@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 = {Alcoholism: Clinical and Experimental Research},
title = {Inflammation, oxidative stress and the gut microbiome perturbation: A narrative review of mechanisms and treatment of the alcohol hangover},
url = {http://dx.doi.org/10.1111/acer.15396},
year = {2024}
}

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TY  - JOUR
AB  - Background: Alcohol is the most widely abused substance in the world and the leading source of mortality in 15-49-year-olds and a major risk factor for heart disease, liver disease, diabetes and cancer. In spite of this, alcohol is regularly and dangerously abused 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 long-term clinical significance by clinicians or consumers.Methods: A critical review of the literature was undertaken to demonstrate the pathophysiological mechanisms of the alcohol hangover.Results: Hereafter, the alcohol hangover is re-defined as a manifestation of sickness behaviour secondary to alcohol-induced inflammation, using the Bradford-Hill criteria to demonstrate causation above correlation. Alcohol causes inflammation through oxidative stress and endotoxaemia. 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. Alcohol metabolism by-products such as acetaldehyde,congeners, sleep deprivation and the activation of non-specific 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, allowingtranslocation of pathogenic bacteria to the systemic circulation (endotoxaemia). This leads to a wellcharacterised cascade of systemic inflammation, additionally activating toll-like receptor 4 to inducesickness behaviour.Conclusions: Considering the evidence, it is suggested that hangover frequency and severity may be predictors of the development of later alcohol-related diseases, meriting formal confirmation in prospective studies. In light of the mechanisms of alcohol-mediated inflammation, research into gut permeabili
AU  - Turner,BRH
AU  - Jenkinson,PI
AU  - Huttman,M
AU  - Mullish,BH
DO  - 10.1111/acer.15396
PY  - 2024///
SN  - 0145-6008
TI  - Inflammation, oxidative stress and the gut microbiome perturbation: A narrative review of mechanisms and treatment of the alcohol hangover
T2  - Alcoholism: Clinical and Experimental Research
UR  - http://dx.doi.org/10.1111/acer.15396
UR  - http://hdl.handle.net/10044/1/112594
ER  - 

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