Navigating the maize between red meat and oncomirs.

High red meat consumption is associated with increased risk of colorectal cancer. Various mechanisms have been proposed, including mutagenesis, alterations of the gut microbiome, and effects on local immunity and inflammation. This lack of well-defined mechanistic explanations for diet and cancer associations coupled with our inability to derive causal inferences from population-based studies allows us to rationalize that burger we ate at lunch or that steak we ate at dinner. The preparation and consumption of red meat is a major social and dining pleasure in the Western culture, so there is resistance to concern ourselves with the cancer risk associated with red meat. In fact, advertisements do not add a rapid-fire statement that consumption of more than half a portion of red meat per day has been associated with increased risk of cardiovascular disease, diabetes, cancer, and even death, because these data are not from randomized controlled trials? Would we heed a warning if there was evidence that burgers and steaks induced the expression of small noncoding RNAs that inhibit the expression of tumor-suppressor genes in our enterocytes? What level of evidence is necessary to convince ourselves that a dietary exposure is sufficiently causal to put a warning label on it? How do we experimentally obtain such evidence? If we knew the mechanism, perhaps we could modify the risk sufficiently such that we can have our steak and eat it too-without the warnings.