Fatty Liver Disease: When You’re Not Consuming Too Much Alcohol, You’re Producing It

It’s common knowledge that your Corona is doing your liver no favours. Heavy alcohol consumption isn’t great for your health.

Reported in Cell Metabolism, new research gets more specific: the gut bacteria that creates alcohol, ethanol-producing microbes, may cause nonalcoholic fatty liver disease, making the name maybe not so apt.

Nonalcoholic Fatty Liver Disease (NAFLD)

Fatty Liver disease is often the result of high alcohol consumption, whereas nonalcoholic fatty liver disease (NAFLD) is the name for the range of liver conditions that effect low to non-drinkers. Those with the disease have too much fat stored in their liver, causing tiredness or pain in the upper right abdomen. It can also be identified by abdominal swelling, enlarged blood vessels and spleen, red palms, and jaundice.

The disease in itself is common: around 1/4 of Americans have it and its correlated with other common health issues such as obesity, type 2 diabetes, and high cholesterol. However, NAFLD is less common, and a severe form of the disease known as nonalcoholic steatohepatitis, or NASH, less still. Because not everyone who gets the disease is consuming high amounts of alcohol, there are questions about why the disease manifests in them. This is the rare part: the people who do not follow the typical pattern of cause and effect.

The New Research

Researchers at the Capital Institute of Pediatrics and the Chinese Center for Disease Control and Prevention in Beijing looked into how gut microbes may play a role, a relationship implicated in past studies. They conducted an experiment that studied the feces of healthy people and those with nonalcoholic fatty liver disease, three quarters of whom had the severe NASH form. While they had similar levels of the gut bacteria, Klebsiella pneumonie, the bacteria of those with the disease were producing medium to high levels of alcohol, at 61% with the disease versus 6.25% of the healthy population, though they did not consume much or any alcohol.

The experiments then tested this on mice, transplanting the bacteria that creates the alcohol from patients with the disease into their body, and found the same inflammation and fatty liver issues. When the alcohol-producing bacteria was selectively removed, the mice had no issues.

This study implies that consuming the alcohol itself is not the only trigger. Alcohol in any form, including self-production, while less common, is linked to the disease.

 


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