Impact of dark chocolate and cocoa powder on heart disease - Cardiovascular Risk Factors - Brief Article

Nutrition Research Newsletter, Nov, 2001

A group of polyphenolic compounds, called flavonoids. occur commonly in fruits, vegetables, tea and red wine. Certain types of cocoa and chocolates are also rich sources of flavonoids, in particular the flavonoids of the subclass known as procyanidins. Previous reports have demonstrated that the catechin and procyanidin content of cocoa and chocolate was correlated with the antioxidant activity of these foods. Oxidative modification of low-density lipoproteins (LDL) has been shown to be crucial in the initiation of atherogenesis. Much research has shown that flavonoids prevent LDL oxidation in vitro through scavenging free radicals or sequestering metal ions. The ability of flavonoids to prevent LDL oxidation does depend on their bioavailability. There are also many conflicting observations in human studies regarding how flavonoids affect platelet function.

In light of the above suggestive evidence that cocoa powder and chocolates may favorably impact oxidation and platelet activity, a study was conducted to evaluate the effect of cocoa powder and dark chocolate rich in catechins and procyanidins on serum antioxidant capacity and risk factors for cardiovascular disease. Twenty-three healthy men and women with a mean age of 36 years participated as subjects. Before the main study took place, investigators carried out a pilot study to evaluate the bioavailability of flavonoids in cocoa powder and dark chocolate. For the long-term study, a ramdomized, two-period, crossover design was employed. The subjects were free living and fed two well-controlled experimental diets. One diet was an average American diet (AAD) that served as the control diet. The experimental diet contained 22 grams of cocoa powder and 16 grams of dark chocolate (CP-DC diet) per day. Subjects consumed each diet for a four-week period, followed by a brief break and then were crossed over to the other diet. Both diets provided similar amounts of total fat (33-34 percent of energy), saturated fatty-acids (15-16 percent of energy). monounsaturated fatty acids (11 percent of energy), polyunsaturated fatty acids (7 percent of energy), cholesterol (330 mg/day), and dietary fiber (18 grams/day). In the CP-DC diet, approximately 75 percent of the flavonoids came from cocoa powder and 25 percent came from dark chocolate. The AAD was poor in procyanidins, which are the predominant flavonoids in chocolate. The cocoa powder and dark chocolate were incorporated in to the CP-DC diet in different ways. including mixing in milk or pudding snacks or baked into cookies or brownies. To control for the contents of caffeine and theobromine provided by the cocoa powder and dark chocolate in the experimental diet, diet cola and a theobromine supplement were added to the AAD. Serum lipids and lipoproteins were analyzed at baseline and following the completion of each diet. LDL oxidation was also determined following each diet period.

The data revealed LDL oxidation lag time was ~8 percent greater (P = 0.01) after the CP-DC diet than after the AAD. Serum total antioxidant capacity measured by oxygen radical absorbance capacity was ~4 percent greater (P = 0.04) following the CP-DC diet than following the AAD and was positively correlated with LDL oxidation lag time (r = 0.32. P = 0.03). After the CP-DC diet, HDL cholesterol was 4 percent higher than after the AAD. Twenty-four hour urinary excretion of thromoxane [B.sub.2] and 6-keto-prostaglandin [F.sub.1]< as well as the ratio of the two compounds were not significantly different between the two diets.

These results appear to indicate a beneficial effect of both cocoa powder and dark chocolate on LDL oxidation and HDL cholesterol concentrations with no adverse effect on prostaglandins.

Y. Wan, J. Vinson, T. Etherton, et al. Effects of cocoa powder and dark chocolate on LDL oxidative susceptibility and prostaglandin concentrations in humans. American Journal of Clinical Nutrition 74:596-602 (November. 2001) [Correspondence: P. M. Dris-Etherton, S-16 Henderson Building, Nutrition Department, University Park, PA 16802. E-mail: PMK3@psu.edu.]