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Studies Find Fungi (Molds) Can Worsen Alcoholic Liver Disease (ALD)

Mar 10, 2026 | Mold Symptoms | 0 comments

A 2017 study by the National Institute on Alcohol Abuse and Alcoholism (NIAAA) had shown that intestinal fungi (molds) such as a Candida may contribute to the development of alcoholic liver disease (ALD or Alcoholic fatty liver disease, Alcoholic hepatitis). A disease that is the 12th leading cause of death in the U.S. and accounts for approximately half of all liver disease deaths.

ALD is characterized by fat deposition in liver cells, inflammation and mild scarring of the liver which is end-stage liver disease, or cirrhosis (liver cell death). ALD has previously been associated with bacterial overgrowth in the intestines, but until thi sstudy, little was known about the role of intestinal fungi in ALD.

“Not only is this the first study to associate fungi and liver disease,” said senior author Bernd Schnabl, MD, associate professor of gastroenterology at UC San Diego School of Medicine, “we might be able to slow the progression of alcoholic liver disease by manipulating the balance of fungal species living in a patient’s intestine.”

The researchers also conducted small preliminary studies with humans to examine intestinal fungi of people with alcohol use disorder and various stages of liver disease.

They observed an overgrowth of a specific fungal species compared to healthy control subjects, as well as less fungal diversity in individuals with alcohol use disorder and ALD.  They also found that the more prevalent the fungal overgrowth in individuals with ALD, the higher the likelihood of mortality.

“This work demonstrates that alcoholic liver disease is exacerbated not only by bacteria, but also by fungi. Therefore, therapeutic strategies that target both need to be translated into clinical practice,” said co-author Derrick Fouts, PhD, professor of genomic medicine at JCVI. “This study suggests a greater role of fungi in modulating the human microbiome than previously appreciated.”

Since that original report, follow‑up studies have confirmed that this “mycobiome” component of the gut–liver axis is not a one‑off finding but a consistent pattern in alcohol‑related liver disease.

Patients with alcohol‑associated liver disease tend to show intestinal fungal dysbiosis—loss of normal fungal diversity with a marked overgrowth of Candida species—as well as heightened immune responses to fungal antigens, indicating that fungal products are crossing the damaged gut barrier and reaching the liver.

These patients often have elevated antibodies against fungal components, and higher antifungal antibody levels have been linked to more advanced liver damage and worse outcomes, which dovetails with the early mortality signal seen in the 2017 work.

One of the most striking newer discoveries is the identification of candidalysin, a pore‑forming toxin produced by certain strains of Candida albicans, as a direct driver of alcohol‑induced liver damage.

A 2019–2020 study found that candidalysin‑producing C. albicans strains were far more common in patients with alcoholic hepatitis than in healthy individuals and people with alcohol use disorder without severe liver disease, and that candidalysin itself could directly injure liver cells in lab experiments and worsen ethanol‑induced liver disease in mice.

In that study, patients carrying candidalysin‑positive C. albicans had higher MELD scores, more severe hepatic inflammation, and higher short‑term mortality, reinforcing the concept that not just the presence of fungi, but the specific fungal toxins they produce, may influence how quickly ALD progresses.

More recent reviews of the gut mycobiome and liver diseases now conclude that fungi are a missing but critical piece of the gut–liver puzzle in alcohol use disorder, sitting alongside bacteria and viruses as key modulators of inflammation, barrier function, and immune activation.

These papers highlight that alcohol‑related changes in the mycobiome—such as expansion of Candida, shifts in other commensal fungi, and increased translocation of fungal cell‑wall components and toxins—can promote fat accumulation in the liver, amplify inflammatory pathways, and accelerate scarring and cirrhosis.

As a result, there is growing interest in therapies aimed at restoring a healthier fungal balance in the gut, including non‑absorbable antifungals, diet and lifestyle interventions, and future microbiome‑based approaches that could complement alcohol cessation, nutritional support, and standard medical treatment for alcoholic liver disease.

Study links

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