Health

Man’s gut bacteria made him ‘drunk’ without alcohol

Researchers studying a Chinese man with a rare condition that causes him to become drunk without consuming any alcohol discovered a certain type of gut bacteria may be to blame for his inebriation … and severe liver damage as a result.

In research recently published in the medical journal Cell Metabolism, researchers detailed the odd case of a Chinese man who had severe liver damage and a rare condition called auto-brewery syndrome. The latter, per Healthline, occurs when the body turns high-sugar foods or carbohydrates into alcohol, causing intoxication.

In the past, auto-brewery syndrome – also known as “drunkenness disease” – has been linked to an excessive amount of yeast in the gut. But those treating the man found no yeast in his gut — discovering instead his gut contained “several strains of a bacteria known as Klebsiella pneumonia.” The bacteria, researchers wrote, produces “high levels” of alcohol.

“K. pneumonia is a common type of commensal gut bacteria. Yet, the strains isolated from the patient’s gut can generate about four to six times more alcohol than strains found in healthy people,” they wrote in a press release regarding the findings.

The bacteria – and the amount of alcohol it produces – may be to blame for the patient’s non-alcoholic fatty liver disease (NAFLD), which has “severely” damaged his liver.

The research team also sampled gut bacteria from 43 patients who also had NAFLD and from 48 healthy patients. By the end, “they found about 60 [percent] of NAFLD patients had high- and medium-alcohol-producing K. pneumonia in their gut, while only 6 [percent] of healthy controls carry these strains.”

“We were surprised that bacteria can produce so much alcohol,” said lead author Jing Yuan, a microbiologist at the Capital Institute of Pediatrics, in a statement. “When the body is overloaded and can’t break down the alcohol produced by these bacteria, you can develop fatty liver disease even if you don’t drink.”

To further test their hypothesis, the team fed the bacteria, extracted from the Chinese patient with auto-brewery syndrome, to healthy mice. After one month, the mice began to develop a fatty liver. At two months, their lives began to scar — a sign that “long-term liver damage had been made,” they wrote.

“The progression of liver disease in these mice was comparable to that of mice fed with alcohol,” they added.

But when treated with a K. pneumonia-killing antibiotic, the condition reversed. The results show that there’s promise in treating patients with bacteria-linked NAFLD.

“In the early stages, fatty liver disease is reversible. If we can identify the cause sooner, we could treat and even prevent liver damage,” Yuan said, noting it’s not yet clear why some people have high-alcohol-producing K. pneumonia while others do not.

“We don’t understand what factors would make someone more susceptible to these particular K. pneumonia and that’s what we want to find out next,” Yuan added.