidative stress and endotoxemia. Alcohol metabolism is oxidative and increased intake causes relative tissue hypoxia and increased free radical generation. Tissue damage ensues through lipid peroxidation and the formation of DNA/protein adducts. Byproducts of alcohol metabolism such as acetaldehyde and congeners, sleep deprivation, and the activation of nonspecific inducible CYP2E1 in alcoholexposed tissues exacerbate free radical generation. Tissue damage and cell death lead to inflammation, but in the intestine loss of epithelial cells leads to intestinal permeability, allowing the translocation of pathogenic bacteria to the systemic circulation (endotoxemia). This leads to a wellcharacterized cascade of systemic inflammation, additionally activating tolllike receptor 4 to induce sickness behavior. Considering the evidence, it is suggested that hangover frequency and severity may be predictors of the development of later alcoholrelated diseases, meriting formal confirmation in prospective studies. In light of the mechanisms of alcoholmediated inflammation, research into
AU  - Turner,BRH
AU  - Jenkinson,PI
AU  - Huttman,M
AU  - Mullish,BH
DO  - 10.1111/acer.15396
EP  - 1465
PY  - 2024///
SN  - 2993-7175
SP  - 1451
TI  - Inflammation, oxidative stress and gut microbiome perturbation: A narrative review of mechanisms and treatment of the alcohol hangover
T2  - Alcohol, Clinical and Experimental Research
UR  - http://dx.doi.org/10.1111/acer.15396
UR  - https://doi.org/10.1111/acer.15396
VL  - 48
ER  - 

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