- Researchers say they may have found a connection between an alcohol-producing bacteria and nonalcoholic fatty liver disease (NAFLD).
- In some people, this bacteria can cause them develop a form of auto brewery syndrome, a condition in which the body turns starchy or sugary foods into alcohol.
- Researchers say this can lead to several serious health conditions such as nonalcoholic steatohepatitis (NASH) and cirrhosis of the liver.
A man in China regularly became so drunk that his blood alcohol content would be equivalent to taking 15 shots of whiskey. Only this man hadn’t been drinking alcohol.
After Chinese researchers took an interest in the man’s situation, they discovered a new potential cause for the most common liver disease in the world.
In new research published
NAFLD is an umbrella term for a group of conditions, the most common of which is fatty liver.
Fatty liver is not necessarily harmful on its own but can progress to serious conditions such as nonalcoholic steatohepatitis (NASH) and cirrhosis of the liver.
While NAFLD is very common, experts say its root cause is varied, but includes several common risk factors including high blood pressure, obesity, and diabetes.
But there are also additional factors that researchers suspect play a role, such as that of the gut microbiome, that have not yet been proven concretely.
The hypothesis of the new research, that a certain bacteria could be involved in NAFLD, fits within the larger theory that the gut microbiome is a factor in the development of the disease.
In the case of the Chinese man who would spontaneously become drunk, researchers found he had severe NASH and auto brewery syndrome, a condition in which the body turns starchy or sugary foods into alcohol. Normally this is caused by an excessive amount of yeast (fungus) in the gut.
But when doctors attempted an antifungal treatment, it had no effect.
“Surprisingly, we found that this effect was due to bacteria, rather than fungi,” said First author Jing Yuan, a molecular biologist at the Capital Institute of Pediatrics, Beijing, China.
“Our observations suggest that [this] patient, although he had no history of alcohol use, showed a similar symptom as alcoholic fatty liver disease in clinic. The potential mechanism of this phenomenon is that some bacteria, named HiAlc Kpn carried in the gut of the patient, could induce the generation of endogenous alcohol, which could accelerate (NAFLD) development,” she said.
The bacteria Klebsiella pneumonia is known to produce high levels of alcohol in the gut. In this particular patient, however, the strains produced four to six times as much as those found in healthy individuals.
To confirm their findings, Yuan and her team sampled the gut microbiota of a Chinese cohort including 43 individuals with known NAFLD and 48 healthy people. They found that in 60 percent of NAFLD patients, a strain of high or medium alcohol-producing Klebsiella pneumonia, which they identify by the name HiAlc Kpn, was present.
HiAlc Kpn was present in only 6 percent of the healthy group.
Additionally researchers used a mouse model to test their hypothesis on the relationship between HiAlc Kpn and the development of NAFLD. They found that mice infected with the bacteria began to develop fatty liver within one month. Scarring of the liver, which indicates long-term liver damage, was present by the second month.
When the team administered an antibiotic to kill the bacteria, liver health began to improve.
As for humans: “We think that targeting these bacteria might provide some benefits for treatment of these patients,” said Yuan.
Others in the field say it is far too early to point the finger at a single bacteria, in this case HiAlc Kpn, as a major culprit of NAFLD.
“I say that this is a very interesting, early study on the gut microbiome but it certainly isn’t the end-all. The take that I would take from this is that there may be some pathways where the microbiome can lead to the development of fatty liver,” said Dr. David Bernstein, chief of hepatology at Northwell Health in Manhasset, New York.
Bernstein suggests that looking at the connection between the gut microbiome and the development of NAFLD (and, in fact many other diseases in the body) is promising but still nascent.
He maintains that NAFLD development is multifactorial, but that bacteria in the gut microbiome could very likely play a role:
“Does altering the gut’s flora change gut permeability? Change the absorption of all different types of substances and then do those substances get to the liver and influence fat deposition, inflammation, fibrosis?” he said.
“This is sort of the overall thought process as to why the gut microbiome might be involved but we have no clear cut mechanism. That’s why this study is interesting: because it offers a potential mechanism.”