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Articles |
1
Northern Ireland Centre for Diet and Health, School of Biomedical Sciences, University of Ulster, Coleraine, County Londonderry, Northern Ireland BT52 1SA, United Kingdom.
2
Institute of Food Research, Colney, Norwich NR4 7UA,
United Kingdom.
a Author for correspondence. Fax 44-2870-324965; e-mail M.Chopra{at}ulst.ac.uk
Background: Epidemiological studies suggest a cardioprotective role for carotenoid-rich foods. Smokers have a high risk of cardiovascular disease and low dietary intake and plasma concentrations of carotenoids. The aim of this study was to determine the carotenoid response of smokers and nonsmokers to increased intake of 300400 g of vegetables and its effect on LDL oxidation.
Methods: After a depletion period of 8 days, 34 healthy females (18 nonsmokers, 16 smokers) were supplemented with ß-carotene- and lutein-rich (green) and lycopene-rich (red) vegetable foods, each for 7 days.
Results: Baseline concentrations (mean ± SD) of plasma ß-carotene (0.203 ± 0.28 µmol/L vs 0.412 ± 0.34 µmol/L; P <0.005) and lutein (0.180 ± 0.10 vs 0.242 ± 0.11 µmol/L; P <0.05) but not lycopene (0.296 ± 0.10 vs 0.319 ± 0.33 µmol/L) were significantly lower in smokers compared with nonsmokers. After supplementation, the change (supplementation minus depletion) in plasma ß-carotene (0.152 ± 0.43 vs 0.363 ± 0.29 µmol/L in smokers vs nonsmokers; P = 0.002) and LDL lutein (0.015 ± 0.03 vs 0.029 ± 0.03 µmol/mmol cholesterol; P = 0.01) was significantly lower in smokers than nonsmokers. Green-vegetable supplementation had no effect on the resistance of LDL to oxidation (lag-phase) in either group. After red-vegetable supplementation, plasma and LDL lycopene concentrations were increased in both groups, but only nonsmokers showed a significant increase in the lag-phase (44.9 ± 9.5 min at baseline, 41.4 ± 6.5 min after depletion, and 49.0 ± 8.9 min after supplementation; P <0.01) compared with depletion.
Conclusions: In this short-term intervention study, a dietary intake of >40 mg/day of lycopene by a group of nonsmoking individuals significantly reduced the susceptibility of LDL to oxidation, whereas an equivalent increase in lycopene by a group of smokers showed no such effect.
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