A new study published in the journal Gut points to deoxycholic acid (DCA), a substance produced when particular gut bacteria chemically transform bile acids made by the liver, as promoting tumor growth:
An international research team led by German institutions combined experiments in genetically modified pigs, mice, and lab-grown human colon tissue with an analysis of microbial data from thousands of people with and without colorectal cancer.
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Most bile acids are later reabsorbed and returned to the liver, but a small proportion reaches the colon. There, bacteria capable of a process called 7-alpha-dehydroxylation can convert primary bile acids into secondary ones, including DCA.
Higher concentrations of DCA and the bacteria that produce it have previously been observed in people with colorectal cancer.
A 2024 study published in Immunity also found that DCA weakened the activity of immune cells that help attack tumors and promoted colorectal tumor growth in mice.
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To investigate this more directly, the researchers first examined genetically modified pigs predisposed to developing polyps in the colon.
When the pigs were fed a Western-style diet, intestinal tumor development worsened. This was accompanied by higher DCA levels in their feces and increased proliferation of the epithelial cells lining the colon.
The researchers then treated some pigs with cholestyramine, a drug that binds bile acids in the digestive tract so they can be removed from the body.
With those bile acids removed, there was less excessive cell proliferation in the colon, strengthening the suspected connection between bile acids and tumor development.
The team next turned to germ-free mice, whose intestinal microbial communities could be precisely controlled.
Adding DCA-producing bacteria, including Clostridium scindens and Extibacter muris, to defined communities of gut microbes led to DCA production and increased the number of colon tumors in two different mouse models of colorectal cancer.
In another experiment, the researchers genetically modified the bacterium Faecalicatena contorta so it could no longer perform the reaction required to produce DCA.
Mice colonized with the genetically altered bacteria developed fewer colon tumors than those carrying the unmodified, DCA-producing strain.
The modified bacteria also caused less epithelial cell proliferation in human colon organoids – miniature, simplified versions of colon tissue grown in the laboratory.
To examine whether the same bacterial machinery was associated with colorectal cancer in people, the researchers analyzed microbial DNA from stool samples collected across several human cohorts. These data comprised 1,034 individuals with colorectal cancer and 1,108 without.
Genes involved in DCA production, particularly those associated with C. scindens and closely related bacteria, were found more frequently in people with colorectal cancer than in those without the disease.
Together, the findings support a possible chain of events: A high-fat Western diet alters bile acid metabolism by promoting certain gut bacteria that convert primary bile acids into DCA, and DCA stimulates abnormal cell proliferation, creating conditions that may support tumor growth.
A “Western diet” in this context may or may not be what Americans actually eat:
High fat, especially saturated fats (e.g., from anhydrous milk fat/butter, hydrogenated palm oil, or lard), often providing ~20–38% of energy from fat (or higher in some high-fat variants).
High refined carbohydrates/sugars, such as sucrose, fructose, white flour, or other simple carbs (replacing complex carbs/starch), contributing a large share of energy (e.g., ~47% from carbs in isocaloric designs).
Elevated cholesterol (e.g., 0.5–1.5% or added purified cholesterol).
Low fiber compared to healthier patterns (e.g., ~7 g/100 g diet vs. higher in whole-grain diets).
Protein at moderate levels (often ~13–15% of energy), plus vitamins/minerals to meet needs.
Overall higher energy density than control/standard diets; feeding may be isocaloric (matched calories) or ad libitum/excess to promote weight gain.