title: Oxygenated Carotenoid Lutein and Progression of Early Atherosclerosis: The Los Angeles Atherosclerosis Study Carotenoids, immunocompetence, and the information content of sexual colors: an experimental test. Some dietary and adipose tissue carotenoids are associated with the risk of nonfatal acute myocardial infarction in Costa Rica. Diabetes mellitus and serum carotenoids: findings of a population-based study in Queensland, Australia. Plasma lycopene, other carotenoids, and retinol and the risk of cardiovascular disease in men. Plasma lycopene, other carotenoids, and retinol and the risk of cardiovascular disease in women. Both alpha- and beta-carotene, but not tocopherols and vitamin C, are inversely related to 15-year cardiovascular mortality in Dutch elderly men. Dietary carotenoids and risk of coronary artery disease in women. Relation between prenatal lipid-soluble micronutrient status, environmental pollutant exposure, and birth outcomes. Effects of lutein and lycopene on carotid intima-media thickness in Chinese subjects with subclinical atherosclerosis: a randomised, double-blind, placebo-controlled trial. Smoking induces insulin resistance--a potential link with the insulin resistance syndrome. Plasma Carotenoids and Tocopherols and Risk of Myocardial Infarction in a Low-Risk Population of US Male Physicians Prospective Study of Plasma Carotenoids and Tocopherols in Relation to Risk of Ischemic Stroke Lutein-fortified infant formula fed to healthy term infants: evaluation of growth effects and safety Serum Retinol and Carotenoids in Association with Biomarkers of Insulin Resistance among Premenopausal Women Low-serum carotenoid concentrations and carotenoid interactions predict mortality in US adults: the Third National Health and Nutrition Examination Survey. Plasma lycopene, other carotenoids, and the risk of type 2 diabetes in women. The effect of lutein- and zeaxanthin-rich foods v. supplements on macular pigment level and serological markers of endothelial activation, inflammation and oxidation: pilot studies in healthy volunteers. Effect of beta-carotene supplementation on the concentrations and distribution of carotenoids, vitamin E, vitamin A, and cholesterol in plasma lipoprotein and non-lipoprotein fractions in healthy older women. Plasma carotenoids and risk of acute myocardial infarction in the Singapore Chinese Health Study. Relation of Consumption of Vitamin E, Vitamin C, and Carotenoids to Risk for Stroke among Men in the United States Assessment of carotenoid status and the relation to glycaemic control in type I diabetics: a follow-up study Associations of serum carotenoid concentrations with the development of diabetes and with insulin concentration: interaction with smoking: the Coronary Artery Risk Development in Young Adults (CARDIA) Study. Uric acid and serum antioxidant capacity: a reaction to atherosclerosis? High plasma levels of alpha- and beta-carotene are associated with a lower risk of atherosclerosis: results from the Bruneck study. Effects of lutein supplement on serum inflammatory cytokines, ApoE and lipid profiles in early atherosclerosis population. Lutein supplementation reduces plasma lipid peroxidation and C-reactive protein in healthy nonsmokers. Low plasma retinol predicts coronary events in healthy middle-aged men: the PRIME Study. Changes in CD4+ cell count and the risk of opportunistic infection or death after highly active antiretroviral treatment
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 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 Many male birds use carotenoid pigments to acquire brilliant colors that advertise their health and condition to prospect i ve mates . The direct means by which the most colorful males achieve superior health has been debated , however . One hypothesis , based on studies of carotenoids as antioxidants in humans and other animals , is that carotenoids directly boost the immune system of colorful birds . We studied the relationship between carotenoid pigments , immune function , and sexual coloration in zebra finches ( Taeniopygia guttata ) , a species in which males incorporate carotenoid pigments into their beak to attract mates . We tested the hypotheses that increased dietary carotenoid intake enhances immunocompetence in male zebra finches and that levels of carotenoids circulating in blood , which also determine beak coloration , directly predict the immune response of individuals . We experimentally supplemented captive finches  with two common dietary carotenoid pigments ( lutein and zeaxanthin ) and measured cell-mediated and humoral immunity a month later . Supplemented males showed elevated blood-carotenoid levels , brighter beak coloration , and increased cell-mediated and humoral immune responses than did controls . Cell-mediated responses were predicted directly by changes in beak color and plasma carotenoid concentration of individual birds . These experimental findings suggest that carotenoid-based color signals in birds may directly signal male health via the immunostimulatory action of ingested and circulated carotenoid pigments Antioxidants , particularly carotenoids and tocopherols , may protect against cardiovascular disease . The objective of this study was to determine whether dietary and adipose tissue carotenoids and tocopherols are associated with the risk of myocardial infa rct ion ( MI ) . Cases ( n = 1456 ) of a first acute MI were identified and matched by age , sex , and residence to r and omly selected population controls ( n = 1456 ) living in Costa Rica .  Carotenoids and tocopherols were measured in adipose tissue using HPLC .  Dietary intake was assessed using a vali date d FFQ . Anthropometrical and lifestyle data were collected using an interviewer-administered question naire . Subjects were distributed into quintiles of intake or adipose tissue concentration of carotenoids or tocopherols . The lowest quintile was used as the referent in conditional logistic regression analyses . Adipose tissue beta-carotene showed a significant inverse relation with MI risk ; the odds ratio ( OR ) comparing the highest to the lowest quintile was 0.70 ( 95 % CI : 0.51 - 0.96 , P for trend = 0.02 ) . Intake of fruits and vegetables that are rich in beta-carotene was also inversely associated with the risk of MI ( OR = 0.74 ; CI : 0.54 - 1.01 , P for trend = 0.09 ) . In contrast , lutein + zeaxanthin in adipose tissue ( OR = 1.46 ; CI : 1.05 - 2.05 , P for trend = 0.02 ) and diet ( OR = 1.18 ; CI : 0.88 - 1.57 , P for trend = 0.02 ) was positively associated with MI risk . MI risk was not associated with any of the other carotenoids or tocopherols in the diet or adipose tissue . Thus , the inverse association between beta-carotene and MI risk suggests that beta-carotene protects against MI or it is a marker of some protective factor in foods containing beta-carotene . The mechanism underlying the positive association between lutein + zeaxanthin and the risk of MI warrants investigation BACKGROUND Epidemiologic evidence suggests that serum carotenoids are potent antioxidants and may play a protective role in the development of chronic diseases including cancers , cardiovascular disease , and inflammatory diseases . The role of these antioxidants in the pathogenesis of diabetes mellitus remains unclear . OBJECTIVE This study examined data from a cross-sectional survey to investigate the association between serum  carotenoids  and  type 2 diabetes .  