Auto-Brewery Syndrome (ABS): When the intestine produces alcohol
If someone roams the streets slurring their words, it is immediately assumed that they have had too much to drink.
But what if the person has not had a glass of alcohol at all?
What if they are drunk through no fault of their own?
In auto-brewery syndrome, those affected develop measurable blood alcohol levels even though they have not consumed alcohol. In the study discussed here, the focus is not on yeasts, but on a functionally altered intestinal microbiome that activates certain metabolic pathways and thus produces ethanol.
It is not so much the specific composition of the intestinal microbiome that is decisive, but rather the unique biochemical interaction of the microorganisms. Under certain conditions, such as high carbohydrate availability, alcohol can be produced in the gut. The syndrome is rare and can be clearly distinguished from classic alcohol consumption. Nevertheless, those affected are often stigmatized.
What was done?
The study examined an observational study with
- 22 patients with auto-brewery syndrome
- 21 unaffected household partners as a control group
This is a classic multi-omics approach.
These were carried out:
- Measurement of ethanol production from stool samples
- Analysis of microbial composition and functional genes with a focus on ethanol-relevant metabolic pathways
- Measurement of central metabolites, including short-chain fatty acids, and correlation with blood alcohol levels
- Fecal microbiota transplantation in a patient with subsequent therapy observation
Why is auto-brewery syndrome dangerous?
Auto-brewery syndrome (ABS) is dangerous because it leads to uncontrolled and often unnoticed production of ethanol in the gut, which poses medical as well as social and legal risks.
A. Physical health and organ damage
1. liver damage: constant exposure to endogenously produced alcohol leads to liver damage, which manifests itself in increased levels of alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (AP) and total bilirubin.
2. cirrhosis: In severe cases, chronic alcohol exposure through the microbiome can lead to liver cirrhosis.
3. metabolic diseases: Pathological ethanol production in the intestine is associated with the development of metabolic steatotic
liver disease (MASLD). Not yet confirmed.
4. neuro-psychiatric symptoms: patients suffer from extreme drowsiness and personality changes such as potentially increased aggression.
B. Dangers in everyday life and legal risks
1. high blood alcohol concentration (BAC): During acute episodes (“flares”), average BAC values of 136 +/- 82 mg/dl were measured, which is well above the US limit for driving ability (80 mg/dl).
2. legal problems: As with alcohol dependence, those affected often experience serious legal consequences, for example by drinking and driving without ever having drunk.
3. unpredictable intoxication: Since alcohol is produced spontaneously by the fermentation of carbohydrates in the intestine, intoxication often occurs completely unexpectedly.
C. Social stigmatization and misdiagnosis
1. suspicion of secret drinking: Many patients are wrongly labeled as “secret drinkers” by doctors or their social environment and are not taken seriously.
2. diagnostic hurdles: Diagnosis is extremely resource-intensive and often not easily accessible or covered by insurance, leaving many sufferers without help for long periods of time.
3. burden on the environment: the disease leads to serious family and social problems that are comparable to the effects of alcohol addiction.
What does that mean?
The study provides strong evidence that auto-brewery syndrome in this cohort is primarily associated with bacterial metabolic pathways. Contrary to previous assumptions, yeasts did not play a dominant role here.
Key observations:
- The production of ethanol was functionally measurable
- The focus was on the pathway level, not on individual species
- Microbial metabolism correlated with blood alcohol levels
- In addition to Escherichia coli and Klebsiella pneumoniae, other taxa, including Ruminococcus gnavus, were also enriched during acute episodes, although their direct role in ethanol production has not been conclusively clarified
This clearly shows that pure sequence data does not tell a story. Only a look at the microbial reality, including the metabolism, reveals the truth.
Not every enrichment of proteobacteria led to ethanol production. Only the combination of substrate availability, enzyme equipment and microbial community dynamics produces the observed effect.
In addition, it was found that acetate in the stool of auto-brewery syndrome patients was significantly increased and correlated strongly with the blood alcohol concentration. Acetate is a central metabolic product in ethanol metabolism.
The focus is therefore clearly on the microbial ecosystem.
What impact will this have one day?
Since bacterial metabolic pathways played a central role in this study, this opens up the possibility of more targeted therapeutic approaches in the future.
In the study, one patient underwent FMT (fecal microbiota transplantation) treatment, with a clear subsequent clinical improvement.
In the long term, the treatment of auto-brewery syndrome could move away from blanket interventions such as non-specific antibiotics towards targeted modulation of microbial metabolic pathways and interactions.
The decisive factor here is the combination of ecological classification and functional analysis. This provides insights that pure sequence data cannot deliver.
In the future, analyses of the microbiome will increasingly focus on holistic approaches. Understanding the entire system is becoming increasingly necessary.
Source:
Hsu, C. L. et al. Gut microbial ethanol metabolism contributes to auto-brewery syndrome in an observational cohort. Nature Microbiology, 2026. DOI: 10.1038/s41564-025-02225-y
The most important facts at a glance
- The auto-brewery syndrome can probably also be caused by proteobacteria and not only by yeasts. In this study, a functional enrichment of proteobacterial metabolic pathways was indeed associated with the phenotype.
- Understanding microbial ecology is necessary to explain complex phenotypes such as ABS.
- In future, ABS patients could be treated in a more targeted and functionally oriented way.
