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COCOA CONSUMPTION DOSE‐DEPENDENTLY IMPROVES FLOW‐MEDIATED DILATION AND ARTERIAL STIFFNESS IN HEALTHY SUBJECTS
Author(s) -
Grassi Davide,
Desideri Giovambattista,
Necozione Stefano,
Di Giosia Paolo,
Cheli Paola,
Barnabei Remo,
Allegaert Leen,
Bernaert Herwig,
Ferri Claudio
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.359.3
Subject(s) - pulse wave velocity , arterial stiffness , medicine , vasodilation , brachial artery , zoology , cardiology , endocrinology , blood pressure , biology
To investigate the effects of different doses of cocoa on endothelial function and arterial stiffness. According to a randomized, double‐blind, controlled, cross‐over design, 20 healthy volunteers were assigned to receive either five treatments with daily intake of 10 g cocoa (0, 80, 200, 500 and 800 mg cocoa flavonoids/day) in five periods lasting 1 week each. Cocoa dose‐dependently increased flow‐mediated dilation (FMD) from 6.2% (control) to 7.3, 7.6, 8.1 and 8.2% after the different flavonoid doses, respectively (p < 0.0001). Compared with control, even 80 mg cocoa flavonoids/day increased FMD (p < 0.0001). The change in FMD after 800 mg/day was not only significant compared with control (p < 0.0001) but also with 80 mg/day (p = 0.0003) and 200 mg/day (p = 0.05). Compared with control, carotid–femoral artery pulse wave velocity (PWV) dose‐dependently ( 0 mg vs. 200 mg: p = 0.0008; 0 mg vs. 500 mg: p < 0.0001; 0 mg vs. 800 mg: p < 0.0001) decreased. Our study showed for the first time that cocoa dose‐dependently improved FMD and decreased PWV. Our findings are clinically relevant, suggesting cocoa, with very low calorie intake, might be reasonably incorporated into a dietary approach representing a consistent tool in cardiovascular prevention. Starting from our findings, the European Food Safety Authority claimed a relationship between cocoa flavanols and endothelial‐dependent vasodilation.