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© 2007 American Society for Nutrition J. Nutr. 137:959-963, April 2007

Nutrient Physiology, Metabolism, and Nutrient-Nutrient Interactions

Change in Plasma Lutein after Egg Consumption Is Positively Associated with Plasma Cholesterol and Lipoprotein Size but Negatively Correlated with Body Size in Postmenopausal Women1

David Waters2, Richard M. Clark2,*, Christine M. Greene2, John H. Contois3 and Maria Luz Fernandez2

2 Department of Nutritional Sciences, University of Connecticut, Storrs, CT 06269 and 3 Liposcience, Inc., Raleigh, NC 27616

* To whom correspondence should be addressed. E-mail: richard.m.clark{at}uconn.edu.


   ABSTRACT
TOP
 ABSTRACT
Introduction
 Materials and Methods
 Results
 Discussion
 LITERATURE CITED
 
We investigated associations between plasma concentrations of cholesterol and lutein after consumption of eggs. Using a crossover design, 22 postmenopausal women (50–77 y) consumed an egg treatment (640 mg/d additional cholesterol and 600 µg/d additional lutein + zeaxanthin) or a baseline treatment (no additional cholesterol or lutein + zeaxanthin) for 30 d, followed by a 3-wk washout period and the alternate diet. The increases in plasma total cholesterol and lutein due to egg consumption were related (r = 0.48, P < 0.05). There was a positive correlation between LDL size (r = 0.45, P < 0.05), HDL size (r = 0.64, P < 0.01), and plasma lutein, but no relation with the number of LDL or HDL particles. The activities of cholesterol ester transfer protein and lecithin cholesterol acyltransferase, although important in the exchange of cholesterol among lipoproteins, were not associated with changes in plasma lutein. Plasma lutein concentrations observed during the baseline period were a strong predictor of the increase in plasma lutein after egg treatment (r = 0.50 P < 0.05). There was a negative association between the change in lutein due to egg consumption and BMI (r = –0.40, P < 0.06) and waist circumference (r = –0.49, P < 0.05). This was particularly evident in individuals with BMI >29. We conclude that the increase in plasma lutein after egg consumption is associated with the change in plasma total cholesterol, but that the effect is diminished by obesity. Lipoprotein size, but not number, also affects plasma response to dietary lutein.


   Introduction
TOP
 ABSTRACT
 Introduction
Materials and Methods
 Results
 Discussion
 LITERATURE CITED
 
Studies have shown that consumption of lutein and zeaxanthin from foods or supplements increases the concentrations of these carotenoids in the blood and the macula of the eye (1–6). This is important for eye health, as the concentrations of lutein and zeaxanthin in the blood and macular pigment are inversely related to risk for age-related macular degeneration (AMD)4 (7,8). Additional clinical studies have shown that lutein supplementation increases macular pigment and may slow the progression of this disease (9). In nearly all cases, the increase in macular pigmentation is related to the serum concentration of lutein and zeaxanthin after carotenoid intervention (1–4). Therefore, understanding dietary and nondietary factors that affect the concentrations of lutein and zeaxanthin in the blood and macula have clinical relevance.

Several studies suggest that eggs are a highly bioavailable dietary source of lutein and zeaxanthin (10–15). As little as 1 egg/d for 5 wk increases serum lutein and zeaxanthin in individuals >60 y old (14), and the consumption of 6 eggs/wk for 12 wk increased macular pigment in women 24–59 y old (15). These studies suggest that a modest consumption of eggs may decrease the risk for AMD. However, not everyone responds to dietary lutein and zeaxanthin.

There is a great deal of individual variation in the plasma response to dietary carotenoids, with some individuals having little or no change in plasma concentration of carotenoids, whereas others display large changes (16). A similar variation in plasma response is observed with dietary cholesterol (17). This led to the concept of hyper- or hypo-responders to dietary cholesterol and carotenoids. In a previous study with healthy young men and women, the change in plasma lutein after egg consumption was associated with the change in plasma cholesterol (10). One of the objectives of this study was to evaluate whether this relation between cholesterol response and lutein could be confirmed in an older population of postmenopausal women. Another objective was to investigate lipoprotein characteristics that may be associated with plasma lutein concentrations after consumption of eggs. Specifically, we tested associations between plasma lutein and the number of LDL and HDL particles, their size, and their cholesterol content. We also investigated the possibility that the activities of cholesterol ester transfer protein (CETP) and lecithin cholesterol acyltransferase (LCAT) may affect the plasma lutein response, because these activities mediate the in vitro movement of lutein between lipoproteins from both trout and humans (18).