DESIGN Study participants were adults aged > or = 25 y ( n = 1597 ) from 6 r and omly selected cities and towns in Queensl and , Australia . Study examinations conducted between October and December 2000 included fasting plasma glucose , an oral-glucose-tolerance test , and measurement of the serum concentrations of 5 carotenoid compounds .  RESULTS Mean 2-h postload plasma glucose and fasting insulin concentrations decreased significantly with increasing quintiles of the 5 serum carotenoids -- alpha-carotene , beta-carotene , beta-cryptoxanthin , lutein/zeaxanthin , and lycopene . Geometric mean concentrations for all serum carotenoids decreased ( all decreases were significant except that of lycopene ) with declining glucose tolerance status . Beta-carotene had the greatest decrease , to geometric means of 0.59 , 0.50 , and 0.42 micromol/L in persons with normal glucose tolerance , impaired glucose metabolism , and type 2 diabetes , respectively ( P < 0.01 for linear trend ) , after control for potential confounders . CONCLUSIONS Serum carotenoids are inversely associated with type 2 diabetes and impaired glucose metabolism . R and omized trials of diets high in carotenoid-rich vegetables and fruit are needed to confirm these results and those from other observational studies . Such evidence would have very important implication s for the prevention of diabetes BACKGROUND Emerging evidence suggests a possible role of lycopene in the primary prevention of cardiovascular disease ( CVD ) . OBJECTIVE We examined whether plasma lycopene concentrations in the Physicians ' Health Study were associated with CVD in a prospect i ve , nested , case-control design . DESIGN Baseline blood sample s were collected starting in 1996 . During a mean follow-up of 2.1 y , we identified 499 cases of CVD ( confirmed myocardial infa rct ion , stroke , CVD death , or revascularization procedures ) and an equal number of men free of CVD and matched for age ( x : 69.7 y ) , follow-up time , and smoking status . We collected self-reported coronary disease risk factors and measured plasma carotenoids , retinol , lipids , and C-reactive protein . RESULTS In matched analyses with additional adjustment for plasma total cholesterol and r and omized treatment , the relative risks ( RRs ) of CVD for men in the lowest to highest quartiles of plasma lycopene were 1.00 ( reference ) , 0.92 , 1.04 , and 0.95 ( P for linear trend = 0.93 ) . With multivariate adjustment , the RRs of total CVD were 1.00 ( reference ) , 1.08 , 0.94 , and 1.03 ( P for linear trend = 0.98 ) . For important vascular events ( 241 cases ) , excluding revascularization procedures , the multivariate RRs remained nonsignificant ( P for linear trend = 0.50 ) . Adding plasma carotenoids , lipids , or C-reactive protein to multivariate models had a minimal effect on the RRs of total CVD for plasma lycopene . Compared with lycopene , higher concentrations of plasma lutein/zeaxanthin and retinol suggested a moderate increase in CVD risk , whereas no association was found for beta-cryptoxanthin , alpha-carotene , and beta-carotene . CONCLUSIONS Higher plasma lycopene concentrations were not associated with the risk of CVD in this study of older men . Further evaluation in diverse population s is necessary BACKGROUND Growing evidence suggests that lycopene has significant in vitro antioxidant potential .  Lycopene has rarely been tested in prospect i ve studies for its role in cardiovascular disease ( CVD ) prevention . OBJECTIVE We examined the association between plasma lycopene and the risk of CVD in middle-aged and elderly women . DESIGN A prospect i ve , nested , case-control study was conducted in 39 876 women initially free of CVD and cancer in the Women 's Health Study . Baseline blood sample s were collected from 28 345 ( 71 % ) of the women . During a mean of 4.8 y of follow-up , we identified 483 CVD cases and 483 control subjects matched by age , smoking status , and follow-up time .  Plasma lycopene , other carotenoids , retinol , and total cholesterol  were measured . RESULTS In analyses matched for age and smoking , with adjustment for plasma cholesterol , the relative risks ( RRs ) and 95 % CIs of CVD in increasing quartiles of plasma lycopene were 1.00 ( referent ) , 0.78 ( 95 % CI : 0.55 , 1.11 ) , 0.56 ( 0.39 , 0.82 ) , and 0.62 ( 0.43 , 0.90 ) . In multivariate models , the RRs were 1.00 ( referent ) , 0.94 ( 0.60 , 1.49 ) , 0.62 ( 0.39 , 1.00 ) , and 0.67 ( 0.41 , 1.11 ) ; those in the upper compared with the lower half of plasma lycopene had an RR of 0.66 ( 0.47 , 0.95 ) . For CVD , exclusive of angina , women in the upper 3 quartiles had a significant multivariate 50 % risk reduction compared with those in the lowest quartile . The stepwise addition of individual plasma carotenoids did not affect the RRs . CONCLUSIONS Higher plasma lycopene concentrations are associated with a lower risk of CVD in women . These findings require confirmation in other cohorts , and the determinants of plasma lycopene concentrations need to be better understood The role of beta-carotene , alpha-tocopherol , and vitamin C in the prevention of cardiovascular diseases ( CVD ) is controversial . Prospect i ve studies on gamma-tocopherol and carotenoids other than beta-carotene are sparse . We assessed relations between the intake of different carotenoids , alpha- and gamma-tocopherol , and vitamin C with  15-y CVD mortality in elderly men who participated in the Zutphen Elderly Study . Information on diet and potential confounding factors was collected in 1985 , 1990 , and 1995 . In 1985 , 559 men ( mean age approximately 72 y ) free of chronic diseases were included in the current analysis . After 15 y of follow-up , comprising 5744 person-years , 197 men had died from CVD . After adjustment for age , smoking , and other potential lifestyle and dietary confounders , relative risks ( RR ) ( 95 % CI ) of CVD death for a 1-SD increase in intake were 0.81 ( 0.66 - 0.99 ) for alpha-carotene and 0.80 ( 0.66 - 0.97 ) for beta-carotene . Carrots were the primary source of alpha- and beta-carotene and their consumption was related to a lower risk of death from CVD ( adjusted RR , 0.83 ; 95 % CI = 0.68 - 1.00 ) . Intakes of carotenoids other than alpha- and beta-carotene were not associated with CVD mortality , nor were vitamin C and alpha- and gamma tocopherol . In conclusion , dietary intakes of alpha-carotene and beta-carotene are inversely associated with  CVD mortality in elderly men . This study does not indicate an important role for other carotenoids , tocopherols , or vitamin C in lowering the risk of CVD death BACKGROUND Numerous studies have shown that higher intakes or higher blood concentrations of carotenes are associated with a lower risk of  coronary artery disease ( CAD ) . Given the null results in trials of beta-carotene supplementation , considerable attention has focused on the potential role of other dietary carotenoids in the prevention of CAD . OBJECTIVE Our objective was to prospect ively examine the relation between dietary intakes of specific carotenoids and risk of CAD in women . DESIGN In 1984 , 73 286 female nurses completed a semiquantitative food-frequency question naire that assessed their consumption of carotenoids and various other nutrients . The women were followed for 12 y for the development of incident CAD ( nonfatal myocardial infa rct ion and fatal CAD ) , and dietary information was up date d in 1986 , 1990 , and 1994 . RESULTS During 12 y of follow-up ( 803 590 person-years ) , we identified 998 incident cases of CAD . After adjustment for age , smoking , and other CAD risk factors , we observed modest but significant inverse associations between the highest quintiles of intake of beta-carotene and alpha-carotene and risk of CAD but no significant relation with intakes of lutein/zeaxanthin , lycopene , or beta-cryptoxanthin .  