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Department of Ophthalmology and Visual Sciences and
* Department of Biostatistics and Medical Informatics, University of Wisconsin at Madison, Madison, WI;
National Cancer Institute, Bethesda, MD;
** Department of Nutritional Sciences, University of Wisconsin at Madison, Madison, WI; and Departments of
Ophthalmology and
Preventive Medicine, University of Tennessee Health Science Center-Memphis, Memphis, TN
2To whom correspondence should be addressed. E-mail: mgruber{at}facstaff.wisc.edu.
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ABSTRACT |
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 TOP ABSTRACT SUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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40 y old, were examined. In a fully adjusted, multiple linear regression model, lower serum lutein + zeaxanthin was significantly associated with smoking, heavy drinking, being white, female, or not being physically active, having lower dietary lutein + zeaxanthin, higher fat-free mass, a higher percentage of fat mass, a higher waist-hip ratio, lower serum cholesterol, a higher white blood cell count, and high levels of C-reactive protein (P < 0.05). The model explained 24% of the variation present in serum lutein + zeaxanthin for the current sample. The correlation between dietary and serum lutein + zeaxanthin was 0.17 and increased to 0.18 after adjusting for the effects of given covariates. Each 10% increase in dietary lutein + zeaxanthin was associated with a 1% increase in serum conditional on other terms in the model. Many factors that influence the level of serum lutein + zeaxanthin remain unknown.
KEY WORDS: • body mass • carotenoids • diet • lutein • smoking • zeaxanthin
Lutein and its structural isomer, zeaxanthin, are 2 carotenoids that are concentrated in tissues of the eye. Some epidemiologic studies suggested that people with lower dietary levels of these carotenoids are at higher risk for common eye diseases associated with aging [age-related maculopathy and cataracts] and for cardiovascular disease, but results are inconsistent across studies [reviewed in (1)].
Supplements containing these carotenoids have also recently become popular, despite the early stage of understanding their relation with chronic disease. Examining the associations between intake of lutein + zeaxanthin and the occurrence of chronic diseases across different populations can provide evidence about their potential protective influence. Serum levels of these carotenoids may provide a biomarker of intake that is independent of reporting errors of individuals or inaccuracies of food databases. However, studies conducted to date indicate that levels of carotenoid in the diet explain very little of the variability in serum levels (2–4). This may be due in part to the variable response of serum carotenoids to given oral doses noted among individuals (5,6). This may also be due to the fact that levels in the serum might also reflect other physiologic or biochemical factors or aspects of lifestyle that could bias associations of carotenoids to diseases or introduce extraneous variability. To understand the associations of carotenoids with diseases, it is important to know which of these potential correlates of serum carotenoids should be measured and adjusted for. Although several previous studies reported dietary and lifestyle correlates of lutein and zeaxanthin, the current investigation was conducted in a sample that represents the American population and has available a broader range of lifestyle, anthropometric, and biochemical measurements that may relate to serum carotenoids. Some potential determinants, such as inflammatory markers, body lean mass, and body fat distribution were not well investigated previously. Thus, the aim of this investigation was to describe a broad range of potential health and lifestyle correlates and determinants of serum lutein + zeaxanthin in a large and representative sample of the U.S. population.
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SUBJECTS AND METHODS |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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40 y old were included in NHANES III. Of these, 11,448 were interviewed and 9737 were examined. After excluding subjects with missing values for tested covariates, a sample population of 7059 persons was selected for analysis. Data collection. Dietary intake of nutrients was determined from responses to a 60-item, FFQ administered during the household interview (7). This questionnaire, which was designed to capture nutrients in fruits and vegetables, was selected to estimate carotenoid intake instead of the 24-h diet recalls that are also available for this sample; this was done to obtain a better estimate of the intake in light of the wide day-to-day variability that exists in carotenoid intake. Nutrient composition databases utilized in creating estimates of intake were developed by using the foods reported in the 24-h recall interviews as described previously (8). Information was recorded according to a coding system from the University of Minnesota Nutrition Coordinating Center (9,10). Carotenoid levels were assigned on the bases of the USDA National Cancer Institute Carotenoid Food Composition Database (11) and a composite carotenoid database (12).
Serum specimens were collected during the mobile examination and stored at –70°C. Serum cholesterol, fibrinogen, and carotenoids were analyzed using reverse-phase HPLC with multiwavelength detection (13,14). Detailed information about the procedures and protocol used for these measurements is provided in the NHANES III documentation (7,15) and in the laboratory procedures used for NHANES III (13,16).
