Summary: Cocoa was originally cultivated by ancient societies in Central and South America, where it was consumed as a fermented beverage for medicinal and ceremonial purposes. Cocoa and chocolate, its fermented byproduct, are rich in flavanols—potent antioxidants associated with a reduced risk of cardiovascular disease and cancer. Two types of flavanols, called catechins and procyanidins, have been shown in experimental studies to reduce markers of inflammation and angiogenesis, two processes closely linked to cancer development. While more study is required, cocoa and chocolate have significant potential for chemoprevention as a dietary supplement.
Cocoa, the seed of the cocoa tree, is believed to have been cultivated over 3,000 years ago by native inhabitants of Central and Northern South America. These inhabitants prepared cocoa as a fermented beverage, similar to tea, which was used for medicinal and ceremonial purposes, and the beans themselves were used as a form of currency. Spanish explorers brought cocoa back to Spain in the early 1500s, and from there it spread to France, Italy, and eventually to Great Britain. In the middle of the 18th Century, chocolate manufacturing was introduced to Massachusetts using cocoa imported from the West Indies and Central America. Commercial chocolate become available in the mid-19th Century when a London company added sugar to chocolate liquor and cocoa butter.
Chocolate, the fermented byproduct from processed cocoa, contains high levels of bioactive flavanoids (polyphenols) that are formed during the fermentation process. Two flavanoids in particular, catechins and procyanidins, are highly concentrated in dark chocolate and cocoa powder. Observational studies indicate that catechins and procyanidins derived from green tea, red wine and soy may protect against a number of chronic diseases, notably cardiovascular disease and cancer.
The cancer-protecting (chemoprotective) activity of catechins and procyanidins is likely related to their ability to inhibit proliferation of cancer cells, remove toxins from the body, reduce inflammation, and suppress angiogenesis.
Angiogenesis, the process by which tumors acquire a blood supply, is a critical process in cancer development. Chronic inflammation is a known risk factor for both cardiovascular disease and many types of cancer. Inflammatory cells create an attractive environment for tumor growth, facilitate cell proliferation and angiogenesis, and promote genetic instability in cancer cells. Markers of inflammation, such as interleukin-2, C-reactive protein, and tumor necrosis factor-µ, have been associated with cancer risk in prospective studies.
Flavanols contained in green tea, soy and other foods have been shown to reduce markers of inflammation and suppress cancer cell proliferation in a number of experimental studies. Catechins and procyanidins inhibit the activation of NFkB, a key regulator of inflammation and the immune response. Relatively few studies have specifically looked at the influence of cocoa on markers of inflammation. However, since dark chocolate and cocoa contain very high concentrations of procyanidins—higher than most other foods—it is quite possible that chocolate may suppress inflammation to an extent equal to or greater than that of other foods. Cocoa has one of the highest concentrations of flavanoids of any food—over 10% of the total weight of cocoa powder.
Prospective studies using cocao as a nutritional supplement will help to better define the anti-inflammatory and chemopreventive potencies of cocoa powder and chocolate. The epidemiological evidence for chocolate is also less extensive than for green tea and other foods. Among two case-control studies that specifically looked at chocolate intake in relation to cancer risk, one found no association between chocolate consumption and colon cancer risk, while the other found a lower prevalence of pre-cancerous colon polyps with higher chocolate intake. Nonetheless, cocoa and chocolate, with its high flavanol content, have substantial potential for chemoprevention and should be studied further in well-designed trials using defined dietary amounts with valid markers of inflammation.
Originally posted on February 21, 2011 by eattodefeat by Roderick Smith, M.S.
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