Stanford Researchers Identify 140+ Common Medications That Disrupt Gut Microbiome and Trigger Cancer-Linked Inflammation
Researchers at Stanford University have identified more than 140 widely used medications capable of reshaping the gut microbiome and causing bacterial imbalances tied to cancer-promoting inflammation. The study highlights how drugs alter the availability of nutrients in the intestine, forcing microbial populations to compete in ways that can permanently shift gut health.
Stanford scientists identify over 140 medications that disrupt the gut microbiome, reshape nutrient competition, and increase inflammation linked to cancer.
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Scientists analyzed how common medications affect diverse gut microbes that influence metabolism, immune activity and overall health. Their findings show that certain drugs eliminate key bacterial strains and change the nutrient landscape, creating conditions where drug-resistant species dominate.
A total of 51 antibiotics, several chemotherapy drugs, antifungal treatments and antipsychotic medications used for schizophrenia and bipolar disorder had the strongest impact on gut communities. These drugs were shown to kill weaker bacterial species, leaving behind sugars, amino acids and molecules that more harmful bacteria rapidly consume.
The new environment allows inflammatory species to grow rapidly, reshaping the microbiome into a state linked to colorectal cancer risk. Surviving microbes alter the balance of the gut ecosystem that typically supports immune defenses and protects against viral threats.
Lead researcher Dr. Handuo Shi explained that drug exposure not only eliminates microbes but also reorganizes the nutrient “buffet,” determining which bacteria are able to persist. Dr. KC Huang added that understanding competition for food sheds light on the collateral damage caused by medications and helps predict which bacteria survive.
The team used a human fecal sample to colonize mice, then recreated a stable microbial community in laboratory conditions. They exposed these communities to 707 medications, one per experiment, and measured survival rates, nutrient shifts and overall bacterial growth.
One example involved two beneficial bacterial species that rely on an iron-containing molecule known as heme. These bacteria survived exposure to the antifungal drug bifonazole when provided heme directly in a test tube. Inside the gut, however, they depend on other bacteria to supply this compound. The drug killed those heme-producing bacteria, cutting off the nutrient source and rendering the beneficial species vulnerable, enabling harmful strains to consume the remaining nutrients.
A total of 141 medications eliminated entire bacterial communities, and many failed to recover even after the drugs were withdrawn. The resulting dysbiosis created chronic inflammation capable of damaging colon cell DNA and contributing to the development of colorectal cancer.
The imbalance also weakened the mucosal barrier that lines the intestines, allowing harmful substances to enter intestinal tissue and intensify inflammation. Certain bacteria, including strains of E. coli, were found to produce colibactin, a compound known to damage colon cell DNA and contribute to cancer formation.
US doctors have reported rising numbers of drug-resistant infections, often called superbugs, driven by bacteria that no longer respond to standard antibiotic treatments. These infections require stronger medications, which may further disrupt the microbiome.
Recent American Cancer Society data shows a rapid increase in colorectal cancer among adults under 55. Cases among individuals aged 45 to 49 jumped from a one percent annual rise before 2019 to 12 percent annually through 2022. A separate analysis showed cases among adults aged 20 to 29 increasing by an average of 2.4 percent each year, positioning colorectal cancer to become the most common cancer among people under 50 by 2030.
The Stanford team’s findings provide researchers with a tool to assess how specific drugs reshape gut bacteria and offer a potential path toward strategies that protect or restore the microbiome during medical treatment. Shi noted that shifting the view of medications from targeting a single microbe to affecting an entire ecosystem may lead to future approaches that combine treatments with diets or probiotics designed to support microbiome health.
The study was published in Cell.
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