For women in the highest compared with the respective lowest quintile of intake , the relative risks for beta-carotene and alpha-carotene were 0.74 ( 95 % CI : 0.59 , 0.93 ) and 0.80 ( 95 % CI : 0.65 , 0.99 ) , respectively . The association between the specific carotenoids and CAD risk did not vary significantly by current smoking status . CONCLUSION Higher intakes of foods rich in alpha-carotene or beta-carotene are associated with a reduction in risk of CAD BACKGROUND Adverse postnatal health effects have been associated with compromised fetal growth , which makes it essential to underst and its determinants . Significant effects of environmental pollutants on birth outcomes have been observed in our study population , and nutritional status may be an additional factor influencing fetal development and effects of environmental toxins . OBJECTIVE The objective of the study was to examine the relations between birth outcomes and lipid-soluble plasma micronutrient concentrations and to explore interactions between micronutrients and environmental pollutant exposure in newborns in Krakow , Pol and . DESIGN In this prospect i ve cohort study , retinol , alpha-tocopherol , and carotenoids were measured in maternal and cord blood sample s obtained at delivery ( 251 maternal-newborn pairs ) , and birth weight , birth length , head circumference ( HC ) , and gestational age were evaluated . Linear regression analysis was used to estimate the effects of micronutrients while covariates were controlled for . Interaction terms assessed whether the effects of polycyclic aromatic hydrocarbons ( PAHs ) , common environmental pollutants , varied by nutrient status . RESULTS Infants whose mothers had low plasma alpha-tocopherol concentrations ( below the median ) weighed 92.9 g less and had 0.41-cm smaller HCs than did infants whose mothers had high alpha-tocopherol concentrations . Infants with low plasma retinol ( below the median ) weighed 125.9 g less and had 0.31-cm smaller HCs . There was no evidence of an interaction between PAHs and micronutrients , although power was limited . CONCLUSION Maternal alpha-tocopherol and cord retinol concentrations were significantly and positively associated with BW and HC . These micronutrients may have direct effects or may be markers for other underlying determinants of these pregnancy outcomes The aim of the present study was to evaluate the effects of lutein and lycopene supplementation on carotid artery intima-media thickness ( C AIM T ) in subjects with sub clinical atherosclerosis . A total of 144 subjects aged 45 - 68 years were recruited from local communities . All the subjects were r and omly assigned to receive 20 mg lutein/d ( n 48 ) , 20 mg lutein/d+20 mg lycopene/d ( n 48 ) or placebo ( n 48 ) for 12 months . C AIM T was measured using  Doppler ultrasonography at baseline and after 12 months , and serum lutein and lycopene concentrations were determined using HPLC . Serum lutein concentrations increased significantly from 0·34 to 1·96 μmol/l in the lutein group ( P < 0·001 ) and from 0·35 to 1·66 μmol/l in the combination group ( P < 0·001 ) . Similarly , serum lycopene concentrations increased significantly from 0·18 to 0·71 μmol/l in the combination group at month 12 ( P < 0·001 ) , whereas no significant change was observed in the placebo group . The mean values of C AIM T decreased significantly by 0·035 mm ( P= 0·042 ) and 0·073 mm ( P < 0·001 ) in the lutein and combination groups at month 12 , respectively . The change in C AIM T was inversely associated with the increase in serum lutein concentrations ( P < 0·05 ) in both the active treatment groups and with that in serum lycopene concentrations ( β = - 0·342 , P= 0·031 ) in the combination group  . Lutein and lycopene supplementation significantly increased the serum concentrations of lutein and lycopene with a decrease in C AIM T being associated with both concentrations . In addition , the combination of lutein and lycopene supplementation was more effective than lutein alone for protection against the development of C AIM T in Chinese subjects with sub clinical atherosclerosis , and further studies are needed to confirm whether synergistic effects of lutein and lycopene exist OBJECTIVES The acute effect of smoking and snuffing on insulin sensitivity was studied in a group of healthy habitual smokers . DESIGN The euglycaemic clamp technique was combined with the subcutaneous injection of a bolus ( 0.1 U kg-1 ) of fast-acting insulin ( Actrapid ) . R and omized subjects smoked either one cigarette per hour for 6 h , took one bag-packed snuff per hour for 6 h or refrained from nicotine for 48 h before as well as during the clamp . SUBJECTS Seven healthy smokers , four females and three males , of normal weight ( BMI , mean + /- SEM , 21 + /- 0.7 kg m-2 with a range of 18.6 - 23.9 ) , aged 31 + /- 2 years ( range 24 - 35 years ) , who had consumed at least 20 cigarettes per day for at least 5 years were studied . They were recruited through an advertisement in a newspaper . RESULTS The steady-state plasma nicotine levels were similar during smoking and snuffing . The insulin and glucose levels were also similar during all three clamps . Smoking , but not snuffing , impaired insulin action ( P < 0.05 ) mainly due to a lower peripheral glucose uptake . The mean growth hormone levels during the 6-h study were more than doubled during smoking ( P < 0.01 ) while no significant differences were seen in the other counter-regulatory hormones . CONCLUSION Smoking ( also in habitual smokers ) acutely impairs insulin action and leads to insulin resistance . Thus , smoking can be of importance for the development of the insulin resistance syndrome associated with risk for cardiovascular disease Background —Increased intake of carotenoids and vitamin E may protect against myocardial infa rct ion ( MI ) . However , prospect i ve data on blood levels of carotenoids other than & bgr;-carotene and vitamin E ( tocopherol ) and risk of MI are sparse . Methods and Results —We conducted a prospect i ve , nested case-control analysis among male physicians without prior history of cardiovascular disease who were followed for up to 13 years in the Physicians ’ Health Study . Sample s from 531 physicians diagnosed with MI were analyzed together with sample s from paired control subjects , matched for age and smoking , for 5 major carotenoids ( & agr;- and & bgr;-carotene , & bgr;-cryptoxanthin , lutein , and lycopene ) , retinol , and & agr;- and & ggr;-tocopherol . Overall , we found no evidence for a protective effect against MI for higher baseline plasma levels of retinol or any of the carotenoids measured . Among current and former smokers but not among never-smokers , higher baseline plasma levels of & bgr;-carotene tended to be associated with lower risk ( P for interaction=0.02 ) . Men with higher plasma levels of & ggr;-tocopherol tended to have an increased risk of MI ( P for trend=0.01 ) . Conclusions —These prospect i ve data do not support an overall protective relation between plasma carotenoids or tocopherols and future MI risk among men without a history of prior cardiovascular