title: Chocolate is a powerful ex vivo and in vivo antioxidant, an antiatherosclerotic agent in an animal model, and a significant contributor to antioxidants in the European and American Diets.
abstract: Chocolate today is often viewed as a food or snack with little nutritional value. The high saturated fat content of chocolate has also contributed to the belief that its consumption increases the risk of heart disease. However, recent human studies have proven that chocolate has beneficial effects on some pathogenic mechanisms of heart disease such as endothelial function and blood pressure. Although the antioxidant properties of chocolate have been known for some time, there has been no examination of its place in the U.S. diet as a source of antioxidants. This paper demonstrates that chocolate makes a significant contribution to U.S. per capita dietary antioxidants and by inference the European Community's. In the U.S. diet chocolate is the third highest daily per capita antioxidant source. An ex vivo study shows that epicatechin, a major polyphenol in chocolate and chocolate extracts, is a powerful inhibitor of plasma lipid oxidation due to polyphenols' ability to bind to lower density lipoproteins. Conversely, the fat from chocolate alone is a pro-oxidant in this model. This is also demonstrated in an in vivo human study. After consumption of dark chocolate and cocoa powder, the lower density lipoproteins isolated from plasma were protected from oxidation compared to the lipoproteins isolated after cocoa butter consumption, which were put under oxidative stress. In an animal model of atherosclerosis, cocoa powder at a human dose equivalent of two dark chocolate bars per day significantly inhibited atherosclerosis, lowered cholesterol, low-density lipoprotein, and triglycerides, raised high-density lipoprotein, and protected the lower density lipoproteins from oxidation. Chocolate has thus been shown to have potential beneficial effects with respect to heart disease.
authors.affiliation: Department of Chemistry, Loyola Hall, University of Scranton, Scranton, PA 18510, USA. vinson@scranton.edu
authors.forename: Joe A
authors.initials: JA
authors.lastname: Vinson
authors.forename: John
authors.initials: J
authors.lastname: Proch
authors.forename: Pratima
authors.initials: P
authors.lastname: Bose
authors.forename: Sean
authors.initials: S
authors.lastname: Muchler
authors.forename: Pamela
authors.initials: P
authors.lastname: Taffera
authors.forename: Donna
authors.initials: D
authors.lastname: Shuta
authors.forename: Najwa
authors.initials: N
authors.lastname: Samman
authors.forename: Gabriel A
authors.initials: GA
authors.lastname: Agbor
mesh_terms: D000328:Adult; D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage / Q000032:analysis*; D050197:Atherosclerosis / Q000517:prevention & control*; D002099:Cacao / Q000737:chemistry*; D002392:Catechin / Q000097:blood / Q000494:pharmacology; D006224:Cricetinae; D004032:Diet; D004195:Disease Models, Animal; D005060:Europe; D005260:Female; D006801:Humans; D015227:Lipid Peroxidation / Q000187:drug effects; D008055:Lipids / Q000097:blood; D008297:Male; D008647:Mesocricetus; D008875:Middle Aged; D010636:Phenols / Q000032:analysis; D014481:United States
chemical_list: D000975:Antioxidants; D008055:Lipids; D010636:Phenols; D002392:Catechin