   Materials and Methods
TOP
 ABSTRACT
 Introduction
 Materials and Methods
Results
 Discussion
 LITERATURE CITED
 
    Materials. Liquid pasteurized whole eggs and cholesterol-free/fat-free eggs (placebo) were purchased from Better Brands Inc. Enzymatic cholesterol and triacylglycerol (TG) kits were obtained from Roche-Diagnostics. Ethyl-ß-apo-8'-carotenoate was obtained from Fluka.

    Subjects. The subjects were postmenopausal women who were participants in a larger study investigating the effect of egg consumption on lipoprotein characteristics (19,20). The men in the original study and women consuming vitamin supplements were not included in this study. The subjects did not have a history of heart disease, diabetes, or kidney disease and were not taking lipid-lowering medication. Anthropometric characteristics of the subjects are presented in Results. The experimental protocol was approved by the University of Connecticut's Institutional Review Board, and written informed consent was obtained from each subject.

    Diet and study design. The study used a randomized, crossover design, with subjects assigned to an egg (EGG) or placebo (Baseline) treatment for 30 d, followed by a 3-wk washout period, after which the second dietary period began. During the EGG treatment period, subjects consumed commercially packaged liquid whole eggs, which contributed ~640 mg of cholesterol and 600 µg of lutein + zeaxanthin to the diet per day. During the baseline treatment period, subjects consumed an egg substitute containing no cholesterol or lutein + zeaxanthin. Once a week, daily amounts of egg or egg substitute were provided in individual containers, and the subjects returned uneaten portions at the end of the week. Suggestions for ways to include eggs in the diet were provided, but the subjects were not required to follow a standard protocol for preparation and use of the eggs or egg substitute. Subjects were asked to maintain their regular diets throughout the experiment and to avoid any egg consumption other than that provided by the study. To ensure compliance, subjects completed seven 24-h dietary records during each treatment period, both of which included 2 weekend days. Dietary analysis was performed using Nutritional Data System for Research software, version 4.0, developed by the Nutrition Coordinated Center, University of Minnesota, Minneapolis, MN.

    Plasma lipid analysis. Plasma samples were collected in the morning (0600–0900) from women who had fasted 12 h. Plasma total cholesterol was determined by enzymatic methods, using Roche-Diagnostics standards and kits (21). HDL cholesterol (HDL-C) was measured in the supernatant, after precipitation of apo-B containing lipoproteins (22), and LDL cholesterol (LDL-C) was determined using the Friedwald equation (23). TG was measured using Roche-Diagnostic kits, which adjust for free glycerol (24).

    Plasma carotenoid analysis. Plasma samples were prepared for HPLC analysis as previously described (25). Briefly, 200 uL of serum was mixed with an equal volume of absolute ethanol, containing butylated hydroxytoluene and ethyl-ß-apo-8'-carotenoate (internal standard). The sample was extracted 3 times with hexane containing butylated hydroxytoluene. The hexane was removed with a stream of nitrogen, and the sample was reconstituted with 2-propanol and placed in HPLC injection vials. Carotenoids were analyzed using a Waters HPLC system. A Varian HPLC column (100 x 4.6 mm microsorb-MN 100–3 C-18), preceded by an Upchurch C-18 guard column (Upchurch Scientific), with an isocratic mobile phase consisting of 80% acetonitrile: 15% dioxane: 2.5% methanol: 2.5% 2-propanol: 0.01% triethylamine: 0.01% ammonium acetate, was used. Detection of the internal standard and lutein was at 450 nm. All solvents used were HPLC grade and were filtered and degassed before use. Standard curves were generated using HPLC purified lutein and ethyl-ß-apo-8'-carotenoate.

    LDL and HDL particle size and number. NMR spectroscopy was used to determine the concentrations and mean sizes of VLDL, LDL, and HDL particles, as previously described (26). Analysis was performed on a 400 MHz NMR analyzer (Bruker BioSpin). Lipoprotein subclasses of different sizes produce a distinct lipid methyl signal, whose amplitude is directly proportional to lipoprotein particle concentration. The weighted mean lipoprotein particle sizes were calculated, based on the diameter of each lipoprotein subclass multiplied by its respective concentration.