disease Background and Purpose — Intake of fruits and vegetables has been related to lower risk of ischemic stroke , but nutrients responsible for this apparent benefit remain ill-defined . Tocopherols ( vitamin E ) have also been proposed to be protective . Methods — We conducted a prospect i ve , nested case-control analysis among male physicians without diagnosed cardiovascular disease followed-up for up to 13 years in the Physicians ’ Health Study . Sample s from 297 physicians with ischemic stroke were analyzed with paired controls , matched for age and smoking , for 5 major carotenoids ( & agr;- and β-carotene , β-cryptoxanthin , lutein , and lycopene ) , retinol , and & agr;- and γ-tocopherol . Results — Baseline plasma levels of & agr;-carotene and β-carotene and lycopene tended to be inversely related to risk of ischemic stroke with an apparent threshold effect . As compared with men whose plasma levels were in the lowest quintile , the multivariate adjusted odds ratios ( ORs ) of ischemic stroke among men with levels in the second through fifth quintiles were 0.59 ( 95 % CI , 0.36 to 0.98 ) for & agr;-carotene , 0.62 ( 95 % CI , 0.38 to 1.01 ) for β-carotene , and 0.61 ( 95 % CI , 0.37 to 1.00 ) for lycopene . A tendency toward an inverse association was found for β-cryptoxanthin , but the result was not statistically significant . No association was found for lutein , retinol , and tocopherols . Conclusion — Our data suggest that higher plasma levels of carotenoids , as markers of fruit and vegetable intake , are inversely related to risk of ischemic stroke and provide support for recommendations to consume fruits and vegetables regularly Background / Objectives Breast milk contains lutein derived from the mother 's diet . This carotenoid is currently not added to infant formula , which has a small and variable lutein content from innate ingredients . This study was conducted to compare the growth of infants fed lutein-fortified infant formula  with that of infants fed infant formula without lutein fortification . Subjects/ Methods This 16-week study was prospect i ve , r and omized , controlled , and double-blind with parallel groups of healthy term infants fed either control formula ( Wyeth S-26 Gold  , design ated as Gold ) or experimental formula ( Wyeth S-26 Gold fortified with lutein at 200 mcg/l , design ated as Gold + Lutein ) . Two hundred thirty-two ( 232 ) infants ≤ 14 days postnatal age were r and omized and 220 ( 94.8 % ) completed the study .  Weight ( g ) , head circumference ( cm ) , and length ( cm ) were measured at Weeks 4 , 8 , 12 , and 16 . The primary endpoint was weight gain ( g/day ) from baseline to Week 16 . Safety was assessed through monitoring of study events ( SEs ) throughout the study and evaluation of selected blood chemistry tests performed at Week 16 . Results Infants in both treatment groups demonstrated appropriate growth . No differences between treatment groups were found in any of the measures of growth at any of the measurement time points . Both study formulas were well tolerated . The mean values of all measured blood chemistry parameters fell within the modified normal ranges for infants , and the values for both groups for any measured parameter were similar . Conclusions Infants fed lutein-fortified S-26 Gold  demonstrated growth equivalent to that of infants fed unfortified lutein formula Objective . The aim of this study was to investigate how serum retinol and carotenoids ( β-carotene , β-cryptoxanthin , lutein/zeaxanthin , lycopene ) are associated with biomarkers of insulin resistance . Research Methods and Procedures . The BioCycle Study ( 2005–2007 ) is a prospect i ve cohort of 259 healthy premenopausal women . Fasting serum sample s were collected at up to sixteen clinic visits , from which  retinol , carotenoids , insulin , glucose , and sex hormone-binding globulin ( SHBG ) were measured . Insulin resistance was estimated by the homeostasis model assessment ( HOMA-IR ) . Linear mixed models were used to determine associations adjusting for age , race , body mass index ( BMI ) , education , smoking , physical activity , triglycerides , and energy intake . Results . Retinol was positively associated with HOMA-IR ( β = 0.19 ( 95 % CI : 0.07 , 0.32 ) ) units per ug/mL increase in retinol ; the relationship was driven by insulin ( β = 0.20 ( 95 % CI : 0.08 , 0.31 ) ) . Retinol was inversely associated with SHBG ( β = −0.22 ( 95 % CI : −0.28 , −0.16 ) ) . Although no significant associations were found between serum carotenoids and HOMA-IR , β-carotene was positively associated with SHBG and β-cryptoxanthin inversely with fasting plasma glucose . Conclusion . Results indicate a possible role for serum retinol in the pathogenesis of type 2 diabetes . However , they do not support a strong association between individual or total serum carotenoids and insulin resistance Evidence regarding the health benefits of carotenoids is controversial . Effects of serum carotenoids and their interactions on mortality have not been examined in a representative sample of US adults . The objective was to examine whether serum carotenoid concentrations predict  mortality among US adults . The study consisted of adults aged ≥20 years enrolled in the Third National Health and Nutrition Examination Survey , 1988 to 1994 , with measured serum carotenoids and mortality follow-up through 2006 ( N = 13,293 ) . Outcomes were all-cause , cardiovascular disease , and cancer mortality . In adjusted Cox proportional hazards models , participants in the lowest total carotenoid quartile ( < 1.01 μmol/L ) had significantly higher all-cause mortality ( mortality rate ratio , 1.38 ; 95 % confidence interval , 1.15 - 1.65 ; P = .005 ) than those in the highest total carotenoid quartile ( > 1.75 μmol/L ) . For α-carotene , the highest quartile ( > 0.11 μmol/L ) had the lowest all-cause mortality rates ( P < .001 ) . For lycopene , the middle 2 quartiles ( 0.29 - 0.58 μmol/L ) had the lowest all-cause mortality rates ( P = .047 ) . Analyses with continuous carotenoids confirmed associations of serum total carotenoids , α-carotene , and lycopene with all-cause mortality ( P < .001 ) . In a r and om survival forest analysis , very low lycopene was the carotenoid most strongly predictive of all-cause mortality , followed by very low total carotenoids . α-Carotene/β-cryptoxanthin , α-carotene/lutein+zeaxanthin and lycopene/lutein+zeaxanthin interactions were significantly related to all-cause mortality ( P < .05 ) . Low α-carotene was the only carotenoid associated with cardiovascular disease mortality ( P = .002 ) . No carotenoids were significantly associated with cancer mortality . Very low serum total carotenoid , α-carotene , and lycopene concentrations may be risk factors for mortality , but carotenoids show interaction effects on mortality . Interventions of balanced carotenoid combinations are needed for confirmation The authors conducted a nested case-control study from 1992 to 2003 among US women aged 45 years or older and free from cardiovascular disease and cancer to examine the prospect i ve association among plasma lycopene , other carotenoids , and the risk of developing type 2 diabetes . During 10 years of follow-up , 470 cases of incident type 2 diabetes were selected and individually matched on age ( + /- 1 year ) and follow-up time to 470 nondiabetic controls .  