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Effect of Cocoa Bran on Low-Density Lipoprotein Oxidation and Fecal Bulking
David J. A. Jenkins, MD;
Cyril W. C. Kendall, PhD;
Vladimir Vuksan, PhD;
Edward Vidgen, BSc;
Evelyn Wong, MSc;
Livia S. A. Augustin, MSc;
Victor Fulgoni III, PhD
Arch Intern Med. 2000;160:2374-2379.
Background Legumes have reported benefits in terms of reduced risk for coronary heart disease and of colonic health. A novel legume fiber, cocoa bran, also may have favorable health effects on serum lipid levels, low-density lipoprotein (LDL) cholesterol oxidation, and fecal bulk.
Methods Twenty-five healthy normolipidemic subjects (13 men and 12 women) (mean ± SEM age, 37 ± 2 years; mean ± SEM body mass index [calculated as weight in kilograms divided by the square of height in meters], 24.6 ± 0.7) ate cocoa-bran and chocolate-flavored low-fiber breakfast cereals for 2-week periods, with 2-week washout, in a double-blind crossover study. The cocoa-bran cereal provided 25.0 g/d of total dietary fiber (TDF). The low-fiber cereal (5.6 g/d TDF) was of similar appearance and energy value. Fasting blood samples were obtained at the start and end of each period, and 4-day fecal collections were made from days 11 through 14.
Results High-density lipoprotein (HDL) cholesterol level was higher (7.6% ± 2.9%; P = .02) and the LDL/HDL cholesterol ratio was lower (6.7% ± 2.3%; P = .007) for cocoa-bran compared with low-fiber cereal at 2 weeks. No effect was seen on LDL cholesterol oxidation. Mean fecal output was significantly higher for cocoa-bran than for low-fiber cereal (56 ± 14 g/d; P<.001) and equal to the increase seen in the same subjects with wheat fiber in a previous study.
Conclusions A chocolate-flavored cocoa-bran cereal increased fecal bulk similarly to wheat bran and was associated with a reduction in the LDL/HDL cholesterol ratio. In view of the low-fat, high-fiber nature of the material, these results suggest a possible role for this novel fiber source in the diets of normal, hyperlipidemic, and constipated subjects.
From the Clinical Nutrition and Risk Factor Modification Center, St Michael's Hospital (Drs Jenkins, Kendall, and Vuksan, Mr Vidgen, and Mss Wong and Augustin), and the Department of Nutritional Sciences, Faculty of Medicine, University of Toronto (Drs Jenkins, Kendall, and Vuksan, Mr Vidgen, and Ms Augustin), Toronto, Ontario; and The Kellogg Company, Battle Creek, Mich (Dr Fulgoni).
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