    Plasma LCAT and CETP activity determinations. Physiologic plasma LCAT activity was determined by measuring the decrease in the mass of endogenous free cholesterol after incubation for 6 h at 37°C. CETP activity is the calculated mass transfer of cholesteryl ester from HDL to apo-B lipoproteins after a 6 h incubation at 37°C (27).

    Statistical analysis. This study was a repeated measures, within-subject design, with the main effects being dietary treatment and a dichotomous classification of subjects, based on plasma response to egg cholesterol (hyper- or hypo-responder). All data were analyzed using PROC MIXED procedure of SAS (SAS Institute). The statistical model included responder classification and dietary treatment as a repeat factor. Statistical significance among individual treatment groups was determined by differences of least squares means with appropriate corrections for multiple comparisons. Pearson Product Moment Correlation was used to assess association between changes in serum lutein and other parameters. The results presented are means ± SD.


   Results
TOP
 ABSTRACT
 Introduction
 Materials and Methods
 Results
Discussion
 LITERATURE CITED
 
Subjects were classified as either hyper- or hypo-responders to egg cholesterol, based on values provided in a meta-analysis of several dietary cholesterol studies (28). Individuals with increases in total plasma cholesterol >0.06 mmol/L per 100 mg dietary cholesterol were classified as hyper-responders and individuals with increases <0.05 mmol/L per 100 mg dietary cholesterol were classified as hypo-responders to dietary cholesterol (28). Using these reference values, 13 women in the study were classified as hypo-responders, and 9 women were classified as hyper-responders to dietary cholesterol.

Hyper- and hypo-responders did not differ in age or anthropometric characteristics. The hyper-responders were 55.1 ± 7.0 y old (range 50–62 y) and had a mean BMI of 27.4 ± 6.0 (range 20.7–37.3) and a waist circumference of 85.5 ± 10.8 cm (range 70–104 cm). The hypo-responders were 59.1 ± 7.9 y old (range 50–77 y) and had a mean BMI of 28.7 ± 6.2 (range 18.5–41. 9) and a waist circumference of 90.4 ± 16.7 cm (61–104 cm).

Analysis of 7-d dietary records collected during each treatment period confirmed that all subjects consumed more cholesterol and lutein + zeaxanthin during the egg treatment period (Table 1). The cholesterol and lutein + zeaxanthin concentrations in the baseline diets consumed by the hyper- and hypo-responder groups did not differ. Throughout the study, individual energy intake was relatively constant and intakes did not differ among the treatment groups.


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  		TABLE 1 Dietary intake and plasma concentrations of lipids, lutein, and zeaxanthin in postmenopausal women classified as hyper- or hypo-responders to dietary egg cholesterol during egg and baseline treatment periods12

 
Plasma concentrations of total cholesterol, LDL-C, HDL-C, and TG did not differ between hyper- and hypo-responders at baseline (Table 1). The hyper-responders had significantly greater plasma total cholesterol, LDL-C, and HDL-C concentrations after the egg treatment. Plasma triglycerides did not change in the hyper-responders. In the hypo-responders, none of the plasma lipids were affected by egg consumption.

Both hyper- and hypo-responders had a significantly higher plasma lutein concentration after egg consumption (Table 1). Individuals classified as hyper-responder had an increase of 0.27 ± 0.23 µmol/L, whereas hypo-responders had an increase of 0.13 ± 0.07 µmol/L (P < 0.05). Therefore, the hyper-responders experienced twice the increase in plasma lutein. Plasma lutein during the baseline period was greater (P < 0.05) in the hyper-responders than in the hypo-responders and the plasma lutein concentration during the baseline period was a strong predictor of the increase due to the egg treatment (r = 0.50, P < 0.05). When the changes in plasma lutein within individuals were compared, 4 of the 9 hyper-responders had increases in plasma lutein >0.30 µmol/L, compared with only 1 of the hypo-responders.

Consistent with the observation that hyper-responders to egg cholesterol had greater increases in plasma lutein, the difference in plasma concentrations of lutein between periods and the difference in total plasma cholesterol concentrations between periods were correlated (r = 0.48, P < 0.05). There was a similar correlation (r = 0.43, P < 0.05) between the difference in plasma lutein and the difference in LDL-C, due to egg consumption. Differences between the periods in plasma HDL-C and lutein were not correlated.