Baseline plasma levels of lycopene , alpha-carotene , beta-carotene , beta-cryptoxanthin , and lutein/zeaxanthin  were similar in cases and controls ( all p > 0.05 ) . A possible crude inverse association between plasma lycopene and risk of type 2 diabetes was attenuated upon multivariate adjustment . After control for plasma total cholesterol and known diabetes risk factors , the multivariate odds ratios of type 2 diabetes in the highest versus the lowest quartile of plasma carotenoids were 1.13 ( 95 % confidence interval ( CI ) : 0.60 , 2.13 ) for lycopene , 1.27 ( 95 % CI : 0.63 , 2.57 ) for alpha-carotene , 1.10 ( 95 % CI : 0.57 , 2.13 ) for beta-carotene , 0.91 ( 95 % CI : 0.46 , 1.81 ) for beta-cryptoxanthin , and 1.35 ( 95 % CI : 0.68 , 2.69 ) for lutein/zeaxanthin . There was no prospect i ve association between baseline plasma carotenoids and the risk of type 2 diabetes in middle-aged and older women The aim of the present study was to compare the effect of lutein- and zeaxanthin-rich foods and supplements on macular pigment level ( MPL ) and serological markers of endothelial activation , inflammation and oxidation in healthy volunteers . We conducted two 8-week intervention studies . Study 1 ( n 52 ) subjects were r and omised to receive either carrot juice ( a carotene-rich food ) or spinach powder ( a lutein- and zeaxanthin-rich food ) for 8 weeks . Study 2 subjects ( n 75 ) received supplements containing lutein and zeaxanthin , β-carotene , or placebo for 8 weeks in a r and omised , double-blind , placebo-controlled  trial . MPL , serum concentrations of lipid-soluble antioxidants , inter-cellular adhesion molecule 1 , vascular cell adhesion molecule 1 , C-reactive protein and F2-isoprostane levels were assessed at baseline and post-intervention in both studies . In these intervention studies , no effects on MPL or markers of endothelial activation , inflammation or oxidation were observed . However , the change in serum lutein and zeaxanthin was associated or tended to be associated with the change in MPL in those receiving lutein- and zeaxanthin-rich foods ( lutein r 0.40 , P = 0.05 ; zeaxanthin r 0.30 , P = 0.14 ) or the lutein and zeaxanthin supplement ( lutein r 0.43 , P = 0.03 ; zeaxanthin r 0.22 , P = 0.28 ) . In both studies , the change in MPL was associated with baseline MPL ( food study r - 0.54 , P < 0.001 ; supplement study r - 0.40 , P < 0.001 ) . We conclude that this 8-week supplementation with lutein and zeaxanthin , whether as foods or as supplements , had no significant effect on MPL or serological markers of endothelial activation , inflammation and oxidation in healthy volunteers , but may improve MPL in the highest serum responders and in those with initially low MPL OBJECTIVE We studied the effect of beta-carotene supplementation on the concentrations and distribution in plasma lipoprotein and non-lipoprotein fractions of carotenoids , alpha-tocopherol , retinol , and cholesterol . METHODS Ten women ingested either 90 mg of beta-carotene or placebo daily for 3 weeks while residing in their homes and eating their usual meals . Carotenoids ( beta-carotene , lycopene , lutein/zeaxanthin ) , retinol , alpha-tocopherol , and cholesterol were measured in plasma lipoprotein and non-lipoprotein fractions before and after treatment . RESULTS In the beta-carotene-supplemented group , total plasma beta-carotene increased 14-fold from 0.48 + /- 0.13 to 6.83 + /- 2.12 mumol/L ( p = 0.04 ) . Although the greatest increase in beta-carotene was in low-density-lipoproteins ( LDL ) , the magnitude of increase was similar in LDL , high-density-lipoproteins ( HDL ) , and very-low-density-lipoproteins ( VLDL ) . Thus , the relative distribution of beta-carotene in lipoproteins was unchanged : approximately 71 % was in LDL , approximately 15 % in HDL and approximately 12 % in VLDL , before and after beta-carotene supplementation . There were no changes in amounts and distribution in lipoproteins of the other carotenoids , alpha-tocopherol , and cholesterol . There was no change in the amount of retinol in lipoprotein-deficient plasma . There were no changes in total plasma triglycerides . Significant positive correlations were found between LDL- or VLDL-cholesterol and alpha-tocopherol in LDL or VLDL , respectively ; between LDL- or VLDL-cholesterol and lutein/zeaxanthin in LDL or VLDL , respectively ; and between HDL-cholesterol and beta-carotene in HDL . CONCLUSIONS beta-Carotene supplementation ( 90 mg/day for 3 weeks ) in healthy older women results in an enrichment of all plasma lipoprotein fractions with beta-carotene , but does not alter the relative distribution of beta-carotene in lipoproteins . beta-Carotene supplementation has no effect on the amounts and relative distribution of lycopene , lutein/zeaxanthin , and alpha-tocopherol in lipoproteins , or of retinol in the non-lipoprotein fraction of plasma . Short-term beta-carotene supplementation has no effect on the concentrations of plasma total triglycerides , total cholesterol , HDL- , LDL- , and VLDL-cholesterol BACKGROUND AND AIM Modification of low-density lipoprotein due to oxidative stress is essential in the development of coronary atherosclerosis . Data of specific carotenoids except β-carotene on cardioprotective effects in humans are limited . METHODS AND RESULTS This study examined the associations between plasma concentrations of specific carotenoids and incidence of acute myocardial infa rct ion . The study included 280 incident cases of acute myocardial infa rct ion and 560 matched controls nested within the Singapore Chinese Health Study , a prospect i ve cohort of 63,257 Chinese men and women aged 45 - 74 years old enrolled in 1993 - 1998 in Singapore . Retinol and carotenoids in prediagnostic plasma were quantified using high-performance liquid chromatography . High levels of plasma β-cryptoxanthin and lutein were associated with decreased risk of acute myocardial infa rct ion after adjustment for multiple risk factors for coronary heart disease . For β-cryptoxanthin , the odds ratio ( 95 % confidence interval ) for the highest ( Q5 ) versus the lowest ( Q1 ) quintile was 0.67 ( 0.37 - 1.21 ) ( P for trend=0.03 ) . For lutein , the odds ratios ( 95 % confidence intervals ) for the combined Q2-Q3 and the combined Q4-Q5 versus Q1 were 0.71 ( 0.45 - 1.12 ) and 0.58 ( 0.35 - 0.94 ) respectively ( P for trend=0.03 ) . There was no statistically significant association between other carotenoids or retinol and risk of acute myocardial infa rct ion . CONCLUSIONS High plasma levels of β-cryptoxanthin and lutein were associated with decreased risk of acute myocardial infa rct ion . The findings of this study support a cardioprotective role of these two carotenoids in humans Considerable evidence supports the hypothesis that vitamin E reduces the risk for atherosclerosis ( 1 ) . Vitamin E inhibits the proliferation of smooth-muscle cells in vitro ( 2 ) and increases the resistance of low-density lipoprotein to oxidation when it is added to plasma or administered to humans ( 3 , 4 ) . Furthermore , platelets from persons taking vitamin E supplements  had markedly reduced adhesiveness to collagen ( 5 ) . Consistent with these findings , vitamin E intake has been inversely associated with risk for coronary heart disease ( 6 - 8 ) and for peripheral arterial disease ( 9 ) and with carotid artery wall thickness ( 10 , 11 ) . Risk for ischemic stroke also increases with atherosclerosis and might therefore be reduced by vitamin E. However , few studies have addressed the relation between vitamin E and risk for ischemic stroke , and those