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But those drugs didn’t work on the Chinese patient. Baffled, a team of doctors, led by Jing Yuan from the Capital Institute of Pediatrics, analyzed the man’s stool samples and found that the alcohol in his body was being produced not by yeast, but by bacteria. During his first episode in the hospital, Klebsiella bacteria had bloomed so vigorously that it made up 19 percent of the microbes in his gut, and became 900 times more common than in healthy people.

Klebsiella pneumoniae is extremely common in both soils and human bodies. Though usually harmless, it’s also an opportunistic pathogen that can cause severe infections if given the chance. And while Klebsiella is not known for intoxicating its hosts, Yuan’s team found that the patient had two particular strains that can churn out alcohol. Many gut microbes do this, but at such low levels that their boozy by-products are easily removed by the liver. The Klebsiella strains in Yuan’s patient were exceptions: At one point, they produced so much of the stuff that it was as if the man had knocked back 15 shots of whiskey. “We were surprised that bacteria can produce so much alcohol,” Yuan says.

Auto-brewery syndrome is extreme, but it has similarities to other, milder and more prevalent conditions. For example, people with nonalcoholic fatty liver disease (NAFLD) build up fatty deposits in their liver in the style of heavy drinkers, despite touching little or no alcohol. This condition is very common, affecting 30 to 40 percent of American adults; the causes are still unclear and likely varied. Yuan wondered if Klebsiella might be involved, and when she analyzed 43 Chinese people with NAFLD, she found that 61 percent had the same high-alcohol strains as the man with auto-brewery syndrome. By contrast, just 6 percent of people with a healthy liver carry those strains.

To see if those strains were actually causing fatty livers, the team fed them to mice that had been raised in sterile conditions and lacked microbes of their own. Within two months, the rodents had signs of liver disease, inflammation, and scarring, comparable to mice that had been drinking alcohol itself. The same thing happened if the team transplanted the stool from an NAFLD patient into germ-free mice, but not if they first removed the alcohol-making Klebsiella using a virus—a phage—that specifically kills those strains. Although studies in mice should be treated with caution, Yuan nonetheless suggests that these strains could be an important cause of NAFLD, through the alcohol they produce.

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Other researchers have suggested this before. In 2000, Anna Mae Diehl from Johns Hopkins University noticed that obese mice often have alcohol on their breath, which goes away after antibiotic treatment. “Intestinal production of ethanol may contribute to the genesis of obesity-related fatty liver,” she speculated. Two groups later showed that alcohol-producing microbes are more common in the guts of people with NAFLD than in those of their healthy peers.