Collection of other covariate data, such as smoking, alcohol consumption, and supplement use were determined from questions asked at the household interview and MEC examination. For these analyses, smoking is categorized as currently smoke (yes/no), never have smoked (yes/no), or smoked at some point in the past (yes/no). Alcohol consumption was categorized as currently having 0 drinks/d (237 mL glass of wine, 355 mL glass of beer, or shot of liquor), having >0 but <2 drinks/d, or 2 drinks/d. Detailed descriptions of questions asked and summary variables created to determine cardiovascular disease, diabetes, hypertension, and supplement use are published elsewhere (7,16). Information concerning health and physical activity status were ascertained during MEC interviews. Information regarding fat-free mass and the percentage of fat mass was derived from equations published elsewhere (17).
Statistical analyses and methods. Correlates of serum and dietary lutein + zeaxanthin were first examined. ANOVA was used to compare quintile means for continuous variables, and Cochran-Mantel-Haenszel tests for general association were used for categorical variables. The mean levels of serum and dietary lutein + zeaxanthin were examined by categorical predictor. Large sample tests, utilizing Z-scores, were used for comparisons of continuous variables and the Cochran-Mantel-Haenszel Test for "General Association" across groups at the 5% significance level was used for comparisons of categorical variables.
A multiple linear regression model was used to test the associations between serum lutein + zeaxanthin and possible dietary and lifestyle determinants. A natural log transformation was made on the response, serum lutein + zeaxanthin, because of the need for normality of the residuals in a linear regression model (18). Preliminary models indicated that 4 subjects had residual values greater than ±3. These subjects were considered outliers (18,19) and were not included in the final analysis. The exclusion of these subjects did not affect the reported results.
Additional transformations were made on the independent variables in the model as well. The dependent variable, serum lutein + zeaxanthin, has a range of values on a small scale (
0.2–0.8 µmol/L), whereas many independent variables have values on a larger scale. Transformations to certain independent variables were done to present coefficients on a large enough scale as they compare to serum lutein + zeaxanthin. For example, each unit increase in age now represents age decades. Dietary lutein + zeaxanthin was analyzed on the logarithmic scale. The coefficients are representative of a model with the response given as ln(serum lutein + zeaxanthin). A variable was considered significant if P 
0.05.
Finally, we evaluated correlates of potential nonresponse to diet lutein + zeaxanthin as defined by subjects who fell into the upper and lower quartiles of diet lutein + zeaxanthin. These subjects were compared with a group of subjects who fell in the upper quartiles of diet lutein + zeaxanthin and serum lutein + zeaxanthin. Large sample tests and Cochran-Mantel-Haenszel tests were used to test predictors of poor serum response to high diet lutein + zeaxanthin levels.
Because of the complex survey design used in NHANES III, traditional methods of analysis, which assume simple random sampling, do not apply. Sample weights are used to make the sample "nationally representative," and variance correction estimation methods must be used to comply with the complex design of the study (20). Software used for the analyses were SAS v8 (SAS Institute) and Sudaan v7.11 (Research Triangle Institute). Values in the text are means ± SD.
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RESULTS |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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12% lower serum levels compared with nondrinkers and moderate drinkers. Women had a 5% higher serum lutein + zeaxanthin concentration than men.
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Factors that were independently associated with lower serum lutein + zeaxanthin (Table 3) included being White, being older or male, having a higher fat-free mass, percentage of fat mass, waist-hip ratio, levels of serum CRP, white blood cell count, lower serum cholesterol, heavy drinking (2 drinks/d), smoking, and not being physically active (all P < 0.05). After further adjustment for all variables in the model, all variables remained significantly associated with serum lutein + zeaxanthin with these exceptions: lower serum levels were associated with being female (rather than male in the model adjusted only for diet); heavy drinking was no longer associated with serum lutein + zeaxanthin. After adjusting for these factors, each 10% increase in dietary lutein + zeaxanthin increased serum by 1%. The correlation between dietary and serum lutein + zeaxanthin was 0.17 (P 0.01) and increased to 0.18 (P 0.01) after removing the effects of the factors included in this model. Overall, the model explained 24% of the variation present in serum lutein + zeaxanthin.
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Next, we evaluated possible predictors of nonresponse of serum lutein + zeaxanthin to high dietary intake of these carotenoids (Tables 4, and 5). This was done by comparing means (for continuous variables) and percentages (for categorical variables) of potential lifestyle, demographic, and physiologic variables in subjects who had serum levels in the low vs. high quartiles among those with dietary lutein + zeaxanthin in the highest quartile. Nonresponse of serum lutein + zeaxanthin to high levels in the diet was associated with being White, smoking, having a history of cardiovascular disease, higher fat-free mass, and lower serum cholesterol values.
