How can you support your liver after drinking alcohol?

Aim of the study: Chronic alcohol consumption is an important cause of liver-related deaths. Specific intestinal microbiota profiles are associated with susceptibility or resistance to alcoholic liver disease in both mice and humans. We aimed to identify the mechanisms by which targeting intestinal microbiota can improve alcohol-induced liver lesions.

Results: Pectin treatment modified the microbiome and metabolome in human microbiota-associated alcohol-fed mice, leading to a specific faecal signature. High production of bacterial tryptophan metabolites was associated with an improvement of liver injury. The AhR agonist Ficz (6-formylindolo (3,2-b) carbazole) reduced liver lesions, similarly to prebiotic treatment. Conversely, inactivation of the ahr gene in alcohol-fed AhR knock-out mice abrogated the beneficial effects of the prebiotic. Importantly, patients with severe alcoholic hepatitis have low levels of bacterial tryptophan derivatives that are AhR agonists. Improvement of alcoholic liver disease by targeting the intestinal microbiota involves the AhR pathway, which should be considered as a new therapeutic target.

Aim of the study: Zinc is an essential trace element required for normal cell growth, development, and differentiation. It is involved in DNA synthesis, RNA transcription, and cell division and activation.

Results: Zinc supplementation has been documented to block/attenuate experimental ALD through multiple processes, including stabilization of gut-barrier function, decreasing endotoxemia, decreasing proinflammatory cytokine production, decreasing oxidative stress, and attenuating apoptotic hepatocyte death. Clinical trials in human liver disease are limited in size and quality, but it is clear that zinc supplementation reverses clinical signs of zinc deficiency in patients with liver disease. Some studies suggest improvement in liver function in both ALD and hepatitis C following zinc supplementation, and 1 study suggested improved fibrosis markers in hepatitis C patients. The dose of zinc used for treatment of liver disease is usually 50 mg of elemental zinc taken with a meal to decrease the potential side effect of nausea.

Aim of the study: Prolonged alcohol consumption disrupts the gut microbiota and the immune system, contributing to the pathogenesis of alcohol-associated liver disease (ALD). Probiotic-postbiotic intervention strategies can effectively relieve ALD by maintaining gut homeostasis.

Results: The heat-killed L. johnsonii provoked immunity helps correct the gut microbiota dysbiosis, specifically by reversing the reduction of butyrate-producing bacteria (such as Faecalibaculum rodentium) and the expansion of opportunistic pathogens (such as Helicobacter sp. and Pichia kudriavzevii) induced by ethanol. The findings provide novel insights into the gut microbiota-liver axis that may be leveraged to enhance the treatment of ALD.

Aim of the study: Alcohol-associated liver disease is the leading cause of cirrhosis in the United States and has become the top indication for liver transplantation since direct-acting antivirals allowed for cure of hepatitis C. The COVID-19 pandemic compounded existing concerns about a rising prevalence of alcohol-associated hepatitis, with a notable increase in women in their 30s and 40s.

Results: Alcohol use screening is essential for all adults. Abstinence from alcohol remains the cornerstone intervention for alcohol-associated liver disease, although pharmacotherapies are under evaluation. Noninvasive liver disease assessment, including serum and imaging modalities, is expanding access to advanced liver disease evaluation in primary care settings. Other causes of substance-based liver injury include prescription and nonprescription medications, herbal products, and dietary supplements.

Aim of the study: Background: Alcoholic liver disease (ALD) refers to a progressive liver injury syndrome induced by chronic excessive alcohol intake. Current treatment options are mainly limited to symptom management, and there are safety risks associated with long-term use.

Results: Conclusions: Consistently, NMDS analysis based on the OTU level showed that the IS-treated groups clustered away from the EtOH group and shifted toward the Control group, indicating a partial restoration of the overall microbial community structure toward that of healthy controls. In terms of species composition, IS treatment enriched beneficial microbial communities and inhibited the proliferation of pathogenic bacteria, efficiently restoring intestinal flora homeostasis. Collectively, these findings suggested that the hepatoprotective effects of IS were closely associated with the amelioration of gut microbiota dysbiosis and intestinal barrier function, pointing to a potential involvement of the gut-liver axis, although its causal contribution remains to be confirmed by further mechanistic studies (e.g., microbiota depletion or fecal microbiota transplantation).