Imagine this: you have a perfectly ordinary lunch—rice, bread, potatoes, meat, and fruit compote. An hour later, you’re stumbling, your speech is slurred, and your breath reeks of alcohol. Yet you haven’t had a single drop. People don’t believe you, doctors suspect hidden alcoholism, and the police strip you of your driving licence. This isn’t science fiction—it’s a real, albeit extremely rare, medical condition: auto‑brewery syndrome (ABS), also known as gut fermentation syndrome. First described in Japan, it has since offered researchers plenty of surprises—including the discovery that not only yeasts but also bacteria can “brew alcohol” inside the human body.

JAPANESE ROOTS: THE WORLD’S FIRST “BREWERY” IN ONE’S OWN STOMACH

The story of the syndrome began long before it got its official name. As early as 1934, Time magazine reported the case of Kozo Ohishi, a Japanese entrepreneur from the small town of Pippu in northern Japan. After a simple snack of bread or potatoes, he felt as if he’d overindulged in sake: he suffered from hangovers, his speech became confused, and for years, acquaintances believed him to be an alcoholic. His reputation was saved only thanks to doctors in Sapporo, who found unicellular fungi, Candida albicans, in his stomach and intestines. These microbes were converting carbohydrates from food into ethyl alcohol.

In the 1950s–1970s, Japanese physicians documented several similar cases and were the first in the world to define this condition as a distinct medical syndrome. In Japanese medical literature, it was called meiteisho—the syndrome of alcoholic autointoxication. Researchers identified three key features: a rise in blood alcohol levels after consuming carbohydrate‑rich food, an overgrowth of yeast fungi in the gut, and the disappearance of symptoms after antifungal treatment.

At first, some Japanese experts even suspected mutant fungi allegedly altered by radiation after the atomic bombings of Hiroshima and Nagasaki—until it became clear that Kozo Ohishi’s case was described a full decade before those bombings.

AN AMERICAN IN JAPAN: A DISEASE THAT ONLY JAPANESE DOCTORS KNEW HOW TO TREAT

Shortly after World War II, auto‑brewery syndrome struck a foreigner on Japanese soil. Charles Swaart, an American working as press secretary for General Douglas MacArthur’s headquarters in occupied Japan, was admitted to hospital with viral hepatitis—and the doctors were stunned: the patient appeared dead drunk, even though no alcohol had entered his ward. He was nearly denied further hospitalization.

When Swaart told a Japanese doctor that he got drunk not from alcohol but from Italian cuisine, the physician recalled the Time article about Kozo Ohishi. Tests revealed that Charles’s digestive system was teeming with colonies of the same Candida albicans fungi. To get rid of them, he had to return to Japan—because at that time, only there did doctors know how to treat meiteisho.

HOW THE “INTERNAL BREWERY” WORKS

The mechanism behind auto‑brewery syndrome is broadly understood. In a healthy person, the gut hosts microorganisms that produce small amounts of ethanol as a by‑product of metabolism. The liver easily handles this, and endogenous alcohol levels remain negligible. Scientific studies confirm this: even in people who don’t drink, traces of alcohol can be found in the blood.

But in auto‑brewery syndrome, this delicate balance collapses. Certain microorganisms proliferate to such an extent that the gut effectively becomes a living brewery: carbohydrates from food are fermented into ethanol, which is absorbed into the то bloodstream. The liver can’t keep up with the load, and the person becomes intoxicated.

Several factors usually contribute to the development of the syndrome: genetic predisposition (impaired function of enzymes that break down alcohol), underlying conditions (diabetes, liver diseases, intestinal inflammations), prolonged use of antibiotics that disrupt normal gut flora, and a high‑carbohydrate diet.

Symptoms fall into three groups: neurological (slurred speech, impaired coordination, seizures, blurred vision, memory loss); gastrointestinal (nausea, diarrhea, abdominal discomfort); and psychiatric (drowsiness, disorientation, depression, confusion). In some patients, constant endogenous intoxication even leads to genuine alcohol dependence. How does this happen? The brain simply gets used to the alcohol that the body produces on its own.

A SCIENTIFIC REVOLUTION: BACTERIA, NOT YEAST

For decades, experts believed that the main “brewers” in the gut were yeasts: Saccharomyces cerevisiae (the same ones used in beer brewing), Candida albicans, and Candida tropicalis. Antifungal medications usually helped.

That changed in 2019, when a paper by a team led by microbiologist Jing Yuan from the Capital Institute of Pediatrics (Beijing, China) was published in Cell Metabolism. They described the case of a 27‑year‑old patient with severe liver damage and intoxication despite no alcohol consumption. Antifungal drugs didn’t work, and tests for yeast came back negative. Researchers then analyzed the patient’s fecal samples and discovered something unexpected: the gut was colonized by Klebsiella pneumoniae bacteria—specifically, special strains capable of producing enormous amounts of alcohol.

“At first, we thought it was due to yeast, but the test results were negative. The antifungal medications didn’t help either, so we assumed the cause must be something else,” Dr. Yuan recalled.

