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Cayenne pepper, which is also known as African pepper or capsicum fruit has a high concentration of a substance called capsaicin which has demonstrated an ability to help kill cancer cells, including prostate cancer cells.
In a laboratory study published in 2007, for example, scientists found that capsaicin slowed growth of prostate cancer cells and encouraged them to “commit suicide” (apoptosis). (Sanchez 2007) In a more recent study, Italian researchers reported that capsaicin can induce apoptosis in prostate cancer cells. (Ziglioli 2009) A study performed at the University of California, Los Angeles, showed capsaicin to have what the researchers called a “profound antiproliferative effect on prostate cancer cells,” inducing cell suicide and leading them to note that capsaicin “may have a role in the management of prostate cancer.” (Mori 2006)
Researchers who conducted a study at Nottingham University and published it in 2007 reported that they found how and why capsaicin kills cancer cells: it attacks the mitochondria, the energy-generating portion of cells. The family of molecules to which capsaicin belongs, called the vanilloids, attach to proteins in the cancer cell mitochondria and trigger apoptosis without harming the surrounding healthy cells. (Athanasiou 2007)
Although cayenne supplements are available, they should be used with caution because they have the potential to cause stomach distress.
References
Athanasiou A et al. Vanilloid receptor agonists and antagonists are mitochondrial inhibitors: how vanilloids cause non-vanilloid receptor mediated cell death. Biochem Biophys Res Commun 2007 Mar 2; 354(1): 50-55.
Mori A et al. Capsaicin, a component of red peppers, inhibits the growth of androgen-independent, p53 mutant prostate cancer cells. Cancer Res 2006 Mar 15; 66(6): 3222-29.
Sanchez AM et al. Apoptosis induced by capsaicin in prostate PC-3 cells involves ceramide accumulation, neutral sphingomyelinase, and JNK activation. Apoptosis 2007; 12(11): 2013-24.
Ziglioli F et al. Vanilloid-mediated apoptosis in prostate cancer cells through a TRPV-1 dependent and a TRPV-1-independent mechanism. Acta Biomed 2009 Apr; 80(1): 13-20
