A diet rich in green and yellow vegetables inhibits atherosclerosis in mice.

Although dietary patterns characterized by a high intake of fruits and vegetables are associated with reduced risk of coronary heart disease, the mechanisms involved are uncertain. We determined the effects of a diet rich in green and yellow vegetables on the development of atherosclerosis, the underlying cause of coronary heart disease, in a mouse model of atherosclerosis, the LDL receptor -/-, apolipoprotein B transgenic mouse. The mice were randomized into 2 diet groups: 1) a vegetable-free control diet (n = 53) and 2) the same diet with 30% (w:w) replaced by an equal-parts mixture of freeze-dried peas, green beans, broccoli, corn, and carrots (n = 54). Mice were fed these diets for 16 wk. Aortic atherosclerosis, as estimated by cholesteryl ester content, was reduced 38% (P < 0.001) in mice fed the vegetable-rich diet. Plasma total cholesterol (-12%), VLDL + ILDL cholesterol (-32%), serum amyloid A (-37%), and body weight (-7%) (all P < 0.01) were also lower in these mice at the end of the treatment period. In a regression model, antiatherogenic effects of the vegetable diet remained largely unexplained by the variation in plasma lipoproteins or body weight. Although the pathway(s) involved remain uncertain, the results indicate that a diet rich in green and yellow vegetables inhibits the development of atherosclerosis and may therefore lead to a reduction in the risk of coronary heart disease.

Vitamin E bioavailability from fortified breakfast cereal is greater than that from encapsulated supplements.

BACKGROUND: Conflicting results from vitamin E intervention studies suggest supplemental vitamin E malabsorption. OBJECTIVE: We compared vitamin E bioavailability from a supplement with that from a fortified breakfast cereal. DESIGN: Vitamin E bioavailability was evaluated by using deuterium-labeled all-rac-alpha-tocopherol in three 4-d trials (2 wk apart). Five fasting subjects sequentially consumed the following (with 236 mL fat-free milk): 400 IU d(9)-alpha-tocopheryl acetate (400-IU capsule), 41 g ready-to-eat wheat cereal containing 30 IU d(9)-alpha-tocopheryl acetate (30-IU cereal), and 45 g cereal containing 400 IU d(9)-alpha-tocopheryl acetate (400-IU cereal). Five months later (trial 4), they consumed a 400-IU capsule with 41 g vitamin E-free cereal. Blood was obtained up to 72 h after the start of each trial. RESULTS: The mean (+/-SD) vitamin E bioavailabilities of the 30-IU cereal and the 400-IU cereal were 6 +/- 2 and 26 +/- 8 times, respectively, the vitamin E bioavailability of the 400-IU capsule. The areas under the 0-72-h d(9)-alpha-tocopherol curves for the 400-IU capsule, the 30-IU cereal, and the 400-IU cereal were 30 +/- 7, 153 +/- 43, and 765 +/- 164 micro mol. h/L (all trial comparisons, P < 0.0001). In trial 4, 3 subjects barely responded and 2 subjects had areas under the curve that were similar to their 400-IU cereal responses. CONCLUSION: The low bioavailability of vitamin E from the 400-IU capsule and the variability observed when the capsule was consumed with cereal suggest that encapsulated vitamin E is poorly absorbed when consumed with a low-fat meal and that bioavailability can be enhanced by food fortification with vitamin E.