The unequal risk of alcoholic liver disease (ALD) suggests that cofactors are involved in the development of the disease. Recent research tends to show the role of microbiota in developing the disease.
Alcohol consumption is responsible for 3.8% of deaths worldwide and 4.6% of the loss of years of life due to premature death1. As for alcoholic liver disease (ALD) itself, there is no direct way to calculate its epidemiology. We can get picture of the disease by studying the mortality rate from hepatic cirrhosis, although bearing in mind that it is difficult to make a distinction between alcoholic and non-alcoholic cirrhosis2.
Associated diseases and pathologies
ALD is diagnosed when excessive consumption of alcohol (more than 30 g/day)1 is observed along with clinical and biological signs indicating steatosis, alcoholic steatohepatitis (ASH), progressive fibrosis, cirrhosis, or even the early signs of hepatocellular cancer.
Role of microbiota
The influence of microbiota on ALD has been known since 1995: it has been observed that the alteration in microbiota produced by antibiotics protects rats from hepatic lesions due to alcohol3. On the one hand, microbiota transforms alcohol into acetaldehyde, which alters the intestinal barrier4 and increases the permeability of the intestinal wall; on the other hand, an increase in the concentration of polysaccharides leads to hepatic inflammation5.
Alcohol and dysbiosis: a connection
The chronic ingestion of ethanol causes dysbiosis in rodents, with a reduction in bacteria of the genera Lactobacillus, Pediococcus, Leuconostoc, and Lactococcus6, and an increase in Proteobacteria and Actinobacteria7. In humans, observations have shown an alteration of the microbiota in alcoholic patients, with a reduction in Bacteroidetes and an increase in Enterobacteriaceae and Proteobacteria8.
Beyond its role in hepatic lesions, the microbiota also seems to influence psychological and psychiatric symptoms associated with ALD9. Its role should not be neglected in treating patients.
1. Directives de pratique clinique de l’EASL: Prise en charge de la maladie alcoolique du foie - Association européenne pour l’étude du foie (EASL) - Journal of Hepatology 2012 vol. 57 | 399–420
2. Rehm J et al. Global burden of disease and injury and economic cost attributable to alcohol use and alcohol-use disorders. Lancet 2009;373:2223–2233. https://www.ncbi.nlm.nih.gov/pubmed/19560604
3. Adachi Y et al. Antibiotics prevents liver injury in rats following long-term exposure to ethanol. Gastroenterlogy 1995 ; 108 : 218-24. https://www.ncbi.nlm.nih.gov/pubmed/7806045
4. Ferrier L. et al. Impairement of the intestinal barrier by ethanol involves enteric microflora and mast cell activation in rodents. Am J Pathol 2006 ; 168 : 1148-54. https://www.ncbi.nlm.nih.gov/pubmed/16565490
5. Mencin et al. Toll-like receptors as targets in chronic liver disease. Hepatology 2009 ; 50 : 638-44. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3721430/
6. Yan et al. Enteric dysbiosis associated with a mouse model of alcoholic liver disease. Hepatology 2011 ; 53 : 96-105. https://www.ncbi.nlm.nih.gov/pubmed/21254165
7. Bull-Otterson L. et al. Metagenomic analyses of alcohol induced pathogenic alterations in the intestinal microbiome ad the effet of Lactobacillus rhamnosus GG treatment. PloS One 2013 ; 8 : e53028. https://www.ncbi.nlm.nih.gov/pubmed/23326376
8. Mutlu et al. Colonic microbiome is altered in alcoholism. Am J Physiol Gastrointest Liver Physiol 2012 ; 302 : G966-978. https://www.ncbi.nlm.nih.gov/pubmed/22241860
9. Leclercq S et al. Intestinal permeability, gut-microbial dysbiosis and behavioral merkers of alcohol-dependence severity. PNAS 2014; 111 : E4485-93. http://www.pnas.org/content/111/42/E4485.full