Have you experienced that burning sensation on your tongue after eating a spicy pepper? This reaction is caused by capsaicin, a colorless and odorless compound present in chili peppers. Spiciness is measured using Scoville heat units (SHU), which are based on the concentration of capsaicin in the pepper. Jalapeños have a range of 3,500 — 10,000 Scoville units, habaneros have a range of 100,000 — 350,000 Scoville units, and the world’s hottest pepper, the Trinidad Moruga Scorpion, has a range of 2,000,000 — 2,200,000 Scoville units. However, they all pale in comparison to pure capsaicin, which scores around 16 million Scoville heat units.
Capsaicin, however, does more than just add heat to your favorite foods; it has also been found to negatively affect important immune cells. In 2014, researchers at the Asan Medical Center in Seoul, South Korea found that capsaicin inhibits natural killer (NK) cells, a type of cell that is important for the surveillance of cancer.1 NK cells use cytokine signaling molecules such as interferon-γ and tumor necrosis factor-α to target and lyse cancer cells.2 Capsaicin directly decreases the cytotoxicity of NK cells by reducing cytokine production. In fact, extended exposure to capsaicin can kill NK cells.1 NK cell malfunctions have been shown to lead to higher rates of tumor formation and cancer metastasis,3 and many patients suffering from cancer exhibit defects in the function of NK cells.4 Since capsaicin has negative effects on NK cells, capsaicin may also have deleterious effects on other immune cells that protect us from cancer and other ailments.
Several studies have suggested some correlation between tumor formation and capsaicin consumption. In one study, five groups of mice were fed different levels of capsaicin for 35 days, with one group being fed no capsaicin as a control. 10% of the mice that were fed varying levels of capsaicin developed adenocarcinomas of the duodenum (gastrointestinal tumors) while no control mice developed tumors.5 Another paper by López-Carrillo et al. studied the correlation between capsaicin intake through chili peppers consumption and gastric cancer incidences in Mexico.6 They found that people who consumed high levels of capsaicin, about 90 — 250 mg daily, were at a statistically higher risk for gastric cancer than those who had a lower consumption rate. 90 — 250 mg of capsaicin, however, corresponds to about 9 — 25 jalapeño peppers every single day, so most people are not at a higher risk.
Despite its apparent carcinogenicity, capsaicin may also have therapeutic capabilities in cancer treatment. Studies have shown that capsaicin is so potent that it can actually inhibit the growth of leukemia, hepatoma, glioblastoma, and colon cancer cells.7 In one study, gastric cancer cells treated with capsaicin at concentrations of 10, 50, and 200 μM actually underwent apoptosis, or programmed cell self-destruction, at a higher rate than normal epithelial cells under the same conditions. Capsaicin is able to induce apoptosis in cells by activating p53, a tumor suppressor gene commonly dubbed as “guardian of the genome.” This gene also functions to activate DNA repair genes, pause the cell replication cycle, and initiate apoptosis when certain triggers are activated. Capsaicin was found to activate one of these triggers, causing the p53 gene to begin apoptosis. These results suggest new possible methods of cancer treatment or prevention.8
Perhaps in the near future, capsaicin can be manipulated for beneficial medical applications. Capsaicin presents an interesting duality—it has promising effects for cancer treatment, yet it can lead to cancer itself. In designing treatments, researchers will have to maximize the benefits of capsaicin’s cancer-fighting abilities while mitigating the potential damage to the body’s healthy cells; this tradeoff is analogous to the one made in chemotherapy today. The correlation between capsaicin and cancer may still be quite concerning. However, with moderation, all of us can continue to enjoy the burn of Sriracha and hot wings without worrying about putting our lives in danger—at least for those who can handle the heat.
References
- Kim, H. S. et al. Carcinogenesis 2014, 35, 1652–1660.
- Long, E. O. et al. Annu. Rev. Immunol. 2013, 31, 227–258.
- Hann, N. et al. J. Immunol. 1981, 127, 1754–1758.
- Saito, H. et al. Gastric Cancer 2012, 15, 27–33.
- Toth, B.; Rogan E.; Walker, B. Anticancer Res. 1984, 4, 177–179.
- López-Carrillo, L. et al. Int. J. Cancer. 2003, 106, 277–282.
- Bode, A. M. et al. Cancer Res. 2011, 71, 2809–2814.
- Chow, J. et al. BBA 2007, 1773, 565-576.
