Search Here

Adding pepper to meals could significantly decrease the risk of colorectal tumors, according to a new study.

Researchers found that the dietary capsaicin, the active ingredient in chili peppers, reduces the risk of colorectal cancer by triggering chronic activation of a receptor or in ion channel called TRPV1, which are abundant in cells lining the intestines of mice. Previous studies reveal that TRPV1, which were originally discovered as sensory neurons acts as a guard against heat, acidity and spicy chemicals in the environment.

"These are all potentially harmful stimuli to cells," Eyal Raz, MD, professor of Medicine and senior author of the study, said in a news release. "Thus, TRPV1 was quickly described as a molecular 'pain receptor.' This can be considered to be its conventional function, which all takes place in the nervous system."

New research also reveals that TPRV1 can also be found in intestinal epithelial cells.  TPRV1 is activated by epidermal growth factor receptor or EGFR, an important driver of cell proliferation in the intestines, in the gut.

"A basic level of EGFR activity is required to maintain the normal cell turnover in the gut," first author Petrus de Jong, MD, of the University of California, San Diego School of Medicine, said in a news release. "However, if EGFR signaling is left unrestrained, the risk of sporadic tumor development increases."

Researchers explain that the interaction between TRPV1 and EGFR lowers the risk of unwanted growth and intestinal tumor development.

The latest study revealed that mice genetically modified to be TRPV1-deficient suffered significantly higher rates of intestinal tumor growths.

"These results showed us that epithelial TRPV1 normally works as a tumor suppressor in the intestines," added de Jong.

Colorectal cancer-prone mice fed capsaicin also experienced a 30 percent longer lifespan than those not given the pepper ingredient.

"Our data suggest that individuals at high risk of developing recurrent intestinal tumors may benefit from chronic TRPV1 activation," Raz concluded. "We have provided proof-of-principle."

The findings are published in The Journal of Clinical Investigation.