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 .
Relation of Consumption of Vitamin E, Vitamin C, and Carotenoids to Risk for Stroke among Men in the United States
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
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 .