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Is chilli good for the colon?

In another context, chili peppers are beneficial. Capsaicin also has an anticancer effect. Besides, ingestion of chili peppers can promote digestive juice to secrete and accelerate bowel movements [21], which may reduce the risk of CRC.

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Capsaicin concentration is related to the variety and maturity of chili peppers and its concentration can change. E-capsaicin is the major capsaicin in chili peppers. A study shows a greater than 25-fold variation in E-capsaicin levels among individual peppers, ranging from about 0.04 μg/mL to 1 μg/mL [15]. In general, the concentration of capsaicin ranges from 0.1 to 1% in chili peppers. The results of some studies suggested that intake of capsaicin may predispose to one or more forms of gastrointestinal cancer. Dietary administration of capsaicin produced duodenal tumors in Swiss albino mice [16]. An epidemiological study conducted in Mexico observed that consumers of chili peppers were at higher risk for gastric cancer than non-consumers [17]. In addition, excessive consumption of chili peppers may irritate colonic mucosa. Ingestion of large amounts of capsaicin has been reported to cause histopathological and biochemical changes, including erosion of gastric mucosa and hepatic necrosis [18]. However, the results of other studies suggested that intake of capsaicin might reduce cancer risk. Studies in the laboratory had observed capsaicin to interfere with the action of some chemical carcinogens, such as aflatoxin B 1 and the tobacco-specific nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone [19], and also to inhibit the proliferation of CRC cells and induce apoptosis and necrosis of cancer cells. Initial work by Hoch-Ligeti showed that rats fed diets containing 10% chili pepper developed liver tumors [20]. The validity of this study, however, was questioned because of possible contamination of the experimental diet with the potent hepatocarcinogen aflatoxin B 1 . Results of Surh and Lee’s preliminary study indicated that repeated application of capsaicin on the shaved backs of female ICR mice following an initial dose of 7,12-dimethylbenz[a]anthracene led to no significant enhancement of papilloma formation in the skin, compared with the control animals that received the carcinogen alone. Summarizing the relevant studies, Surh and Lee suggested that although a minute amount of capsaicin displays few or no deleterious effects, heavy ingestion of the compound has been associated with necrosis, ulceration, and even carcinogenesis [18]. According to previous studies, capsaicin has both carcinogenic and anticancer effects. In our study, we did not observe a significant difference in chili peppers: compared to persons consuming chili peppers no more than twice each week, the relative risk in those whose weekly intake was 3–7 times and > 7 times was 1.2 (95% CI 0.75–2.0) and 1.4 (95% CI 0.84–2.2), respectively. In fact, the relationship between chili peppers and CRC was indeed complex. The chili pepper is a spicy food, and excess consumption may damage to colonic mucosa. The long-term damage is related to the occurrence of CRC. In addition, capsaicin may play the weak carcinogenesis role in causing CRC. In another context, chili peppers are beneficial. Capsaicin also has an anticancer effect. Besides, ingestion of chili peppers can promote digestive juice to secrete and accelerate bowel movements [21], which may reduce the risk of CRC. Generally, there was little difference in the size of the OR associated with consumption of chili peppers across different subgroups, though we did observe an increased risk associated with weekly consumption of chili peppers 3–7 times (OR = 1.2 95% CI 0.78–2.0) and > 7 times (OR = 1.6 95% CI 1.1–2.5) among persons with a relatively low consumption of cured meat. With our existing knowledge, we considered it suggested a link or an interaction between chili pepper and cured meat. Lots of capsaicin may weakly suppress the chemical carcinogens, such as PAH found in cured meat. It needs further study to elucidate the mechanism associated with this observation.

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Interpretation of the results must take into account some limitations of our study. First, family members responding to proxy respondents about diet habits over the past 10 years is a limitation. And the study collected dietary information only for the past 10 years, which may be less relevant to risk than intake earlier in life. Second, even for intake during the past 10 years, there can be non-differential misclassification of exposure status when interviews are used to obtain the information on frequency of intake. Third, the study measured only the times of chili peppers intake, not the quantity consumed. Finally, the referent category used in our analysis included some persons who did consume chili peppers, just at a lower frequency than 3 times per week. However, an analysis in which the referent category has no chili pepper intake could not be done, due to the fact that among the study participants, there was virtually no one who did not consume chili peppers.

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