that have been done were small , had little variation in vitamin E intake , or did not distinguish between ischemic and hemorrhagic stroke ( 12 - 15 ) . Risk for hemorrhagic stroke is unlikely to be reduced by high doses of vitamin E and could even be increased by the reduced platelet adhesion that these doses cause ( 5 ) . The most informative previous studies a large r and omized trial in men ( 16 , 17 ) and a prospect i ve investigation in women (6)supported a modest beneficial effect of vitamin E with respect to ischemic stroke , but the results were not statistically significant . Moreover , in the trial in men ( 16 ) , this apparent benefit was offset by an increased risk for hemorrhagic stroke . Like vitamin E , vitamin C and carotenoids have antioxidant properties ( 18 , 19 ) and have been hypothesized to reduce risk for stroke , but epidemiologic evidence to support these hypotheses is limited ( 14 - 17 , 20 - 22 ) . Of the carotenoids , we considered -carotene , -carotene , lutein , and lycopene because they are present in relatively large amounts in the diet and have distinct antioxidant properties ( 23 ) . Our primary hypothesis was that high intake of these antioxidants would reduce risk for ischemic stroke . We report here the associations between intakes of vitamin E , vitamin C , and specific carotenoids and risks for ischemic and hemorrhagic stroke in a large cohort of men in the United States . Methods Study Sample The Health Professionals Follow-up Study began in 1986 , when 51 529 health professionals 40 to 75 years of age [ 24 ] completed a 131-item food-frequency question naire and supplied information about medical history and lifestyle . Follow-up question naires were sent every 2 years so that we could up date information on potential risk factors , including use of vitamin supplements , and identify newly diagnosed cases of stroke and other diseases . We excluded from analysis 1595 men who did not have 1 ) a daily caloric intake between 800 and 4200 kcal and 2 ) fewer than 70 blanks ( among 131 listed food items ) on the food-frequency question naire . We also excluded men with previous myocardial infa rct ion , angina , coronary artery surgery , stroke , transient ischemic attack , peripheral arterial disease , or diabetes . We followed the 43 738 eligible men for incidence of stroke for 8 years . The average response rate for the 2-year follow-up cycles was more than 94 % . Nonresponding participants who were not matched to the National Death Index were assumed to be alive . This study was approved by the institutional review board of the Harvard School of Public Health . Assessment of Diet and Other Exposure Variables On the 1986 question naire , we asked about 1 ) the average frequency of intake over the previous year of specified portions of 131 foods and 2 ) the use of vitamin and mineral supplements . We specifically asked about dose and duration of use of multivitamin , vitamin E , and vitamin C supplements . Nutrient calculations took into account the specific br and s of breakfast cereal and multivitamin supplements reported by each participant . We assessed the question naire 's validity in a r and om sample of 127 men who completed two 1-week diet records ( 25 ) ; 121 of these men also provided blood sample s ( 26 , 27 ) . The correlations between the food-frequency assessment s of intake and plasma concentrations were 0.51 for -tocopherol , 0.47 for -carotene and lycopene , 0.35 for -carotene , and 0.40 for lutein . These correlations were similar to those seen between plasma levels of these nutrients and intake of these nutrients as estimated by the two 1-week diet records ( 25 ) , and they support the validity of the food-frequency question naire . Even if dietary measurements were perfect , vitamin intake and plasma levels would not be highly correlated because multiple factors contribute to between-person variations in plasma vitamin levels . The correlation between the food-frequency and diet-record assessment s was 0.92 for both vitamin C and vitamin E ( 25 ) . In 1986 , in addition to reporting on diet , participants were asked to report their usual systolic and diastolic blood pressures and whether they had physician-diagnosed hypertension . The validity of these variables has been documented ( 28 ) . Other potential risk factors for stroke that were assessed at baseline and in the follow-up question naire included smoking history , body mass index , history of hypercholesterolemia , physical activity , parental history of myocardial infa rct ion , and alcohol consumption . Events End points were fatal or nonfatal stroke occurring between the return of the baseline question naire and 31 January 1994 . If a participant reported an incident stroke on a follow-up question naire , we asked for permission to review that participant 's medical records . Strokes were confirmed if they were characterized by a typical neurologic defect of sudden or rapid onset that lasted at least 24 hours and was attributable to a cerebrovascular event . Strokes caused by infection or neoplasia were excluded . Review s were conducted by physicians who had no knowledge of participants ' risk factor status . Strokes were subclassified , according to the criteria of the National Survey of Stroke , as due to ischemia ( embolism or thrombosis ) , subarachnoid hemorrhage , intracerebral hemorrhage , or an unknown cause ( 29 ) . If no records could be obtained , a stroke was considered probable if it necessitated hospitalization and was corroborated by additional information provided in a letter or interview . Deaths were initially reported by next-of-kin , coworkers , postal authorities , or the National Death Index . Fatal strokes were confirmed by medical records ( 84 % ) or autopsy reports ( 2 % ) or were considered probable if medical records or autopsy reports could not be obtained and stroke was listed as the underlying cause of death on the death certificate ( 14 % ) . Statistical Analysis Participants contributed follow-up time from the return of the 1986 question naire to the occurrence of a confirmed stroke or death or 31 January 1994 . Men who had nonfatal myocardial infa rct ion or coronary surgery during the follow-up period were retained in the analysis . Intake of vitamin E and other nutrients was energy-adjusted to 2000 kcal/d ( 30 ) . Relative risks were calculated by dividing the incidence of stroke among men in each quintile of energy-adjusted vitamin E intake at baseline by the incidence of stroke among men in the lowest quintile of intake . Similar calculations were done for the other nutrients . Quintiles were used to avoid assumptions about the shape of the dose-response relation and to provide sufficient power to compare men in the extreme categories of intake . For vitamin E , vitamin C , and -carotene , additional analyses separately considered supplemental and dietary intake . We adjusted relative risks for age ( in 5-year categories ) ( 31 ) and used the Mantel extension test ( 32 ) to test for linear trends . To adjust for other risk factors , we used pooled logistic regression with 2-year intervals . Where the probability of an event within an interval is small , this method is equivalent to a Cox proportional-hazards analysis ( 33 ) . The multivariate models included the following as covariates : calendar time ( in 2-year intervals ) , total energy intake ( continuous variable ) , smoking ( current ; past ; or 1 to 14 , 15 to 24 , and 25 cigarettes/d ) , alcohol