The baseline plasma zeaxanthin concentration was significantly greater in hyper-responders than in hypo-responders. After the egg treatment, plasma zeaxanthin was significantly greater in the hyper-responders and was not affected in the hypo-responders (Table 1). When all the subjects were combined for statistical analysis, there was a strong association between the change in plasma total cholesterol and the change in plasma zeaxanthin, due to egg consumption (r = 0.717, P < 0.01).

Both BMI and waist circumference were negatively associated with the baseline plasma lutein concentrations and its change due to egg consumption. The plasma lutein concentration was negatively correlated with BMI (r = –0.44; P < 0.05) and, as BMI increased, increases in plasma lutein due to the egg treatment tended to decrease (r = 0.40, P < 0.06) (Fig. 1A). This was particularly evident in individuals with a BMI >29. Waist circumference was negatively correlated with the baseline plasma lutein concentration (r = 0.45, P < 0.05) and negatively associated with the change in plasma lutein after the egg treatment (r = 0.49, P < 0.05) (Fig. 1B).


Figure 1
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  		Figure 1  Negative correlations in postmenopausal women between the differences in plasma lutein after 30 d of consuming eggs, contributing 600 µg/d lutein + zeaxanthin, compared to the baseline diet with no added lutein, and BMI (A) and waist circumference (B).

 
The NMR analysis of lipoproteins provided information on the number and size of the LDL and HDL particles. The LDL particle concentration for all subjects was 1200 ± 467 nmol/L, with a mean size of 21.5 ± 1.0 nm. The concentration of HDL particles for all subjects was 35.9 ± 7.4 mmol/L, with a mean size of 9.4 ± 0.4 nm. The number and size of lipoprotein particles did not differ between treatment periods or between hyper- and hypo-responder groups. However, the plasma lutein concentration during the egg period was correlated with LDL (r = 0.45, P < 0.05) (Fig. 2A) and HDL particle size (r = 0.64, P < 0.01) (Fig. 2B). The numbers of LDL and HDL particles were not correlated with plasma lutein.


Figure 2
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  		Figure 2  Positive correlations in postmenopausal women between plasma lutein concentrations after 30 d of consuming eggs, contributing 600 µg/d lutein + zeaxanthin, and LDL (A) and HDL (B) particle size.

 
CETP and LCAT, which are important in the movement of cholesterol among lipoproteins, did not differ between treatment periods and were not associated with the baseline plasma lutein concentration or its change due to egg consumption (data not shown).


   Discussion
TOP
 ABSTRACT
 Introduction
 Materials and Methods
 Results
 Discussion
LITERATURE CITED
 
Fifty years ago Krinsky et al. (29) found that xanthopylls (lutein and zeaxanthin) were primarily transported with LDL and HDL. Subsequent studies have confirmed these observations and, although different methods have been used to isolate lipoprotein fractions, most studies find the xanthophylls evenly distributed between LDL and HDL, with small amounts associated with VLDL (30–34). As the lutein and zeaxanthin are primarily transported in the cholesterol rich lipoproteins, it is not surprising that several studies have found a positive correlation between plasma total cholesterol and lutein (35–38). Plasma HDL-C and non-HDL cholesterol also have been found to be associated with plasma lutein (14,15,36–39). Consistent with previous observations, concentrations of plasma total cholesterol and LDL-C in postmenopausal women were significantly associated with plasma lutein. However, we did not find the expected correlation between plasma HDL-C and lutein, which is probably due to the narrow range of HDL-C concentrations in these subjects.

To our knowledge, this is the first study to investigate the relation between both the number and size of LDL and HDL particles and plasma lutein concentrations. We found that the sizes, but not the numbers, of LDL and HDL particles were positively correlated with circulating lutein (Fig. 2). Larger LDL and HDL particles carried more lutein. Lutein and zeaxanthin are thought to associate with the surface layer of the lipoprotein (34), and the larger particles provide more surface for incorporation of xanthophylls. However, our observations are not consistent with a previous study that reported that more lutein and zeaxanthin associated with small HDL3 particles than with the larger HDL2 particles (32). Additional work is needed to clarify the relation between lipoprotein size and carotenoid transport in the blood.

