A new study that investigated the influence of gut bacteria on cancer development has come to more than one surprising conclusion. The project’s main finding was that antioxidant-rich foods (chocolate, black tea, berries, nuts) may provide the perfect bacterial environment in the colon for cancer development. To understand how the research team came to that conclusion, however, we’ll have to start from the beginning.
First off, researchers from The Hebrew University of Jerusalem have discovered that mutated cells actually work to defend against cancer in certain areas of the body. Yes, you read that last sentence correctly.
What makes certain mutated cells cancer-friendly and others anti-cancer? The number of local gut bacteria nearby. When it comes to gastrointestinal cancers, colon (large intestine) cancer is much more common than small intestine cancer. This fact in and of itself has always puzzled doctors and scientists alike; why is cancer seen much more frequently in the colon? Now, researchers have an explanation.
The colon contains tons of gut bacteria, whereas the small intestine houses a much smaller bacterial community. Via a complex cellular experiment, the team at HUJ successfully showed that it is indeed the high levels of bacteria in the colon that promote cancer growth.
But, this observation led to the next logical question; why does the gut microbiome often encourage cancer development? Further experiments led the research team to their next breakthrough. If an individual eats lots of antioxidant-rich foods their gut bacteria will produce more antioxidant metabolites. These metabolites appear to be the difference-maker when it comes to determining if a mutated cancer cell will be helpful or hurtful.
That was a bit of a long and winding scientific road, but in short, the research team has discovered a legitimate possible link between antioxidant-rich foods and higher colorectal cancer risk.
“Scientifically speaking, this is new territory. We were astonished to see the extent to which microbiomes affect cancer mutations–in some cases, entirely changing their nature,” explains Professor Yinon Ben-Neriah, on the study’s main authors, in a release.
“Scientists are beginning to pay more and more attention to the role gut microbiomes play in our health: both their positive effects and, in this case, their sometimes pernicious role in aiding and abetting disease,” he adds.
At the center of this study was the common gene known as TP53. This gene is found in every cell in your body. Normally, TP53 produces a protein called p53 that acts as a protective barrier against genetic mutations for the cell. When it’s functioning normally TP53 is a cancer-protective gene. However, in the event a TP53 gene becomes damaged, it can start to encourage cancer growth.
So, the research team decided to use TP53 to test their hypothesis that gut bacteria impacts cancer development. A series of mutated p53 proteins were introduced into the guts of a group of lab mice. Within the rodents’ small intestines, the mutated proteins were actually quite helpful, and acted as cancer “super-suppressors.” Inside the rodents’ colons, though, the mutated cells promoted cancer and tumor growth.
“We were riveted by what we saw,” Ben-Neriah comments. “The gut bacteria had a Jekyll and Hyde effect on the mutated p53 proteins. In the small bowel they totally switched course and attacked the cancerous cells, whereas in the colon they promoted the cancerous growth.”
To confirm that it was indeed the gut bacteria that influenced the mutated proteins in this way, the researchers then gave the mice some antibiotics that effectively killed all the bacteria in their colons. Sure enough, after the bacteria had been neutralized the p53 proteins no longer fostered cancer growth.
Finally, a closer examination of the microbiomes within each rodent’s colon (before the antibiotics) revealed their bacterial communities were producing high levels of antioxidant metabolites. Moreover, when the mice were fed a diet high in antioxidants, their gut bacteria produced more metabolites and the mutated p53 proteins “accelerated” their pro-cancer behaviors.
For as noteworthy and potentially groundbreaking as these findings are, they are also preliminary. More research is warranted on this topic before any conclusive statements can be made. That being said, the study’s authors say people with a family history of colorectal cancer may want to start re-examining their diets.
The full study can be found here, published in Nature.