On May 26, 2009, Robert Lustig gave a lecture called “Sugar: The Bitter Truth,” which was posted on YouTube the following July. Since then, it has been viewed well over 800,000 times, gaining new viewers at a rate of about 50,000 per month, fairly remarkable numbers for a 90-minute discussion of the nuances of fructose biochemistry and human physiology.
Lustig is a specialist on pediatric hormone disorders and the leading expert in childhood obesity at the University of California, San Francisco, School of Medicine, which is one of the best medical schools in the country. He published his first paper on childhood obesity a dozen years ago, and he has been treating patients and doing research on the disorder ever since.
The viral success of his lecture, though, has little to do with Lustig’s impressive credentials and far more with the persuasive case he makes that sugar is a “toxin” or a “poison,” terms he uses together 13 times through the course of the lecture, in addition to the five references to sugar as merely “evil.” And by “sugar,” Lustig means not only the white granulated stuff that we put in coffee and sprinkle on cereal — technically known as sucrose — but also high-fructose corn syrup, which has already become without Lustig’s help what he calls “the most demonized additive known to man.”
It doesn’t hurt Lustig’s cause that he is a compelling public speaker.
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.
Flavokawain B, a kava chalcone, induces apoptosis via up-regulation of death-receptor 5 and Bim expression in androgen receptor negative, hormonal refractory prostate cancer cell lines and reduces tumor growth
Limited success has been achieved in extending the survival of patients with metastatic and hormone-refractory prostate cancer (HRPC). There is a strong need for novel agents in the treatment and prevention of HRPC. We have shown that flavokawain B (FKB), a kava chalcone, is about 4- to 12-fold more effective in reducing the cell viabilities of androgen receptor (AR)-negative, HRPC cell lines DU145 and PC-3 than AR-positive, hormone-sensitive prostate cancer cell lines LAPC4 and LNCaP, with minimal effect on normal prostatic epithelial and stromal cells. FKB induces apoptosis with an associated increased expression of proapoptotic proteins: death receptor-5, Bim and Puma and a decreased expression of inhibitors of apoptosis protein: XIAP and survivin. Among them, Bim expression was significantly induced by FKB as early as 4 hr of the treatment. Knockdown of Bim expression by short-hairpin RNAs attenuates the inhibitory effect on anchorage-dependent and – independent growth and caspase cleavages induced by FKB.