Purpose of review: Colorectal cancer (CRC) is the third most common cancer and the second most common cause of cancer-related deaths. Of the various established risk factors for this aggressive condition, diet is a notable modifiable risk factor. This review aims to summarize the mounting evidence to suggest the role of diet, the microbiota and their cross-talk in modulating an individual's risk of developing CRC.
Recent findings: Specifically, the metabolism of bile acids and its symbiosis with the microbiota has gained weight given its basis on a high meat, high fat, and low fibre diet that is present in populations with the highest risk of CRC. Bacteria modify bile acids that escape enterohepatic circulation to increase the diversity of the human bile acid pool. The production of microbial bile acids contributes to this as well. Epidemiological studies have shown that changing the diet results in different levels and composition of bile acids, which has in turn modified the risk of CRC at a population level. Evidence to identify underlying mechanisms have tied into the microbiota-led digestions of various foods into fatty acids that feedback into bile acid physiology as well as modulation of endogenous receptors for bile acids.
Summary: There is adequate evidence to support the role of microbiota in in the metabolism of bile acids, and how this relates to colorectal cancer. Further work is necessary to identify specific bacteriome involved and their underlying mechanistic pathways.
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