Baseline concentrations of lutein were a strong predictor of the plasma lutein response to dietary lutein in eggs. Individuals with higher baseline levels of lutein had significantly greater increases in plasma lutein. Plasma concentrations of carotenoids are determined by rates of absorption, removal from plasma to tissues, and efflux from tissues. The mechanisms controlling these processes are poorly understood. Recent reports that membrane transporters such as SR-BI (scavenger receptor class B type I) and CD 36 (cluster determinant 36) affect absorption of carotenoids (40–42), and that ABCG5 polymorphisms may play a role in individual plasma responses to lutein from eggs (43), suggest that some of the factors controlling plasma levels of lutein are under genetic control. It is likely that the physiological factors that cause increased levels of lutein during the baseline diet period would also favor a greater response to lutein from egg.

Several cross-sectional studies have reported an inverse relation between BMI and plasma carotenoids (2,35,36,39). The relation is most evident in subjects with a BMI >27 (2,44). We also found a negative association between baseline levels of plasma lutein and BMI. A few studies have reported a negative association between BMI and the change in plasma carotenoid concentrations after carotenoid supplementation (45) or dietary interventions (46). Yeum et al. (46) found an inverse correlation of plasma carotenoids with fat mass in older women, but not in younger women or men. We also found an inverse relation with postmenopausal women, but, in an identical study with younger women, we did not find a correlation between BMI and the plasma lutein response to egg consumption (10). This may be because the range of BMI was smaller in the younger subjects or there may be inherent differences in carotenoid metabolism in postmenopausal women.

The activities of CETP and LCAT affect the distribution of the major lipid classes (TG, cholesterol, and phospholipids) in lipoproteins and have been reported to mediate movement of lutein between lipoproteins. Tyssandier et al. (18) found bidirectional exchange of carotenoids between VLDL and HDL from trout and bidirectional transfer of lutein between VLDL and HDL from human plasma. The transfer was sensitive to CETP and/or LCAT inhibitors. However, in earlier reports, Cornwell et al. (30) argued against such an exchange and Romanchik et al. (34) found no evidence for net exchange of carotenoids between lipoproteins of humans.

We did not find correlations between LCAT and CETP activities and plasma lutein. Romanchik et al. (34) suggested that the small amount of carotenoids, relative to cholesterol and cholesterol esters in the lipoproteins, make carotenoids a poor substrate for CETP and LCAT activities. They estimated that there were only 4 carotenoids/VLDL molecule, 1 carotenoid/LDL molecule, and 25 carotenoids/1000 HDL molecules. Our data support these estimates. Assuming the distribution of lutein to be 10% VLDL, 46% LDL, and 44% HDL (31), and using the plasma lutein concentration and particle number data from our study, we calculated the numbers of lutein molecules per lipoprotein to be ~2 lutein molecules/VLDL particle, 3 lutein molecules/10 LDL particles, and 7 lutein molecules/1000 HDL particles. The small number of carotenoid molecules per lipoprotein particle would make carotenoid exchange very difficult to measure. Although LCAT and CETP might mediate transfer of carotenoids between lipoproteins, the physiological relevance of these enzymes remains unresolved.

In conclusion, we confirm our earlier report (10) that plasma responses to dietary cholesterol and lutein from eggs are related. Individuals who are hyper-responders to dietary cholesterol have greater increases in plasma lutein and zeaxanthin due to eggs. We found also that BMI was negatively associated with baseline levels of lutein and with the change in plasma lutein due to the consumption of eggs. From an application standpoint, this may mean that individuals who want to reduce their risk for AMD will have to lose weight before they respond to lutein interventions. Finally, it appears that the size of the LDL and HDL particles, not their number, affects plasma lutein.

Additional studies on the effect of lipoprotein composition and size on carotenoid transport may provide insights into the turnover and metabolism of carotenoids by the body.


   FOOTNOTES
 
1 Supported by The American Egg Board, USDA National Research Initiative Grant 02-35200-12312. Back

4 Abbreviations used: AMD, age-related macular degeneration; CETP, cholesterol ester transfer protein; HDL-C, high density lipoprotein cholesterol; LCAT, lecithin cholesterol acyltransferase; LDL-C, LDL cholesterol; TG, triacylglycerol. Back

Manuscript received 21 November 2006. Initial review completed 28 December 2006. Revision accepted 1 February 2007.


   LITERATURE CITED
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 Introduction
 Materials and Methods
 Results
 Discussion
 LITERATURE CITED
 

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