The literature on risk factors for cardiometabolic diseases showed that lutein might be beneficial for atherosclerosis and inflammatory markers , but there were inconsistent associations with blood pressure , adiposity , insulin resistance , and blood lipids .
CONCLUSIONS Our findings suggest that higher dietary intake and higher blood concentrations of lutein are generally associated with better cardiometabolic health .
BACKGROUND The antioxidant lutein is suggested as being beneficial to cardiometabolic health because of its protective effect against oxidative stress , but evidence has not systematic ally been evaluated .
OBJECTIVE We aim ed to evaluate systematic ally the effects of lutein ( intake or concentrations ) on cardiometabolic outcomes in different life stages .
Oxygenated Carotenoid Lutein and Progression of Early Atherosclerosis: The Los Angeles Atherosclerosis Study
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 r and omly sample d 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
The literature on risk factors for cardiometabolic diseases showed that lutein might be beneficial for atherosclerosis and inflammatory markers , but there were inconsistent associations with blood pressure , adiposity , insulin resistance , and blood lipids .
CONCLUSIONS Our findings suggest that higher dietary intake and higher blood concentrations of lutein are generally associated with better cardiometabolic health .
BACKGROUND The antioxidant lutein is suggested as being beneficial to cardiometabolic health because of its protective effect against oxidative stress , but evidence has not systematic ally been evaluated .
OBJECTIVE We aim ed to evaluate systematic ally the effects of lutein ( intake or concentrations ) on cardiometabolic outcomes in different life stages .