consumption ( < 5 , 5 to 9 , 10 to 14 , 15 to 29 , or 30 g/d ) , history of hypertension , history of hypercholesterolemia , parental history of myocardial infa rct ion before 65 years of age , profession , and quintiles of body mass index and physical activity . In these models , we evaluated monotonic trends by using the median value of each category and modeling it as a continuous variable . Analyses were also conducted to up date dietary intake and other covariates during follow-up . In these analyses , the incidence of stroke in 1986 - 1990 was related to vitamin and carotenoid intake reported in 1986 , whereas the incidence of stroke in 1990 - 1994 was related to the average intake reported in 1986 and 1990 . Because dietary changes made after the development of intermediate end points , such as coronary heart disease , peripheral arterial disease , transient ischemic attacks , diabetes , and hypercholesterolemia , may confound the associations between diet and disease ( 34 ) , we repeated the analyses without updating information on diet for men who reached an intermediate end point before completing the 1990 dietary question naire . All P values are two-sided . Role of the Funding Source The National Institutes of Health had no role in the collection , analysis , or interpretation of the data or in the decision to su bmi t the paper for publication . Results During 323 394 person-years of follow-up , we documented 328 strokes : 210 ischemic , 70 hemorrhagic , and 48 unclassified . Fifty of the 328 strokes were fatal . The distribution of risk factors for stroke differed somewhat by vitamin E , vitamin C , and -carotene intake ( Table 1 ) . Men in the top quintiles of vitamin E or vitamin C intakemost of whom used multivitamin or specific vitamin supplementswere less likely to smoke , were more likely to use aspirin , and were Objective : To assess the carotenoid status in young type I diabetic patients and its relationship to the glycaemic control of the disease . Design : A follow-up study . Setting : Hospital Universitario Puerta de Hierro , Health Area VI of Madrid (Spain).Subjects : Forty-seven type I diabetic patients , followed for 2.5 years . Interventions : Coinciding with physical examination and laboratory tests , serum levels of carotenoids were analysed by HPLC , and dietary intake of carotenoids was evaluated by a semiquantitative food frequency question naire and 3-day prospect i ve dietary records . Results : In type I diabetic patients , average intake , serum levels and correlations between diet and serum levels of carotenoids were comparable to those in reference non-diabetic groups . Between-subjects seasonal variations were observed for β-cryptoxanthin intake and serum levels ( higher in winter ) and serum lycopene ( higher in summer ) . Significant within-subjects seasonal changes were shown for dietary and serum β-cryptoxanthin and serum β-carotene . Serum carotenoids were unrelated to glycaemic control markers . Subjects with clinical ly acceptable glycaemic control showed lower lycopene intake than those with unacceptable control . Intake of carotenoids did not explain variance in insulin dose , fasting glycaemia , fructosamine or HbA1c . With the exception of lycopene , serum carotenoids were predicted by dietary intake , but in no case by fasting glycaemia , HbA1c or fructosamine . Conclusion : In type I diabetic patients , serum carotenoid concentrations and their variance are determined by dietary intake patterns , and are unrelated to the glycaemic control of the disease , as assessed by biochemical markers Smoking is associated with low serum carotenoid concentrations . Prospect i ve studies have found lower diabetes risk among persons with high-carotenoid diets . Whether diabetes risk is low in the rare smoker who has high serum carotenoid levels is unknown . The authors investigated the interaction of serum carotenoid concentrations and smoking with diabetes mellitus in 4,493 Black and White men and women aged 18 - 30 years in the Coronary Artery Risk Development in Young Adults ( CARDIA ) Study . The authors assessed 15-year ( 1985 - 2001 ) incident diabetes  ( 148 cases ) , insulin concentration , and insulin resistance  ( homeostasis model assessment ) in smokers and nonsmokers according to baseline levels of serum alpha-carotene , beta-carotene , zeaxanthin , beta-cryptoxanthin , and lycopene . Diabetes incidence was inversely associated with the sum of carotenoid concentrations in nonsmokers ( per st and ard deviation ( SD ) increase , relative hazard = 0.74 , 95 % confidence interval : 0.55 , 0.99 ) but not in current smokers ( relative hazard = 1.13 , 95 % confidence interval : 0.83 , 1.53 ) ( p for interaction = 0.02 ) . Similarly , year 15 insulin and insulin resistance values , adjusted for baseline levels , were inversely related to sum of carotenoids only in nonsmokers ( per SD increase in insulin level , slope = -0.46 ( p = 0.03 ) ; per SD increase in insulin resistance , slope = -0.14 ( p = 0.01 ) ) . In CARDIA , higher serum carotenoid concentrations are associated with lower risk of diabetes and insulin resistance in nonsmokers but not in smokers BACKGROUND the evidence of a potential beneficial role of antioxidants in preventing atherosclerotic disease is not entirely consistent . OBJECTIVE to assess the longitudinal association of serum total antioxidant capacity and serum antioxidants with the presence of sub clinical carotid atherosclerosis . METHODS Prospect i ve case-control study nested within an historical cohort . Cases were 150 individuals with elevated carotid intimal-medial thickness measured by B-mode ultrasound at the first two examinations of the Atherosclerosis Risk in Communities Study ( 1987 - 92 ) . Controls were 150 age-gender-matched individuals with low carotid intimal-medial thickness .  Serum antioxidant vitamins , uric acid , and serum total antioxidant capacity  were measured in frozen serum sample s collected from the same  individuals  in 1974 ( 13 - 15 years prior to the determination of case-control status ) . RESULTS Compared to controls , atherosclerosis cases had significantly higher levels of serum total antioxidant capacity in 1974 than controls . This difference was almost entirely explained by increased serum concentration of uric acid in cases . In contrast with cross-sectional results , uric acid serum concentration in 1974 , was significantly higher in cases than in controls , even after adjusting for the main cardiovascular risk factors . Cases had significantly lower levels of alpha-carotene in the 1974 sera than controls , but no other differences in serum antioxidant vitamin concentrations were observed . CONCLUSIONS The higher serum uric acid concentration seemed associated with elevated total serum antioxidant capacity among individuals with atherosclerosis . This finding is consistent with experimental evidence suggesting that hyperuricemia may be a compensatory mechanism to counteract oxidative damage related to atherosclerosis and aging in humans BACKGROUND AND PURPOSE A large number of studies have contributed to the hypothesis that carotenoids , vitamins A and E are protective against atherosclerosis by acting as antioxidants . The aim of this study was to assess the relationship between plasma levels of carotenoids ( alpha- and beta- carotene , lutein , lycopene , zeaxanthin , beta-cryptoxanthin ) ,  vitamins A and E  , and atherosclerosis in the carotid and femoral arteries . METHODS This prospect i ve and cross sectional study involved a r and omly selected population sample of 392 men and women aged 45 - 65 years .  