Oxygenated carotenoid lutein and progression of early atherosclerosis: the Los Angeles atherosclerosis study.

Notes: 

Those with highest blood levels of lutein had the healthiest blood vessels, with no atherosclerosis. (Lutein an indicator of green vegetable consumption.)

TitleOxygenated carotenoid lutein and progression of early atherosclerosis: the Los Angeles atherosclerosis study.
Publication TypeJournal Article
Year of Publication2001
AuthorsDwyer JH, Navab M, Dwyer KM, Hassan K, Sun P, Shircore A, Hama-Levy S, Hough G, Wang X, Drake T, Merz CN, Fogelman AM
JournalCirculation
Volume103
Issue24
Pagination2922-7
Date Published2001 Jun 19
ISSN1524-4539
KeywordsAdult, Animals, Apolipoproteins E, Arteriosclerosis, beta Carotene, Carotid Arteries, Cell Movement, Cells, Cultured, Coculture Techniques, Cohort Studies, Culture Media, Conditioned, Disease Models, Animal, Disease Progression, Dose-Response Relationship, Drug, Endothelium, Vascular, Female, Humans, Lipoproteins, HDL, Lipoproteins, LDL, Los Angeles, Lutein, Male, Mice, Mice, Knockout, Middle Aged, Monocytes, Muscle, Smooth, Vascular, Oxidation-Reduction, Risk Factors
Abstract

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 receptor-null 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 receptor-null 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.

Alternate JournalCirculation
PubMed ID11413081
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