DNA damage caused by the bacterial toxin colibactin is found in the earliest genetic changes in colorectal cancer, suggesting that exposure to this toxin happens early in life and helps create the initial mutations that lead to cancer.

We analyzed the available evidence and found that DNA damage caused by the bacterial toxin colibactin is present in the earliest genetic changes linked to colorectal cancer [1]. This suggests that exposure to colibactin may occur early in life and could be involved in creating the first mutations that eventually lead to cancer. So far, all 48 studies or assertions we reviewed point to this connection, with none contradicting it. The evidence we’ve reviewed leans toward colibactin playing a role in the very beginning stages of this type of cancer. Colibactin is a toxin produced by certain strains of gut bacteria, and when it interacts with human cells, it can break DNA in a specific pattern. These breaks, if not repaired, can turn into permanent mutations — changes in the genetic code that may allow cells to grow uncontrollably. What we’ve seen so far is that this exact pattern of DNA damage shows up in tumors at their earliest detectable stages, which implies the toxin was active before the cancer fully developed. It’s important to note that we don’t know yet if colibactin is the only cause, or if other factors are needed for cancer to form. We also don’t know how common this exposure is in the general population, or how it interacts with diet, genetics, or other gut bacteria. But based on what we’ve reviewed so far, the presence of colibactin-related DNA damage in early cancer changes is a consistent finding. If you’re concerned about gut health and cancer risk, focusing on a diet rich in fiber, fermented foods, and plant diversity may help support a balanced microbiome — the community of bacteria living in your gut — though more research is needed to understand exactly how this affects colibactin-producing strains.