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40 y old) was used due to nonparticipation or missing values for variables integral to the analyses. To evaluate this bias, we compared characteristics of subjects who were included and those who were excluded from these analyses. Participants who were included were slightly older than those who were excluded (57 ± 14 vs. 56 ± 15 y, P = 0.04). Those included tended to be less likely to currently smoke (19 vs. 21%, P = 0.09), more likely to be moderate drinkers (44 vs. 35%, P < 0.01), more likely to be physically active (59 vs. 52%, P < 0.01) and less likely to have a history of cardiovascular disease (13 vs. 17%, P < 0.01). Participants who were included also had lower white blood cell count (7.1 ± 2.3 x 10–9/L vs. 7.3 ± 2.8 x 10–9/L, P < 0.01), lower intake of dietary lutein + zeaxanthin (2217 ± 2957 vs. 2362 ± 3120 µg/d, P < 0.01), and slightly lower levels of serum lutein + zeaxanthin (0.41 ± 0.24 vs. 0.43 ± 0.32 µmol/L, P < 0.01). |
DISCUSSION |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Some determinants of serum lutein + zeaxanthin may reflect differences in dietary intake of carotenoids. One such determinant is ethnicity, which had a large effect on dietary lutein + zeaxanthin estimates. Mean intakes in non-Hispanic Blacks were >2 times higher than in non-Hispanic Whites and 3 times higher than in Mexican-Americans (data not shown). After adjusting for diet lutein + zeaxanthin, differences in serum lutein + zeaxanthin between non-Hispanic Blacks and Mexican-Americans did not remain. However, serum levels in non-Hispanic Whites remained lower. In other studies, higher levels of serum lutein + zeaxanthin in non-Hispanic Blacks were observed (2,23). Mexican-Americans had lower levels of lutein + zeaxanthin in the diet despite higher levels of these carotenoids in the serum than non-Hispanic Whites. The diet questionnaire used in NHANES may have been limited in its ability to capture complete sources of dietary carotenoids. It is possible that ethnic differences in food preparation, or in combinations of foods eaten together, could enhance or inhibit the absorption of lutein + zeaxanthin, and thereby limit our ability to estimate true intake from a FFQ. Genetic factors, including the gastrointestinal absorption mechanisms of lutein + zeaxanthin, may also influence absorption and/or the turnover of lutein + zeaxanthin in the serum, and may also account for some of the differences we observed. It seems likely that there are several dietary, genetic, and environmental factors unique to each ethnic group that affect serum lutein + zeaxanthin levels. Further studies that can better account for these differences are warranted.
After controlling for dietary lutein + zeaxanthin, both higher lean mass and the percentage of fat mass were associated with lower levels in serum. The association with lean mass is the first to be reported to our knowledge and possibly reflects the dilution of serum levels by distribution over a larger tissue pool. The inverse association with fat mass was reported previously (27–29) and may reflect a propensity to accumulate lutein preferentially in adipose tissue over serum. Interestingly, an inverse association between levels in adipose tissue and serum was observed in quail for lutein but not zeaxanthin (30). This suggests the possibility that the relation between levels in the serum and adipose differs between these 2 different isomers.
Higher waist-hip ratios were associated with lower serum lutein + zeaxanthin (Table 5). This is the first observation of an association between serum lutein + zeaxanthin and body fat distribution. Preliminary data from another study (28) showed that lutein concentrations differed among body fat sites (abdomen, buttocks, and thigh). Abdominal adipose tissue may concentrate lutein more highly than adipose tissue in other regions of the body.
Smokers were more likely to have low levels of lutein + zeaxanthin in their diets, as reported by others (2,22). Serum lutein + zeaxanthin remained lower in smokers after adjusting for dietary lutein + zeaxanthin. Similar results were shown by Rock et al. (2). It is possible that smoking increases the turnover of lutein because of the oxidant load it imposes.
Having high levels of C-reactive protein, a marker of inflammation, was associated with lower levels of lutein + zeaxanthin in serum. A similar observation was made previously in a sample of younger (25–55 y old) NHANES III participants who were nonsmokers (31). Higher white blood cell count was also associated with lower serum lutein + zeaxanthin as well, which remains consistent with other studies (31). However, plasma fibrinogen was not associated with lutein + zeaxanthin in the crude or fully adjusted model. Because of the oxidative burst associated with the inflammatory response (32), it is possible that lower levels of lutein + zeaxanthin and other serum antioxidants reflect the higher level of oxidative stress that is associated with chronic inflammation. However, it is also possible that the lower serum lutein in persons with high levels of C-reactive protein reflects a relation of both to some unknown factor.