Carotid and femoral artery atherosclerosis was assessed by high-resolution duplex ultrasound . RESULTS alpha- and beta- carotene plasma levels were inversely associated with the prevalence of atherosclerosis in the carotid and femoral arteries ( P=0.004 ) and with the 5-year incidence of atherosclerotic lesions in the carotid arteries ( P=0.04 ) . These findings were obtained after adjustment for other cardiovascular risk factors ( sex , age , LDL ( low density lipoproteins ) , ferritin , systolic blood pressure , smoking , categories of alcohol consumption , social status , C-reactive protein ) . Atherosclerosis risk gradually decreased with increasing plasma alpha- and beta-carotene concentrations ( P=0.004 ) . No associations were found between vitamin A and E plasma levels and atherosclerosis . CONCLUSIONS This study provides further epidemiological evidence of a protective role of high alpha- and beta- carotene in early atherogenesis AIM The purpose of this study was to determine the effects of lutein supplement on serum cytokines , apoE and lipoprotein profiles in early atherosclerosis population . METHODS Early atherosclerosis patients ( n= 65 ) were r and omized to receive placebo ( A+P , n= 31 ) or 20 mg/d lutein ( A+L , n= 34 ) for 3 months . RESULTS Serum lutein increased significantly compared to baseline after lutein supplements in A+L group ( p<0.001 ) . Lutein supplements result ed in a significant decrease in serum interleukin-6 ( IL-6 ) and monocyte chemoattractant protein-1 ( MCP-1 ) at 3 month in A+L group ( p<0.05 ) . Intragroup comparison revealed a significant difference in the changes of serum MCP-1 between A+L and A+P groups ( p= 0.021 ) . The serum low-density lipoprotein ( LDL ) and triglyceride ( TG ) significantly decreased in A+L group ( p<0.05 ) . The changes in serum lutein were negatively associated with those in serum LDL in A+L group ( r=-0.384 , p=0.043 ) , while no such relationship was observed in A+P group ( r= 0.087 , p= 0.685 ) . CONCLUSION An increase in serum lutein after supplementation can reduce inflammatory cytokines and regulate serum lipids , which may pay important roles in early atherosclerosis OBJECTIVE The aim of this study was to determine whether lutein affected biomarkers related to cardiovascular diseases ( CVD ) in healthy nonsmokers . METHODS A r and omized , double-blind , placebo-controlled trial of lutein supplementation was conducted in healthy nonsmokers . 117 eligible subjects were r and omly assigned to receive 10 or 20 mg/d of lutein or placebo for 12 weeks . Levels of plasma carotenoid concentrations , total antioxidant capacity ( TAOC ) , the lipoprotein profile , and antioxidant enzymes activities were determined at baseline and at 6 , and 12 weeks after the initiation of treatment . Biomarkers of oxidative damage to protein and lipids , and C-reactive protein ( CRP ) concentrations were measured at baseline and after supplementation . RESULTS Plasma lutein and TAOC significantly increased in both active treatment groups during 12 weeks . A significant reduction was found in malondialdehyde in the 20 mg lutein group . CRP concentration decreased in a dose-dependent manner for lutein supplementation , and there was a significant between-group difference in CRP between the 20 mg lutein and the placebo group . Serum CRP was directly related to the change in plasma lutein and TAOC for both active treatment groups . CONCLUSION The results support the possibility that lutein supplementation reduce biomarkers of CVD risk via decreased lipid peroxidation and inflammatory response by increasing plasma lutein concentrations and antioxidant capacity The role of plasma retinol and carotenoids in coronary heart disease ( CHD ) remains unclear . The PRIME Study prospect ively evaluated these in France and Northern Irel and in 9758 men aged 50 - 59 years who were free of CHD at baseline . After five years ' follow-up 150 incident cases of CHD ( non-fatal myocardial infa rct ion and fatal CHD ) were compared with 285 controls matched for age , date of blood collection and study centre .  Geometric means of major carotenoids did not differ significantly between cases and controls ( P>0.05 ) , whereas the absolute and lipid-st and ardized plasma retinol levels were 9 % lower in cases than controls in both countries ( P<0.002 ) , without correlation with carotenoids . After adjusting for risk factors , the relative risks ( RRs ) of CHD in the first four quintiles of retinol distribution in controls ( < or = 601 , -683 , -760 , and -846 microg/l ) were 2.65 ( P=0.0009 ) , 1.70 , 1.03 , and 1.12 ( all P>0.05 ) respectively , relative to the top quintile ( retinol > or = 846 microg/l ; linear trend P=0.0001 ) . The 10th percentile of lipid-st and ardized retinol ( < or = 544 microg/l ) predicted an RR of 4.7 ( P<0.001 ) . The risk associated with low retinol was comparable to strong risk factors ( e.g. HDL-cholesterol , Interleukin-6 ) and behaved additively . In conclusion , plasma retinol levels of < 601 microg/l in a fifth of middle-aged European men place them at an approximately threefold RR of developing CHD . Thus the intake of vitamin A might be too low in middle-aged men . These findings must be confirmed Objective : To study the relationship between the CD4 + cell response after initiation of protease inhibitors and the occurrence of opportunistic infections and survival . Design : Prospect i ve observational cohort study . Methods : HIV-1-seropositive subjects followed-up in HIV centres of Bordeaux University Hospital , Southwest France who were prescribed at least one available protease inhibitor between January and December 1996 were included in this analysis . A Cox model estimated the independent effect of baseline covariates and CD4 + cell response , considered as a time-dependent covariate , on the occurrence of new AIDS-defining opportunistic infection , new AIDS-defining events , new AIDS-defining opportunistic infection or death . Results : A total of 556 HIV-positive patients were prescribed at least one protease inhibitor : 34 % saquinavir , 52 % indinavir , and 14 % ritonavir .  Median CD4 + cell count at baseline was 95 × 106/l and mean plasma HIV RNA was 5.0 log10 copies/ml . After a median follow-up of 230 days , 65 patients experienced a new episode of opportunistic infection , 79 patients experienced at least one AIDS-defining event , and 24 had died . On average , the increase in CD4 + cell count was 42 × 106/l ( SD , 74 ) after a median of 49 days . In the multivariate analysis of opportunistic infection or death , each 50 % higher CD4 + cell count at baseline was associated with a 23 % reduction [ 95 % confidence interval ( CI ) , 14–30 ] of risk . Each 50 % increase in CD4 + cell count during follow-up was associated with a 9 % reduction ( 95 % CI , 2–15 ) of risk , adjusted for the presence of AIDS prior to protease inhibitor therapy ( hazard ratio , 3.76 versus absence of AIDS ; P < 0.01 ) and haemoglobin level ( hazard ratio , 0.48 if ≥ 11 g/dl versus < 11 g/dl ; P < 0.01 ) . Conclusion : Our results show , at least indirectly , how protease inhibitors might produce clinical stabilization . This result may be due to improved functionality of CD4 + cells in patients started on protease inhibitors
target: 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: 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 .