The numbers astonished the researchers. The abundance of Klebsiella pneumoniae in the patient’s gut exceeded the norm by 900 times and accounted for about 19 % of the entire gut microbiota. These bacteria produced 4–6 times more alcohol than strains found in healthy individuals. At peak levels, the patient’s blood alcohol concentration reached values equivalent to having consumed roughly 15 shots of whiskey.

“We were amazed that a bacterium could produce so much alcohol,” Yuan admitted.

Klebsiella pneumoniae is a common gut bacterium present in most people and usually harmless. But the patient harbored two specific strains that turned his intestine into an ethanol factory.

LINK TO FATTY LIVER DISEASE

This discovery led to another breakthrough. Dr. Yuan wondered whether these bacteria might be responsible for non‑alcoholic fatty liver disease (NAFLD)—a condition where fat accumulates in the liver similarly to what happens in heavy drinkers, even though the person doesn’t consume alcohol. NAFLD affects 30–40 % of adults in developed countries, and its causes long remained a mystery.

Researchers analyzed the microbiota of 43 NAFLD patients and 48 healthy individuals. About 60 % of NAFLD patients carried high‑alcohol‑producing strains of Klebsiella pneumoniae, compared to only 6 % among healthy subjects.

To confirm a causal link, scientists inoculated germ‑free mice (those without their own microbiota) with the bacteria isolated from the patient. Within a month, the rodents developed fatty livers; by two months, signs of scarring—indicating long‑term damage—appeared. The picture resembled that of mice given pure alcohol. When the mice were treated with an antibiotic targeting Klebsiella, their liver condition improved.

“These bacteria damage your liver just like alcohol does—the only difference is that you have no choice in the matter,” Dr. Yuan described vividly.

DIAGNOSIS: A YEARS‑LONG INVESTIGATION

Diagnosing auto‑brewery syndrome is no easy task. Because the condition is so rare (fewer than 100 documented cases worldwide), doctors rarely consider it when making a diagnosis. Patients are often first treated for alcoholism, referred to psychiatrists, or suspected of hiding their drinking.

A striking example is the case of a 50‑year‑old Canadian woman described in the Canadian Medical Association Journal. For two years, she visited doctors complaining of drowsiness: she could fall asleep right in the middle of work or while cooking. Her family noticed the smell of alcohol on her breath, and her blood ethanol levels reached 62 mmol/L. Her family doctor diagnosed alcohol intoxication, and she was treated under a narcology protocol by psychiatrists. Only after her seventh visit was she referred to a gastroenterologist, who finally made the correct diagnosis: auto‑brewery syndrome.

The diagnostic process typically includes: ruling out alcohol and drug use, blood tests to measure alcohol levels, gastrointestinal endoscopy with sampling for culture, and determining microbial sensitivity to medications. The final step is in‑hospital observation for 24 hours: the patient is given a high‑carbohydrate diet and a glucose tolerance test, then doctors check whether their blood alcohol level rises.

TREATMENT: DIET, ANTIBIOTICS, AND FECAL TRANSPLANTATION

The core treatment strategy depends on which microorganism is driving the syndrome. If fungi are to blame, antifungal drugs and a low‑carb diet are prescribed. If bacteria are the culprit—as in Dr. Yuan’s patient—antibiotics, probiotics, and drastic carbohydrate restriction are used. Dr. Yuan’s patient responded to antibiotics and a no‑carb diet over three weeks—his intoxication symptoms disappeared.

In 2026, a paper in Nature Microbiology by an international research group confirmed the role of bacteria—Escherichia coli and Klebsiella pneumoniae—in the pathogenesis of auto‑brewery syndrome. The team analyzed the microbiota of 22 patients with confirmed ABS. One patient with severe symptoms underwent fecal microbiota transplantation—the transfer of gut flora from a healthy donor. After two transplants and supportive therapy, the patient remained in stable remission for more than 16 months.

THE SYNDROME AND THE LAW: DRUNK AT THE WHEEL WITHOUT FAULT

Auto‑brewery syndrome creates paradoxical legal situations. In 2024, a 40‑year‑old man in Belgium was acquitted of driving under the influence after proving that his own gut had produced the alcohol detected in his blood. The breathalyzer showed 0.91 mg/L, even though he hadn’t consumed a drop.

Researchers emphasize that any person who denies drinking but has elevated blood alcohol levels or a positive breathalyzer result should be examined for auto‑brewery syndrome—including those arrested for drunk driving.

Auto‑brewery syndrome is a vivid example of how a disruption in the delicate balance of gut microbiota can lead to dramatic consequences. From the Japanese entrepreneur Kozo Ohishi, whose hangover from bread puzzled doctors in the 1930s, to the Chinese scientists who discovered a bacterium capable of “getting a person drunk” like fifteen shots of whiskey—this is a story of how complex and surprising the world inside us can be. And perhaps this is just the tip of the iceberg: if a gut bacterium can produce enough alcohol to cause fatty liver disease in a non‑drinker, what else might our microbiota be capable of?

Editor‑in‑Chief of the journal
World Community,
Vice‑Rector of the University
of Natural and Humanitarian Sciences
(Moscow)