Serum cholesterol was directly associated with levels of lutein + zeaxanthin in serum as observed by others previously (2,22,23). Lutein + zeaxanthin are distributed equally on LDL and HDL (33). Thus, factors that influence serum levels of lipoproteins may also influence levels of these carotenoids.
People who reported being physically active had higher intakes and serum levels of lutein + zeaxanthin in the fully adjusted model even after adjusting for diet lutein + zeaxanthin and other determinants. A mechanism whereby physical activity could directly influence lutein+ zeaxanthin distribution in the serum has not been described. This association may reflect other, unknown factors that directly influence serum lutein + zeaxanthin.
Previous experimental studies demonstrated that the serum response to an oral dose of carotenoids is quite variable among individuals and that some individuals appear not to experience an increase in serum carotenoids with increasing oral doses. We attempted to provide clues to possible predictors of nonresponse by describing persons within the sample who had low levels (i.e., lowest quartile) of lutein + zeaxanthin in the serum, despite having high levels in the diet (i.e., highest quartile). Potential nonrespondents characterized in this way were more likely to be non-Hispanic Whites, smokers, and have low levels of serum cholesterol. Future investigations comparing absorption of lutein + zeaxanthin may further advance our understanding of potential factors that influence absorption of these carotenoids.
The low coefficient of determination (0.24) in our model indicates that much of the variability is due to variables not yet known. In a similar study (2) a coefficient of determination of 0.24 was found. This is despite the larger number of additional determinants (inflammatory markers, comorbid conditions, and supplement use) that were considered in this fully adjusted model compared with other studies (2). This may reflect the greater diversity in this representative sample of the U.S. population. The high level of unexplained variability may also be due in part to the single serum sample available, which reflects only 1 time point. As previously mentioned, serum values tend to reflect diet over the past few weeks, whereas the FFQ and diet records taken in NHANES III reflect diet over the past few months. Moreover, there appear to be diurnal (34) and hormonal (27) variations in serum carotenoids that were not accounted for in this study. Other studies (35,36) showed that exposure to UV light significantly reduced the amount of serum carotenoids and vitamins in vivo. Variation in serum lutein + zeaxanthin, related to intake, may be caused by the competition of serum, tissues, and the retina for these carotenoids or other unknown endogenous or external factors that influence their absorption or distribution. Because of the low coefficient of determination in this and other studies, the levels of carotenoids in the diet and serum appear to provide a large degree of independent information regarding carotenoid exposure.
The uncertainty in using serum lutein + zeaxanthin as a surrogate measure of the retinal lutein + zeaxanthin bioavailability and content may explain in part the inconsistency of epidemiologic observations with chronic diseases. For example, relations between lutein + zeaxanthin in serum and the occurrence of age-related macular degeneration are inconsistent in epidemiologic studies, despite a strong biologic rationale that supports a protective influence of these carotenoids on this age-related condition (30,37–39). The lack of adjusting for determinants and correlates of serum lutein + zeaxanthin in published epidemiologic studies may explain some of the inconsistency.
In summary, we observed that serum lutein and zeaxanthin in middle-aged and older Americans reflected dietary intake, but to a minor extent. Other factors that independently influenced levels in the serum included sex, ethnicity, smoking, alcohol intake, physical activity, lean and fat body mass, waist-hip ratio, level of serum CRP, and white blood cell count. Measuring and adjusting for these factors will improve the ability to consider levels of lutein + zeaxanthin in the serum as a marker of intake in epidemiologic studies of the middle-aged and elderly, but the considerable amount of unexplained variability limits the ability to predict exposure using a single serum measurement. There is a need to better understand other potential determinants of serum lutein + zeaxanthin to further investigate the associations of these carotenoids with chronic disease in epidemiologic studies.
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FOOTNOTES |
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Manuscript received 20 January 2004. Initial review completed 17 March 2004. Revision accepted 9 June 2004.
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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J. A Mares, T. L LaRowe, D M. Snodderly, S. M Moeller, M. J Gruber, M. L Klein, B. R Wooten, E. J Johnson, R. J Chappell, and for the CAREDS Macular Pigment Study Group and Inv Predictors of optical density of lutein and zeaxanthin in retinas of older women in the Carotenoids in Age-Related Eye Disease Study, an ancillary study of the Women's Health Initiative. Am. J. Clinical Nutrition, November 1, 2006; 84(5): 1107 - 1122. [Abstract] [Full Text] [PDF]
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J. D. Burke, J. Curran-Celentano, and A. J. Wenzel Diet and Serum Carotenoid Concentrations Affect Macular Pigment Optical Density in Adults 45 Years and Older J. Nutr., May 1, 2005; 135(5): 1208 - 1214. [Abstract] [Full Text] [PDF]
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