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Oxygenated Carotenoid Lutein and Progression of Early Atherosclerosis. Circulation 103, 2922-7
| Dwyer J., Navab, M, Dwyer, KM, Hassan, K, Sun, P, Shircore, A, Hama-Levy, S, Hough, G, Wang, X, Drake, T, Bairey Merz, CN, Fogelman, AM (2001).
| Background—Carotenoids are hypothesized to explain some of the protective, effects of fruit and vegetable intake on risk of cardiovascular disease., The present study assessed the protective effects of the oxygenated, carotenoid lutein against early atherosclerosis., , , Methods and Results—Epidemiology: Progression of intima-media thickness, (IMT) of the common carotid arteries over 18 months was determined, ultrasonographically and was related to plasma lutein among a randomly, sampled cohort of utility employees age 40 to 60 years (n=480). Coculture:, The impact of lutein on monocyte response to artery wall cell modification, of LDL was assessed in vitro by quantification of monocyte migration in a, coculture model of human intima. Mouse models: The impact of lutein, supplementation on atherosclerotic lesion formation was assessed in vivo by, assigning apoE-null mice to chow or chow plus lutein (0.2% by weight) and, LDL receptornull mice to Western diet or Western diet plus lutein. IMT, progression declined with increasing quintile of plasma lutein (P for, trend=0.007, age-adjusted; P=0.0007, multivariate). Covariate-adjusted IMT, progression (mean±SEM) was 0.021±0.005 mm in the lowest quintile of plasma, lutein, whereas progression was blocked in the highest quintile, (0.004±0.005 mm; P=0.01). In the coculture, pretreatment of cells with, lutein inhibited LDL-induced migration in a dose-dependent manner (P<0.05)., Finally, in the mouse models, lutein supplementation reduced lesion size, 44% in apoE-null mice (P=0.009) and 43% in LDL receptornull mice (P=0.02)., , , Conclusions—These epidemiological, in vitro, and mouse model findings, support the hypothesis that increased dietary intake of lutein is, protective against the development of early atherosclerosis.
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