• Capsaicin and Gut Tumors

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    Capsaicin and Gut TumorsChili peppers have been known as a fiery spice. It has been used in cooking to add heat and additional dimension of flavor to dishes. But aside from these, chili peppers have been believed to have beneficial effects on health – if you have tumor cells in the gut.

    Nutrition wise, chili peppers contain vitamins A and C and have fiber as well.

    The heat produced by the pepper is because of the phytochemicals called capsaicinoids. Capsaicin is the chief that is responsible for the pepper's health benefits particularly in cancer.

    Researchers at the University of California, San Diego School of Medicine report that dietary capsaicin – the active ingredient in chili peppers – produces chronic activation of a receptor on cells lining the intestines of mice, triggering a reaction that ultimately reduces the risk of colorectal tumors.

    The findings are published in the August 1, 2014 issue of The Journal of Clinical Investigation.

    The receptor or ion channel, called TRPV1, was originally discovered in sensory neurons, where it acts as a sentinel for heat, acidity and spicy chemicals in the environment. “These are all potentially harmful stimuli to cells,” said Eyal Raz, MD, professor of Medicine and senior author of the study. “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.”

    But Raz and associates discovered that TPRV1 is extracted by epithelial cells of the intestines and is then activated by epidermal growth factor receptor or EGFR. EGFR is a central driver of cell spread in the intestines, whose epithelial lining is substituted roughly every four to six days.

    “A basic level of EGFR activity is required to maintain the normal cell turnover in the gut,” said Petrus de Jong, MD, first author of the study. “However, if EGFR signaling is left unrestrained, the risk of sporadic tumor development increases.”

    The scientists found out that TRPV1, once actuated by the EGFR, commences a direct negative response on the EGFR, stifling the latter to decrease the risk of undesirable growth and intestinal tumor growth.

    They found that mice genetically modified to be TRPV1-deficient suffered higher-than-normal rates of intestinal tumor growths.

    “These results showed us that epithelial TRPV1 normally works as a tumor suppressor in the intestines,” said de Jong. In addition, molecular studies of human colorectal cancer samples recently uncovered multiple mutations in the TRPV1 gene, though Raz noted that currently there is no direct evidence that TRPV1 deficiency is a risk factor for colorectal cancer in humans.

    “A direct association between TRPV1 function and human colorectal cancer should be addressed in future clinical studies,” he said.

    If that would be the conclusion, the latest study proposes one potential remedy might be spicy capsaicin, which acts as a nuisance in mammals, causing a burning feeling in contact with tissue.

    Capsaicin is now widely used as a pain killer in topical creams where its characteristics as an irritant rout nerves, making them incapable to register pain for long periods of time. It's also the main component in pepper spray.

    The researchers fed capsaicin to mice genetically prone to developing multiple tumors in the gastrointestinal tract. The treatment resulted in a reduced tumor burden and extended the lifespans of the mice by more than 30 percent. The treatment was even more effective when combined with celecoxib, a COX-2 non-steroidal anti-inflammatory drug already approved for treating some forms of arthritis and pain.

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

    Though more research still has to be done, testimonies have been done in the lab to prove the powers of spicy chilies to be powerful against tumors in the gastrointestinal tract.

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